1
1
1 REPORTERS RECORD
2 VOLUME 6 OF 11 VOLUMES
3 TRIAL COURT CASE NO. 2004-03963
4
5 IN RE: ASBESTOS : IN THE DISTRICT COURT OF
6 : HARRIS COUNTY, T E X A S
7 : 11TH JUDICIAL DISTRICT
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14 MDL HAVNER HEARINGS
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19 On the 9th day of June, 2005, the
20 following proceedings came on to be heard in the
21 above-entitled and numbered cause before the
22 Honorable Mark Davidson, Judge presiding, held in
23 Houston, Harris County, Texas.
24 Proceedings reported by Machine
25 Shorthand.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
2
1 A P P E A R A N C E S
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3 Attorneys for the Plaintiffs:
4 MR. PETER KRAUS
MR. JEFFREY SIMON
5 Waters & Kraus
3219 McKinney
6 Dallas, Texas 75204
7
MR. JOHN SPILLANE
8 Baron & Budd, PC
3102 Oak Lawn Avenue, #1100
9 Dallas, Texas 75219
10
MR. AARON DeLUCA
11 The Lanier Law Firm, PC
6810 FM 1960 West
12 Houston, Texas 77069
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MR. RICHARD NEMEROFF
14 Nemeroff Law Firm
4514 Cole Avenue, #806
15 Dallas, Texas 75205
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17 Attorneys for the Defendant, Georgia Pacific:
18 MR. BRUCE J. BERGER
MR. FRANK LEONE
19 Spriggs & Hollingworth
1350 I Street, Nw
20 Washington, DC 20005
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Attorneys for the Defendant, Garlock:
22
MR. RAY HARRIS
23 MR. CARY SCHACHTER
Schachter Harris, PC
24 600 N. Pearl Street, #2300
Dallas, Texas 75201
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TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 MR. MITCHELL CHANEY
Rodriguez, Colvin, Chaney & Saenz, LLP
2 1201 East Van Buren St.
Brownsville, Texas 78522
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4 MR. JOHN A. LaBOON
Segal McCambridge
5 100 Congree Ave., #700
Austin, Texas 78701
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7 For the Defendant, Owens Illinois:
8 MR. PETER MOIR
Quilling, Selander, Cummiskey & Lownds
9 2001 Bryan Street, #1800
Dallas, Texas 75201
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TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 I N D E X
2 WITNESSES
3 For Plaintiff: Page
4 Dr. Ronald Dodson
Direct Examination by Mr. Simon 8:11
5 Cross-Examination by Mr. Leone 113:12
Cross-Examination by Mr. Schachter 155:5
6 Redirect Examination by Mr. Simon 179:24
Recross-Examination by Mr. Leone 194:14
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8
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10 EXHIBITS
11 For Defendants:
12 48
Received 146:11
13
14
15 For Plaintiff:
16 39
Received 30:7
17
40
18 Received 37:14
19 41
Received 70:15
20
43
21 Received 76:24
Received 90:13
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25
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
5
1 P R O C E E D I N G S
2 June 9, 2005 Havner Hearings
3 THE COURT: Good morning, everybody.
4 Please be seated. Mr. Simon, you look to be in
5 the pole position.
6 MR. HARTLEY: Your Honor, I have one
7 matter to bring up we havent been able to resolve
8 completely.
9 At the deposition of Dr. Case last
10 weekend on Saturday, I asked some questions about
11 — and this is the excerpt from the transcript –
12 I asked some questions of Dr. Case about what he
13 was relying on for his opinions about tremolite
14 content in various chrysotile deposits. He said
15 he was relying on a thesis that he had, and I
16 asked for it and they said they would produce it.
17 We have been given part of the thesis by Mr.
18 Schachter. Mr. Schachter represented to me today
19 after many attempts he is trying to get the rest
20 of it.
21 I am very concerned because I have my
22 last witness coming in tomorrow that we are being
23 prejudiced by this. I ask, A, that Dr. Case
24 produce his full, complete copy of this; and
25 secondly, we would reserve our right to offer
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 rebuttal testimony if this thesis bares out what I
2 think it does.
3 THE COURT: Mr. Schachter said he
4 would get it. I have every confidence that he
5 will succeed.
6 MR. SCHACHTER: I have gotten him what
7 we promised him (inaudible). Dr. Case said — we
8 have an electronic copy I think we have printed
9 out. I have given him the electronic copy. It
10 turns out these are big files. Pages 1 through 40
11 arent in that copy. I am going to do everything
12 I can today to find it and find out if Case really
13 does have those cases, and obviously we will get
14 it to them.
15 THE COURT: You are entitled to
16 everything Case has. I cant make him fly off to
17 Paris to get it. But if you need somebody to fly
18 off this weekend, sign me up. Just pay my
19 airfare.
20 MR. HARTLEY: The thing I am concerned
21 about here is that we are putting on our last
22 witness tomorrow. This is something I asked for
23 more than a week ago. I got part of it recently.
24 THE COURT: You are entitled to what
25 is in Dr. Cases file.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 MR. HARTLEY: Thank you, Your Honor.
2 THE COURT: I am confident you will
3 get it. Please call your next witness, Mr. Simon.
4 MR. SIMON: At this time the
5 respondents would call Dr. Ronald Dodson.
6 (WITNESS SWORN IN)
7 THE COURT: Please be seated.
8 DR. RONALD DODSON,
9 called as a witness, testified upon his oath as
10 follows:
11 DIRECT EXAMINATION
12 QUESTIONS BY MR. SIMON:
13 Q Please state your full name.
14 A Ronald Franklin Dodson.
15 Q Are you the Dr. Dodson referred to by
16 witnesses as, Go ask Dr. Dodson, I think he
17 knows, Dr. Dodson?
18 A Unfortunately, probably so. Yes, sir.
19 Q I know the Court is well aquatinted with
20 your background, education, and training in
21 previous proceedings, but I just want to hopefully
22 hit the highlights. You have a Ph.D.; is that
23 correct?
24 A That is correct, sir.
25 Q What is that Ph.D. in?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A In the life sciences with an emphasis in
2 biological electron microscopy.
3 Q What is the transmission electron
4 microscope?
5 A The transmission electron microscope is
6 the instrument that has the highest resolution of
7 any magnifying and defining instrument that we
8 have accessible for biological and other
9 applications.
10 Q How commonly do you use that instrument?
11 A I have used it as the primary instrument
12 in my career.
13 Q How long have you been using that kind of
14 instrumentality to answer biological questions?
15 A Since I entered the doctoral program in
16 65.
17 Q Do you specialize in lung biology?
18 A I do. Yes.
19 Q Do you hold yourself out as an expert in
20 the bioscience of lung disease?
21 A Particularly with emphasis in
22 pneumoconiosis and asbestos-related diseases.
23 Q What is pneumoconiosis, sir?
24 A Pneumoconiosis is a long term for
25 dust-induced diseases of the lung.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 Q To what degree, if any, has your interest
2 in research over the years focused on
3 asbestos-related pneumoconiosis?
4 A The major focus of my research has been in
5 asbestos-related issues. Rather inclusive,
6 obviously I have done a lot of work in quantifying
7 tissue burden for asbestos by light and electron
8 microscopy.
9 I have also done animal modeling and I
10 work with tissue culture studies and molecular
11 biology type applications.
12 Q How long has asbestos disease in one form
13 or another been a focus of your research interest?
14 A Since 1977.
15 Q Do you have some training and some
16 certification in asbestos-related industrial
17 hygiene?
18 A Well, I previously directed or been the
19 director through initially approval by EPA, and
20 subsequently after the approval was transferred to
21 the Texas agency for the Department of Health for
22 Environmental Occupational Training Division. I
23 also sat for the state exams as licensed for
24 supervisor/contractor and inspector management
25 planner.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 Q Did you pass those exams?
2 A Yes, I did.
3 Q When licensed as a supervisor/contractor
4 of asbestos abatement, just in laypersons terms,
5 just tell us what that is.
6 A Well, it essentially equates with a
7 confident person under OSHA definition. It
8 simplistically means a person who can control the
9 work and the workplace.
10 Q In order to reduce the asbestos-related
11 hazards, if any, in that workplace?
12 A Proper application of techniques to do
13 just that. Yes.
14 Q You have been here for the testimony of
15 several witnesses in this proceeding; is that
16 true?
17 A I have.
18 Q I want to just ask you whether you agree
19 or disagree, based on your experience in asbestos
20 disease, with some of the testimony.
21 Number one, that approximately 95
22 percent of the chrysotile — excuse me, of the
23 asbestos fiber used in products in the United
24 States was chrysotile rather than the commercial
25 amphibole type?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A I have written that in some of my own
2 texts.
3 Q Where did amocite come from?
4 A The amocite used commercially in this
5 country came predominantly from South Africa.
6 Q Where did crocidolite come from?
7 A Crocidolite came from South Africa with a
8 very small amount from Bolivia.
9 Q There are some doctors and/or scientists
10 who have expressed the opinion that chrysotile
11 fibers have not been demonstrated to be a cause of
12 mesothelioma. True?
13 A Yes.
14 Q So the proposition that I want to ask you
15 about is the likelihood that all asbestos-related
16 mesotheliomas in the United States are caused by
17 some form of asbestos other than the type of
18 asbestos that constituted 95 percent of that which
19 was consumed here. Okay?
20 A Okay.
21 Q What in general terms percentage of
22 mesotheliomas in adult men in the United States do
23 you believe are demonstrably attributable to
24 asbestos exposure with enough research involved?
25 A I think the answer that was given earlier
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 by witnesses is a reasonable one. We look at the
2 Hillerdal concept of one to two per million
3 without definitive proof that those one to two
4 didnt occur from some exposure that was unknown.
5 I think that is a reasonable concept until proven
6 otherwise.
7 Q The number was put out that at least 80
8 percent of all mesotheliomas in adult men in the
9 U.S. are demonstrably attributable to asbestos.
10 From your experience in your understanding of the
11 medical and scientific literature, does that sound
12 about right, too high, or too low?
13 A I think all the literature agrees that the
14 majority of mesotheliomas in our society are
15 asbestos related or in the world, with the
16 exception of some possible areas of some unique
17 exposures.
18 Q The testimony was given that asbestos
19 fibers cause asbestosis and there is no dispute
20 about that. Do you agree or disagree with that
21 proposition as stated?
22 A I agree.
23 Q There was also testimony that asbestos
24 fibers themselves can cause lung cancer and that
25 is there is no dispute about that. Do you agree
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 or disagree with that proposition?
2 A I agree.
3 Q There has always been testimony that
4 asbestos fibers cause asbestos-related pleural
5 plaques and there is no dispute an about that. Do
6 you agree or disagree with that proposition?
7 A I agree.
8 Q Do you believe that there are well-done
9 studies in the medical and scientific literature
10 in which the authors have concluded that
11 chrysotile fibers also cause diffuse malignant
12 mesothelioma in humans?
13 A Yes.
14 Q Have you written some of that literature?
15 A I have written some of that and referred
16 to some of that.
17 Q Based on your experience in the study of
18 asbestos disease going back to 1977, taking all of
19 that into account, the amount of chrysotile as a
20 percentage of the asbestos used in this country;
21 the fact, as you have stated it, that the majority
22 of mesotheliomas are asbestos-related; the fact
23 that chrysotile fibers, indisputably by your
24 testimony, cause asbestosis, lung cancer, and
25 asbestos-related pleural plaques; and that there
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 are studies that you consider to be well done in
2 the peer-reviewed literature in which authors
3 conclude that chrysotile fiber do cause
4 mesothelioma in humans. What is your opinion
5 about whether or not, within reasonable scientific
6 probability, chrysotile fibers can cause diffuse
7 malignant mesothelioma in humans?
8 A My opinion is that they can.
9 Q How well accepted among experts in
10 asbestos disease with whom you deal do you believe
11 that opinion to be held?
12 A I think there is a large body of
13 scientists that agree with that opinion. Clearly
14 there is a large group of individuals, be they
15 regulators or scientists internationally, that
16 agree with it because meso is one of the reasons
17 that bans have been put in place in other
18 countries.
19 Q Lets talk about that for a moment. Has
20 there been regulation of asbestos use in the
21 workplace in the United States for some number of
22 years?
23 A Yes.
24 Q For example, when was OSHA, the
25 Occupational Safety and Health Administration,
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 created?
2 A Functionally in the early 70s.
3 Q What was the first workplace hazard OSHA
4 addressed?
5 A OSHA set a PEL for asbestos.
6 Q A PEL is what?
7 A Permissible exposure limit.
8 Q Has that level gone down over the years?
9 A It has gone down over the years with logic
10 being that they have tried to reduce significant
11 risk, as they define significant risk, for a
12 population of exposed individuals.
13 Q As that level has gone down, when it
14 followed, have we as a country been able to
15 eradicate new cases of asbestosis?
16 A The primary focal point of that change has
17 been heavy dose exposure, which is asbestosis.
18 Q Does it take more or less or the same
19 amount of exposure to asbestos to cause asbestosis
20 as it does mesothelioma?
21 A I believe there is a concurrence that
22 individuals develop asbestos preferentially with
23 higher dose exposures.
24 Q Between lung cancer and mesothelioma, does
25 one take more asbestos exposure than the other,
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 typically speaking?
2 A Between?
3 Q Mesothelioma versus lung cancer.
4 A Mesothelioma has been defined by a number
5 of investigators as a lower-dose-exposure disease
6 with a number of instances, a link to a longer
7 latency period. Conceptually you dont get enough
8 exposure to die from the asbestosis risk. You
9 live longer and, therefore, have elevated
10 potential for lung cancer. Ultimately those
11 people that are better exposed at some level,
12 usually a lower level based on the literature, at
13 some longer period of time develop meso.
14 Q Are there some doctors and/or scientists
15 who have written that asbestos-related lung cancer
16 does not occur if a person doesnt have enough
17 exposure to cause asbestosis?
18 A Well, there has been a debate about that
19 and a number of communications back and forth over
20 an article that Dr. Churg wrote stating that he,
21 in essence, would like to define pathologically
22 asbestosis before linking a causation of the
23 asbestos to the lung cancer. There were obviously
24 those who took exception to that for logical
25 reasons.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 Q If I understood you correctly, asbestosis
2 requires more exposure than what would be
3 necessary to induce mesothelioma, generally
4 speaking?
5 A That is generally, conceptually true.
6 Yes.
7 Q Lung cancer requires more exposure
8 generally speaking to be asbestos related than
9 necessary to induce mesothelioma?
10 A In most instances, that is reasonable.
11 Q Some researcher have said it actually
12 takes as much exposure to induce asbestosis as it
13 would take to induce lung cancer, correct?
14 A Some have.
15 Q I am not asking you to observe whether you
16 agree or disagree. I am trying to get that
17 concept out there.
18 As the permissible exposure level has
19 gotten lower and lower and lower, you stated the
20 goal was to prevent asbestosis, correct?
21 A The concept is to prevent disease during a
22 workers lifetime with obvious emphasis on
23 reduction of exposure, eliminating the more
24 heavier-dose diseases at the beginning of the
25 concept. Yes.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 Q Can we for the most part prevent new cases
2 of asbestosis and asbestos-related lung cancer by
3 regulating it rather than simply banning the use
4 of asbestos?
5 A It is more reasonably attainable with
6 asbestosis. Its an open-ended question for lung
7 cancer because of the regulations that govern a
8 measurable type of fiber. There are many more
9 fibers in most environments that dont fall into
10 that category. Certainly if the ultimate
11 determinant of exposure is the human lung. Those
12 fibers are the ones we know are in the lung and,in
13 fact, in extrapulmonary sites outside the lung.
14 Q Do we know of a level of exposure to
15 asbestos too low to induce mesothelioma?
16 A No.
17 Q You heard the testimony that a number of
18 countries have banned the use of chrysotile
19 asbestos?
20 A Yes.
21 Q From that biological point of view, if by
22 regulating the use of chrysotile asbestos by
23 keeping the dust levels really low we can pretty
24 much prevent new asbestosis cases and pretty much
25 prevent lung cancer cases, why ban it?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A Because the great unknown is how many
2 people will develop mesothelioma from low levels
3 of exposure. Therefore, the target is to make as
4 low as possible a background or an exposure for
5 people to test how many over 40, 50 years will get
6 the disease.
7 Q If chrysotile fibers cannot cause
8 mesothelioma, would it be necessary to ban it
9 rather than just regulate it?
10 A Repeat that, please.
11 Q Sure. If chrysotile fibers cant cause
12 mesothelioma and you can prevent new asbestosis in
13 lung cancer cases by simply regulating it, would
14 you need to ban it?
15 MR. LEONE: Objection, Your Honor.
16 There is no foundation. It calls for speculation
17 as to why other countries do things.
18 THE COURT: Sustained.
19 QUESTIONS BY MR. SIMON:
20 Q If by regulating exposures we could
21 prevent asbestosis and lung cancer, and chrysotile
22 fibers cant cause mesothelioma, apart from the
23 question of banning it, would we need to eliminate
24 the use of chrysotile asbestos to prevent these
25 two diseases?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 MR. LEONE: Objection. There has been
2 no foundation this witness is an electron
3 microscopist and he is speculating.
4 THE COURT: Sustained.
5 QUESTIONS BY MR. SIMON:
6 Q Let me go back then. To what extent in
7 your career, Dr. Dodson, have you focused upon
8 asbestos-related disease from the standpoint of
9 bioscience and lung pathology?
10 A Much of my work is related to that very
11 subject.
12 Q In your work in industrial hygiene, for
13 which you were certified by the State of Texas,
14 have you had to deal with the balancing of
15 regulatory issues with health-related issues
16 involving asbestos?
17 A Well, the public building law in the state
18 of Texas was written as a focal point to try to
19 protect public health.
20 Q Have you written on the difference between
21 aspects of asbestos-related in diseases which are
22 regulatory in nature versus disease causing in
23 nature and where they compare and contrast?
24 A I have in point, in fact, commented on
25 regulated fibers and what I consider that
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 definition served versus concerns about real
2 exposures in human beings as indicated by tissue
3 burden.
4 Q In order to perform your services for the
5 State of Texas in compliance with the
6 Environmental Protection Agency regulations
7 dealing with asbestos, did you familiarize
8 yourself with those regulations?
9 A I have looked at the regulations from the
10 governmental agencies. Yes.
11 Q With that background, heres my question.
12 If regulating rather than eliminating the use of
13 chrysotile fiber can eliminate new asbestosis in
14 lung cancer cases, why eliminate the use of
15 chrysotile fiber, if at all?
16 A Well, we are still talking about the
17 lowest dose disease potential among those that you
18 have outlined, mesothelioma. We dont know what
19 those lower doses are.
20 Q In your opinion, does the elimination of
21 the use of chrysotile fiber target the
22 elimination, if possible, of new mesothelioma
23 cases?
24 MR. LEONE: Objection, Your Honor. It
25 calls for speculation.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 THE COURT: Overruled.
2 A (By the witness) I think the elimination
3 of asbestos attempts to target all of those
4 issues, in particular mesothelioma.
5 QUESTIONS BY MR. SIMON:
6 Q Now, you mentioned in a previous matter in
7 this Court that you were a member of the advisory
8 committee that wrote the guidelines for asbestos
9 abatement in public buildings, correct?
10 A I was on that for a couple of sessions,
11 yes, as a member.
12 Q You also said today that you were director
13 of the asbestos training division that taught
14 asbestos health issues to those required to comply
15 with EPA guidelines; is that correct?
16 A Its a little more complex than that. The
17 programs they teach involve all facets of asbestos
18 abatement. A part of that is requirement to
19 understand health effect issues associated with
20 exposures, which is why the courses are put
21 together to begin with because there is a causal
22 relationship to disease that we have outlined.
23 Q Does the Texas Department of Health
24 regulate asbestos-related health issues in
25 compliance with EPA guidelines?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A They are the agency under subcontract to
2 apply the NESHAPS regs. They also — Texas is not
3 an OSHA state, but they do have certain
4 responsibilities under the model accreditation
5 program that carries them into some industry
6 sector and they are responsible for public
7 buildings, including the AHERA governance of
8 activities related to asbestos in schools.
9 Q I would like to show you what I have
10 marked as Plaintiffs Exhibit No. 39 and just ask
11 you if you are familiar with that statute from the
12 Texas Administrative Code?
13 A Yes.
14 Q I would like to look at what it provides,
15 if anything, about chrysotile asbestos. Is this
16 the Department of State Health Services to which
17 you refer?
18 A Yes.
19 Q It says: Adoption by reference. This is
20 in Section 295.33. The Texas Department of Health
21 department adopts by reference the following
22 federal laws and regulations as amended in the
23 Code of Federal Regulations.
24 Where are EPA guidelines — not
25 guidelines, regulations published?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A In the code.
2 Q In Section C it says: State versus
3 Federal Standards. In certain instances a state
4 requirement in a Texas Asbestos Health Protection
5 Act and/or these sections are more stringent than
6 the federal standards listed in Subsection A of
7 this section. In such cases the state
8 requirements shall prevail.
9 Do you see that?
10 A Yes.
11 Q I would like to look then at what is
12 addressed about the subject of mesothelioma in
13 those Environmental Protection Agency Rules and
14 Regulations of Asbestos Worker Protection from
15 Wednesday, November 15, 2002. Number one, it says
16 the primary root of human exposure is through the
17 respiratory system where asbestos fibers may cause
18 carcinoma of the lung, malignant mesothelioma of
19 pleura and peritoneum, asbestosis and other
20 illnesses.
21 From a biological and pathological
22 point of view, do you consider that observation to
23 be correct or incorrect?
