Document 2jDZ3jQdDgy6rOe7QRDM4bxbp

1 STATE OF WEST VIRGINIA 2 IN THE CIRCUIT COURT FOR THE COUNTY OF HARRISON 3 4 LENORA PERRINE, CAROLYN HOLBERT, 5 WAUNONA MESSINGER CROUSER, 6 REBECCAH MORLOCK, ANTHONY BEEZEL, 7 MARY MONTGOMERY, MARY LUZADER, 8 TRUMAN R. DESIST, LARRY BEEZEL, 9 and JOSEPH BRADSHAW, Individuals 10 Residing in West Virginia, On 11 Behalf Of Themselves And All 12 Others Similarly Situated, 13 Plaintiffs, 14 vs. Case No. 04-C-296-2 15 E.I. DU PONT NEMOURS AND COMPANY, 16 a Delaware Corporation Doing 17 Business In West Virginia, 18 MEADOWBROOK CORPORATION, a 19 Dissolved West Virginia 20 Corporation, MATTHIESSEN & HEGELER 21 ZINC COMPANY, INC., a Dissolved 22 Illinois Corporation Formerly 23 Doing Business In West Virginia, 24 NUZUM TRUCKING COMPANY, a West 25 Virginia Corporation, T.L. 89 1 DIAMOND & COMPANY, INC., a 2 New York Corporation Doing 3 Business in West Virginia, 4 and JOE PAUSHEL, an Individual 5 Residing in West Virginia, 6 Defendants. 7 ___________________________ 8 9 10 The Telephonic Videotaped Deposition of 11 DAVID GARABRANT, M.D., VOLUME II, 12 Taken at 2900 South State Street, 13 Ann Arbor, Michigan, 14 Commencing at 9:04 a.m., 15 Friday, June 8, 2007, 16 Before Leisa M. Pastor, CSR-3500, RPR, CRR. 17 18 19 20 21 22 23 24 25 90 1 APPEARANCES: 2 3 AMANDA SLEVINSKI (via telephone) 4 Levin, Papantonio, Thomas, Mitchell, Echsner & Proctor, P.A. 5 316 South Baylen Street, Suite 600 6 Pensacola, Florida 32502 7 (850) 435-7000 8 Appearing on behalf of Plaintiffs. 9 10 CLAYTON PATTERSON (via telephone) 11 Law Office of Gary W. Rich, L.C. 12 Brock, Reed & Wade Building 13 212 High Street, Suite 223 14 Morgantown, WV 26505 15 (304) 292-1215 16 Appearing on behalf of Plaintiffs. 17 18 TIMOTHY S. DANNINGER 19 Squire, Sanders & Dempsey, L.L.P. 20 Two Renaissance Square, Suite 2700 21 40 North Central Avenue 22 Phoenix, Arizona 85004-4498 23 (602) 528-4000 24 Appearing on behalf of Defendant DuPont. 25 91 1 WILLIAM SCOTT WICKLINE 2 Allen, Guthrie, McHugh & Thomas, P.L.L.C. 3 500 Lee Street East, Suite 800 4 Charleston, West Virginia 25301 5 (304) 720-4234 6 Appearing on behalf of Defendant DuPont. 7 8 ALSO PRESENT: 9 John Asher - Video Technician 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 92 1 Ann Arbor, Michigan 2 Friday, June 8, 2007 3 9:04 a.m. 4 5 VIDEO TECHNICIAN: We are now on the 6 record. This is the videotaped deposition of David 7 Garabrant being taken on Friday, June the 8th, 2007. 8 The time is now 9:04 and 28 seconds a.m. We are 9 located at 2900 State Street, Ann Arbor, Michigan. We 10 are here in the matter of Lenora Perrine, et al., 11 versus E.I. DuPont Nemours And Company, et al. This is 12 case No. 04-C-2962. This matter is being held in the 13 Circuit Court of Harrison County, West Virginia. My 14 name is John Asher, video technician. Will the court 15 reporter swear in the witness and the attorneys 16 briefly identify themselves for the record, please. 17 DAVID GARABRANT, M.D., 18 was thereupon called as a witness herein, and after 19 having first been duly sworn to testify to the truth, 20 the whole truth and nothing but the truth, was 21 examined and testified as follows: 22 MS. SLEVINSKI: Amanda Slevinski for the 23 plaintiffs. 24 MR. PATTERSON: Clayton Patterson on behalf 25 of Law Office of Gary Rich for the plaintiffs. 93 1 MR. DANNINGER: Tim Danninger, Squire, 2 Sanders and Dempsey for DuPont. 3 MR. WICKLINE: Scott Wickline, Allen, 4 Guthrie, McHugh & Thomas also on behalf of DuPont. 5 MS. SLEVINSKI: Y'all set? 6 MR. DANNINGER: We are here. 7 THE WITNESS: Yes. 8 EXAMINATION 9 BY MS. SLEVINSKI: 10 Q. All right, good morning, Dr. Garabrant. Yesterday 11 afternoon, we left off, we'd been discussing some of 12 the research you had been involved with. Today I'd 13 like to focus on your report that you submitted in 14 this particular case. Your report, well, actually, do 15 you have it handy? It was Exhibit No. 151? 16 A. Yes. 17 Q. Okay, and do you have the completed version that had 18 the complete page 4 that you can refer to? 19 A. Yes. 20 Q. Okay, now your report is divided into general main 21 sections; am I correct? That one is opinions 22 regarding Dr. Werntz's proposed cancer screening 23 program, there's another main section that is opinions 24 regarding Dr. Werntz's proposed screening for 25 noncancer effects; is that correct? 94 1 A. Yes. 2 Q. And under -- within those two main topics, there's 12 3 subopinions that you go into more detail about, 4 correct? 5 A. Yes. 6 Q. Okay, let's go ahead and start on page 3 of your 7 report, No. 1. 8 A. Okay. 9 Q. Your opinion No. 1 says that Dr. Werntz' basis for 10 claiming increased cancer risk around smelter sites is 11 not reliable; is that correct? Does that correctly 12 state your opinions? 13 A. Yes. 14 Q. And you set out your reasons below there are for that 15 in the narrative portion; is that correct? 16 A. Yes. 17 Q. And you set out the basis for that opinion, the 18 materials you relied upon in reaching it, correct? 19 A. Yes, yes. 20 Q. Okay, I'm going to go ahead and ask you to go step by 21 step through the meat of your opinion. You start out 22 talking about the Tokudome study, and you state that 23 by -- and states that this is one of the references -24 COURT REPORTER: Could you please slow down 25 because I don't have the documents in front of me so I 95 1 can't follow along so I'm trying to just go based on 2 how you're speaking. 3 (Discussion off the record at 9:08 a.m.) 4 (Back on the record at 9:08 a.m.) 5 BY MS. SLEVINSKI: 6 Q. You started out discussing four studies that Dr. 7 Werntz cited in his proposed medical -- and it's your 8 opinion that these materials Dr. Werntz cited are not 9 reliable, correct? 10 A. No, it's not that they're not reliable, it's that they 11 don't support his opinion. 12 Q. Could you explain how they don't support his opinion? 13 In general, we'll go through it individual -- like 14 take it apart, is there a brief way you can summarize 15 why they don't support his opinions in general? 16 A. Yes, the first is that the Tokudome study has nothing 17 to do with residents around a smelter site; it's a 18 study of workers at a smelter. 19 Q. Okay. Well, let's start with that. 20 A. And it shows no increased risk of stomach cancer, so 21 it doesn't support Dr. Werntz's opinion that stomach 22 cancer is a disease that should be monitored for. 23 Q. Okay, well, let's take a look. 24 MS. SLEVINSKI: Could you please hand 25 Dr. Garabrant No. 137? 96 1 MARKED BY THE REPORTER: 2 DEPOSITION EXHIBIT NUMBER 137 3 9:09 a.m. 4 COURT REPORTER: Okay, I've done so. 5 MS. SLEVINSKI: Thank you. 6 BY MS. SLEVINSKI: 7 Q. Dr. Garabrant, if you -- this is the Tokudome; is that 8 how it's pronounced, Tokudome? 9 A. Well, I'm not an expert in Japanese, but that's how I 10 think it's pronounced. 11 Q. I'll just go from there. Does this appear to be the 12 study we are, in fact, talking about? 13 A. Yes. 14 Q. All right. All right, now you say that it does not 15 support Dr. Werntz's opinions but there is an 16 increased risk of cancer generally surrounding smelter 17 sites and specifically for this article, stomach 18 cancer, am I following you correct? 19 A. No, you're not following me -20 Q. Okay. 21 A. -- correctly. 22 Q. Well, could you clarify then, please? 23 A. Okay. This is a study of smelter workers. It doesn't 24 have any relationship to cancer risks around smelter 25 sites. 97 1 Q. So in your opinion, if the particular study is not an 2 exact replica or, you know, an exact same situation, 3 it's not a valuable or it's not evidence or 4 information that should be considered in reaching a 5 conclusion? 6 MR. DANNINGER: Objection to form. 7 A. That's not my opinion. 8 BY MS. SLEVINSKI: 9 Q. So if there was not an exact match as far as the study 10 is concerned -- strike that. If you -- we're going to 11 rely upon a study of smelter workers, what aspects of 12 it would make you more inclined to say it was a good 13 study as far as extrapolating it to a community around 14 the smelter? 15 A. Well, there would be a long list of things that I 16 would consider before I would extrapolate from a 17 population of smelter workers to a population of 18 community residents; do you want me to start listing 19 them? 20 Q. Yes, sir, would you, please? 21 A. Okay, well, the first is that I would want to ensure 22 that both -- both populations had comparable 23 demographics, so in terms of age distribution, sex, 24 race, ethnicity, those sorts of factors. And 25 secondly, and probably most importantly, I would want 98 1 to be sure that the exposures of the smelter workers 2 were comparable to the exposures of the community 3 residents, and there's absolutely no reason to believe 4 that's true in this instance. The Tokudome study is a 5 study of copper smelters in Ooita Prefecture in Japan. 6 Now, how in the world you could extrapolate 7 that to the general population of West Virginia, I 8 think is a startlingly inappropriate comparison. 9 Q. Can I interrupt you for just one second to ask a 10 question, please? So you don't believe that using a 11 study that focused on a population in a different 12 country is appropriate, the results from that study 13 are appropriate to use in comparison to a U.S. 14 population? 15 MR. DANNINGER: Objection, form. 16 A. That's not my opinion. 17 BY MS. SLEVINSKI: 18 Q. Well, you just said that this study that was conducted 19 in an area of Japan was not appropriate to compare to 20 a U.S. population in West Virginia? 21 A. I just said that I think it is inappropriate to 22 compare smelter workers, copper smelter workers in 23 Japan, to the general population of West Virginia. 24 Q. Is it inappropriate to compare Japanese smelter 25 workers to a population that lives in -- or somebody 99 1 very near a smelter, a zinc smelter in West Virginia? 2 A. I'm sorry, could you repeat that? 3 Q. Yes. Do you think it's inappropriate to compare the 4 results of a study that focused on Japanese smelter 5 workers to a situation in the United States where the 6 people are living in an area very near a zinc smelter? 7 A. Well, there's a lot you'd have to know before you 8 could make such a comparison reliably. I would 9 consider that a study of copper smelter workers in 10 Japan might be relevant to a study of copper smelter 11 workers in the United States provided that I knew that 12 the exposures were comparable, that the structure of 13 the populations were comparable, and provided that I 14 had some understanding of -- for each of the diseases 15 under study whether there was a relationship between 16 the different ethnicities of those populations and 17 risk of that disease. 18 In other words, if there's some other 19 factor related to ethnicities that is a cause of the 20 disease under study, then one would have to account 21 for that and adjust the results before it would be 22 appropriate to simply compare results from those two 23 smelter populations. Now, that answer does not in any 24 way suggest that it's appropriate to compare a working 25 population in Japan to the general population in West 100 1 Virginia without knowing a tremendous amount more than 2 we know, that sort of comparison is simply not 3 reliable in the absence of additional information. 4 Q. Would it be appropriate in your opinion to compare a 5 working population, a study of a working population 6 with those results to a nonworking population in 7 general? 8 A. There's no in-general answer; it depends on the issue. 9 Q. Okay, well, not even focusing on Japan. If you were 10 looking at a U.S. study of smelter workers somewhere, 11 would it be appropriate in your opinion to compare the 12 results of the U.S. smelter workers study to a 13 nonoccupational area but residents that live around a 14 smelter so it would be comparing smelter workers to 15 residents living in an area surrounding a smelter? 16 A. Well, it's typical in doing cohort studies to compare 17 the cohort of interest to the general population of 18 the county or state or region or country in which that 19 population exists, and that's typically done by 20 calculating a standardized mortality ratio. 21 However, when that calculation is done, one 22 still has to appropriately consider whether there are 23 meaningful differences between those two populations 24 in terms of other risk factors for the diseases under 25 study. I'll give you an example. When we did our 101 1 cohort mortality study of aircraft manufacturing 2 workers in San Diego which you and I discussed 3 yesterday, we compared those workers to the San Diego 4 county population, and we also compared them to the 5 U.S. general population. 6 We got very different SMR results for many 7 causes of death, and the reason we got many different 8 results is that the San Diego general population is 9 very different in terms of its ethnicity, in terms of 10 its risk factors for cardiovascular disease, risk 11 factors for cancer, risk factors for many diseases 12 than is the U.S. general population. So the use of 13 different comparison populations or different referent 14 populations dramatically altered the findings in that 15 study. 16 That's exactly the issue that concerns me 17 here. If you were to take copper smelter workers in 18 Japan and calculate the SMRs using the U.S. general 19 population or the West Virginia general population 20 rather than the Japanese general population, you are 21 very likely to get substantially different results, 22 and so those comparisons are not necessarily reliable. 23 Q. Okay. The next sort of portion of your opinion on the 24 Tokudome study says that it contradicts Dr. Werntz's 25 opinions regarding stomach cancer in relation to 102 1 smelter exposures, and you indicated that this study 2 does not support Dr. Werntz's beliefs that stomach 3 cancers are at risk in that area; am I correct? 4 A. I'm just trying to -- yes, that is correct. 5 Q. If you'd look at Exhibit 137, the actual article, did 6 you have any hesitation or did it concern you at all 7 that there were actually some increased risks of 8 cancer in this copper smelter study in Japan? 9 A. I didn't have any hesitation. 10 Q. Would you turn to page 312 of that article, the page 11 numbers are in the top, left corner. 12 A. Yes. 13 Q. All right, under the results column on the right-hand 14 side, the results say that among copper smelters, 15 significantly increased SMRs -- that's standardized 16 mortality ratios, correct? 17 A. Yes. 18 Q. -- were observed for total malignant neoplasms, and 19 malignant neoplasms of the -20 COURT REPORTER: Slow down, please, slow 21 down. Malignant neoplasms? 22 BY MS. SLEVINSKI: 23 Q. -- of the large intestine, except rectum, abbreviated 24 as colon cancer, malignant neoplasm of respiratory 25 systems, and malignant neoplasm of trachea, bronchus 103 1 and lung -2 COURT REPORTER: Trachea, bronchus and what 3 was that? Trachea, bronchus, and? 4 MS. SLEVINSKI: Lung. 5 MR. DANNINGER: Lung. 6 BY MS. SLEVINSKI: 7 Q. Hereafter abbreviated as lung cancer, do you see that, 8 Dr. Garabrant? 9 A. Yes. 10 Q. Now, it says the increase was most marked for lung 11 cancer. How did that fact affect your opinion on this 12 study of reliability. 13 A. It had no effect on my opinion about the reliability 14 of the study. We don't typically judge the 15 reliability of a study by its results. We judge it by 16 its methods. 17 Q. Well, isn't lung cancer, in fact, one of the issues in 18 this situation in Spelter, West Virginia? 19 MR. DANNINGER: Object to form. 20 BY MS. SLEVINSKI: 21 Q. Is lung cancer not one of the diseases that we're 22 concerned about the residents seeing an increased risk 23 of developing in Spelter, West Virginia? 24 MR. DANNINGER: Object to form. 25 A. I believe that Dr. Werntz is concerned about lung 104 1 cancer in his report. 2 BY MS. SLEVINSKI: 3 Q. So in so much as you criticize his reliance upon this 4 study because it contradicted his opinions regarding 5 study cancer in relation to smelter exposure, did you 6 not find it necessary to discuss or to evaluate the 7 fact that it did, in fact, find an increase of lung 8 cancer? 9 A. Well, I could certainly have discussed each and every 10 finding in each and every one of the 148 papers that I 11 cited in my bibliography. My point regarding the 12 Tokudome study is that it has nothing to do with 13 community residents around a smelter. It has to do 14 with people who work in the smelter and who likely had 15 very high exposure to some hazardous materials in the 16 smelter. That has nothing to do with living in a 17 community where there's no evidence of excessive 18 exposure, whatsoever, such as in Spelter. 19 Q. So -20 A. And so it's a meaningless comparison, it's nonsense. 21 Q. So I understand that is your opinion but you went on 22 to point out that it was contradictory because it 23 didn't talk about an increased risk of stomach cancer, 24 so why was -- why did you not mention or consider that 25 it found increased risk of other cancers that are of 105 1 concern? 2 A. Well, I think the more important question is why Dr. 3 Werntz didn't mention that his references didn't 4 support his opinions on stomach cancer. 5 Q. This -6 A. And Dr. Werntz seems to have missed that his point 7 that his own references don't support his position on 8 numerous issues. The fact that they might support his 9 opinions on some issues, if you make inappropriate 10 comparisons, doesn't in any way argumentative that his 11 opinions are well-founded. His own references don't 12 support him on issues such as stomach cancer, and he 13 doesn't bother to explain how the Tokudome study 14 supports his position on stomach cancer because it 15 doesn't. 16 Q. Would you agree that the Tokudome study supports the 17 positions that lung cancer is at -- at -- excuse me 18 increased risk of lung cancer in smelter sites? 19 A. Well, I don't know what you mean by at a smelter site. 20 The Tokudome study supports there's an increased risk 21 of lung cancer in copper smelter workers in Japan, or 22 at least in this one prefecture in Japan -23 Q. Would -24 A. -- I'm still speaking. It doesn't in any way support 25 that there's a risk of lung cancer in a community 106 1 around a smelter, anywhere. 2 Q. Is it your understanding that Dr. Werntz cited those 3 specifically to say that this Tokudome study, excuse 4 me, was cited specifically for -- as meaning that 5 residents near a smelter were at increased risk of 6 cancers? 7 A. Well, let's go back and look at Dr. Werntz's exact 8 wording and see what he said about it. 9 Q. Can you please answer my question? 10 A. Well, your question asked me for what it was my 11 understanding Dr. Werntz said, and the best -12 Q. To Dr. Werntz's report, that's what I'm asking. 13 A. Well, I'm going to get Dr. Werntz's report, and we'll 14 read it. 15 Q. Dr. Garabrant? 16 A. Yes. 17 Q. I'm asking the questions right now, I'm not asking to 18 go dig out Dr. Werntz's report, I'm asking what your 19 understanding was from your review of his report 20 because you did mention in your materials review list 21 that was one of the ones you used in forming your 22 opinions on this matter? 23 MR. DANNINGER: Amanda, Dr. Werntz -- Dr. 24 Garabrant, excuse me, has stated that it will refresh 25 his recollection and give him the ability to answer 107 1 your question if he turns to the report. If you 2 refuse to allow him to turn to the report, then I'm 3 going to object to any questions that you're asking 4 based on the report without him being allowed to 5 review it and that's what I think he's asking to be 6 able to do the review of the report to adequately 7 respond to your question. 8 MS. SLEVINSKI: Okay, thank you, we're not 9 going to go through Dr. Werntz's report right now. 10 MR. DANNINGER: Okay, then I object to any 11 question you asked based on the report that he's not 12 allowed to review the report in answering. 13 MS. SLEVINSKI: All right, thank you. 14 MR. DANNINGER: Dr. Garabrant, you can 15 attempt to answer the question if you're able. 16 A. Well, I don't recall exactly what Dr. Weren't said 17 word for word in his report without looking at it. 18 BY MS. SLEVINSKI: 19 Q. Okay, the next issue that you address was Dr. Werntz' 20 reliance upon the ATSDR public health assessment study 21 of National Zinc Company in Bartlesville, Oklahoma. 22 MS. SLEVINSKI: Could you please hand Dr. 23 Garabrant No. 6? 24 MARKED BY THE REPORTER: 25 DEPOSITION EXHIBIT NUMBER 6 108 1 9:28 a.m. 2 COURT REPORTER: All right, he has it. 3 MS. SLEVINSKI: Thank you. 4 BY MS. SLEVINSKI: 5 Q. In your opinion, this particular study was not 6 reliable because it did not find that the occurrence 7 of lung and kidney cancer was as expected from state 8 rates; is that correct? 9 A. No. 10 Q. I'm sorry, no? 11 A. No, that's not my opinion. 12 Q. Okay, what is it then, please? 13 A. My opinion is that the ATSDR study of the Bartlesville 14 plant found that the occurrence of lung and kidney 15 cancer was virtually identical to the State rates. 16 There was no evidence that residents in the area 17 around the zinc smelter were at increased risk of 18 cancer and that contradicts Dr. Werntz's opinion that 19 residents around a smelter are at increased risk of 20 cancer. 21 Q. So your belief from his study that there was no 22 increased risk of cancer, whatsoever? 23 MR. DANNINGER: Object to form. 24 A. It's my opinion that there was no evidence in this 25 report that the residents around the smelter were at 109 1 increased risk of cancer. 2 Q. Would you please, sir, turn to page 13 of 17, bottom 3 left-hand corner where the payment numbers appear. 4 A. Yep, just a moment. 5 Q. Okay. 6 A. Okay. 7 Q. On this page, where they discuss the cancer mortality 8 data, and in fact, there was an increased risk of 9 cancer in this area, was it not? 10 A. To what are you referring? 11 Q. If you look under No. 2 cancer mortality rate of the 12 third paragraph. There were -- there was an increased 13 risk of cancer there? 14 A. Well, what -- what you're pointing to is an increased 15 risk of ovarian cancer and multiple myeloma. 16 Q. Correct. 17 A. But those are not at issue in this litigation as far 18 as I understand. 19 Q. Well, I'm just trying to clarify your opinions and how 20 you stated your opinions in your report because that 21 sentence clearly says there was no evidence that the 22 residents in the area around the zinc smelter were at 23 increased risk of cancer, and that is not, in fact, 24 what this says, so I'm just trying to clarify how you 25 formed your opinions and where you got this 110 1 information, how you processed it. I -- is there a 2 reason why you didn't consider that there were other 3 types of cancers or I'm just trying to figure out why 4 there's a lack of specificity? 5 MR. DANNINGER: Object to form. 6 A. Well, yes, if you read the Bartlesville study here's 7 what it says, of the 30 anatomical sites evaluated the 8 number of deaths for multiple myeloma and ovarian 9 cancer in Washington county was greater than what 10 would be expected from the numbers for the State of 11 Oklahoma. Now what they're talking about is they did 12 30 comparisons, right of the observed number of 13 cancers to the expected number of cancers. Out of 14 those 30, two were elevated. Now, given that we 15 calculate 95 percent confidence limits or we calculate 16 P values and consider those with values less than .05 17 to be statistically significant, we would expect 5 18 percent of those comparisons to be statistically 19 significant by chance alone. 20 They found two out of 30. Now, 2 out of 30 21 is roughly 6 percent, okay? Pretty close to what you 22 expect by chance alone, okay? And then they go on to 23 say the available data on cadmium and lead do not 24 identify ovarian cancer or multiple myeloma as 25 possible health outcomes, we're not talking about 111 1 probable or known we're talking about not even 2 possible health outcomes human I'm quoting again, 3 human studies do not identify any cancers associated 4 with exposure to lead. So the ATSDR holds the opinion 5 that lead is not known to cause cancer in humans. 6 Occupational studies indicate that cadmium may be a 7 weak lung carcinogen, and so what they're saying is 8 well, we had these two findings, they don't make any 9 sense because these -- the chemicals involved had 10 never been thought to cause these, and they simply 11 discounted them. 12 My -- my additional point to you is if you 13 take any reasonable estimate of the probability of 14 getting significant positive associations by chance 15 alone, 2 out of 30 is not unexpected in any way, so 16 nobody at the ATSDR who wrote this report gave any 17 credence to the idea that multiple myeloma or ovarian 18 cancer was causally associated with living near the 19 smelter, and as far as I can tell, Dr. Werntz doesn't, 20 either, because he never cited that multiple myeloma 21 or ovarian cancer were in any way related to living 22 near the Spelter facility. 23 Q. Okay, and you said that there's -- ATSDR does not 24 consider lead a carcinogen? 25 A. I read it to you. 112 1 Q. Right, well, if you would look up just a couple of 2 paragraphs, three paragraphs down from the top of the 3 page says cancer considered a biological plausible 4 health outcomes because cadmium or lead are considered 5 probable human carcinogens and because both 6 contaminants are in completed air and soil human 7 exposure pathways. Significant exposure -8 COURT REPORTER: I'm sorry, I'm not getting 9 you that fast. 10 MS. SLEVINSKI: Oh, I'm sorry, where do you 11 want me to start from? 12 COURT REPORTER: Go back a sentence. 13 MS. SLEVINSKI: I'm sorry? 14 COURT REPORTER: Just go back one sentence. 15 MR. DANNINGER: Maybe just start the 16 paragraph over, Amanda. 17 BY MS. SLEVINSKI: 18 Q. Cancer is considered a biologically plausible health 19 outcome because cadmium and lead are considered 20 probable human carcinogens and because those 21 contaminants are in completed air and soils human 22 exposure pathways. 23 Now, Dr. Garabrant, that appears to be that 24 the ATSDR considered lead and cadmium as posing a 25 definite risk of cancer in humans. Does it not appear 113 1 that way to you? 2 A. Well, that's not what it says. You just read it. 3 Cancer is considered a biologically plausible health 4 outcome because cadmium and lead are considered 5 probable human carcinogens. Nowhere in that sentence 6 does it say that these are known carcinogens and 7 nowhere in that -- in that sentence does it say they 8 cause cancer. 9 It says well, they're probably carcinogens, 10 and it's plausible that they cause cancer and then if 11 you drop down three or four paragraphs to what I read 12 to you from the ATSDR report, it says human studies do 13 not identify any cancers associated with exposure to 14 lead, that's true. So they're saying well, it's 15 possible, but it -- but the human studies don't 16 identify any cancers associated with lead. 17 Q. All right, thank you. 18 A. You're welcome. 19 Q. The next study you mentioned, the Pershagen study. 20 MS. SLEVINSKI: Can you please get 21 Dr. Garabrant No. 121? 22 MARKED BY THE REPORTER: 23 DEPOSITION EXHIBIT NUMBER 121 24 9:37 a.m. 25 COURT REPORTER: Okay. 114 1 BY MS. SLEVINSKI: 2 Q. Now, Dr. Garabrant, what about this study do you 3 conclude made it unreliable as far as Dr. Werntz to 4 support his opinions that people around cancer -- I 5 mean excuse me people around smelter sites are at 6 increased risk of cancer? 7 A. Well, the author, Dr. Pershagen says, quote, no firm 8 conclusions can be drawn on the cause of excess lung 9 cancer risk in the smelter area. 10 Q. All right, and that's on the front page in the 11 abstract? 12 A. Right. In other words, the author, himself, is 13 reluctant to say that the excessive lung cancer in the 14 smelter area was caused by the smelter. 15 Q. Now, that sentence doesn't end where you could you 16 read after the comma, after where you left off please? 17 A. Sure, then Dr. Pershagen goes on to say but it seems 18 plausible that the very substantial emissions to air 19 from the smelter, especially of arsenic may have 20 played a role. So he says it's plausible it could 21 have happened. 22 Q. Would you please turn to page 692 of the second -23 well, no, actually -- third to the last page on the 24 article. 25 A. Yes. 115 1 Q. The last paragraph in the right-hand column, where it 2 starts in conclusion; do you see that? 3 A. Yes. 4 Q. Would you please read the first three sentences of 5 that paragraph? 6 A. Sure. In conclusion, the results show that men living 7 in the vicinity of a large copper smelter have an 8 increased risk of lung cancer. The excess risk also 9 remains after standardization for smoking habits and 10 occupational background. It is plausible that the 11 very substantial air emissions from the smelter, EG, 12 of arsenic may have played a role, no firm conclusions 13 can be drawn. 14 Q. That's -15 A. Especially in view of the inadequate exposure data. 16 Q. Thank you. Now, focusing on the portions, the first 17 several sentences prior to where they state no firm 18 conclusions, what about that conclusory paragraph 19 leads you to say that there was no clearly increased 20 risk of lung cancer in the community? 21 A. Well, the authors, themselves, say it's plausible that 22 the emissions may have played a role and no firm 23 conclusions can be drawn. 24 Q. What in the study as far as the methods, the results, 25 the meat of this study, what about it led you to say 116 1 there was no clear risk, increased risk? 2 MR. DANNINGER: Object to form. 3 A. The relative lack of exposure information precluded 4 any analysis that showed a relationship between 5 exposure and lung cancer risk. I agree with Dr. 6 Pershagen in his conclusion that no firm conclusion 7 can be drawn, particularly in light of the inadequate 8 exposure data. 9 BY MS. SLEVINSKI: 10 Q. What does it mean to you when you read a study that 11 uses that phrase, no firm conclusions can be drawn? 12 A. It means no firm conclusion can be drawn. 13 Q. You can't elaborate on that, frequently risks in these 14 types of studies? 15 A. It speaks for itself. 16 MR. DANNINGER: Object to form. And 17 foundation, belated. 