Document QXNo89N069NyozOEEdXapxeEL

1 IN THE UNITED STATES DISTRICT COURT FOR THE EASTERN DISTRICT OF TEXAS 2 MARSHALL DIVISION 3 CHARLES WILSON and ) LAURA WILSON, ) 4) Plaintiffs ) 5) vs. ) CIVIL ACTION NO.2:06-CV-286 6) RYCOLINE PRODUCTS, INC.; ) 7 et al., ) ) 8 Defendants ) 9 10 ******************************************************** 11 ORAL DEPOSITION OF 12 DR. WAYNE SNODGRASS 13 September 14, 2007 ******************************************************** 14 15 ORAL DEPOSITION of DR. WAYNE SNODGRASS, produced 16 as a witness at the instance of the Plaintiff, and duly 17 sworn, was taken in the above-styled and numbered cause 18 on September 14, 2007, from 9:47 a.m. to 1:07 p.m., 19 before Brenda L. Kaplan, CSR in and for the State of 20 Texas, reported by Stenographic method, at the Tremont 21 House Hotel, 2300 Mechanic Street, Galveston, Texas 22 77550, pursuant to the Texas Rules of Civil Procedure 23 and the provisions stated on the record or attached 24 hereto. That the deposition shall be read and signed by 25 any notary public. 1 1 APPEARANCES 2 3 4 FOR THE PLAINTIFF: 5 Mr. Keith Patton SCHMIDT & CLARK 6 2911 Turtle Creek Boulevard, Suite 1400 Dallas, Texas 75219 7 8 9 FOR THE DEFENDANTS, RYCOLINE PRODUCTS: 10 Mr. Jonathan Shoebotham THOMPSON & KNIGHT 11 333 Clay Street, Suite 3300 Houston, Texas 77002 12 13 14 15 16 17 18 19 20 21 22 23 24 25 2 1 INDEX PAGE 2 Appearances . . . . . . . . . . . . . . . . . 2 3 Stipulations . . . . . . . . . . . . . . . . 4 4 DR. WAYNE SNODGRASS 5 Examination by Mr. Patton . . . . . 4 Examination by Mr. Shoebotham . . . 113 6 Re-Examination by Mr. Patton. . . . 120 7 Signature and Changes . . . . . . . . . . . . 124 8 Reporter's Certificate. . . . . . . . . . . . 122 9 10 EXHIBITS NO. DESCRIPTION PAGE 11 1 Report of Dr. Wayne Snodgrass 26 12 2 List of High-Quality Data 29 13 3 Testimony List of Dr. Wayne Snodgrass 61 14 4 Deposition Notice With Subpoena Duces Tecum 103 15 5 Curriculum Vitae of Dr. Wayne Snodgrass 103 16 6 Harrison's Principles of Internal Medicine 17 16th Edition 103 18 7 Copies of the Strom Study 103 19 8 "Evolving Classifications of the Myelodysplastic Syndromes," by Dr. Komrokji, from the "Current 20 Opinion in Hematology" journal, 2007 103 21 9 Institute of Medicine Article Entitled "Gulf War and Health," dated 2003, Volume 2, "Insecticides 22 and Solvents" 103 23 10 American Cancer Society Statement Regarding Long-term Workplace Exposure to Benzene 103 24 25 3 1 WAYNE R. SNODGRASS, 2 having been first duly sworn, testified as follows: 3 EXAMINATION 4 BY MR. PATTON: 5 Q. Please introduce yourself for the record. 6 A. All right. My name is Wayne Snodgrass. 7 Q. And, Dr. Snodgrass, what kind of doctor are 8 you? 9 A. I'm a physician and a toxicologist. 10 Q. What kind of physician are you? 11 A. I'm a -- I have a sub-specialty practice in 12 medical toxicology and clinical pharmacology. 13 Q. You were hired as an expert in this case by 14 Ashland, correct? 15 A. Yes. 16 Q. What was your objective, or what was your job 17 or purpose in serving as an expert in this case, as you 18 understand it? 19 A. What I agreed to is just telling what I 20 thought, just what my opinion was about the information. 21 Q. Opinions on what information? 22 A. Mr. Wilson's disease and his exposure to 23 chemicals. 24 Q. Is it your opinion in this case that 25 Mr. Wilson's disease -- well, first of all, do you 4 1 dispute the diagnosis or do you dispute that Mr. Wilson 2 has myelodysplastic syndrome? 3 A. Yes. That is not an accurate diagnosis. 4 Q. What do you believe his diagnosis to be? 5 A. His diagnosis is refractory anemia with ringed 6 sideroblasts, which is a distinct diagnostic entity. 7 Myelodysplastic syndrome is just simply a collection of 8 different diseases. 9 Q. So, his disease is RARS? 10 A. Yes. 11 Q. And do you consider that to be a type of 12 myelodysplastic syndrome? 13 A. Not particularly, no. It's a -- it's a 14 distinct disorder. It's classified with that many 15 classifications. But that's all that MDS is; it's a 16 listing of different types of diseases. 17 Q. Is it your opinion in this case and would you 18 testify at trial in this case that benzene exposure does 19 not cause RARS? 20 A. That's correct. 21 Q. Would you testify at trial in this case that 22 Mr. Wilson's exposure to benzene, whatever that exposure 23 might be, was in no way any type of cause of his 24 disease? 25 A. That's also correct. 5 1 Q. Okay. So, just to ask it sort of one more time 2 with a couple of different words: Is it your opinion 3 that benzene played absolutely zero role as a causative 4 factor of Mr. Wilson's disease? 5 A. Yes. 6 Q. Okay. What did cause Mr. Wilson's RARS? 7 A. Medicine, in 2007 does not know the exact 8 molecular origin of many diseases, including RARS. It's 9 a spontaneous event in the genetic control of his cell 10 production. 11 Q. I want to make a list of all of the things that 12 cause RARS. 13 A. Okay. 14 Q. What would we put on that list? 15 A. The list in the future, when we get such 16 information, perhaps might include some of the 17 following, but to my knowledge, there's no publication 18 or data on these factors I'm about to list. They might 19 include any disorganization or -- or disregulation of 20 the precursor cells for the erthrocyte; they might 21 include disregulation genetically of mitochondrial 22 function that results in iron accumulation in 23 mitochondria that then localize around the nucleus. 24 And it may include relationships to the 25 genes that control aging and how aging occurs in the 6 1 relationships, in other words, what we call "linked 2 loci," on that. And those are yet all to be determined 3 as spontaneous causes. 4 Q. So, the real cause of RARS, which you believe 5 will be figured out in the near future -- or some time 6 in the future, is going to be some type of disregulation 7 of the cells or some type of other genetic event that 8 happens, correct? 9 A. Yes. 10 Q. Is it your belief, is it your opinion, that 11 environmental factors play zero role in disturbing or 12 disregulating cells or genes? 13 A. With regard to RAS, specifically? 14 Q. No, with regard to anything. 15 A. No. 16 Q. Okay. Where are we missing each other? 17 A. That's a very broad question you asked. So, 18 does the environment have any influence on genes? Yes. 19 Q. Okay. Does the environment have any influence 20 on cells? 21 A. Yes. 22 Q. Do chemicals have any influence on genes? 23 A. Just as a broad question, yes. 24 Q. Do chemicals, as a broad question, have any 25 influence on cells? 7 1 A. Yes. 2 Q. Does benzene have any influence on genes? 3 A. At some sufficient dose, as a broad question, 4 yes. 5 Q. Okay. So, benzene can affect the genes? 6 A. At some sufficient dose, yes. 7 Q. And there's a debate about what that dose might 8 be? 9 A. It's above the circulating background that we 10 all have currently in our body of benzene, which is 11 200 nanograms per ml of benzene in our serum. 12 Q. Can you repeat at that one more time, the 13 measurement, again? 200 -14 A. Nanograms per ml of benzene in our serum. We 15 all have that as a background level. 16 Q. So, we're all walking around with a little bit 17 of benzene in our body? 18 A. Yes. 19 Q. And you know this as a medical toxicologist and 20 clinical pharmacologist? 21 A. Yes, sir. 22 Q. Can that little bit of benzene that floats 23 around in all of our bodies, 200 nanograms or so, can 24 that have an adverse effect on cells or genes? 25 A. Not that I'm aware of anybody's demonstrated in 8 1 in experimental data. 2 Q. How do we get that benzene in our body? That 3 background 200 nanogram level, how do we get it inside 4 of us? 5 A. There is benzene in the air from man-made 6 sources. There's benzene in egg yolk. There's a 7 variety of sources. 8 Q. What are some of the other sources? Egg yolk, 9 man-made sources? 10 A. Cigarette smoke, even if it's passive. 11 Q. Second-hand cigarette smoke? 12 A. Second-hand smoke would be included. 13 Q. So, if I was sitting in a room where a lot of 14 people were smoking, I would get additional -- I would 15 inhale benzene into my body from that second-hand smoke, 16 correct? 17 A. That's detectible, yes. 18 Q. Okay. Detectible, such that it would 19 contribute, or maybe even raise that 200 nanogram 20 level? 21 A. It -- in an individual, depending on where they 22 start and depending on how much is in the room, perhaps 23 it might raise in the body. It's, generally also 24 reported as just part of your background exposure. 25 Q. Okay. What are the other sources of the 9 1 200 nanograms or so of benzene in a person's body? 2 A. It's a small amount -- it's not quantitated as 3 to the contribution to the 200 number, but there's a 4 small amount that we produce from other normal body 5 metabolism. 6 Q. Are some people walking around with more than 7 200 nanograms of benzene in their body? 8 A. Yes. 9 Q. And what would cause a person to have more than 10 that baseline -- can I call it a baseline level? 11 A. Yes. 12 Q. What would cause a person to have more than 13 that 200 baseline level? 14 A. The most characterized that I'm aware of is 15 cigarette smoking. 16 Q. Because if someone smokes cigarettes, they're 17 essentially inhaling a little bit of benzene into them 18 every day? 19 A. Yes. 20 Q. What if someone were, like, a bartender and 21 they worked in a bar where somebody -- where people 22 smoked all day and all evening, would that bartender 23 then get an increased level by inhaling benzene daily in 24 their work? 25 A. Compared to the 200 number? 10 1 Q. Yes. 2 A. I'm not aware of data that's looked at that 3 question. If the dose were sufficiently high, perhaps 4 it might be above 200. 5 Q. So, is it your testimony that someone being 6 exposed to second-hand smoke doesn't necessarily have a 7 higher level above the 200 nanogram baseline? 8 A. It would depend on the dose in the air. 9 Q. What if someone worked in a refinery where 10 benzene was present, would they have a higher level than 11 the 200 ppm -- or 200 nanograms? 12 A. Currently, most refineries, one would predict 13 they would not, because refinery workers are less 14 exposed than, let's say, distributors, for example. 15 Q. What do you mean by "distributors"? 16 A. Well, for example, the truck drivers that 17 deliver gasoline or things like that. 18 Q. People who deliver gasoline for a living, 19 they're going to be exposed to a little bit of benzene 20 on a daily basis by working with or around that 21 gasoline, correct? 22 A. Yes. 23 Q. So, they might have higher than a 200-baseline 24 dose? 25 A. They might. I've never seen data. 11 1 Q. Okay. Well, whether or not you've seen 2 data, is it your opinion -- would you expect someone 3 working with gasoline to have higher than the 4 200-nanogram dose? 5 A. It would depend on the dose exposure, which 6 depends in part on their handling characteristics. 7 Q. Stuff like if it's windy outside or how far 8 their nose is from the source of the liquid? 9 A. And the actual benzene content of the gasoline, 10 itself, yes. 11 Q. So, benzene content, proximity, ventilation, 12 things of that nature, elements like that would go into 13 the evaluation to determine whether or not that person 14 might have a level of benzene above 200 nanograms. Fair 15 statement? 16 A. Yes. 17 Q. What if somebody worked with a 18 benzene-containing solvent on a daily basis at arm's 19 length, indoors, in a room with less than ideal 20 ventilation, would you expect them to have a level of 21 benzene in their body above the 200 nanograms? 22 MR. SHOEBOTHAM: Objection, form. 23 A. And what is the concentration of benzene in the 24 solvent? 25 Q. (BY MR. PATTON) Well, what is the 12 1 concentration of benzene in gasoline? 2 A. Nowadays, it's about half a percent or less. 3 Q. So, it's about 500 ppm or less? 4 MR. SHOEBOTHAM: Objection, form. 5 A. I'd have to go through the numbers to come up 6 with it. However, you may be right; I haven't sat down 7 to convert it. 8 Q. (BY MR. PATTON) I think it's .1 percent equals 9 1,000 ppm. That's my understanding. 10 A. Okay. 11 Q. Do you believe that to be correct? 12 A. Yes. 13 Q. Okay. So, if someone were working with a 14 product that had half of 1 percent, that would be .5 15 or -16 A. It would be approximately that, yes. 17 Q. Well, that would actually be 5000 ppm? 18 A. (No response.) 19 Q. Let's just get this straight real quick. 20 .1 equals 1000 ppm, true? And then 1 percent would 21 equal 10,000 ppm. So, .5 percent would equal 5000 ppm. 22 I think that's correct. 23 A. I'll assume it is. 24 Q. All right. 25 A. I haven't done the calculation, but I assume it 13 1 is. 2 Q. So, if we presume that gasoline has 5000 ppm 3 benzene in it, your testimony, as you just stated, is 4 that a gasoline worker could, under certain conditions, 5 as working as a gasoline-distribution worker, experience 6 daily exposures to benzene via that liquid such that it 7 would increase the amount of baseline benzene in his 8 body above 200 nanograms? 9 MR. SHOEBOTHAM: Objection, form. 10 Q. (BY MR. PATTON) Is that a fair statement? 11 A. Not actually, because the only dose response 12 data I can relate to this is that years ago when there 13 was much more benzene in gasoline and individuals used 14 to pump gas, it wasn't self-service stations -- so, 15 5 percent benzene or more even, '60s, '70s, even 16 earlier, that the urinary metabolite of that -- one of 17 the metabolites of benzene could be increased only when 18 they were very closely working with that, spilling it, 19 and in the area of a clearly high level of exposure. 20 So, that was considerably more than .5 in 21 order to -- .5 percent in order to get a change in your 22 urine metabolites. So, that's the only data I know, 23 relevant to that assessment. 24 Q. So, your testimony is that besides that little 25 piece of data that you're aware of, there's no evidence 14 1 to indicate that people working with benzene daily would 2 have an increase in their 200-nanogram baseline rate? 3 A. To my knowledge -- there may be data, but I'm 4 not aware of it. I'm not aware of data that has 5 specifically been gathered to answer that question and 6 published. 7 Q. How many studies in the literature are you 8 aware of that examine benzene as a causative factor of 9 RARS? 10 A. The Strom study is the only one I'm aware of. 11 Q. Strom 2005? 12 A. Yes. 13 Q. Okay. What about studies that deal with 14 benzene as a causative factor of refractory anemia with 15 excess blasts, or RAEB? 16 A. To my knowledge, the Strom study is the only 17 one that addresses that. 18 Q. The Strom study looks at MDS sub-types, 19 correct? 20 A. It looks at -- one way of describing it is as 21 you did, is the -- MDS, again, is a list of different 22 disorders. They've looked at the various types that are 23 often listed in that description. 24 Q. Is it your professional opinion in this case, 25 that the whole body of literature which discusses 15 1 benzene and MDS is totally irrelevant when examining and 2 exploring benzene as a cause of RARS, the disease that 3 my client has? 4 MR. SHOEBOTHAM: Objection, form. 5 A. It depends what you mean by "totally 6 irrelevant." But in terms of specifying a particular 7 disease, I -- the -- just the terminology "MDS" does not 8 do that. 9 Q. (BY MR. PATTON) Do you believe it is a fair 10 and prudent method to examine the body of literature, 11 which discusses benzene and bone marrow disease, any 12 bone marrow disease, when examining causation in the 13 instance of Charles Wilson? 14 MR. SHOEBOTHAM: Objection, form. 15 A. If I understand your question correctly, "Is it 16 useful" -17 Q. (BY MR. PATTON) That would be a good question. 18 Is it useful in some way, to examine -- let me start 19 over. 20 When examining causation of Charles 21 Wilson's illness and whether or not that can be 22 connected to benzene exposure, is it useful to look at 23 the world's literature which discusses benzene and bone 24 marrow diseases generally? 25 MR. SHOEBOTHAM: Objection, form. 16 1 A. It may be useful to be able to -- to look at 2 that and see what does or what does not appear to relate 3 to Mr. Wilson. 4 Q. (BY MR. PATTON) Is it useful to look at the 5 studies that deal with benzene and MDS -- outside of the 6 Strom study, is it useful to look at those studies when 7 examining benzene as a possible causative factor of 8 Charles Wilson's disease? 