24 A It is correct.
25 Q It says: Human exposure to asbestos.
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
25
1 Asbestos is found in building products, such as
2 insulation, ceiling and floor tiles, spackling
3 tape for drywall, and roofing products. In
4 general, asbestos-containing materials in good
5 condition do not pose a risk of exposure, but if
6 the matrix of asbestos fibers is disturbed or
7 deteriorates, fibers may be released into the air.
8 Workers may be exposed to asbestos during new
9 construction, asbestos abatement, renovation,
10 building maintenance, custodial activities, and
11 brake and clutch repair work. Building occupants
12 including school children may be exposed to
13 asbestos fibers as a result of activity taking
14 place in their building.
15 To what extent was your training and
16 certification in the state of Texas on asbestos
17 industrial hygiene and abatement issues targeted
18 to deal with that issue?
19 A Well, it is the focal point of those
20 issues, to protect workers, protect public health,
21 as is the guidelines of EPA and OSHA.
22 Q In the same section it says: The issue of
23 the risk from chrysotile asbestos has been raised
24 and considered in previous EPA and OSHA rule
25 makings and both agencies have declined to
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 distinguish between asbestos fiber types in
2 performing risk assessment for regulatory
3 purposes.
4 Do you see that?
5 A Yes.
6 Q Furthermore, EPA reviewed the literature
7 available in what year?
8 A 99.
9 Q So was it just back in 1986 never to be
10 looked at again or was it reviewed more recently
11 than that?
12 A It was reviewed more recently than that.
13 Q On asbestos hazards: In order to assist
14 in the preparation of the United States
15 third-party submissions to a dispute resolution
16 panel of the World Trade Organization regarding
17 the French asbestos ban.
18 What fiber did the French ban?
19 A The major emphasis of that entire
20 controversy with the French was chrysotile,
21 Canadian chrysotile.
22 Q According to the EPA, did it find anything
23 in that literature that persuasively contradicted
24 the risk assessment approach followed by EPA and
25 OSHA?
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 A It says it did not.
2 Q What did EPA conclude in its risk
3 assessment back in the day about whether
4 chrysotile causes mesothelioma in humans?
5 A It maintained the same position.
6 Q Which was?
7 A It does.
8 Q Same question for OSHA.
9 A The same answer.
10 Q Now, what I would like to lastly look at
11 from this is, what factors did EPA look at in
12 making its determination? How inclusive or
13 inconclusive was it? Do you see here it says:
14 EPA considered the health effects of asbestos, the
15 magnitude of human exposure to asbestos — what is
16 that?
17 A The amount.
18 Q The environmental effects of asbestos and
19 the magnitude of the exposure of the environment
20 to asbestos. What is that?
21 A What we might call background.
22 Q The benefits of asbestos for various uses
23 and the availability of substitutes for those
24 uses.
25 A That means looking at the benefits/risks
TERRI W. ANDERSON
301 FANNIN, SUITE 212 HOUSTON, TEXAS 77002
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1 ratio in the sum applications, kind of questioning
2 whether it can be replaced has been one of the
3 subjects of dialogue.
4 Q The reasonable ascertainable economic
5 consequences of this rule. After consideration of
6 the effect on the national economy, small
7 business, technological innovation, the
8 environment, and public health, and the social
9 impacts of the rule. Do you see that?
10 A I do.
11 Q From your experience in dealing with
12 regulatory bodies on the subject of asbestos
13 health, do you find that when it comes to asbestos
14 health regulatory bodies, such as the
15 Environmental Protection Agency or the Texas
16 Department of Health which adopts its provision,
17 can just pass rules, regulate the use of asbestos
18 willie-nillie without consideration of its health
19 effect, the available literature, the economic
20 consequences, the technological feasibility of
21 substitutes, and the other factors described?
22 A No. They are obviously both logical as
23 well as considerable political ramifications, as
24 well as rule making processes that prevent that.
25 MR. SIMON: Your Honor, at this time I
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1 would ask for the admission of Plaintiffs Exhibit
2 39, which is the statute from the Texas Department
3 of Health.
4 MR. SCHACHTER: No objection.
5 THE COURT: I will receive it into
6 evidence.
7 (PLAINTIFFS EXHIBIT NO. 39 RECEIVED)
8 QUESTIONS BY MR. SIMON:
9 Q Have you published any of your work on
10 asbestos-related health issues?
11 A Yes.
12 Q In peer-reviewed literature?
13 A Yes.
14 Q About how many?
15 A 80 or 85 probably. Two or three more in
16 press.
17 Q Have you written textbooks and/or chapters
18 in them regarding asbestos-related health issues?
19 A I have written chapters in the textbooks
20 and I have a book coming out in a matter of a few
21 months.
22 Q Because its obligatory, I am going to pay
23 for your time today, arent I?
24 A Yes.
25 Q What do you expect to be paid for your
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1 time?
2 A When I am actually in court, $800 an hour.
3 Q You have been retained by both plaintiffs
4 and defendants in asbestos-related cases before?
5 A Yes.
6 Q Do you charge differences depending on
7 whom you are retained by?
8 A No.
9 Q There was some comment yesterday about
10 some testimony Dr. Roggli gave in some case — I
11 believe it was the Innerarity case — about
12 whether pure chrysotile had been demonstrated to
13 cause mesothelioma in humans. Were you here for
14 that?
15 A I think I was. Yeah.
16 Q I would like to look at a context in which
17 Dr. Roggli, under oath, set out opinions about
18 pure chrysotile and the role of chrysotile in
19 causing mesothelioma and discuss them with you.
20 Okay?
21 I have marked as Plaintiffs Exhibit
22 40 an affidavit by Dr. Roggli, which is dated May
23 29, 2001. On Page 2 of his affidavit, Dr. Roggli
24 testifies to some things and I want to ask you
25 whether you agree or disagree with the
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1 propositions as he stated them. Mesothelioma is
2 a relatively rare disease.
3 A I agree.
4 Q Science has not demonstrated any cause of
5 mesothelioma in the workplace other than exposure
6 to all forms of asbestos dust which makes it a
7 signal malignancy, i.e., an epidemiological marker
8 for exposure to asbestos.
9 A That has been stated in the literature in
10 several places before.
11 Q Do you agree or disagree?
12 A I agree.
13 Q Once a patient is diagnosed with
14 mesothelioma, the first question to resolve is
15 where and when he or she was exposed to asbestos.
16 Do you agree or disagree?
17 A That is reasonable.
18 Q Because asbestos dust is so strongly
19 associated with mesothelioma, proof of significant
20 exposure to asbestos dust is proof of specific
21 causation.
22 Do you agree or disagree with that?
23 A I think that is a reasonable conclusion.
24 It is actually the same concept in the Helsinki
25 report.
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1 Q The overwhelming world scientific
2 consensus is that dust from all three commercial
3 types of asbestos incorporated in products
4 manufactured in the United States, amocite and
5 crocidolite from South Africa and chrysotile from
6 Canada, are all capable of causing mesothelioma.
7 Do you agree or disagree?
8 A I agree.
9 Q Indeed the causal relationship between
10 exposure to all forms of asbestos dust and the
11 development of mesothelioma is so firmly
12 established in the medical and scientific
13 literature that it is accepted as scientific fact.
14 In that respect, it is like the relationship
15 between smoking and lung cancer, HIV and AIDS, or
16 even water in the lungs and drowning.
17 Do you agree or disagree that the
18 proof is that compelling?
19 A I agree.
20 Q While there is no question among experts
21 in the field that chrysotile dust causes the
22 disease, mesothelioma, there is some dispute
23 regarding whether it is the chrysotile itself or
24 the tremolite contaminant of the chrysotile dust
25 or both that causes the mesothelioma.
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1 Do you agree that there is some
2 dispute depending on who one talks to about how
3 that issue lays out?
4 A Yes. There are people that have different
5 perspectives on that. That is correct.
6 Q The resolution of that dispute is however
7 purely an academic exercise.
8 Here he says: Furthermore, the
9 physical evidence supports the continued
10 contamination of chrysotile after it is
11 incorporated into finished products.
12 He says at the bottom: Accordingly,
13 based upon all the foregoing, the existence of
14 pure chrysotile is a theoretical concept that does
15 not exist in the real industrial world.
16 Now, can you summerize what you
17 understand to be Dr. Rogglis opinion about how
18 ubiquitous, if at all, tremolite is in products
19 that contain Canadian chrysotile?
20 MR. LEONE: Objection. Speculation.
21 Calls for this witness to summarize another
22 witnesss opinion.
23 THE COURT: Overruled.
24 A (By the witness) I believe Dr. Roggli
25 believes tremolite is a component of the
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1 commercial chrysotile and carries with it the
2 products.
3 QUESTIONS BY MR. SIMON:
4 Q If asked the question — put it this way.
5 If it were true, if Dr. Roggli is correct that
6 there is no such thing in the real world as pure
7 chrysotile, if thats true, then could it be
8 proven that pure chrysotile is a cause of
9 mesothelioma?
10 A Rephrase that, please.
11 Q If there is no such real thing as pure
12 chrysotile, if he is right about that, then can
13 you prove that pure chrysotile causes
14 mesothelioma?
15 A Well, I think that there is two answers,
16 there are several answers to that actually. It is
17 not quite as simple as that concept.
18 First, many of the mines, apparently,
19 in Canada have tremolite. Some of the mines I
20 have been advised do not or have low tremolite
21 component. NIOSH did not find tremolite in the
22 material they purchased from the Jeffrey mine in
23 the 80s to make a sample for — used by
24 scientists around the world or in this country for
25 studies.
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1 But from the standpoint of a direct
2 issue as raised with that statement, these are,
3 after all, chrysotile mines. They are not
4 tremolite mines that have a chrysotile
5 contamination, even if the tremolite is there.
6 It certainly is not the reason they mine it. They
7 mine it for the chrysotile, which I dont think
8 anyone would refute is the major component, there
9 being some minor percent in some of those mines of
10 tremolite apparently. At least in the dykes.
11 Q You said something there that we are going
12 to talk about in a little bit. It does raise the
13 threshold issue. When we talk about in a
14 chrysotile miner or miller is it the chrysotile
15 fiber and/or the tremolite fiber, is there any
16 doubt that chrysotile is the predominant asbestos
17 exposure?
18 A Not that I am aware of.
19 Q So going back to this, according to this,
20 does Dr. Roggli believe that there is such a thing
21 as a pure chrysotile product upon which we can
22 prove that pure chrysotile causes mesothelioma?
23 A He indicates he doesnt.
24 MR. SIMON: Your Honor, we ask that
25 Plaintiffs Exhibit 40 be admitted.
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1 MR. SCHACHTER: May I ask one question
2 on voir dire?
3 THE COURT: Yes.
4 MR. SCHACHTER: On Plaintiffs Exhibit
5 40, you actually believe Dr. Roggli is wrong that
6 there is such a thing as pure chrysotile. You
7 have written that, right?
8 THE WITNESS: Yes. He didnt follow
9 all the world literature on chrysotile apparently
10 when he made that statement, sir.
11 MR. SCHACHTER: No objection.
12 THE COURT: I will receive Plaintiffs
13 40.
14 (PLAINTIFFS EXHIBIT NO. 40 RECEIVED)
15 QUESTIONS BY MR. SIMON:
16 Q What is your opinion about whether or not
17 pure chrysotile within reasonable scientific
18 probability can cause mesothelioma in humans and
19 has done so?
20 A My opinion is that asbestos causes meso
21 and chrysotile in the asbestiform habit can cause
22 meso.
23 Q Have you been consulted both by plaintiffs
24 and defendants in asbestos cases to do tissue
25 burden analysis?
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1 A Certainly.
2 Q In order to render what opinions?
3 A Well, the primary thrust of the request
4 are generally in regard to determining the present
5 numbers of ferruginous bodies in asbestos fibers
6 in a sample of tissue.
7 I would not be fair by not including
8 that I have also had some involvement with
9 particularly some defense attorneys in looking at
10 product composition, which has nothing to do with
11 looking at a piece of tissue, but has something to
12 do with looking at material they requested me to
13 assess for them.
14 Q When you are asked to look at tissue
15 burden analysis, you are consulted for your
16 opinion as to what asbestos is there; is that
17 right?
18 A Yes.
19 Q And in what number?
20 A Yes.
21 Q Anything else?
22 A Sure. What dimensions the asbestos is in.
23 That usually or that does result in a report.
24 After that report, then I am asked in some form
25 for interpretation of what the report means.
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1 Q From the standpoint of causation?
2 A Yeah. Sure.
3 MR. LEONE: Objection. Leading.
4 THE COURT: Sustained.
5 QUESTIONS BY MR. SIMON:
6 Q You were asked to interpret based on the
7 burden that appears what?
8 A I am asked to interpret all facets of
9 information concerning the burden as it relates to
10 the potential for causation or in the case of
11 product analysis, potential causation.
12 Q We have talked a lot about tissue burden
13 analysis. And I want to talk for a moment, if we
14 could, about its connection, if any, to general
15 causation.
16 If you look in my lungs and I had
17 mesothelioma, and I have a level of chrysotile in
18 my lungs that is above background, and there is
19 appropriate latency for the development of my
20 mesothelioma, what conclusion, if any, would you
21 draw about whether or not chrysotile was a cause
22 of my mesothelioma?
23 A Well, I would suggest first that I would
24 tell you that there was an asbestos exposure. I
25 would define that exposure based on the number of
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1 fibers per gram of tissue. I would tell you
2 something about the fibers dimensionally. Then I
3 would tell you that provides a snapshot of the
4 lung content at that time with a realization that
5 particularly shorter fibers can relocate to
6 extrapulmonary sites, including those where mesos
7 develop.
8 Q Well, we are going to talk about that
9 issue in a little more detail in a moment. What
10 you see when you open the lungs is only partial of
11 what was once there, correct?
12 A That is correct.
13 Q We are going to talk about whether or not
14 looking in the lungs is necessarily the place to
15 look for causation of mesothelioma through tissue
16 burden analysis, right?
17 A Okay.
18 Q My question is just assuming I have
19 mesothelioma, you look in my lungs and I have a
20 heavy chrysotile asbestos burden in my lungs.
21 What, if anything, does that tell you whether
22 chrysotile was a cause of my mesothelioma?
23 A That you have a type of asbestos there.
24 Asbestos of that type could be relocated as with
25 any other type to the sites where mesos develop.
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1 Q Within reasonable scientific probability,
2 would you consider that asbestos fiber found at a
3 level above background in my lungs having
4 mesothelioma as a cause of that disease?
5 A I would certainly tell you it was an
6 indicator of exposure. I would suggest that it
7 links to causation.
8 Q Now, if chrysotile can cause mesothelioma
9 in somebody as confirmed by tissue burden
10 analysis, what, if anything, does it tell us about
11 whether or not it is capable of causing
12 mesothelioma in humans generally?
13 A I think we went over that earlier. I
14 consider chrysotile can be a cause of meso.
15 Q I want to talk about history of asbestos
16 exposure. Tissue burden analysis, Dr. Hammar told
17 us, was a means of looking in tissue and seeing
18 direct evidence of exposure. Do you agree or
19 disagree with that?
20 A Yes.
21 Q In your experience is enough tissue always
22 available to do a tissue burden analysis in a
23 person with mesothelioma?
24 A In the context of how mesos are now
25 diagnosed with smaller and smaller samples of
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1 biopsies, generally there is not enough tissue to
2 work with for a diagnosis unless there is samples
3 collected at autopsy.
4 Q Let me make sure I understand that about
5 diagnosis as you put it.
6 One way to diagnose mesothelioma is
7 through a needle biopsy; is that right?
8 A Through a needle biopsy of cytology
9 analysis of fluid collected, emitted from the
10 tumors with cells that are cast off from the tumor
11 essentially.
12 Q I want to set that out. There is
13 procedures for diagnosing mesothelioma by looking
14 at fluid drawn from the pleural space, right?
15 A They look at the cytology of the cells
16 that are collected from that fluid to determine
17 characteristics of a cell, including potential
18 cancerous-type patterns.
19 Q Needle biopsy. Is that just taking tissue
20 with a needle?
21 A Yes. In the case of mesothelioma, one is
22 trying to determine that it is a meso. Generally
23 they do that for intervention persistence mode.
24 So the concept of that is to take a very small
25 piece of the target site where the tumor is.
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1 Q Has the ability to diagnose mesothelioma
2 through cytology fluid and needle biopsy gotten
3 better or worse in the last number of years?
4 A Well, there have been constant
5 improvements in the specificity of diagnosis,
6 which can, in many instances, be made with smaller
7 and smaller pieces of tissues.
8 Q Do these diagnostic tools yield enough
9 tissue to do the diagnosis of mesothelioma in many
10 cases?
11 A Yes.
12 Q Do they yield enough tissue to do a tissue
13 burden analysis?
14 A No. I wouldnt do one on them.
15 Q How typical is it that somebody living
16 with mesothelioma, being treated for mesothelioma,
17 has been diagnosed with mesothelioma with the
18 tools that permit that, but dont yield enough
19 tissue for tissue burden analysis?
20 A It is common.
21 Q For you to have enough tissue on a living
22 person, what kind of procedures would need to
23 happen?
24 A Well, one would have to have a highly
25 evasive procedure in which you took a piece of
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1 tissue, large enough piece of tissue to work with.
2 That is basically unethical if you can make a
3 diagnosis from a moderately or mild invasive
4 procedure to get a smaller sample that would give
5 you a conclusive definition of a type of tumor.
6 There is no reason to do that.
7 Q Is there a type of treatment sometimes
8 administered called extrapleural pneumonectomy?
9 A Yes.
10 Q That is where they take out half the
11 chest?
12 A Try to take out the tumor and the tissue.
13 Yes.
14 Q If you dont have an open biopsy because
15 the doctors didnt consider it appropriate, and
16 you didnt have a extrapleural pneumonectomy
17 sample because the patient wasnt a candidate for
18 it, how can you determine if that person did have
19 a history of asbestos exposure sufficient to cause
20 mesothelioma?
21 A It gets back into a thorough history of
22 the background of the individual and has to go
23 into great detail to define potential places,
24 locations, and opportunities for asbestos
25 exposure.
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1 Q How well accepted is it, not in the
2 courtroom, just in the field of science, that an
3 appropriate history of exposure to asbestos absent
4 tissue burden analysis is a sufficient basis in
5 order to determine if a persons mesothelioma is
6 related to asbestos and specifically to what type
7 or types?
8 MR. SCHACHTER: Objection, Your Honor.
9 It is calling for medical opinions. This
10 gentleman is not a medical doctor.
11 THE COURT: Overruled.
12 A (By the witness) I think it is extremely
13 important and the thoroughness of that history is
14 critical.
15 QUESTIONS BY MR. SIMON:
16 Q What does the Helsinki Criteria say about
17 the appropriateness of using history of exposure
18 to asbestos to determine how, if at all, to
19 attribute to the cause of mesothelioma?
20 A They use a specific example of chrysotile,
21 and the reason they use that is their awareness
22 that it clears from the lung. It may clear to
23 other parts of the body simultaneously with
24 clearing up and out of the lungs. But they made
25 the point that history, a thorough, documented
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1 history may be the only source in some instances
2 of linking causation to exposure.
3 Q So history of asbestos exposure can be
4 more reliable in appreciating actual exposure than
5 tissue burden analysis if what type of asbestos
6 fiber is being considered?
7 A Their reference point was chrysotile.
8 Q Now, you have been here –
9 THE COURT: Stop. Their reference
10 point was chrysotile. I dont understand that
11 answer.
12 THE WITNESS: You want me to explain
13 the logic of that?
14 THE COURT: You better. Say what you
15 want. I dont understand the meaning of what you
16 just said. If I dont understand it, it doesnt
17 do anybody a lot of good.
18 THE WITNESS: Right. Their exact
19 reference was chrysotile because it is the type of
20 asbestos that is inhaled in a shorter form and,
21 therefore, one, it can be more readily eliminated
22 from the lung.
23 But that doesnt have anything to do,
24 which is the logic for their conclusion, with what
25 exposure may have occurred in the past, what had
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1 transpired before it got there. Therefore, the
2 history may be a better indicator because you may
3 not find it in the lung. It had been there and
4 induced possibly changes in the lung, but also
5 likely then relocated out to the sites outside of
6 the lung where the meso occurs.
7 If you use the lung as an indicator
8 only, which was their tissue burden reference, you
9 may not find any, and yet there may have been a
10 heavy exposure that has simply been eliminated by
11 the time the person got the disease.
12 THE COURT: Got it. Now I understand.
13 THE WITNESS: Yes, sir.
14 QUESTIONS BY MR. SIMON:
15 Q I just want to bring into focus the
16 Helsinki Criteria as it relates to those issues.
17 Is this the one to which we refer?
18 A It is. Yes.
19 Q According to the Helsinki group by
20 consensus, what is the most reliable measure of
21 occupational asbestos exposure?
22 A It states the history.
23 Q Involving structured questionnaires,
24 check lists, trained interviewers can identify
25 persons with a work history compatible with
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1 significant asbestos exposure.
2 Do you agree or disagree with that?
3 A I think I would agree with all that is
4 stated there with the exception that I would add
5 the work history, hobbies, and other factors in
6 the background of the person.
7 Q Where they observed: Chrysotile fibers do
8 not accumulate within lung tissue to the same
9 extent as amphiboles because of faster clearance
10 rates, therefore, occupational histories, fiber
11 years of exposure, are probably a better indicator
12 of lung cancer risk for chrysotile than fiber
13 burden analysis is.
14 Is that a similar or a different
15 concept than what you were expressing?
16 A That is exactly what I just went over with
17 the Judge.
18 Q What I want to do is talk about what
19 scientists, such as yourself, mean when we say
20 that chrysotile is more easily cleared from the
21 lung.