18 BY MS. SLEVINSKI: 19 Q. I mean if no firm conclusions can be drawn, you can't 20 rule out a possibility of increased risk, can you? 21 A. Well, there is -- there are an infinity number of 22 things that are possible in the universe. We have to 23 move forward, we have to base our opinions, we have to 24 base our -- our science on authentication that are 25 reasonably proven to be true, not on speculation that 117 1 it might be true. 2 Q. You would agree that if no firm conclusions can be 3 drawn from the results of a particular study, that's 4 not saying either way what is possible can happen? 5 MR. DANNINGER: Object to foundation. 6 A. I would agree that when the authors say no firm 7 conclusions can be drawn, that your characterization 8 that it might be true is nothing more than 9 speculation -10 BY MS. SLEVINSKI: 11 Q. -- mentioned that the exposure data in this study was 12 inadequate; is that correct? 13 A. That's what the authors said. 14 Q. That -- does the fact that there's inadequate exposure 15 data, does that render the entire study the results 16 unreliable, does it make it not a piece of evidence 17 that you would like to rely upon? 18 A. The lack of exposure data does not invalidate the 19 study for what it is. The lack of exposure data means 20 that it is unclear whether the excess risks of lung 21 cancer has anything to do with exposure. It doesn't 22 invalidate the study, it just says it doesn't prove up 23 what you want it to prove up which is that the excess 24 risk of lung cancer has to do with exposure from the 25 smelter. 118 1 Q. All right, thank you. Now, the last sentence in that 2 paragraph addresses the Brown study. 3 MR. DANNINGER: Are you in the -- his 4 report again? 5 MS. SLEVINSKI: Yes, sir, I'm. 6 MR. DANNINGER: Okay. 7 BY MS. SLEVINSKI: 8 Q. Back to your report on page 4 of Dr. Garabrant's 9 report. 10 MR. DANNINGER: Okay. 11 BY MS. SLEVINSKI: 12 Q. Top paragraph, last sentence -13 A. Just a moment. 14 Q. -- refers to the Brown study. 15 MS. SLEVINSKI: Would you please hand the 16 witness No. 18? 17 MARKED BY THE REPORTER: 18 DEPOSITION EXHIBIT NUMBER 18 19 9:44 a.m. 20 COURT REPORTER: Okay, he has that. 21 MS. SLEVINSKI: Thanks. 22 BY MS. SLEVINSKI: 23 Q. Now, Dr. Garabrant, this particular study does that 24 found an increased risk of lung cancer in an area 25 where a zinc smelter site; is that correct? 119 1 A. I'm just looking. 2 Q. Okay. 3 A. Okay, this study found an excess risk of lung cancer 4 associated with residents near the zinc smelter. 5 Q. Thank you, and where was the zinc smelter located, it 6 was in the United States, wasn't it? 7 A. It was in eastern Pennsylvania. 8 Q. Okay. Now, what did you find about this study that 9 was unreliable or not good enough to compare to the 10 situation in Spelter, West Virginia? 11 MR. DANNINGER: Object to form. 12 A. I didn't say that the study was unreliable, I said 13 that the authors concluded that the limited size of 14 the study precluded causal interpretation. 15 BY MS. SLEVINSKI: 16 Q. Was there anything about this when you went through 17 and reviewed it to write your report that you could 18 find to criticize it on except for the limited size of 19 the report I mean of the sample? 20 MR. DANNINGER: Object to form. 21 A. My point regarding the Brown study is that the 22 authorize, themselves, were not willing to conclude 23 there was a causal association between living near the 24 smelter site and lung cancer, that's all. 25 BY MS. SLEVINSKI: 120 1 Q. Other than them not being able to say that there was a 2 definite causal association, you don't have any other 3 criticisms of this particular study? 4 MR. DANNINGER: Object to form. 5 A. I mean we could -- I could go back and critique it in 6 detail. My point in writing my report is that Dr. 7 Werntz failed to note that the authors of the report, 8 themselves, were unwilling to conclude a causal 9 association existed. 10 BY MS. SLEVINSKI: 11 Q. Can you please turn to page 260, 260 of the report, 12 second to last page. 13 A. Yes. 14 Q. Final paragraph, in conclusion, would you please read 15 that? 16 A. Yes. In conclusion, our results raised the 17 possibility of an increased lung cancer risk 18 associated with environmental exposure to high 19 concentrations of heavy metals including arsenic and 20 cadmium. The small sample size and limited 21 environmental data preclude causal interpretation, but 22 suggest the need for further research in other 23 polluted areas of the United States and there has been 24 further research which I cited and which Dr. Werntz 25 failed to cite which does not show increased cancer 121 1 risks around smelter sites. 2 Q. We're going to get into that in the very next 3 paragraph in just a second. Would you please explain 4 or elaborate what it means when a study is unable to 5 make a causal interpretation from its results? 6 A. Yes, it means the authors are unwilling to conclude 7 that there is a cause and effect relationship between 8 exposure and the health outcome, in this case, lung 9 cancer, in their study. That's what it means. It 10 speaks for itself. 11 Q. Do you refer into science -- oh, excuse me, strike 12 that. 13 Are the authors of this study, Brown, 14 Pottern, and Blot, are they unable to draw scientific 15 causation, or is that what they're referring to? 16 MR. DANNINGER: Foundation. 17 A. I don't know what your question is about. These 18 authors are scientists at the national -- they were 19 scientists at the National Cancer Institute. They 20 work in the realm of science. I believe that their 21 conclusions have to do with what they feel are 22 scientifically reliable standards of evidence. 23 BY MS. SLEVINSKI: 24 Q. All right. The next paragraph section, I guess, where 25 it starts furthermore, in your report, I'm sorry, 122 1 excuse me. 2 MR. DANNINGER: Thank you. 3 BY MS. SLEVINSKI: 4 Q. Page 4. Now, Dr. Garabrant, what was the reason that 5 you researched, did your, you know, liter -- excuse 6 me, literature search and found these? 7 MR. DANNINGER: Form objection. 8 A. Well, I think that it is appropriate when a scientist 9 is trying to address a question in science to research 10 the topic and to gather the relevant scientific 11 literature. I sought to find the relevant scientific 12 literature regarding cancer risks in communities 13 around smelters in which soil is contaminated with 14 arsenic, cadmium or lead. Dr. Werntz apparently 15 didn't do that, I did. And he neglected to find or 16 cite the studies that didn't go his way. 17 BY MS. SLEVINSKI: 18 Q. Let's discuss the ones that you've selected as not 19 going Dr. Werntz's way. 20 MS. SLEVINSKI: Could you please get Dr. 21 Garabrant No. 5? 22 COURT REPORTER: All right. 23 MARKED BY THE REPORTER: 24 DEPOSITION EXHIBIT NUMBER 5 25 9:52 a.m. 123 1 BY MS. SLEVINSKI: 2 Q. Before we get into the instance of this particular 3 exhibit, is it correct to say that because you offered 4 these several studies we're about to go through in 5 this section, these are evidence of no apparent cancer 6 risks in communities near smelters or where there is 7 soils contaminated with arsenic cadmium or lead; is 8 that correct? 9 A. Yes. 10 Q. So you would have subjected these particular studies 11 to the same risk analysis that you put to the ones to 12 Dr. Werntz through, wouldn't you? 13 A. Yes. 14 Q. Could you look at No. 5, that's another ATSDR public 15 health assessment. 16 A. Is that -17 Q. Now you stated that it found no apparent public health 18 hazard it concluded that health effects from arsenic, 19 cadmium, or lead are unlikely due to limited exposures 20 to these metals. The public health assessment doesn't 21 provide a whole lot of information. What in this 22 particular document did you rely upon that led you to 23 make that conclusion? 24 A. I relied on the report from the ATSDR that they 25 investigated a smelter site and found no evidence of 124 1 health effects in the community as a result of 2 arsenic, cadmium or lead because there was limited 3 exposure to those metals. 4 Q. Now, where in this document did you glean that 5 information? There are some very conclusory 6 statements in there but there's no information on 7 exposure data which you have recently said was 8 important in making a determination as to whether the 9 results are something that you can rely upon or 10 something that you can work from, so this -- I don't 11 see anything in here that is much more conclusory 12 statements, do you? 13 MR. DANNINGER: Object to form. 14 A. This report gives the conclusions of a public health 15 assessment of a smelter site in Utah and says that 16 health effects are unlikely due to limited exposure to 17 arsenic, cadmium and lead. The point of this study is 18 that smelter sites do not necessarily carry any health 19 risks to the community. 20 BY MS. SLEVINSKI: 21 Q. What particular information -22 A. And the -23 Q. -- about this community in this smelter site do you 24 have to compare it to any other situation? 25 MR. DANNINGER: Amanda? 125 1 BY MS. SLEVINSKI: 2 Q. The situation in West Virginia there's nothing in here 3 that tells you what levels were present? 4 MR. DANNINGER: Amanda, the doctor wasn't 5 finished. 6 MS. SLEVINSKI: I'm sorry. 7 MR. DANNINGER: He should be allowed to 8 finish. 9 A. Yeah, I was still speaking, thank you. The point is 10 this, before it is reliable to make any conclusions 11 about health effects in communities related to 12 industrial sites, you have to have evidence of 13 exposure adequate to have caused health effects and 14 you have to have evidence of health effects. There is 15 no basis for a conclusion in the absence of such 16 evidence that a smelter facility such as the one in 17 salt lake county, Utah, or such as the one in Spelter 18 West Virginia has any adverse effects in the 19 community. You can't make that assumption. 20 You have to have evidence of exposure. My 21 point in citing the public health assessment of the 22 Murray smelter site is here's a big smelter where the 23 government -- the Federal Government came in, they 24 investigated and they found no apparent public health 25 hazard. You cannot draw the conclusion as Dr. Werntz 126 1 seems to that smelters are adversely affecting the 2 communities around them unless you have evidence of 3 exposure and evidence of adverse effects. 4 Q. With respect to Exhibit No. 5 of -- dealing with the 5 Murray smelter in Utah, this contains no information, 6 whatsoever, about the exposure levels, no evidence of 7 the exposure, no evidence of the extent of operations 8 of this facility so I'm trying to figure out how you 9 determined that this was a good example of no increase 10 risk of cancer around the smelter sites, you have 11 stated previously this morning that evidence of 12 exposure is critical, that you know you can't compare, 13 you know, two different populations or areas without 14 having more information to rule out any other risk 15 factors that might be affected one or the other so I'm 16 just trying to figure out based on this exhibit how 17 you're able to analyze this the same way you analyzed 18 the studies we previously spoke about this morning? 19 A. The study is what it is. Okay? It's a public health 20 assessment by the Federal Government, the agency for 21 toxic substances and disease registry. It's a smelter 22 site, they found no evidence of a public health 23 hazards. My point is simply that you cannot conclude 24 that smelter sites are public health hazards or are 25 associated with adverse health effects in communities 127 1 unless you have evidence that those communities have 2 been overexposed and evidence that there's increased 3 risk of disease in the community, and that's the point 4 that Dr. Werntz doesn't seem to follow. 5 Q. Looking at this Exhibit 5, what were the levels of 6 exposure or the levels of contaminants at the Murray 7 smelter in Murray salt lake county Utah? 8 A. The report does not give the numbers. It simply says 9 there was limited exposure to arsenic, cadmium, and 10 lead. So it -- you know, if -- if you want to make 11 this into a key piece, I'll go back and get the entire 12 public health assessment and then we can discuss it in 13 more detail. 14 Q. I'm just trying to figure out where you're able to -15 what apparent to -- I just don't see from this 16 document what sort of information that you've already 17 said is critical where -- where he found it from his 18 document? 19 MR. DANNINGER: Object to form. Are you 20 asking him where he found it in the document? 21 MS. SLEVINSKI: I'm just -- I'm asking Dr. 22 Garabrant he said on numerous occasions this morning 23 there's various aspects of studies that are important 24 in determining whether you can compare it to another 25 situation or just whether it's a good study in 128 1 general, example 5 noted exposure levels and said to 2 me and does not indicate that he has any background on 3 that sort of information that he's already said needs 4 to be addressed in a study, a particular study to 5 determine whether it's adequate evidence of his 6 results. 7 MR. DANNINGER: So what's your question 8 then? 9 MS. SLEVINSKI: I'm asking him -10 MR. DANNINGER: Well, I'm aware of what 11 you're asking him, but you're not asking a question. 12 What's your actual question to the doctor? 13 BY MS. SLEVINSKI: 14 Q. Did you -- Dr. Garabrant, did you have any sort of 15 outside exposure levels or documentation of lead to 16 this Murray smelter? 17 A. No. 18 Q. Are you saying that there weren't high exposures in 19 this area? 20 A. I'm saying what the ATSDR said there was limited 21 exposure to those metals. 22 Q. In the first paragraph under conclusions, the last 23 sentence beginning with therefore, can you please read 24 that? 25 A. I don't see where you're -- oh, the first paragraph, 129 1 okay. Well, that -- reading just that last sentence 2 takes it out of context. I think we have to read the 3 paragraph in order to understand what they're saying. 4 A sentence that starts -- a sentence that starts with 5 therefore has a premise, and the premise isn't stated 6 in the sentence so we have to go back and get the 7 premise. 8 Q. Can you just read the sentence, please? 9 A. You want me to just take something out of context 10 that's misleading? 11 Q. Just please -- well, please do as I ask and read the 12 sentence. 13 MR. DANNINGER: Object on the basis that 14 the doctor's already said it's out of context, but 15 doctor, you can read the sentence. 16 A. Well, I'm going to give the context because reading 17 the sentence would be misleading. The context is that 18 the results of this investigation indicated that 19 health effects due to arsenic, cadmium and lead were 20 unlikely due to limited exposure to those metals. 21 That conclusion was based on a talks logic evaluation 22 of the worker exposures at the smelter which indicated 23 the exposure levels were too low to result in health 24 effects. The authorize then pointed out that if the 25 exposure circumstances changed so that the amount of 130 1 exposure increased significantly, health effects would 2 be possible. 3 Then they say, and I'll read your sentence, 4 therefore, remediation of contaminated soil should be 5 done based on the potential for health effects as 6 indicated by the soil levels of these metals. In 7 other words, if they were to find elevated levels of 8 metals in soil, they should remediate those soils 9 based on evidence that there would be a likelihood of 10 adverse health effects. That's what they're saying. 11 But if you read the sentences before it, there wasn't 12 any. There's no evidence of excessive levels in the 13 soil and there was no evidence of adverse health 14 effects. 15 BY MS. SLEVINSKI: 16 Q. Are you finished? 17 A. Yes. 18 Q. I don't want to interrupt you. 19 MR. DANNINGER: He's finished. 20 MS. SLEVINSKI: All right, we've been going 21 a little bit over an hour. Is it okay to take about a 22 five, ten-minute break real quick? 23 MR. DANNINGER: Of course it is. That's 24 just fine with us, Amanda. 25 MS. SLEVINSKI: Okay. 131 1 MR. DANNINGER: We'll plan on being back 2 about 15 after? 3 MS. SLEVINSKI: Sounds good. 4 MR. DANNINGER: Okay. 5 MS. SLEVINSKI: Thanks. 6 VIDEO TECHNICIAN: We are going off the 7 record, the time is 10:05 and 5 seconds a.m. 8 (Recess taken at 10:05 a.m.) 9 (Back on the record at 10:18 a.m.) 10 VIDEO TECHNICIAN: We are now back on the 11 record. This is the beginning of tape No. 2. The 12 time is 10:18 and 15 seconds a.m. 13 BY MS. SLEVINSKI: 14 Q. Dr. Garabrant, we left off on page 4 of your report, 15 the paragraph where you were discussing different 16 studies that in your -- your conclusions that show no 17 apparent excess cancer risk in communities with 18 smelter sites or where there's contaminated soils. 19 Another study you discussed was -- is study by an 20 author Wong, An Ecologic Study of Skin Cancer and 21 Environmental Arsenic Exposure; do you recall that 22 study? 23 A. Can we get it out? I don't recall it offhand. 24 Q. It's No. 146. 25 MS. SLEVINSKI: Would you please hand that 132 1 to Dr. Garabrant? 2 MARKED BY THE REPORTER: 3 DEPOSITION EXHIBIT NUMBER 146 4 10:19 a.m. 5 COURT REPORTER: Okay. 6 BY MS. SLEVINSKI: 7 Q. Dr. Garabrant, you in your report shows that skin 8 cancer rates, well, first of all let me back up, 9 strike that, excuse me, this is an ecologic study of 10 skin cancer, correct, according to the title? 11 A. Yes. 12 Q. Would you describe briefly what an ecological study 13 design is? 14 A. Yes, an ecological study design typically is one in 15 which the exposures are assessed at some aggregate 16 level, typically a population level or a community 17 level, and then they are linked to health effects or 18 health conditions either at the individual level or at 19 the group or community level. 20 Q. All right, so part of the design of an ecologic study 21 doesn't allow for individualized data collection for 22 the various people that are being studied, correct? 23 A. Well, typically, an ecological study does not have 24 individual level data for all variables. It may have 25 individual level data for some. 133 1 Q. Okay. This particular study, No. 146, by Otto Wong, 2 you refer to it in order to show that there was skin 3 cancer rates within the range for other locations in 4 the United States and they were comparing it to with 5 an area with environmental arsenic exposure; is that 6 correct? 7 A. Yes, the study showed that skin cancer rates in an 8 area where the soil was contaminated with arsenic were 9 in the range for other areas in the U.S. 10 Q. Now, when you were going through the study and 11 evaluating it and -- and you decided to include it in 12 a portion of your report, did you take into 13 consideration the limitations of the study that are 14 cited? 15 A. What limitations are you referring to? 16 Q. If you turn to the final page of the article, 241, 17 starting in the left-hand column, the first full 18 sentence starts with however, does this-- this page 19 has several limitations discussed and described by the 20 authors. Would those limitations affecting this 21 study, did they come into play when you decided to use 22 this in a portion of your report? 23 A. I'm not sure what limitation you're talking about. 24 Could you clarify? 25 Q. Sure. On that final page, the authors start out -- 134 1 well, the acknowledge the many confounding factors 2 they couldn't account for because of the study design 3 such as individuals', you know, tendencies for sun 4 exposure this is looking for skin cancer, correct? 5 A. Yes. 6 MR. DANNINGER: Object to form. 7 MS. SLEVINSKI: I'm sorry? 8 MR. DANNINGER: Me or him? 9 MS. SLEVINSKI: Oh, no, I...going on... 10 BY MS. SLEVINSKI: 11 Q. Can you -- just one moment. 12 A. Are you waiting for me or -13 Q. No, sir, I'm reading something. 14 A. Oh, okay. 15 Q. I apologize. The authors they discuss the details, 16 the different factors of different varying levels of 17 exposure to skin cancer. It's the, I guess, the 18 second paragraph from the top where it says additional 19 issues? Do you see that? 20 A. Yes. 21 Q. That discusses another factor that could have impacted 22 their finding of no association with skin cancer and 23 environmental arsenic exposure, different diagnostic 24 procedures. The final paragraph to conclude, in that 25 column, do you see that? 135 1 A. Yes. 2 MR. DANNINGER: Object to form. 3 BY MS. SLEVINSKI: 4 Q. Conclude the age adjusted annual to conclude, the age 5 adjusted annual skin cancer incidence rates were found 6 to be higher in the control county than in the two 7 exposed counties. So Dr. Garabrant, do you read that 8 to interpret saying there's no increased risk of skin 9 cancer in arsenic exposed areas? 10 A. I read that to mean that the age adjusted annual skin 11 cancer incidence rates were higher in the controlled 12 counties than in the two exposed counties. In other 13 words, there was not evidence that exposures in the 14 exposed counties led to any increased risk of skin 15 cancer. 16 Q. Because they were not able to account for individual 17 sun exposures and individual diagnostic differences, 18 does that in your opinion or in your review of this an 19 important factor in whether this is a good example of 20 the findings of no association between environmental 21 arsenic and skin cancer? 22 MR. DANNINGER: Object to form. 23 A. Well, the authors point out that the issue of 24 diagnostic criteria is not likely to be a major factor 25 for basal cell carcinomas and squamous cell carcinomas 136 1 of the skin and I agree with that so although they 2 raise the issue, I think they're correct in saying 3 this -- this is unlikely to cause any substantial 4 difference in the skin cancer incidence in these 5 different areas. 6 BY MS. SLEVINSKI: 7 Q. Would you agree, though that arsenic is a known human 8 carcinogen, correct? 9 A. Well, I agree that arsenic can cause certain types of 10 cancer. It can cause skin cancer if you ingest 11 arsenic typically in drinking water, that -- that is 12 well established. 13 Q. So you agree, arsenic is a known human carcinogen? 14 A. I just answered that question. -- arsenic is known to 15 cause skin cancer in situations where people ingest 16 arsenic contaminated -17 Q. The question, Dr. Garabrant -18 MR. DANNINGER: No, Amanda, let him finish 19 his answer. 20 A. Yeah. Ms. Slevinski, your question is so vague that 21 it demands a precise answer. Arsenic can cause cancer 22 in humans, and it's important to specify the root and 23 circumstances of exposure and what cancers arsenic is 24 linked to, okay? So arsenic in drinking water is 25 linked to skin cancer in areas of the world where 137 1 there is -- where there are very high arsenic levels 2 in drinking water. Arsenic by inhalation is not known 3 to be linked to skin cancer. 4 BY MS. SLEVINSKI: 5 Q. Is arsenic by inhalation known to be linked to lung 6 cancer? 7 A. In settings such as in arsenic smelting operations, 8 yes. 9 Q. Only in arsenic smelting operations in your opinion? 10 A. No, the issue is dose in settings where people have 11 high and prolonged inhalation exposures to inorganic 12 arsenic compounds, it has been linked to increased 13 risk of lung cancer. 14 MS. SLEVINSKI: Number -- could you please 15 get Dr. Garabrant No. 60? 16 MARKED BY THE REPORTER: 17 DEPOSITION EXHIBIT NUMBER 60 18 10:29 a.m. 19 COURT REPORTER: Okay. 20 BY MS. SLEVINSKI: 21 Q. All right, Dr. Garabrant, this is another study that I 22 cited and discussed briefly in your report. You said 23 that -- well, the study also says this is a study of 24 an environmental arsenic exposure situation in 25 Australia, correct? 138 1 A. Yes. 2 Q. And why did you decide to use this article here? 3 MR. DANNINGER: Hay, Amanda, I don't want 4 you to lose your point, I just want to raise something 5 with you that I just noticed. 6 MS. SLEVINSKI: Okay. 7 MR. DANNINGER: Dr. Garabrant inadvertently 8 highlighted on your Exhibit 146. If you'd like, I did 9 not highlight the copy that I received. If you'd 10 like, we can use that and insert that as the exhibit, 11 and I'll take the highlighted version. It's up to 12 you, I don't -- I just -13 MS. SLEVINSKI: No, that's fine, use the 14 highlighted version. 15 MR. DANNINGER: Okay, then I'll leave that 16 in there, I just wanted you to be aware of that. I'm 17 sorry to interrupt. 18 MS. SLEVINSKI: No, no problem. 19 MR. DANNINGER: The court reporter may be 20 able to read that back to you. 21 BY MS. SLEVINSKI: 22 Q. I was just asking Dr. Garabrant the reasons for which 23 he decided to use this particular study at this point 24 in his report. 25 A. Well, because the Hinwood study is a study in which 139 1 they looked at soil and water arsenic concentrations 2 in relation to cancer risks. 3 Q. And this was an ecological study design, as well, 4 wasn't it? 5 A. I think that's fair to say, yes. 6 Q. Now, when you were reviewing this, did you take note 7 of any of the limitations that were noted by the 8 authors that -- to this study? 9 A. Could you give me some guidance on what it is you're 10 referring to? 11 Q. Well, you could turn to page 139, please, first full 12 paragraph. 13 A. Yes. 14 Q. Now, this paragraph states that this study was -15 several limitations that it has small numbers to 16 enable appropriate subanalysis. Did that affect your 17 evaluation of this in any way? 18 A. Well, I don't think that that comment really applies 19 to the cancers at issue in this litigation. That's 20 not true for lung cancer for which there were 749 21 cases for bladder cancer for which there were 303 22 cases, for kidney cancer, where there were 134 cases, 23 for stomach cancer where there were 228 cases, one 24 moment. Yeah, I guess those are the ones I need to 25 address. No, this is quite a large study for those 140 1 specific types of cancer, it's a very large study. 2 Q. Now, the next sentence says in discussing the 3 limitations, it says the analysis based on postcodes 4 is likely to be biased toward a negative result 5 because of the inevitable misclassification of many 6 unexposed persons in the areas as exposed. 7 Negatives -- likely to be biased towards a negative 8 result, does that mean likely to find no associations? 9 A. Yes. That is one of the -- one of the concerns in 10 ecological study designs is that typically, people's 11 exposures are assigned at the population level and in 12 instances where there is variation in exposure between 13 individuals they are classified as having the same 14 exposure level, and that may bias toward the null, a 15 negative result, although, it's well recognized that 16 in some circumstances, it can bias away from the null, 17 so you can end up creating positive associations as 18 well. 19 Q. So in this particular study, though, there was no, you 20 no he, individual exposure data available for these 21 people, correct? 22 A. I believe that's correct and that's -- that's. 23 Q. -- more reliable or a better example of a 24 nonassociation without having exposure, I'm -- I'm 25 sorry, strike that. 141 1 You're citing this as supporting your 2 position that there is no excess risk of cancer aren't 3 smelter sites or around arsenic or lead or cadmium 4 contaminated soils, how is it that this study's lack 5 of exposure -- still renders it a better example than 6 other studies you've discussed this morning that you 7 said is one of the first things you had was lack of 8 exposure data for the people that it wasn't an 9 adequate or good representative study of the situation 10 that we're discussing here in West Virginia? 11 A. I'm not sure -12 MR. DANNINGER: Object to form. 13 A. I'm not sure that I understand what your question is. 14 BY MS. SLEVINSKI: 15 Q. I'm asking what makes this study better to support 16 your position eastbound though it has several 17 limitations including lack of exposure data which is 18 something you criticize in the report Dr. Werntz cited 19 so I'm trying to figure out what makes this one a 20 better or more reliable example as opposed to another 21 study that Dr. Werntz relied upon that you criticized 22 that didn't have exposure data? 23 MR. DANNINGER: Object to form. 24 A. They study has exposure data, it has a lot of exposure 25 data and it is used appropriately. 142 1 BY MS. SLEVINSKI: 2 Q. I believe you just said that it didn't have individual 3 exposure data? 4 A. Well, it doesn't have exposure data at the individual 5 level. In other words, they didn't test the water of 6 each and every person in the census areas, but it does 7 have exposure data on soil, arsenic, and water arsenic 8 in those areas, it just doesn't have it for each and 9 every property and each and every water source which 10 would be an extraordinary study if such data existed, 11 but it doesn't. The point is they do have soil 12 arsenic and water arsenic concentrations in many 13 communities throughout Australia where this study was 14 done and they found no evidence of increased risk of 15 any of the tumors at issue in this litigation. 16 Q. If you turn to page 138 on that study -17 A. Yes. 18 Q. -- I guess it would be the third paragraph from the 19 top, the last sentence, well, the second to last 20 sentence, the authors mention that the current use in 21 that area of contaminated water is limited to a small 22 percentage of the population in any given area due to 23 reliance on rainwater tanks for domestic consumption, 24 and this is a study looking into people developing 25 skin cancers via arsenic containment drinking water 143 1 and they acknowledge the fact that there's likely not 2 very many people that are drinking the water that they 3 tested that's being contaminated; is that not correct? 4 MR. DANNINGER: Object to form. 5 A. Well, they point out that current usage of 6 contaminated water is limited, and then they point out 7 past usage of contaminated supplies may have been 8 greater. 9 BY MS. SLEVINSKI: 10 Q. All right. Thank you. Then the final -- looking at 11 your report, page 4 again, the final sentence on that 12 paragraph that we've been discussing, you also looked 13 at a report by -- No. 50. 14 MS. SLEVINSKI: Would you please get 15 Dr. Garabrant Exhibit 50? 16 MARKED BY THE REPORTER: 17 DEPOSITION EXHIBIT NUMBER 50 18 10:39 a.m. 19 COURT REPORTER: Okay. 20 BY MS. SLEVINSKI: 21 Q. Now, Dr. Garabrant, you state in your report that this 22 study, the authors found there's no evidence of 23 increased lung cancer risk in the communities exposed 24 to the smelter's arsenic emissions. Now, is this an 25 arsenic smelter in the United States? 144 1 A. Yes. 2 Q. Now, that statement in your report is that there is 3 evidence of increased lung cancer risk is that your 4 opinion of what the study showed or was that the 5 author's conclusion? 6 A. Well, that's taken from the paper, from the authors. 