9 MR. SHOEBOTHAM: Objection, form. 10 A. Unfortunately, it's not. 11 Q. (BY MR. PATTON) So, then, the only study that 12 matters is Strom 2005? 13 A. Short answer is "yes." 14 Q. What's the long answer? 15 A. The long answer is that the other studies don't 16 separate out the distinct disease entities. 17 Q. So, they don't matter? 18 MR. SHOEBOTHAM: Objection, form. 19 A. You can't -- you can't make any conclusions 20 from them. 21 Q. (BY MR. PATTON) Are there -- if we agree -22 well, first of all, do you agree with me that RARS is a 23 sub-type or variation of MDS? 24 A. No. I would say it's a distinct, different 25 disease. 17 1 Q. Okay. 2 A. It may be listed under -- MDS is simply a 3 collection of listing of different disorders. 4 Q. What is AML? 5 A. AML is acute myelogenous leukemia. 6 Q. Is that one distinct disorder? 7 A. As we learn more about it, it may become 8 sub-divided. Currently, most people consider it one 9 disorder. 10 Q. But it has sub-types, doesn't it? 11 A. Yes. 12 Q. Like M6, M4? 13 A. There are sub-types beginning to be defined, 14 yes. 15 Q. Let's talk about ML a little bit. When were 16 AML sub-types first defined? 17 A. You know, I'm not a hematologist or oncologist, 18 so I'm going to have to defer to Dr. Natelson or 19 someone. I don't remember the time line. 20 Q. How many different sub-types of AML are there, 21 approximately? 22 A. I don't know at the moment. 23 Q. Okay. Is there a range that you could 24 estimate? 25 A. It would be better to ask someone like an 18 1 oncologist, hematologist. 2 Q. Have you ever testified as an expert in a case 3 involving AML? 4 A. Yes. 5 Q. And benzene? 6 A. Yes. 7 Q. An AML/benzene case, you've been an expert in 8 that type of case, right? 9 A. I think so. 10 Q. Did you look at the sub-type of AML when 11 examining the evidence on causation in that case? 12 A. There was one case. The one I'm recalling, I 13 think, was the -- it was a different sub-type than would 14 be compatible with benzene, and I -- promyelocytic 15 leukemia, as I recall. 16 Q. That's a sub-type of AML? 17 A. It used to be considered that. It's beginning 18 to be classified more as its own distinct entity. 19 Q. Well, let's talk about MDS again, then. Let's 20 say someone has RARS, as Charles Wilson. Okay? 21 Mr. Wilson does not have any cytogenetic or chromosomal 22 abnormalities, correct? 23 A. That's correct. 24 Q. Okay. So, he has RARS with no abnormalities, 25 true? 19 1 A. True. He has a loss of a Y chromosome, but 2 that's not relatable. 3 Q. Okay. Do some RARS patients have chromosomal 4 abnormalities? 5 A. I don't know for certain. I think a 6 possible -- a very few may. 7 Q. Okay. Well, let's say someone has RARS with 8 chromosomal abnormalities, like a Inversion 16 or a 9 deletion of the 5 or 7 chromosome. Okay? Let's just 10 take that for example. 11 Would the Strom study be instructive on 12 each of those two different types of RARs? 13 MR. SHOEBOTHAM: Objection, form. 14 A. No. 15 Q. (BY MR. PATTON) So, the Strom study wouldn't 16 be useful for an RARS with chromosomal abnormalities? 17 A. It would be. 18 Q. It would be? 19 A. For that question, the answer is "yes." 20 Q. Okay. And would the Strom study be useful for 21 examining a person alleging benzene exposure as a cause 22 of RARS with no chromosomal abnormalities? 23 A. Yes. 24 Q. So, the Strom study is useful for both, with or 25 without chromosomal abnormalities? 20 1 A. At this stage and this time in the history of 2 science simply because it doesn't make that distinction. 3 It includes both. 4 Q. Okay. Well, before 2005, the relevant 5 literature on benzene in MDS, it didn't make the 6 distinctions of sub-types such as RARS or RAEB, did it? 7 A. Typically, no. 8 Q. All right. So, at that stage, it was all 9 relevant, wasn't it? 10 MR. SHOEBOTHAM: Objection, form. 11 A. No. 12 Q. (BY MR. PATTON) So, in 2004 -- let's say you 13 were asked to look at this case, this Wilson case, in 14 2004 and there's no Strom study, would your opinion be, 15 "Well, there's just no relevant literature to support 16 benzene as a cause of RARS, because RARS has never been 17 examined in the literature in relation to benzene 18 exposure"? Would that be your testimony? 19 MR. SHOEBOTHAM: Objection, form. 20 A. No. 21 Q. (BY MR. PATTON) Well, your testimony today is 22 that the Strom study is the only relevant study because 23 it deals with RARS specifically, which you call a 24 "distinct disease." 25 A. Yes. 21 1 Q. So, where -- what am I missing you? 2 A. You're missing the disconnect that occurs 3 between amounts of benzene exposure in the general 4 population and the demographics of MDS, if you want to, 5 you know, call MDS as a -- just put all of those 6 categories together, what is the demographics of MDS, 7 and how does that fit with benzene, and there's a major 8 disconnect in the general demographics. 9 Q. Okay. 10 A. There are isolated cases, yes, but in the 11 general demographics, it's not connected, because MDS 12 has characteristics such as age of onset and benzene 13 characteristics such as what is the population exposure 14 that could reasonably lead to anything like MDS or 15 leukemia, and those frequencies are markedly different. 16 Q. Does benzene cause MDS? 17 MR. SHOEBOTHAM: Objection, form. 18 A. If you put all categories together, based on 19 some older literature at some sufficiently significantly 20 high dose, then, yes, in the general rubric of how you 21 use the word "MDS." 22 Q. (BY MR. PATTON) We happen to have "Harrison's 23 Principles of Internal Medicine" on the table with us 24 here today, and there's a hematology textbook that 25 Dr. Haas talked about, "Wintrobe's," I believe? 22 1 A. Yes. 2 Q. Wintrobe's hematology text talks about benzene 3 is a causative factor of MDS. Do you disagree with 4 Wintrobe? 5 A. Yes. 6 Q. So, Wintrobe's wrong? 7 A. Well, if you went to that author today and 8 showed him this same information -9 Q. Showed him Strom 2005? 10 A. Sure. Would he rewrite that chapter, sentence? 11 Greater than a 51 percent chance he would, because it's 12 new, better information. 13 Q. Are you aware of anyone who has written to 14 Wintrobe and said, "Hey, here's the Strom 2005 study. 15 Now this chapter in your 9th or 10th edition of your 16 hematology/oncology text is wrong, you need to rewrite 17 it"? 18 Has anybody brought that to his attention 19 that you know of? 20 A. Not specifically that, no. 21 Q. Have you brought that to his attention? 22 A. No. 23 Q. Will you? 24 A. No. There's so many things to change in each 25 edition, it would take a full-time job to do that. 23 1 Q. So, even though you admit that benzene can 2 cause a disregulation of the cells and you admit that 3 benzene can cause a disregulation of genes, you do not 4 believe that benzene can cause RARS, true? 5 A. Well, let's extend that logic. If benzene at 6 some sufficiently high dose caused some disregulation of 7 some sort of gene function, why aren't all cancers due 8 to benzene? Why should it just pick AML? Should be -9 every cancer should be due to benzene, right? 10 Q. Do you think all cancers are related to 11 benzene? 12 A. No. 13 Q. Do you believe Charles Wilson was exposed to 14 benzene? 15 A. Yes. 16 Q. And what were the sources of his exposure to 17 benzene? 18 A. Well, one that he's contending here has to do 19 with the -20 Q. I'm not asking you what he's contending. I'm 21 asking you what you believe Charles Wilson's sources of 22 exposure to benzene are, based on your review of the box 23 of materials that you reviewed for this case? 24 A. Various solvents were used in the printing 25 area. 24 1 Q. So, do you believe that some of those solvents 2 contained benzene? 3 A. At some level, at some detectible level. 4 Q. Okay. And you believe that that benzene was a 5 source of Charles Wilson's exposure, correct? 6 A. He had some exposure. 7 Q. Okay. 8 A. Probably. 9 Q. Okay. So, you agree with me that Charles 10 Wilson had exposure to benzene via use of printing 11 solvents? 12 A. It's -- even small amounts of benzene, perhaps, 13 were still in those solvents that would be measurable at 14 some analytical level, yes. 15 Q. Okay. All right. So, when we're making a list 16 of Charles Wilson's exposure to benzene, he had exposure 17 to benzene in printing solvents. What else was a source 18 of exposure to benzene for Charles Wilson? 19 A. I don't recall information about other 20 individuals smoking or in the break room. And I don't 21 recall the -- to my recollection, he did not have a 22 history, himself, of cigarette smoking; so, I don't 23 recall that as a possible exposure source. 24 There may be in -- even today, in some 25 plastics or some materials in construction and other 25 1 sources, electrical wiring and things, there may be 2 tiny, tiny amounts of benzene even in the other aromatic 3 solvents that off-gas in these kinds of construction or 4 building materials that we'd all be exposed to. 5 Some benzene in foods, as I mentioned 6 before. 7 Q. Like egg yolk? 8 A. Yes. 9 Q. How much benzene was in the Ashland printing 10 solvents that Charles Wilson used? 11 MR. SHOEBOTHAM: Objection, form. 12 A. My estimate would be somewhere -- if you looked 13 at Mr. Whitlock's information, somewhere in the 14 approximately 2 and-a-half to 5 ppm is a possibility. 15 (Snodgrass Exhibit No. 1 marked.) 16 Q. (BY MR. PATTON) I'm marking as Exhibit 1, your 17 report. Can you turn to Page 5, please -- rather, Page 18 3. Can you read that last sentence of the first 19 paragraph? 20 A. "Unpublished information regarding Ashland 21 Blend 3078 D and Blend 7650, indicate considerably lower 22 benzene content compared to the assumptions of 23 Dr. Nicas." 24 Q. Okay. Who gave you that information -- well, 25 first of all, what unpublished information are you 26 1 referencing? 2 A. I'm referencing information that I requested 3 from Morgan Gaskin. 4 Q. Okay. 5 A. And she checked with someone and called me back 6 and gave me some information. 7 Q. What information did she give you -- Morgan 8 Gaskin is a lawyer for Ashland, right? 9 A. Yes. Yes. 10 Q. What information did she give you? 11 A. In that it was in the -- somewhere in the 12 approximate 5 or less part-per-million range. 13 Q. Well, hold on. What unpublished information 14 did Morgan Gaskin identify? 15 A. I assumed she talked to somebody at Ashland. 16 Q. Did she identify for you the unpublished 17 information? 18 A. No. 19 Q. When you say "considerably lower benzene 20 content," what do you mean by that? Why did you choose 21 those words? 22 A. If you go back to Dr. Nicas's report, he has -23 it's actually confusing -- at least, it was to me. He 24 talks about unit weight percent, and then he talks about 25 weight per weight and equates them. And so, I -- in 27 1 going back over that report, my estimate is that he's 2 talking about .00175 percent, which is 1,750 -- I'm 3 sorry -- .175 percent, which is 1,750 ppm. 4 Q. Are you a chemist? 5 A. Not now. 6 Q. How much benzene did Morgan Gaskin tell you the 7 unpublished information indicated was in the Ashland 8 solvent blends? 9 A. Somewhere in the range of less than 5 ppm. 10 Q. Okay. Do you believe that's a sound scientific 11 method, for you to put that sentence in your report 12 based on what Ashland's lawyer tells you? 13 A. It doesn't reflect Hill criteria, but it does 14 have relevance to the case. 15 Q. So, Ashland's lawyer telling you that there's 16 5 ppm or less benzene in these solvents, that has 17 relevance to the case; the body of MDS literature, 18 pre-2005, outside of Strom, doesn't have relevance to 19 the case. Is that your testimony? 20 MR. SHOEBOTHAM: Objection, form. 21 A. The body of the literature prior to 2005 may 22 have some relevance, but it depends on how you want to 23 twist the data and interpret it. 24 Q. (BY MR. PATTON) You only like to use 25 high-quality data when you examine the relevant benzene 28 1 literature; is that true? 2 A. That would be the preference. 3 Q. Okay. What does "high-quality data" mean? 4 A. It could be data that perhaps approximates 5 Level 1-A or 1-D or 1-C or 1-B or 2-A or 2-B, 2-C or 6 3-A or -7 Q. Slow down, Doctor, please. 8 A. All right. 9 Q. Let's start over. Okay? 10 A. It could be levels of -11 Q. Hang on. I'm going to start -- ask a new 12 question. 13 Okay. Page 6 of your report, do you see 14 the last sentence before your Summary of Conclusions? 15 You say, "There are no" -- can you read that for us? 16 A. "There are no published high-quality data that 17 true MDS develops at lower cumulative dose exposures." 18 Q. Okay. I've written down on this piece of paper 19 here -- and I'll mark this as Exhibit 2 to your 20 deposition. 21 (Snodgrass Exhibit No. 2 marked.) 22 Q. (BY MR. PATTON) I've written on here: 23 "High-quality data according to Dr. Snodgrass." And as 24 it relates to your opinions on the data that my experts, 25 or Plaintiffs' experts, rely on in their opinions, I'd 29 1 like you to make a list of what makes something 2 high-quality data on Exhibit 2. And you can talk about 3 it as you write. 4 A. Cochrane levels defined. 5 Q. Okay. What is a Cochrane level? 6 A. So, it is a -- they are defined as Levels 1, 7 with Sub-Types A, B and C and D; and 2 A, B, C and D; 8 3 A, B, C and D; 4 A, B, C and D; and the various 9 characteristics of scientists, physician/scientists, 10 assessing published data as to its quality. 11 Q. Can you write that down? 12 A. Okay. 13 Q. "Cochrane levels defined." And you wrote 14 "Characteristics of quality of data." Is that what you 15 wrote? 16 A. Yes. 17 Q. Okay. Who is Cochrane? 18 A. Don't recall. It's a database nowadays. It 19 may have been named after an individual. I don't recall 20 who the individual was. 21 Q. Okay. What is a Cochrane level? 22 A. It's a way of categorizing the quality of 23 information. 24 Q. Now, are there -- you said there are four 25 different levels, one, two, three, and four? 30 1 A. Yes. 2 Q. And then, there's four divisions within each 3 Cochrane level? 4 A. Yes. 5 Q. A, B, C and D? 6 A. Yes. 7 Q. So, it's essentially 16 different levels in 8 evaluating the quality of data -9 A. Yes. 10 Q. -- or the quality of a study? 11 A. Yes. 12 Q. Okay. So, that's to say that a scientist who 13 would read up and learn about Cochrane levels would be 14 able to take any study -- let's take the Strom study. 15 Okay? He could evaluate the Strom study and give it a 16 rating, so to speak, within the Cochrane levels, the 17 16 different Cochrane levels? Is that a fair statement? 18 A. Yes. 19 Q. Okay. So, high-quality data has a defined 20 Cochrane level, whatever that level may be? 21 A. Yes. 22 Q. So, it's like a grade, 1 through 16? 23 A. Yes. 24 Q. How do we grade the Strom study -- well, before 25 I ask that, is there a -- does each published study in 31 1 the scientific literature, whatever the subject may be, 2 does it receive a grade, or a Cochrane level? 3 A. No. 4 Q. Why not? 5 A. It's not routine, working practice for the 6 scientific community. 7 Q. So, evaluating and grading scientific 8 literature under the Cochrane level guidelines is not 9 common practice in the scientific community, correct? 10 A. It's common practice for those who deliberately 11 set out to assess information. It's -- it's not as 12 formally applied by reviewers and editors to put a 13 number on it, but it's definitely the equivalent of it 14 as applied by reviewers, who then tell an editor "yes" 15 or "no" to accept an article for publication. 16 Q. The Strom study was published in The Leukemia 17 Journal? 18 A. Yes. 19 Q. So, if I were to go to the editor of The 20 Leukemia Journal, I would -- I could say, "Hey, Editor, 21 you defined or you graded every study before you put it 22 in your journal, and you gave each one a Cochrane 23 level," and he'd say, "Yes, I did"? 24 A. No, he would not say that, because he didn't do 25 it. 32 1 Q. Okay. Well, did somebody else do it and then 2 tell the editor of The Journal of Leukemia? 3 A. No. No. The way the process works is that, 4 for reviewing articles for peer-reviewed publications, 5 the editor will receive the journal article being 6 submitted by the authors and the editor will determine 7 whatever he thinks or she thinks is -- who are expert in 8 the area and send it to them. 9 Q. Peer reviewers? 10 A. It's called "peer review." 11 Q. Okay. So, the editor sends the paper to a 12 reviewer? 