22 A Okay.
23 Q What does that mean to you, according to
24 your research?
25 Q First, smaller structures, whatever they
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1 are, have a greater likelihood of being eliminated
2 by our defense mechanisms up and out the way they
3 came in essentially in what has been described
4 already as muco-ciliary escalator. If you
5 consider chrysotile has a likelihood of being
6 curved as it gets longer, then you have to also
7 grant that most fibers that are inhaled that are
8 chrysotile will likely be shorter in the lung than
9 the equivalent type dose of amphiboles that are
10 straight.
11 That puts them in the category I just
12 described. From the perspective of the tissue
13 response, the defense mechanisms can eliminate at
14 the lower levels of the lungs small things faster
15 than they can large things.
16 Q If its a short tremolite fiber, will it
17 be more easily cleared than a long one?
18 A Yes. Short matter, yes, will readily
19 clear the lungs in the same time as asbestos or
20 any other material.
21 Q This concept that short fibers are more
22 readily cleared from the lung isnt unique to
23 chrysotile as opposed to other forms of asbestos?
24 A No. That is why I made the point of
25 smaller, short things.
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1 Q When we say, cleared, where do they go?
2 A In the sense that most people use the term
3 when they are talking about clearance, they are
4 really, I think, talking about elimination, which
5 means they pass up the airways, and we either
6 swallow them or you cough them up and eliminate
7 them.
8 Q One way in which the short fibers are
9 cleared is that our defense mechanisms eliminate
10 them, correct?
11 A Out of the lung, yes. But their other
12 process is they can be relocated to other sites in
13 the body.
14 Q What is that concept known as?
15 A Some people have used the term
16 translocation. It is still clearing it from the
17 lungs somewhere else.
18 Q Some short fibers can be eliminated from
19 the lung, but not translocated, and some are
20 eliminated from the lung and are translocated?
21 A That is possible. Yes. Both of those are
22 active processes of disease.
23 Q Which size fibers are more readily
24 translocated to the lining of the lung where
25 mesothelioma occurs, long or short?
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1 A Well, actually it is not the lining of the
2 lung necessarily. It is the lining of the chest
3 cavity and the lining of the abdominal components.
4 It is equivalent to the one in the chest.
5 But from the data that we know what
6 fibers are found in those spots, they are short
7 fibers, vast majority. Some long ones can reach
8 those sites, but the majority are short fibers.
9 Q By fiber type, if that distinction can be
10 made based in science, which type of asbestos
11 fiber most readily translocates to the sites where
12 mesotheliomas occur?
13 A According to Sebastiens article in 80,
14 it was a preferential relocation for chrysotile,
15 short chrysotile.
16 Q Have you published on this?
17 A I have published on that, and I concur
18 with Sebastiens findings that preference, at
19 least for the predominant fiber in the pleura, is
20 chrysotile. But differs in that I acknowledge
21 that fibers of amphiboles can reach those sites,
22 too. Again, favoring short fibers.
23 I might add so did Suzuki publish on
24 this subject.
25 Q Why is it biologically significant, if at
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1 all, that chrysotile fibers and short ones in
2 general are the ones which are most readily
3 translocated to the extrapulmonary sites like the
4 mesothelial lining when they are cleared from the
5 lung?
6 A Well, the clearance process is an ongoing
7 process. It is a highly effective one in most of
8 us most of the time. However, when a traffic jam
9 occurs in that ability to eliminate that freeway,
10 then other escape routes for the freeway exist in
11 the lung. One of those to meet the overload is
12 through the drainage system, the interstitium, to
13 the lymphatics and the lymph nodes. Then that
14 water is shed out to the pleural lymphatics and
15 other parts of the body.
16 That is basically what Brody was
17 talking about when he gave his deposition.
18 Q I just want to get your opinion on this.
19 Some chrysotile fibers more readily relocate to
20 the organs where mesotheliomas arise. So what?
21 Why is that biologically significant?
22 A Well, you have an entity that is
23 considered to cause cancer. I think everyone has
24 agreed that I have heard it can cause lung cancer.
25 If it can cause lung cancer, it reaches a site
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1 where another cancer develops, mesothelioma. I
2 guess it seems reasonable that a carcinogen at the
3 site could be a contributor to the development of
4 cancer.
5 Q How long have you been publishing in
6 peer-reviewed literature on exactly that issue?
7 A I published the paper on the lymph nodes
8 and pleural plaque tissue back in 80 — in 90.
9 I am sorry.
10 Sebastien published it in 80. He
11 actually went as far as saying in his paper that
12 the lung may not be a good place to look to get an
13 assessment of what is in the extrapulmonary sites,
14 such as the pleura.
15 Q Lets break that down for a moment. In a
16 person with mesothelioma, if I look at the
17 asbestos fibers found in their lung, can I infer
18 that those fibers got to the pleura to cause
19 disease there?
20 A By looking at what is in the lung?
21 Q Uh-huh.
22 A I would say what you could confirm is that
23 that confirms a past exposure.
24 Q If I can look in pleural plaques, for
25 example, can I confirm which fibers actually got
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1 to where those pleural scars occur?
2 A That is the site of the action. Yes.
3 Q Have you published on that?
4 A Yes, as did Sebastien and Suzuki.
5 Q What types of asbestos fibers did you find
6 in the pleural plaques of people you studied?
7 A The predominant form we found was
8 chrysotile with some amphiboles, all which were
9 basically short.
10 Q What conclusions did you draw in this
11 paper, which was approved for publication?
12 THE COURT: Wait. Chrysotile with
13 some other fibers that have amphiboles?
14 THE WITNESS: Amphiboles, the other
15 category. If they are short, they get there, too.
16 THE COURT: I thought the amphiboles
17 were the little things that were on the other
18 kinds of fibers. I thought chrysotile could not
19 have amphiboles.
20 THE WITNESS: The question was just
21 asked by Your Honor about the coating that we
22 talked about earlier in the other hearing on
23 asbestos fibers. That was actually the coating
24 that can form on any fiber if its over 8 microns
25 long, and thats called a ferruginous body. Those
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1 are formed in the lung basically.
2 QUESTIONS BY MR. SIMON:
3 Q Just at least for the record, amphiboles
4 are the amocite, crocidolite, tremolite type
5 fibers and chrysotile is the serpentine type; and
6 if a fiber is long enough, it can form a
7 ferruginous body in the lung where it gets coated
8 with iron, is that right?
9 A The concept of a chrysotile and the
10 amphiboles is mineralogical families that just fit
11 into different mineralogical groupings.
12 Q Lets talk about that for just a minute.
13 Can I see a ferruginous body with a light
14 microscope?
15 A Yes.
16 Q Can I see an uncoated asbestos fiber with
17 a light microscope?
18 A A large number of those, the majority you
19 cant.
20 Q If I use a light microscope to tell me how
21 much asbestos is in that lung and what type, is it
22 a sensitive tool for that?
23 A A light microscope?
24 Q Yes.
25 A You cant define type with a light
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1 microscope.
2 Q Will I be able to see really long
3 chrysotile fibers if they are not coated with iron
4 in that lung with a light microscope?
5 A It depends on their thickness. Most of
6 them you would not because you cant inhale, for
7 the reasons we went over earlier, long chrysotile
8 fibers that are that thick because dimensionally
9 they are too large and dont go down deeply.
10 Q The short asbestos fibers, such as
11 chrysotile, that more readily relocate to the
12 pleura, can I see those in lung tissue with a
13 light microscope?
14 A It is exceedingly difficult to see any
15 fiber in lung tissue with a light microscope
16 because of the interference of the tissue around
17 fiber. You cant see the ferruginous bodies
18 because they are great big dumbbell things on the
19 longer fibers.
20 Q What types of asbestos fibers do
21 ferruginous bodies tend to form around?
22 A They tend to preferentially form on
23 amphiboles, which also are the type fibers inhaled
24 in the longer form. They form only on longer
25 things.
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1 Q Just to bring that to a head, if I am
2 looking with a light microscope to see if the
3 person has a lot of uncoated chrysotile fibers in
4 there, will a light microscope tell me that?
5 A No, sir.
6 Q So we talked about the fact that in terms
7 of translocation, the short fibers are the ones
8 which typically do that. Okay?
9 A Yes.
10 Q But when we get back to the general
11 concept of which fibers are more readily cleared
12 from the lung, to what extent, if any, does the
13 amount of asbestos and the number of times over
14 and over and over that a person is expose affect
15 the lungs ability to clear those fibers?
16 A That the impact of repetitious exposure is
17 one that was looked at with Coin and several other
18 people, Brody, Roggli in a paper. Basically
19 because of what we have already talked about with
20 chrysotile being more likely inhaled in a short
21 form, that an animal model with a one-time
22 exposure, most of the dust gets out of the lung
23 quickly.
24 If you give repetitious exposure to
25 those same animals, I think it is three exposures,
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1 there was an accumulation of some of that dust in
2 the interstitium which didnt clear. Those are
3 preferentially, I think, longer fibers in that
4 study.
5 Q What is the interstitium?
6 A That is the area underneath the epithelium
7 and the lining of the lungs. So that means it is
8 in its first stage of going to a place that causes
9 a more lasting problem. And thats what they
10 found that did indeed cause DNA breaks, which is
11 the genetic change in cells in the area,
12 beginnings of fibrosis, which is scarring, which
13 is more of a permanent-type response. If its
14 caused by asbestos, it asbestosis. And the
15 presence of fibers that were not eliminated
16 because they werent on the fast track to get out
17 anymore. They were entrapped inside the tissue,
18 not on the surface of it.
19 Q Let me then try to pull those concepts
20 together. Do you believe that in all people the
21 long asbestos fibers are the ones most responsible
22 for causing their mesothelioma?
23 A I think I believe that all the asbestos
24 fibers are contributors that reach the site where
25 the mesothelioma develops. The data that exist in
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1 the literature, including our labs, Sebastien, and
2 Suzuki, indicate that the short fibers are the
3 prevalent form that tend to get out there.
4 Q So when we talked about the factors that
5 cause a fiber to cause cancer, one of them was it
6 translocation potential if we are talking about
7 mesothelioma, correct?
8 A From the lung, yes.
9 Q What are the other factors?
10 A To cause a tumor?
11 Q Yes, sir.
12 A Well, one that we have discussed or had
13 discussed here is the chemical composition of the
14 fiber.
15 Q I am going to call that chemical
16 reactivity.
17 A That is fine.
18 Q All right. Okay.
19 A That would include potentially surface
20 charge of the fiber as well as the actual makeup
21 chemically of the fiber, which differs between
22 fibers as potential incubators, if you will, of
23 reactions, chemical reactions.
24 Q How much chemical is out there?
25 A Well, the fibers are in contact with cell
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1 components, and it depends on what cells. If they
2 are in contact with the defense cells, the
3 macrophages, they come out on the surface to try
4 to attack the fiber, enclose it, to try to help
5 get it in the process to either detox it, which
6 they cant do, or move it up the trachea for
7 clearance, if they get on that process of
8 elimination.
9 One of the concepts of damage to the
10 lung is that these are bundles of enzymes,
11 chemical enzymes waiting to attack in most of us,
12 particularly me right now, bacterial infection.
13 But in the case of a rock, they dont do much with
14 it. So they simply initially die and dump their
15 contents, which can contribute to damage to the
16 lung surface.
17 In the context of the cells that form
18 the tumors, lining cells, be it the lung or the
19 mesothelial lining-type cells, the chemical
20 reactivity as we have already heard is the same in
21 both those areas in one facet, and thats the
22 potential for producing radicals, which are
23 charged particles waiting for a place to cause a
24 reaction that should occur; or the other facet,
25 particularly in those lining cells, is that it is
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1 a physical entity, a presence.
2 So you have two components if you happen
3 to have those fibers taken up in a dividing cell,
4 a cell that is capable of reproducing itself. One
5 of those is chemical reactions that may cause
6 damage within that cell. That is some of the
7 complex genetic or protein complexes that are
8 required for cell division. The other is a
9 simple, logical one that you have an entity in
10 there stuck in a place it is not suppose to be,
11 which may, in fact, physically alter the
12 capability of the cell to create two equal cells
13 because they cant get a distribution by physical
14 presence.
15 Q I want to make sure I understand what we
16 are saying. Is surface area a factor?
17 A Surface area is one issue for some of the
18 chemical reactivity.
19 THE COURT: I am going to give Terri a
20 10 minute break. Well take 10 minutes.
21 (RECESS)
22 THE COURT: Please proceed.
23 QUESTIONS BY MR. SIMON:
24 Q Dr. Dodson, where I am going in trying to
25 understand the factors that are in play in the how
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1 and why asbestos fibers cause cancers like
2 mesothelioma is to talk more directly about your
3 research that deals with long versus short fibers
4 and their role in causing mesothelioma. You have
5 been writing upon that subject for a number of
6 years; is that true?
7 A Yes, sir.
8 Q From your review of the literature, why is
9 it that some authors write that long fibers are
10 more potent for causing mesothelioma?
11 A Well, long fibers are more potent than
12 short fibers for causing mesothelioma if you stick
13 them directly at the site where the mesothelioma
14 develops. So most of that is based on studies by
15 Stanton and Pott or other intraperitoneal or
16 intrapleural injections. I dont think anyone
17 would argue that a long fiber one-on-one is
18 probably more dangerous than a short fiber
19 one-on-one.
20 But thats not the distribution you
21 get in the air stream and in the environment. It
22 is not the distribution you get in the tissue. It
23 is not the distribution you find in the
24 extrapulmonary sites.
25 Q Would a long fiber when compared to a
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1 short fiber if it got to the targeted site have
2 more surface area there than a short fiber?
3 A If it were one-on-one, yes.
4 Q Would it have more surface area from which
5 to exact chemical reactivity in area cells?
6 A If it were one-to-one.
7 Q So lets go back a step then. If you put
8 the fiber in the place where mesothelioma
9 originates, are long fibers on a one-to-one basis
10 more potent for reasons like this?
11 A Thats what the experimental studies have
12 indicated.
13 Q More surface area, more chemical
14 reactivity therefore?
15 A And maybe even more just physical irritant
16 because it is a big thing jabbing stuff.
17 Q Presence?
18 A Yes, but that is not intracellular.
19 Q We will talk about that in a minute.
20 To what extent is the hypothesis that
21 long fibers are more potent for mesothelioma than
22 short fibers based on animal models rather than
23 human exposure data?
24 A Well, the entire concept that has been
25 written about with the Stanton hypothesis based on
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1 that very idea of the test. Sometimes it is
2 misquoted a little bit. Because he did find some
3 tumor in implants with fibers that were 4 microns
4 in length. That doesnt have anything to do with
5 the other guy who did the work, which we ignore in
6 this country mostly, Dr. Pott in Germany.
7 Q Firstly, were short fibers demonstrated to
8 cause mesothelioma in those very same animal
9 studies?
10 A Pott did exactly that with milled
11 chrysotile that was short, 99.8 or something
12 percent less than 5 microns, and he got, I think,
13 30 percent tumors in his animal model.
14 Q When we then go to watching the biological
15 processes in humans, actual asbestos exposures
16 played out in tissue burden analysis, is it the
17 case that those long fibers that are more potent
18 one-to-one are the ones which as readily relocate
19 to the pleura where mesotheliomas occur?
20 A The data that exist thus far from
21 Sebastien, Suzuki, and our lab is that you are
22 more likely to find short fibers there.
23 Q Talking for just a moment about animal
24 data, in animal data has it been demonstrated or
25 has it not that pure chrysotile, that is, no
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1 demonstrable tremolite in it or any other
2 amphibole or asbestos-formed mineral, can cause
3 mesothelioma in animals?
4 A Yes.
5 Q UICC B chrysotile, what is that?
6 A That was a preparation that was made for
7 use in scientific investigations essentially and
8 experimental models collected from multiple mines
9 in Canada.
10 Q Has the question of whether that fiber can
11 cause mesothelioma in humans been addressed in the
12 literature?
13 A Well, you dont get a UICC B exposure to
14 humans. You get the exposure from the various
15 mines from which the samples were collected to
16 make it.
17 Q I didnt say that right. In animal
18 studies, has UICC B chrysotile been used in
19 connection with whether or not mesothelioma
20 arises?
21 A In animal studies, yes.
22 Q With what end, what result?
23 A Mesos and tumors developing, yes.
24 Q Have you analyzed UICC B to see if the
25 fiber that caused mesothelioma in animals was, in
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1 fact, free of amphibole asbestos?
2 A Actually we looked at the sample just to
3 determine what percent the amphibole/tremolite
4 would be present or if we could find it.
5 Q What did you find?
6 A The limits of our exploration of that, we
7 didnt find it.
8 Q So Dr. Roggli is of the opinion that
9 tremolite prevents the description of pure
10 chrysotile, true or not true?
11 A Repeat that, please.
12 Q I am trying to compare and contrast Dr.
13 Rogglis opinion as stated in the affidavit about
14 whether there is in the real world a pure
15 chrysotile, at least compared to what you have
16 seen experimentally.
17 A In that particular analysis we conducted,
18 we didnt find any tremolite.
19 In the second one, the Jeffrey
20 material, there was an extensive study by NIOSH of
21 1,000 pounds, I believe it was, that was obtained
22 from the Jeffrey mine for distribution to
23 researchers as a standard prep. If you look at
24 their data that Campbell presented, he didnt find
25 tremolite as a contaminant, if I recall, in the
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1 samples they analyzed by several ways, light and
2 EM and a couple of other methodologies.
3 Q EM is electron microscope?
4 A Yes, electron microscope.
5 Q In the medical and scientific literature
6 with which you are familiar has mesotheliomas
7 arising from the works in the Jeffrey mines been
8 documented?
9 A As I recall, they have.
10 Q So now I want to go back to talking about
11 if there is a difference between whether or not on
12 a one-to-one implanted basis an asbestos fiber is
13 more potent if it is longer rather than shorter to
14 what can happened to people in real world
15 exposures. Okay?
16 A Yes.
17 Q What distinction, if any, have you seen in
18 tissue burden of the extrapulmonary sites in that
19 evaluation?
20 A Well, in the pleura the data that we have
21 observed, as well as Sebastien reported, was that
22 short fibers are the predominant type fiber that
23 reaches the pleura.
24 Q If there is a lot more short fiber than
25 long fiber in the extrapulmonary sites, what
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1 effect does that have on which fiber has more
2 surface area in the targeted zone?
3 A Well, I dont think that has any
4 difference there that Dr. Churg stated several
5 years ago when he cautioned people to ignore short
6 fibers and their contribution in lung tissue.
7 That is, if you get a number of short ones, youre
8 going to make up for the impact of one long one.
9 The number of the parameters we discussed for
10 interactions.
11 Q Just in a real world example, a
12 hypothetical real world example, if I have a few
13 long fibers in my pleura and a whole lot of short
14 fibers in my pleura, which size fiber, long or
15 short, is creating or existing as more asbestos
16 surface area in that organ?
17 A The short fibers ultimately.
18 Q If the short fibers represent the
19 abundance of surface area, which type of fiber
20 will be exerting the abundance of chemical
21 reactivity?
22 A All of them, but preferentially the
23 majority of the surface would be of a small, short
24 fiber type if thats what reaches there.
25 Q Does saying that a long fiber on a
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1 one-to-one basis is more potent for mesothelioma
2 mean that if a person is exposed to a whole lot of
3 chrysotile rather than just some long fiber
4 amphibole, the long fiber amphibole is still the
5 more potent cause of mesothelioma in that person?
6 A Under the condition you described, that
7 would not be a situation because you also would be
8 exposed to short amphiboles. The answer is, no,
9 as you described it. No. It would not make
10 logical sense.
11 Q Would I also be exposed to long
12 chrysotile?
13 A In many scenarios you would. Yes.
14 Q Do asbestos exposures with any type of
15 fiber come only as long or only as short?
16 A Obviously in experimental scenarios that
17 has been reported as part of the model concept
18 where there has been separation of fibers in
19 length, including work from our lab. But in the
20 real world, most of it is a mixture.
21 Q You indicated that short fibers are more
22 readily translocated to extrapulmonary sites
23 through the lymphatic system, correct?
24 A Or through the body.
25 Q Have you ever looked at the lymphatic
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1 system to see if asbestos fibers do get out there?
2 A Looked at the lymph nodes, which are the
3 waste stations in the lymphatic system.
4 Q What did you find?
5 A Asbestos.
6 Q In your paper, Asbestos Content of Lung
7 Tissue, Lymph Nodes and Pleural Plaques from
8 Former Shipyard Workers dated March 5, 1990 –
9 THE COURT: Is that in evidence?
10 MR. SIMON: I will put it in right
11 now. That is Plaintiffs Exhibit 41. I will
12 offer it at this time as Plaintiffs Exhibit 41.
13 THE COURT: I will receive it into
14 evidence without objection.
15 (PLAINTIFFS EXHIBIT NO. 41 RECEIVED)
16 QUESTION BY MR. SIMON:
17 Q Dr. Dodson, is this a peer-reviewed paper
18 for which you are the lead author?
19 A Yes.
20 Q What did you look at in this paper and
21 what did you find that was of biological
22 significance worth reporting?
23 A We looked at lung tissue, lymph nodes, and
24 pleural plaque material from people who had
25 exposure in Italy in a shipyard working
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1 environment.
2 Q What questions were you asking and what
3 answers did you find?
4 A The fundamental question is what type of
5 asbestos was in the site at each of the sites.
6 What were the dimensions of the asbestos and, I
7 guess, at the beginning were there ferruginous
8 bodies or asbestos bodies in the sites, which you
9 do by light microscopy. That is the big things.