7 Q. Could you show me where they've specified there was no 8 evidence of increased lung cancer risks? 9 A. Yes, on page 150, left hand column, first paragraph 10 under results. 11 Q. Sorry? 12 A. Okay. 13 Q. Page 150, sir. 14 A. Page 150, right-hand column. 15 Q. Yeah. 16 A. Down near the bottom, under results, reading that 17 first paragraph starting at the second sentence, in 18 neither the Rustin area nor the remainder of Tacoma 19 did the total number of observed deaths exceed the 20 expected. The relative risks for lung cancer given 21 residence in the Rustin area is 0.82 and for the 22 remainder of Tacoma, it is 0.98. For the total Tacoma 23 Rustin area the relative risk is 0.94 with an upper 24 one-sided 95 percent confidence interval of 1.08. 25 Q. Can I stop you right there and ask a question? 145 1 A. Yes. 2 Q. All right. The relative risks are below 1.0, correct, 3 and that indicates a nonassociation? 4 A. It does not indicate a positive association, that's 5 correct. 6 Q. My question is because the 95 percent confidence 7 interval includes the value of 1.0, doesn't that 8 indicate to you these results are not statistically 9 significant? 10 A. That's correct. 11 Q. So that, in your opinion, a clear finding of no 12 increased risk? 13 A. That's a finding that there is not evidence of 14 increased risk. 15 Q. Okay, would you please go to the next paragraph keep 16 reading that where you left off. 17 A. Okay. In residual Pierce County, lung cancer rates 18 were significantly below expected, P less than .01. 19 since residual Pierce County was primarily rural 20 during this time period and since lung cancer rates in 21 rural areas tend to be lower than in urban areas, the 22 deficit of lung cancers in residual Pierce County is 23 not surprising. 24 Q. Okay, let me stop you right there. When you -- you 25 might want to I don't know if you recall this from 146 1 when you first reviewed this study, now, Pierce County 2 was one of the portions -- one of the areas they 3 studied that was the county with the lowest exposure 4 anticipated, correct? 5 A. I have to look back and review the methods here. 6 Q. Are you ready to continue are Dr. Garabrant? 7 A. Yes, go ahead, what was your question? 8 Q. This county, this particular area where they found 9 significantly lower lung cancer rates, that was an 10 area from 6 to 40 miles outside away from the smelter 11 plant, wasn't it? 12 A. Yes. 13 Q. It was a pretty large area of low exposure. Is that 14 what you're relying upon to say there's no increased 15 risks near a smelter? This includes people 40 miles 16 away. 17 A. No, no, I'm relying on the results from the two areas 18 close to the smelter from Tacoma and Rustin. 19 Q. Okay, but those are not statistical significant. Is 20 that the fact that those results were not 21 statistically significant that doesn't affect your 22 opinion as to whether those are adequate results or an 23 adequate representation of what might be the true 24 state of the situation of the population? 25 MR. DANNINGER: Object to form. 147 1 A. It's difficult to interpret your question. 2 BY MS. SLEVINSKI: 3 Q. Okay. 4 A. There was no evidence of increased risk of lung cancer 5 in the two areas closest to the smelter, period. 6 There was just no evidence. I'm not sure what your 7 understanding of statistical significance is. The 8 point is they were not significantly elevated. In 9 fact, they were slightly below one entirely consistent 10 with there being no association between exposure to 11 that arsenic smelter and increased risk of lung 12 cancer. 13 Q. So generally speaking, you don't find statistical 14 significance as an important factor in determining 15 whether the results of a study are an adequate 16 representation of what might be the true association 17 between the disease and the agent in the population? 18 MR. DANNINGER: Object to form. 19 A. I have no idea what your question was. Part of it has 20 a premise that I don't rely on statistical 21 significance. I've certainly do rely on statistical 22 significance or much more appropriate measures of the 23 role of chance which are confidence intervals, I rely 24 on them considerably. I always take them into 25 consideration. The rest of your question, I don't 148 1 understand. 2 BY MS. SLEVINSKI: 3 Q. Okay, well, then, how -- what effects does a 4 competent -- you said you rely on confidence levels. 5 Here, in this particular situation, it's not 6 statistically significant. I -- I don't see how, you 7 know, that -- I'm trying to understand how you 8 interpret studies that have results that are not 9 statistically significant and use those to support a 10 certain position because -- I want you to explain how 11 you rely on statistical significance. 12 A. Well, I rely on statistical significance in the 13 following way: When you use the term statistical 14 significance in the scientific community, that 15 customarily means that you have calculated a P value. 16 The P value is a -- represents the probability that 17 you could have gotten the data you obtained by chance 18 alone when there is no true association between the 19 factors under study. Okay? And I routinely look at P 20 values and rely on them. When the P value is greater 21 than .05, it is customary in the scientific community 22 to conclude that there is a reasonable chance that you 23 could have gotten the data that you got by chance 24 alone when there is, in fact, no true association 25 between the exposure and the outcome under study. 149 1 Okay. 2 Confidence intervals indicate something 3 different than P values. Confidence intervals tell 4 you the range within which the measure of association 5 is likely to fall 95 percent of the time if you were 6 to repeat the exact same study over and over and over 7 again a very large number of times or an infinite 8 number of times, so it gives you a sense for the role 9 of chance and how it might cause the measure of 10 association to vary under the assumption that the data 11 you got was, in fact, an estimate of the true 12 association and that it varied from the truth only 13 because of random error in the data? 14 Q. Okay, are you finished? 15 A. Yes. 16 Q. Okay. Back to your report, you said that there was no 17 evidence of increased lung cancer and we've just gone 18 through the numbers that you relied upon in making 19 that opinion. If we turn to the last page of this 20 article -21 A. Yes. 22 Q. -- the final paragraph -23 MR. DANNINGER: Are you still there, 24 Amanda? 25 VIDEO TECHNICIAN: You want to go off the 150 1 record? We're going off the record. The time is 2 10:50 and 22 seconds a.m. 3 (Recess taken at 10:50 a.m.) 4 (Back on the record at 11:01 a.m.) 5 VIDEO TECHNICIAN: We are now back on the 6 record. The time is 11:01 and 15 seconds a.m. 7 BY MS. SLEVINSKI: 8 Q. Dr. Garabrant, before the break, we were discussing 9 Exhibit No. 50, it was a study on lung cancer among 10 women near an arsenic emitting smelter. If you go 11 back to the final page once again, this study-- the 12 author said we produced mix results. What does that 13 mean in your opinion, a study that produces mixed 14 results? 15 MR. DANNINGER: Object to form. 16 A. Well, that phrase, mixed results, is so vague, I -- I 17 can't interpret it without putting some context around 18 that. 19 BY MS. SLEVINSKI: 20 Q. Okay, well, on page 151 of Exhibit 50 under discussion 21 the first sentence says the findings of this study 22 appear to be mixed. It goes on to say about an 23 elevated incidence of lung cancer was not -24 COURT REPORTER: Slow down. 25 BY MS. SLEVINSKI: 151 1 Q. An elevated incidence of lung cancer was not detected 2 in comparing observed with expected lung cancer rates. 3 However, the arsenic exposure indices were higher in 4 cases than in age-matched controls. The difference is 5 not significant at the .05 level. Several factors 6 could explain mixed results and the inability of the 7 study to detect an effect of arsenic exposure on lung 8 cancer incidence. 9 Did I read that correctly? 10 A. Yes. 11 Q. What does the fact that this had mixed results in an 12 overall inability to detect any effect of arsenic 13 exposure on lung cancer, how does that factor into 14 your decision that this was an appropriate study to 15 cite here? 16 A. Okay, well, as I said earlier in this deposition, we 17 don't judge the reliability of a study based on the 18 findings, okay? That's circular reasoning and so 19 that's not an appropriate way to figure out if a study 20 is reliable. We judge the reliability of the study by 21 reading the methods by which the study was done, and I 22 think this is a reliably done study. 23 Q. Okay, well, the fact that -24 A. I hadn't -- I hadn't finished. 25 Q. Sorry. 152 1 A. Okay. What this study shows is that when the 2 population that lived closest to the copper smelter 3 and the arsenic processing facility was compared to 4 the general population of the United States, there was 5 no excess of lung cancer in the population that lived 6 closest to the facility and which -- and which was 7 believed to have been exposed to arsenic from that 8 facility. 9 The study then goes on to do a case control 10 analysis within the population and that study found no 11 significantly increased relative risk of lung cancer, 12 and so the -- the author stated that the arsenic 13 exposure indices were higher in cases than in matched 14 controls but the difference was not significant at the 15 .05 level, so what we have here is a study that fails 16 to find statistically significant evidence of an 17 association between arsenic exposure in a community 18 near a smelter and arsenic refining facility and risk 19 of lung cancer. 20 Q. Are you finished? 21 A. Yes. 22 Q. Okay. So you said you judge the reliability of a 23 study on its methods, not on the actual results. 24 Would methods include by study design, how they 25 designed the study and actually carried out the study? 153 1 A. Yes. 2 Q. So here, it says the study is unable to detect an 3 affective arsenic exposure on lung cancer incidents 4 wouldn't that go to the reliability of the study as 5 designed is unable to detect arsenic effect on lung 6 cancer incidence? 7 A. No, no, no. No. 8 Q. Would you please explain then for me what that means 9 the inability of the study to detect and effective 10 arsenic exposure on lung cancer incidents? 11 A. It means the study didn't find it, it doesn't mean 12 there's anything wrong with the study. It says we 13 were unable to find that there was anything there. 14 The authors aren't implying that their work is 15 unreliable, they're saying we couldn't find anything. 16 Q. You couldn't find anything? 17 A. Right. 18 MR. DANNINGER: Object to form. 19 A. We were unable to find evidence of increased risk. 20 BY MS. SLEVINSKI: 21 Q. The -22 A. Their -- they're not commenting that their study is 23 improperly or unreliably done, they're commenting that 24 they didn't find reliable, in other words 25 statistically reliable evidence of increased risk. 154 1 Q. The last paragraph of the article says by the 2 limitations, the study argued against large excess 3 lung cancer risks for communities exposed to ambient 4 arsenic. The results may be consistent with a small 5 elevated lung cancer risk for people who resided close 6 to the smelter for a period of over 20 years. 7 Now, does that -- did I read that 8 correctly, first of all? 9 A. Yes, you did. 10 Q. Does that say there is no risk of lung cancer in the 11 community near the arsenic emitting plant? 12 A. No, it says what it says. Let me try and explain 13 what -- what these authors are -- are saying because 14 this is how epidemiologists typically and correctly 15 phrase their findings. We talked about confidence 16 intervals a few minutes ago. Okay, so let's say just 17 hypothetically we have a study that shows a 1.1 fold 18 association between exposure and lung cancer risks 19 with a confidence interval that goes from, let's say, 20 9 to 1.35. okay. How -- how would an epidemiologist 21 interpret those results? 22 Well, the 1.1 says the data we collected, 23 the data we observed shows a weak positive association 24 between exposure and lung cancer. However, the 25 confidence interval tells us that the data are 155 1 reasonably compatible with that -- the true 2 association being somewhere between .9 and 1.35, 3 values below .9 are really not compatible with the 4 data we got, values above 1.35 are really not 5 compatible with the data we got, values in between are 6 reasonably compatible. 7 What we conclude from that is that the true 8 association is likely to lie in the range of .9 to 9 1.35 with the most likely estimate being 1.1 which is 10 exactly what we observed. Okay. So that means that 11 it is possible there's no association, it's also 12 possible that there is a weak positive association and 13 of course our best estimate is a 1.1 fold association. 14 It's not a statistically significant finding because 15 it's reasonably possible or reasonably likely that the 16 true association is really 1.0, meaning no 17 association. 18 That's the way epidemiologists typically 19 phrase their results. That's exactly what Frost and 20 his colleagues are saying in this last paragraph. In 21 other words, the study argues against large excess 22 lung cancer risks. In other words, the confidence 23 limits on their measures of relative risk tell us that 24 it's very unlikely that there are large excess risks, 25 there could be small ones, okay? And the next 156 1 sentence says exactly that. These -- the results may 2 be consistent with a small elevated lung cancer risk 3 for people who resided close to the smelter for the 4 period of over 20 years, in other words, a small 5 elevated risk is within the 95 percent confidence 6 interval, that's possible. However, no association is 7 also possible. That's really what they're saying. 8 Q. Have you spoken with the authors, with Dr. Frost at 9 all about this, about what they were saying? 10 A. No, I haven't spoken with Dr. Frost. I'm -- I'm an 11 epidemiologist, and this is what -- this is the way 12 epidemiologists interpret relative risks and 13 confidence intervals. 14 Q. Well, is that the way you interpret these results, 15 these confidence intervals, relative risks? 16 A. Well, that's the way I interpret them based on 35 or 17 36 years of experience as a practicing occupational 18 environmental epidemiologist who does studies similar 19 to this, calculates relative risks and confidence 20 intervals, and publishes papers interpreting them, and 21 I believe my views are entirely consistent with 22 textbooks in epidemiology that use very similar 23 terminology and very similar understanding of relative 24 risks, P values, and confidence intervals. 25 Q. Do you speak for all epidemiologists? 157 1 A. I don't speak for all epidemiologists, I speak for the 2 mainstream of epidemiologists who understand these 3 concepts and-- largely agree to what they mean. 4 Q. You speak for yourself direct though Dr. Garabrant 5 yourself as an epidemiologist? 6 A. Well, if you would like, I would refer you to Rothman 7 and Greenland's textbook titled Modern Epidemiology. 8 I would refer you to Clayton and Hill's Statistical 9 Methods In Epidemiology. I would refer you to Charles 10 Hennekens' and Julie Buring's textbook, Clinical 11 Epidemiology. I'd refer you to Ross Brownson's 12 textbook on epidemiology, I would refer you to two 13 IARC publications, one on statistical methods in 14 cohort studies written by Nicholas Day and Norm 15 Breslow, the other being Statistical Methods In Case 16 Control Studies, also written by Breslow and Day. I 17 could easily put together ten textbooks that would 18 concur in exactly what I just told you. 19 MS. SLEVINSKI: I'm going to object and 20 move to strike. That is nonresponsive. Could I have 21 my question read back to Dr. Garabrant? 22 MR. DANNINGER: Dr. Garabrant's question 23 (sic) was completely responsive. He's serving as an 24 expert in this case and he's giving the basis for his 25 opinions and his response as an expert in the field of 158 1 epidemiology. 2 COURT REPORTER: Hold on one second while I 3 go back to the question, please. 4 (The requested portion of the record was 5 read by the reporter at 11:15 a.m.) 6 MR. DANNINGER: Are you still there, 7 Amanda? 8 MS. SLEVINSKI: I am. I'm sorry, I don't 9 know what the feedback is. Hello? 10 MR. DANNINGER: Yeah, we're still here. 11 MS. SLEVINSKI: Okay. 12 MR. DANNINGER: It sounds like it's -- it's 13 kind of going in and out. We'll let you know if we 14 don't understand something you ask. 15 MS. SLEVINSKI: Okay. 16 MR. DANNINGER: Did you want the doctor to 17 respond to the question that was read back by the 18 reporter? 19 MS. SLEVINSKI: Yes, I would like a 20 response. 21 MR. DANNINGER: Okay, and I'll object that 22 it's been asked and answered, but go ahead, Doctor. 23 A. I've already answered that question, Ms. Slevinski. I 24 don't speak for all epidemiologists. I speak for the 25 mainstream of epidemiologists, and I believe that I am 159 1 correctly stating what is widely accepted among 2 epidemiologists as the correct way to interpret P 3 values, relative risks, and confidence intervals. 4 BY MS. SLEVINSKI: 5 Q. All right. We'll go ahead and move on. The 6 conclusion of this first opinion in your report, you 7 state that Dr. Werntz's conclusion appear to be based 8 upon incomplete consideration of design literature, 9 selective review of favorable articles, and occasional 10 mischaracterizations of their contents. Did you in 11 your preparation for your report completely consider 12 all the available scientific literature? 13 MR. DANNINGER: Object to form. 14 A. Well, I -- completely considered a far larger body of 15 literature than Dr. Werntz did, and I considered 16 everything I could find. It is possible there are 17 additional studies that I was unable to find, but I 18 had certainly did a far more thorough job than 19 Dr. Werntz. 20 BY MS. SLEVINSKI: 21 Q. Did you do a more thorough job than Dr. Werntz or your 22 research assistant did a more thorough job than 23 Dr. Werntz? 24 MR. DANNINGER: Object to form, that's 25 argumentative. 160 1 A. I did a far more thorough job than Dr. Werntz. 2 BY MS. SLEVINSKI: 3 Q. You say that Dr. Werntz occasionally mischaracterized 4 the contents of the literature. And by 5 mischaracterization, do you mean that Dr. Werntz 6 interpreted or reached a different opinion on the 7 matter as you -- as opposed to you or that he asserted 8 something that was not in fact in that study? 9 A. He asserted something that was wrong. He said, and 10 this is a quote, there have been several studies 11 documenting increased cancer risk around smelter sites 12 where similar exposures have occurred, and he 13 references the Brown, the Pershagen, the Bartlesville, 14 the Tokudome studies. As we've discussed, the 15 Tokudome study was not a study around a smelter site 16 and in none of those studies does he have any basis 17 for saying that similar exposures have occurred. 18 Q. So you -19 A. I think that's a mischaracterization of the contents 20 of those studies. 21 Q. So you disagree with the way he interpreted the 22 studies or your opinion he mischaracterized the 23 results of these studies? 24 MR. DANNINGER: Objection, asked and 25 answered. 161 1 A. I've already answered that question. He 2 mischaracterized what those studies were about, and he 3 made statements that were factually incorrect. 4 MS. SLEVINSKI: Are you hearing a little 5 bit of the crackling? It might be just from past 6 experience, it might be a Blackberry. Mine's not on 7 in here so I don't -- I'm not sure if someone else has 8 one or... 9 MR. DANNINGER: Yeah -- all -- all the 10 Blackberrys here are away from the table. 11 MS. SLEVINSKI: Okay, well, I -12 MR. DANNINGER: Yeah, we'll -- we'll watch 13 out for it. 14 MS. SLEVINSKI: But that might be a reason 15 for the crackling. Sorry for the interpretation. 16 MR. DANNINGER: No, that's all right. 17 Thank you for the insight. 18 BY MS. SLEVINSKI: 19 Q. Dr. Garabrant, that's -- spoke -- I wanted to discuss 20 with you so far about your first opinion in your 21 report. Are there any other materials like the ones 22 you've referenced here section in relying upon in 23 stating your opinions? 24 A. To the extent I am aware of it, I cited the materials 25 I rely upon in my report. 162 1 Q. And the reasons set out in your report formed the 2 entirety of your opinion on this particular issue; is 3 that correct? 4 A. I don't understand that question. I don't know what 5 you mean by the reasons set out. Forgive me. 6 Q. Well, your explanation in the narrative portion that 7 we just spent a couple hours going through, are those 8 the reasons and support and basis for your entire 9 opinions, No. 1, the first opinion we went through, 10 the studies Dr. Werntz relied upon were not reliable. 11 A. Well, my -- my overall opinion No. -- opinion 1, is 12 that Dr. Werntz does not have a reliable basis for 13 claiming increased cancer risks around smelter sites. 14 The basis that he cites for his opinion is those four 15 studies we just discussed, Brown, Pershagen and 16 Bartlesville and Tokudome, so he does not have a basis 17 in his report for claiming increased cancer risk. 18 I would have to add to what I've written 19 here is that it is my understanding that there is not 20 reliable evidence of exposure to arsenic, lead or 21 cadmium in the Spelter -- in the community around the 22 smelter site that would put people at any -- any 23 meaningfully increased risk of any type of cancer. 24 Q. Okay, so are there any other reasons for your first 25 opinion that we haven't already discussed or is not 163 1 included in your report? 2 A. Yes, my understanding of the expert opinions by Dr. 3 Rodericks', Dr. Valberg's, and by the scientists at 4 Gradient who wrote a report that I -- that we 5 discussed yesterday. 6 Q. How are you relying on all those reports that are 7 listed the different defense expert... 8 A. I'm relying on them because they give a thorough and 9 rigorous appraisal of plaintiff's evidence regarding 10 exposure to arsenic, lead and cadmium in the community 11 and they show that plaintiff's evidence is not 12 reliable. 13 Q. Well, you mentioned Dr. Valberg, volume bearing, you 14 said yesterday you viewed his report after you wrote 15 your report in this case. Is that correct? 16 A. I believe that's correct. 17 Q. Nevertheless you're relying upon Dr. Valberg's report 18 in forming your opinions on this report? 19 A. Well, I'm relying on Dr. Valberg's report in forming 20 my opinions that I'm giving you here today. 21 MR. DANNINGER: Hay, Amanda, with that 22 crackling? 23 MS. SLEVINSKI: Yes. 24 MR. DANNINGER: Just to let you know, 25 nobody's touched anything in this room, and it's come 164 1 back, so I don't know if it might be where you are or 2 where Clayton is. 3 MS. SLEVINSKI: Okay, I'm not sure. If it 4 gets extremely interruptive, we'll figure something 5 out. 6 MR. DANNINGER: Well, the videographer said 7 that it will come through on the DVD and that he's 8 hearing it in his headphones so just so you know. 9 MS. SLEVINSKI: All right. Well, Clayton, 10 if you're on -- oh, I'm sure you are, but if you have 11 a Blackberry on, maybe cut it off or take it further 12 away from the speakerphone. 13 MR. PATTERSON: Okay, I'm listening and I 14 have -15 MS. SLEVINSKI: Okay, well, if anyone has 16 their Blackberrys, please part with them and turn them 17 off and take them away, so we don't get too much 18 feedback on the video. 19 MR. DANNINGER: Good deal. 20 MS. SLEVINSKI: Thanks. 21 MR. DANNINGER: Thank you, Amanda. 22 BY MS. SLEVINSKI: 23 Q. Dr. Garabrant, the next opinions in your report, 24 No. 2, it says lead is not known to be carcinogenic, 25 and the medical monitoring proposed by Dr. Werntz 165 1 related to lead exposure has no scientific foundation. 2 Did I read that accurately? 3 A. Yes. 4 Q. And similarly, below which there's a narrative portion 5 is that where you set out your reasons for this 6 opinion? 7 A. Yes. 8 Q. And you also have set out the bases you relied upon in 9 forming this opinion and the materials upon which 10 you're relying; is that correct? 11 A. Yes. 12 Q. What degree or amount of evidence relating to 13 carcinogenicity of a particular agent would you 14 consider to be adequate to support a conclusion of 15 causation or carcinogenicity? 16 MR. DANNINGER: Amanda, can you just repeat 17 the first few words in there? I missed what you 18 asked, what degree was that? 19 MS. SLEVINSKI: Sorry. 20 BY MS. SLEVINSKI: 21 Q. What degree or how much evidence relating to the 22 carcinogenicity of a particular agent would you 23 consider to be adequate to support a conclusion that 24 that agent is, in fact, carcinogenic to humans? 25 MR. DANNINGER: Thank you, objection to 166 1 form. 2 A. Considerably more than there is for lead. 3 BY MS. SLEVINSKI: 4 Q. Okay. How much more? 5 A. Well, it's hard to quantify that. I think that Austin 6 Bradford Hill laid out a series of considerations that 7 give guidance on how to assess whether there's a 8 causal association between an environmental agent and 9 cancer risk and I follow those considerations. Lead 10 doesn't measure up, and I am not aware of any 11 scientific body that has concluded that lead is known 12 to cause cancer in humans. There are none to my 13 knowledge and I don't think Dr. Werntz found any, 14 either. 15 Q. Are you finished? I'm sorry. 16 A. Yes. 17 Q. So you've mentioned it yesterday, I assume you're 18 familiar with the IARC system of classifying agents 19 based upon their likelihood to cause cancer in humans; 20 are you familiar with that? 21 A. Yes. 22 Q. And is it correct that the IARC groups the agents 23 based on their carcinogenicity of groups 1 to 4, 1 24 being known carcinogens and 4 being probably not 25 carcinogenic; is that correct? 167 1 A. Yes. 2 Q. You mention in your report about the issue of the 3 carcinogenicity of lead that Dr. Werntz relied upon 4 the evaluation of the IARC for his opinion regarding 5 the carcinogenicity of lead. IARC indicates there's 6 limited evidence in humans for the carcinogenicity of 7 inorganic lead compounds. Hello? 8 A. Yes. 9 Q. Okay, sorry. The fact that IARC has classified 10 inorganic lead compounds in category 2-A means, by 11 definition, there is not sufficient evidence of 12 carcinogenicity of humans to classify lead as being a 13 human carcinogen. Group 2-A is classified as probable 14 human carcinogen, correct? 15 A. That's the definition. 16 MS. SLEVINSKI: Okay. Now, would you 17 please get Dr. Garabrant Exhibit No. 73? 18 MARKED BY THE REPORTER: 19 DEPOSITION EXHIBIT NUMBER 73 20 11:28 a.m. 21 MR. DANNINGER: Amanda, was this one that 22 we sent a supplemental larger one? I'm just not sure. 23 MS. SLEVINSKI: I'm not sure. 24 MR. DANNINGER: Okay, I don't think it was, 25 actually, for some reason. Sorry to interpret you. 168 1 MS. SLEVINSKI: That's okay. 2 BY MS. SLEVINSKI: 3 Q. Do you have the exhibit, Dr. Garabrant? 4 A. Yes, I do. 5 Q. Several pages into it, I have as page No. 22 at the 6 top, left-hand corner, that's where they discuss 7 the different conclusions of the chemicals; could you 8 turn to that page, please? 9 A. Yes. 10 Q. All right. Group 1, it says have used when there's 11 sufficient evidence of carcinogenicity in humans. 12 Does that mean they are known carcinogens? 13 A. It means there is sufficient evidence of 14 carcinogenicity in humans. 15 Q. Now, group 2 is divided into subcategories being 2A 16 and 2B, and that's based on different levels of 17 evidence of carcinogenicity; is that correct? 18 A. Yes. 19 Q. Now, the first paragraph under group 2, it says this 20 category includes agents for which at one extreme the 21 degree of evidence of carcinogenicity in humans is 22 almost sufficient as well as those for which at the 23 other extreme there are no human data but for which 24 there is evidence of cars in experiment... and it goes 25 on to describe on who to how this probably dried them 169 1 into carcinogen group 2-A or 2 P, probably 2 carcinogenic signifying a higher level of evidence 3 than possibly carcinogenic. Does that application 4 mean to you that there's -- that lead is not-- is not 5 a carcinogenic agent? 6 MR. DANNINGER: Object to form. 7 A. What that classification means is that the evidence is 8 not sufficient in humans to say that lead is 9 carcinogenic to humans. 10 BY MS. SLEVINSKI: 11 Q. It does say that it's almost sufficient in humans, 12 though, doesn't it? 13 A. No. 14 Q. It does not? 15 A. No. 16 Q. First sentence under group 2 says this category 17 includes agents for which at one extreme the degree of 18 evidence of carcinogenicity in humans is almost 19 sufficient. 20 A. Well -21 Q. That wouldn't -22 A. -- you're -- you're completely missing the boat, okay? 23 If you go to the IARC monograph, volume 87 on 24 inorganic and organic lead compounds and you read the 25 evaluation, here's what it says. There is limited 170 1 evidence in humans for the carcinogenicity of 2 inorganic lead compounds. So it doesn't say almost 3 sufficient, it says limited. 4 Q. What are you reading from, Dr. Garabrant? 5 A. I'm reading from IARC monograph volume 87 titled 6 Inorganic And Organic Lead Compounds at page 377. 7 And I want to go on because what's directly 8 relevant to this Spelter litigation is the evidence 9 regarding different types of arsenic compounds, okay? 10 There is inadequate evidence in experimental animals 11 for the carcinogenicity of lead oxide and lead 12 arsenate. So we're in a situation where for the 13 compounds at issue, not only is there limited evidence 14 in humans, there's inadequate evidence in animals. 15 Okay? That is clearly woefully inadequate to say that 16 these compounds pose a cancer risk to humans. I 17 should add to that on page 378 of that IARC monograph 18 there is inadequate evidence in experimental animals 19 for the carcinogenicity of lead powder and so the 20 forms of arsenic that are at issue in this litigation 21 are ones where there is not even adequate evidence in 22 animals, much less adequate evidence in humans, there 23 is neither. 24 Q. Does the word probably carcinogenic, probably does 25 that carry with it more weight than possibly 171 1 carcinogenic? 2 MR. DANNINGER: I just want to clarify, I 3 believe the doctor might have misspoke and said 4 arsenic instead of lead when we were speaking. 