13 A. Yes. 14 Q. And then what? 15 A. And then the peer reviewers either accept or 16 reject or they accept with modifications and tell the 17 editor that, and then the editor makes a decision. 18 Q. And then where does the -- where does the 19 Cochrane level come into that? 20 A. In that process, not formally, no. 21 Q. Informally? 22 A. Informally, in the sense, perhaps -- they're 23 not thinking of Cochrane, typically; but in the sense of 24 they think they know what is quality information, and 25 they just say, yes, it's good data or it's not good 33 1 data; or it's a good paper, or it's not; or they have 2 other reasons for either accepting it or not accepting 3 it. 4 Q. Have you ever been excluded from testifying in 5 a civil lawsuit? 6 A. No. 7 Q. What is the Cochrane level grade of the Strom 8 2005 paper? 9 MR. SHOEBOTHAM: Objection, form. 10 A. I don't have all the 16 criteria right in front 11 of me, so I don't have them memorized. This is not a 12 prospective, randomized, controlled trial; so, 13 therefore, it's not a 1-A, and probably not even a 1-C 14 or D. 15 Q. (BY MR. PATTON) The ones that are the highest 16 quality? 17 A. Yeah -- well, it can't be if it's not a -- it 18 can't be a 1-A or perhaps a 1-B if it's not a 19 prospective, randomized, controlled trial, which this is 20 not, because it's an epidemiology study. By definition, 21 epidemiology studies, even cohorts, are going to be a 22 lower level. 23 Q. So, the Strom study is a low-quality study? 24 MR. SHOEBOTHAM: Objection, form. 25 A. Did I say that? 34 1 Q. (BY MR. PATTON) I'm asking you. 2 A. I'm asking you: Did I say that? 3 Q. No, you didn't. 4 My question is this: Is the Strom study a 5 low-quality study? 6 A. No. 7 Q. It's a high-quality study? 8 A. Yes. 9 Q. Okay. What makes it a high-quality study? 10 A. Because they have appropriate controls and they 11 have a specific -- if you want to call it "hypothesis," 12 a specific goal in looking at the relationship of 13 benzene to specific types of erythroid dysplasia. 14 Q. You said on Page 6 of your report: "There are 15 no published high-quality data that true MDS develops at 16 lower cumulative dose exposures." 17 Do you see that on Page 6 of your report? 18 A. Yes. 19 Q. Okay. Dr. Parent is one of Plaintiff's experts 20 in this case, correct? 21 A. Yes. 22 Q. Dr. Infante is one of the plaintiff's experts 23 in this case, correct? 24 A. Yes. 25 Q. You reviewed both of their reports, right? 35 1 A. Yes. 2 Q. You reviewed the citations of the authority 3 that they used to support their opinions in this case, 4 right? 5 A. Yes. 6 Q. You reviewed their depositions, right? 7 A. Yes. 8 Q. Is it your position that Plaintiff's experts 9 rely upon no high-quality data in reaching their 10 conclusion that Mr. Wilson's RARS form of MDS was caused 11 by exposure to benzene? 12 A. They rely on data that in some cases is about 13 as good a quality as it could be based on the way that 14 study was designed and done, but it -- the 15 interpretation and the ascribance of significant of that 16 data is not appropriate. 17 Q. So, that makes it low-quality data? 18 A. No, it made -- the authors may have done as 19 quality a job as they could do based on the 20 characteristics of how they designed the study, but the 21 interpretation and application to come and get a 22 conclusion is not reasonably possible to make the 23 conclusions that they did. 24 Q. I'm not talking about the conclusions. I'm 25 talking about the data, itself, because you say: "There 36 1 are no published, high-quality data that true MDS 2 develops" -- what is "true MDS"? 3 A. Well, it would be -- if you want to look at all 4 the listings of -- within the categories of MDS that are 5 listed here, I think there are five or six different 6 sub-types. 7 Q. Is RARS a true MDS? 8 A. I think, no, in 2007 and onward, because it's 9 going to become clear that this is a distinct disease. 10 Q. Your report is dated July 5th, 2007, right? 11 A. Yes. 12 Q. And you say: "There are no published, 13 high-quality data that true MDS develops at lower 14 cumulative dose exposure." 15 Why are you even talking about true MDS, 16 when my client has RARS, which you don't believe to be 17 MDS? 18 A. Simply to address the question. 19 Q. Is RARS true MDS? 20 A. No. 21 Q. So, your opinion has no relevance to this case, 22 because you're talking about true MDS, not RARS, right? 23 MR. SHOEBOTHAM: Objection, form. 24 A. I would disagree. 25 Q. (BY MR. PATTON) Why would you disagree? 37 1 A. My opinion does have relevance. He has RARS, 2 and that is not caused by benzene. 3 Q. Did you go through all or each of Dr. Parent's 4 pieces of authority that he sites in support of his 5 opinions, all 186 of them? 6 A. No. 7 Q. Did you evaluate -- did you evaluate any of 8 them to give them a Cochrane level grade to -- so that 9 you could determine whether or not they were high 10 quality or low quality? 11 A. That's already been done in a different way, 12 but no, I did not do it. 13 Q. Who did that in a different way? 14 A. The Shatner article. 15 Q. What does the Shatner article say? 16 A. Well, what the Shatner article does is to look 17 at over 300-some published -- over 400 published 18 articles and studies related to benzene, and AML 19 particularly, and he is able to divide them out into 20 studies that meet various quality criteria that I've 21 listed in my report. 22 Q. At the -- and that's -- in Page -- on Page 5, 23 on the bottom half of your report, right? 24 A. Yes, sir. 25 Q. Near the bottom of the second to last paragraph 38 1 on Page 5, starting "Highest quality," can you read that 2 for us? 3 A. "Highest quality data show that cumulative 4 benzene exposure 200 ppm-years is the threshold for 5 increased risk of AML. There are no published 6 high-quality data that true MDS that is caused by 7 benzene exposure develops at lower cumulative benzene 8 dose exposure." 9 Q. And that's the same sentence that you repeated 10 in the next paragraph at the bottom, too, right? 11 A. Yes. 12 Q. So, because you give such credence to the 13 Cochrane levels and to Shatner and to high-quality data, 14 if there were an instance where someone has AML and they 15 had 201 ppm-years of exposure, you would agree that the 16 benzene caused that person's AML? 17 MR. SHOEBOTHAM: Objection, form. 18 Q. (BY MR. PATTON) True? 19 A. That's as a misconception of what the 20 information means. 21 Q. The information would mean there's an increased 22 risk, right? 23 A. Yes. 24 Q. Okay. So, if someone had 201 ppm-years 25 exposure to benzene and they had AML, your opinion would 39 1 be, generally speaking, that that person had an 2 increased risk of AML from exposure to the 201 ppm-years 3 of benzene, true? 4 A. It might be a small risk, but it might -- but 5 it would be increased compared to the general 6 population, yes. 7 Q. Would you believe that the 201 years -8 ppm-years of benzene exposure were a substantial 9 causative factor in that person's AML? 10 MR. SHOEBOTHAM: Objection, form. 11 A. "Substantial causative factor at 201 ppm-years 12 based on all the information available" -- from a lay 13 perspective, no. 14 Q. (BY MR. PATTON) Are there any circumstances 15 under which you could opine that a person's AML was 16 caused by benzene exposure? 17 A. Yes. 18 Q. What are those circumstances? 19 A. It's a dose response phenomenon: As you 20 increase the dose, the risk the likelihood that AML was 21 caused by benzene becomes greater. So, certainly, at -22 above 400 ppm-years, that risk begins to increase 23 significantly. 24 Q. So, if I, as a plaintiff's lawyer, had a case 25 in which I could show you evidence that someone was 40 1 exposed to 401 ppm-years of benzene exposure and they 2 had AML, would you support my case that benzene exposure 3 was a substantial causative factor of that person's AML? 4 MR. SHOEBOTHAM: Objection, form. 5 A. If the sub-typing of AML, in a sense, were the 6 appropriate type, yes. 7 Q. (BY MR. PATTON) So, we've got to go back into 8 sub-type again? 9 A. Likely, for AML, yes. 10 Q. Okay. And we would have to look, then, only to 11 the studies of AML that examine AML and sub-type; is 12 that your testimony? 13 A. That examine -- sub-types that examine 14 cytogenetic abnormalities, the factors that are 15 associated with benzene, and in the future that examine 16 oxidoreductase quinone metabolism and allele's. 17 MR. PATTON: I'll object to the 18 nonresponsive portion of your answer. 19 Q. (BY MR. PATTON) If I had a client that I could 20 show you had 401 ppm-years of benzene exposure and they 21 had AML, you would not be able to support causation in 22 that case unless there were certain sub-types, true? 23 MR. SHOEBOTHAM: Objection, form. 24 A. Most likely, yes. 25 Q. (BY MR. PATTON) Okay. So, you would have to 41 1 take a look at that plaintiff's -- or that patient's 2 sub-type and then do the analysis, and then looking -3 you would only look to the relevant literature of 4 sub-type, right? 5 MR. SHOEBOTHAM: Objection, form. 6 A. Let me ask you what -- to be more clear on that 7 answer, if there were information about cytogenetics, 8 that would be very helpful. 9 Q. (BY MR. PATTON) Let's say -- we'll call him 10 "Plaintiff X." Okay? 11 A. Yes. 12 Q. Let's say Plaintiff X has AML-M4. Okay? 13 A. Yes. 14 Q. A non-smoker. 401 ppm-years of benzene 15 exposure. Okay? No cytogenetic abnormalities. Could 16 you support benzene as a cause of that disease? 17 MR. SHOEBOTHAM: Objection, form. 18 A. No cytogenetic abnormalities. So, what that 19 does is that stratifies the risk differently. 20 Q. (BY MR. PATTON) What do you mean "stratifies"? 21 A. Okay. It makes -22 Q. Because I don't think I've ever heard that 23 word. 24 A. Okay. "Stratify" means you separate into 25 groupings. So, if you showed me -- and let me make the 42 1 comparison here. I'm not even thinking about M1, M4, 2 M6. I'd have to go back to the literature, and a 3 hematologist can you tell you better than I on that. 4 But if you're thinking about what is known 5 about benzene and its effects on the body or on cells, 6 and if you have -- and it is well-understood and 7 accepted that benzene tends to cause chromosome 8 aberrations. Chromosome aberrations can be a gain of 9 chromosomes, it can be a loss of chromosomes, it can be 10 something we call polypolidy -- p-o-l-y-p-l-o-i-d-y -11 and other differences. 12 So, if you find -- and I may not have this 13 memorized correctly -- but if you find an addition or a 14 deletion, like a 5-7 or a 17-18 or 17-19, those -- and 15 that that were the case of the gentleman you were 16 describing with AML and he had those, then -- and you 17 have a 400 and -- I think it becomes, perhaps, more 18 likely than not with that degree of benzene exposure. 19 Q. Tell me again what "stratify" means? 20 A. Stratify means to divide out or split out into 21 various groupings. 22 Q. So, when something like a hematology text 23 indicates that benzene causes AML, for you to give an 24 opinion on benzene causing AML you would need to further 25 stratify AML; you would need to put it in separate 43 1 groups? 2 A. Yes. 3 Q. Okay. And so, then, once you put it into the 4 separate groups -- I wish I knew offhand how many 5 sub-types there were, because -- I know there's about 6 five in MDS -- but given your position on MDS, I think 7 it's a better context of AML. 8 Do you know approximately how many sub -9 MR. SHOEBOTHAM: Objection, form. 10 MR. PATTON: Forgive the sidebar. 11 Q. (BY MR. PATTON) Do you know approximately how 12 many sub-types of AML there are? I'm not going to hold 13 you to this. 14 A. All right. 15 Q. Just so we can talk about it. 16 A. I can't remember, actually. I'm sorry. 17 Q. Okay. But you, as an expert in examining 18 causation, you would want to stratify AML? You would 19 want to look at sub-type and then you would want to look 20 at chromosomal aberrations within each sub-type, 21 correct? 22 A. Yes. 23 Q. And then you would want to look at the specific 24 chromosomal aberrations within each sub-type. So, you 25 would further stratify it as far as you possibly could 44 1 in examining causation. That's the way you would work, 2 right? 3 A. Yes. 4 Q. That is your methodology, to stratify to the 5 lowest -- or most specific possible manner, right? 6 A. To -- my methodology is to base my approach on 7 the best available data, which now, compared to 30 years 8 ago, we have much more information on what these 9 disorders are like. 10 Q. Page 7 in your report. It has references. 11 What does the Bjork reference stand for, 12 generally. 13 A. These are last names of the first author of 14 papers. 15 Q. Sure. 16 A. And I didn't have time to finish it, putting 17 all the specific information in; so, I don't recall 18 the Bjork paper without looking at it. 19 Q. Were you under a time crunch when you were 20 writing this report? 21 A. Yes. 22 Q. When were you first given the Wilson case to 23 review and opine on? 24 A. Plenty of time to write a report. I was under 25 time issues from my other workload. 45 1 MR. PATTON: Objection, nonresponsive. 2 Q. (BY MR. PATTON) When were you given the -3 A. Oh. I don't remember. I can find a -- I 4 apologize. I can find the -- a letter that was sent to 5 me, perhaps. 6 Q. I think it's back in the box. And it's all 7 right. We can continue. 8 MR. PATTON: Let's take a break. Off the 9 record. 10 (Short break.) 11 Q. (BY MR. PATTON) Doctor, we took a short break; 12 and I want to finish out talking about Exhibit 2. When 13 want made a list of what is "high-quality data," 14 according to you, you talked about your deference, or 15 respect, should I say, for the Cochrane levels, correct? 16 A. Yes. 17 Q. And what is the next part? 18 A. That within those 16 various categories, which 19 I don't have here and I don't have memorized -- if we 20 had those, we could list those as the way one applies 21 this to individual studies. 22 Q. Is there a level within that 16 Cochrane 23 grades, so to speak, that you make it a cutoff, that 24 something is above the line and, therefore, high quality 25 or below the line and, therefore, low quality, or how 46 1 does that work? 2 A. It's a continuum. 3 Q. Some are higher than others? 4 A. Yes. 5 Q. Okay. And then, what's this part you wrote 6 here that I can't read (indicating)? 7 A. "Characteristics of quality of data." 8 Q. Okay. That's something that -9 A. It's defined in each of the -- in the actual 10 formal listings -11 Q. Okay. 12 A. -- if we had a copy of it. 13 Q. So, "high-quality data," that phrase, for you 14 is all about the Cochrane levels, right, and those 15 things set forth within the Cochrane levels? 16 A. High-quality data is sort of a qualitative 17 descriptive term. The Cochrane is an attempt to try to 18 semi-quantitatively apply some numerics to that. 19 Q. Okay. Do you consider each of the references 20 on Page 7 of your report to be high-quality data? 21 A. They have -- and I've not done this, but they 22 would have varying levels of -- if you tried to write 23 them by the Cochrane approach -- varying levels of 24 Cochrane category. Some are higher -- depends on what 25 you mean by "high quality." 47 1 If you mean overall, then maybe they're 2 high quality with regard to what they had to work 3 with -- excuse me -- and maybe they simply are unable to 4 be higher quality because of the nature of the design of 5 the study or the limitations in the data that was 6 accessible. 7 Q. But isn't it true that all scientific 8 literature is going to have varying levels of 9 quality? You know, for instance, well, this is a real 10 positive for the study or -- and at the same time, 11 another issue is a real negative for the study? 12 It's kind of like the weather. Yes, it's 13 sunny out, which is nice; but it's humid, which is 14 unfavorable. I mean, can't each study be looked at to 15 have some positive attributes or strengths and some 16 weaknesses? 17 A. Within a range, perhaps. 18 Q. And then do some studies just fall out of that 19 range such that they have so many weaknesses that they 20 just don't pass muster for any type of appreciable 21 quality? 22 A. Sometimes I have seen that occur. 