10 Q In this paper, one of the observations you
11 make is that: Chrysotile has been noted as the
12 predominant asbestos form in parietal pleura.
13 This observation is of particular interest since
14 the lower limits of fiber length used in this
15 study would have preferentially excluded many of
16 the shorter chrysotile fibers included in the .5
17 micron greater or equal to limits set in the
18 present study.
19 What does that mean?
20 A Dr. Sebastien used the transmission
21 electron microscope and included short fibers.
22 The point made there, as well as in a number of
23 our other papers, that if you use a counting
24 scheme which preferentially excludes the short
25 fibers, you will miss the majority of the asbestos
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1 in tissue.
2 Q You then write: The data of both studies
3 indicate that chrysotile can accumulate in the
4 pleural regions. Several other studies have
5 indicated that chrysotile makes up a majority of
6 these short, uncoated fibers. An explanation of
7 this stems from length being a determinant of
8 which fibers were relocated to the pleural
9 regions.
10 How long ago did you write this paper?
11 A 1990.
12 Q So I guess what I am asking you is, is
13 this just some new methodology, some new
14 introduction to the peer-reviewed literature?
15 A No. As a matter of fact, the reference
16 point is Dr. Sebastien who did it 10 years before,
17 one site.
18 Q Now, in Dr. Cases deposition in this
19 case, a transcript was prepared and I gave you a
20 copy.
21 A Yes.
22 Q Have you read it?
23 A Yes.
24 Q Do you recall whether or not he made
25 observations about whether you could conclude that
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1 fibers that got to pleural plaques got there from
2 the lymph system as opposed to contamination from
3 the lung at the point of autopsy? Do you remember
4 that discussion?
5 A I did see that.
6 Q Just so we can clarify what the issue is,
7 if the fibers that you found got to pleural
8 plaques carried through the lymph system, for
9 example, that would be very different in terms of
10 its significance than if it is just fibers from
11 the lung which at the point of autopsy somehow
12 just got over into the pleural samples, right?
13 A Yes.
14 Q Did you account for that possibility?
15 A Sure.
16 Q How?
17 A When my colleagues took the samples, they
18 took them from the tissue or from the body and put
19 them in separate containers in their own fixative.
20 There was no cross-mixing. They say they stayed
21 that way until they got to our lab. I dont think
22 Dr. Case critiqued any of our techniques as being
23 his point of contamination.
24 But in assessment of the material, we
25 carried as the paper states all of the samples
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1 separately through the processing obviously.
2 Everything we did was with prefiltered solutions
3 in our own labs and we do quality controls. We
4 actually report.
5 In the case of the lymph nodes and the
6 pleural plaque material, we state that we both
7 vigorously rinsed them with refiltered water, and
8 then trimmed the outside of them to even further
9 assure continuity.
10 I was a bit taken by Dr. Cases
11 comment because if he wants to talk about
12 chrysotile contamination, he probably would have
13 had to have gone the other way from the lymph
14 nodes and the pleural tissue to the lung because
15 if you look at the table, one of the samples were
16 below detectable limits in the lung. We didnt
17 find any and it was positive for chrysotile in the
18 lymph nodes and the pleural plaques. It would be
19 rather hard, I guess to begin with, to envision
20 that the fibers could go from a sealed container
21 to another sealed container.
22 Furthermore, that in this case that
23 the lung could have totally dumped all of its
24 chrysotile somehow into those other two samples.
25 Q Lets break that down. Looking at Sample
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1 No. 8, and this is on Page 845, this is a person
2 with pleural plaques where you look at the
3 question what asbestos fibers, if any, are in
4 their lung? What asbestos fibers, if any, are in
5 there pleural plaques?
6 A Yes, sir.
7 Q Right. What was the asbestos load in
8 their lungs?
9 A Below our detectable limits for chrysotile
10 in that sample.
11 Q What was the asbestos load in the pleural
12 plaques?
13 A In the plaque it was 21 million, I believe
14 it is, and then in the nodes it was 5.5 million.
15 Q We are talking about somewhere over 26
16 million asbestos fibers in the lungs and lymph
17 nodes taken together, correct?
18 A That is what that would indicate. Yes,
19 sir.
20 Q Based on the controls you put in place and
21 your understanding of the biological processes by
22 which fibers move around the body, what is the
23 likelihood that all of those 26-million-plus
24 asbestos fibers are asbestos fibers which just
25 through contamination each and every one of them
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1 leaked out from lung tissue into these
2 extrapulmonary sites during the autopsy process
3 such that you couldnt find any asbestos fibers in
4 the lung when you looked at them?
5 A Doesnt make much sense. I think Dr.
6 Case acknowledges it was a possibility.
7 Q Do you therefore feel comfortable or not
8 comfortable with your observation that the process
9 involved in relocating asbestos fibers to these
10 extrapulmonary sites results in disposition of a
11 typically shorter uncoated fiber rather than
12 contamination from your autopsies?
13 A Yes, sir.
14 MR. SIMON: I would like to mark as
15 Plaintiffs Exhibit 42 a paper on which you were
16 the lead author entitled, Asbestos Fiber Length as
17 Related to Potential Pathogenicity, a Critical
18 Review from the American Journal of Industrial
19 Medicine, 2003 and offer it into evidence at this
20 time, Your Honor.
21 MR. SCHACHTER: We have no objection.
22 THE COURT: I will receive 43 into
23 evidence.
24 (PLAINTIFFS EXHIBIT NO. 43 RECEIVED)
25 QUESTIONS BY MR. SIMON:
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1 Q Is this a peer-reviewed paper that you
2 successfully published in this journal?
3 A It is.
4 Q Now, this is a review paper, right?
5 A Yes, sir.
6 Q What does that mean?
7 A That means its an accumulation of
8 information on a given subject.
9 Q Did you review your own data and published
10 literature?
11 A Yes.
12 Q Did you review other publications?
13 A I did.
14 Q Did you compare and contrast the two?
15 A Yes.
16 Q You make some observations on Page 293
17 about fiber size and its role in causing disease.
18 You reference a Stanton and a Pott. Are those the
19 animal models on fiber size we discussed earlier?
20 A Yes. They are two individuals who really
21 did some outstanding work in looking at fiber
22 pathogenicity in animal models, pleural implants,
23 and peritoneal exposure models. Stanton was in
24 this country, the National Cancer Institute. Pott
25 is a German investigator. A number of their
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1 conclusions are similar and some are different.
2 Q What did you find to be the significance,
3 if any, that even in the Stanton models shorter
4 fibers cause disease?
5 A Well, the Stanton model is often quoted.
6 People tend to stop before they get to that level
7 and only talk about the Stanton fiber as being one
8 that is 8 microns long and less than or equal to
9 0.25.
10 That wasnt all he said. He said –
11 just as I quote — gave the higher probability of
12 tumor development in the animal model. But he did
13 induce them with the others, which were shorter.
14 Q What did you find to be the significance
15 of the fact that Pott found that fibers shorter
16 than 10 microns in length could induce tumors?
17 That in one set of experiments they used milled
18 chrysotile, which contained few fibers longer than
19 10 microns in length, and 99.8 percent of the
20 fibers shorter than 5 microns in length. What is
21 the significance of that to you?
22 A Well, the significance of that to me is
23 what we have discussed. That long fibers carry a
24 risk, which one can compare one-on-one with a
25 shorter fiber, and talked about differences. But
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1 that the cumulative impact of shorter fibers can,
2 in point of fact, cause tumors. He said a lot
3 more actually in his studies including sort of
4 what we went over earlier that there is a lot of
5 factors other than dimensions that play off the
6 toxicity of fibers.
7 Q What, if anything, did Dr. Churg report
8 about whether it is only long fibers that cause
9 disease in humans, specifically mesotheliomas?
10 A Dr. Churg is one of those people who has
11 always counted shorter fibers as we have, which
12 makes it, I think, legitimate for us to talk about
13 shorter fibers rather than if we had
14 preferentially excluded them and then make
15 conclusions based upon what we do include rather
16 than what we excluded.
17 In the context of his conclusions, as
18 shown in that material that I took direct, his
19 lung data from his study in that particular
20 project indicated meso was not something he could
21 link to long fibers in the lung. And that they
22 were probably associated with lower aspect ratio
23 fibers, meaning basically shorter fibers. Given
24 that his lung tissue — but at the same token I
25 think his conclusions are valid and he has written
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1 those before. Essentially says dont jump to
2 total exclusion of short fibers. Most fiber
3 exposures in humans are mixed.
4 Q Dr. McDonald of McGill University who has
5 written extensively on the tremolite/amphibole
6 hypothesis as the cause of Canadian miners and
7 millers mesotheliomas, what has he observed about
8 whether short fibers cause mesothelioma in humans?
9 A Well, basically his conclusions are just
10 about the same as Pott with animal models. In
11 this case, it is lung material and in this case he
12 included shorter fibers in the analysis. He
13 preferentially didnt cut them out of the act by
14 not including them in a count.
15 What the synopsis is is that the
16 longer fibers tend to be associated with meso with
17 a higher incidence followed by the median by his
18 definition of 6 to 10 microns. Then the mesos
19 with the relationship to the shorter fibers he
20 found in the tissue, or his colleague actually
21 did, which was less than 6 microns.
22 Q What is the significance to you that he
23 found and reported that even fibers shorter than 6
24 microns correlate with the inducement of
25 mesothelioma?
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1 A Again, we are talking lung tissue and with
2 the realization that we have already discussed
3 that they are preferentially the ones that can be
4 relocated more readily, that that acknowledgement
5 indicates that they were there in the lung and the
6 potential for them to therefore be out at the
7 pleura exists.
8 Q What is the geometric mean?
9 A I am not a statistician, but basically it
10 is the root of N. N is based on a number of cases
11 or units measured. To put that as I understand it
12 from my statisticians over the years into more
13 reasonable terms, it is using a methodology to
14 look at a mathematical model to which rather than
15 taking an arithmetic mean, which is simply taking
16 the numbers and adding and then dividing, you are
17 dealing with units of numbers on either side of
18 what will ultimately be your medium that have
19 variabilities. And, therefore, you can
20 extrapolate those as a more meaningful number by
21 using a geometric mean.
22 Q I want to ask you about a concept I
23 understood Dr. Craighead to say, ultimately the
24 record will bear out whether I understood it
25 right, I understood him to say that if you look in
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1 tissue, lung for example, and you find chrysotile
2 fibers there, it has to be a recent exposure.
3 That it has to have just been there within the
4 half life of chrysotile of a few weeks to a few
5 months, and cant be some representative portion
6 of exposure that occurred back in the past. Does
7 that sound correct to you?
8 A No, sir.
9 Q Why not?
10 A Well, when we look at tissue, any of us
11 that do that type of work, it is because the
12 material has been obtained oftentimes in autopsy
13 or because a disease is in progress. Certainly if
14 its an autopsy that means oftentimes the person
15 has either had lung cancer or mesothelioma. If
16 you track some of those people within their
17 history once that has been diagnosed, they go
18 through a very long period of time in which they
19 have very limited activity or totally no activity
20 because of the status of their health. So it is
21 rather illogical.
22 By the time I got one of those
23 samples, our pathologist took one of those
24 samples, and the person had been sick for a year
25 or two years after diagnosis before they passed
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1 away, that they would have found a way to get more
2 asbestos exposure. Most of them are simply trying
3 to survive day-to-day.
4 Q Let me play that out a little bit. The
5 Canadian miners and millers exposed to chrysotile
6 dust and did get mesothelioma as discussed in
7 various papers, correct?
8 A Yes.
9 Q Any doubt that exposure to the chrysotile
10 dust causes mesothelioma?
11 A No, sir.
12 Q How early in time did some of that cohort
13 start working?
14 A In the early 20s. It varies with mine.
15 Q These were men born in the 1891 to 1920
16 range, at least in this paper, right?
17 A Yes.
18 Q That is our frame of reference. Do these
19 people typically represent a working population
20 where they literally went to miners and millers to
21 see if they had mesothelioma, or are they people
22 who were generally retired years past the work who
23 got mesothelioma?
24 A A number of those usually are people that
25 are retired. So, its been a period of time since
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1 they — as with most mesothelioma cases, that
2 occurs usually over a period of time after they
3 quit work.
4 Q With a latency period of 30 or 40 years,
5 how common is it for people with mesothelioma to
6 get the disease in their 70s?
7 A Very common.
8 Q How about their 80s?
9 A Sure.
10 Q What is the mean life expectancy for
11 somebody with mesothelioma from the point of
12 diagnosis, give or take?
13 A Best projections are usually about 18
14 months.
15 Q Just in general terms, a lot or a little,
16 within background levels or above it, how much
17 chrysotile was found in the lungs of some of these
18 people that died of mesothelioma?
19 A I dont remember this particular study.
20 In some of the cases it is skewed with amphibole.
21 Q Let me go back a step then. Have you
22 found in the lungs of some people with
23 mesothelioma significant amounts of chrysotile?
24 A You can find that. Yes.
25 Q How high have you found it to be in some
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1 instances?
2 A Remember chrysotile continues to clear.
3 Q Right.
4 A Therefore its a variable.
5 Q I guess what I am saying is, if you have
6 found it in high concentrations before?
7 A Yes.
8 Q What do you mean by high, for example?
9 A Because chrysotile clears so readily, when
10 you find chrysotile in numbers it generally
11 implies a more recent exposure or it implies a
12 residual — for lack of a better description, a
13 tip of the iceberg for what had been there.
14 Q Sometimes it is a recent exposure and
15 sometimes its a –
16 A Residual amount left over from what has
17 been cleared over the years.
18 Q If you find asbestos there that is
19 chrysotile in some concentration, what do you know
20 about how much chrysotile exposure they could have
21 had in the past, where those fibers are no longer
22 in the lungs but have cleared entirely or
23 translocated to the pleura?
24 A That is the whole concept of having
25 historical information to supplement.
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1 Q Does it seem reasonable to you that it
2 would always be the case that somebody gets
3 diagnosed with mesothelioma, all right, and they
4 then pass away and when they — doctors look in
5 their lungs they find a lot of chrysotile, which
6 does happen sometimes, right?
7 A Sometimes yes.
8 Q In each instance what that is is the
9 person got diagnosed with mesothelioma and then
10 somehow found their way into a work setting or
11 some other way of getting exposed where they got
12 exposed to so much chrysotile again since
13 diagnosis of mesothelioma that that is the
14 chrysotile that is being observed in their lungs?
15 A These individuals are not in a condition
16 that they are pursuing activities of that type.
17 Yes. That is correct.
18 Q Talking about the Canadian miners and
19 millers studies. We talked about people exposed
20 to chrysotile dust get mesothelioma. I just want
21 to talk about what the possibilities are there.
22 The possibilities are that chrysotile
23 causes mesothelioma. That is one, right?
24 A Yes.
25 Q That tremolite causes mesothelioma. That
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1 is one of them?
2 A Correct.
3 Q And the possibility that they do it
4 together?
5 A Correct.
6 Q And then the possibility that it is
7 tremolite only, right?
8 A Yes.
9 Q I am going to refer to tremolite only as
10 the amphibole hypothesis. Are you familiar with
11 that term?
12 A Not as it applies only to tremolite, but,
13 yes.
14 Q I want to show you an observation from Dr.
15 Cases deposition in this case, May 28, 2005. At
16 Page 58, Line 2, he is asked: You agree that
17 through the early 1980s a reasonable and prudent
18 researcher looking at the medical and scientific
19 literature at that time would have concluded that
20 chrysotile fibers can cause mesothelioma in
21 humans?
22 His answer is: Yes.
23 And then he goes on to explain, but he
24 changed his mind, right?
25 A Yes.
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1 Q I asked him at Line 20: For how long did
2 you testify that chrysotile fibers cause
3 mesothelioma in humans?
4 He observes at Line 22: For at least
5 10 years, and probably a bit longer than that.
6 Do you see that?
7 A Yes.
8 Q You have been studying asbestos disease
9 since the late 1970s. In the early 1980s, did you
10 have the same or different view that you have now
11 about whether chrysotile fibers can cause
12 mesothelioma in humans?
13 A I had basically the same view.
14 Q I want to provide a context, a historical
15 context. When Quebec miners and millers were
16 getting mesothelioma that was being documented in
17 the literature in the 70s and early 80s, as you
18 recall, what conclusion was generally drawn from
19 that exposure and that result?
20 A That chrysotile asbestos was the cause of
21 the disease.
22 Q In fairness, did a school of thought amid
23 some researchers begin to take hold of the idea
24 that it is the tremolite in that dust that
25 exclusively causes that disease?
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1 A I dont know how the time frame of
2 exclusively was used, but they began to define the
3 presence of tremolite as a questionable
4 contributor to some level. I might add, too,
5 something called tremolite, which may or may not
6 be asbestos.
7 Q Just in terms of general time frame, am I
8 accurate that, as Dr. Case says, in the early 80s
9 chrysotile causes mesothelioma, look at the miners
10 and millers. Then a hypothesis emerged among some
11 that it was really a contaminant form of asbestos
12 causing disease?
13 A That was the premise, yes, that some
14 reported or suggested.
15 Q Do all papers that have looked at those
16 miners and millers attribute the mesothelioma to
17 the tremolite to the exclusion of the chrysotile?
18 A No.
19 Q Are you familiar with the Begin paper,
20 Work-Related Mesothelioma in Quebec, published in
21 the American Journal of Industrial Medicine in
22 1992?
23 A I am.
24 MR. SIMON: Which, Your Honor, I would
25 now offer as Plaintiffs Exhibit 28.
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1 MR. SCHACHTER: No objection. It has
2 probably been in three times.
3 THE COURT: I think it is in already.
4 I dont mind getting one more copy. I just cant
5 promise you I am going to read it every time, one
6 for every time you give it to me.
7 MR. SIMON: Your Honor, can I remark
8 it as 42?
9 THE COURT: He says 43.
10 MR. SIMON: Can I reoffer it as 43?
11 THE COURT: I will receive 43 into
12 evidence.
13 (PLAINTIFFS EXHIBIT NO. 43 RECEIVED)
14 QUESTIONS BY MR. SIMON:
15 Q Looking at these populations of miners and
16 millers from one mining area to the other, Page
17 540, to what do the authors attribute the apparent
18 number of more mesotheliomas in one mining area of
19 the Quebec than to another?
20 A Well, their conclusion that it was likely
21 not the tremolite contamination that was the
22 difference between the mesothelioma occurrence in
23 the areas. But rather the number of people
24 working in those areas, in that exposure setting.
25 Q What does that mean?
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1 A Well, I believe their conclusions were
2 based on levels of tremolite in the ore and/or air
3 in that area versus the area with the higher,
4 supposedly higher incidence of meso. They are
5 relating it to exposed numbers of workers, I
6 think, in their conclusion.
7 Q Do the authors — the authors observed in
8 the abstract: In the mining towns of Thetford and
9 Asbestos the incidence of mesothelioma was
10 proportional to the workforce, thus suggesting
11 that the tremolite air contamination, which is
12 seven-and-a-half times higher in Thetford, may not
13 be a significant determinant of the disease in
14 these workers.
15 What does that mean?
16 A I think that is what I tried to say in
17 more simplistic terms possibly. Number of people
18 exposed in a work force.
19 Q If more people have exposure in one area
20 than in another, there is more opportunities for
21 mesothelioma to arise?
22 A Yes.
23 Q But it says: Furthermore, a recent study
24 of Canadian cases of mesothelioma attributed the
25 disease to amphiboles in the lung tissue –
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1 MR. SCHACHTER: What page are you on
2 now?
3 MR. SIMON: I am sorry. I am on 537.
4 QUESTIONS BY MR. SIMON:
5 Q — either in association with
6 contamination of chrysotile ore or of amphibole
7 tremolite or the contamination of the worksite by
8 occupational use of amphiboles, such as
9 crocidolite, in quality control procedures.
10 Citing McDonald.
11 A major factor in the data
12 interpretation of this study was the small number
13 of cases coming from the primary industry in
14 Asbestos where amphibole was not a significant
15 contamination of the ore, and the fact that
16 asbestos fibers, other than chrysotile, had been
17 used only sporadic in quality control procedures.
18 Citing Case.
19 These observations have lead to the
20 suggestion that chrysotile alone has little or no
21 mesothelioma-producing potential.
22 When I refer to the amphibole
23 hypothesis in this setting, do you understand I
24 mean essentially that hypothesis?
25 A Well, yes. As he states, they have
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1 included in that scenario commercial amphiboles
2 other than just tremolite. He said crocidolite
3 somewhere I think in there.
4 Q Opposite views have also been published.
5 Churg has noted in his review that some cases of
6 malignant mesothelioma are likely produced by
7 chrysotile asbestos. Berry noted at least 10
8 cases of mesothelioma that were acceptable
9 examples of chrysotile-induced mesotheliomas.
10 Are you familiar with that Berry
11 paper?
12 A Yes.
13 Q And more precisely, on May 28, 2005, at
14 Page 132, Line 7 of his deposition, Dr. Case says
15 in response to this question: But what makes
16 sense to you is that there is a legitimate
17 question here about whether chrysotile causes
18 mesothelioma on which qualified, well-intended
19 scientists exist on both sides of that conclusion?
20 His answer is: That is fair. Yeah.
21 You agree with that?
22 A Yes. I agree that there are people with
23 differing opinions on that subject, but that
24 happened to be as I stated in my opinion.
25 Q Did this hypothesis that only the amocite
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1 is at work in causing the mesotheliomas in Quebec
2 miners and millers culminate in some papers
3 published in 1997?
4 A You may have misspoken. I think you said
5 amocite. You mean tremolite?