5 THE WITNESS: Oh, what -- I'm sorry. What 6 did I say? 7 MR. DANNINGER: I think you might have said 8 arsenic. 9 THE WITNESS: Everything I was talking 10 about was about lead, not about arsenic. My apologies 11 if I misspoke. 12 MR. DANNINGER: It could have been that I 13 misheard you say arsenate. 14 THE WITNESS: Well, I said lead arsenate, 15 but the rest of it was all about lead oxide and lead 16 powder for which the animal evidence is inadequate 17 regarding carcinogenicity of those compounds. 18 BY MS. SLEVINSKI: 19 Q. Regardless of that, IARC still classifies lead as a 20 group 2 probable human carcinogen, yes or no? 21 A. Well, group 2 -22 Q. Say -23 A. -- includes agents for which at one extreme the degree 24 of evidence is almost sufficient as well as at the 25 other extreme, there's no human data but which there's 172 1 evidence of carcinogenicity in experimental animals, 2 what I'm trying to point out is that for the lead 3 compounds at issue in this case, it doesn't satisfy 4 even that extreme where there is no human data but 5 there is evidence of carcinogenicity in experimental 6 animals. IARC's decision regarding classification of 7 inorganic lead appears to be driven largely by the 8 evidence in experimental animals for lead acetate, 9 lubs -- lead subacetate, lead chromate, and lead 10 phosphate, not the chemicals at issue in this case. 11 And so you're reliance on the IARC 12 classification for lead compounds does not take into 13 account and does not properly consider the difference 14 in carcinogenicity or the difference in evidence of 15 carcinogenicity for different lead compounds. The 16 compounds at issue do not show adequate evidence even 17 in animals to say that they are carcinogenic in 18 animals, and there is not adequate evidence in humans 19 to say that they are human carcinogens, either. 20 Q. Inorganic lead is at issue in this current case; isn't 21 it Dr. Garabrant? 22 A. Yes, it is. 23 MS. SLEVINSKI: Could I ask you to please 24 give Dr. Garabrant Exhibit 72? 25 MARKED BY THE REPORTER: 173 1 DEPOSITION EXHIBIT NUMBER 72 2 11:36 a.m. 3 COURT REPORTER: Okay. 4 BY MS. SLEVINSKI: 5 Q. Dr. Garabrant, is this the same IARC inorganic lead 6 monograph you were reading from just now? 7 A. Yes. 8 Q. Okay, just making sure I have the same thing I dug out 9 of my box here. If you would turn to page -- I don't 10 have -- numbers on mine -- section 5.5, my version 11 doesn't have page numbers, I apologize. 12 A. Yeah, I'm at 5.5. this is the section from which I 13 was just reading. 14 Q. Where it says overall evaluation, inorganic lead 15 compounds are probably carcinogenic to humans group 16 2-A, is that what it reads? 17 A. Yes. 18 Q. Thank you. The report also addresses the way the EPA 19 classifies the carcinogenicity of lead and lead 20 compounds. You state that the EPA considers the 21 available human evidence to be inadequate to refute or 22 demonstrate any potential carcinogenicity for humans 23 for lead exposure. That's not the complete 24 description given by the EPA, is it, Dr. Garabrant? 25 A. Well, we'd have to pull that reference and look. I 174 1 don't recall from memory. 2 MS. SLEVINSKI: Would you please hand 3 Dr. Garabrant No. 46? 4 MARKED BY THE REPORTER: 5 DEPOSITION EXHIBIT NUMBER 46 6 11:38 a.m. 7 COURT REPORTER: Okay. 8 BY MS. SLEVINSKI: 9 Q. Page 5 of 11, Dr. Garabrant. 10 A. Yes. 11 Q. Would you identify what this document is before we get 12 that to that final page, please? 13 A. This is the EPA IRIS document titled Lead and 14 Compounds Inorganic, Cass Registration No. 7439-92-1. 15 Q. All right, and I misspoke it's page 6 of 11, please. 16 A. Okay. 17 Q. Is that the second paragraph from the top, is that 18 where you got the first -- the last sentence of the 19 second paragraph, is that where you got your quotation 20 in your report? 21 A. I believe it is. 22 Q. Would you read that complete sentence, please? 23 A. Yes. Thus, the available human evidence is considered 24 to be inadequate to refute or demonstrate any 25 potential carcinogenicity for humans from lead 175 1 exposure. 2 Q. Now this is classified by the EPA as probably 3 carcinogenic to humans, and when they say the evidence 4 is inadequate to refute or demonstrate, by refute or 5 demonstrate, that's not saying that it is not a 6 carcinogen, is it? 7 MR. DANNINGER: Foundation. 8 A. No, it says that the evidence is inadequate to 9 establish whether it is or is not. 10 BY MS. SLEVINSKI: 11 Q. So it's -- it's probably a human carcinogen? 12 A. No. No. That sentence says the human evidence is 13 inadequate to make any conclusion. Now, I would point 14 out that EPA is relying, as does IARC, on animal 15 evidence, and if you look at the animal evidence, 16 which is summarized on page 6 right below the 17 paragraph we were reading, you will see exactly what 18 they said. Okay? 19 Animal carcinogenicity data, sufficient. 20 The carcinogenic potential of lead salts, primarily 21 phosphates and acetates, administered via the oral 22 root or by injection has been demonstrated in rats and 23 mice by more than ten investigators. We're not 24 talking about the chemicals at issue in Spelter. The 25 chemicals at issue in Spelter are oxides. Okay? So 176 1 acetates and phosphates are not what we're talking 2 about. So while those lead compounds may be 3 carcinogenic in animals, what we've already discussed 4 is that the compounds at issue here are not known to 5 be carcinogenic in animals or in humans. 6 Q. The fact remains though that the EPA and IARC both 7 consider lead to be a probable human carcinogen, do 8 you disagree with that classification? 9 MR. DANNINGER: Object to form. 10 A. To the extent that IARC and EPA have to make 11 classifications for broad categories of compounds, I 12 do not disagree with it. But when you come to an 13 issue that is pointed and important such as in Spelter 14 where we're talking about oxides, then you have to 15 look back at the original evidence. 16 The original evidence is quite clear. Lead 17 oxides are not known to be carcinogenic in animals and 18 they are not known to be carcinogenic in humans, so 19 it's not appropriate to rely on an umbrella 20 designation when you actually are talking about 21 specific compounds, you should talk about the evidence 22 for those specific compounds. 23 Q. Are lead oxides inorganic lead compounds? 24 A. They are. And what we see in both the IARC and the 25 EPA documents is that the evidence is dramatically 177 1 different for different forms of inorganic lead 2 compounds. 3 Q. Your report you go on to discuss that you say that 4 unknown still whether people exposed to lead are at 5 increased risk of cancer, consequently there's no 6 justification for medical monitoring for lung cancer, 7 stomach cancer, kidney cancer or any other cancer 8 Dr. Werntz alleges is related to lead. 9 Is it your opinion that medical monitoring 10 is not justified in this situation, or would it never 11 be justified in a situation where lead was alleged to 12 be causing cancer? 13 A. Well, it's my opinion that Dr. Werntz's medical 14 monitoring program has absolutely no scientific 15 foundation with respect to lead. He wants to monitor 16 for cancers that are not known to be caused by lead, 17 that's nonsense. 18 Q. In your opinion, are any cancers caused by lead? 19 A. There is not adequate human evidence to reach a 20 conclusion that cancer is caused by lead in humans. 21 Q. What's the next page of your report, page 5? 22 A. The first paragraph, you are -- you have several a 23 whole string of studies listed and you say that these 24 studies failed to show consistent excessive any cancer 25 site failed to show evidence of those response and are 178 1 potentially compounded by other concurrent exposures. 2 What -- are those all evidence of, you know, each one 3 of those things you listed excessive failed he to show 4 excess cancer sites failed to show evidence of dose 5 response or are they divided up somehow to represent 6 different aspects of that statement. 7 MR. DANNINGER: Form. 8 A. Well, what I'm really alluding to is the Austin 9 Bradford Hill considerations. I'm pointing out that 10 the body of evidence regarding cancer risks in 11 relation to lead exposure do not show associations in 12 any consistent pattern. Austin Bradford Hill would 13 tell us that you have to have evidence of association 14 and that strong associations are less likely to be due 15 to bias and confounding than are weak associations. 16 Here we don't even have consistent evidence of 17 associations. I'm pointing out that we don't see dose 18 response. 19 Austin Bradford Hill says there ought to 20 be, as he calls it, biological gradient. People who 21 have greater exposure should have higher risks of 22 cancer than those at low exposure. We don't see that 23 in the lead literature. Austin Bradford Hill points 24 out that before we accept the studies as showing 25 associations, we -- we must evaluate whether the 179 1 authors have adequately considered confounding and 2 bias as possible explanations for those associations. 3 I'm pointing out that in some of the published studies 4 of lead exposure, there were other exposures such as 5 to arsenic that could have confounded those 6 associations. 7 MR. DANNINGER: Amanda, just so you know, 8 we have about five minutes left on the videographer's 9 tape so just take that into consideration. 10 MS. SLEVINSKI: Okay. 11 BY MS. SLEVINSKI: 12 Q. Dr. Garabrant -- free (ph.) that not all factors -13 all the Bradford Hill factors are required as present 14 to prove causation, do they? 15 MR. DANNINGER: I think we might have 16 missed the beginning of that because the noise is 17 back, and nobody's doing anything here. So we're -18 it's really bad this time. 19 MS. SLEVINSKI: Yeah, it's pretty loud. 20 Let me -21 MR. DANNINGER: We missed that. 22 MS. SLEVINSKI: It's not coming from -23 we've got -- working on it. Why don't we go ahead and 24 change the tape. Maybe y'all make sure -25 MR. DANNINGER: Well, we're going to dial 180 1 back in. Why don't you and Clayton also dial back in 2 so that we can -3 MS. SLEVINSKI: Again. 4 MR. DANNINGER: -- try having a new -- a 5 new line. 6 MS. SLEVINSKI: A ten-minute -- ten-minute 7 break and get this resolved, okay. 8 MR. DANNINGER: Let's all dial back in. 9 MR. WICKLINE: Hey, Amanda? 10 VIDEO TECHNICIAN: Okay, we're -- going off 11 the record? 12 MR. WICKLINE: Yes. 13 VIDEO TECHNICIAN: We're going off the 14 record. The time is 11:48 and seconds a.m. 15 (Recess taken at 11:48 a.m.) 16 (Back on the record at 12:36 p.m.) 17 VIDEO TECHNICIAN: We are now back on the 18 record. This is the beginning of tape No. 3, the time 19 is 12:36 and 42 seconds p.m. 20 BY MS. SLEVINSKI: 21 Q. Dr. Garabrant, before lunch, we had started to get 22 into your second opinion regarding lead not being 23 known to be carcinogenic and the medical monitoring 24 proposed by Dr. Werntz related to lead exposure has no 25 scientific foundation. 181 1 On page 5 of your report at the top, we had 2 started to briefly touch on that page that you have 3 cited there. I'd like to go through those and I've 4 got some questions to ask on a couple of those. 5 MS. SLEVINSKI: So if the court reporter 6 could please hand Dr. Garabrant Exhibit No. 2. 7 COURT REPORTER: Okay. 8 MARKED BY THE REPORTER: 9 DEPOSITION EXHIBIT NUMBER 2 10 12:38 p.m. 11 BY MS. SLEVINSKI: 12 Q. Dr. Garabrant, this particular study, the nervous 13 system cancer among workers exposed to lead, do you 14 recognize this as one of the studies you, in fact, 15 cited in this paragraph that we're discussing? 16 A. Yes. 17 Q. What did you cite this particular article as the 18 basis, what how does this support your opinion, this 19 particular article? 20 A. Well, what we saw when we looked at the IARC material 21 a few minutes ago and also the EPA material a few 22 minutes ago was that some lead compounds and I think 23 it was lead acetate and subacetate were associated 24 with increased risk of brain tumors in rats and that 25 that was part of the basis for the decision that lead 182 1 compounds show some carcinogenicity in animals, and I 2 wanted to point out that in humans, we don't see 3 evidence of brain cancer, so the human evidence is 4 different than the animal evidence. 5 Q. So with this particular study, if you're looking at 6 the front page of the italicized abstract the final 7 sentence or the second to last sentence states the 8 results suggest that there may be an association 9 between occupational lead exposure and the risk of 10 gliomas; is that correct? 11 MR. DANNINGER: Form objection. 12 A. I'm sorry, I wasn't following exactly where you were 13 reading. Would you show me? 14 BY MS. SLEVINSKI: 15 Q. Okay, it's the abstract, the italicized abstract it's 16 the second to last sentence? 17 A. Yes. Okay. Go ahead. 18 Q. And gliomas, those are -- is that a brain tumor? 19 A. Yes. 20 Q. And this would have been a study focusing on human 21 beings being exposed to lead in the workplace? 22 A. That's correct. 23 Q. So I'm not following how this does not -- how this 24 supports your position that there's not evidence in 25 humans of increased risk of cancer from lead. 183 1 A. Well, the sentence you read is followed by a sentence 2 that says no firm conclusions can be drawn because of 3 the small number of cases and loss of material. 4 One of the themes that is important for you 5 to recognize in my report and in my testimony is that 6 I don't pick and choose, the studies that go my way, I 7 report them all, and so whereas my criticism of Dr. 8 Werntz is that he picks and chooses only the favorable 9 studies, I try to do a thorough review of the 10 literature and I include studies that show 11 associations between exposure and cancer risks as well 12 as those that do not, and I try to summarize them 13 fairly, and so here's a study that suggests an 14 association. It's not very strong and the authors, 15 themselves, say no firm conclusion can be drawn. 16 Q. And just to clarify, we are -- we are not worried 17 about any sort of brain tumors in this particular 18 case, are we, that's not at issue? 19 A. Well -20 MR. DANNINGER: Foundation. 21 A. -- to the extent I'm aware of it, your expert, 22 Dr. Werntz, has not claimed that the people in the 23 Spelter area or the class area are at increased risk 24 of brain cancer. However, Dr. Werntz is relying on 25 the IARC and EPA classification for his opinion that 184 1 lead is a carcinogen, and as I pointed out, much of 2 that evidence comes from lead compounds that are not 3 at issue in this case, and one of the results of the 4 animal studies relates to brain cancer, so I felt that 5 I had to deal with that issue, we were talking about 6 compounds that aren't at issue and we're talking about 7 a tumor that's not at issue and that's what Dr. Werntz 8 is basing his opinions on. 9 BY MS. SLEVINSKI: 10 Q. All right. You also described -- well, cited a 11 discussion of studies, No. 36, 35, and 37. 12 MS. SLEVINSKI: Would you please hand those 13 three to Dr. Garabrant, and we'll talk about those 14 briefly? 15 MARKED BY THE REPORTER: 16 DEPOSITION EXHIBITS NUMBERED 35-37 17 12:43 p.m. 18 COURT REPORTER: Okay they have them. 19 MS. SLEVINSKI: Great, thanks. 20 BY MS. SLEVINSKI: 21 Q. Dr. Garabrant, just so I'm clear, these three studies 22 were conducted by several different researchers but 23 the main one on each one were the Clark -- W. Clark 24 Cooper, and they, No. 36, Exhibit No. 36, from what I 25 understand, is actually the initial study that he did; 185 1 can you confirm that for me? 2 A. No. 36 is the first publication of those three to the 3 extent I'm aware, it was the initial report. 4 Q. Okay, that's what I'm just making sure. And then No. 5 35 would actually be the second -- well, the next one 6 in that succession, correct? 7 A. Yes. 8 MR. DANNINGER: Foundation. 9 BY MS. SLEVINSKI: 10 Q. And then Exhibit 37 is the file in the succession as 11 there -- as you have them cited in your reports, do I 12 have that clear? 13 A. I believe that's correct. 14 Q. Okay. Now, what -- did you consider these like 15 altogether their results or the fact that they were, 16 you mow, a study and then several follow-up studies, 17 how did that of an effect your opinion, in the section 18 of your report? 19 MR. DANNINGER: Form objection. 20 A. I -- I'm not sure what you're asking. The 1985 21 publication in the Scandinavian Journal of Work, 22 Environment and Health, Exhibit 37, I believe, is the 23 most recent one. 24 BY MS. SLEVINSKI: 25 Q. Well, then focusing on No. 37, the most recent, would 186 1 you explain to me how this particular article factored 2 into your opinion? 3 A. Well, I considered it with all of the other literature 4 on lead in forming my opinion about cancer risks 5 related to lead exposure. 6 Q. Did you consider the results of these three as they 7 progressed starting from the first one to the second 8 to the third, or did you only look at, for example, 9 No. -- Exhibit No. 37, the final study? 10 MR. DANNINGER: Can you repeat that for my 11 edification, Amanda? 12 MS. SLEVINSKI: Well, could you just have 13 it read back, please? 14 (The requested portion of the record was 15 read by the reporter at 12:47 p.m.) 16 A. I considered all three of them. 17 BY MS. SLEVINSKI: 18 Q. Do you believe that these studies either separately or 19 when considered together show an excess risk of cancer 20 associated with lead exposure? 21 A. Well, I think that the third study, the one in the 22 Scandinavian Journal, is based on a larger number of 23 person years at risk, and gives somewhat more stable 24 findings than the earlier two publications, and this 25 study provides some evidence of increased cancer risks 187 1 among men employed in lead battery plants for at least 2 a year back in the 1940s, up through the 1960s. 3 Q. And among some of the cancer sites that they examined, 4 stomach cancer, as well as lung cancer were cited as 5 possible for having contributed to excess in cancer 6 mortality; is that correct? 7 A. That's correct. 8 MS. SLEVINSKI: Could you please hand 9 Dr. Garabrant 39? 10 MARKED BY THE REPORTER: 11 DEPOSITION EXHIBIT NUMBER 39 12 12:49 p.m. 13 COURT REPORTER: Okay. 14 BY MS. SLEVINSKI: 15 Q. Dr. Garabrant, Exhibit No. 39, mortality among 16 firefighters extreme northwestern United States cities 17 was also cited in the section where you're adding the 18 carcinogenicity of lead in humans. Could you tell me 19 how this particular article addressed the issue of 20 carcinogenicity of lead in human beings? 21 A. That article should not have been on my reference 22 list. I think I pulled in the wrong citation number. 23 I don't think this one has anything to do with lead. 24 I apologize, I -- must have written the wrong number 25 down when I prepared my bibliography. 188 1 Q. Okay, well just to confirm, this article, in fact, 2 does not address any sort of effects from lead on -3 in its cancer capabilities in people, correct? 4 A. To the best of my knowledge, that's correct and I 5 apologize for having it listed it on my bibliography. 6 Q. Well, it wasn't just in the bibliography, it was 7 actually also in the body of your report. 8 A. Well, I cited it, and I should not have cited it, it 9 doesn't belong. 10 Q. Okay, and it should be taken out then of your report 11 in the reference section, sir? 12 A. Yes. 13 MS. SLEVINSKI: Okay. Could you please 14 hand Dr. Garabrant Exhibit No. 87? 15 MARKED BY THE REPORTER: 16 DEPOSITION EXHIBIT NUMBER 87 17 12:51 p.m. 18 COURT REPORTER: Okay. 19 BY MS. SLEVINSKI: 20 Q. Dr. Garabrant, this is reference No. 87, as well as 21 Exhibit 87, and it's the Linkage Study of Cancer Risks 22 on Lead Exposed Workers in New Jersey. How does this 23 study in particular contribute to your rendering an 24 opinion in this section of your report? 25 A. Well, this study looks at adults who have elevated 189 1 blood leads using the ABLES program in New Jersey, and 2 follows them over time to calculate their cancer 3 mortality, and this study fails to show that there is 4 any clear excess of stomach cancer, colorectal cancer, 5 lung cancer, kidney cancer, and so in contrast to the 6 studies we just talked about by Clark Cooper where 7 there were some excesses of some of those cancers, 8 this study shows a different results showing no excess 9 of those types of cancer, so I correctly weighed this 10 in my overall opinion. 11 Q. When you were assessing this particular article, 12 again, this has several limitation mentioned by the 13 authors real quickly in the abstract where it says 14 conclusion, it lists various -- call numbers, large 15 percentages of workers without age information, the 16 short full of time, lack of vital status information, 17 and the cancer incidents in this cohort is expected to 18 be low due to the healthy worker effect and the young 19 age. Would those were those limitations considered in 20 evaluating you know whether there was a good example 21 of a study showing no association between lead and 22 cancer? 23 A. Yes. 24 Q. How did you -- how did you consider those factors? 25 A. Well, first off, it has to be noted that they're also 190 1 some important strengths of this study, one of which 2 is that this study is of a cohort of men who had 3 documented evidence of increased body burdens of lead, 4 they all had blood lead levels over 25. That makes 5 them a very important group of people to study because 6 this is not a study where we are speculating about 7 exposure, this is not a study where we're looking at 8 communities of people and thinking well, perhaps they 9 have some level of exposure to inhalation of 10 compounds, this is a study where the body burden was 11 actually measured, and that's a very important 12 strength. 13 In this study, there was no evidence of 14 increased risk of any of the cancers at issue in this 15 case. Now, the principal limitation of this study is 16 that it was relatively small and for uncommon cancers, 17 that could reduce the potential to find statistically 18 significant positive associations if they were present 19 but for the more common cancers, particularly lung 20 cancer, this study had plenty of power to find an 21 excess risk of lung cancer if there was one and there 22 was not, so I think it's an important study. 23 The -- the discussion of limited size and 24 limited amount of follow-up is an important 25 consideration for the uncommon cancers but it's not as 191 1 important for the more common cancers. 2 Q. So did you -- okay, I'm making sure I heard your 3 answer correctly, and part of that answer, you said 4 that there was exposure data available in the form of 5 the blood lead levels and that they wouldn't have 6 other confounding exposures and risk factors; did you 7 say that? 8 A. No. 9 Q. With respect to this particular study, would you 10 agree, though, that the study doesn't prove or 11 disprove causation with respect to lead and cancer? 12 A. Well, the point this study and the point of each study 13 individually is that it provides important evidence 14 that must be considered in a determination of whether 15 lead is known or is not known to cause cancer in 16 humans. I considered this study, I would point out 17 that I don't think that Dr. Werntz considered this 18 study. 19 In fact, I don't think Dr. Werntz 20 considered the vast majority of relevant literature 21 that is necessary to provide a scientific foundation 22 for his opinions, he doesn't do it. I went to the 23 trouble of finding the literature and considering it. 24 This is a study that's very good because we had 25 documented blood lead levels, and it happens to show 192 1 no evidence of increased cancer risk in this cohort of 2 men. 3 MS. SLEVINSKI: All right, could you please 4 hand Dr. Garabrant Exhibit 94? 5 MARKED BY THE REPORTER: 6 DEPOSITION EXHIBIT NUMBER 94 7 12:58 p.m. 8 COURT REPORTER: Okay. 9 BY MS. SLEVINSKI: 10 Q. Thank you. Dr. Garabrant, do you recognize this 11 Exhibit No. 94, Blood Lead Levels And Mortality, as 12 one of the articles you cited and relied upon in this 13 section of your report? 14 A. Yes. 15 Q. Generally to the other questions I've been asking, 16 what portion of this report did you find significant 17 in forming your opinions? 18 A. This study suggests that there was a nonsignificantly 19 increased mortality due to nonlung cancers and a 20 nonsignificantly increased mortality due to lung 21 cancers among individuals who have blood lead levels 22 of 20 to 29 micrograms per deciliter. 23 Q. So this study found an association between lead and 24 lung cancer incidence of these individuals? 25 A. Well, it found an association that was positive but 193 1 compatible with chance. It was not statistically 2 significant. 3 Q. And this was not an occupational exposure situation, 4 was it? This was a different type of study? 5 A. This was a study based on the National Health And 6 Nutrition Examination Survey which is a multi-stage 7 stratified random sample of the United States 8 population, and this was restricted to participants 9 aged 30 to 74 years who had blood lead measurements. 10 MS. SLEVINSKI: Would you please hand 11 Dr. Garabrant No. 104? 12 MARKED BY THE REPORTER: 13 DEPOSITION EXHIBIT NUMBER 104 14 13:01 p.m. 15 COURT REPORTER: Okay. 16 BY MS. SLEVINSKI: 17 Q. Dr. Garabrant, Exhibit 104, the carcinogenicity of 18 lead was this cited in support of your opinion that 19 lead is not a human carcinogen? 20 MR. DANNINGER: Objection, form. 21 A. I cited this study as one of the articles I considered 22 in reaching my opinions. This is a review article on 23 the carcinogenicity of lead, and it concludes that 24 there is not proof that lead may cause cancer in man. 25 BY MS. SLEVINSKI: 194 1 Q. By review article, is it fair to say that that means 2 the authors gathered a lot of whatever evidence they 3 could find and on the subject matter reviewed it and 4 wrote an article on it? 5 A. Well, it means that they gathered the published 6 literature relevant to the issue and reviewed it and 7 summarized it and wrote up that summary. 8 Q. This article was published in 1979, correct? 9 A. Yes. 10 Q. And so this was, in your opinion, a good piece of 11 information regarding the state of scientific 12 knowledge of the carcinogenicity of lead? 13 A. Well, as of 1979, I think that would be a fair 14 statement, yes. 15 Q. What about as of 2007? 16 A. As of 2007? There is a tremendous amount of in your 17 scientific literature which when considered in its 18 entirety fails to show sufficient evidence that lead 19 is associated with increased cancer risk in humans. 20 And I think we just reviewed that looking at the most 21 recent IARC document which just came out, that book 22 just came out within the past month or so, and also 23 looking at the EPA IRIS document. 24 Both of those agencies made conclusions 25 entirely consistent with mine and as we pointed out, 195 1 the evidence in animals that lead is carcinogenic is 2 based principally on compounds that are not at issue 3 in this case, the evidence in animals regarding lead 4 oxides is not sufficient to conclude that those 5 materials cause cancer in animals, much less humans. 6 MS. SLEVINSKI: Could you please hand 7 Dr. Garabrant Exhibit No. 128? 8 MARKED BY THE REPORTER: 9 DEPOSITION EXHIBIT NUMBER 128 10 1:05 p.m. 11 COURT REPORTER: Okay. 12 BY MS. SLEVINSKI: 13 Q. Dr. Garabrant, could you explain to me what part of 14 this exhibit you used in forming your opinions here 15 and how you used it? I just -- I don't understand. 16 A. Okay. This is part of a monograph written by 17 Professor Siemiatycki. Dr. Siemiatycki did a very 18 large population based case control study where he 19 looked at ten different types of cancer, sorry, 11 20 different types of cancer, and essentially did a 21 series of case control studies for each of those 11 22 types of cancer in which he interviewed cases and 23 interviewed controls and reconstructed their lifetime 24 working histories and history of exposure to many 25 different chemical agents. 196 1 He wrote an entire book on the results, and 2 I have Xeroxed for you in Exhibit 128 the results for 3 the various lead exposures in his study, and so if 4 you'd turn to page 152, you will see for all of the 5 following cancers, esophagus, stomach, colon, rectum 6 pancreas, prostate, bladder, kidney, skin melanoma, 7 and non-Hodgkins lymphoma odds ratios and 90 percent 8 confidence intervals for exposure to lead compounds 9 right in the center, top section of page 152. 10 What -- and we see that he's also 11 classified exposure into any exposure versus none and 12 substantial exposure versus none. What you see is for 13 the substantial exposure column, for each of those 14 types of cancer with the exception of stomach cancer, 15 there is no significant association between 16 substantial lead exposure and those types of cancer, 17 so for example, looking at lung cancer, the odds ratio 18 is 1.2 with a 90 percent confidence interval of .9 to 19 1.7 so no significant association. 20 For bladder cancer, 1.1, not significant, 21 for kidney cancer, 0.8, not significant. For stomach 22 cancer, he did find a positive association odds ratio 23 of 1.8, and his 90 percent confidence interval was 1.1 24 to 2.8. now -- so he found a moderate association. 25 His use of 90 percent confidence intervals is a bit 197 1 unusual. Most scientists use 95 percent confidence 2 intervals. I can't tell you whether that is actually 3 statistically significant or not at the 95 percent 4 level because he didn't calculate his results in that 5 manner. 6 What this study does show, however, is that 7 for all of the cancer sites at issue in this case, 8 except for stomach, there's no clear association 9 between substantial exposure to lead compounds and 10 increased cancer risk. 11 If we then look at the next set of columns 12 to the right, where he looks at basic lead carbonate, 13 another form of inorganic lead and scan down those 14 odds ratios under substantial exposure, there's not a 15 single one that is statistically significant. If we 16 look at the set of columns at the lower left, lead 17 crow mat, there's not a single one that's 18 statistically significant. 19 If we look at the next set of columns 20 labeled lead fumes, there's not a single one that is 21 statistically significant. And so this is a very 22 important study because it is widely regarded in the 23 epidemiologic community as a -- a watershed study, 24 Jack Siemiatycki is widely respected for this work, 25 and it really fails to show any pattern of increased 198 1 cancer risk related to exposure to lead compounds, 2 basic lead carbonate, lead chromate, or lead fumes. 