23 Q. Well, for instance, today could be 24 characterized as something of a high-quality day, 25 because it's sunny out, it's warm, it's not raining, 48 1 it's generally pleasant, it's not too windy. Whereas, 2 if you had a day where there's, like, a tropical storm 3 coming through, as in a few days ago, most people would 4 agree that is a -- an unfavorable day or a bad day 5 weather-wise? 6 Do you understand my analogy? 7 A. Yes. 8 Q. Okay. Are there some studies that when you 9 take a look at them, you can say, you know what, that's 10 just a bad study. It's like a day where there's a 11 tropical storm coming through; it's just not good, it's 12 not favorable, and it's just below muster, it's below 13 the line of something that anyone would appreciate or 14 like? 15 MR. SHOEBOTHAM: Objection, form. 16 A. Well, then, it would be a dis -- "favorable" 17 may be favorable to the case, in a legal setting. 18 Whether it's good or not or bad or not in a quality 19 sense, may be a different distinction of terms or what 20 were their methods, what were the data sets that they 21 had to work with. 22 Q. (BY MR. PATTON) What are your criticisms of 23 Dr. Parent and Dr. Nicas's -- I'm sorry -- Dr. Parent 24 and Dr. Infante's opinions as it speaks to their 25 reliance upon data of whatever quality that may be? 49 1 A. My critiques are very similar to what would be 2 in the Institute of Medicine Report that looks at that 3 information. And that is that -- and also similar to 4 Shatner's with regard to a different end point. And 5 that is that your -- there's issues of -- very specific 6 kinds of issues a variety of more than I can recall, but 7 issues of misclassification, of confounding of the 8 design of the study and how strong a conclusion one can 9 make from that type of design or study; and so, that, 10 they take a variety of studies and don't really talk 11 about the limitations or weaknesses of those studies. 12 Q. Well, you cite -- you cite 18 references on 13 Page 7 of your report. 14 A. Yes. 15 Q. In your report, do you discuss the strengths 16 and weaknesses of each -17 A. No. 18 Q. -- study? 19 A. I do not. 20 Q. Did you review each of the 186 references by 21 Dr. Parent and sort of check them off, so to speak, and 22 say, you know what, that one has too many weaknesses or 23 that other one has too many weaknesses or that other one 24 is just bad science or -- did you go through and 25 individually critique each of their -- each of 50 1 Plaintiff's expert's references? 2 A. No. 3 Q. Nor did you go through and grade them, so to 4 speak, per the Cochrane levels, true? 5 A. Correct. 6 Q. You just didn't do that, right? 7 A. That's correct. 8 Q. Okay. So, how do you reach the conclusion, 9 then, that Plaintiff's experts, Dr. Parent and 10 Dr. Infante, their opinions are based on no published 11 high-quality data? 12 A. Because if you'd look at the kind of studies 13 they look at, and you want to answer the question, "yes" 14 or "no," does benzene cause RARS, they do not address 15 the issue, specifically; they do not show dose response 16 data; they do not describe dose response data; they do 17 not address that even as a factor. 18 Q. Does the Strom 2005 discuss dose response? 19 A. No. 20 Q. What's the strength of the data in the Strom 21 study? 22 A. Its strength is that it looks at RARS 23 specifically. 24 Q. Okay. What are the weaknesses of the Strom 25 study? 51 1 A. There -- part of what any kind of case control 2 study would have -- or retrospective case control study 3 cannot be as -- the same strength of evidence as, say, a 4 prospective cohort study would be. 5 Q. So, you think prospective cohort studies are 6 the best studies under which to examine benzene as a 7 causative factor in a given type of bone marrow disease, 8 true? 9 A. Well, that's just general epidemiology 10 information, yes. 11 Q. Prospective cohort studies are the best? 12 A. Yes. 13 Q. Which prospective cohort studies are cited in 14 your report? 15 A. To my knowledge, I don't recall any of them 16 being prospective cohort studies. 17 Q. So, you don't cite any prospective cohort 18 studies for your conclusion that benzene doesn't cause 19 MDS and benzene was in no way a causative factor of 20 Charles Wilson's MDS? 21 A. I'm not aware of any published prospective 22 cohort studies that address benzene and RARS or MDS. 23 Q. Okay. So, then what's the next best type of 24 study out there, highest quality? 25 A. What's available by design would be a case 52 1 control-type study. 2 Q. Okay. Case control studies, those are 3 reliable -- that's a reliable methodology? That's a 4 relevant piece of scientific literature that's respected 5 in the scientific community? 6 A. It's regarded as to what it is. 7 Q. It's going to have strengths and weaknesses? 8 A. Yes. 9 Q. Each case control study will have strengths and 10 weaknesses, right? 11 A. Often, yes. 12 Q. You cite some case controlled studies? 13 A. Yes. 14 Q. Okay. They all have strengths and weaknesses, 15 don't they? 16 A. Yes. 17 Q. Some of them look at dose response, some don't? 18 A. Yes. 19 Q. Okay. What's the problem with -- or what are 20 your criticisms of Plaintiff's experts in terms of the 21 types of studies they use? Do they point to any 22 prospective cohort studies? 23 A. No. 24 Q. All right. Do Plaintiff's experts rely on any 25 case control studies? 53 1 A. Yes. 2 Q. And your position is the case control studies 3 they rely on do not support benzene as a cause of RARS, 4 true? 5 A. Correct. 6 Q. Do you believe the case control studies that 7 Plaintiff's experts rely on support benzene as a 8 possible causative factor in MDS, generally? 9 A. When you use that terminology, then the answer 10 to that would be there's older literature at 11 sufficiently high dose of exposure, years ago for 12 benzene, that some AML cases are preceded by what would 13 be then, in those days, termed "MDS." And I think it 14 would be general agreement that at sufficiently high 15 dose, a long enough period of time, that benzene can 16 lead to AML, could, in some of those cases, have 17 produced what is -- was then, in those days, called 18 "MDS." 19 Q. Okay. Do you believe Dr. Infante misinterprets 20 some studies in relying upon them in support of his 21 opinions? 22 A. Yes. 23 Q. Which studies does he misinterpret? 24 A. If you look at Page 10 of Dr. Infante's report, 25 on the bottom half of that page he cites a 1970 paper by 54 1 Girard and Revol, and this is under the section that is 2 entitled "Epidemiological Studies Subsequently Provided 3 Evidence That Benzene Caused AML and MDS." 4 And in that study is -- he states near the 5 bottom of that paragraph that the -- he's indicated that 6 the frequency of benzene exposure was statistically 7 significantly elevated for patients admitted with acute 8 leukemia and aplasia. 9 Q. What's aplasia? 10 A. Aplasia is the opposite of MDS. So, it would 11 be a matter of whether you want to include that as 12 something related to MDS or not, as to how you interpret 13 that study -- or to use that study to relate it to MDS. 14 Q. What other criticisms do you have of 15 Dr. Infante's opinions in this case, either expressed in 16 his report or through his deposition? 17 A. On Page 13 of his report in the first full 18 paragraph, which starts: "For dose response 19 analyses" -- he's talking about Hays, et. al, in 1997 -20 he makes the statement that reflects that he is not 21 dividing MDS into the actual different disease 22 categories that it is; and he states: "Simply because 23 MDS is a precursor to AML..." 24 Some distinct disorders may be a precursor 25 to AML, but not necessarily and not necessarily 55 1 specifically that. 2 Q. The Hays study didn't stratify sufficiently for 3 your taste, correct? 4 A. It just didn't divide into RARS or other 5 distinct disorders, no, it did not. 6 Q. How far -- if we look at Page 7 of your report, 7 in your references, how far stratified, so to speak, are 8 each of these studies that you cite, the 18 studies, or 9 authority that you cite? 10 A. None, to the extent that Strom is. 11 Q. It's unusual for a -- for a benzene-type study 12 or study that discusses benzene to stratify as far as 13 Strom, isn't it? 14 A. Well, I will correct my response. It's -- the 15 Wong studies have done that. 16 Q. How far did they stratify? 17 A. And what they did was not related to MDS. It 18 was related to leukemia, AML. 19 Q. Did Wong look at all leukemia or did Wong look 20 at only AML? 21 A. That's the point. He looked at AML 22 specifically. 23 Q. Did he look at AML by sub-type? 24 A. No. 25 Q. So, you rely on the Wong study because it talks 56 1 about AML and the cumulative dose necessary, according 2 to Dr. Wong's study, to increase the risk of AML from 3 exposure to benzene; but the Wong study doesn't stratify 4 beyond AML, correct? 5 A. Correct. 6 Q. And so -- remember when I was talking about 7 "Plaintiff X" earlier, my potential client who had 401 8 ppm-years exposure to benzene? 9 A. Yes. 10 Q. Would the Wong study at all be helpful to you 11 in opining in that type of case? 12 A. Yes. 13 Q. Even though he doesn't stratify? 14 A. Yes. 15 Q. Can you explain that? 16 A. Because -- because the hypothetical individual 17 you've mentioned is -- I think you mentioned 401 -- that 18 is above 400, which is a higher risk. And 200 is a very 19 conservative estimate; it's above 200. So, it says that 20 he would definitely have some risk of benzene being a 21 cause of his AML if we don't know the sub-types. 22 Q. So, he's above 400. So, all AMLs are caused by 23 benzene exposure above 400? 24 MR. SHOEBOTHAM: Objection, form. 25 A. No. We don't know that. In fact, we know the 57 1 opposite. We know to some extent that some types would 2 not be because of the type of cytogenetic findings you 3 have. 4 Q. (BY MR. PATTON) So, when Dr. Wong says that 5 excess of 200 ppm-years exposure to benzene causes an 6 increased risk of AML, it's not really an accurate 7 statement; you would need to look, then, further to the 8 sub-types of AML before you could say that 200 -- excess 9 of 200 ppm-years exposure would cause a given sub-type, 10 correct? 11 MR. SHOEBOTHAM: Objection, form. 12 A. Let me be sure I understand your question. 13 Wong's study looked at the data available, and it did 14 not have sub-type information for him to be able to make 15 any kind of classification like that. So, all he could 16 say, it was AML; so, that's the extent of what can be 17 concluded from the data he had available. 18 Q. (BY MR. PATTON) Don't you think you're trying 19 to have it both ways in this case? You're trying to say 20 that benzene doesn't cause RARS, and here's one study 21 that's ultra-stratified and that's the end of the 22 inquiry. 23 Meanwhile, when you talk about benzene 24 generally is a cause of other bone marrow diseases, 25 you're willing to opine that it takes significantly 58 1 higher exposures than one might opine Mr. Wilson had; 2 and the basis for that is a really low, if at all, 3 stratified study like Wong. 4 MR. SHOEBOTHAM: Objection, form. 5 Q. (BY MR. PATTON) How do you reconcile that as a 6 scientist? 7 A. There's no need to reconcile anything. They're 8 all very consistent with the data that's available, and 9 when you have dose response information, that's very 10 relevant to making an assessment about an individual 11 person's likelihood or not likelihood to have a disorder 12 related to benzene or not related to benzene exposure. 13 Q. But the dose response data from Wong says, 14 "Excess of 200 ppm-years equals increased risk of AML," 15 right? 16 A. Yes. It starts as a threshold at that point. 17 Q. Okay. So, then once you're above that 18 threshold, you would still need to further stratify or 19 sub-divide a given patient's AML before you could then 20 say, "Okay. Wong is right, because this patient has 21 this certain sub-type that's shown in other literature"? 22 A. Wong's 1995 data did not address sub-types. 23 Q. Did Crump '94 examine sub-types? 24 A. Of AML, no. Of leukemia, yes. 25 Q. What types of leukemia did Crump look at? 59 1 A. So, lymphocytic leukemias versus myelocytic 2 leukemia. 3 Q. What about Ward '96, does that look at -- how 4 far does that stratify? 5 A. I would have to look at the study. I don't 6 recall it without looking at the data. 7 Q. Can we look it up? I don't think it's in that 8 box, to be honest. 9 A. I don't think I have it here. 10 Q. Okay. We can move on. 11 You work at a poison control center, 12 right? 13 A. Yes. 14 Q. You're the medical director at the Texas Poison 15 Center in Santa Fe? 16 A. No, it's the Texas Poison Center that serves 17 Houston and Galveston, and it's located here in 18 Galveston. 19 Q. Do you give opinions in your clinical work as 20 to a specific substance causing a specific disease? 21 A. In a general sense, that is a question that 22 sometimes is asked, yes. 23 Q. And do you go to a textbook or some other type 24 of medical or toxicological authority that talks about, 25 okay, substance "X" causes illness "Y," or do you just 60 1 take that for what it is or do you then dive into the 2 literature and start stratifying to give the opinion 3 that, yes, "X" caused "Y," or, no, "X" did not cause 4 "Y"? How far do you dig when you give a causation 5 opinion in your clinical practice? 6 A. Well, the context and setting is very different 7 than here in a legal setting. So, much of the time, if 8 not a far majority of the time, it's something that's 9 relatively well-known or accepted; so, cause is sort-of 10 already understood. The question is in that individual 11 patient -- in a general sense, cause is understood. The 12 question is in that individual patient is that what's 13 doing it to this patient or are there other factors 14 involved or, if it is causing it, how do we manage this 15 and how do we treat it. So, the setting is actually 16 rather different. 17 Q. I know I'm bouncing around a little this 18 morning, Doctor; and I think I'll wrap it up at some 19 point, but I want to next talk about the list of cases 20 that you've testified in. Is that okay? 21 A. Yes. 22 (Snodgrass Exhibit No. 3 marked.) 23 Q. (BY MR. PATTON) I've marked as Exhibit 3, a 24 list of testimony in the last four years. And this is a 25 list that you've faxed to the lawyers at Thompson 61 1 Knight, correct? 2 A. Yes. 3 Q. Okay. How many of these cases did you testify 4 on behalf of a plaintiff? 5 A. Approximately, I'd say, typically, around 6 40 percent. 7 Q. 40 percent of your work is with plaintiffs? 8 A. Yes, sir. 9 Q. How many of these cases involve benzene? And 10 can you tell me which one, so I can write "benzene" next 11 to it on my list? 12 A. Well, this is from memory. I know I've 13 testified or at least had a deposition in a benzene case 14 or -- one or more. I see a xylene case listed. The 15 fourth case is Martinez. That was not benzene. I'm 16 trying to recall, see if I can recall a benzene case. 17 I apologize. I know I have in the past; I 18 just don't remember them. 19 Q. Can you estimate approximately how many benzene 20 cases you've testified in? 21 A. I'd say at least two and maybe three or four. 22 Q. Two to four benzene cases? 23 A. I would estimate that number at this point. 24 Q. How many cases have you testified in on behalf 25 of Ashland? 62 1 A. To my recollection, none. 2 Q. How many cases have you testified in involving 3 Mr. Shoebotham or his firm? 4 A. Two, or perhaps three or four. 5 Q. So, each of your benzene cases were with his 6 law firm, Thompson & Knight? 7 A. I'm not certain. I -- there may have been one 8 or two. Perhaps, it was with different attorneys. 9 Q. Which cases on here involved Mr. Shoebotham and 10 his law firm? 11 A. None of them. 12 MR. PATTON: Mr. Shoebotham, just for 13 the -14 MR. SHOEBOTHAM: I -15 MR. PATTON: -- ease of clarification -16 MR. SHOEBOTHAM: I can -17 MR. PATTON: -- do you have any input on 18 this? 19 MR. SHOEBOTHAM: I can tell you one from 20 memory that I think may have just been omitted from the 21 list. It was a case called Scott versus Pharmacia in 22 which Mr. Snodgrass testified, and I was one of the 23 lawyers that retained him. 24 And I don't see that on the listing. So, 25 I would ask Dr. Snodgrass to supplement his list orally 63 1 with that deposition. That deposition took place in 2 either late 2005 or early 2006. 3 MR. PATTON: Who was the plaintiff's 4 lawyer? 5 MR. SHOEBOTHAM: Mike Kesky. 6 MR. PATTON: That was that Scott case? 7 MR. SHOEBOTHAM: That's the only one that 8 springs to mind, just looking at the list. 9 Q. (BY MR. PATTON) You've never testified on 10 behalf of a plaintiff in a benzene case, correct? 