6 Q Yes. Let me rephrase the question.
7 Did this hypothesis that its the
8 tremolite alone at work in causing mesothelioma in
9 Quebec miners and millers, purportedly anyway
10 according to the authors, reach a conclusion in
11 1997?
12 A I think thats what it was presented or
13 thereabouts the accumulation of several papers and
14 some observations.
15 Q What was the general methodology of those
16 papers? In other words, they look at these two
17 populations. Do they also look in their lung
18 tissue?
19 A There was some tissue burden analysis.
20 Q Which purported to show what?
21 A Residual tremolite.
22 Q This paper, Mesothelioma in Quebec
23 Chrysotile Miners and Millers, Epidemiology and
24 Etiology by McDonald and Case and Churg and Gibbs
25 and Sebastien and McDonald, published in 1997 in
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1 the Annals of Occupational Hygiene. Are you
2 familiar with this paper?
3 A Yes. I have seen the paper.
4 Q In the abstract they say that: There was
5 no indication that risks were affected by the
6 level of dust exposure.
7 That is their conclusion, correct?
8 A Yes.
9 Q Then they go on and say that:
10 Geographical differences both in the Thetford
11 region and between it and Asbestos suggests the
12 explanation is mineralogical. Lung tissue
13 analysis showed that the concentration of
14 tremolite fibers was much higher in Area A than in
15 Area B, a finding compatible with the geologic
16 knowledge of the region.
17 Lung tissue analysis. Number one,
18 according to the paper, do the authors know which
19 fibers were actually in the pleura of these people
20 that got mesothelioma?
21 A I guess there was one issue when I read
22 the paper that was of interest. Sebastien was a
23 coauthor, I believe, and had written the 80 paper
24 saying that the lung may not be a good indicator
25 of what gets to the pleura where the mesos
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1 develop.
2 Q Next, I want to look at what these authors
3 conclude can and cant be drawn actually –
4 significantly about the tissue burden analysis
5 they did based on the methodology they employed.
6 Page 712: Of the 27 cases of mesothelioma for
7 which there was an autopsy, electron microscopic
8 analysis of dried lung tissue had been made in 19
9 miners and millers, including 5 from Asbestos and
10 2 factory workers. Detailed results are in Table
11 1. Given the possible effects of selection, small
12 numbers, inevitable uncertainty of diagnosis, and
13 the absence of control were denominators,
14 questions of risk and causation cannot be
15 addressed.
16 According to the authors, based on the
17 methodology they employed, can they draw causal
18 distinctions based on the differing tremolite
19 levels they found in one autopsy versus the other?
20 A I say no.
21 MR. SCHACHTER: Your Honor, for
22 optional completeness, may I read the rest of it
23 into the record?
24 THE COURT: You may.
25 MR. SCHACHTER: Continuing the
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1 sentence: Nevertheless, the findings summarized
2 in Table 2 are informative. It is fairly clear
3 that tremolite fibers were predominant in the
4 lungs of miners and millers who died of
5 mesothelioma, especially in Thetford mines,
6 although these men were exposed overwhelmingly the
7 chrysotile. However, in the two factory workers
8 and in three of the five miners and millers from
9 Asbestos, there were substantial concentrations of
10 crocidolite.
11 QUESTIONS BY MR. SIMON:
12 Q According to Begin in the 92 paper, the
13 higher incidence of mesothelioma in the Thetford
14 mine as opposed to the Asbestos mine was
15 attributable to what?
16 A Number of exposed individuals.
17 Q Now, you made the point that when you
18 publish on tissue burden analysis, you publish
19 your methodology, correct?
20 A That is correct.
21 Q What kinds of things do you publish on so
22 the reader knows how to interpret your results?
23 A Well, there are a number of things, one of
24 which is the technique used for tissue
25 preparation. The other is what fibers you
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1 include. For example, if you use a count scheme
2 of 5 microns and longer, you would preferentially
3 target the exclusion of chrysotile from a count
4 scheme. One has to also know magnification that
5 you use, and like I said it is very important to
6 know what you include and what you exclude as far
7 as the counted materials unless you skew what you
8 are trying to present or interpret.
9 Q From reading this document, in order to
10 find methodology, would I know whether the
11 electron microscope referred to is a scanning
12 electron microscope or a transmission electron
13 microscope?
14 A Unless there is a methods, I havent seen
15 it. I mean unless there is a methods section
16 somewhere.
17 Q Would I know which asbestos fibers, in
18 terms of length, they counted and which ones they
19 didnt?
20 A I havent seen that indicated in the
21 paper.
22 Q Would I know if the people in Asbestos had
23 a whole lot more chrysotile than tremolite in
24 their lungs or tremolite in their lungs than the
25 Thetford population, but they were of a certain
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1 length that the authors just didnt count? Would
2 I know that?
3 A That is why it is important to define what
4 you include in the count. Yes.
5 Q Would I know whether or not they prepared
6 the autopsy samples in the same way where they
7 chemically digested some but ashed others?
8 A It would be useful information.
9 Q Would I know what their limits of
10 detection were, not just as to length but also as
11 to diameter so if there were lots and lots of
12 really long chrysotile fibers in those lungs that
13 were too narrow for the detection of the electron
14 microscope they used, they wouldnt know they were
15 there, would I know that?
16 A Not unless that was defined.
17 Q Do I know what their controls are? Do I
18 know what they are comparing as the tremolite
19 burden compared to what I am supposed to find so
20 that I can draw conclusions about whether its the
21 tremolite or not?
22 A They indicated an absence of controls, if
23 I read that correctly. Of course, we certainly
24 want to make sure they guarded against
25 cross-contamination.
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1 Q There is an epidemiological component to
2 the paper as well. I am not going to ask you to
3 express epidemiology opinions. I just want to ask
4 you since you are familiar with the paper what
5 confidence interval they used in this paper?
6 A It says 90 percent.
7 Q Whether or not their confidence interval
8 includes 1 in three out of the four calculations?
9 A I dont see that.
10 Q 0.95. 0.27. 0.36.
11 A Sorry. Yes. I certainly would like to
12 have seen the detection limit.
13 Q In the companion paper, Chrysotile
14 Tremolite and Carcinogenicity. Are you familiar
15 with this paper?
16 A I think I have seen this paper.
17 Q Published in 1997 in the Annals of
18 Occupational Hygiene?
19 A Yes. I have seen the paper.
20 Q The authors discuss: Confusion was
21 created by the inevitable difficulty in
22 interpreting findings in workers usually exposed
23 to amphibole chrysotile mixtures in manufacturing
24 and product use. This, in turn, gave rise to much
25 bigger controversy. There were those
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1 investigators of chrysophiles who believe the
2 evidence to show a major difference between the
3 relatively low carcinogenicity of chrysotile and
4 the much higher risk, particularly of
5 mesothelioma, usually associated with amphibole
6 exposure. Others, the chrysophobes, concluded
7 from much of the same evidence that all types of
8 asbestos were equally dangerous.
9 Do you see that?
10 A Yes.
11 Q Is it the same evidence according to the
12 authors or different evidence upon which
13 well-qualified people can reach different
14 conclusions?
15 A Thats what they said.
16 Q Now, the McDonalds, as we saw, reached the
17 conclusion that its tremolite, right?
18 A Yes.
19 Q There is an epidemiological component, is
20 there not, to the work?
21 A I believe there was.
22 Q Done to what confidence interval in
23 reaching the conclusion that it is tremolite at
24 work based upon on achieved epidemiological
25 differences between Area A and Area B?
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1 A It says 90 percent.
2 Q If it is the case legally, I am not asking
3 you to assume it is, I am just saying if it is,
4 that epidemiological data is not valid at 90
5 percent, such that is the distinction being drawn
6 here it is tremolite at work based on
7 epidemiological data that is not valid, then where
8 are we?
9 A I am not an epidemiologist, but I have
10 fundamental questions about data fed into the
11 process to generate the conclusions, particularly
12 when we are using tissue samples and leave out the
13 things we have already talked about as important
14 parameters for description.
15 Q Where were we, at the very least, in the
16 early 1980s on the observation of chrysotile
17 exposure causes mesothelioma in these people?
18 A In the early 1980s?
19 Q Yes.
20 A That it did.
21 Q The fibers themselves?
22 A Yes.
23 Q The Berman & Crump paper, have you read
24 it?
25 A Not in entirety.
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1 Q Have you read portions of that from which
2 you have drawn opinions?
3 A I have looked at some of the executive
4 conclusions of it, I think.
5 Q What concerns, if any, do you have about
6 it as to the portions you have read?
7 A Well, I will not speak to the modeling
8 aspects.
9 What concerned me was the data input
10 or more specifically the data that wasnt provided
11 as an input in that short fiber studies or fibers
12 that show short fibers are present in the sites
13 where mesos develop, for example, was not factored
14 in as I could tell.
15 Q I am not sure I understand your answer.
16 What was not factored in that you
17 think is significant in a risk calculation — I
18 mean the pathological component to it — in a risk
19 calculation about the role of fiber length in
20 causing mesothelioma?
21 A Well, if you are going to reach some
22 conclusions about recommending even longer fibers
23 fall under regulated auspices, it seems reasonable
24 to me to make very sure you include every
25 potential scientific publication that spoke to the
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1 potential of short fibers, which I dont believe
2 they included my data. I dont think they looked
3 at Suzukis. There may be a footnote for
4 Sebastien and his data.
5 I attended the first conference in
6 Oakland and brought up some of these issues from
7 before. In that forum found no one who would
8 refute the fact or be in agreement that the short
9 fibers are the ones that tend to be found more
10 likely in the extrapulmonary sites.
11 Q Let me make sure I understand. You went
12 to a meeting in Oakland where this panel was
13 convened?
14 A Yes.
15 Q What did you do there?
16 A I was in the audience with a number of
17 other people that went there to hear some various
18 presentations. There was a brief period of
19 comment section. At the end — actually I am not
20 sure the long fiber issue arose until late in the
21 day when there seemed to be a concurrence among
22 the more vocal people that longer fibers are all
23 that carry a risk. At that point I simply pointed
24 out to the previous studies of Sebastien and our
25 own studies. I think Suzuki had occurred at that
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1 time.
2 In any case, the scientists did not
3 disagree with me that the short fibers are the
4 ones that preferentially relocated from the lungs
5 to the sites where mesothelioma occurred.
6 Q Then what happened in terms of their risk
7 calculation? Did they build in that body of work
8 demonstrating the role of short fibers?
9 A To my knowledge, they didnt.
10 Q The document is in evidence, the Berman &
11 Crump document. I just want you to assume, as was
12 discussed yesterday, that the Suzuki and Yuen
13 paper from 2001, published in Industrial Health,
14 purported to show that chrysotile fibers alone
15 were the cause of mesothelioma in about 23.3
16 percent of mesotheliomas studied.
17 The Yano paper, published in the
18 American Journal of Epidemiology, purported to
19 show a strong association between pure chrysotile
20 and the development of mesothelioma in two cases
21 were not built into the risk calculation of Berman
22 & Crump. Will you just assume that?
23 A Okay.
24 Q Just as a logical matter, if studies
25 purporting to show strong risk for mesothelioma or
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1 actual causation through tissue burden for the
2 role of chrysotile fibers in causing mesothelioma
3 are not built into the risk calculation, what will
4 that do to the analysis of whether pure chrysotile
5 can cause mesothelioma?
6 MR. LEONE: Objection, Your Honor.
7 There is no foundation. It hasnt been
8 established that the witness is expert enough to
9 answer that question.
10 THE COURT: I think I know the answer
11 to that question anyway. I will see you after
12 lunch. Sustain your objection.
13 (LUNCH RECESS)
14 THE COURT: Please be seated.
15 Mr. Simon.
16 MR. SIMON: Thank you, Your Honor.
17 QUESTIONS BY MR. SIMON:
18 Q Dr. Dodson, what I intend to end with
19 before letting other lawyers ask you some
20 questions for just a couple of issues you discuss
21 in your 2003 paper, Asbestos Fiber Length as
22 Related to Potential Pathogenicity, a Critical
23 Review, because those concepts touch upon some
24 issues you discussed earlier and some issues that
25 other witnesses have discussed.
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1 Here on Page 292 you discuss what is a
2 fiber, as that word is used in the context of
3 asbestos; is that correct?
4 A Yes.
5 Q What is the subject here?
6 A The subject is a regulated fiber as
7 defined under the federal regulations.
8 Q Versus what?
9 A Well, the implications of it being a
10 health-related fiber dimension.
11 Q You say: As a result of the proven role
12 of asbestos in the induction of disease in man,
13 federal agencies have established work practices
14 and exposure levels based on measurements of
15 regulated fibers. The terms, regulated fiber and
16 pathological active fiber, are often liberally and
17 erroneously interchanged.
18 What do you mean by, erroneously
19 interchanged?
20 A The implication is sometimes made that
21 that fiber selection length was based on some kind
22 of a health-related issue.
23 Q What was it actually based upon?
24 A I think it is up at the other part of the
25 next page. It was based as Dr. Langer has defined
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1 on developing a scheme for the light microscope
2 that can allow you to count fibers and get
3 reproducible information within the parameters of
4 the count scheme as can be applied to the same
5 sample between multiple labs.
6 Q How practical would it have been to have
7 required counting asbestos fibers with the
8 transmission electron microscope given the cost
9 and nature of that instrumentality, how practical
10 is that?
11 A It is both costly and there are a limited
12 number of labs that do it. It was defined under
13 another federal regulation, the AHERA rule,
14 governing asbestos work in schools as the
15 instrument for final clearance in most projects in
16 school-related activities. In those conditions a
17 fiber was defined by other dimensions so that
18 basically the same could be achieved. A
19 reproducible based on information between labs on
20 the same standard could be achieved with a count
21 scheme using the transmission electron microscope.
22 Q What problems, if any, do you believe
23 arise if we refer to a regulated fiber as the
24 definition of a fiber that can cause disease
25 instead of considering anything else?
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1 A Well, if you use those dimensions, you
2 exclude a large percent of the fibers, the
3 majority in most cases of the fibers you find in
4 the human lung tissue and other sites. They are
5 shorter than that.
6 Q Are most of the fibers one finds in lung
7 tissue doing tissue analysis fibers which are of
8 a, lets say, smaller dimension than a regulated
9 fiber?
10 A In any of the studies or the vast majority
11 of those that use transmission electron
12 microscopes and count shorter fibers, the data in
13 the tissue reflects that there often is a
14 predominance of fibers less than 5 microns.
15 Q If I am doing tissue analysis and I only
16 count fibers that are 5 microns in length, what
17 types of fibers am I likely to miss?
18 A You are likely to miss the more easily
19 respirable short fibers. You are also likely to
20 miss the long, thin fibers because the light
21 microscope has a detection limit based on the
22 diameter of something it can detect, and they can
23 be quite long and still not be counted even though
24 they exceed the 5 microns. They are too thin.
25 Q Can you have an 80 micron long asbestos
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1 fiber that is not a regulated fiber because it is
2 too narrow to be seen with the light microscope?
3 A Sure. If it could not be included in the
4 count scheme, you cant see it.
5 Q Is there any doubt that an 80 micron long
6 asbestos fiber is the kind of fiber that can cause
7 asbestos disease?
8 A No.
9 Q You talk about the distinction, if any,
10 between a chrysotile fiber and a chrysotile
11 fibril. Dr. Craighead talked about that, too.
12 What is that difference?
13 A Well, a fiber — a fiber is often a term
14 used for the light microscope definition of seeing
15 something. It conforms to the count scheme
16 defining a fiber.
17 Essentially you dont see fibrils with
18 the light microscope. They are too thin, no
19 matter what the length is. That requires you to
20 go to the next level of instrumentation to be able
21 to determine their presence.
22 Q Can there be in the lung lots of
23 chrysotile fibrils that are long, but narrow?
24 A Yeah, there can be. In fact, Dr. Langer
25 has commented in several of his papers that he
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1 considers — I dont know — I dont agree with
2 this totally — he considers bundles of fibers
3 breathed in can go in the lung and break down into
4 thinner and thinner units and become fibrils.
5 Q Can fibrils cause asbestos disease?
6 A They are the ones that you often find in
7 the extrapulmonary sites and, in fact, in tissue.
8 Q Is the chemical composition of a fibril
9 any different than the chemical composition of the
10 fiber?
11 A No, just simply the single unit structure
12 of thickness.
13 Q Lastly, on Page 294 you talk about the
14 fact that: Consideration between — of the
15 relationship between fiber length and the risk for
16 the development of disease frequently includes
17 allowance for the fact that short fibers are
18 cleared more readily from the lungs. However,
19 this is am extrapolation that is of less
20 importance when there are constant infusions of
21 short fibers and result in eventual dust overload
22 which can compromise clearance.
23 Who is the author of that paper?
24 A Castanova.
25 Q Was Castanova one of the panel members?
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1 A That is correct.
2 Q Of the EPA report?
3 A I think that is correct. Yes.
4 Q Going back to your differences with Dr.
5 Craighead on whether a chrysotile fiber load in
6 tissue would have to be recent exposure, my
7 question is if that load came as a result of
8 constant infusions of short fibers, what is going
9 to happen to the clearance rate of chrysotile as
10 breathed into the lung?
11 A There is going to be an impact on the
12 clearance rate, and if in point of fact we accept
13 the concepts that I think most people have agreed
14 with that chrysotile can cause asbestosis, once
15 you begin to get interstitial fibrosis, you get
16 entrapment of materials in place including fibers.
17 Q If we speak in general terms about the
18 fact that short fibers are more readily cleared
19 from the lung, we talked about the fact that
20 cleared may very well mean translocated, right?
21 A Could, yes.
22 Q Must we also account for what if it is a
23 heavy dose exposure and how that is going to
24 affect our assumptions about clearance rates?
25 A And included in the heavy dose exposure
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1 would be repetitious exposures.
2 Q In that regard, does the concept that a
3 short fiber clears more readily exist independent
4 of dose?
5 A I think its a fact given as an exposure
6 under conditions. That has to be reconsidered
7 when you add the variables that we have just
8 spoken about.
9 MR. SIMON: That is all I have at this
10 time.
11 THE COURT: Mr. Leone.
12 CROSS-EXAMINATION
13 QUESTIONS BY MR. LEONE:
14 Q Good afternoon, Dr. Dodson.
15 A Good afternoon, sir.
16 Q You have given a number of opinions this
17 morning and I just want to first establish what
18 you are and are not an expert in. You are not an
19 expert in epidemiology, correct?
20 A That is correct, sir.
21 Q You are not a biostatistician?
22 A That is correct, sir.
23 Q You are not a medical doctor or
24 pathologist?
25 A That is correct.
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1 Q You are not a toxicologist?
2 A That is correct.
3 Q You have talked about industrial hygiene,
4 but you are not a certified industrial hygienist,
5 are you?
6 A That is correct.
7 Q You testified that fiber burden or tissue
8 burden analysis provides you information regarding
9 the number and type and size of fibers found in
10 tissue, right?
11 A Yes, sir.
12 Q The purpose of the tissue burden analysis
13 then is to determine the number of fibers and
14 compare it to a background rate to determine if
15 there was a significant exposure; is that right?
16 A Well, that is part of it. I guess the
17 first question to answer is, is there any asbestos
18 there.
19 Q The first question is, is there any
20 asbestos. The second question would be, how much?
21 A And what type.
22 Q And what type?
23 A Yes, sir.
24 Q Then there are standards, for example, set
25 forth in the Helsinki Criteria that you mentioned
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1 in terms of asbestos bodies or number of fibers in
2 lung tissue which you can then compare someones
3 exposure; is that right?
4 A You can then compare your findings with
5 other people who have published their findings as
6 long as they use the same methods and count the
7 same thing.
8 Q So your opinion at least would be that
9 then you can identify the number of fibers,
10 compare it to a standard, and using that attribute
11 a disease, a mesothelioma, for example, to an
12 exposure in a specific causation kind of way,
13 right?
14 A Well, that is part of it. I think I also
15 included the type fibers and the dimensions of
16 fibers as having some important contributing
17 factors to understand exposure.
18 Q In terms of discussing the relationship
19 between tissue burden studies and causation, you
20 essentially take it as a given that asbestos and
21 all asbestos fiber types cause mesothelioma,
22 correct?
23 A I think they all have the potential to
24 cause mesothelioma. Yes, sir.
25 Q So when you are doing — you are not
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1 relying on the fiber burden analysis to determine
2 that asbestos fibers in general cause
3 mesothelioma. You are just applying it in a
4 specific case, right?
5 A In a specific case to learn what is in the
6 tissue. Yes.
7 Q But your assumption underlying all of that
8 is that all asbestos fibers cause mesothelioma?
9 A Asbestos-related diseases including
10 mesothelioma. Yes.
11 Q A tissue burden analysis can show
12 exposure, but in and of itself it cannot prove
13 that a substance is a carcinogen, right?
14 A It would prove exposure to a substance
15 that had been defined as a carcinogen, I guess.
16 Q If there is a prior definition that a
17 substance is a carcinogen, then you can use the
18 tissue burden analysis to prove exposure, right?
19 A Yes.
20 Q I know the Court has heard about SV40.
21 But, for example, that is a substance that is
22 found in mesothelial tissues. The fact it is
23 found in the tissue doesnt prove it causes the
24 disease, in this case, mesothelioma, correct?
25 A Fair.
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1 Q When you do your tissue burden analysis,
2 you dont just find asbestos fibers. You find a
3 lot of fibers and dust in tissue, correct?
4 A You do generally find other types of dust.
5 Yes.
6 Q The presence of a dust in lung tissue or
7 even pleural tissue or lymph nodes or the other
8 places you look, that doesnt prove that material
9 causes a disease, does it?