3 Q. Okay, is that it? Thank you. 4 A. We could also look at the previous page or page 149 5 where we are looking at the upper left soldering fumes 6 and we see very similar findings, soldering fumes 7 typically involves lead and we see no significant 8 increased risk of any type of cancer with the 9 exception of non-Hodgkins lymphoma in that table but 10 there's no-- no clearly increased risk for stomach 11 cancer, colon, rectum, lung, bladder, or kidney. 12 Q. Okay, now I understand, I didn't even understand the 13 basis of that exhibit, thank you. 14 A. You're welcome. 15 MS. SLEVINSKI: Can you please get 16 Dr. Garabrant Exhibit 51? 17 MARKED BY THE REPORTER: 18 DEPOSITION EXHIBIT NUMBER 51 19 1:11 p.m. 20 COURT REPORTER: Okay. 21 BY MS. SLEVINSKI: 22 Q. Dr. Garabrant, Exhibit No. 51 is actually No. 51 on 23 your reference list, and this is a meta-analysis from 24 1995. It's entitled Cancer And Occupational Exposures 25 Inorganic Lead Compounds and then Analysis Of 199 1 Published Data. Now, you listed this in your 2 reference section as something you reviewed in 3 preparation for rendering your opinions but you did 4 not discuss this in the body of your report. Why was 5 this one excluded from the discussion portion of your 6 report? 7 A. It was not excluded from the discussion portion of my 8 report. I cited this with all of the other studies in 9 my report, as the body of scientific evidence origin 10 the carcinogenicity of lead in the human populations. 11 Q. Would you please show me, sir, where 51 is? I was not 12 able to find it if the body of your report, it is in 13 your reference section but it was not cited in your 14 report, the body of it. 15 A. Well, then all that is wrong is on page 5 in the first 16 paragraph, line 2, I should have included reference 51 17 in that list of studies. I apologize for not having 18 done that. 19 Q. All right, so that's -- another mistake, it needs to 20 be added to that section citing the study, correct? 21 MR. DANNINGER: Objection, form. 22 A. It would be appropriate to include that on page 5 23 first paragraph line 2 as part of the large body of 24 scientific evidence on the carcinogenicity of lead in 25 human populations, and I would note that Dr. Werntz 200 1 apparently cited none of this literature. It's not 2 clear he had ever read any of it. 3 BY MS. SLEVINSKI: 4 Q. Would you please read just from the abstract portion 5 of the conclusion, the first sentence of the 6 conclusion in the abstract. 7 A. Yes. The findings from the workers with heavy 8 exposure to lead provided some evidence to support the 9 hypothesis of an association between stomach and lung 10 cancer and exposure to lead. So what that means is 11 almost exactly what IARC has discussed that there is 12 some evidence but not adequate evidence, to support an 13 association between some types of cancer and exposure 14 to lead. 15 You are probably aware that Dr. Paolo 16 Boffetta is a scientist at IARC, and he actually heads 17 the unit of analytical epidemiology at IARC, and his 18 work was cited in the IARC monograph in their 19 consideration of the human evidence, and I think that 20 IARC's conclusion that the human evidence is not 21 adequate to support a conclusion that lead causes 22 cancer in humans derives, in part, from Dr. Bufeta's 23 work. 24 Q. Dr. Garabrant, Dr. Boffetta, who you're referring to, 25 he is on the scientific advisory board for the Dow 201 1 Dioxin study that you are working on right now; is 2 that correct? 3 A. I don't know what the Dow dioxin study is that you're 4 referring to. 5 Q. The study that the University of Michigan is -- you 6 are one of the researchers on it for the presence of 7 dioxins in an area in Michigan through -- that have 8 been attributed through a Dow plant up there? 9 A. If you're referring to the University of Michigan 10 dioxin exposure study, yes, I -- I know what you're 11 talking about, and Dr. Boffetta is on the scientific 12 advisory board to that study. 13 Q. Thank you. That -- as far as we have spoken about the 14 business process so far, is that the reasons of for 15 relying upon those studies that we've talked about 16 thus far? 17 MR. DANNINGER: Objection, form. 18 A. I don't understand your question, I'm sorry. 19 BY MS. SLEVINSKI: 20 Q. Okay, I'm sorry, I'll try and rephrase it. The 21 articles we've just spent an hour or so discussing, 22 are those -- do you have anything to add to why they 23 have contributed to your opinion in this case? 24 MR. DANNINGER: Objection, form. 25 A. Well, these studies represent the published peer 202 1 reviewed literature on the carcinogenicity of lead to 2 humans. I tried to consider the evidence, and I would 3 point out again that there's no evidence that Dr. 4 Werntz did anything such as this at any point in 5 forming his opinions. He doesn't cite the literature. 6 BY MS. SLEVINSKI: 7 Q. Are there any other materials besides the ones that 8 are cited there in your report that you've relied upon 9 in forming this opinion? 10 MR. DANNINGER: Objection, form. 11 A. Are we talking about opinion 2 now? 12 BY MS. SLEVINSKI: 13 Q. Yes, that -14 A. No, I think that they are cited in my report. 15 Q. And the reason -- you set forth the reasons for your 16 opinions in the narrative portions of that section of 17 your report? 18 MR. DANNINGER: Objection, form. 19 A. Well, I have set forth the scientific foundation for 20 my opinion that lead is not known to be carcinogenic 21 to humans, and I believe I have set forth that since 22 it's unknown whether people exposed to lead are at 23 increased risk of cancer, there's no justification for 24 medical monitoring for lung cancer, stomach cancer, 25 kidney cancer, or any other cancer Dr. Werntz alleges 203 1 are related to lead, yes. 2 BY MS. SLEVINSKI: 3 Q. If lead were -- if lead -- the classification of lead 4 was changed to be a human carcinogen, would that 5 change your opinion? 6 A. Well, if the evidence changes, I would certainly 7 consider the new evidence, and I might change my 8 opinion, of course, that's what good scientists do. 9 Q. Similarly, if lead were determined to be a human 10 carcinogen, would medical monitoring be appropriate 11 for these cancers? 12 MR. DANNINGER: Objection, form. 13 A. That's a very complicated question. If lead was a 14 human carcinogen, and at the moment, it is not known 15 to be one, it would be critically important to 16 determine whether the lead compounds that provided the 17 scientific foundation for that determination of 18 carcinogenicity were, in fact, the lead compounds at 19 issue in the Spelter class area. If they were not the 20 same compounds, no, it would not provide an adequate 21 basis for medical monitoring. If they were the same 22 compounds and as I've already pointed out, the 23 compounds at issue in this lawsuit are ones for which 24 there is really not either humor animal evidence that 25 they are carcinogens, it would then be important to 204 1 consider the circumstances of exposure of the 2 population including exposure intensity, duration, 3 frequency, root of exposure, bioavailability, and dose 4 before it would be possible to calculate risks of 5 cancer related to those potential exposures and the 6 calculation of those risks would be a necessary 7 foundational point in determining whether it made 8 sense to do medical monitoring. 9 If it was clear that there was increased 10 risk of some type of cancer, then it would also be 11 important to determine whether screening tests for 12 that cancer are sufficiently reliable to be used, what 13 the sensitivity specificity and positive predictive 14 value of those tests are, whether the utilization of 15 those tests resulted in any net gain in life or any 16 net benefit to the screened population, what the risks 17 of those tests are to balance their benefits, and it 18 would be important to consider many issues regarding 19 technical feasibility as to whether those tests could, 20 in fact, be implemented in a community setting 21 including whether the subjects would participate, the 22 percent participation, whether it would be feasible to 23 follow people up, whether the necessary medical 24 services were in place to follow-up positive findings, 25 and considerations such as that. 205 1 Q. Is that the conclusion of your answer? 2 A. Yes. 3 Q. Okay, thank you, I didn't want to cut you off. 4 The next opinion in your report, No. 3, it 5 states Dr. Werntz does not properly consider exposure 6 pathways, dose, and latency in designing his medical 7 monitoring program. Am I correct in stating that that 8 is your opinion on this particular discussion? 9 A. Yes. 10 Q. Do you believe that the individuals living in the 11 Spelter area have been or are still being exposed to 12 arsenic, cadmium, and lead? 13 MR. DANNINGER: Foundation. 14 A. I am not aware that there is any reliable evidence 15 that exposures in the class area around Spelter are 16 meaningfully different than the background exposures 17 in other areas of West Virginia. 18 BY MS. SLEVINSKI: 19 Q. What are you basing that upon? 20 A. I'm basing that on the reports written by 21 Dr. Rodericks and by Gradient Corporation. 22 Q. Are those the two? I don't want to cut you off. 23 A. Yes. 24 Q. Are you aware that Dr. Rodericks in his report relied 25 upon the sampling results that were taken by our 206 1 experts in the case? 2 A. I am aware that Dr. Rodericks considered those 3 sampling results taken by your experts and raised 4 grave concerns about the validity of those sampling 5 results. 6 Q. Are you aware of any other sampling results that are 7 available from the class area be it soil, dust, taken 8 by any -- any parties? 9 MR. DANNINGER: Objection, form. 10 A. It will take me a minute. 11 BY MS. SLEVINSKI: 12 Q. All right. 13 A. I am aware that there was a study in 1996 that looked 14 at blood lead measurements among children in the town 15 of Spelter and found only 1 child out of 25 had a 16 blood lead above 10 micrograms per deciliter, and so I 17 think this is direct evidence of a lack of exposure to 18 excessive amounts of lead in the pediatric population 19 in Spelter. 20 Q. A sample size of 25 is an adequate size in your 21 opinion to reach that conclusion, 25 individuals? 22 A. Well, it is what it is. The point is that the 23 government of the State of West Virginia felt that 24 that was an adequate sample size, and I guess it 25 was -- sorry, it was ATSDR, sorry, not the government 207 1 of West Virginia. They felt it was an adequate sample 2 size to evaluate whether there had been excessive 3 exposure. 4 Q. Now, with respect to the ATSDR study we were just 5 talking about, the blood lead levels, would you agree, 6 though, that it's not sufficiently powered to reach a 7 reliable conclusion? 8 MR. DANNINGER: What was the word there 9 that you used? Specifically what? 10 BY MS. SLEVINSKI: 11 Q. Related to the ATSDR study we just mentioned, the 12 blood lead levels, would you agree that it's not 13 specifically powered to reach a reliable conclusion? 14 MR. DANNINGER: Objection, form. 15 A. No, I would not agree with that. What do you mean by 16 sufficiently powered? 17 BY MS. SLEVINSKI: 18 Q. Was the study of a power that allows you to reach a 19 reliable conclusion based on its results? 20 A. Well, when you pose a question such as that, you have 21 to specify what you mean by -- by sufficient power. 22 Q. Statistically speaking, the power of a study. 23 A. I understand statistically speaking the power of the 24 study, but you have to specify what power it is you 25 think is adequate. 208 1 Q. I'm asking you if this would be adequate, 25 people 2 would be adequate for the power of a study? 3 A. The answer is ATSDR felt this was adequate. I do, 4 too. I don't know how to answer your question because 5 it is lacking in detail adequate for me to know what 6 it is you are asking. 7 Q. All right. Dr. Garabrant, what do you believe are the 8 exposure pathways in the class area in this case? 9 MR. DANNINGER: Foundation. 10 A. I was not asked to identify the exposure pathways in 11 the class area. I am aware that plaintiff's expert, 12 Dr. Brown, has purported to do so, and that other 13 defense experts have given expert opinions on the 14 adequacy of Dr. Brown's work. I will defer to the 15 other defense experts in the issue of which of those 16 exposure pathways are valid and which are not. 17 BY MS. SLEVINSKI: 18 Q. Do you have an opinion on the exposure pathways in 19 this case? 20 A. I have an opinion that the work done by Dr. Brown and 21 the work done by Dr. Flowers is not sufficiently 22 reliable to conclude that there is evidence of 23 exposure to lead, arsenic, or cadmium from the Spelter 24 site that is meaningfully different from the 25 background exposures in that region of West Virginia. 209 1 Q. What are you basing that opinion on? 2 A. Dr. Rodericks' report and the report from Gradient 3 Corporation. 4 Q. Is that all? 5 A. Well, and also having read Dr. Brown's report and 6 Dr. Flowers' report, yes, that's all. 7 Q. Anything else? 8 A. Well, and my experience in the field of occupational 9 environmental epidemiology and in doing assessments of 10 chemical exposures to humans and exposure pathways in 11 humans. 12 Q. All right, is that it? 13 A. Yes. 14 Q. Dr. Garabrant, if there are some arsenic laden dust 15 particles about ten microns in size, if that's inhaled 16 by a person, will travel through a person's 17 respiratory system, is that correct, ten microns? 18 A. Ten microns is at the limit of what is defined as 19 respirable. A particle of that size would stand a 20 very good chance of simply being filtered out in the 21 nose, and it would not be inhaled deeper into the 22 respiratory tract. 23 Q. What about a particle say 15 microns? 24 A. 15-micron particle has a very high probability of 25 being captured in the nose and never being inhaled any 210 1 deeper than that. 2 Q. How about 20 microns? 3 A. Even higher probability of being filtered out in the 4 nose and not getting into the body beyond the nasal 5 passages. 6 Q. What happens, say, whichever size is necessary for 7 this dust particle to travel through the respiratory 8 system to the lungs, can you explain where -- when it 9 travels from the nose into the lungs the pathway it 10 will take? 11 A. I'm not quite sure what you're asking. Do you want me 12 to talk about the anatomy of the respiratory tract? 13 Q. Not in too much detail, just how it enters the lungs 14 and it can travel from, you know, their lungs to other 15 areas of their body? 16 MR. DANNINGER: Form. 17 A. So you want me to talk about the anatomy of the 18 respiratory tract in not much detail and how particles 19 get from the lungs to other areas of the body? 20 BY MS. SLEVINSKI: 21 Q. Yes, and you know in simple detail, you don't need a 22 superlong information about -- just enough to 23 understand? 24 MR. DANNINGER: Form. 25 A. Is this a test of my understanding of inhalation 211 1 toxicology? I'm happy to do that if you really want 2 it -3 BY MS. SLEVINSKI: 4 Q. -- a test, I'm just asking you to answer the question 5 Dr. Garabrant? 6 A. Okay, well, could you give me some more focused 7 questions? The answer to your question is the subject 8 of numerous textbooks, and I -- I'll go through it if 9 you want but I think perhaps more focused questions 10 would be more productive. 11 Q. Thank you. I'll give you some more focused questions. 12 Let's say, for example, an arsenic laden dust particle 13 is inhaled and it travels to the lungs if it's 14 sufficient in size. Once it's in the lungs, can it 15 get caught in the mucus, and are there bodies in the 16 lungs that helps the particle travel that will even 17 take the particle out of the lungs and it will become 18 embedded? What happens in there? 19 MR. DANNINGER: Objection, form. 20 A. Well, the answer to your first part of the question is 21 yes. 22 BY MS. SLEVINSKI: 23 Q. Okay, just -- is that your answer? You're not going 24 into detail? Don't want to cut you off. 25 A. Well, I'm not sure -- the question's so vague and so 212 1 comprehensive in scope, it's hard to know what you 2 want. If you want me to recite my entire 3 understanding of inhalation toxicology, I'll do it. 4 I -5 Q. I don't need -6 A. That could go on for two hours, I teach this. 7 Q. Of course. 8 A. I could go on for six hours. In fact, I teach this 9 material. I teach pathophysiology of the respiratory 10 tract to graduate students, and if you want to hear 11 it, I'll give it to you. 12 Q. No, I'm not really looking to hear that -- that big of 13 an explanation, but thank you. Is it possible for a 14 dust particle to go into the lungs, be removed from 15 the lungs and travel, maybe, get coughed up in sputum 16 or mucus and then swallowed, and is it possible to 17 travel through the stomach into the digestive tract? 18 A. Yes. 19 Q. Do you have an opinion about the size of a dust 20 particle that would travel into the lungs and not be 21 trapped in the nose or expelled through the nose? 22 A. Yes, I do. 23 Q. What would that be, sir? 24 A. Typically, particles greater than ten microns in 25 aerodynamic diameter are officially filtered out in 213 1 the nose, so particles larger than that, only a small 2 proportion of them get beyond the nasal passages. The 3 larger they are above ten microns, the lower is the 4 proportion of them that get beyond the nose. 5 As we get down into particles less than ten 6 microns, an increasing proportion of them can travel 7 down through the conducting airways. Particles that 8 are between one and ten microns are captured in the 9 mucus that lines the conducting airways with varying 10 efficiency, and it depends on particle size, the 11 bigger particles tend to be captured in the mucus more 12 efficiently than the small particles. 13 As we get down to particles in the range of 14 two or three microns, we begin to see that an 15 appreciable part of them get down into the alveoli, 16 and we also see that an appreciable part of particles 17 in that size range are actually exhaled without being 18 captured by the body at all. 19 When we get down into particles lower -20 smaller than one micron in size range, so submicron 21 range, they very efficiently reach the alveoli, but 22 they also very efficiently are exhaled, so in that 23 size range, if I had to give you a ballpark number, 24 I'd say perhaps 60 percent of submicron range 25 particles reach the alveoli and are exhaled again. 214 1 A good illustration of that would be 2 watching a smoker inhale deeply and then exhale. What 3 you notice in much of cigarette smoke is in the 4 submicron size range. What you see is that an 5 appreciable part of the smoke they inhale, they 6 exhale. The particles come right out again. 7 Of the particles that are retained, those 8 in the submicron range, a small proportion of them are 9 caught in the mucus, but the larger proportion of them 10 actually impact in the alveoli where they are 11 deposited and are eventually taken up by the alveolar 12 macrophages. 13 Does that answer your question. 14 Q. Yes, thank you very much, Dr. Garabrant. What's your 15 understanding of the historical source of drinking 16 water in the class area? 17 BY MS. SLEVINSKI: 18 A. I do not know comprehensively what the historical 19 source of drinking water is in the class area. It is 20 my understanding that your experts, Dr. Brown, do not 21 believe that drinking water is an exposure pathway in 22 this litigation. 23 MR. DANNINGER: Amanda, when you get to a 24 point, you don't have to do it right now, but just a 25 break would be nice here in the next few minutes. 215 1 MS. SLEVINSKI: Okay, I'll be ready in just 2 a minute. 3 MR. DANNINGER: Yeah, no problem. 4 BY MS. SLEVINSKI: 5 Q. Dr. Garabrant, are you -- do you have any knowledge as 6 to whether the west fork river was ever used as a 7 source of drinking water in the class area? 8 A. I do not. 9 Q. Do you know about any impact of the site contaminants, 10 arsenic, cadmium, and lead, have had on the West Fork 11 River? 12 A. I do not. 13 Q. If you were told that the people in and around Spelter 14 and the class area had consumed water contaminated 15 with arsenic, would your opinion change on the skin 16 cancer pathway? 17 A. Well, I guess if your experts don't think they drank 18 that water, there's no reason for me to think it. 19 Q. That's not really what I asked. 20 MS. SLEVINSKI: Could you please read the 21 question? 22 (The requested portion of the record was 23 read by the reporter at 1:39 p.m.) 24 A. Well, if you told me something that I thought had 25 absolutely no factual basis, I would not speculate as 216 1 to what might be true. 2 MS. SLEVINSKI: I'm going to move to strike 3 as nonresponsive. Please read the question back, and 4 Dr. Garabrant, answer the question. 5 MR. DANNINGER: Amanda, it's responsive. 6 He's answering to the best of his ability. He's 7 saying that he's not going to speculate on something 8 that your experts say isn't factually positive, so I 9 mean you can go through it again, and he may give you 10 the same answer, but I'm just -- I mean this moving to 11 strike his answers is just getting a little bit old in 12 this. 13 BY MS. SLEVINSKI: 14 Q. Dr. Garabrant, would you answer that question for me 15 as posed in a hypothetical? Hypothetically speaking, 16 if you were told that residents in the class area had 17 consumed water contaminated with arsenic, would that 18 change your opinion on the skin cancer pathway in this 19 case? 20 A. I am happy to answer your question. If you give me a 21 hypothetical that I believe has absolutely no 22 relationship to the plausible facts in the case, I 23 think that giving an answer would simply be 24 speculation, and it would be nonsense. It is my 25 understanding that your experts do not believe that 217 1 drinking water is an exposure pathway in this case. I 2 am not aware of any evidence that has been presented 3 by your experts or by defense experts that would 4 suggest that drinking water containing arsenic or lead 5 or cadmium is an issue in this case. 6 Q. So is your answer to my question no? 7 MR. DANNINGER: Form. 8 A. My answer to your question is I believe that I should 9 not speculate regarding hypothetical questions that 10 have no relationship to any plausible set of 11 circumstances. 12 BY MS. SLEVINSKI: 13 Q. Okay, Dr. Garabrant, what difference does the media 14 make in an exposure evaluation? And by media, I mean 15 whether it's -- the contaminants are, you know, 16 ingested via soil, air, water, what difference does 17 that make in an exposure evaluation? Exposure 18 pathway. 19 A. Well, it makes all the difference in the world. You 20 know, it's very clear from things we've already 21 discussed today that the evidence regarding inhalation 22 of arsenic compounds and cancer risks is very 23 different than the evidence regarding drinking arsenic 24 contaminated water. 25 In those areas of the world such as Taiwan 218 1 where there are areas where there is very heavy 2 arsenic contamination of drinking water, we see a 3 pattern of cancer risks that is entirely different 4 than the pattern of cancer risks among men who have 5 worked in arsenic smelters in the United States or in 6 Japan or in other areas of the world. And so 7 inhalation of arsenic poses a completely different set 8 of risks than ingestion of arsenic in drinking water. 9 Q. Are you finished? 10 A. Yes. 11 Q. Okay. In your report, I'm looking at page 5. You say 12 that skin cancer likely to be linked to arsenic 13 contaminated drinking water but not to soils, 14 ingestion, or inhalation of arsenic. You cite in your 15 report the studies relating to arsenic and -- arsenic 16 and drinking water, but what do you base your opinion 17 on there's never been a link to soil and inhalation of 18 arsenic? 19 A. The lack of evidence that it's been linked to those 20 pathways. 21 Q. Are there no art fees -- saying there's no articles 22 that address that issue? 23 A. Well, if you have some in mind, I would be happy to 24 discuss them with you. 25 Q. I'm just asking you. 219 1 A. Well, I'm not aware of literature that would support 2 that but again, if you have -- if you have some that 3 you'd like to discuss, I'd be happy to do that. 4 MR. DANNINGER: Just remember, Amanda, 5 we're waiting on a break, too. 6 MS. SLEVINSKI: I know. Actually, yeah, 7 this will be a good time, we can good ahead and take a 8 break. 9 MR. DANNINGER: Okay, say five to ten 10 minutes? 11 MS. SLEVINSKI: Sounds good. 12 MR. DANNINGER: Thanks. 13 MS. SLEVINSKI: Mm-hmm. 14 VIDEO TECHNICIAN: We are going off the 15 record. The time is 1:43 and 48 seconds p.m. 16 (Recess taken at 1:43 p.m.) 17 (Back on the record at 2:00 p.m.) 18 VIDEO TECHNICIAN: We are now back on the 19 record. This is the beginning of tape No. 4. The 20 time is 2:00 and 56 seconds p.m. 21 BY MS. SLEVINSKI: 22 Q. Dr. Garabrant, before the break, we left off, we were 23 at the bottom of page 5, basically, on your report, 24 going back to that section, the last paragraph on 25 page 5, it starts out, you say, bladder cancer is not 220 1 associated with exposure to cadmium or lead. Is it 2 your understanding that Dr. Werntz proposed or 3 mentioned at all that cadmium and lead were, in fact, 4 associated with an increased risk of bladder cancer? 5 A. No. 6 Q. I'm sorry, the phone cut off; did you say no? 7 A. I said no. 8 Q. Okay. You go on to mention about bladder cancer only 9 being linked to drinking water containing excessive 10 arsenic, and then the last sentence starts bladder 11 cancer is not known to be linked to either inhalation 12 or soil ingestion of arsenic; is that your opinion? 13 A. Yes. 14 Q. What do you base that on that bladder cancer is not 15 linked to soil or inhalation of arsenic? 16 MR. DANNINGER: Objection, form. 17 A. A lack of evidence linking bladder cancer to 18 inhalation or soil ingestion of arsenic. 19 BY MS. SLEVINSKI: 20 Q. Lack of evidence meaning articles that have actively 21 researched that issue or you just have not looked at 22 any? 23 A. I found no evidence that would suggest that bladder 24 cancer was causally associated with arsenic inhalation 25 or ingestion of soil containing arsenic. 221 1 Q. Okay, by no evidence I'm just trying to clarify you 2 mean you found no articles that discuss an association 3 between ingested or inhaled arsenic and bladder 4 cancer? 5 MR. DANNINGER: Objection, form. 6 A. That's not what I said. The sentence stands for 7 itself, it's quite clear what it means. There's 8 simply no evidence to support a conclusion that 9 bladder cancer is linked to inhalation of arsenic or 10 linked to ingesting soil containing arsenic, and we've 11 talked about these various environmental studies when 12 we started today. I can't find any evidence that 13 would support a claim that bladder cancer is 14 exposed -- is associated with those exposure pathways, 15 and I would point out that Dr. Werntz has not provided 16 any evidence that would support those exposure 17 pathways even though he claims that the people in the 18 class area are at increased risk of bladder cancer due 19 to their alleged soil ingestion or inhalation 20 exposures. 21 Q. Dr. Werntz, you agree that -- excuse me, 22 Dr. Garabrant, I apologize, do you agree that lung 23 cancer has been associated with inhaled arsenic and 24 cadmium in occupationally exposed individuals? 25 A. Yes. 222 1 Q. Is it your opinion in this case that lung cancer has 2 not been reliably shown with community exposures to 3 arsenic and cadmium? 4 A. Yes. 5 Q. What's your basis for that opinion? 6 A. We discussed that this morning. We went through, I 7 don't know, eight or ten studies that examined that 8 very issue starting with Tokudome and the Bartlesville 9 study, the Pershagen study, Brown, ATSDR study at the 10 Murray smelter, the study in Australia, the ASARCO 11 smelter in Washington state, the Wong study, that's 12 what we just went through for, I don't know, an hour 13 and a half, two hours. 14 Q. In preparation of your report, did you review any 15 literature that dealt with exposure to arsenic, 16 cadmium, lead, and cancerous effects that were in an 17 environmental exposure, not an occupational exposure 18 setting? 19 A. Yes. We've already discussed those, that's what I 20 just recited to you. 21 MS. SLEVINSKI: Well, how about -- would 22 you please hand Dr. Garabrant Exhibit No. 56? 23 MARKED BY THE REPORTER: 24 DEPOSITION EXHIBIT NUMBER 56 25 2:06 p.m. 223 1 BY MS. SLEVINSKI: 2 Q. Dr. Garabrant, do you recognize this as one of the 3 items you have in your reference list of your report, 4 correct? 5 A. Yes. 6 Q. However, I do not -- you referenced it you didn't 7 discuss this in the body of your report and I want to 8 ask you a couple of questions on some items in it. 9 Would you turn to page 372? It's the second page, 10 please. 11 A. Yes. 12 Q. Now, this article is looking at the carcinogenicity of 13 metals in humans, and this is the section dealing with 14 arsenic, and look on the right-hand column, the last 15 paragraph. It says analysis came from the U.S., 16 Quebec -- in Canada -- Sweden and China showed an 17 increased lung cancer among residents near arsenic 18 producing industrial operations; although, some 19 investigations have been negative. 20 Now, it lists the United States, Canada, 21 Sweden, and China, and it also has some other studies 22 noted, cited there. Did you look up those studies 23 during your research to see what they talked about, 24 the increase in lung cancers for residents near 25 arsenic producing industries? 224 1 A. Yes. 2 Q. And which ones were those? 3 A. Well, okay, you see in that sentence analysis from the 4 U.S. and then they cite references 4, 33, and 34, 4 is 5 the Brown study. 6 Q. Didn't you reference that because it was first you 7 were responding to Dr. Werntz's use of it in his 8 report? 9 A. No, I referenced it because it was relevant to the 10 issue. 11 Q. Didn't Dr. Werntz cite that in his report as one of 12 his studies showing an increased risk of cancer in 13 smelter sites? 14 A. Yes, and so did I. The point is it was relevant to 15 the issue. Unlike Dr. Brown, I actually got -- I'm 16 sorry, Dr. Werntz, I went out and got a much larger 17 body of evidence that addressed the issue so -18 Q. Okay, well, let's look at, in this particular study, 19 No. 33 in the reference list, it appears to be a Blot, 20 W.J. Fraumeni, I didn't see that in your reference 21 list. Did you overlook that one, Arsenical Air 22 Pollution And Lung Cancer? 