11 A. I don't believe I have been asked -- or seen 12 data that was sufficient for causation. I -- correct, 13 I've not. 14 Q. Have you ever reviewed cases involving benzene 15 exposure for a plaintiff's attorney? 16 A. I think I may have been asked, yes, but I am 17 trying to remember. It's been more than -- probably 18 more than three or four years ago. 19 Q. How much are you being paid for your time in 20 this case? 21 A. $350 per hour for review. 22 Q. And how much for deposition or trial testimony? 23 A. It's 750 per hour. 24 Q. How much time did you spend reviewing materials 25 in this case? 64 1 A. I spent 44 hours. 2 Q. And you know that from memory? 3 A. Yes. 4 Q. You don't have any time cards or time sheets or 5 invoices with you today? 6 A. No. 7 Q. Have you created any type of time sheet or 8 invoice? 9 A. No. 10 Q. How do you know it's 44 hours? 11 A. I keep track in my mind. 12 Q. Is that an effective way of getting paid? I'm 13 joking, partially. 14 A. It's just what I do. 15 Q. $350 an hour, and you don't write down your 16 time spent at that rate? 17 A. It's 44 hours. 18 Q. Okay. And it's not written down anywhere? 19 A. Correct. 20 Q. Okay. What's 44 times 350? You went to school 21 longer than I did, not that that automatically makes you 22 more qualified. $15,400? 23 A. Yes. Yes. 24 Q. For the record, I got it before you did. 25 A. That's correct. 65 1 MR. SHOEBOTHAM: Also for the record, no 2 one had a calculator. 3 Q. (BY MR. PATTON) Okay. Have you been asked to 4 testify at trial in this case? 5 A. Yes. 6 Q. Do you know when the trial is scheduled? 7 A. In a relatively shorter period of time, in the 8 next several weeks. 9 Q. Do you know where trial is at? 10 A. I don't know specifically. 11 Q. Is there any other information that you would 12 like to review in forming or revisiting or confirming 13 your opinions in this case that you have not been 14 provided? 15 A. I can't think of any information at this point 16 in time. 17 Q. What about the benzene content of the Ashland 18 solvent blends? Remember how in your report you said 19 there's unpublished information? 20 A. Yeah. 21 Q. Would you like to see published information on 22 benzene content? 23 A. I -- if there was some information available, 24 that would be of interest to see, yes. 25 Q. And I'm talking about that line on Page 3 of 66 1 your report. 2 A. Yes. 3 Q. Tell me again about the basis for your 4 opinion -- or statement, rather, that unpublished 5 information indicates considerably lower benzene content 6 compared to the assumptions of Dr. Nicas. Was it just 7 that one phone conference with Morgan Gaskin? 8 A. Yes. And then, of course, subsequently, it's 9 Dr. Whitlock's deposition. 10 Q. Does it bother you that the -- that this case 11 involves benzene exposure, involves benzene alleged as a 12 constituent or contaminant in the Ashland solvent 13 blends? You're working for Ashland in this case, but 14 Ashland can't tell you how much benzene is in that 15 product. Does that bother you? 16 MR. SHOEBOTHAM: Objection, form. 17 A. Well, I think that Dr. Whitlock would have an 18 accurate idea of what was in there. 19 Q. (BY MR. PATTON) But don't you think Ashland -20 wouldn't you expect Ashland to have documents supporting 21 Mr. Whitlock's assertions? 22 MR. SHOEBOTHAM: Objection, form. 23 A. You know, an industrial hygienist can answer 24 that question. I -- I don't know about those issues, 25 actually. 67 1 Q. (BY MR. PATTON) Do you always take your 2 client's word for it, or do you ask for documents or 3 other proof to back up their statements? 4 A. Well, I often ask for other information if it's 5 available. 6 Q. And did you ask for other information in this 7 case? 8 A. Yes. 9 Q. Because you wanted to see more than just 10 Whitlock's statements, true? 11 A. Well, I wanted to see if there was other 12 information, yes. 13 Q. And continuing on Page 3, you talk about 14 approximately one-half of the amount of benzene inhaled 15 is absorbed into the body. Approximately one-half of 16 absorbed benzene is excreted, unchanged, via the lungs 17 over a 36-hour period, depending on exercise level and 18 amount of body fat. So, is that to say that in a given 19 day if a person were to inhale one unit of benzene, 20 okay, half that unit would go right back out within 21 36 hours? 22 A. Yes. 23 Q. Can you explain that more for me? I guess I 24 should try to get it in your words, rather than me 25 reading your sentence. 68 1 Tell us about your opinions and your 2 understanding of how benzene comes in the body and then 3 leaves the body and what the bases of those opinions 4 are. 5 A. It's actually very simple, that benzene has 6 a -- what we call a "vapor pressure" so that a solution 7 of benzene in a container, an open container, will have 8 a little bit of vapor of benzene above it going into the 9 air. So, if you inhale some air that has benzene in it, 10 then your body will absorb about a half of that. The 11 other half comes right back out in the next breath. 12 And then of the one-half that you have now 13 absorbed, over 36 hours half of that comes back out of 14 the body if you're no longer exposed, being exhaled 15 through the lungs. 16 Q. So, 25 percent of what was originally inhaled 17 stays in? 18 A. Approximately, yes. 19 Q. Okay. And then does that ever go back out? 20 A. Yes. It's handled by the body. It's excreted 21 by the kidneys. It's excreted in the bowel movement. 22 It's metabolized in metabolites, and go out the kidney. 23 Q. All humans metabolize things differently, 24 right? 25 A. Within range, yes. 69 1 Q. I could go to McDonald's and eat a Big Mac and 2 you can eat -- go to McDonald's and sit next to me and 3 eat a Big Mac, and our bodies would metabolize the 4 substances in that Big Mac differently, right? 5 A. We might generate different amounts of body 6 heat from that fuel source, that's correct. 7 Q. And then, as far as the amount of time that it 8 would take for all the ingredients or substances in that 9 Big Mac to come back out of our body or to stay or 10 whether it goes to the liver or the kidneys, my body 11 would handle that differently than your body would, 12 correct? 13 A. Within a somewhat narrow range, yes. 14 Q. Okay. And the point that I'm trying to segue 15 into here is: All individuals handle and metabolize 16 products or substances a little bit differently, 17 correct? 18 A. That's true. That's why the genetics becomes 19 important. 20 Q. Have you testified in any cases involving, 21 like, alcohol or drugs? 22 A. Yes. 23 Q. Okay. And so, different people respond to 24 alcohol and drugs differently than others, right? 25 A. Again, within a somewhat narrow range, yes. 70 1 Q. I could drink a bottle of whiskey here today 2 and you drink a bottle of whiskey today, and our bodies 3 would react differently to that? 4 A. Depending on what reaction is measured, it 5 might be somewhat different -6 Q. Okay. 7 A. -- possibly. 8 Q. Some people are more susceptible to feel the 9 effects of a given substance, so to speak, true? 10 A. Within a range, yes. 11 Q. Okay. And just as some people are allergic to 12 cats and dogs, other people are not allergic to cats and 13 dogs, true? 14 A. That's allergy, which is not really dose 15 response. 16 Q. Okay. 17 A. That's a different process. 18 Q. When we talk about dose response, though, 19 let's -- coming back to Plaintiff X, who had 401 20 ppm-years of benzene exposure. If you had two different 21 people, Person 1 and Person 2, and let's say that 22 they -- each of them worked side by side their whole 23 life with benzene and one had 2000 ppm-years of benzene 24 cumulative dose and the other had 2000 ppm-years 25 cumulative dose, one person might get AML -- even though 71 1 both are at an increased risk, one person might get AML, 2 one person might not get AML, true? 3 A. That's true. 4 Q. Okay. Why the individual difference? 5 A. It's genetics. 6 Q. Some people are more genetically susceptible to 7 feel the effects of a dose response relationship than 8 others, true? 9 A. Within a range, yes. 10 Q. Do the studies that talk about benzene as a 11 causative factor of bone marrow diseases -- do they talk 12 genetic susceptibility? 13 A. Only the more recent ones begin to address that 14 somewhat. 15 Q. Do any of the studies cited by your report talk 16 about individual genetic susceptibility? 17 A. Tunca and Zhang approach that, yes. 18 Q. What do they say about it, generally? I mean, 19 we could all go read the report, but what are your 20 opinions on what they say or -21 A. Well, what we've talked about before, which is 22 the chromosome aberrations, whether you can have a 23 chromosome gain or chromosome loss within cells, or 24 polyploidy, those types of phenomenon. 25 MR. PATTON: Let's take a short break. 72 1 (Short break.) 2 MR. PATTON: Back on the record. 3 Q. (BY MR. PATTON) We were talking on the break 4 about the list of cases that you've testified in, 5 Dr. Snodgrass, and it's my understanding there's some 6 discrepancy between Exhibit 3 and what you've actually 7 testified in. Could you or your attorney explain that 8 for us? 9 A. Yes. There is a case called "Scott" that 10 involved benzene, and also a case entitled "Boren," 11 B-o-r-e-n, that involved benzene. 12 Q. And you were working with Ashland's law firm in 13 this case on both of those cases, right? 14 A. Yes. 15 Q. All right. And in each of those cases was it 16 your testimony that benzene was not a causative factor 17 in the plaintiffs' diseases? 18 A. Yes. 19 Q. Do you know what the diseases at issue in each 20 of those cases were? 21 A. I don't, actually, at the moment. 22 Q. But in any event, it was your testimony that 23 benzene played absolutely no role in causing the 24 individuals -- workers, in those two cases? 25 A. That's correct. 73 1 Q. And you have never testified in a case that 2 benzene played any causative role in a person's bone 3 marrow disease, true? 4 A. I have not been presented a case that way, yes, 5 correct. 6 Q. In your opinion, does the Strom study tell us 7 definitively that benzene exposure does not cause RARS? 8 MR. SHOEBOTHAM: Objection, form. 9 A. It -- the data would -- I would interpret it to 10 say it's highly -- highly likely, highly likely that it 11 does not cause RARS. 12 Q. (BY MR. PATTON) Okay. And which part of the 13 study tells you that or do you interpret that way? 14 A. Well, it's an overall result from the study, or 15 you could find some of the -- for example, Table 6 has 16 data that's -- lists that information. 17 Q. Okay. Which part is it? 18 A. Right there (indicating). 19 Q. Okay. 20 A. So, on Table 6, you'll see a section of benzene 21 or solvents or gasoline exposure; and then the -22 they're looking at what we call a -- "an odds ratio." 23 And the odds ratio could be significant. The lower 24 limit of the confidence interval has to be above 1.0 -25 Q. Okay. 74 1 A. -- otherwise, it's not significant. 2 And so that what you see is that -- for 3 the RARS group, that none of the odds ratios for having 4 that, either refractory anemia or RARS -- first of all, 5 none of those odd ratios are above 2, which is generally 6 accepted to be a more significant odds ratio; and 7 secondly, the confidence intervals are -- you know, the 8 lower limit is always below 1. 9 And then, the trend for the significance 10 of the test in the case of the refractory anemia with 11 excessive blasts, which can go on to become leukemia in 12 a greater percentage -- perhaps maybe 20 percent or more 13 of those, perhaps, can go on to become, for example, a 14 leukemia; whereas, with the RARS, much of the data says 15 less than 1 percent -- the trend for the test is not 16 significant. There's a number here of .34. Whereas, 17 for the excessive blasts, it's significant, which is a 18 value less than .001. That's a statistical test. 19 Q. In Table 6 here, they examine -- well, first of 20 all, how many people in this RARS category are 21 investigated or explored? 22 A. There are -- there were a total of 354 cases of 23 all types together, and there were 67 that have 24 refractory anemia and there were 38 that had RARS. 25 Q. Okay. And so, this column -- this first column 75 1 here in Table 6 at the bottom where you're talking about 2 benzene, that's exploring 67 people with RA, 38 people 3 with RARS, right? 4 A. Yes. 5 Q. And they asked those people what kind of 6 benzene solvent or gasoline exposure they had, None, 7 Low/Medium, or High, correct? 8 A. Yes. 9 Q. And how much benzene solvent or gasoline 10 exposure is meant in the "None" category? 11 A. There was something called the "job exposure 12 matrix" -- they list it as "JEM" -- which is developed 13 by the National Cancer Institute, and it assigns a level 14 of intensity of exposure for job titles. And it's None 15 or Low or Medium or High, and it was -- it was asked to 16 them in a questionnaire. 17 Q. So, how much benzene were the people in the 18 Low/Medium category exposed to? 19 A. They do not have actual air level data or 20 milligram-amount exposure information. 21 Q. So, on Table 6, we don't know what dose of 22 benzene/solvent/gasoline any of the 67 RA people or 23 38 RARS people were exposed to, true? 24 A. You actually have an estimate of the dose, you 25 don't have a specific measurement of it. 76 1 Q. Okay. Do we have an estimate -- do we know 2 what the estimated dose is for each of these categories? 3 A. It's not specified in the paper, no. 4 Q. Okay. Do you know how they went about 5 estimating dose? 6 A. They estimated it based on the -7 Q. On the job category? 8 A. Yes, in that reference. I would have to go 9 back and show you to explain it. It's the Dosemeci in 10 1994. 11 Q. What footnote is that? 12 A. That's Reference 16 in the -- to that Strom 13 paper. 14 Q. Okay. So, what does it mean when the result of 15 Table 6 here is not statistically significant? What 16 does that mean to us? 17 A. It means it's not related. 18 Q. Okay. And then what's the problem with the 19 odds ratio here? 20 A. It just shows it's not related. 21 Q. Okay. So, this tells us that 22 benzene/solvent/gasoline exposure is not related, 23 statistically, significantly to RARS for the 67 people 24 who filled out a questionnaire and happened to be at 25 M.D. Anderson, as well as the 38 people with RARS who 77 1 filled out the questionnaire and happened to be at 2 M.D. Anderson at this time frame when the study was 3 conducted, true? 4 A. Yes. 5 Q. Okay. So, putting aside the -- well, how many 6 years of literature do you think there are out there 7 that talk about benzene and leukemia and bone marrow 8 diseases? 20, 30, 40 years of literature out there? 9 A. Yes. 10 Q. So, in forming your opinions in this case, you 11 essentially chose to put aside the 20, 30, 40 years of 12 literature and focus on one study from 2005 examining 13 67 refractory anemia patients and 38 with refractory 14 anemia with ringed sideroblasts patients who happened to 15 be at M.D. Anderson at some point in the mid 2000s and 16 filled out a questionnaire which asked them how much 17 benzene/solvent/gasoline they were exposed to, and 18 determined that there was no statistically significant 19 relationship? That's your opinion? 20 MR. SHOEBOTHAM: Objection, form. 21 A. No. 22 Q. (BY MR. PATTON) Where am I wrong? 23 A. I looked at enormous amounts of literature 24 going back many years. 25 Q. And all that literature tells you that there's 78 1 just no way benzene was a causative factor in Charles 2 Wilson's MDS/RARS, true? 3 MR. SHOEBOTHAM: Objection, form. 4 A. That's correct. 5 Q. (BY MR. PATTON) Have you reviewed any 6 quantitative exposure data concerning Charles Wilson's 7 benzene exposure in forming your opinions in this case? 8 A. I have reviewed the testimony of the chemist, 9 but nothing further. 10 Q. Do you have any opinions as we sit here today 11 as to what level of exposure to benzene Charles Wilson 12 experienced by use of the Ashland solvents and other 13 printing solvents in his 26 years of work as a printer? 