10 A Not specifically.
11 Q You were asked your questions about lung
12 cancer, and how asbestos fibers cause lung cancer,
13 and then asbestos fibers can travel to the pleura.
14 Cigarette smoke also causes lung cancer, correct?
15 A Yes.
16 Q Cigarette smoke contains a great number of
17 carcinogenic substances, right?
18 A Thats true.
19 Q Substances like PAHs?
20 A Yes.
21 Q Do those sorts of substances also make it
22 to the lymph nodes in the pleura and
23 extrapulmonary sites?
24 A I am not sure about the measurements of
25 those sites. They make it to extrapulmonary
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1 sites. Yes. Yes.
2 Q There you have substances that are known
3 carcinogens, they are in extrapulmonary cites, but
4 you would not say cigarette smoking causes
5 mesothelioma, would you?
6 A They transfer through the blood — through
7 the blood, if I recall correctly with that
8 particular one, to other sites. Was your question
9 then about the meso? I am sorry.
10 Q Does cigarette smoking cause mesothelioma?
11 A Not that we know of. No.
12 Q Typically in your tissue burden studies
13 you find both amphiboles and chrysotile, right?
14 A We generally do. That is correct, sir.
15 Q Are you familiar with an article that we
16 have marked it as Defendants Exhibit 8 by Boutin
17 on black spots?
18 A Yes, sir.
19 Q Let me just show you a copy. It is
20 Defendants Exhibit 8.
21 THE COURT: I have a copy.
22 QUESTIONS BY MR. LEONE:
23 Q You are familiar with this study, Dr.
24 Dodson?
25 A Yes, sir.
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1 Q You dont have any criticisms of the
2 methodology use by the authors of this study, do
3 you?
4 A I dont recall I do.
5 Q You are familiar with the authors work and
6 you regard it as good, scientific work?
7 A Yes.
8 Q The investigators of this study were
9 testing the hypothesis that asbestos fibers might
10 congregate in certain parts of parietal pleura
11 called black spots?
12 A Well, they become black spots because of
13 the pigmentation that locates there. Yes. Thats
14 what they are called after the fact.
15 Q In doing that analysis, they found that
16 they said — in the abstract it says, second
17 sentence: We hypothesized that the distribution
18 of the asbestos fibers in the pleura was
19 heterogeneous and they might concentrate in
20 certain areas, as does coal dust in patients
21 showing anthracotic black spots of the parietal
22 pleura during thoracoscopy.
23 Then what they found here was that
24 amphiboles outnumbered chrysotile fibers in all
25 the samples, right?
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1 A Yes, sir. Including the lung, if I
2 recall.
3 Q They found, also, just in the abstract
4 here a total of 22.5 percent of the fibers were
5 greater than 5 microns in length in the black
6 spots, right?
7 A Yes.
8 Q Looking solely at patients with
9 mesothelioma on Table 3, they found that 100
10 percent of the fibers in the diseased pleural
11 tissue hot spots were amphibole fibers?
12 A Yes.
13 Q So although you have talked about short
14 chrysotile fibers being found in the pleura and
15 certainly your studies show that, this study, for
16 example, find long amphibole fibers in the pleura
17 including with people who have mesothelioma,
18 right?
19 A Sure. In this study it includes people
20 that have — that had considerable amphiboles in
21 their lungs.
22 We also indicated, as I said as an
23 exception to the other two studies, that
24 amphiboles reach the pleura in our study, too.
25 Q In general, you cannot determine a
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1 particular source or a product from which an
2 asbestos fiber comes by looking at tissue burden
3 samples, right?
4 A Generally, thats true. Yes, sir.
5 Q You have done studies on backgrounds, that
6 is, asbestos fibers present in the lungs of people
7 without occupational exposure, right?
8 A Thats true.
9 Q For example, you did a study of folks in
10 East Texas that has been published?
11 A Yes, sir.
12 Q You found that 23 of 33 people had
13 asbestos fibers in their lung?
14 A Of some type, yes, sir.
15 Q Those who had asbestos in their lung had
16 an average concentration of 120,000 fibers per dry
17 gram, right?
18 A For the ones that had asbestos in their
19 lungs, yes, that is correct.
20 Q Even people without mesothelioma can have
21 chrysotile fibers in their lungs, right?
22 A 14 out of the 33 were positive in that
23 study.
24 Q I think you stated that all members of our
25 society are exposed to asbestos-containing
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1 environments and indeed have asbestos fibers in
2 their lungs?
3 A Well, actually I said there were 26 out of
4 the 33 that were positive, which meant there were
5 some that I had no known within the detection
6 limit found in their tissue. The first of part of
7 that is, yes, we have products around us and have
8 had. The second part I am not as sure of now that
9 all of us have asbestos fibers in our lungs.
10 MR. LEONE: Go ahead and mark this as
11 the next exhibit. This is 47.
12 QUESTIONS BY MR. LEONE:
13 Q Doctor, this is an article that you wrote?
14 A Long time ago, yes.
15 Q The second sentence of the abstract
16 states: Since all members of our society are
17 exposed to asbestos-containing environments and
18 indeed have asbestos fibers in their lungs, the
19 concern exists as to its significance in
20 contributing to the incidence of lung cancer.
21 At that time did you write that all
22 members of society have asbestos fibers in their
23 lungs?
24 A I probably believed that more then. Yes.
25 Q The presence of chrysotile in lung tissue
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1 doesnt mean that chrysotile in and of itself
2 causes mesothelioma, right?
3 A No. In this group they were also
4 primarily blue color workers, which you would
5 expect to have more opportunities for exposures.
6 Q You talked about counting fibers and how
7 you count all fibers over .5 microns in length?
8 A Yes, sir.
9 Q Other labs like Dr. Rogglis lab, for
10 example, only count fibers longer than 5 microns,
11 right?
12 A Dr. Roggli counts those longer than 5
13 microns that he can see within the magnification
14 and the technique that he uses, which he uses –
15 as I said to count a fiber whatever length you
16 have set, you have to be able to first see it.
17 There are limits to the SEM.
18 Q You believe it is legitimate to have
19 different approaches to counting fibers in tissue
20 burden studies, dont you?
21 A Different approaches?
22 Q Yes.
23 A Could you define that? I am sorry.
24 Q Sure. Well, during your deposition we
25 discussed the different methodologies. There are
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1 a number of different methodologies for tissue
2 burden analysis?
3 A There are different options. Yes.
4 Q You choose to count shorter fibers. But
5 it is legitimate just to count longer fibers as
6 long as you report thats what you are doing,
7 right?
8 A I think as long as you report what you
9 included, which means diameter as well as length.
10 Then not try to extract information that applies
11 to someone who has done a different type of count
12 scheme. You have to be very careful with that
13 kind of comparison.
14 Q You believe it is appropriate to compare
15 different count schemes of the different methods?
16 A Yes, sir. I do.
17 Q You dont calculate any sort of error
18 range or confidence intervals in the results of
19 the tissue burden analyses that you do, do you?
20 A I think in some of our papers the
21 statisticians have.
22 Q Your deposition in this case was taken May
23 21, 2005. On Page 103 in that deposition I asked
24 you, Dr. Dodson: Have you calculated an error
25 range or confidence intervals on the results that
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1 you report in your studies?
2 Your answer was: No. That is simply
3 what we find.
4 Right?
5 A We report what we find. We also report
6 detection limits. That indicates the level of
7 sensitivity of the method.
8 Q But you dont calculate error ranges or
9 confidence intervals, right?
10 A I think in a couple of papers the
11 statisticians probably did.
12 Q When I asked you that in your deposition
13 that was your answer?
14 A I did give you that answer.
15 Q I believe in your direct testimony you
16 indicated that fiber burden analysis is
17 essentially a snapshot in time, and that tells you
18 — may tell you what fibers were present at the
19 time the analysis is being done. But that doesnt
20 necessarily tell you what was going on 40 years
21 earlier, right?
22 A Thats true.
23 Q You indicated that chrysotile fibers are
24 cleared quickly. So it may be that the chrysotile
25 fibers that you are seeing in the lung are ones
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1 that have been there for a long time resulting
2 from the large exposure or they may be ones that
3 came in relatively recently, right?
4 A That is fair.
5 Q Amphiboles clear over time as well, but
6 much more slowly; is that right?
7 A If they are of the same length, there is
8 no logical reason why they couldnt clear.
9 Q Sometimes there are fiber burden analyses
10 that dont find any amphiboles present with people
11 we know were exposed to amphibole-containing
12 products, right?
13 A I am trying to think the reference point
14 you are making. Is it possible?
15 Q Because amphiboles can clear or because
16 sampling errors simply might not identify the
17 fibers, right?
18 A Either of those are possibilities. Yes,
19 sir.
20 Q I believe in your direct you actually
21 talked about some of the limitations on fiber
22 burden studies including that there are — you are
23 looking at just a small piece of tissue, right?
24 A What I said was you ideally try to take
25 multiple sites to sample to cover yourself for
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1 random sampling issues as best you can. Yes, sir.
2 Q It is important that laboratories have
3 quality control procedures to avoid contamination
4 of samples. You talked about some of that on your
5 direct as well, right?
6 A Yes, sir.
7 Q Because, in fact, tap water reagents,
8 paraffin filters, and other materials may be
9 contaminated with asbestos fibers, particularly
10 short chrysotile fibers, right?
11 A People have suggested that.
12 Q That is why you have gone through these
13 steps to make sure that in your studies your
14 samples are not contaminated, right?
15 A Not just chrysotile, but any other type of
16 asbestos-containing material.
17 Q Lets talk about pleural analysis. You
18 have published some studies that talk about –
19 that analyze for asbestos fibers in lymph nodes
20 and pleural plaques, right?
21 A Yes, sir.
22 Q You have not done — you have not
23 published any studies that talk about asbestos
24 fiber in the pleura, other than in pleural
25 plaques, correct?
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1 A I think thats true.
2 Q We will talk in a minute about Dr.
3 Suzukis article, but there are not a large number
4 of studies that replicate that kind of analysis,
5 are there?
6 A In the pleura?
7 Q Yes.
8 A That is correct.
9 Q I wont go into details, but basically
10 your testimony earlier was that you found in lymph
11 nodes, pleural plaques, and the peritoneum short
12 chrysotile fibers, but you also found long
13 amphiboles fibers?
14 A A population is what I testified to. Yes.
15 Q In one of the documents that you were
16 shown, the 1990 shipyard study, I want to ask you
17 a follow-up question about that. It is
18 Plaintiffs Exhibit 41. I just have one question
19 about Sample No. 8 there. That was PL is pleura
20 and this is pleural plaque, right?
21 A Yes.
22 Q LU is lung?
23 A Yes.
24 Q NO is lymph node.
25 This was one that Mr. Simon pointed
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1 out that had no chrysotile — chrysotile fibers
2 there — no chrysotile fibers in the lung and 21
3 million in the pleural plaque?
4 A Yes, sir.
5 Q How many fibers did you count to come up
6 with the number of 21 million in the pleural
7 plaque?
8 A I dont know what the detection limit was,
9 if its stated there or not, sir.
10 Q I will give you the article.
11 A Thank you. I have to go back to the data.
12 I cant immediately find that.
13 Q Can you give me a rough estimate? To
14 estimate 21 million fibers, do you need to count 1
15 million fibers or 100 fibers or 3 fibers?
16 A No. Usually our count scheme is 10 grid
17 squares on 3 separate grids to get the count area,
18 which is about 1.32 millimeters, square
19 millimeters.
20 Q How many actual fibers might that turn
21 into, might you actually be counting to come up
22 with a figure of 21 million?
23 A As I said, I would have to get our
24 detection limit. It doesnt seem to be in this
25 paper immediately.
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1 Q Could it be less than 10?
2 A Likelihood is it was not.
3 Q Could it be less than 20?
4 A I would have to guess. I am not going to
5 guess.
6 Q It is something considerably less than 21
7 million?
8 A Yes. There is a multiplier.
9 Q One of your — another study that I
10 believe you were asked about earlier today,
11 Asbestos in Extrapulmonary Sites. This was
12 looking at the peritoneal area. It is Defendants
13 Exhibit 6.
14 In the discussion of that paper you
15 indicated that: Heavier inhaled exposures,
16 especially as evidenced by increased FB counts,
17 and to a lesser extent total amphibole burden,
18 tended to favor the migration of amphibole fibers
19 to these extrapulmonary sites.
20 FB is a ferruginous body or asbestos
21 bodies that we talked about?
22 A Yes, sir.
23 Q Then you concluded that: In this cohort
24 there is a considerable amphibole burden in all
25 asbestos-positive sites sampled. Right?
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1 A That is right. These were amocite-exposed
2 people by and large.
3 Q You found that 67.2 percent of the
4 asbestos fibers in the omentum and 70.5 in the
5 mesentery were greater than 5 microns in length.
6 You also found that asbestos fibers in these sites
7 were predominantly longer amphiboles, particularly
8 amocite, correct?
9 A Thats right.
10 Q That indicates that although you talked
11 this morning about short chrysotile fibers getting
12 to these sites, in fact, significant numbers of
13 longer amphibole fibers get to these sites as
14 well?
15 A I think we were talking about the pleura.
16 This is sort of a different area. The
17 omentum/mesentery is the abdominal.
18 Q Do the asbestos fibers to get to the
19 abdominal area follow the same path of going from
20 the lung to the pleural — to the lymph system and
21 then reaching the peritoneal area?
22 A They follow the same general pathway,
23 although Dr. Kain has shown some rather large
24 pores in the diaphragm that might explain why you
25 can get longer ones in the peritoneum.
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1 Q Nevertheless, in your analysis of pleural,
2 not peritoneal tissue, you have also found long
3 amphibole fibers?
4 A We found some. Yes.
5 Q There was a discussion about the Helsinki
6 Criteria in your testimony this morning. The
7 Helsinki Criteria states: In discussing fiber
8 burden analysis more information is needed
9 regarding the interpretation of fiber burdens in
10 the pleura where samples of tumor tissue before
11 these measures can be used for the purposes of
12 attribution.
13 Although the Helsinki Criteria talks
14 about using lung burden analysis, is it correct
15 that it does not approve using tumor or pleural
16 burden analysis as a means of attribution?
17 A It indicates that more information was
18 needed. I think some of that came out in Suzukis
19 work.
20 Q Do you know if there was ever a revised
21 Helsinki Consensus document that says it is okay
22 to use pleural burden analysis for purposes of
23 attribution?
24 A I dont think there has been a new one.
25 Q Talking about Dr. Suzuki, he uses a
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1 preparation method which is different from yours
2 for some of the samples at least, right?
3 A Well, it appears that he uses some
4 digestion procedures and some ashing procedures
5 both.
6 Q You have testified that ashing can break
7 up fibers into — and fiber bundles into smaller
8 fibers?
9 A I dont use it.
10 Q That is why you dont use it?
11 A Yes. It concerns with whether you may do
12 trauma to the material.
13 Q In terms of Dr. Suzukis article that you
14 mentioned, when he talks about pleural tissue, you
15 dont know whether he is talking about diseased or
16 nondiseased tissue, right?
17 A The paper, as I recall, and I havent read
18 it in a while, talks about tumor tissue,
19 mesothelioma tissue. Then I saw his deposition
20 that said he looked at some control pleura, too, I
21 think.
22 Q In the people with mesothelioma, do you
23 think he just looked at the mesotheliomas or did
24 he look at other pleural tissues as well?
25 A He outlined what he looked at. I am
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1 saying I dont recall specifically what he said.
2 Q This has been marked as Defendants 7
3 apparently. This is the 1991 article by Dr.
4 Suzuki that we are talking about?
5 A These are two of his articles. This is
6 one. Yes.
7 Q He talks about mesothelial tissues, but he
8 never says exactly what the nature of the
9 mesothelial tissues are that he is looking at,
10 does he?
11 A Well, on Page 153, if I read this
12 correctly, it says that he took material from
13 lung, mesotheliomatous tissue, meaning the tumor
14 and hyaline plaque.
15 Subsequently below he does say in lung
16 plaque and in tumor.
17 Q So it is your understanding he is just
18 looking at tumor and diseased tissues?
19 A He says plaque and tumor and lung.
20 Q In your fiber burden analysis, you have
21 never looked at tumorous tissue, have you?
22 A No, sir.
23 Q You try to avoid looking at diseased
24 tissue, right?
25 A We do for tissue burden in the lung. Yes.
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1 Q Are you aware of any published background
2 levels or reference standards for pleural tissue?
3 A The parietal pleura I think he mentioned
4 in either this or in his deposition. I dont
5 recall which one. That he had look at some normal
6 pleura, normal appearing pleura and/or normal
7 pleura.
8 Q Do you know if there were controls that
9 were matched to the mesothelioma cases that he
10 looked at?
11 A Again, in one of those sources he quoted
12 controls. Some of the Mount Sinai studies.
13 Q Do you know if he looked at controls that
14 were matched to the cases that he looked at?
15 A No. I dont know specifically if he
16 matched them.
17 Q Now, substances other than asbestos can
18 cause mesothelioma, correct?
19 A In animal models.
20 Q I believe you testified earlier that there
21 are a certain percentage of mesotheliomas that are
22 idiopathic that cant be attributed to any
23 specific exposure, including asbestos exposure?
24 A I hope what I said is there is a certain
25 number that do not have a correlation with
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1 asbestos exposure but that do not exclude that may
2 have occurred.
3 Q You have noted that it has been published
4 that 15 to 40 percent of mesotheliomas may be
5 idiopathic?
6 A There is a range.
7 Q In addition to ones where you cant
8 confirm an exposure, you do believe there are
9 spontaneous mesotheliomas, right?
10 A I think I said that that possibility
11 exists.
12 Q Now, are people who have — given the
13 common finding of chrysotile in the lungs, are
14 there some people with spontaneous mesotheliomas
15 who may also have at least low levels of
16 chrysotile in their lungs?
17 A You cant exclude that possibility.
18 Q You talked this morning a little about
19 mechanisms. Is it fair to say that we dont know
20 the mechanism by which mesothelioma develops?
21 A Well, mesothelioma develops from dividing
22 cells that are abnormal. Is that what you are
23 asking? I am sorry.
24 Q That would be true of any cancer?
25 A Sure. Yes.
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1 Q We dont know the mechanism by which
2 asbestos may give rise to that situation, correct?
3 A We outlined some options this morning.
4 Q There were some options, but you cant say
5 it is the physical interference or generation of
6 oxygen radicals or both?
7 A Or accumulation of all, sure.
8 Q You talked this morning about how it might
9 be related to asbestos surface area and in
10 reaction from asbestos surface area, but you dont
11 know that is the case, right?
12 A No. It is just one of the various
13 parameters that can induce responses.
14 Q Right. There are differences between
15 reactivity of surface and amphiboles and
16 chrysotile, right?
17 A Yes, different charges and different
18 elemental compositions.
19 Q And, in fact, amphiboles are much more
20 likely to give rise to reactive oxygen species
21 that you talked about this morning because they
22 contain higher levels of iron in their molecular
23 structure?
24 A There is a Molecular Biology article in
25 99 that took exception to that. The amphiboles,
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1 some of them, have iron as part of their elemental
2 composition. But there is apparently a surface
3 iron in low level on chrysotile and the added
4 charges were picking up more iron once it hits the
5 tissue, at least according to that persons
6 study.
7 Q Nevertheless, iron is something that is
8 related to the generation of reactive oxygen
9 species, correct?
10 A It is one mechanism for driving a Fenton
11 reaction. Yes.
12 Q A number of other substances also generate
13 reactive oxygen species, right?
14 A Yes.
15 Q I believe that you testified that we dont
16 know if a fiber needs to be in direct contact with
17 the pleura itself in order to contribute to a
18 mesothelioma, correct?
19 A In regard to the parietal pleura?
20 Q Sure.
21 A It would seem logical that it would have
22 to be at the site thinking about that issue.
23 Q Do you know if the asbestos fiber has to
24 be in direct contact with the cell in order to
25 give rise to a mesothelioma?
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1 A Well, the models in inducing tumors have
2 resulted from contact of fibers with cells.
3 Q In your deposition I asked you, and I can
4 show you: For an amphibole asbestos to give rise
5 to a mesothelioma, does that fiber have to be in
6 direct contact with the cell or do we know?
7 Your answer was: I think we have to
8 answer those questions you already asked more
9 definitively before we can say that.
10 Do you recall that testimony?
11 A There is a list of those questions
12 including that. I think the answer I gave you now
13 was not different than the ones I gave you then.
14 Q You cant say as you sit here today that
15 the fiber needs to be in direct contact with the
16 cell for mesothelioma to arise, can you?
17 A If we are talking about the physical
18 aspect as one of the parameters, the answer is
19 yes.
20 Q You dont know if its the physical
21 aspects or the chemical aspects that give rise?
22 A Or a combination.
23 Q Assuming it is the physical aspect, yes,
24 the fiber needs to be in physical contact. You
25 dont know if that is the mechanism?
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1 A No. But on the others we have to come up
2 with some different explanations of how that
3 process would occur to not denature the product by
4 the time it got there.
5 Q You have talked earlier today about the
6 differences between amphibole and chrysotile, and
7 amphiboles tend to be longer and straighter and
8 chrysotile is curly, and therefore amphiboles can
9 go deeper into the lung, correct?
10 A The longer chrysotile tends to be curly.
11 Yes, sir.
12 Q In your studies you typically find more
13 long amphibole fibers than long chrysotile fibers,
14 correct?
15 A Yes. In a control study they were pretty
16 equal in size. But, yes, in occupational-exposed
17 individuals, amphiboles tend to be longer.
18 Q Amphibole fibers are more durable in the
19 lung and in tissue, correct?