23 MR. DANNINGER: Objection, form. 24 A. I didn't cite that one. You will notice that Blot is 25 the same Blot in the Brown study. That study came 225 1 from the environmental epidemiology group at the 2 National Cancer Institute with Bill Blot, I think -3 no, actually, Joe Fraumeni headed that, and so I 4 think -- the blood study was published in The Lancet 5 in 1975. 6 BY MS. SLEVINSKI: 7 A. The Brown study was published in 1984. So I didn't -8 I didn't cite the Blot study. 9 Q. You didn't review it though either because it wasn't 10 in your reference list? 11 MR. DANNINGER: Objection, form. 12 A. I actually have that reference, I have read it, I 13 probably should have put it in my reference list, I 14 may have forgotten. 15 BY MS. SLEVINSKI: 16 Q. So we have one more mistake, one more thing we need to 17 add to your reference list? 18 MR. DANNINGER: Objection, form. 19 A. I'm not sure it's a mistake. It is by the same author 20 on the same issue, and it's nine years earlier. 21 BY MS. SLEVINSKI: 22 Q. In a completely different journal and has a completely 23 different title? 24 MR. DANNINGER: Is there a question there? 25 BY MS. SLEVINSKI: 226 1 Q. Is that correct? 2 A. It's published in The Lancet, and it's about arsenical 3 pollution and lung cancer, whereas, the Brown study is 4 published in environmental research and it's about 5 lung cancer, and you will recall it's about arsenic. 6 Q. How about reference No. 34, Matanoski? Mat -7 Matanofsky? I'm probably butchering that. 8 A. It's Matanoski. 9 Q. That also was not included in your reference list. Is 10 this another one that you did, in fact, review and 11 neglected to include in your reference list? 12 MR. DANNINGER: Objection, form. 13 A. I don't know the Matanoski study, I'll have to look at 14 that one. 15 BY MS. SLEVINSKI: 16 Q. No. 35, Courtier and Toureau (ph.), that also was not 17 included in your reference list; is that of the same 18 caliber, forgotten but reviewed? 19 MR. DANNINGER: Objection, form. 20 A. I -- I don't recall the Courtier study. I believe I 21 have read it in the past, it's possible that I -- I 22 missed that one in my review. 23 BY MS. SLEVINSKI: 24 Q. And No. 36, you did actually review the Pershagen 25 study, one of them, and that was also one that was 227 1 cited by Dr. Werntz, correct? 2 A. That's correct, and I reviewed the Frost study, 3 No. 37, and -4 Q. I'm not asking about that; I was just asking about 5 those particular ones because they were related to the 6 previous question. 7 MR. DANNINGER: I don't believe the doctor 8 was finished with his answer. 9 MS. SLEVINSKI: Would you please hand 10 Dr. Garabrant Exhibit No. 113? 11 MARKED BY THE REPORTER: 12 DEPOSITION EXHIBIT NUMBER 113 13 2:12 p.m. 14 COURT REPORTER: Okay. 15 BY MS. SLEVINSKI: 16 Q. Dr. Garabrant, as you look at the paragraph -- well, 17 go to page 6 of your report, the second paragraph from 18 the top, it deals with lung cancer, and it says lung 19 cancer has been associated with inhalation of arsenic 20 and cadmium among workers and industries, again picked 21 up -- not reliably associated with community arsenic 22 to arsenic or cadmium. Exhibit 113, do you recognize 23 this as one of the materials you reviewed in the 24 preparation for your report? 25 A. Yes. 228 1 Q. This was referenced but it was not discussed in the 2 body of your report. Can you explain why? 3 A. I didn't discuss each and every one of the 148 4 references I cited in the body of my report. The 5 purpose of my report, among others, was to point out 6 that Dr. Werntz had never considered the science that 7 he needed to consider as a basis for his 8 recommendations for medical monitoring, and so it 9 appears that I've brought to your attention the large 10 body of science relevant to his opinions. My opinions 11 are that Dr. Werntz didn't do his job. He didn't find 12 the scientific evidence, he didn't consider it, he 13 didn't structure his medical monitoring program to 14 reflect the scientific evidence that would have to 15 underpin such recommendations. 16 Q. Are you finished? 17 A. Yes. 18 Q. Okay, well, let's take a look at Exhibit 113. Now, 19 this is an environmental exposure to cadmium and risks 20 of cancer a prospective population based study, did I 21 read that correctly? 22 A. Yes. 23 Q. Now, this study, it followed a population, a group of 24 people in Belgium who live right around the zinc 25 smelter; isn't that correct? 229 1 A. Yes. 2 Q. Okay. Did that factor into your decision to omit this 3 from the discussion portion of your report? It seems 4 to be pretty similar to the situation at hand. 5 MR. DANNINGER: Objection, form. 6 A. Well, I should point out to you, I was the one who 7 included this in my report. I don't see that 8 Dr. Werntz even included it in his. 9 BY MS. SLEVINSKI: 10 Q. I'm not asking about Dr. Werntz; I'm asking you about 11 your opinions and your reasons in support for your 12 report. Did you -13 MR. DANNINGER: So what's your question? 14 MS. SLEVINSKI: Could the court reporter 15 please read my question back? 16 (The requested portion of the record was 17 read by the reporter at 2:16 p.m.) 18 MR. DANNINGER: Objection, form. 19 A. I'm sorry, what's the question? 20 MS. SLEVINSKI: She just read it back, did 21 you not hear it? 22 MR. DANNINGER: Do you want the court 23 reporter to reread it, or do you want to ask the 24 question again? 25 MS. SLEVINSKI: I would like to have her 230 1 reread it, please. 2 MR. DANNINGER: Okay. 3 (The requested portion of the record was 4 read by the reporter at 2:16 p.m.) 5 MR. DANNINGER: Objection, form. 6 A. I included this publication in my report. 7 BY MS. SLEVINSKI: 8 Q. You included it in the reference section; you did not 9 include it in the body of your report where you 10 discussed other studies. Let's take a look closer. 11 This study says we aim to discuss the association 12 between environmental exposure for cadmium and cancer. 13 That's the same situation -- strike that. 14 MR. DANNINGER: Where were you reading 15 from? Or where are you reading from? 16 MS. SLEVINSKI: Okay, under -- on the first 17 page of the article, it's the very first paragraph 18 under the black word summary. 19 MR. DANNINGER: Okay. 20 BY MS. SLEVINSKI: 21 Q. The last sentence, we aim to assess the association 22 between environmental exposure to cadmium and cancer. 23 Is it not true, Dr. Garabrant, that there is 24 environmental exposure to cadmium in Spelter, West 25 Virginia. 231 1 A. I am not aware of any reliable evidence that shows 2 there is environmental exposure to cadmium from the 3 smelter site that is any different than the background 4 levels in that region of West Virginia. 5 MR. DANNINGER: Belated foundation 6 objection. 7 BY MS. SLEVINSKI: 8 Q. Do you agree that at issue in this case is the class 9 residents' exposure to cadmium in and around the 10 Spelter facility? 11 MR. DANNINGER: Foundation. 12 A. I'm sorry, I didn't understand, say -- would you 13 repeat that or have the reporter read it back? 14 MS. SLEVINSKI: Would you please read my 15 question back? 16 (The requested portion of the record was 17 read by the reporter at 2:18 p.m.) 18 MR. DANNINGER: Foundation. 19 A. It is my understanding that the class of plaintiffs 20 alleges that the smelter site has caused cadmium 21 exposures to occur via inhalation pathways. 22 BY MS. SLEVINSKI: 23 Q. Okay, would you please turn to page 125, it's the 24 second to last page of this article. 25 A. Yes. 232 1 Q. At the very bottom right-hand column, it reads in 2 conclusion, consistent with indirect evidence 3 currently available we have shown a significant 4 association between risks of lung cancer and 5 environmental exposure to cadmium. Did I read that 6 correctly? 7 A. Yes. 8 Q. In this study that was looking into the possible 9 association between cadmium and cancer, and the 10 population of people that live near a zinc smelter 11 facility did, in fact, find, this said, a significant 12 association. Is that true? 13 A. That's what the authors say, and it is to their 14 knowledge the first time such an association has been 15 reported in an environmentally exposed population. 16 Now, my point is that this finding -- and I should 17 point out, I brought this reference to your attention, 18 Dr. Werntz didn't, as far as I can tell, he never 19 cited it, didn't -- didn't take any role in his 20 thinking. 21 My point is that okay here's a positive 22 study, you know here's the defendant's expert pulling 23 up the positive studies, this hasn't been replicated. 24 Q. It also wasn't discussed in the body of your report; 25 is that correct? 233 1 A. I'm the one who cited it in my report. 2 Q. I'm not asking you if you cited it. Dr. Garabrant, 3 did you discuss it in the body of your report, yes or 4 no? 5 MR. DANNINGER: Form, he's answered it. 6 A. I did not insert the citation after a single sentence 7 on page 6 where I discussed the evidence. If that's 8 what you're asking, should I have put citation No. 113 9 in paragraph 2, no, I didn't do that. I cited this 10 study in my report, I brought it to your attention as 11 relevant literature on the issue of cadmium exposure 12 and lung cancer risk. 13 BY MS. SLEVINSKI: 14 Q. Okay, so you found the study, brought it to our 15 attention, you read it, and you didn't discuss it in 16 your report because it showed a positive association 17 between cadmium and cancer, correct? 18 MR. DANNINGER: Objection, form. 19 A. I cited it because it is relevant regardless of what 20 it showed. That's the whole point. Dr. Werntz didn't 21 cite the literature. He's the guy that's got the 22 opinions that medical monitoring is required, and he 23 doesn't have any foundation for his opinions. 24 BY MS. SLEVINSKI: 25 Q. Thank you, Dr. Garabrant. You also discussed the 234 1 relationship of kidney cancer and exposure to cadmium 2 or lead in the next paragraph down in your report. Do 3 you see that on page 6 -4 A. Yes. 5 Q. -- that page. Okay, and is it your opinion that 6 kidney cancer is not associated with cadmium? 7 A. Yes. 8 Q. Is it your opinion that there's no exposure pathways 9 in the class area that would suggest residents to an 10 increased risk of kidney cancer from cadmium? 11 MR. DANNINGER: Foundation. 12 A. It is my understanding that plaintiff's experts have 13 alleged that the exposure pathways of concern involve 14 inhalation, they do not include drinking water and I 15 am aware of no evidence that inhalation of cadmium is 16 linked to increased risk of kidney cancer in humans. 17 BY MS. SLEVINSKI: 18 Q. And you -- one article that -- or excuse me, one 19 reference cited, and that is No. 22, could you please 20 actually -- no, I won't need that one, sorry, strike 21 that. 22 You don't have any information in there 23 cited as what you based your opinion on kidney 24 cancer's association with cadmium. What -- what did 25 you base that opinion on? 235 1 A. The lack of evidence of an association. There is a 2 small body of literature on that that I'd be happy to 3 discuss with you. There is a study by Kolonel in 4 1976, a study by Mandel in 1995, a study by Pesch, 5 P-e-s-c-h, in 2000, a study by Armstrong in 1983, a 6 study by Hu, H-u, in 2002. I'm still looking. 7 Q. Are you looking through your reference list? 8 A. I'm looking through my references. 9 Q. Okay, that's just what I was trying to establish. 10 A. Yeah, those would be the studies that I have looked at 11 on that issue. 12 Q. For cadmium and renal cancer? 13 A. Yes. 14 Q. Any others? 15 A. I don't recall whether the other references in my 16 bibliography address that. I have to look through 17 them now to answer that. 18 Q. Are you -19 A. I'm -20 Q. Not being in front of you, are you looking for it 21 still or -22 MR. DANNINGER: Yeah, he's still looking, 23 Amanda. 24 A. Hold on, it will take -- it will take a few minutes 25 for me to do that. And you want just kidney cancer? 236 1 BY MS. SLEVINSKI: 2 Q. Kidney cancer and cadmium. 3 A. Right. Yeah, I think we would have to include the 4 reference by Anderson. Hold on, I'll go through and 5 give you the exhibit numbers as I do this. Exhibit 6 No. 1. Okay. That was a mortality study among 7 cadmium and nickel exposed workers in a Swedish 8 battery factory. That study clearly ascertained 9 cadmium cancer in that cohort, and the results were 10 not of sufficient interest for them to bother 11 reporting it. They clearly had it and they reported 12 kidney disease other than kidney cancer, so that's a 13 study that is relevant and provides no evidence of 14 increased risk. 15 Armstrong, reference No. 3, the mortality 16 of cadmium workers, clearly had the ability to observe 17 kidney cancer, clearly ascertained deaths due to that 18 cause if there were any, and did not report the 19 results out, so that's a study that fails to show 20 evidence of increased risk. 21 Q. Dr. Garabrant, in the interest of time, could we 22 just -- you tell me which ones they are and not do the 23 description. Just -- so which ones you relied upon -24 A. Sure. 25 Q. -- for your opinion? Okay, just the number and the 237 1 exhibit for the references, so that will be sufficient 2 if you wouldn't mind doing that, please. 3 A. Okay, just a second. 4 MR. DANNINGER: Well, he's not going to be 5 able to give you the exhibit number because we don't 6 have those exhibits, so he'll give you the number on 7 his reference list. 8 MS. SLEVINSKI: That's why -- I'm sorry, I 9 wasn't clear. 10 MR. DANNINGER: Yeah, no, no, no, but to 11 the extent that it may disagree with your future 12 exhibits, I just don't want you to think that we're 13 giving you exhibit numbers. 14 MS. SLEVINSKI: Okay, no problem. 15 BY MS. SLEVINSKI: 16 Q. Just go down your reference list by number, 17 Dr. Garabrant. 18 A. Okay. It takes a while. 19 Q. Okay. 20 A. Okay, reference 4 by Assaul (ph.) is one I considered. 21 Reference 40 by Elander (ph.), reference 75, Iliasoba 22 (ph), reference 76 by Inskip (ph.), reference 77 by 23 Gerrup (ph.), reference 85 by Kazansas (ph.), 24 reference 132 by Sorahan (ph.), reference 136 by Toon 25 (ph.). I think that's it. 238 1 Q. Okay, so those are the references that you relied upon 2 in forming your opinions on the relationship between 3 cadmium and kidney cancer; is that correct? 4 A. That's correct. 5 Q. Okay, thank you. Okay, Dr. Garabrant, the bottom of 6 the last paragraph, I guess, of your report on page -7 you state that Dr. Werntz hasn't considered latency in 8 designing his cancer screening program. 9 MR. DANNINGER: Amanda, it cut out, we lost 10 the page number there. 11 MS. SLEVINSKI: Oh, I'm sorry, page 6 of 12 his report, last paragraph. 13 MR. DANNINGER: Okay. 14 COURT REPORTER: Did she ask a question? 15 MR. DANNINGER: Yeah, we're -- we were kind 16 of lost at that point. Can you repeat your question? 17 MS. SLEVINSKI: Oh, sure, okay, I 18 apologize. 19 MR. DANNINGER: That's okay. 20 BY MS. SLEVINSKI: 21 Q. I'm just asking Dr. Garabrant to explain in more 22 detail his statement that Dr. Werntz hasn't considered 23 latency in designing his cancer screening program. 24 A. Yes, Dr. Werntz did not consider latency in designing 25 his cancer screening program. Carcinogens or agents 239 1 that cause cancer do not cause cancer on the day of 2 the exposure. 3 There is usually a lag time between the 4 onset of exposure and the point at which there is 5 increased risk of cancer. That lag time is commonly 6 referred to as latency. It makes no sense to screen 7 for cancer during time periods when there is no 8 increased risk of cancer because you cannot possibly 9 detect cancers related to exposure during that time 10 period. 11 Dr. Werntz seems never to have considered 12 that fact in designing his program. So his proposal 13 to do cancer screening for a period of 40 years never 14 takes into account for his postulated increased risk 15 of cancer during -- at what point in these various 16 class plaintiffs' lives they would actually be at 17 increased risk of various cancers he believes are due 18 to these exposures, and so what he has proposed is to 19 do cancer screening during time periods when people 20 are not known to be at increased risk or are not at 21 increased risk and during which he could not detect 22 any cancer related to these exposures. 23 Q. What is your understanding as to how long people have 24 been living in the community surrounding the zinc 25 smelter? 240 1 A. Well, I -- I don't know the entire occupational 2 history of the population, I'm not aware that any of 3 the plaintiff experts have actually shown what that 4 distribution is. I do know that some individual 5 plaintiffs have lived there for as long as 65 years. 6 I don't know what the distribution of first years of 7 residence is in the various class areas. I don't know 8 the age distribution, I don't know how people have 9 moved in and out of the area. 10 All of those factors have to be considered 11 by Dr. Werntz, and he didn't. I mean if you're going 12 to design a cancer screening program that makes sense 13 that has a scientific basis, you have to target people 14 who are at increased risk and you have to target them 15 during the period when they are at increased risk. 16 Otherwise, your program is nonsense. 17 Dr. Werntz did not make any effort to 18 target people during the period he believes they would 19 be at increased risk of cancer. 20 Q. When in your opinion was the residence in the class 21 year be at an increased risk of cancer due to their 22 exposure? 23 MR. DANNINGER: Foundation, form. 24 A. Never, they're not. There's not a this read of 25 evidence that they're at increased risk of cancer as a 241 1 result of anything from the Spelter site. 2 BY MS. SLEVINSKI: 3 Q. What are you relying upon to establish your -- a 4 latency period? 5 MR. DANNINGER: Form. 6 A. Your question presumes I've established a latency 7 period. I'm not sure what you're talking about. 8 BY MS. SLEVINSKI: 9 Q. If you look at your report on page 6, I guess it would 10 be the one, two -- third sentence, this suggests that 11 screening for lung cancer in relation to inhaled 12 arsenic will not reveal any arsenical cancers until at 13 least 35 to 40 years after first exposure. Is that 14 correct? 15 A. That's what my report says. 16 Q. Where -- what basis are you relying on for your 35 to 17 40 years there? 18 A. My report says quite clearly in the previous sentence 19 in the Tokudome study upon which he, meaning Dr. 20 Werntz, relies the latency from first exposure to 21 arsenic to lung cancer was 37.6 years. I'm pointing 22 out in that sentence that Dr. Werntz never considered 23 latency, and that's his reference. That's a reference 24 that Dr. Werntz relied on. He never considered 25 latency in designing his screening program, so he 242 1 proposes to screen people during periods when based on 2 his own references it's not clear that they have any 3 increased risk, and that's simply not scientifically 4 tenable. That is not a defensible cancer screening 5 program. 6 Q. Do you -- in that paragraph, you go on to say that 7 much of the cancer screening and proposals will be 8 done during periods when the class members are at no 9 increased risk of cancer from their alleged exposures, 10 and, therefore, his screening cannot -- the screening 11 programs cannot provide any benefit, whatsoever, 12 during these periods. Did I read that correctly? 13 A. Yes. 14 Q. And confirm for me, you don't believe the residents 15 will ever be at an increased risk of cancer from 16 exposure; is that correct? 17 MR. DANNINGER: Objection, form. 18 A. It is my opinion that your experts have presented no 19 reliable evidence that exposures from the Spelter site 20 have placed people in the class at any meaningfully 21 increased risk of cancer of any type. 22 BY MS. SLEVINSKI: 23 Q. Do you agree they've been exposed to these 24 contaminants from the site? 25 MR. DANNINGER: Objection, form. 243 1 A. It's not clear that there is reliable evidence of 2 exposure from this site. That's the whole point. 3 That's what Dr. Rodericks' report discusses. That's 4 what the Gradient report discusses. Dr. Valberg 5 refers to that issue in his report. Your experts 6 don't provide any reliable evidence of exposure. 7 BY MS. SLEVINSKI: 8 Q. Dr. Garabrant, those are not our experts, though; am I 9 correct? Those are defense experts you just referred 10 to? 11 A. The people to which I referred are defense experts 12 commenting on your expert's evidence which appears not 13 to be reliable. 14 Q. In your opinion, are residents at no increased risk of 15 cancer while they're still being exposed to 16 contaminants in and around the smelter community? 17 MR. DANNINGER: Objection, form, 18 foundation. 19 A. It depends on the latency from first exposure. I 20 could probably illustrate it by example. We agree I 21 think universally within the scientific community that 22 ultraviolet from the sun is a cause of skin cancer. 23 We do not believe that you get skin cancer on the day 24 you get a sunburn. There is latency involved from 25 time of first exposure to the development of skin 244 1 cancer, and I think the same is true for arsenic and 2 cadmium. 3 BY MS. SLEVINSKI: 4 Q. So would the length of time these people have been 5 living in this community near this Spelter -- I mean, 6 excuse me, near this smelter, that would not factor 7 into the latency period of diseases associated with 8 cadmium and arsenic? 9 MR. DANNINGER: Foundation. 10 A. That's exactly the point. Of course it factors in, 11 and Dr. Werntz didn't consider it. 12 MS. SLEVINSKI: Would y'all want to take a 13 quick break here before I move on to another topic? 14 Is this a good time? It's been about an hour. 15 MR. DANNINGER: That's perfectly all right 16 if you'd like one, that's -- that's with us. It gives 17 us a little time to stretch our legs, too. 18 MS. SLEVINSKI: Okay. 19 MR. DANNINGER: So we'll say about five or 20 ten minutes? 21 MS. SLEVINSKI: Yeah. 22 MR. DANNINGER: Okay. 23 MS. SLEVINSKI: I mean closer to five if 24 possible. 25 MR. DANNINGER: Okay, sounds good. 245 1 VIDEO TECHNICIAN: We're going off the 2 record. The time is 2:47 and 5 seconds p.m. 3 (Recess taken at 2:47 p.m.) 4 (Back on the record at 2:58 p.m.) 5 VIDEO TECHNICIAN: We are now back on the 6 record. The time is 2:58 and 40 seconds p.m. 7 BY MS. SLEVINSKI: 8 Q. Dr. Garabrant, before our break, we had been 9 discussing latency as it relates to the cancer 10 screening program, and you mentioned that -- well, in 11 your report, you're relying on the Tokudome study to 12 say that there are no lung cancers associated with 13 arsenic until at least 35 to 40 years after first 14 exposure; is that correct? 15 MR. DANNINGER: Objection, form. 16 A. I said there were no arsenic related lung cancers. 17 BY MS. SLEVINSKI: 18 Q. Okay, and that was based on the reference to the 19 Tokudome -- excuse me, Tokudome study? 20 A. Yes. 21 Q. Would you get -- look back at that Exhibit No. 137, 22 please? Do you still have that handy? 23 A. Yes, I do. 24 Q. Do you have it back in front of you? 25 A. I do. 246 1 Q. Okay. Now, you would agree that this report, this 2 Tokudome, the 37.6 year latency period was an average 3 of the cases reported; is that correct? 4 A. I would. 5 Q. Can you please turn to page 315 of that article? 6 A. Yes. 7 Q. In the left-hand column, towards the top, it discusses 8 latent period of lung cancer seen among public 9 smelters in that column; do you agree that the average 10 included cases, both above and below the 37.6 years 11 from first exposure? 12 A. Yes. 13 Q. In fact, this study it shows here that the first 14 exposure was -- excuse me, strike that. 15 It shows here that the first case was 13 16 years from first exposure; do you agree? 17 A. Yes. 18 Q. And that over 20 years below the 35 to 40-year range 19 that was stated in your report; is that correct? 20 A. Well, my report simply points out that in the Tokudome 21 study, the latency was 37.6 years. I do not believe 22 that Tokudome study alone provides a thorough 23 assessment of the latency between arsenic inhalation 24 and the onset of lung cancer or any other cancer, but 25 it's clear that Dr. Werntz's medical screening program 247 1 has not adequately considered latency. 2 I don't hold my report out as establishing 3 the latency period for arsenic and lung cancer. The 4 point of my report is to say there is information in 5 the literature, and Dr. Werntz never considered it, 6 and that is a failing in his basis for his medical 7 monitoring program. 8 Q. Would you agree, though, that I've just asked -- the 9 same question, that is the first case seen at 13 years 10 over 20 years below the 35- to 40-year range that's 11 stated in your report, correct? 12 A. 13 is more than 20, less than 35, that is correct. 13 Q. And the Tokudome study is a measurement from first 14 exposure to death from cancer; isn't that correct? 15 MR. DANNINGER: Form, foundation. 16 A. I believe that's how they calculated latency. It 17 should be pointed out that the average survival in 18 lung cancer is on the range of about a year, so 19 latency from first exposure to onset of clinical 20 cancer is roughly the same as latency from onset of 21 exposure to death. 22 BY MS. SLEVINSKI: 23 Q. That's not found in the Tokudome study, is it, though? 24 A. What's not found in -25 Q. What you just said about the death of lung cancer 248 1 and... 2 A. No, that's from my knowledge of that disease process 3 as a practicing physician, and that's fairly easy to 4 find. 5 Q. The Tokudome study gives no data as to when people 6 were first diagnosed; is that correct? 7 A. I don't understand your question. I'm sorry. 8 Q. In the Tokudome study, there's no data as to when the 9 people, the cases were first diagnosed; is that 10 correct? 11 MR. DANNINGER: Form. 12 A. Well, I'll have to look, I haven't considered that 13 issue. It doesn't talk about when they were first 14 diagnosed. It's a mortality study that studies 15 deaths. 16 BY MS. SLEVINSKI: 17 Q. Thank you. Dr. Garabrant, is it also your opinion 18 that Dr. Werntz's program does not provide for 19 termination of the screening program he proposes? 20 A. He does not consider that there is a -- an end to the 21 period at which people are at increased risk from 22 exposure, so again, it's not part of his consideration 23 in designing his program. The -- the window of time 24 when people are at increased risk of cancer from some 25 exposure to a carcinogen has a beginning and has an 249 1 end, and Dr. Werntz hasn't considered that. 2 Q. Would you agree, though, that the period of risk would 3 continue as long as exposure to the contaminants 4 continues? Would you agree with that, sir? 5 A. If the exposure put people at increased risk, the 6 period of increased risk would begin after adequate 7 latency had passed and would continue for as long as 8 exposure continued plus whatever the latency period 9 is. 10 In other words, latency is nothing more 11 than a lag time, and so if -- if exposure begins on 12 year 10 and latency is 20 years, then risk begins on 13 year 30. If exposure stops on year 20 and the end of 14 the increased risk period lags the end of exposure by 15 20 years, then risk would stop on year 40. 16 Q. Is that the end of your answer? I don't want to cut 17 you off? 18 A. Yes. 19 Q. Okay. If you'd turn, please, sir to page 7 of your 20 report continuing on to opinion No. 4? 21 A. Yes. 22 Q. Now, your opinion is cancer risks alleged from these 23 exposures are too small to be detectable in relation 24 to background cancer risks; is that accurate? 25 A. Yes. 250 1 Q. You -- the sentence is, Dr. Werntz failed to properly 2 consider the risk of cancer related to the exposures 3 he alleges. Can you explain how he failed to properly 4 consider the risks? 5 A. Yes, the risks calculated by Dr. Brown and reiterated 6 by Dr. Werntz are so small that a medical screening 7 program could -- would -- would not uncover more than, 8 perhaps, at most one or two cancers, and so he's going 9 to -- Dr. Werntz proposed to screen a population of 10 thousands of people for 40 years -- sorry, just a 11 moment, now I'm blanking out -- yes, for 40 years past 12 the end of exposure, and it's clear that he will 13 discover not more than one or two cancers in that 14 entire time related to the exposures that he alleges 15 have occurred. He will discover in addition to those 16 one or two cancers that might be related, perhaps, 1 17 or 2,000 cancers that have no relationship to the 18 exposure. 19 That type of misguided medical monitoring 20 indicates that he has not thought carefully about the 21 magnitude of these risks and whether it is sensible to 22 screen for cancer in this population. 23 Q. Okay, Dr. Garabrant, are you aware that the United 24 States EPA considers a 1-in-10,000 risk in developing 25 cancer due to exposure a significant risk? 251 1 A. I'm not aware that they've used those terms, and it is 2 quite clear that the U.S. EPA has never recommended 3 screening for a 1-in-10,000 cancer risk. 4 Q. What do you base that on? 5 A. My reading of U.S. EPA documents. You've never seen 6 anything that suggests that screening should be done. 7 I've never seen any guidelines for cancer screening 8 that have suggested that screening under those 9 circumstances is justified. And one of the federal 10 agencies that is responsible for developing medical 11 surveillance guidelines for populations exposed to 12 hazardous waste, the ATSDR has developed screening 13 guidelines, and they do not recommend screening for 14 cancer risks as low as this. 15 Q. Would you agree with the EPA's classification of a 16 1-in-10,000 risk of developing cancer due to exposure 17 as a significant risk? 18 A. You would -19 MR. DANNINGER: Objection, foundation. 20 A. You would have to show me the document in which the 21 EPA says that before I could comment on it. 22 BY MS. SLEVINSKI: 23 Q. Okay. Going a little further in your report, you 24 compared the incremental lifetime cancer risk as 25 calculated by Dr. Brown to the lifetime cancer risk in 252 1 the U.S. general population; is that correct? 2 A. Yes. 3 Q. Now, the lifetime cancer risk that you used on your 4 calculations now, is that the risk for developing all 5 cancers or a select few? 6 A. All cancers. 7 Q. All cancers. And what is your understanding of the 8 cancers that Dr. Brown accounted for his incremental 9 cancer risk calculations? 