14 A. I think the industrial hygienist will address 15 that better than I for -- for an air level. I -- I 16 don't recall his numbers at the moment. I did look at 17 some of that. 18 It's a low air level exposure. So, it 19 would be -- if you look at how Dr. Nicas calculated his 20 18.1, that -- this would be considerably below that. 21 Q. So, do you have a number that you're relying 22 upon that you consider to be Charles Wilson's level of 23 exposure to benzene in this case? 24 A. I think the best number will come from 25 Mr. Spencer. I would defer to him to give you that 79 1 information, but I think it's going to be a much, much 2 lower level than the 18. 3 Q. What information -- I don't want to know what 4 information he gives me. What information did he give 5 you? 6 A. I'll have to look at his material. 7 Q. Well, let me back up. In forming your opinions 8 prior to your report, what did you understand to be the 9 level of exposure that Charles Wilson experienced, less 10 than 18.1 and that was it? 11 A. It would be that -- less than 5, say, 12 2-and-half parts per million in the benzene content of 13 the solvent; therefore, that would translate into a low 14 air level exposure. 15 Q. What if someone came out with study tomorrow 16 and it -- we'll call it the "Jones study." Okay? Let's 17 say, the Jones study -- well, let's call it "Strom 2." 18 Okay? 19 Let's say a second Strom study came out 20 and it had this same Table 6. What number would have to 21 be in these benzene/solvent/gasoline categories for you 22 to feel that there was a positive correlation or a 23 statistically significant causal relationship between 24 benzene/solvent/gasoline exposure and RARS for you to 25 give the opinion that benzene exposure can be related to 80 1 RARS? 2 A. What you would want to see would be data that's 3 statistically significant and, therefore, relatable. 4 Q. Okay. 5 A. So, the odds ratio would be above 2, and the 6 confidence interval would be -- the lower limit of the 7 confidence interval would be greater than 1.0. 8 Q. So, let's say the Strom 2 study comes out 9 tomorrow and it has an OR above 2 and a CI with the 10 lower limit above 1.0 -11 A. Yes. 12 Q. That would be enough for you to say, "I, 13 Dr. Snodgrass, believe there is a positive correlation 14 between benzene exposure and RARS and that benzene 15 exposure is a possible causative factor of RARS"? 16 MR. SHOEBOTHAM: Objection, form. 17 A. Yes. 18 Q. (BY MR. PATTON) Okay. So, how would you 19 reconcile having the Strom 1 study which says no 20 correlation and the Strom 2 study which has a 21 correlation? Why do you pick Strom 2? 22 MR. SHOEBOTHAM: Objection, form. 23 A. Well, I might not have picked it, if it's weak 24 enough. If it's -- I would look at these various 25 characteristics, some of which are included in the 81 1 Cochrane kind of criteria: What are the numbers of 2 persons; what are the other characteristics of 3 information that are available for them; what are the 4 confounders; and probably try to look for additional 5 information -- perhaps in the second paper there might 6 be more additional information about the -- something 7 related to the dose exposure; and put all that together 8 and say, "Which is the better quality paper?" 9 Q. (BY MR. PATTON) What if it's the same, same 10 number of people, same information or lack of 11 information on dose, same confounders? 12 A. Right. Then -- and the conservative approach 13 would be to say there's a risk. 14 Q. So, then you -- then you could opine, yes, 15 there is a risk of an increased chance? 16 A. Yes. Biologically, that's not likely to 17 happen, but I understand your question. 18 MR. PATTON: I'll object to that last part 19 as nonresponsive. 20 Q. (BY MR. PATTON) Have you had any conversations 21 with any industrial hygienists as it relates to exposure 22 levels Charles Wilson would have experienced of benzene? 23 A. No. 24 Q. You didn't talk to John Spencer, correct? 25 A. That's correct. 82 1 Q. Did you talk to Buddy Whitlock? 2 A. No. 3 Q. Did you talk to Tom Keenan? 4 A. No. 5 Q. Did you talk to anyone at Ashland? 6 A. No. 7 Q. Did you talk to anyone besides Ashland 8 attorneys in forming your opinions in this case? 9 A. No. 10 Q. Did you talk to any of your colleagues about 11 this case? 12 A. No. 13 Q. Did you talk to any hematologists about this 14 case? 15 A. No. 16 Q. Did you talk to any oncologists about this 17 case? 18 A. No. 19 Q. Did you ask to be put in touch with someone 20 from Ashland to discuss this case and the chemicals at 21 issue? 22 A. No. I just asked for that information we 23 discussed earlier. 24 Q. Through Ashland's attorney? 25 A. Yes. 83 1 Q. The citations on Page 7 of your report. 2 A. Yes. 3 Q. Did Ashland provide any of those studies to 4 you? 5 A. No. 6 Q. Did Ashland provide you with any literature 7 that discusses what Ashland believes to be the 8 relationship between benzene exposure and bone marrow 9 diseases? 10 A. I don't recall any, no. 11 Q. They didn't give you any studies or any other 12 authority on the subject, true? 13 A. That's true. 14 Q. The studies you rely upon in forming your 15 opinions, those come from your own library and your own 16 experience, right? 17 A. Yes. 18 Q. Did you ask Ashland what additional studies or 19 what additional literature they might have that perhaps 20 would talk about these specific solvent blends and the 21 incidence of leukemia or the incidence of bone marrow 22 diseases in relation to the use of those solvent blends? 23 MR. SHOEBOTHAM: Objection, form. 24 A. I had the MSDS sheets. No, I did not ask 25 Ashland. 84 1 Q. (BY MR. PATTON) Have you ever been to a 2 printing facility? 3 A. Yes. 4 Q. Tell us about that. 5 A. It's been quite a few years ago. I visited a 6 printing facility for one of the large newspapers in 7 Washington, D.C. 8 Q. Have you ever been to any Ashland facility? 9 A. Not that I know of, no. 10 Q. Outside of the context of this case, which I 11 understand you said you didn't talk to anyone from 12 Ashland, have you ever otherwise spoken to anyone from 13 Ashland? 14 A. Not that I know of, no. 15 Q. In the course of your clinical work, have you 16 ever encountered a printer who was having some type of 17 ill effects from exposure to solvents? 18 A. That is possible. I don't recall a specific 19 case, but I get a lot of referrals from physicians. So, 20 it's possible, but I don't recall a case. 21 Q. What kind of -- can you tell us about the type 22 of referrals that come to mind that you were thinking of 23 there? 24 A. Well, there are numbers of times where 25 physicians, family practitioners or internists, are 85 1 seeing a person who is having some sort of symptoms or 2 health complaints and the patient may believe it's 3 related to some exposure at work or non-work; and 4 because it's involving a chemical and -- though, I'm not 5 trained in that area, they will refer the patient for me 6 to evaluate. 7 Q. Did anyone else help you in forming your 8 opinions or writing your opinions or writing your report 9 or performing your research, anything of that nature? 10 A. No. 11 Q. You did this all by yourself? 12 A. Yes. 13 Q. Do you have a typist or someone, or do you type 14 it yourself? 15 A. No, I type it. 16 Q. You have ten fingers that type as well as mine 17 do? 18 The other cases that you've testified in 19 as reflected on Exhibit 3, subject to the verbal 20 amendment that we've had here today, did you have more 21 than one piece of authority supporting your opinions in 22 those other cases? 23 A. Sometimes. 24 Q. I mean, is it a fair statement that you're 25 relying very heavily on the Strom study in supporting 86 1 your opinion that no causation of Charles Wilson's 2 MDS/RARS by benzene exposure? You're relying very 3 heavily on the Strom study, true? 4 A. Well, yes, it's true I -- I'm using that study 5 because that's the most relevant to his diagnosis. 6 Q. And when you worked as an expert in these other 7 litigation cases, did you rely in a similar fashion 8 heavily on a given -- on one single given study because 9 it was so specific to that person's diagnosis? 10 A. Most of those other chemicals or drugs involved 11 have a lot more published data that was relevant to the 12 question of the individual. Whereas, in this case, 13 we -- in 2007, I'm only aware of this one paper that's 14 this specific. 15 Q. This Strom study, it says here on the front 16 page cases where patients registered at M.D. Anderson 17 Cancer Center between 1999 and 2003 with no restrictions 18 on age, gender, or ethnicity, right? 19 A. Yes. 20 Q. Okay. So, this is a four-year window of 21 patients they took a look at, correct? 22 A. Yes. 23 Q. Did they go through and pull every RA patient 24 and every RARS patient and then do the questionnaire or 25 find the other information with each such RARS patient 87 1 during that four-year time period? 2 A. Yes. 3 Q. That's your understanding of the study? 4 A. Yes. 5 Q. Okay. You would agree with me, as a scientist, 6 that if M.D. Anderson were to use a different four-year 7 window for this study, let's say '95 to 1999, they would 8 probably have different results, wouldn't they? They 9 wouldn't have the exact numbers in Table 6, you wouldn't 10 be inclined to believe, would you? 11 A. They might not have those same numbers, but the 12 statistics would be likely the same. 13 Q. Why do you think the statistics would likely be 14 the same? 15 A. That's why you do statistics, because now, once 16 you've got this set of data, even if you don't take into 17 account the biology, the likelihood that another set 18 being not reproducible to this is very low, much less -19 much less than 5 percent. So, it's a 95 percent or 20 greater likelihood that the next set of patients will 21 give you similar odds ratios and confidence interval 22 information. 23 Q. Well, what if the sampling had -- instead of 38 24 RARS patients, what if it had 380 RARS patients? 25 A. Then you would get even tighter intervals 88 1 likely. So that the confidence interval might be -2 probably not quite up to the 2.3 and the 3.3 you see 3 there, but would probably be down in the low 2s, for 4 example, you know, at the upper limit of the confidence 5 interval. And so, that's -- that would be the effective 6 numbers. 7 Q. But if there were 380 RARS patients examined in 8 another study during a different four-year time period, 9 the other -- the new 300, so to speak, they could 10 possibly answer differently or inconsistent with the 11 data that led to this table, right? 12 MR. SHOEBOTHAM: Objection, form. 13 A. That turns out not to be correct, because if 14 you look at the statistical trend analysis here, the 15 .001 for the RAEV -- so, it's not even 95 -- it's more 16 than even 95 percent likely you'll get the same data. 17 It's probably 99-something percent likely you'll get the 18 same data and odds ratios, in that it is not 19 significantly associated. 20 So, as you add more numbers, this will 21 tighten up to even more significance that there is not 22 an association. 23 Q. So, you believe this sampling of 38 RARS 24 patients plus, combined with 67 RA patients, gives us a 25 pretty reliable baseline on what would be found in any 89 1 other study? 2 A. Yes, sir. For this type of statistics. I had 3 a minor in statistics when I did my Ph.D. And for this 4 type of statistics, when you've got an "N" of 30 or 5 greater, you're getting into the 95 percent confidence 6 for your data, often. 7 Q. Even though they only took a snapshot of a 8 little over 100 people? 9 A. That's right. And so, the likelihood of that 10 being repeated on different time windows is quite high. 11 Q. Have you reviewed Dr. Haas's deposition in this 12 case? 13 A. Yes. 14 Q. And what opinions or -- opinions and/or 15 criticisms do you have of what Dr. Haas had to say about 16 Mr. Wilson's disease? 17 MR. SHOEBOTHAM: Objection, form. 18 MR. PATTON: How can I fix that question? 19 MR. SHOEBOTHAM: It's really broad. I 20 don't know. The answer is: I don't know how to fix the 21 question, but I think it's overly broad. 22 MR. PATTON: You just think it's a bad 23 question? 24 MR. SHOEBOTHAM: I think it's overly broad 25 and -- 90 1 Q. (BY MR. PATTON) How about I ask a couple of 2 more specific questions and that might help us get 3 through. 4 Did you review Dr. Haas's deposition? 5 A. Yes, I did. 6 Q. When did you review it? 7 A. Yesterday. 8 Q. When did you receive it? 9 A. Day before that. 10 Q. Okay. And did anything stand out -- I mean, I 11 see you flipping through the pages. And first of all, 12 you didn't take any notes on his deposition -13 A. No. 14 Q. -- did you? 15 A. I did not. 16 Q. Did anything stand out? 17 MR. SHOEBOTHAM: Objection, form. 18 A. I agree with him about there's probably going 19 to be a reclassification in RARS as a distinct entity 20 and that type of thing. What I'm looking for -- there 21 was some part of this about the relationship to benzene, 22 as I recall. He thought it was related to benzene, and 23 I would disagree with that. 24 Q. (BY MR. PATTON) Because you disagree with 25 Wintrobe, who Haas -- Dr. Haas calls the "godfather of 91 1 hematology/oncology," correct? 2 MR. SHOEBOTHAM: Objection, form. 3 A. Yes. 4 Q. (BY MR. PATTON) You disagree with the 5 godfather of hematology and oncology? 6 MR. SHOEBOTHAM: Objection, form. 7 A. On that one sentence, the way it's stated, yes. 8 Q. (BY MR. PATTON) Because you think the 9 godfather of hematology and oncology should be given a 10 copy of the Strom study and revise his paragraph on 11 benzene as a causative factor for MDS, true? 12 MR. SHOEBOTHAM: Objection, form. 13 A. Well, let's just say Dr. Wintrobe is no longer 14 living, but he would be the first to look at new data 15 and evaluate it carefully. 16 Q. (BY MR. PATTON) And he would take a look at 17 this new data in the Strom study and the 105 people who 18 were examined with the combined category of RA/RARS and 19 he would say, "That's enough. Time to revise the 20 textbook"? Is that your position? 21 MR. SHOEBOTHAM: Objection, form. 22 A. It's the best data we have, yes. 23 Q. (BY MR. PATTON) It's a small amount of data, 24 isn't it? Isn't the Strom study a small amount of data, 25 because it speaks to benzene as a cause of MDS and 92 1 benzene as a cause of the various sub-types? 2 A. It's a well-designed study, so it provides a 3 lot of information. The numbers are not that small, 4 necessarily. You would like to see larger numbers, but 5 you also, in science, want to see reproducibility, and 6 that will come with the next study. 7 Q. Okay. Other criticisms or opinions of 8 Dr. Haas's testimony in this case? 9 A. Well, the one I'm recalling was the issue of 10 relating it, benzene, as a cause of RARS, and I 11 disagreed with that. That's all I recall. 12 Q. Okay. Do you believe Dr. Infante uses a sound 13 methodology in formulating his opinions in this case? 14 A. Not entirely, no. 15 Q. What are your complaints in that regard or 16 criticisms in that regard? 17 A. My criticisms are that he disregards other 18 information regarding the strengths of -- and related to 19 the quality of the information he's got and how you 20 interpret that information; and in interpreting or 21 incorporating, as an example, perhaps one or two cases 22 of lymphocytic leukemia as saying that that's now 23 relevant to benzene, when the majority of your 24 scientists disagree with doing that. 25 Q. Couldn't some similar criticisms be made of 93 1 your opinions and your methodologies, though, in sort of 2 boxing out much of the world of literature and focusing 3 so strongly and heavily on Strom? Someone could make a 4 similar criticism of you in that regard, couldn't they? 5 MR. SHOEBOTHAM: Objection, form. 6 A. No, because this is very focused on the 7 specific diagnosis and it's separating out a 8 dose-response relationship. 9 Q. (BY MR. PATTON) What's the dose in the Strom 10 study? 11 A. They classified it as Low or Medium or High. 12 Q. How many ppm-years is Low, Medium, or High? 13 A. They don't have that information listed there. 14 Q. So, they don't really classify out the dose, do 15 they? 16 A. It's not given a number, that's correct. 17 Q. Do you consider yourself a public health 18 professional? 19 A. In a broad sense, yes. 20 Q. Do you agree that workers who have been exposed 21 to benzene have a right to know about the hazards 22 associated with that exposure? 