20 A They tend to be less readily removed.
21 Q Now, you are not an expert in
22 epidemiology, and you have said that epidemiology
23 is not your field, right?
24 A Yes, sir.
25 Q You did talk about regulations earlier
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1 this morning, right?
2 A I did.
3 Q You were asked some questions about bans
4 of chrysotile that had been adopted, and
5 plaintiffs have talked about those sort of steps
6 being taken in various places around the world.
7 You havent been involved with any such actions,
8 right?
9 A In what regard?
10 Q Any bans of chrysotile in Northern Ireland
11 or Gabon or anyplace?
12 A Not directly. Only through e-mail
13 communications and questions and answers.
14 Q Then you talked about OSHA and how it does
15 not distinguish between fiber types. In 1986 when
16 the regulations were adopted, was it proven that
17 anthophyllite asbestos was a cause of
18 mesothelioma?
19 A From the standpoint of OSHA preamble?
20 Q Yes.
21 A I dont know if the Finish article had
22 been published by then. It was probably
23 suggested. It was an open issue.
24 Q But OSHA regulated anthophyllite the same
25 as all the other asbestos fibers, right?
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1 A They did.
2 Q You mentioned limitations on optical
3 microscopy. The analytical method for that
4 specified under OSHA is phase contrast microscopy,
5 correct?
6 A For counting fibers on a filter, yes.
7 Q Does that methodology distinguish between
8 chrysotile and amphibole fibers?
9 A It doesnt distinguish between any fiber.
10 Count the fiber as a fiber.
11 Q Counts cellulose fibers as fibers?
12 A If it conforms to the definition of a
13 fiber. Yes, sir.
14 Q If OSHA were to require — if OSHA were to
15 have a distinction between fiber types in its
16 regulations, would people have to use a different
17 analytical methodology to determine fiber
18 counting?
19 A Yes, sir. They would.
20 Q So as a practical matter in an
21 occupational setting, did OSHA determine that it
22 made sense to regulate all fibers the same?
23 A Well, they made the decision that their
24 methodology could not distinguish. Therefore,
25 they set a standard for a count scheme.
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1 Q Now, do you know the basis for these
2 government regulatory findings that treat all
3 types of asbestos as being the same in terms of
4 disease?
5 A I think those are covered in the preamble
6 in the discussion for reviewers or input from the
7 public or other people.
8 Q Do you know if OSHA looked at any studies
9 based on chrysotile only cohorts to make its risk
10 assessment?
11 A I think they looked at those that were
12 reported to be chrysotile only, but I cant quote
13 the specific reference to you.
14 Q Can you identify any of those studies?
15 A In the OSHA documents preamble, no, not
16 from memory.
17 Q As you sit here, are you aware of any
18 chrysotile-only cohorts?
19 A Well, depending on which mine, I guess the
20 Canadian experience could be chrysotile only, the
21 miners.
22 Q Some Canadian miners might be chrysotile
23 only?
24 A That is what is suggested.
25 Q Then earlier Mr. Simon took you through a
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1 1997 article, and he had a number of criticisms of
2 it, but nevertheless it did show that the miners
3 in Asbestos and Thetford did have tremolite in
4 their lungs, right?
5 A That is what was reported.
6 Q So that indicates they were at least
7 exposed to tremolite?
8 A Some were, yes, sir.
9 Q Now, I believe you agreed this morning
10 that long, thin fibers pose the greatest risk of
11 mesothelioma on a fiber-per-fiber basis?
12 A What I think I said, I hope I said was
13 they do if you give them directly to the site.
14 That is the basis upon which that concept has been
15 generated the Pott and Stanton-type models.
16 Q You agree there are respected scientists
17 in the field who believe that fibers less than 5
18 microns in length are not pathogenic for
19 mesothelioma?
20 A Some people have said that.
21 Q We talked about OSHA and how it only
22 regulates fibers longer than 5 microns, right?
23 A We went over the definition of a regulated
24 fiber. Yes, sir.
25 Q We talked about Dr. Roggli earlier in the
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1 day. He believes fibers less than 5 microns do
2 not cause mesothelioma, right?
3 A I dont know that he believes that. I
4 know that is what he counts. But that is an
5 instrument-related phenomena, I think.
6 Q Let me just ask you about a couple of
7 documents. One is an exhibit that we tried to
8 introduce as Exhibit 2 a long time ago. It didnt
9 get introduced and we would like to offer it now.
10 MR. LEONE: We are marking it as
11 Exhibit No. 48. This is the ATSDR Report on Short
12 Fibers. We would like to offer it.
13 THE COURT: Under the current rules,
14 can I let it in?
15 MR. SIMON: Let me just make an
16 objection for the record. I understand the
17 Courts ruling, for example, with respect to the
18 Mamo paper and other papers where an objection was
19 made by one party or another. Gee, this is not in
20 a peer-reviewed journal. It has not been proved
21 up as a learned treatise.
22 THE COURT: Its an e-mail.
23 MR. SIMON: Its an e-mail. But I
24 dont want to waive the objection if that ever
25 ends up being the right objection depending on the
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1 exhibit. Let me go ahead and make the objection.
2 THE COURT: If that was the right
3 objection, this hearing is reversed 17 ways from
4 Sunday by either side. If the Supreme Court
5 decides I should have been excluding hearsay and
6 nonauthenticated documents all along, then I was
7 right and all of you were wrong.
8 I will respectfully overrule your
9 objection and receive Defendants 48 into
10 evidence.
11 (DEFENDANTS EXHIBIT NO. 48 RECEIVED)
12 QUESTIONS BY MR. LEONE:
13 Q Dr. Dodson, you have seen this document
14 before, right?
15 A I have seen it.
16 Q Its a report prepared for the ATSDR,
17 which is the Agency for Toxic Substances and
18 Disease Registry, which is a branch of the
19 Department of Health and Human Services, correct?
20 A Yes.
21 Q Its a report of an expert panel on the
22 health effects of asbestos and synthetic vitreous
23 fibers as it relates to the influence of fiber
24 length, correct?
25 A Yes.
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1 Q It reflects the discussions of a panel
2 that consisted of Bruce Case, Morton Lippmann,
3 James Lockey, Ernest McConnell, Brooke Mossman,
4 Guenter Oberdorster, and William Wallace, right?
5 A Yes.
6 Q These are people whose work you respect,
7 correct?
8 A I am aware of their work and have quoted
9 it.
10 Q Let me ask you about just a couple of
11 passages. On Page V, the fifth page into the
12 document. It says –
13 A Is that 316?
14 Q Page V. Let me show you my copy.
15 A All right, sir.
16 Q On Roman Numeral V it states, Factors that
17 Influence Toxicity, and it says: Health effects
18 from asbestos and SVFs ultimately are functions of
19 fiber dose, fiber dimension (length and diameter),
20 and fiber durability or persistence in the lung
21 (as determined by the mineral type, the amorphous
22 or crystalline structure, or surface chemistry).
23 Correct?
24 A Yes.
25 Q You agree with that statement, right?
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1 A Basically.
2 Q Then let me just put it up here. This
3 expert panel considered the cancer effects of
4 short fibers and it states: Given findings from
5 epidemiologic studies, laboratory animal studies,
6 and in vitro genotoxicity studies, combined with
7 the lungs ability to clear short fibers, the
8 panelists agreed that there is a strong weight of
9 evidence that asbestos and SVFs shorter than 5
10 microns are unlikely to cause cancer in humans.
11 Do you see that?
12 A I see it.
13 Q Let me ask you about another document
14 then. This is the Berman & Crump final draft,
15 Exhibit 15. You were asked about this document in
16 your direct, and I believe you indicated that you
17 had not read it, correct?
18 A I think I said I have seen the executive
19 summary.
20 Q Let me ask you how this came about. You
21 mentioned that you were in a conference in
22 Oakland. When was that?
23 A It was several years ago. I dont
24 remember which. It was the first one they had to
25 start these discussions, as I understood it.
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1 Q On the first page of the document in the
2 executive summary it states, second paragraph:
3 The current report is a revision to a version
4 originally submitted on September 4, 2001 which
5 was the subject of a peer-reviewed consultation
6 held in San Francisco on September 25-26, 2003.
7 Is that the meeting you attended or do
8 you think there was a different one?
9 A I think there was a preliminary meeting to
10 that.
11 THE COURT: What page were you on?
12 MR. LEONE: Page 1.1 of the executive
13 summary, the second paragraph.
14 THE COURT: Yes.
15 QUESTIONS BY MR. LEONE:
16 Q There was a meeting. There was a draft
17 that was submitted or a report prepared on
18 September 4, 2001. Then there was a peer-review
19 paneling in 2003. Then in the fall of 2003 this
20 document came out, right?
21 A Yes.
22 Q This was meant to be an update of EPAs
23 risk assessment which had originally been adopted
24 in 1986, correct?
25 A The EPA is periodically mandated to review
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1 that.
2 Q Its appropriate for EPA every 15 or 20
3 years to take a look at the data underlying their
4 risk assessments including for asbestos, right?
5 A Sure.
6 Q In terms of fiber size, this report, Page
7 6128, the top of the page, there is a discussion
8 of fiber length. It concludes that fibers less
9 than a minimum length, between 5 and 10 microns,
10 do not appear to contribute to risk, correct?
11 A Yes. Thats what they say.
12 Q That is based on a number of things
13 including analysis of animal studies, right?
14 A Some animal studies.
15 Q They refer in here to the Stanton
16 hypothesis that you mentioned?
17 A Yes.
18 Q They also refer to Dr. Pott, who you also
19 mentioned?
20 A They did mention Pott.
21 Q They looked at the animal data that you
22 also looked at, correct?
23 A Some of it. Yes.
24 Q In addition to looking at the animal data,
25 however, they also as indicated on Page 1.3, the
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1 bottom of the page, they talk about epidemiology
2 studies, and say: The existing asbestos
3 epidemiology database consists of approximately
4 150 studies, of which approximately 35 contain
5 exposure data sufficient to derive quantitative
6 exposure response relationships.
7 And this report provides an analysis
8 of those epidemiological studies. But that is not
9 something you have looked at or can comment on,
10 correct?
11 A No.
12 Q Finally, there was a — you had raised the
13 issue that Berman & Crump did not look at Dr.
14 Suzukis analysis?
15 A I didnt recall they did.
16 Q Exhibit B to what you have there is the
17 report of the peer-consultation workshop, page 315
18 of that document. Maybe I can pull it out and
19 help you find it. There is a lot there.
20 Q Page 315 of the peer-reviewed report
21 indicates, the third paragraph from the top:
22 During this discussion one panelist reviewed a
23 publication, Suzuki and Yuen 2001, that was
24 mentioned in the workshop. The publication
25 documents the amounts and types of asbestos fibers
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1 measured in samples of pleural plaques and tumor
2 tissue collected from legal cases.
3 Then this analysis lists several
4 criticisms of the study, including that the
5 samples were analyzed using a nonstandard
6 technique without any controls. Questioned the
7 major finding of fibers in the pleura because it
8 was actually tumor tissue. Noted the Boutin study
9 that we talked about.
10 Does this indicate at least that
11 Berman & Crump were aware of the Suzuki and Yuen
12 study, correct?
13 A It indicates this panel, as best as I
14 could tell, did not include Sebastien or my study.
15 Did not like Suzukis study. But Boutin, I dont
16 think he had controls he liked. He selectively
17 picked which one he liked out of the group.
18 Q But nevertheless, the authors of the
19 Berman & Crump study were aware of those analyses,
20 right?
21 A Those two. They apparently were not aware
22 of Sebastiens and mine.
23 Q Included also in the Berman & Crump
24 analysis there is a discussion of human pathology
25 studies, right?
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1 A There is a section, as I recall.
2 Q But your criticism is they just — they
3 mentioned a number of studies, but they dont
4 mention yours?
5 A I think the number of the studies they
6 rely on count longer fibers. That will set you up
7 with a bit of a bias if you include longer fibers
8 as part of the findings and dont count all the
9 fibers.
10 Q Do you know if the Berman & Crump analysis
11 as it relates to fiber length was based on fiber
12 tissue burden analysis as opposed to animals and
13 epidemiological studies?
14 A Supposedly originally it included all
15 factors. I cant tell you now that it did from
16 all factors without going through it.
17 Q If there is no threshold for mesothelioma,
18 and if certain scenes of Canadian chrysotile
19 contained 1 percent tremolite, could that 1
20 percent tremolite account for the mesotheliomas
21 that have been found in the Canadian mines?
22 A That is a very tough call. Thats what
23 people have tried to present. Particularly some
24 of my Canadian colleagues. Obviously that is a
25 minority fiber. Majority being chrysotile.
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1 Q Nevertheless, I think you have agreed that
2 amphiboles are more likely to bio-accumulate in
3 the lungs, right?
4 A Depending upon the size that you breathe
5 in of the amphiboles. They are longer fibers. In
6 the population of exposed material, yes. Yes.
7 Thats true.
8 Q Now, at the very beginning you were
9 discussing American sources of crocidolite. Was
10 any crocidolite imported from Australia to
11 America?
12 A I dont recall how much, if there was.
13 Q You indicated that you charge $800 for
14 your hour — per hour for your time when you are
15 in court. You have been here for a good deal of
16 this week. Are you billing at the $800 rate?
17 A No. I bill $250 an hour when I am sitting
18 around.
19 Q Your hourly fee has doubled over the last
20 six years, right?
21 A It has gone up. I dont know if its
22 doubled or not.
23 Q You have been testifying in asbestos cases
24 more or less continuously since the 1970s?
25 A Not continuously. Over that period of
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1 time I have testified, yes.
2 Q Thank you very much.
3 A Yes, sir.
4 THE COURT: Mr. Schachter.
5 CROSS-EXAMINATION
6 QUESTIONS BY MR. SCHACHTER:
7 Q Sir, I would like to start with your
8 discussion of the McDonald studies, and I put up
9 what we showed before. You and Mr. Simon focused
10 on this paragraph from the 1997 publication. Just
11 so we have the record clear, this is an article
12 that appeared in the Annals of Occupational
13 Hygiene, Volume 41, No. 8, at Page 707-729 in
14 1997, correct?
15 A Yes, sir.
16 Q This was one of the major articles that
17 was published at the time by the McDonalds on
18 Mesothelioma in Quebec Chrysotile Miners and
19 Millers, Epidemiology and Etiology, correct?
20 A Yes.
21 Q Many of your criticisms focus on this one
22 paragraph; is that correct?
23 A Well, I think my criticism was a comment
24 that I didnt know exactly how they did their
25 analysis. I can expand on that, if you like.
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1 Q I think I got most of it.
2 What you said is you didnt even know
3 what kind of microscope they had used?
4 A I know what Dr. Churg uses and I know what
5 he includes in his counts on past publications.
6 Q You said you could not tell what kind of
7 microscope was used by the researchers who did all
8 this analysis, correct?
9 A I think the question was, could I
10 determine from that? The answer is, no, sir, not
11 from that only because I know the people.
12 Q Are you basically saying that this isnt
13 good science because the methodology by which the
14 lung tissue analysis was done was not set out?
15 A Well, no. What I am saying is that Dr.
16 Case and Dr. Churg sometimes count different
17 things. Quite often actually.
18 Q You would want some explanation of that,
19 right?
20 A If we are going to make conclusions and
21 Dr. Churg counts short fibers, which to my
22 knowledge he always has, and Dr. Case sometimes
23 includes only 5 microns and longer, which he often
24 does, then to make those conclusions I think it
25 would be helpful to have that information
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1 comparison. I dont know that as we sit here.
2 Q Is it your testimony to the Court that
3 when these results were published, the authors did
4 not make known their methodology for the lung
5 tissue analysis?
6 A I am only speaking from the paper. I
7 didnt see it in the paper as it was shown to me.
8 Q You are aware, are you not — I am going
9 to show you another article that was published in
10 the same journal in the supplement to the same
11 edition. That is, the Annals of Occupational
12 Hygiene, Volume 41, September 1, Supplement 1,
13 Page 231, 1997. You, of course, were aware when
14 you gave your past testimony that this article was
15 published at the same time, were you not?
16 A I think I recall that.
17 Q You recall then that this article provided
18 a detailed discussion of precisely what methods
19 were used by these researchers when they did their
20 tissue burden analysis?
21 A No, sir. I dont recall that.
22 Q For example, on your criticism of the
23 microscope where you said you didnt know which
24 microscope was used, in their methods section,
25 they explained in the second paragraph that:
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1 Fiber identification was performed using energy
2 dispersive x-ray spectrometry, EDS, coupled with
3 transmission electron microscopy, TEM. Correct?
4 A Yes, sir. Thats what they say.
5 Q In terms of the fiber analysis and methods
6 they explain that: Detailed methods of fiber
7 analysis are available in the references cited.
8 Correct?
9 A Thats what it says.
10 Q They do — at the end of the article do
11 you recall that they included footnotes or
12 references that had each of the citations where
13 they had taken their analysis?
14 A No. I was only commenting about the other
15 article. I did not recall that from this. No,
16 sir.
17 Q They also said: All analysis but one
18 included fibers of all lengths greater than 3.1.
19 Basically they went through exactly
20 how they had done this. They solicited results
21 from others who had already published on members
22 of this cohort. They went through in detail what
23 their methodology was.
24 A It actually says there they included
25 filter bleach digestion and low temperature
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1 ashing. Not to be picky, but I dont think Andy
2 Churg uses ashing. He uses just bleach, as far as
3 I know.
4 Q Where are we talking about?
5 A Bottom of that first paragraph before we
6 have fiber indication highlighted. Right above
7 that.
8 Q All analysis include filtered bleach
9 digestion. Low temperature ashing had also been
10 use in specimens prepared in the McGill
11 laboratory.
12 A Right.
13 Q They have explained that some of the
14 specimens came from McGill. Some came from other
15 researchers, right?
16 A Yes.
17 Q They were very clear to try to explain it,
18 and in the references — among the references they
19 have an article by Dr. Churg, Churg, A., Wright,
20 L., Wright and Vedal, 1993, and that article also
21 sets forth in detail what the counting methods
22 were and what the analysis was. That is Exhibit
23 50. Let me hand that to you. Would you agree
24 with that?
25 A Dr. Churg generally does. Yes.
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1 Q This is Exhibit No. 49, Defendants
2 Exhibit No. 49.
3 MR. SCHACHTER: May I give the
4 Court a copy of 50 and 40?
5 THE COURT: Sure.
6 QUESTIONS BY MR. SCHACHTER:
7 Q And, in fact, not only was this published
8 in the supplement of the same volume, but in the
9 materials that you referenced in the portion of
10 the earlier article on lung tissue analysis where
11 they talked about their methodology, the authors
12 of the McDonald study specifically referenced the
13 Case, et al, 1997 paper that set out the
14 methodology, didnt they?
15 A That is what it says.
16 Q If you really wanted to know what kind of
17 microscope was used, all you had to do was turn to
18 the supplement in the same volume and that
19 information was there, correct?
20 A If you track that down it was. Yes.
21 Q You are not fussing at these scientists
22 for putting the details of their lung tissue
23 analysis in a supplement, are you, to the main
24 volume where their general conclusions appear?
25 A No. I think the answer to my question was
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1 from that it wasnt obvious. If the supplement
2 includes it, then that explains it. There is
3 still a difference in the supplement of technique.
4 Q When you were going through the direct
5 examination with Mr. Simon, and I heard his
6 question that how very precise it was, how based
7 on this document alone –
8 (PAUSE)
9 THE COURT: I am sorry. Go ahead.
10 QUESTIONS BY MR. SCHACHTER:
11 Q When you were preparing for your direct
12 examination during the days that you have been
13 sitting here waiting to testify, was that part of
14 your preparation for this that the question would
15 focus on this document alone so that you wouldnt
16 be asked about what was in the supplement, or were
17 you simply unaware there was a supplement?
18 A No. I wasnt asked about that. Im not
19 sure I was asked about this document per se.
20 Q Doctor, there was another point where I
21 thought the question perhaps didnt allow you to
22 give all the information you have.
23 You were discussing why you would not
24 be able to determine whether there were fibers of
25 asbestos in the tissue from a person who had
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1 mesothelioma, do you recall earlier, in
2 Mr. Simons direct examination?
3 A Well, if they are there, you should be
4 able to determine that they are there. I am
5 sorry. Maybe I didnt understand your question.
6 Q I apologize. I am done with the articles
7 that you are holding in your hands.
8 There was a discussion about cytology,
9 where pathologists get fluid, put a needle into
10 the pleura, get fluid, and then they do certain
11 tests. That is one technique pathologists can use
12 to diagnose mesothelioma. Do you recall that?
13 Q Sure. That is cytology.
14 Q Cytology does not provide sufficient
15 specimens to allow a fiber burden analysis to
16 occur, right?
17 A I dont think anyone has ever looked at
18 it. I would not consider it to be a useable
19 sample to disperse cells.
20 Q There is something else called a needle
21 biopsy, correct?
22 A Yes, sir.
23 Q That gets a very small specimen, and it,
24 too, does not give you enough material to see what
25 kind of fibers are in the lung, correct?
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1 A Well, it is not of the lung. It is
2 actually of the –
3 Q Of the tumor?
4 A Of the tumor, yes, sir, which is outside
5 of the lung.
6 Q Is that also called aspiration biopsy
7 specimens?
8 A No. That is a washing generally.
9 Q You are aware that pathologists also have
10 other tools that are not as invasive as doing a
11 full incision and taking out the lung? That
12 extrapleural pleural(sic) pneumonectomy that you
13 and Mr. Simon talked about, correct?
14 A I think that was a treatment mode we were
15 talking about or intervention mode.