10 A. Hold on, I'll have to get Dr. Brown's report out. 11 Dr. Brown used the U.S. EPA cancer slope 12 factor in calculating his risks. The cancer slope 13 factors are based on all cancers caused by that agent 14 in the opinion of the EPA. So that would include all 15 possible cancer outcomes. 16 Q. Dr. Brown's model uses calculation of the 30 years of 17 exposure for a life based on 70 years, correct? 18 A. Could you refer me to exactly where you're -- what 19 you're referring to? 20 MS. SLEVINSKI: You -- I mean do you know 21 that that's what Dr. Brown's 30-year calculation is 22 based on? 23 MR. DANNINGER: Form. 24 A. Well, I don't know it exactly the way you stated it, 25 and those things have to be stated correctly, and you 253 1 should refer me to exactly where in his report you're 2 talking about. 3 BY MS. SLEVINSKI: 4 Q. In your calculation, the 45 percent risk for the male 5 population, that includes people over the age of 70; 6 is that correct? 7 MR. DANNINGER: Form. 8 A. No, I think that that actually is the cumulative 9 lifetime cancer risk to age 70 or 72, I'd have to get 10 that document out to remember exactly what the upper 11 age cutoff was. It's typically 70 or in the low 70s, 12 so it's lifetime cancer risk to that age. 13 BY MS. SLEVINSKI: 14 Q. Dr. Garabrant, moving on to opinion No. 5 in your 15 report -16 A. Yes. 17 Q. -- your opinion states Dr. Werntz's proposed medical 18 monitoring has not known to be effective for some 19 cancers under any circumstances. Did I read that 20 accurately? 21 A. Yes. 22 Q. In your opinion, is the only goal of medical 23 monitoring to reduce deaths from diseases caused by 24 harmful exposures, or would early detection of 25 diseases be an equally important goal? 254 1 MR. DANNINGER: Form. 2 A. Well, you know, that's a really thorny issue. I think 3 that early detection may, in some circumstances, be 4 desirable to individuals. The difficulty is, I think, 5 that few individuals would be willing to trade their 6 longevity just to find out that they got cancer 7 younger. 8 In other words, if the screening program 9 actually incurs risks such that on average, the people 10 screened suffer a loss of life, it is difficult for me 11 to justify how any individual would say oh, I'm 12 willing to have my life shortened so I can find out 13 sooner that I've got cancer. 14 Q. What, in your opinion is required to make a 15 determination that a particular medical monitoring 16 program is effective for cancers? 17 A. Well, one of the things that you have to consider is 18 whether the medical monitoring reduces mortality in 19 the screened population. That's a very important 20 thing to know. 21 Q. Is there anything else? 22 A. It's important to know whether screening results in 23 earlier diagnosis that can be coupled to effective 24 treatment. There's no benefit to screening for a 25 disease for which there is no treatment option that is 255 1 of benefit to the person. It's important to know 2 whether the risks attendant to screening are -- it's 3 important to know what the risks are and to balance 4 those against the benefits of screening. 5 It's quite clear that many screening 6 activities carry substantial risks with them, either 7 risks that are direct consequences of the screening 8 activity or that are indirect consequences because of 9 the medical testing and diagnostic procedures that 10 follow positive screen results, so it's important to 11 know what those risks are. I think those would be the 12 major issues. 13 Q. Do you have an opinion, Dr. Garabrant, as to whether 14 early detection of any of the cancers that are at 15 issue in this lawsuit -- early detection lead to a 16 better prognosis? 17 MR. DANNINGER: Form. 18 A. Well, I think I've laid my opinions out on that issue 19 on page 7. For lung cancer, there is no evidence that 20 early detection leads to a better prognosis, and 21 that's true today in 2007 as it has been true for 22 decades, sadly. For bladder cancer, there is no 23 screening program that has been endorsed by the 24 medical community as being beneficial, and so it's 25 simply not done, even in people who are known to be at 256 1 high risk for bladder cancer such as heavy smokers, 2 the medical community has never endorsed screening for 3 bladder cancer in that population. 4 I think the same is true for kidney cancer, 5 the medical community has never endorsed screening for 6 kidney cancer, even in high-risk populations. Stomach 7 cancer, the medical community does not endorse 8 screening for stomach cancer, and so as we go through 9 the list of cancers that Dr. Werntz wants to screen 10 for, I'm not aware that the medical community has 11 endorsed that screening under any circumstances much 12 less the circumstances at issue in this class. 13 BY MS. SLEVINSKI: 14 Q. What about skin cancer, Dr. Garabrant? 15 A. Screening for skin cancer clearly is or can be 16 beneficial under some circumstances, but as I pointed 17 out, skin cancer's not an issue in this case because 18 skin cancer is related only to arsenic exposure from 19 contaminated drinking water which is not part of this 20 case. 21 Q. Okay, Dr. Garabrant, we're going to move on to the 22 second sort of section your report was divided into, 23 and the general title is My Opinions Regarding Dr. 24 Werntz's Proposed Screening for Noncancer Effects. Do 25 you see that on page 8, sir? 257 1 A. Yes. 2 Q. Opinion No. 6, exposure assessment must establish that 3 subject has been adequately exposed to be at increased 4 risk of the disease in order to justify medical 5 monitoring. Is that a correct statement of your 6 opinion, sir? 7 A. Yes. 8 Q. If a precise dose of an agent that is alleged to cause 9 harmful effects is unknown but the agent is known to 10 have toxic effects, does that mean that medical 11 monitoring is not appropriate under any circumstances 12 of exposure? 13 MR. DANNINGER: Form. 14 A. Well, it leaves you in a netherworld where you have no 15 basis for a recommendation. I would point out, for 16 example, that we're all exposed to small amounts of 17 cadmium, arsenic, and lead in the general environment 18 of the United States. Those things are present in 19 food, they're present in the air, they're -- some of 20 them are present around roadways, some of them are 21 present in occupational settings. 22 If you don't have any sense for the 23 exposure levels, you have no basis for a decision to 24 screen or not to screen, and so if -- if you simply 25 say oh, if they're present, we should screen, then I 258 1 guess you should screen the whole world because we're 2 all exposed at some level. You have to have a basis 3 for determining that the exposure levels are adequate 4 to put people at increased risk of some disease as a 5 foundational concept to justify medical monitoring. 6 Q. Is that the end of your response? 7 A. Yes. 8 Q. Okay. ...your report you stated that exposure 9 assessments must establish that subjects have been 10 adequately exposed in order for them to be at 11 increased risk to justify medical monitoring. In your 12 opinion, what would it take to establish adequate 13 exposure? 14 MR. DANNINGER: Form. 15 A. It would take far more than is present in this case in 16 which you have no evidence, no reliable evidence of 17 exposure to arsenic cadmium or lead from the Spelter 18 site in any area of the exposure or of the litigation 19 class. 20 BY MS. SLEVINSKI: 21 Q. What would be reliable evidence in your opinion? 22 A. It's entirely dependent on the circumstances of the 23 alleged exposure. I -- you know, that's a 24 hypothetical that's so broad, I can't answer it for 25 this site. 259 1 Q. Well, then for this particular case, this situation? 2 MR. DANNINGER: Form. Foundation. 3 A. Well, I think the type of evidence that would be 4 extremely valuable would be blood/lead tests, urinary 5 cadmium, blood cadmium, urinary arsenic excretion, 6 that would establish that the plaintiffs actually have 7 received doses that exceed the range in the nonexposed 8 population of comparable age and sex -9 BY MS. SLEVINSKI: 10 Q. Establishing -11 A. I wasn't finished. 12 Q. Okay, sorry. 13 A. Wasn't finished. In -- in addition to evidence that 14 those exposures came from the smelter site that is 15 alleged to have led to their exposure. In other 16 words, what I would regard here is, you know, some -17 some estimates or measurements, even better, of 18 internal dose that say yes, we know these people have 19 been overexposed, and then you have to have a -- a 20 solid scientific foundation to say and yes, we know 21 those exposures came from the Spelter site, and that's 22 entirely lacking. 23 In fact, the single plaintiff who had a 24 blood lead test had a lead test that is at the low end 25 of the normal range. It was two micrograms per 260 1 deciliter, and that woman lives immediately adjacent 2 to the tailings pile. 3 Q. Dr. Garabrant, would using, like you said, blood lead 4 levels, urinary cadmium levels, are those effective 5 measures of exposure that occurred in the past -- and 6 I mean ten years ago for these people -- or do those 7 more accurately reflect acute exposures? 8 A. Well, just a moment ago you asked me about ongoing 9 exposures implying that these exposures are still 10 continuing. Those -- those tests are certainly best 11 for recent exposures. There's no question about that, 12 so if you're looking at urinary arsenic, yes, that -13 that reflects current exposure. 14 If you're looking at blood lead tests, 15 those largely reflect exposure in the most recent few 16 months, although in someone who is heavily leaded and 17 has an appreciable bone lead burden, the blood lead 18 tests may remain elevated for many, many years after 19 exposure ceases. 20 For cadmium, the picture is a bit more 21 complex. Blood cadmium levels typically represent 22 recent exposure within a few months, and urine cadmium 23 levels fluctuate depending on the amount of cadmium 24 bound in the proximal convoluted tubule. They are 25 most reliable in the setting of concurrent or recent 261 1 exposure. But the point is it's important to have 2 some way of showing that the population has been 3 overexposed. 4 In this setting, it is alleged that these 5 people were overexposed to lead. If that were true, I 6 would expect that there would be ways to assess that. 7 Assessing bone lead burden is a technique that's 8 available, and it looks at body stores of lead that 9 are persistent for many, many years. I would expect 10 that plaintiffs would have done that to show that 11 these people were exposed. 12 Q. Is that the end of your response? 13 A. Yes. 14 Q. So in your opinion, you think -- you would like to see 15 actual increased levels in the human body, and 16 increased levels of these various contaminants from 17 the environment would not be an adequate 18 representation of exposure? 19 MR. DANNINGER: Form. 20 A. No, that's not what I said. What you don't have, what 21 plaintiffs don't have in this case is any reliable 22 evidence of environmental exposure levels that are 23 unusual for West Virginia, and they don't have any 24 evidence of increased body burden in the plaintiffs. 25 Lacking both of those foundations, you have no 262 1 evidence of exposure that would in any way justify any 2 sort of medical monitoring for adverse health effects 3 from arsenic, lead, or cadmium. 4 BY MS. SLEVINSKI: 5 Q. Dr. Garabrant, do you know what the half life for 6 arsenic is in the body? 7 A. Well, I think I just told you about that. In the 8 blood, it has a half life on the order of, perhaps, 60 9 hours. 10 Q. Okay. Urine? 11 A. In the urine, I think it's roughly comparable, I don't 12 know the exact number, but it's -- it's typically in 13 the matter of hours, you know, hours to a few days at 14 most. 15 Q. Hair? 16 A. Well, hair, it -- ingested arsenic is incorporated 17 into the hair as the hair grows, and it stays in the 18 hair for as long as it's on the head. So for a woman 19 who has hair down to her waist in the back, 20 theoretically, you can get evidence of excessive 21 exposure to arsenic going back years. For someone 22 with a buzz cut, you're stuck with perhaps a few 23 weeks. 24 Q. Okay, so what about the half life of cadmium in the 25 human body? 263 1 A. I believe cadmium follows a two-compartment model. 2 The blood levels typically have a short half life, 3 typically expressed in hours, I think perhaps a 4 hundred hours. The long-term tissue compartment, I 5 believe, has a half life that's measured in years. 6 MR. DANNINGER: Hay Amanda, just to let you 7 know, we have probably about two or three minutes left 8 on the tape. 9 MS. SLEVINSKI: Okay, let's go ahead and 10 change it real quick and just keep going. 11 MR. DANNINGER: Okay. 12 MS. SLEVINSKI: Off the record change it. 13 MR. DANNINGER: Yeah, it will probably take 14 about five minutes or so. 15 MS. SLEVINSKI: Okay. 16 VIDEO TECHNICIAN: We're going off the 17 record. This is the end of tape No. 4. The time is 18 3:33 and 5 seconds p.m. 19 (Recess taken at 3:33 p.m.) 20 (Back on the record at 3:38 p.m.) 21 VIDEO TECHNICIAN: We are now back on the 22 record. This is the beginning of tape No. 5. The 23 time is 3:38 and 53 seconds p.m. 24 BY MS. SLEVINSKI: 25 Q. Dr. Garabrant, right before the break, we've been 264 1 discussing the half life of the various constituents 2 that we were concerned with and different body fluids, 3 body parts. We left off on cadmium. So if you could 4 please pick up where you left off about cadmium, sir. 5 A. I think I had finished cadmium. 6 Q. Did you -- the half life of cadmium in the urine? 7 A. I'd have to look that up. It's complex because in the 8 early stages of cadmium exposure, cadmium in the urine 9 accurately reflects cadmium in the blood, so I believe 10 it has about the same half life. So what -- what is 11 in the blood and passes through the kidney is 12 effectively filtered out into the urine. 13 As time passes, that cadmium begins to bind 14 to the proximal convoluted tubule cells and 15 accumulates. When you get a sufficient amount of 16 binding, then you begin to have preclinical effects on 17 the kidney such that some tubular proteins begin to be 18 excreted in the urine. 19 At that point, urinary cadmium excretion 20 may actually rise so that you excrete more than is -21 you excrete it at a higher concentration than is 22 present in the blood. If cadmium exposure continues, 23 damage to the convoluted tubules increases, and you 24 develop tubulointerstitial disease which results in 25 damage to the glomeruli and a fall in glomerular 265 1 filtration. And at that point, cadmium excretion in 2 the urine may actually drop and be less than what's in 3 the blood. So it's really sort of a three-phase 4 model. There's no simple answer to the urinary half 5 life. 6 Q. Okay. What about the cadmium half life in human hair? 7 A. I believe that cadmium that is incorporated into the 8 shaft of the hair as the hair is formed stays in the 9 hair, so it's the same answer as for arsenic. 10 Q. Okay, thank you. Now what about for lead? What is 11 the half life of lead, and we'll do the same different 12 bodily, I guess, parts and fluids, starting with lead 13 in the blood, sir. 14 A. Well, lead in the blood has a half life of about 30 15 days. 16 Q. What about lead in the urine? 17 A. It follows lead in the blood. 18 Q. And how about lead in human hair? 19 A. Same answer as for cadmium and arsenic. If lead is 20 incorporated into the hair shaft, it persists in the 21 hair shaft for as long as the hair is on the head. 22 Q. So from our discussion just now, it seems that all 23 these chemicals have a fairly short half life in the 24 urine and blood; is that correct? 25 A. With the exception of the discussion on cadmium, 266 1 certainly for arsenic and lead, that's correct. 2 Q. Okay. Now what ways would you use or suggest to use 3 to assess exposure over the time period that these 4 people have lived in the communities for these -5 these heavy metals because the half life in the blood 6 and urine, excluding cadmium, as you mentioned, is so 7 short? 8 MR. DANNINGER: Form and foundation. 9 A. Well, you know, clearly this is a situation where 10 cortical bone x-ray fluorescence would establish quite 11 clearly whether these people have excessive body 12 burdens of lead and then knowing from environmental 13 sampling, the ratios between lead and arsenic and lead 14 and cadmium, it might be possible to make some 15 inferences about past exposure. 16 I'd been surprised that plaintiffs had done 17 no biological monitoring with the exception of the one 18 lead test on Ms. Perrine which showed that she was at 19 the dramatically low end of the normal population for 20 her blood lead in spite of living adjacent to the 21 tailings pile. Clearly, it's not appropriate to do 22 medical monitoring on this population in the absence 23 of evidence of exposure as is the situation in this 24 case. 25 Q. Okay, thank you. Give me one second, I'm looking at 267 1 my notes. 2 A. Okay, you're welcome. 3 Q. Dr. Garabrant, you can't say that blood and urine 4 tests would show anything to a reasonable degree of 5 scientific certainty, can you? 6 MR. DANNINGER: Form. 7 A. Well, here's the issue, Ms. Slevinski, if there is 8 ongoing exposure in this class area, yes, I would 9 think that blood in urine tests would be invaluable to 10 show that. If there is not ongoing exposure in this 11 community, then your experts simply need to say oh, 12 the exposure ceased, and to give some estimate of when 13 it ceased, and then that would have some important 14 implications for whether medical monitoring for past 15 exposures makes sense, but they've done neither, so 16 here you've got Dr. Werntz proposing medical 17 monitoring for health effects and we're talking 18 noncancer effects now related to arsenic, cadmium, and 19 lead whereas these exposures cease at some point in 20 the past, this monitoring is nonsense. If these 21 exposures are ongoing, then he ought to be asking for 22 biological monitoring for arsenic, cadmium, and lead. 23 BY MS. SLEVINSKI: 24 Q. Dr. Garabrant, would you agree with me that these 25 exposures are cumulative in the exposures to arsenic, 268 1 cadmium, and lead? 2 A. I'm sorry, I missed one of your words because of a 3 noise in the room here. 4 Q. Okay. 5 A. I didn't hear it. 6 Q. Do you agree that exposures to arsenic, cadmium, and 7 lead are cumulative? 8 A. No. No, exposures to lead may accumulate in cortical 9 bone. Arsenic is not cumulative. Arsenic is excreted 10 with a fairly short half life, and there are no tissue 11 stores of arsenic, and as we discussed for cadmium, 12 cadmium can accumulate in the kidney under 13 circumstances of excessive exposure, but there's a 14 threshold for that, and there's a threshold for 15 impairment of the kidney as a result of cadmium. 16 Q. Okay, thank you, Dr. Werntz -- I'm sorry, 17 Dr. Garabrant. Next opinion No. 7. Before I move on, 18 there's nothing cited in your section of opinion No. 19 6, no studies or articles that you have cited here as 20 being relied upon. Can I take that to believe that 21 you are relying upon your experience and education and 22 your reading of Dr. Werntz's report? 23 A. No, you can take it to indicate exactly what it says, 24 that Dr. Werntz's proposed plan is not grounded in 25 consideration of the dose or duration of exposure 269 1 adequate to cause any of the conditions he 2 allegations. The point is Dr. Werntz proposes to 3 screen for all these diseases and he has provided no 4 evidence that he adequately considered the dose 5 adequate that cause those diseases. My -- my -- my 6 comments are that his plan are nonsense, it has no 7 scientific foundation. I don't need references to say 8 he doesn't have any references. 9 Q. Okay. Let me see if I can be a little more clearer 10 with my question. I'm just trying to establish that 11 for your opinion No. 6, you have nothing cited as an 12 outside resource, so you won't be showing up at trial 13 saying that you've got this particular article or book 14 or what have you that says, you know that Dr. Werntz 15 is wrong I'm just establishing that you have no 16 outside materials you're relying on for that opinion; 17 is that correct? 18 MR. DANNINGER: Form. 19 A. Of course I have outside references. I didn't realize 20 it would be necessary to provide references for 21 fundamental principles of science. 22 Okay. I would cite to the textbook by 23 Alice Ottoboni, The Dose Makes The Poison. I would 24 cite to a number of basic toxicology textbooks such as 25 Ellenhorn and Barceloux, E-l-l-e-n-h-o-r-n, 270 1 B-a-r-c-e-l-u-u-x. I would site to Casarett and 2 Doull's Textbook of Toxicology. I would cite to 3 Lowrey's Textbook On Biological Monitoring which has a 4 marvelous chapters on lead, cadmium, and arsenic 5 biological monitoring. 6 I would cite to the two-volume textbook on 7 the toxicity of metals by, it has a blue cover, and 8 I'm blocking out the first author's name. All of 9 those -- I'll come up with it as we talk. All of 10 those materials would substantiate my opinion that it 11 is accepted scientific practice to quantify exposure 12 levels from measurements of exposure, and that 13 assessing whether people have been -- are at increased 14 risk of disease from arsenic, cadmium, or lead has to 15 be based in measurements that they have either been 16 exposed via environmental pathways or biological 17 monitoring that would establish that they had internal 18 doses that had been adequate to put them at increased 19 risk of disease. 20 Q. Is that the end of your response? 21 A. Yes. 22 MS. SLEVINSKI: Scott, can I ask you a 23 quick question? I'm looking at the clock and 24 realizing it's 3:50 your time. How long are you able 25 and Dr. Garabrant to go this afternoon? 271 1 MR. DANNINGER: Well, we were going to talk 2 to you about that because we have to get a cab set up. 3 We were thinking that we would give you a little more 4 time depending on how much you need over five o'clock, 5 but -6 MS. SLEVINSKI: I wouldn't need much over 7 five o'clock. I mean I just I want to be able to 8 gauge -9 MR. DANNINGER: What do you need, you tell 10 us what you need. 11 MS. SLEVINSKI: 5:30 would be sufficient 12 and appreciate that that's -13 MR. DANNINGER: 5:30's just fine. Doctor, 14 is 5:30 okay for you? 15 THE WITNESS: Yes. 16 MR. DANNINGER: Yes, 5:30 is fine, Amanda. 17 MS. SLEVINSKI: Thank you, sorry for that. 18 MR. DANNINGER: Hey, that's all right, I'm 19 glad you brought it up. We were going to bring it up. 20 BY MS. SLEVINSKI: 21 Q. Dr. Garabrant, back to opinion 7, I jumped around, 22 opinion No. 7 in your report says Dr. Werntz fails to 23 consider dose response relationships and latency; is 24 that correct? 25 A. Yes. 272 1 Q. That's your opinion on Dr. Werntz's medical monitoring 2 program, correct? 3 MR. DANNINGER: Form. 4 BY MS. SLEVINSKI: 5 Q. Towards the bottom of page 8, the final paragraph, 6 there's a sentence he has provided no scientific basis 7 for his assumptions that such effects would persist 8 for the remaining life times of all the plaintiffs and 9 thereby necessitate 40 years of medical monitoring as 10 he proposes. Can you explain that statement and your 11 reasons behind it in a little more detail for me, 12 please? 13 A. Well, Dr. Werntz proposes a medical monitoring program 14 that will continue for 40 years, okay? And I'll -15 I'll read from page 4 of his report. Medical 16 monitoring shall continue until 40 years past the end 17 of exposure. Generally, this would be either 40 years 18 beyond moving out of the class area or 40 years after 19 their residence is remediated. This is based on the 20 usual latencies of the diseases of interest. Okay, 21 that's the end of the quote. 22 So what he's saying is I'm assuming that 23 these diseases go on for 40 years beyond the end of 24 exposure or that these people are at increased risk of 25 these diseases for 40 years after the end of the 273 1 exposure. He's provided no basis for that statement, 2 there's not a single reference in his report that 3 would substantiate that paragraph in his plan, and it 4 has no scientific rationale. 5 Q. Now, Dr. Garabrant, similar to opinion 6, since there 6 is no actual materials cited in opinion 7, you're 7 going to base that on your education, your experience, 8 and would there be any outside sources as -- you know, 9 support for your opinions here, sir? 10 A. Ms. Slevinski, I don't -- I'm confused by your point. 11 The point of my report is that Dr. Werntz cites to 12 nothing, he has no basis for his opinions. He 13 proposes a medical monitoring program that is nonsense 14 because he doesn't know how long these diseases 15 persist, he doesn't -- he hasn't specified the 16 circumstances under which people at increased risk, he 17 doesn't specify when their period of increased risk 18 starts or ends. 19 There's no reference that I need to point 20 out that he doesn't have a basis for his opinions. 21 There's no basis for his report. 22 Q. I'm just -23 A. I'm still speaking. 24 Q. I'm just trying to establish that -25 A. I'm still speaking. 274 1 Q. Go ahead. 2 A. Okay? I read your paragraph from page 4 of his 3 report. There is not a single footnote that a 4 companies that part of his plan. My report simply 5 says gee, he doesn't seem to have a basis for his 6 opinions. There's no -- there's no textbook that's 7 going to document that Dr. Werntz doesn't have a basis 8 for his opinions. Dr. Werntz's report has no 9 foundation, it's speculation. 10 Q. Are you finished? 11 A. Yes. 12 Q. I was just saying I don't have a point to the 13 question, per se, except that I'm just trying to 14 establish that as evidenced by this section of your 15 report, you will not be coming later on at trial and 16 say with some material that you say support your 17 opinions in that section. That's all I was asking, 18 just verify that. 19 A. Well, I can certainly provide references that 20 establish the fundamental principals that need to be 21 met in order to perform medical monitoring. I'm happy 22 to do that, so the United States preventive 23 services -- preventive health services task force 24 report, I -- I'll certainly provide that, in fact, I 25 cite that in my references. There are textbooks on 275 1 medical monitoring, the textbook by Alan Morrison on 2 cancer screening, I will cite to that. A whole series 3 of papers published in the journal of occupational 4 meds, to complete issues of that journal some years 5 ago that examined many, many aspects of medical 6 monitoring of populations and screening of populations 7 exposed to chemicals, I will cite to that set of 30 or 8 40 papers. There's a textbook by David Eddy that lays 9 the foundational concepts for cancer screening that I 10 will cite to that was published in about 1980 or 1982, 11 and formed the foundation for the American Cancer 12 Society's recommendations on cancer screening for 13 years, it's still valid. 14 I'm blocking out the citations to two other 15 textbooks I have on my shelves that have to do with 16 medical monitoring and cancer screening, so yes, I 17 will -- I've already given you a bibliography to 18 support my opinions in section 7. 19 Q. Okay, thank you, Dr. Garabrant. Now, moving on in 20 your report to No. 8, cadmium and renal disease, do 21 you agree with me that when a person is exposed to 22 cadmium it accumulates in the kidney; is that correct? 23 MR. DANNINGER: Form. 24 A. At some points in the period of exposure, yes, it can, 25 depends on the amount of exposure they have. 276 1 BY MS. SLEVINSKI: 2 Q. So like over time if a person is continuously exposed 3 to cadmium, it will eventually build up in the kidney? 4 MR. DANNINGER: Form. 5 A. Depends on the levels. I mean we've all been exposed 6 to cadmium, we're all exposed daily, it's in foods. 7 BY MS. SLEVINSKI: 8 Q. In your report, you state that there's published 9 studies according to threshold for the adverse effects 10 of cadmium on renal function that there's a -- that 11 second paragraph in the section; do you see that? 12 A. Yes. 13 Q. Now, I have the report that you cited in there. Would 14 you explain how those taken together indicate there is 15 a threshold of cadmium exposure below which no clear 16 risk of adverse renal effects? 17 MR. DANNINGER: Form. 18 A. Yes, the first study referenced 107, which is by 19 Nakadaira, N-a-k-a-d-a-i-r-a, shows that subject 2 had 20 a blood cadmium level in the range of .38 to .41 21 micrograms per deciliter were not at increased risk of 22 renal dysfunction than were nonexposed subjects who 23 had blood cadmium levels were roughly half of that. 24 That indicates that at those exposure levels, there's 25 no increased risk of renal dysfunction, okay? Ikeda, 277 1 I-k-e-d-a, found that urine cadmium concentrations of 2 4 micrograms of cadmium per gram of creatinine was a 3 threshold above which there was increased excretion of 4 urinary beta 2 microglobulin, and below that, there 5 was not. 6 Q. Wouldn't you agree, sir, that urinary B2 microglobulin 7 is the most sensitive -8 COURT REPORTER: I'm sorry, can you please 9 start that over again? 10 MS. SLEVINSKI: Yes, I'm sorry. 11 BY MS. SLEVINSKI: 12 Q. And you would agree, wouldn't you, that urinary B2 13 microglobulin is the most sensitive indicator of renal 14 damage? 15 A. Of renal dysfunction. 16 Q. Okay. Go on, please, with your explanation for this. 17 A. Okay. And then a third study, No. 81 in my 18 references, they actually calculated the 5 percent 19 BMDL, the benchmark dose limit, and found that that 20 limit for renal tubular dysfunction was in the range 21 of 3 to 4 micrograms of cadmium per gram of creatinine 22 excretion, so a finding very similar to that from 23 Ikeda. 24 So clearly, these investigators show that 25 there are levels of cadmium exposure and cadmium 278 1 excretion below which there's simply no evidence of 2 any adverse effect on the kidney. Now that's really 3 important because in order for Dr. Werntz to justify 4 screening people for evidence of renal dysfunction, he 5 has to have evidence that these people are exposed at 6 levels such that renal dysfunction would occur. 7 Otherwise, there's no reason to do it. 8 Q. Dr. Werntz's screening program does, in fact, call for 9 use of urinary B2 microglobulin; is that correct? 10 A. Yes, it does. 11 Q. Thank you. Now, when we were talking about cadmium 12 accumulation in the kidneys, at what point does the 13 cadmium start building up? Is there a specific amount 14 of exposure that has to occur? 