23 A. I'm not an expert on right-to-know laws, but as 24 a general rule, yes. 25 Q. And as a general rule, you would also agree 94 1 with me that a responsible chemical company should know 2 how much benzene is in the products it sells, true? 3 MR. SHOEBOTHAM: Objection, form. 4 A. I'm not an expert in all that. Again, I think 5 Mr. Spencer or others can answer that question better 6 than I. 7 Q. (BY MR. PATTON) If someone were to come in 8 your poison control center and, say, they had a bottle, 9 okay, and the bottle came from "Company Z," and it was a 10 beverage, okay, and they told you they were feeling sick 11 and they showed symptoms of -- whatever disease, but 12 acute, serious symptoms that required emergency medical 13 attention, okay, would you want to know what chemicals 14 or what ingredients were in the bottle that that person 15 drank from Company Z? 16 A. We might, yes. 17 Q. Would you believe that you could go to 18 Company Z and say, "Hey, I have a person here in our 19 clinic who is sick; and he drank your product, and we 20 think it might be related. Tell us what's in your 21 product that he drank" -- you would expect a responsible 22 product manufacturer to be able to give you that type of 23 information, wouldn't you? 24 A. This was something made for drinking? 25 Q. Sure. 95 1 A. They would have some idea of what was in their 2 product, yes. 3 Q. What if someone came into your clinic and they 4 were exposed acutely to some type of solvent and they 5 were having severe ill effects that required emergency 6 medical treatment, would you want to know what was in 7 the solvent they were working with? 8 A. For acute care, it often doesn't really matter 9 if general solvents, but it would be useful information 10 to have. 11 Q. Okay. And who would you -- where would you go 12 to get that useful information? Where would be the 13 first person you would go to? 14 A. If the source of the exact material were 15 available and the manufacturer were known and one could 16 contact the manufacturer, yes. 17 Q. That would be the first place you'd go, ask the 18 manufacturer, because it's his product, right? 19 A. Unless it's a generally-recognized product, it 20 might have other information that's published, 21 generally, yes. 22 Q. But in any event, one of the first places you 23 would look would be the manufacturer of that product, 24 because you would believe that a reasonable, prudent, 25 and safe manufacturer of chemicals would know what's in 96 1 that product, true? 2 MR. SHOEBOTHAM: Objection, form. 3 A. Depending on the percentages and all that, 4 within range, yes. 5 Q. (BY MR. PATTON) You know there's benzene in 6 stoddard solvent, right? 7 MR. SHOEBOTHAM: Objection, form. 8 Q. (BY MR. PATTON) You know that as a scientist, 9 don't you? 10 MR. SHOEBOTHAM: Objection, form. 11 A. In the older formulations, yes. 12 Q. (BY MR. PATTON) Do you know that there's 13 benzene in xylene, as a scientist? 14 MR. SHOEBOTHAM: Objection, form. 15 A. Well, again, Mr. Spencer can tell you more 16 about that. That's very much dependent on the -- just 17 to say there's some there, well, you know, is it a very, 18 very small amount, or a very large amount, it's going to 19 depend on the processes and how it's made. 20 Q. (BY MR. PATTON) So, like, for stoddard 21 solvent, the benzene content would depend on -- the 22 benzene content of a given sample of stoddard solvent 23 would depend on a variety of factors: Where it's made, 24 how it's treated, how it's blended, its reaction with 25 other chemicals, those sort of things, right? 97 1 MR. SHOEBOTHAM: Objection, form. 2 A. Right. And you'd have to know those things in 3 the time frame of the manufacturer. 4 Q. (BY MR. PATTON) Are you kind of skeptical of 5 Buddy Whitlock's testimony that there's less than 10 ppm 6 benzene in some of the chemicals at issue in this case? 7 A. No. 8 Q. But you acknowledge that that benzene range 9 would differ, depending on refining methods, location, 10 years, things of that nature, right? 11 MR. SHOEBOTHAM: Objection, form. 12 A. Correct. 13 MR. PATTON: Let's take another short 14 break. 15 (Short break.) 16 Q. (BY MR. PATTON) Dr. Snodgrass, we've -- I've 17 marked all the documents that I want to use as 18 exhibits -- attached as exhibits to your deposition; and 19 I want to go through those with you, quickly, for the 20 court reporter's sake. 21 Exhibit 1, that is your report in this 22 case, dated July 5, 2007, correct? 23 A. Yes. 24 Q. Exhibit 2, this was the list you and I were 25 making of high-quality data. 98 1 And I had a follow-up question on that: 2 Are there any publications that -- within which 3 Plaintiff's experts cite papers as authority which you 4 feel to be unreliable publications? For instance, 5 there's citations to the American Journal of Industrial 6 Hygiene or Journal of Environmental Medicine or Leukemia 7 or Blood or other journals like that. 8 Did you make any type of review of Dr. -9 of the references cited by Dr. Parent or Dr. Infante and 10 their accompanying journals and say to yourself, "You 11 know what, that journal is just unreliable," or "They'll 12 publish anything," or "They publish low-quality data," 13 things like that? 14 A. I don't recall seeing any journals of that 15 type. 16 Q. Would you agree with me that the journals that 17 contain the articles that Dr. Infante relies on and 18 Dr. Parent relies on, they generally are respected, 19 peer-reviewed scientific journals or other authority, 20 the authority speaks for itself, that if they're 21 publishing a report, that report is at least of some 22 high enough quality, that it is relevant to the 23 pertinent scientific community? Would you agree with 24 that? 25 MR. SHOEBOTHAM: Objection, form. 99 1 A. Not as worded. The peer-reviewed literature is 2 as good as the peer reviewer so that you have a range on 3 that. So, I think it's -- I haven't sat down to do just 4 that, what you've mentioned, which is to go through 5 their references and look at the journals as -- because 6 I probably would come up with, say, there's some 7 journals here that are recognized, generally, not to 8 have as generally high a quality papers just by common 9 knowledge among scientists, but it doesn't mean that 10 it's not peer reviewed. 11 Q. Some of the journals are like Ivy-League 12 caliber journals, whereas, some might be lesser 13 journals; is that a fair statements? 14 A. It's much more -- yes, it's much more difficult 15 to get a paper accepted for publication in the journal 16 called Science than it would be for, maybe, the 17 International Archives of Occupational Medicine, for 18 example. 19 Q. So, when you conclude that much of the data 20 that Plaintiff's experts rely on is not high-quality 21 data, you're not necessarily faulting the journal, 22 correct? 23 A. Correct. It has nothing to do with the 24 journal. It has to do with the paper itself and the 25 data. 100 1 Q. Exhibit 3 -- well, first of all, is there 2 anything else we should include on our list of what 3 high-quality data means to you besides the Cochrane 4 levels and their characteristics of quality data? 5 A. There are other categorization schemes, as well 6 as the Cochrane, that list quality; but -- levels of 7 evidence. There are those types of listings. But the 8 Cochrane is one, as well. Cochrane and Oxford is one, 9 as well, that's known. 10 Q. When you use the term "high-quality data," as 11 you did a couple of times in your report, is that a 12 phrase that you commonly use when opining in similar 13 cases? 14 A. I don't know how common it is, but I perhaps 15 have used it, yes. 16 Q. I mean, when you look at any given 17 case-controlled study or other piece of scientific 18 authority for the relevant field of benzene and blood or 19 bone marrow disorders, it's real easy to go through and 20 talk about the strengths and the weaknesses of each 21 study. Isn't it pretty easy to just go through and make 22 a blanket statement like, "The plaintiff's experts don't 23 rely on high-quality, relevant data"? 24 MR. SHOEBOTHAM: Objection, form. 25 Q. (BY MR. PATTON) Isn't that a pretty easy 101 1 criticism to throw out there? 2 MR. SHOEBOTHAM: Objection, form. 3 A. It's a short, few words. I think, for me, it 4 means that -- what is the strength of that data; what's 5 the consistency of that data; what's the data source; 6 what -- how does that relate to how we understand the 7 biology and the dose issues; and, you know, how good is 8 that study. 9 Q. (BY MR. PATTON) But you did not look at or 10 review each and every study cited by Dr. Parent and 11 Dr. Infante and review the individual strengths and 12 weaknesses and quality, so to speak, according to 13 Cochrane and/or others, and reach a conclusion each one 14 of those was low quality, therefore, Plaintiff's experts 15 failed to rely on high-quality data; is that a fair 16 statement? 17 A. No. What I did was I realized that there was 18 very few data on RARS regarding benzene and limited 19 data, very limited data, on the whole grouping of 20 various diseases called "MDS" and benzene compared to 21 the enormous amount of data on benzene and AML; and 22 therefore, when I used the information that 23 Dr. Shatner's paper did, which was to go through -- and 24 that paper went through over 400 articles -- and they -25 and I spell that out in my report, is that they listed 102 1 their criteria for what would be essentially 2 high-quality information regarding AML. 3 And you can apply similar kinds of 4 specifics, as listed in my report, where either the MDS 5 type of category or RARS and benzene, and that's what I 6 attempted to do. 7 Q. Okay. And the only RARS/benzene study is 8 Strom? 9 A. That's selective and specific for the RARS, 10 itself, yes. 11 Q. Exhibit 3 is a true and correct copy of your 12 list of testimony, subject to the verbal modifications 13 today, right? 14 A. Yes. 15 (Snodgrass Exhibit No. 4 through 16 11 marked.) 17 Q. (BY MR. PATTON) Exhibit 4 is your Deposition 18 Notice, and I included a subpoena duces tecum asking you 19 to bring everything essentially bearing on your opinions 20 and what you relied on and reviewed in this case. Have 21 you done that? 22 A. Yes. 23 Q. You don't have any handwritten notes? 24 A. No. 25 Q. No summaries of any information? 103 1 A. No. 2 Q. Is there any other literature that you will 3 rely on in expressing your opinions to a jury in this 4 case, other than what you've brought with you today to 5 your deposition or what you've cited in your report? 6 A. Not that I think of, unless a different type of 7 question triggers a different type of memory and some 8 other issue comes up, no. 9 Q. Doctor, I'm generally familiar with the 10 18 citations on Page 7 of your report -- come to think 11 of it, I might not be positive as to which any of these 12 are. If I were to convey a question to your attorney as 13 to, you know, "What is the Rathman study," because that 14 just doesn't ring a bell for me, today, right now, as we 15 sit here, would you be happy and willing to provide that 16 information so that it could be conveyed to me with a 17 citation? 18 A. Yes. 19 Q. Okay. Exhibit 5 is your curriculum vitae, 20 correct? 21 A. Yes. 22 Q. And this was in July 2007, but it's still 23 current as we sit here today? 24 A. Yes. 25 Q. Have you published anything on benzene? 104 1 A. No. 2 Q. Have you ever made any presentations specific 3 to benzene? 4 A. I don't recall any at this time. 5 Q. Have you authored any journal articles on 6 benzene? 7 A. No. 8 Q. And you are a reviewer for journals, correct? 9 A. Yes. 10 Q. Have you reviewed, in the course of your peer 11 review duties, any articles relating to benzene? 12 A. Not in terms of peer review. The prior 13 question about any articles, I don't recall if we've 14 published the data. It was -- I was specifically 15 involved in animal work in the 1970s at the National 16 Institutes of Health. 17 One of the chemicals we studied, we did a 18 fair bit of work on, was benzene and bone marrow in an 19 animal model and looking at some of the bio-chemical 20 effects. And I just don't recall if we ever got that 21 published. So, I -- but that's not -- it would not -22 so, the answer to your question would be: There were no 23 publications, I can recall. 24 Q. Who funded the study that you just talked 25 about? 105 1 A. The U.S. Government. 2 Q. Has the chemical industry or any chemical 3 company ever funded any of your work besides expert work 4 in litigation? 5 A. I had one drug study for a medication funded 6 partially by a drug company years ago. 7 Q. For instance, the Chemical Manufacturers 8 Association or Ashland or Dow or any company like that, 9 or organization of that nature has never funded any of 10 your work besides litigation, correct? 11 A. Correct. 12 Q. What percentage of your income is derived from 13 testifying as an expert in litigation? 14 A. 10 percent, 15 percent. 15 Q. What percent of your professional time is spent 16 working on litigation matters such as this one? 17 A. I'd say around 10 to 15 percent. 18 Q. I marked as Exhibit 6, "Harrison's Principles 19 of Internal Medicine, 16th Edition." I found this in 20 your box. What is this document and its relevance in 21 relation to your opinions in this case? 22 A. This is a couple of pages from a textbook of 23 general internal medicine. In those pages, they discuss 24 myelodysplasia, and it lists the various categories 25 under the WHO -- World Heath Organization's 106 1 classification of myelodysplastic syndromes. And it 2 simply list those, and including in that list would be 3 RARS. 4 Q. Okay. Do you believe Harrison's Principles of 5 Internal Medicine to be a reliable piece of authority in 6 matters of medicine? 7 A. It has good information, generally. 8 Q. And just so that all of us lawyers have 9 16 copies of the Strom study, I went ahead and marked 10 that as Exhibit 7 to your deposition, too. Okay? 11 A. Yes. 12 Q. And Exhibit 8 -- well, I also marked it, 13 because we talked about it so much. 14 A. Yes. 15 Q. I marked as Exhibit 8 to your deposition, 16 Evolving Classifications of the Myelodysplastic 17 Syndromes. This is an article offered by Komrokji -18 K-o-m-r-o-k-j-i -- and this appears to be from the 19 Current Opinion in Hematology Journal, 2007; is that 20 right? 21 A. Yes. 22 Q. How did you come across this article? 23 A. I -- like I did for the rest of it. I searched 24 for articles relevant to this diagnosis. 25 Q. What is the value of this article in your 107 1 opinions in this case? 2 A. It -- the value is simply that it's -- it says, 3 as we know now, that these are becoming -- as we get 4 more information, that diagnoses like RARS are a 5 distinct category, distinct diseases. 6 Q. Is it possible and even perhaps probable that 7 the myelodysplastic syndromes could be reclassified in a 8 different way in the next, say, five years such that the 9 Strom study would be difficult to interpret or view as 10 instructive on issues of benzene causation specific to 11 the different MDSs or MDS sub-types? 12 A. No. What -- in the next five years -- it would 13 just be my, of course, estimation of what might 14 change -- but you may get some bio-markers that may 15 correlate with the diagnosis, and then you could begin 16 to apply some of those as blood tests. 17 Q. So, you could further stratify, as you would 18 say? 19 A. Yes. Or support the stratification with a 20 bio-marker, for example. 21 Q. What is the -- well, first of all, I'll 22 identify, for the record, Exhibit 9 is the Institute of 23 Medicine article entitled Gulf War and Health, dated 24 2003; and this is from Volume 2, Insecticides and 25 Solvents, correct? 108 1 A. Yes. 2 Q. What is the value of this article on your 3 opinions in this case? 4 A. The value is simply that a literature search 5 was done and a review was done by an independent 6 committee of scientists regarding benzene and its 7 causation, including myelodysplastic syndromes. And 8 they looked at many of the same studies that Dr. Infante 9 and others looked at, and that one of their conclusions 10 is, as stated here: "The committee concludes from its 11 assessment of the epidemiologic literature, that there 12 is inadequate/insufficient evidence to determine whether 13 an association exists between chronic exposure to 14 benzene and myelodysplastic syndromes." 15 Q. And that's on Page 330 of Exhibit 9? 16 A. Yes. 17 Q. What is the importance of Exhibit 10 in your 18 opinions? 19 A. This was simply -- I went to the American 20 Cancer Society website to see what they would say, and 21 one of their comments about MDS is they -- similar to 22 the past edition of Wintrobe's textbook, they have a 23 statement about: Long-term workplace exposure to 24 benzene and certain chemicals used in the petroleum and 25 rubber industries can increase your risk of developing 109 1 MDS. 2 So, it's a general -- they used just a 3 general wording of "MDS." 4 Q. And you don't like that general wording of 5 "MDS"? 6 A. I think if it were more accurate, it would -7 it would separate out the different diseases. 8 Q. Exhibit 11, what is the value of this in your 9 opinions? 10 A. This is the Surgeon General -- part of a 11 Surgeon General's report from three years ago, and 12 it's -- it really relates mostly to AML leukemia, not to 13 RARS or any of the other myelodysplastic-type listings. 14 Q. Is this the article that attributes the benzene 15 from cigarette smoke to increased leukemia, or am I 16 thinking of a different Surgeon General article? 17 A. I think that may have occurred earlier, but 18 this one does go into that data, yes, it does. 19 Q. I want to talk about this other stack of 20 materials, and I'm not going to mark this as exhibits; 21 but you had in your file an Ashland document called 22 Health Hazard Determination Guidelines? 23 A. Yes. 24 Q. And this appeared to be Bates 25 No. Ashland-Wilson 3530-3594. Did you review this 110 1 document? 2 A. Yes. 3 Q. And how did that bear on your opinions or what 4 opinions, if any, do you have on that? 5 A. This is just general information about 6 chemicals, and some of it's just general chemical 7 information about toxicology and how you do rating 8 systems, for example. It's just sort of general 9 toxicology background; so, there's a lot of different 10 kind of information in here, but it's not necessarily 11 only selective for benzene. 12 Q. It talks about the hazard determination that 13 they use for all their solvents, correct? 14 A. Yes. 15 Q. Did you see a lot of documents from Ashland 16 evidencing compliance with those guidelines? 17 A. Probably Mr. Spencer is in a better position to 18 answer that. I saw MDS sheets -- MSDS sheets. 19 Q. Okay. Did you review the -20 A. Yes. 21 Q. -- report letter by Dr. Kopstein? 22 A. Yes. 23 Q. What opinions, if any, do you have on that? 24 A. I -- I simply disagree with his -- his overall 25 conclusion. He's relating his support of the estimates 111 1 from Dr. Nicas. 2 Q. Doesn't he also point out some of the 3 shortcomings or inconsistencies of Ashland's position, 4 per the testimony of Whitlock, as it comports with the 5 peer-reviewed literature on benzene content for these 6 products? 7 A. I'm going to leave that up to Mr. Spencer or 8 Dr. Whitlock to really address those issues. 9 Q. Okay. The Toxicological Review of Benzene, 10 this is just something from your general benzene 11 library? 12 A. Yes, it is. 13 Q. And this is from September 1998, CAS 14 No. 71-43-2? 15 A. Yes. 16 Q. What bearing does this have on your opinions, 17 other than -- well, what bearing does it have? 18 A. It provides a lot of the background information 19 on benzene. 20 Q. And the next one you have, can you read that 21 for us? 22 A. The carcinogenic Effects of Benzene and Update. 23 This is April of 1998. This is from the EPA. 24 Q. And then what's the next one? 25 A. This is the -- this next one is the 112 1 Toxicological Profile for Benzene, 1997. This is by the 2 ATSDR, which is part of the Centers for Disease Control. 3 Q. And those are documents that you rely on, 4 generally, in your opinions as they relate to benzene? 5 A. They contain a lot of useful toxicology 6 information about benzene that's independently written, 7 yes. 8 Q. Okay. Do you have any other opinions in this 9 case or do you intend to testify at trial about anything 10 else besides what we've talked about today? 11 A. Not that I can anticipate at this time. 12 Q. Thank you for your time. 13 MR. PATTON: That's all I have for now. 14 MR. SHOEBOTHAM: I have a few questions 15 about Exhibit 5, which we'll define as the "CV." 16 First of all, before I ask the questions, 17 can we just agree that there's a box of documents that 18 he brought with him that haven't been marked as 19 exhibits? 20 MR. PATTON: Right. Yes. 21 MR. SHOEBOTHAM: All right. 22 E X A M I N A T I O N 23 BY MR. SHOEBOTHAM: 24 Q. Okay. All right. Dr. Snodgrass, I just want 25 to ask you some questions about Exhibit 5. What is 113 1 that? 2 A. That's my curriculum vitae. 3 Q. And what is a curriculum vitae? 4 A. It's like a resume. It just lists your past 5 employment and, in my case, publications and teaching 6 and research and patient care activities. 7 Q. Is that a true and correct copy of your current 8 curriculum vitae? 9 A. Yes. 10 Q. And does this truly and accurately summarize 11 your professional background and experience? 12 A. Yes. 13 Q. I'd like to ask you, if you would, could you 14 tell the jury about your educational background? 15 A. I have a bachelor of science degree in 16 chemistry from Butler University in Indianapolis, 1968; 17 I have a masters in pharmacology from Indiana 18 University, 1971; received my M.D. from a medical school 19 in Indiana in 1972; and I have a Ph.D. in 20 pharmacology/toxicology in 1976. 21 Q. Okay. Are you a medical doctor? 22 A. Yes. 23 Q. And where are you licensed? 24 A. In the State of Texas and the State of Indiana. 25 Q. And is your medical license current and on file 114 1 with the appropriate authorities? 2 A. Yes. 3 Q. In addition to being a medical doctor, do you 4 have qualifications in the area of pharmacology? 5 A. Yes. 6 Q. What is pharmacology? 7 A. Pharmacology is the study of substances or 8 drugs or medications that have a beneficial effect for 9 treating diseases or illnesses. 10 Q. Would you describe for the jury your 11 qualifications in the area of pharmacology? 12 A. I have a Ph.D. and a master's degree in 13 pharmacology, and I'm also board certified by the 14 sub-board called the American Board of Clinical 15 Pharmacology. 16 Q. Do you have qualifications in the area of 17 toxicology? 18 A. Yes. 19 Q. What is the science of toxicology? 20 A. Toxicology is the area that deals with the 21 adverse or toxic effects of chemicals or drugs. 22 Q. And would you describe for the jury your 23 qualifications and experience in the area of toxicology? 24 A. I have a Ph.D. that's in 25 toxicology/pharmacology, and I also have -- am board 115 1 certified by the American Board of Medical Toxicology, 2 and I'm the past president of the American Academy of 3 Clinical Toxicology. 4 I'm currently the medical director for one 5 of the 60 certified regional poison control centers in 6 the United States. 7 Q. Right. Now, tell the jury, if you would, about 8 that activity. What is your current position with 9 regard to the Houston/Galveston poison control center? 10 A. I'm the medical director for the Texas Poison 11 Center that serves Houston and Galveston and surrounding 12 5 million population. 13 Q. And what are your duties in connection with 14 that position? 15 A. That's a 24-hour-a-day, seven-day-a-week 16 service. I have 12 nurses and pharmacists who rotate 17 shifts to answer the telephone from the public, as well 18 as from physicians and nurses and hospitals, regarding 19 either acute, or even chronic, exposures or concerns 20 about exposures to substances. And so, I provide that 21 information. When the -- it's beyond the level of a 22 nurse or pharmacist to talk with either a person calling 23 there or a physician, I will help provide information or 24 management for helping to manage patients who are ill 25 due to these substances. 116 1 Q. And are these patients people who are calling 2 into the Poison Control because of concerns about some 3 possible exposure to a drug or a chemical? 4 A. Yes. 5 Q. And so, that's something that you deal with on 6 a daily basis in your position as the medical director 7 of the Houston/Galveston poison control center? 8 A. Yes. 9 Q. Do you hold any medical board certifications? 10 A. Yes. 11 Q. What are those? 12 A. I am -- my subspecialty -- the two 13 sub-specialties were the American Board of Medical 14 Toxicology and the American Board of Clinical 15 Pharmacology, and then my primary board specialty is the 16 American Board of Pediatrics. 17 Q. Do you have any position with the University of 18 Texas? 19 A. Yes. 20 Q. What is your position with the University of 21 Texas? 22 A. I'm a professor of pharmacology-toxicology, 23 professor of pediatrics, and a professor of obstetrics 24 and gynecology at the medical school. 25 Q. And where is that medical school located? 117 1 A. In Galveston. 2 Q. And do you have any teaching responsibilities 3 at the University of Texas? 4 A. Yes. 5 Q. Would you describe those for the jury? 6 A. My teaching includes teaching resident 7 physicians who are in training; teaching medical 8 students; providing seminars or teaching to CME, 9 continuing medical education, meetings for physicians in 10 practice; teaching graduate students, who are in 11 training for their Ph.D. in pharmacology and toxicology. 12 Q. Do you have any positions as a reviewer for any 13 medical journals? 14 A. Yes. 15 Q. Would you describe for the jury some of the 16 medical journals that you are a reviewer for? 17 A. I've been a reviewer for the New England 18 Journal of Medicine; the Journal of Toxicology, Clinical 19 Toxicology; the Drug Metabolism Disposition Journal; 20 Journal of Pediatrics; Toxicology & Applied Pharmacology 21 Journal; Developmental Pharmacology Therapeutics. The 22 Poisondex Information System, I've been a reviewing 23 editor. 24 I've been an invited reviewer for the 25 United States Environmental Protection Agency for 118 1 particular issues, such as "Pesticides", in the past. 2 Those are an example of some of the reviewer's 3 activities. 4 Q. Do you currently hold any positions in which 5 you have been requested by the United States Government, 6 to serve on committees or be available to serve on 7 committees, if necessary? 8 A. Yes. I'm an immediate past voting member for 9 the Nonprescription Drug Advisory Committee to the FDA, 10 and an immediate past temporary voting member for the 11 Anesthetics & Life Support Drugs Committee for the 12 Advisory Committee to the FDA. 13 I'm a current member of the Advisory 14 Committee for Lead Poisoning and Prevention in Childhood 15 for the Centers For Disease Control. 16 Q. Dr. Snodgrass, have you formed an opinion 17 within reasonable medical probability as to whether the 18 chemical, benzene, can cause the illness, refractory 19 anemia with ringed sideroblasts, the disease that 20 Mr. Wilson has? 21 A. Yes. 22 Q. What is that opinion? 23 A. Benzene is not a cause of RARS. 24 Q. And what is the basis for that opinion? 25 A. The basis for that opinion is -- includes the 119 1 Institute of Medicine Review, it also includes data 2 published by Strom and others, showing no relationship. 3 MR. SHOEBOTHAM: I'll pass the witness. 4 RE-EXAMINATION 5 BY MR. PATTON: 6 Q. If we didn't have the Strom 2005 study with us 7 today, you would not be able to give the opinion that 8 you just gave, that you just -- what you just said to 9 Mr. Shoebotham, correct? 10 A. There would not be that specificity of RARS 11 versus just a general listing of all the types of 12 substances -- disorders that are MDS, yes. 13 Q. In the course of your years of professional 14 work in the field of toxicology, have you encountered 15 Plaintiff's expert, Dr. Parent, before? 16 A. I've heard the name, but I don't know him. 17 Q. Have you ever spoken to him? 18 A. No. 19 Q. Do you have any criticism -- did you review 20 Dr. Parent's curriculum vitae that was attached to the 21 Plaintiff's expert disclosures? 22 A. Yes. 23 Q. Do you have any criticisms of Dr. Parent's 24 qualifications to serve as an expert in this case to the 25 same subjects that you're serving as an expert on? 120 1 MR. SHOEBOTHAM: Objection, form. 2 A. No. 3 Q. (BY MR. PATTON) Okay. 4 MR. PATTON: Mr. Shoebotham, can we have 5 the agreement that I'll take the exhibits and make 6 copies of them and send them back to you, and then you 7 can make copies and return to your expert? 8 MR. SHOEBOTHAM: I agree. 9 MR. PATTON: Okay. 10 MR. SHOEBOTHAM: If that's all right with 11 you, Dr. Snodgrass. 12 THE WITNESS: That's fine, yes. 13 MR. PATTON: That's all I have. 14 MR. SHOEBOTHAM: That's all I have. 15 (At the hour of 1:07 p.m., the 16 deposition was concluded.) 17 * * *SIGNATURE REQUIRED* * * 18 19 20 21 22 23 24 25 121 1 CHANGES AND SIGNATURE 2 WAYNE R. SNODGRASS 9-14-07 3 PAGE LINE CHANGE REASON 4 ________________________________________________________ 5 ________________________________________________________ 6 ________________________________________________________ 7 ________________________________________________________ 8 ________________________________________________________ 9 ________________________________________________________ 10 ________________________________________________________ 11 ________________________________________________________ 12 ________________________________________________________ 13 ________________________________________________________ 14 ________________________________________________________ 15 ________________________________________________________ 16 ________________________________________________________ 17 ________________________________________________________ 18 ________________________________________________________ 19 ________________________________________________________ 20 ________________________________________________________ 21 ________________________________________________________ 22 ________________________________________________________ 23 ________________________________________________________ 24 ________________________________________________________ 25 ________________________________________________________ 122 1 ________________________________________________________ 2 JURAT 3 I, WAYNE R. SNODGRASS, have read the 4 foregoing deposition and hereby affix my signature that 5 same is true and correct, except as noted above. 6 ______________________ 7 8 THE STATE OF TEXAS ) COUNTY OF HARRIS ) WAYNE R. SNODGRASS 9 10 Before me,__________________, on this 11 day personally appeared WAYNE R. SNODGRASS, known to me 12 (or proved to me under oath or through ________________) 13 (description, identity card or other document) to be the 14 person whose name is subscribed to the foregoing 15 instrument and acknowledged to me that they executed the 16 same for the purposes and consideration therein 17 expressed. 18 19 Given under my hand and seal of office 20 this _____day of_________, _________ 21 ___________________________ 22 NOTARY PUBLIC IN AND FOR 23 THE STATE OF________________ 24 25 123 1 IN THE UNITED STATES DISTRICT COURT FOR THE EASTERN DISTRICT OF TEXAS 2 MARSHALL DIVISION 3 CHARLES WILSON and ) LAURA WILSON, ) 4) Plaintiffs ) 5) vs. ) CIVIL ACTION NO.2:06-CV-286 6) RYCOLINE PRODUCTS, ) 7) Defendants ) 8 9 10 REPORTER'S CERTIFICATION DEPOSITION OF WAYNE R. SNODGRASS 11 September 14, 2007 12 13 I, Brenda L. Kaplan, Certified 14 Shorthand Reporter in and for the State of Texas, hereby 15 certify that the facts stated by me in the caption 16 hereto are true; that the foregoing deposition 17 transcript of WAYNE R. SNODGRASS, the witness 18 hereinbefore named, was at the time mentioned taken by 19 me in stenograph, the said witness having been by me 20 first duly cautioned and sworn upon his oath to tell the 21 truth, and later transcribed from stenograph under my 22 supervision. 23 I further certify that I am neither 24 attorney or counsel for, nor related to or employed by 25 any of the parties to the action in which this 124 1 deposition is taken, and further that I am not a 2 relative or employee of any attorney or counsel employed 3 by the parties hereto, or financially interested in the 4 action. 5 I further certify that the above and 6 foregoing deposition transcript as set forth in 7 typewriting is a full, true and correct transcript of 8 the proceedings had at the time of taking said 9 deposition. 10 WITNESS MY HAND, this the ________ day 11 of _______________, ___________. 12 13 ________________________________ BRENDA L. KAPLAN, Texas CSR 6977 14 Expiration Date: 12/31/08 U.S. Legal Support/Miller Parker 15 Registration No. 343 5910 North Central Expressway, Suite 100 16 Dallas, Texas 75206 17 18 19 20 21 22 23 24 25 125