15 A. Yes. 16 Q. What is that? 17 A. Hold on, it's going to take me a minute. 18 Q. Okay. 19 A. When cadmium in the renal tubular cells exceeds a 20 threshold in the range of about a hundred to 300 21 micrograms of cadmium per gram of wet weight of renal 22 tissue, that's when cell damage begins and function -23 functional impairment begins. 24 Q. Where did you get that information from, sir? 25 A. I'm reading that from the chapter on cadmium in 279 1 Rosenstock and Cullen's textbook of Clinical 2 Occupational and Environmental Medicine. 3 Q. Is that on your reference list? 4 A. That chapter is not, although, I authored two chapters 5 in this book that are immediately adjacent to that 6 one. I didn't realize that you were going to ask me 7 about the distribution and excretion of cadmium as it 8 related to the kidney, so I didn't -- in fact, I 9 didn't prepare a report on that, but since you've 10 asked me about it, I'm happy to respond. 11 Q. Thank you, shouldn't that particular chapter of that 12 textbook be added as a reference? 13 A. Well, if you're going to go into areas such as you 14 just have, yes. 15 Q. Is it true that urine cadmium levels will not start to 16 go up until the cadmium levels in the kidney have 17 reached the point where renal dysfunction is 18 occurring? 19 A. I don't know what you mean by go up. 20 Q. You won't start detecting cadmium in the urine until 21 the levels of cadmium in the kidney have already 22 reached a point where they can cause renal dysfunction 23 and renal damage; is that correct? 24 A. No, that's not correct. 25 Q. Okay. What are you basing that on? 280 1 A. My understanding of cadmium excretion. 2 Q. Were you looking at something to refresh your 3 knowledge on cadmium excretion? 4 A. Yes, I was. I was looking at the chapter in 5 Rosenstock and Cullen to refresh my memory. 6 Q. Okay, thank you. In urinary B2 microglobulin and the 7 urinary cadmium levels, are they essentially measuring 8 the same thing? 9 MR. DANNINGER: Form. 10 A. No. The answer is no. 11 BY MS. SLEVINSKI: 12 Q. How -- how -- what -- what is the B2 microglobulin 13 measuring and what is urinary cadmium, what is that 14 level measuring? 15 MR. DANNINGER: Form. 16 A. It's beta 2, not B2, beta 2 microglobulin is a -- a 17 protein that comes from the cells of the proximal 18 convoluted tubule in the kidney. It is a marker of 19 tubular dysfunction. It's telling you that the cells 20 are being adversely affected. Urinary cadmium is a 21 measure of cadmium. It tells you how much cadmium is 22 being excreted in the urine. 23 They're not the same things. One is a 24 marker of dysfunction in tissue, the other is a marker 25 of excretion of a material. Other things besides 281 1 cadmium will also cause beta 2 microglobulin 2 excretion. Basically, anything that damages or any of 3 a number of materials that damage the proximal 4 convoluted tubule will lead to excretion of beta 2 5 microglobulin, doesn't have to be cadmium. 6 Q. Okay. In your report, you state that lead has been 7 linked to decreased renal function and renal failure, 8 and you say that the disorder has been seen in 9 industrial settings and in circumstances of prolonged, 10 high exposure; is that correct? 11 MR. DANNINGER: Can you just tell us where 12 you are in this -13 MS. SLEVINSKI: Oh, I'm sorry, on page 9 of 14 Dr. Garabrant's report, third paragraph down. 15 MR. DANNINGER: Okay, thank you. Form. 16 MS. SLEVINSKI: Sorry? 17 MR. DANNINGER: Form objection. 18 A. What you said roughly paraphrases my report. 19 BY MS. SLEVINSKI: 20 Q. Do you know what levels of lead are necessary to 21 induce renal dysfunction? 22 A. I haven't gone back to look that up. Fairly high 23 dysfunction. We don't see evidence of renal 24 dysfunction in -- I don't know where the threshold is, 25 I've never seen it in someone who, with a blood lead 282 1 under 40, in fact, I don't recall seeing it in people 2 with blood leads in the 50s and 60s, so it's -- it 3 requires a fairly high blood lead level before that is 4 observed. Are you there? 5 Q. Yeah, I'm thinking. You said you don't recall seeing 6 it personally. You mean by personally as not recall 7 seeing it in patients or in studies or articles you've 8 read? 9 A. No, no, no, I'm talking about in patients. As I 10 mentioned to you, I -- I used to do the medical 11 monitoring program for a couple of brass foundries. 12 Q. Right, okay. 13 A. And I saw hundreds of people who had lead exposure. 14 Some of them with very high blood lead levels, and I 15 don't recall ever seeing evidence of renal dysfunction 16 in any of them. In fact, my colleagues and I did a 17 research study in one of those foundries looking to 18 see whether we could detect excessive excretion of 19 beta 2 microglobulin retinol binding protein and 20 N-acetyl glucose aminidase, or NAG, and we were unable 21 to show there was any increased excretion of any of 22 those proteins in that population, and these were 23 people who routinely had blood leads in the 30s and 24 40s, and some of them up into the 50s. 25 Q. Okay, thanks, Dr. Garabrant. You also discussed the 283 1 and we have a little bit earlier today discussed buy 2 owe monitoring. Is it your opinion that biomonitoring 3 is the best measure or best way to quantify exposure 4 to these metals in the class areas? 5 A. Well, it depends. If the exposures are still ongoing, 6 then yes, biomonitoring for arsenic, lead, or cadmium 7 would be a valuable way to establish whether people 8 had evidence of internal doses that were excessive -9 Q. Would -10 A. I'm not done. 11 Q. Sorry. 12 A. And that biomonitoring would preclude any other type 13 of medical testing unless it was demonstrated that 14 these people had exposures adequate to put them at 15 increased risk of disease and then the medical 16 monitoring program could be fashioned that would be 17 aimed at detecting those diseases once we knew that 18 people were adequately exposed to be at increased 19 risk. 20 Now, if the subjects -- and I should 21 mention it would be important in addition to that 22 monitoring to establish through environmental 23 measurements that the source of exposure came from the 24 Spelter site. And so if -- if the plaintiffs believe 25 that there's ongoing exposure, I would have expected 284 1 them to have shown via biological monitoring that 2 there was evidence of internal dose. If the exposures 3 have ceased, I do not believe that biological 4 monitoring for urine cadmium or arsenic or blood 5 cadmium is likely to be useful. And I do not believe 6 that blood lead measurements would be useful. I think 7 -- I'm surprised in fact that the plaintiffs have not 8 done cortical bone x-ray fluorescence studies to 9 demonstrate that the plaintiffs have increased body 10 burdens of lead, that's feasible to do. 11 If there is not evidence through biological 12 monitoring or through environmental samples that the 13 class in this litigation has evidence of excessive 14 exposure from the Spelter site, then it would be my 15 opinion that there is no medical monitoring and no 16 biological monitoring program that makes any sense at 17 all, and since I have not seen any reliable evidence 18 that this class has been exposed in any manner that's 19 unusual for that region of West Virginia, it seems to 20 me that there's no reason for medical monitoring or 21 for biological monitoring. 22 Q. Is that the end of your response? 23 A. Yes. 24 Q. So if exposure were ongoing, would biomonitoring be 25 able to detect the degree of past exposure, by past 285 1 exposure being ten years ago, 20 years ago, something 2 further in the past? 3 A. Well, I think I've answered that question. I just 4 answered it. And I think you've asked it now three 5 times in different ways that the urine arsenic, urine 6 cadmium, blood cadmium and blood lead levels relate 7 most clearly to ongoing exposure, those are not good 8 tests for distant past exposure. 9 Q. That's all I was asking, that -- thank you. 10 A. Yes, and -- and let me point out again that if 11 plaintiffs have a sincere interest in estimating 12 distant past exposure, cortical lead x-ray 13 fluorescence would clearly establish whether these 14 people have been overexposed or not. 15 Q. Okay, is that the end of your response for that? 16 A. And that would need to be done one time only in each 17 Pesch person to establish their body burden and I 18 would have thought that would be a foundational test 19 for Dr. Werntz before he could possibly give opinions 20 that these people have been overexposed to lead and he 21 hasn't done it. 22 Q. Are you finished? 23 A. Yes. 24 Q. Okay. If you flip to page 10 of your report, opinion 25 No. 9 on bone fragility, do you see that, sir? 286 1 A. Yes. 2 Q. These subtitles aren't as apparent, so would you 3 please tell me what your opinion is in this case with 4 respect to bone fragility? 5 A. Well, my opinion is exactly what I wrote. Dr. Werntz 6 alleges that lead has been linked to bone fragility. 7 Lead is not known to be associated with this disorder 8 and Dr. Werntz has provided no scientific basis for 9 his claim. Moreover, he proposes no tests to screen 10 for bone fragility. Okay, those are my opinions, so 11 he's -- I think he's just got it wrong. Lead's not 12 linked to bone fragility. He hasn't proposed any 13 tests for bone fragility. 14 Q. Okay. Now, the second paragraph addresses cadmium. 15 What about for cadmium and bone fragility, your -16 A. Okay, Dr. Werntz alleges that cadmium has been linked 17 to bone fragility. Cadmium can interfere with bone 18 mineralization because of damage to the kidneys. When 19 cadmium has accumulated in the proximal convoluted 20 tubule to the point where it is causing clinically 21 apparent nephropathy. It also interferes with vitamin 22 D metabolism, and people do not make enough vitamin D. 23 Vitamin D is important in calcification of bones, and 24 at the point where people begin to suffer 25 tubulointerstitial disease, they may also have defects 287 1 in bone calcification. 2 However, there's no scientific basis, 3 whatsoever, for a conclusion that the exposure levels 4 alleged to have occurred in the class area would have 5 caused this disorder in the community. Dr. Werntz has 6 shown no evidence that anybody in this class has 7 kidney damage consistent with cadmium toxicity. He's 8 shown no evidence of beta 2 microglobulin urea. He's 9 shown no evidence of albuminuria, he's shown no 10 evidence of increased blood creatinine levels, he's 11 shown no evidence of any evidence of any impairment of 12 kidney function which would be a prerequisite before 13 it is likely that anyone has suffered bone fragility 14 in relation to cadmium. 15 Q. Dr. Garabrant, do you agree, though, that Dr. Werntz 16 did not propose in his report to conduct any sort of 17 monitoring for bone fragility; would you agree with 18 that? 19 A. Well, I would agree with that, and -20 Q. Dr. Garabrant? 21 A. No, I'm just looking back at his report where on page 22 5, he mentions bone fragility as a disease considered 23 to be related to the exposures from the Spelter site, 24 and it strikes me as flawed reasoning to opine that 25 that has occurred when he has failed to do the testing 288 1 that would establish whether people have evidence of 2 renal dysfunction that would be a necessary 3 prerequisite before they could develop bone fragility 4 from cadmium. 5 Q. Thank you, sir. I just was asking for you to confirm 6 your understanding if you do understand it, that 7 Dr. Werntz did not, in fact, propose to monitor for 8 bone fragility in his medical monitoring plan? 9 MR. DANNINGER: Form, foundation. 10 A. That's correct, he did not. 11 BY MS. SLEVINSKI: 12 Q. If you look -- well, in the interests of time, these 13 last several subopinions we're talking about back 14 here, we'll try and get through them kind of quickly. 15 The bone fragility, is it correct that the substance 16 in the narrative portion here is your complete opinion 17 with respect to bone fragility in this case? 18 MR. DANNINGER: Form. 19 A. Well, I've certainly given you my opinions regarding 20 Dr. Werntz's claim that bone fragility is related to 21 the exposures from the Spelter site. It is my opinion 22 that there is no evidence to support Dr. Werntz's 23 claim, and the evidence that is readily within his 24 grasp that would substantiate his claim he has simply 25 failed to collect. Now, other than that, my opinions 289 1 are written down. 2 BY MS. SLEVINSKI: 3 Q. That's what I'm asking, just a sum of your opinions on 4 this matter, No. 9. 5 MR. DANNINGER: Form. 6 A. Well, if you were to ask me additional questions 7 related to this topic of bone fragility, I would be 8 happy to give you more opinions. 9 BY MS. SLEVINSKI: 10 Q. Do you intend to offer any other opinions other than 11 the ones you have written out here on bone fragility? 12 A. If I am asked about issues in addition to these, I 13 will respond to the best of my ability. 14 Q. As of today, do you intend to offer any other opinions 15 on bone fragility as it relates to this case? 16 MR. DANNINGER: Form, asked and answered at 17 least three times. 18 A. I -- I have not been asked by defense counsel to 19 prepare any additional opinions, but if they ask me to 20 respond to some of the issues you've raised in this 21 deposition, I may have to. 22 BY MS. SLEVINSKI: 23 Q. That's all I'm asking. Opinion No. 10, is the opinion 24 you've written here, the sum of your opinion you plan 25 to offer as of today in this case? 290 1 MR. DANNINGER: Form. 2 A. Well, what I've written in opinion 10 is self evident. 3 It is what it is. Do you have any questions about my 4 opinion there. 5 Q. I'm just asking if this is the sum of your opinions? 6 Are you going to be adding anything else to this an as 7 of today that you know of? 8 A. I haven't been asked to add any additional opinions 9 about loss of teeth. 10 Q. And the materials you have cited in that paragraph, 11 those are the materials that you relied upon in 12 forming that opinion, correct? 13 A. Yes. 14 Q. No. 11, hypertension. The information you have, is 15 that the paragraph that extends from page 10 onto 11, 16 is that the sum of your opinion as of today that you 17 plan on offering in this case? 18 MR. DANNINGER: Form. 19 A. Yes, unless I'm asked additional questions. 20 Q. And the reference materials in this portion that 21 you've cited are the materials you've relied upon in 22 forming this opinion as of today? 23 A. Well, the reference materials are the reference 24 materials attached as the bibliography to my report. 25 It is possible that I did not cite all of them under 291 1 opinion 11 that are relevant to opinion 11, so my 2 references are the 148 references cited. 3 Q. No. 12, criminal activity. That portion, that 4 paragraph the sum of your opinions that you plan on 5 offering in this case as of today? 6 MR. DANNINGER: Form. 7 A. Unless I am -- these are my opinions. If I am asked 8 additional questions in this area or asked to do 9 additional work, I may well do so. But at the moment, 10 those are my opinions. 11 MS. SLEVINSKI: I'm going to try and get 12 this sped up. Can we take a ten-minute break or so, 13 so I can make sure I've covered all my topics and 14 reconvene, and hopefully get this wrapped up soon? Is 15 that okay with you, Scott? 16 MR. DANNINGER: That's fine. 17 MS. SLEVINSKI: All right, we'll go ahead 18 and take about a ten-minute break. 19 VIDEO TECHNICIAN: Okay. We are going off 20 the record. The time is 4:31 and 4 seconds p.m. 21 (Recess taken at 4:31 p.m.) 22 (Back on the record at 4:43 p.m.) 23 VIDEO TECHNICIAN: We are now back on the 24 record. The time is 4:43 and 50 seconds p.m. 25 BY MS. SLEVINSKI: 292 1 Q. Dr. Garabrant, just kind of to go back to matters from 2 yesterday, do you have daily time sheets that you 3 enter your time on? 4 A. I don't know what you mean by daily time sheets. I 5 write my time down on pieces of paper. 6 Q. Do you have a specific, you know, method of keeping 7 track of your times so you have it all in order when 8 you submit it to your client? 9 MR. DANNINGER: Form. 10 A. Yes, when I spend time on an issue, I write it down on 11 a piece of paper. 12 BY MS. SLEVINSKI: 13 Q. Okay. What happens to the piece of paper you wrote it 14 down on? 15 A. I throw them away after I send the bill. 16 Q. You had no original record of the time you spent on 17 certain items it's just you write them on a piece of 18 paper, then throw it away? 19 A. Yeah. 20 MR. DANNINGER: Form. 21 A. I -- I write them on a piece of paper and then when I 22 get around to do billing, I put them in order on a 23 bill, and after I've checked to be sure that I've 24 added them up properly and got everything listed, I 25 throw the pieces of paper away and male the bill. 293 1 BY MS. SLEVINSKI: 2 Q. Any additional of these pieces of paper relating to 3 this case since the last bill you submitted? 4 A. Yes, yesterday, I wrote down my time on a piece of 5 paper. 6 MS. SLEVINSKI: Would you please hand 7 Dr. Garabrant Exhibit No. 162? 8 MARKED BY THE REPORTER: 9 DEPOSITION EXHIBIT NUMBER 162 10 4:46 p.m. 11 COURT REPORTER: All right. 12 BY MS. SLEVINSKI: 13 Q. Dr. Garabrant, do you recognize Exhibit No. 162 as an 14 e-mail sent from your e-mail account DHG 3 at Comcast? 15 A. Yes. 16 Q. And this is an e-mail you sent on Wednesday, 17 May the 9th, 2007, to Mr. Mitch Akler; is that 18 correct? 19 A. Yes. 20 Q. The subject reads Perrine, is that also accurate? 21 A. Yes. 22 Q. The attachments, as indicated on this e-mail, say 23 GarabrantPerrinemedlineZ9.doc. Did you create the 24 title of that document you attached to this e-mail? 25 A. Yes. 294 1 Q. What does the Z9 stand for, a Z at the end of a title? 2 A. Version 9. 3 Q. So there were eight previous versions? 4 A. Yes. 5 Q. Have you provided those to DuPont and then to us? 6 A. I haven't provided them to anyone, they don't exist. 7 Q. What happened to them? 8 A. Well, typically, when I work on a document, I label 9 the first version Version 1, and when I stop working 10 on it, I save it, and then the next time I work on it, 11 I call it Version 2, and when I am finished, I save 12 it, and then I delete version 1. 13 Q. Do you delete the version or are you renaming the 14 file? 15 A. I save it with a new name, and then I delete the old 16 one. 17 Q. Okay, that's all I was just trying to understand. The 18 body of the e-mail says Michigan I've attached my 19 report regarding Perrine, please review to be sure 20 I've covered the issues. Best wishes. Is that -21 A. Yes. 22 Q. Now, if you flip to the next page of this exhibit, 23 there is attached the version of your report that was 24 attached to that e-mail, is that correct, do you see 25 that? 295 1 A. Yes. 2 Q. Now, you also have the -- the final version of your 3 report that you've been working off of in front of 4 you, it's Exhibit No. 151, but I know that had a 5 messed up page, so you've been working off your 6 personal copy. Do you have that handy, as well? 7 A. I do. 8 Q. Let's compare the version you attached to the May 9th 9 e-mail, and the version that was actually signed on 10 May the 10th, signed by you on May 10th and submitted 11 in this case. The first page is the same, if you'd 12 turn to page 2 of the report, however, on -- there 13 is -- the changes that you made, from the May 9th 14 version and the May 10th version, if you look, the 15 second paragraph from the bottom on page 2, it starts 16 with Dr. Werntz alleges, the final sentence -- well, I 17 guess that is one long sentence, I'm going to read 18 this to you and tell me if it's correct. 19 Dr. Werntz alleges that plaintiffs have 20 been exposed to hazardous levels of the following 21 chemicals from the zinc smelter as a result of plant 22 emissions, soil contamination, exposure to fugitive 23 emissions from waste piles, contaminated household 24 dust, incidental soil and dust ingestion, consumption 25 of contaminated vegetables and contaminated drinking 296 1 water, and there's a colon. Now, did I read that 2 accurately? 3 A. Yes. 4 Q. Okay, and if you look over on the final version of the 5 report you submitted on the same page, you deleted the 6 portion starting with consumption of contaminated 7 vegetables and contaminated drinking water; do you see 8 that? 9 A. Yes. 10 Q. Why did you remove that final portion? 11 A. I think I removed that -- those two phrases because 12 Mr. Axler reminded me that plaintiffs were making no 13 claims about drinking water or contaminated vegetables 14 in this case. And I looked back at my materials and 15 realized he was right. So I deleted them. 16 Q. And similarly, you removed the three bullet points 17 arsenic, cadmium, and lead; is that correct? 18 A. Yes. 19 Q. Was there a reason behind removing those? 20 A. I'm not sure. I think that those were redundant with 21 page 3 where I talk about arsenic, cadmium, and lead, 22 so I think that was -- I realized that was just a 23 redundancy. 24 Q. Okay. The final paragraph on that page, the May 9th 25 version, third line down, starting with he, he 297 1 concurred? 2 A. Yes. 3 Q. You stated he concurs with most of his recommendations 4 but made several changes to the monitoring test. Now 5 if you look on the final version, the -- there is 6 several changes where you changed the pronounce to 7 Dr. Werntz and then Dr. Kornberg, but you changed -8 you -- instead of made several changes you put 9 numerous significant changes. Why did you change the 10 wording to reflect that? 11 A. Because I thought that that was a more appropriate 12 description of the changes. 13 Q. Did anything prompt you to make those changes to 14 figure out the -- was that after you spoke with 15 Mr. Axler? 16 MR. DANNINGER: Form. 17 A. I don't recall. To the best of my recollection, 18 the -- the issue was that I cleaned up that sentence 19 because it was poorly constructed or the -- the part 20 where he concurs with most of his recommendations, I 21 realized that the reference to who he and his were was 22 unclear, and then I felt that the changes to the 23 monitoring tests were numerous and they were 24 significant. 25 BY MS. SLEVINSKI: 298 1 Q. Okay. Moving on to the next page, page 3, May 9th 2 version of the report states the diseases that Dr. 3 Werntz considers to be related to exposure from the 4 smelter sites are, there's a colon, and then it goes 5 into the list; is that correct? 6 A. Yes. 7 Q. Okay, and if you look at the final version, you added 8 a sentence to that which says as the following 9 discussion demonstrates Dr. Werntz did not adhere to 10 his own criteria for medical monitoring. Did I read 11 that correct? 12 A. Yes. 13 Q. What was the -- what prompted you to add that sentence 14 to this portion of the report? 15 A. Because as I reread it, I realized that Dr. Werntz had 16 criteria and he wasn't even following them, so I put 17 that in to emphasize that here's this expert who lays 18 out his criteria I'm only going to test for diseases 19 clearly associated with arsenic cadmium and lead and 20 I'm going to limit testing to diseases and medical 21 tests clearly supported by the literature or general 22 medical practice, and as I thought back over my 23 report, I realized, you know, he doesn't even follow 24 his own rules. 25 Q. All right, go to page 5, please. You made some 299 1 changes starting in opinion No. 3, the references in 2 your May 9th version of your report to Spelter 3 community, Spelter population, do you see those two 4 references in the first paragraph? 5 A. Yes. 6 Q. Similarly in the second paragraph two references to 7 Spelter community, do you see those? 8 A. Yes. 9 Q. Now in the final version, you changed those references 10 to class area, is that -- was there a reason behind 11 changing it to that? 12 A. Yes. 13 Q. What was that, sir? 14 A. Because I discussed with Mr. Axler the issue of what 15 was the legal issue here and he clarified for me that 16 it was the class area, it's not the Spelter 17 population, and so that was a distinction that hadn't 18 been clear to me, so I went back through and edited 19 the report to indicate uniformly that I was talking 20 about the class area so that this report would really 21 be focused on the group of people who were involved in 22 the litigation, not the population of Spelter that 23 might or might not be in the litigation. 24 Q. All right, if you turn to page 7, please. On the May 25 9th version, just below -- oh, in opinion No. 4, I'm 300 1 sorry, just below where you have the bullet point zone 2 1, zone 2, and zone 3, do you see the paragraph 3 immediately below? 4 A. Yes. 5 Q. You removed a significant portion of that paragraph 6 and the three bullet points immediately below the 7 second paragraph. Why did you remove those? 8 MR. DANNINGER: Form. 9 A. Because they were somewhat redundant, and it just -10 it -- I think that the final report was more clearly 11 written than the draft. 12 BY MS. SLEVINSKI: 13 Q. Also, at the bottom of page 7, the final paragraph, 14 starting with even with Dr. Werntz's assumptions, do 15 you see that? 16 A. Yes. 17 Q. Okay. And that -- that paragraph continuing on to 18 page 8 was deleted all the way to point No. 5. 19 A. Yes. 20 Q. For what reason did you delete that paragraph? 21 MR. DANNINGER: Form. 22 A. Again, clarity, I was able to compress my opinions 23 down to one paragraph. I don't think -- I didn't feel 24 that all that additional material actually added 25 anything to the point of the paragraph that begins 301 1 with comparison of these alleged incremental lifetime 2 cancer risks. 3 BY MS. SLEVINSKI: 4 Q. Dr. Garabrant, at the conclusion of yesterday and 5 today, have we covered all the opinions that you 6 intend to offer on this case of an of today? 7 A. I believe we've covered all of the opinions in my 8 report. If I am asked to offer additional opinions 9 and they're within my area of expertise, I may well do 10 so. At the moment I have not been asked to do any 11 additional work. 12 MS. SLEVINSKI: All right, thank you, I 13 don't have any further questions at this time, 14 Dr. Garabrant. 15 THE WITNESS: Thank you. 16 MR. DANNINGER: And we have no questions 17 here. 18 MR. WICKLINE: We'll read. 19 MR. DANNINGER: So Dr. Garabrant will read 20 and sign. 21 MS. SLEVINSKI: Scott, before we go off the 22 record, can we ask that you get us a copy of the book 23 chapters that he was referring to that weren't 24 actually included on the reference list for his 25 report? 302 1 MR. DANNINGER: I believe that you all have 2 that book. If you'd like, we can try to arrange that, 3 or I can give you the ISBN number. 4 MS. SLEVINSKI: I believe it's the cadmium 5 chapter he was reading from and possibly the lead. 6 MR. DANNINGER: He didn't read from the 7 lead, he only read from the cadmium chapter. 8 MS. SLEVINSKI: Okay, well, will we be able 9 to get a copy of that chapter? Because I'm not aware 10 that we have it. I mean if we do, we can resolve it 11 but -12 MR. DANNINGER: We will try. Yeah, I mean 13 I don't know why we can't -14 MS. SLEVINSKI: Okay. 15 MR. DANNINGER: -- but I just don't want to 16 promise you the world and not be able to deliver. 17 MS. SLEVINSKI: Okay. 18 MR. DANNINGER: So we'll do our best. At 19 the very least, we'll be able to provide you the ISBN 20 number so that if you do want to get the book, you 21 can. 22 MS. SLEVINSKI: Okay. 23 MR. DANNINGER: But the reason I say that 24 is someone told me you had a copy of Rosenstock for 25 some reason. 303 1 MS. SLEVINSKI: I'm not aware of it, but we 2 don't have to hash it out right now, but we'll figure 3 it out. 4 MR. DANNINGER: No problem. 5 MS. SLEVINSKI: That's it. Okay, madam 6 court reporter, will you be able to provide a rough? 7 COURT REPORTER: Yes, this evening. 8 MS. SLEVINSKI: Thank you. Okay. 9 COURT REPORTER: The same format as last 10 night? 11 MR. DANNINGER: Yeah. 12 MS. SLEVINSKI: That sounds great, thanks. 13 VIDEO TECHNICIAN: This concludes today's 14 deposition. The time is 5:00 and 38 seconds p.m. 15 (The deposition concluded at 5:00 p.m. 16 Signature of the witness was requested.) 17 18 19 20 21 22 23 24 25 304 1 LENORA PERRINE, et al., 2 Plaintiffs, 3 vs. Case No. 04-C-296-2 4 E.I. DU PONT NEMOURS AND COMPANY, 5 et al., 6 ___________________________ 7 8 VERIFICATION OF DEPONENT 9 10 I, having read the foregoing deposition 11 consisting of my testimony at the aforementioned time 12 and place, do hereby attest to the correctness and 13 truthfulness of the transcript. 14 15 16 _____________________________ 17 DAVID GARABRANT, M.D. 18 Dated: 19 20 21 22 23 24 25 305 1 CERTIFICATE OF NOTARY 2 STATE OF MICHIGAN ) 3 ) SS 4 COUNTY OF MONROE ) 5 6 I, LEISA M. PASTOR, a Notary Public in and 7 for the above county and state, do hereby certify that 8 the above deposition was taken before me at the time 9 and place hereinbefore set forth; that the witness was 10 by me first duly sworn to testify to the truth, and 11 nothing but the truth; that the foregoing questions 12 asked and answers made by the witness were duly 13 recorded by me stenographically and reduced to 14 computer transcription; that this is a true, full and 15 correct transcript of my stenographic notes so taken; 16 and that I am not related to, nor of counsel to either 17 party nor interested in the event of this cause. 18 19 20 21 ___________________________ 22 LEISA M. PASTOR, CSR-3500, CRR 23 Notary Public, 24 Monroe County, Michigan 25 My Commission expires: 9/7/13 306 1 INDEX TO EXAMINATIONS 2 3 Witness 4 DAVID GARABRANT, M.D. 5 6 EXAMINATION BY MS. SLEVINSKI 7 8 9 INDEX TO EXHIBITS 10 11 Exhibit 12 (Exhibits attached to transcript.) 13 14 DEPOSITION EXHIBIT NUMBER 137 15 DEPOSITION EXHIBIT NUMBER 6 16 DEPOSITION EXHIBIT NUMBER 121 17 DEPOSITION EXHIBIT NUMBER 18 18 DEPOSITION EXHIBIT NUMBER 5 19 DEPOSITION EXHIBIT NUMBER 146 20 DEPOSITION EXHIBIT NUMBER 60 21 DEPOSITION EXHIBIT NUMBER 50 22 DEPOSITION EXHIBIT NUMBER 73 23 DEPOSITION EXHIBIT NUMBER 72 24 DEPOSITION EXHIBIT NUMBER 46 25 DEPOSITION EXHIBITS NUMBERED 35-37 Page 94 Page 194 196 199 223 228 294 309 309 309 309 309 309 307 1 DEPOSITION EXHIBIT NUMBER 2 2 DEPOSITION EXHIBIT NUMBER 39 3 DEPOSITION EXHIBIT NUMBER 87 4 DEPOSITION EXHIBIT NUMBER 94 5 DEPOSITION EXHIBIT NUMBER 104 6 DEPOSITION EXHIBIT NUMBER 128 7 DEPOSITION EXHIBIT NUMBER 51 8 DEPOSITION EXHIBIT NUMBER 56 9 DEPOSITION EXHIBIT NUMBER 113 10 DEPOSITION EXHIBIT NUMBER 162 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 308 309 309 309 309 309 309 309 309 309 309