16 Q You are aware that specimens can be
17 obtained by a thoracoscopy, correct?
18 A Yes.
19 Q That involves taking a tube and putting it
20 into the lung, getting to the place where the
21 tumor exists, and taking a specimen that way,
22 right?
23 A That is a lung cancer, I think, you are
24 talking about there.
25 Q Can that also be used for mesothelioma?
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1 A I dont know that one would use that for
2 mesothelioma because you would puncture the lung
3 going in the wrong direction.
4 Q Maybe they dont come in through the lung.
5 Maybe they go through the skin and get there. Are
6 you familiar with a procedure that just uses a
7 little tube that is inserted?
8 A Camera assisted?
9 Q Yes.
10 A You can do that. Yes.
11 Q The notion that there wouldnt be tissue,
12 wouldnt you agree in most cases of mesothelioma,
13 the medical authorities now recommend getting a
14 tissue specimen in order to secure the diagnosis,
15 not merely relying on cytology or needle biopsy?
16 A Well, the biopsy, if taken in the right
17 place, is a specimen of the tumor tissue.
18 Q Let me ask you if agree or disagree with
19 this from Rogglis textbook: Although with the
20 now commonplace usage of immunocytochemistry in
21 the evaluation of cytologic material, the
22 pathologist may become highly suspicious of the
23 diagnosis of mesothelioma, it remains our practice
24 and that of others to treat exfoliative and
25 aspiration biopsy specimens as screening tests and
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1 to rely on tissue specimens to secure diagnosis.
2 Would you agree with me that that is
3 the current state of the art in 2004 and 2005 from
4 this book, that in most cases the doctors try to
5 get a specimen for the diagnosis?
6 A But that specimen because of the
7 sensitivity that Dr. Roggli describes, it can be
8 done with a needle biopsy in many of the centers
9 such as his.
10 Q We have a disagreement about what a needle
11 biopsy is?
12 A How much it is.
13 Q You have, however, done tissue digestion
14 analysis on specimens secured through the
15 procedure where they get an extra — when they use
16 the procedure that just goes in and gets a small
17 specimen, not a needle biopsy, but the procedure
18 that gives you a bigger sample?
19 A The specimens we have looked at from less
20 invasive methods are lavage that washes the lung
21 or an associated biopsy with a small cutting
22 device. I dont remember we have done one as you
23 have described.
24 Q From a thoracoscopy?
25 A I dont remember we have done anything
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1 with a small sample before.
2 Q We will get to that.
3 THE COURT: We will get to a lot of
4 things starting in ten minutes.
5 (RECESS)
6 THE COURT: Please be seated. Please
7 proceed, Mr. Schachter.
8 QUESTIONS BY MR. SCHACHTER:
9 Q In any event, these authors of the
10 McDonald papers, these are authors for whom you
11 have a great deal of respect; is that correct?
12 A I have quoted them in a number of my
13 articles. Yes, sir.
14 Q You do have a great deal of respect for
15 Dr. Case as someone with whom you have worked?
16 A And communicate.
17 Q And communicate. You have a great deal of
18 respect for him?
19 A We have had a number of interactions, sir.
20 Q These are among the finest scientists in
21 the world who have been investigating asbestos and
22 disease, correct?
23 A They have been working on the Canadian
24 chrysotile issue for a while.
25 Q Now, I think — I have done a very poor
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1 job, I am sure, of drawing this diagram. As I
2 understand it, mesothelioma, although we dont
3 know a lot about mechanisms, is believed to start
4 in mesothelial cells, correct?
5 A Yes, sir.
6 Q Mesothelial cells are on the lining of the
7 pleura, correct?
8 A There are the thin lining. Yes.
9 Q They are about one cell thick, the
10 mesothelial tissues?
11 A Essentially, that is correct.
12 Q So we are talking about a size that is
13 less than 10 microns?
14 A They are flattened, so that is fair. Less
15 than that. Yes.
16 Q So it is a very small thing. Then there
17 is connective tissue in the pleura underneath
18 them, right?
19 A Yes.
20 Q And no one so far as you are aware in the
21 entire peer-reviewed medical literature has ever
22 examined what the number of fibers are in the
23 mesothelial cells, in the healthy mesothelial
24 cells of a mesothelioma victim, correct?
25 A I dont remember if Suzuki said he did or
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1 not. I dont recall.
2 Q You are not going to tell the Court that
3 you recall seeing a study where the unaffected
4 mesothelial cells have been examined to see what
5 kind of fibers are sticking in them, right?
6 A Not at this time. There will be one
7 before very long.
8 Q There have been no controlled studies
9 examining fibers in the pleura that have looked at
10 — for the mesothelial cells that have looked at a
11 control population and a diseased population to
12 see if the number of fibers of any kind in the
13 pleura are elevated in mesothelial patients,
14 correct?
15 A I think you asked me this in the
16 deposition, and at that point I told you that if I
17 understood Suzukis answer in his deposition, that
18 he had looked at some control, hadnt published it
19 though.
20 Q There havent been any published studies?
21 A That is correct.
22 Q There is a reference to unpublished
23 controls, seven New Yorkers, correct?
24 A Yes. I think that is right.
25 Q We dont have information in the
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1 unpublished — in the reference to unpublished
2 controls that would allow us to say that Dr.
3 Suzuki looked at the mesothelial tissue of healthy
4 individuals, correct? We just dont know?
5 A Well, anyone that looks at it would also
6 look at the interstitium. That layer you have
7 drawn has not been looked at that I am aware of in
8 the controls yet.
9 Q One thing you hope to do in the future is
10 conduct a controlled study where you look at
11 people who have mesothelioma and determine what
12 the fiber level of chrysotile, amocite,
13 crocidolite, and tremolite is in their uninvolved
14 mesothelial tissues, and compare that with the
15 tissue of matched persons, similar age and
16 experience, who dont have mesothelioma, correct?
17 A Well, I think what I said was one step at
18 a time. It is rather labor intensive and time
19 intensive. So we will tell you more eventually
20 about what is in the tissue of the people with
21 meso.
22 Q As we stand here in 2005, we dont have
23 the control studies that can tell us about the
24 fiber burden in the mesothelial tissues? You
25 havent done them yet, right?
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1 MR. SIMON: Objection. Vague as to
2 which mesothelial tissues. Exhibit No. 36 and 37.
3 THE COURT: Overruled.
4 A (By the witness) What I told you in the
5 deposition was Suzuki said he had done some
6 unpublished, and that I had looked at some random
7 samples and found no fibers.
8 Q What you said in your deposition was that
9 you havent completed your controlled studies and
10 they are not ready for prime time and you werent
11 going to come here and tell the Court that you had
12 formed a scientific conclusion about the levels in
13 any of these studies. Is that still correct?
14 A That is still correct.
15 Q Thank you.
16 This proposition — your basic theory
17 is that short fibers may be involved in causing
18 mesothelioma, correct?
19 A Well, my basic theory is that asbestos is
20 involved in causing mesothelioma.
21 Q Yes.
22 A And that short fibers reach the sites as
23 well as some longer fibers.
24 Q You are aware in the current edition of
25 Dr. Rogglis book, he has commented upon your work
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1 and the work of Dr. Suzuki finding short fibers in
2 pleural plaques and other tissues, correct?
3 A I think that is correct.
4 Q Just so the Court is clear, a pleural
5 plaque is something different than the mesothelial
6 tissues themselves, correct?
7 A Pleural plaque is an organized area of
8 essentially scarring.
9 Q It is not the mesothelial tissue, correct?
10 A It started there as a scar. Yes. Its a
11 scarred area on the surface.
12 Q Let me put this up and see how much, if
13 any, of it you can agree with. Lets go to the
14 top of the paragraph there: It should be noted
15 that most of the studies of fiber burden in
16 mesothelioma patients have examined lung
17 parenchyma.
18 That means the lung tissue itself,
19 correct?
20 A That is correct.
21 Q Would you agree with that statement, that
22 most of the studies have looked at lung fiber
23 burden?
24 A I think it is totally correct with the
25 slight modification that the visceral pleura is
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1 oftentimes attached to what they work with.
2 Q Next it says: It is reasonable to assume
3 that fibers actually reaching the pleura are the
4 ones responsible for pleural disease, and the
5 dimensions and types of fibers accumulating in the
6 pleura are of interest in this regard.
7 That is certainly a sentence with
8 which you agree, correct?
9 A Yes.
10 Q You mentioned Sebastien earlier.
11 Sebastien, et al, reported: That individuals
12 exposed to mixtures of fibers, short chrysotile
13 fibers less than 5 microns, tend to accumulate in
14 the pleura whereas longer amphiboles fibers
15 accumulate in the lung parenchyma.
16 Correct?
17 A Thats what it says.
18 Q You agree with that?
19 A Basically.
20 Q Suzuki and Yuen also reported primarily
21 short chrysotile fibers in the pleura and in
22 mesothelial tissues. Those are the studies you
23 have been talking about, correct?
24 A Yes, sir.
25 Q Churg, et al — and, of course, you
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1 respect Churg. He is a very famous scientists in
2 this area, correct?
3 A Andrew Churg is a good scientist.
4 Q Churg, et al, on the other hand found no
5 difference in the length, diameter, or type of
6 fibers isolated from peripheral versus central
7 lung parenchyma in Canadian chrysotile workers.
8 You are aware of those findings, correct?
9 A Yes. We just skipped from the pleura to
10 the parenchyma, but go ahead. Yes.
11 Q Dodson, et al — that is you — found
12 long commercial amphibole fibers in samples of
13 pleural plaque from asbestos workers. And Gibbs,
14 et al, also identified similar fibers in pleural
15 samples of patients with diffuse visceral pleural
16 thickening.
17 Correct?
18 A Somehow in that translation you left out
19 there were short chrysotile fibers there, also.
20 Q It is clear that he is aware of the same
21 literature you have been citing, correct?
22 A Which brings up the question why he left
23 out part of our conclusions and observations.
24 Q Boutin, et al, found a preferential
25 concentration of long commercial amphibole fibers
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1 in black spots on the parietal pleural — I am
2 sorry. We already read that. No. That is
3 another one.
4 Then he says: Dodson, et al, recovered
5 long commercial amphibole fibers from samples of
6 peritoneum and mesentery.
7 Correct?
8 A Once again he left out the fact that there
9 were short fibers there. Yes, sir.
10 Q He had read your studies. Clearly fibers
11 of the type and size known to be associated with
12 the greatest risk of mesothelioma do, in fact,
13 migrate to the pleural tissues. You would agree
14 with that, right?
15 A Some longer fibers in a predominant short
16 fiber population. Yes, sir.
17 Q Then he says this: The identification of
18 short chrysotile fibers in these tissues is of
19 questionable relevance since there is no
20 convincing data that these fibers are pathogenic.
21 Before analysis of pleural tissues can be
22 substituted for lung tissue analysis, proper
23 controls will have to be established including
24 values expected for normal pleura from nonexposed
25 individuals and for metastatic tumor to the pleura
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1 in patients with malignancies not known to be
2 asbestos-related.
3 Actually, you agree with much of that
4 last sentence, correct?
5 A Well, its an observation that sounds
6 reasonable with the exception of the fact that we
7 do know they are pathologically active, which is
8 what my review paper stated with references.
9 Q You would agree, however, that we dont
10 yet have the controls, and thats what you hope to
11 establish in your future research?
12 A I think that is a reasonable thing that
13 needs to be done.
14 Q Thank you, sir.
15 A Yes, sir.
16 Q Now, on the issue of what you found, I
17 want to go to your shipyard workers study that is
18 Dodson — Plaque from Former Shipyard Workers.
19 That was in 1990. You have a table, Table 4, that
20 identifies what you found in an extra — outside
21 the lung. It says: Uncoated chrysotile and
22 amphibole fibers — that is Table 4, correct?
23 A Yes.
24 Q So when you went to this site outside the
25 lung, was that — where is that, pleural plaques?
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1 A Plaques, lungs, and nodes in each column.
2 Q These are areas close to the mesothelial
3 areas, right, some of them? The plaques are?
4 A They are all in the pleura. Yes.
5 Q The plaques are on the pleura.
6 When it came to amphibole fibers –
7 lets go to that first. The amphibole fibers are
8 listed as the second highlighted entry. Amphibole
9 fibers on the plaque, you identified them by those
10 fibers that were of greater than 5 microns and
11 those that are greater than 10 microns, correct?
12 A Sure.
13 Q You found for amphiboles that there were
14 whatever the quantity that is 10 represents. What
15 does 10 represent in that context?
16 A 10 percent greater than 5 microns.
17 Q 10 percent of the amphibole fibers you
18 found on the plaque were greater than 5 microns,
19 and 8 percent of the fibers you found were greater
20 than 10 microns at the pleural plaque level,
21 right?
22 A Yes.
23 Q Those were of the amphiboles.
24 For the chrysotile fibers, you found
25 3.1 percent that was greater than 5 microns,
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1 correct?
2 A Yes.
3 Q You found absolutely none that were
4 greater than 10 microns, correct?
5 A That is correct.
6 Q So if, in fact, those who say fibers have
7 to be longer than 10 microns are correct, this
8 would be at least some support for the proposition
9 that the fibers that cause the disease arent
10 found at the plaque area, correct?
11 A Arent found at the plaque area?
12 Q There are not in this study?
13 A Sure. There is 8 percent.
14 Q I am sorry. Of the amphiboles?
15 A Of the amphiboles.
16 Q If we are looking for chrysotile fibers
17 that get to that place and stay there long enough
18 to be found by you, we dont find any, correct?
19 A Which was the point I made earlier. The
20 same as the black spots story. If you look at
21 what is in the lung and available for relocation,
22 the amphiboles in the lung are longer and there is
23 a greater percent of them that are longer,
24 capable, therefore, of being relocated.
25 Q In your omentum and mesothelial article we
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1 looked at yesterday, you found at every one of the
2 locations amphiboles longer than 10 microns at
3 that place, correct?
4 A There are long amphiboles that are in the
5 lung in numbers that can be relocated.
6 Q If we need long amphiboles to cause the
7 disease, your research shows that the long
8 amphiboles get there, correct?
9 A They get there as well as short fibers.
10 My concept, it requires asbestos to cause the
11 disease.
12 Q When you publish your conclusions for the
13 scientific community, the way you phrase it and
14 when you carefully phrase it — this is in your
15 article — is: The data presented argue that
16 asbestos fibers of all lengths induce the
17 pathogenic responses and that caution should be
18 exerted when attempting to exclude any population
19 of inhaled fibers.
20 Correct?
21 A That is correct.
22 Q You are not to the point where you can
23 tell us that the evidence is so strong with
24 controlled studies under your analysis that we can
25 definitely include those short fibers that until
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1 now have not even been regulatorilly defined as
2 fibers, can you?
3 A Sure. I think thats what that paper was
4 about. The data that is presented was short
5 fibers and the perspective of what is known about
6 them. Certainly there is plenty about long
7 fibers.
8 Q In fact, in the peritoneal tissue, the
9 most common fibers you found in your study were
10 the long amphibole fibers?
11 A The amphiboles are the longest fibers in
12 population found in the lung. Not unlike the
13 Boutin study.
14 Q I think the last thing just so we are
15 clear, you were shown an affidavit from Dr.
16 Roggli. If someone were to contend there is no
17 such thing as pure chrysotile, you would certainly
18 say your data indicates to the contrary, correct?
19 A From what I understand and what we have
20 looked at, it appears there are areas of pure
21 chrysotile. Yes, sir.
22 Q Thank you very much.
23 THE COURT: Mr. Simon.
24 REDIRECT EXAMINATION
25 QUESTIONS BY MR. SIMON:
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1 Q Just so we understand the context in which
2 we find fibers in the pleura, for example pleural
3 plaques, or in the peritoneum, you have said and
4 Dr. Hammar said there is a correlation to what you
5 find at those sites based on what you found in the
6 lungs. Why is that important?
7 A Well, the population to get somewhere else
8 has to start in the lungs.
9 Q If you look at people who have exposure to
10 a lot of long fiber amphiboles as evident in their
11 lungs, would it surprise you to find that it
12 predominates in the extrapulmonary sites?
13 A It didnt surprise me to find that they
14 were located and reached there. They were, by the
15 way, thin.
16 Q If the exposure is to predominantly
17 chrysotile, what would you expect to find in the
18 extrapulmonary sites?
19 A The predominance of the chrysotile in the
20 lung is short. Therefore, that is the population
21 that can be relocated.
22 Q In your papers on omentum and mesentery,
23 to what extent did you do exactly what Mr.
24 Schachter has described? I took a control
25 population. I took people with mesothelioma. I
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1 looked at what was in the lung of both. I looked
2 at what was in the extrapulmonary sites of both.
3 I had a frame of reference, and I made a
4 comparison.
5 A I said basically what we did.
6 Q What did you find? If people had
7 significant exposures to chrysotile, what did you
8 find in the peritoneum?
9 A You found a relocation of chrysotile
10 fibers at those sites.
11 Q If it was amocite, what did you find?
12 A Same thing.
13 Q If it was both, what did you find?
14 A A mixture.
15 Q If it was long fibers, what did you find?
16 A Some long fibers.
17 Q If it was short, what did you find?
18 A A number of short fibers.
19 Q Is there any scientific basis that you
20 consider compelling upon which to say, so what
21 about the chrysotile fibers?
22 A No, sir. I dont have a favorite length.
23 Q How about so what about the short fibers?
24 Any compelling scientific basis?
25 A I cant say that, obviously.
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1 Q Dr. Churg — the Boutin paper, what were
2 those peoples predominant source of asbestos
3 exposure as found in their lungs?
4 A Amphiboles. I mentioned that early.
5 Q 99.9 percent?
6 A Yes.
7 Q If 99.9 percent of the fibers found in the
8 lungs were there, what would you expect to find in
9 the extrapulmonary sites?
10 A If something is going to be relocated,
11 there is a pretty good chance it has to be an
12 amphibole.
13 Q Now Dr. Andrew Churg was discussed with
14 you in connection with a few things, but one was
15 just citations from Dr. Rogglis book. I have
16 some testimony from Dr. Churg, and I want to just
17 ask you about it. This is from the Anderson case
18 in March 13, 1987.
19 MR. SCHACHTER: Your Honor, I am going
20 to object to this. It is totally irrelevant and
21 outdated testimony. He is not a witness in this
22 proceeding.
23 THE COURT: I will overrule. Although
24 it occurs to me a criminal conviction, if a
25 conviction for murder more than 10 years old isnt
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1 valid, neither should testimony be used to
2 impeach. But I will allow it under our relaxed
3 Rules of Evidence.
4 MR. SIMON: Unless it doesnt change,
5 Your Honor, which is coming next.
6 QUESTIONS BY MR. SIMON:
7 Q He is asked at Page 24, Line 14: And you
8 have been asked about amphiboles, and you have
9 been asked about chrysotile.
10 Now, tremolite is an amphibole, right?
11 A Yes, sir. It is.
12 Q How do you interpret chrysotile here?
13 Chrysotile fiber or chrysotile/amphibole?
14 A That is a chrysotile asbestos fiber.
15 Q But to make sure, chrysotile can cause
16 mesothelioma?
17 What was his answer?
18 A Chrysotile can cause mesothelioma.
19 Q That is 1987.
20 Fifteen years later, we have gone
21 through the McDonald papers trying to explain
22 their perception of the amphibole hypothesis and
23 so forth. Dr. Andrew Churg, March 27, 2002 from
24 the Brock case, in the Superior Court of the State
25 of California for the County of Los Angeles. Page
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1 42, Line 5: You would agree with me that in order
2 to say that a mesothelioma was induced by
3 chrysotile, you dont need to see asbestosis?
4 Answer: No. You dont need to see
5 asbestosis. You merely have to have exposure up
6 to that level.
7 Now, first of all, Dr. Churg thinks it
8 takes a lot of exposure to chrysotile to cause
9 mesothelioma. Fair?
10 MR. SCHACHTER: Objection. He is just
11 making a speech.
12 THE COURT: Sustained.
13 QUESTIONS BY MR. SIMON:
14 Q According to this testimony as you
15 interpret it, what does Dr. Churg conclude simply
16 about whether or not at some dose chrysotile can
17 cause mesothelioma?
18 MR. SCHACHTER: Objection, Your Honor.
19 He is not qualified to interpret the testimony of
20 another witnesses.
21 THE COURT: He can say what he
22 concluded, which is what the question was. But
23 you may answer the question.
24 A (By the witness) What he said is up to
25 that level of exposure, he makes a correlation of
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1 potential.
2 QUESTIONS BY MR. SIMON:
3 Q I was asking you about methodological
4 strengths and limitations in the McDonald paper as
5 cited or not cited by the authors. Do you recall
6 that?
7 A Yes, sir.
8 Q I want to ask you in the context in which
9 I asked Dr. Case about it just so the record is
10 clear about those citations. I asked him at Page
11 101: Is it your testimony that if I read
12 references on Page 236 of this paper, the lung
13 fiber content for mesothelioma, I will be able to
14 discern from each of the 21 mesotheliomas for
15 which lung tissues analysis was done the amount of
16 tissue that was sampled?
17 Then we have a discussion on Page 102
18 about what I can and cant tell if I do that. Do
19 you see that?
20 A Yes.
21 Q He tells me that there are some things
22 that I will learn if I go read those cites, right?
23 A Yes.
24 Q I asked him at Line 12: Will I be able to
25 determine all the quality controls which are
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1 employed or not employed?
2 His answer was what?
3 A That I am not sure of.
4 Q At Line 19 I ask him: Will I be able to
5 understand the nature, if any, of the inter-lab
6 variations that work there simply by reading those
7 cites?
8 His answer was: No. You couldnt do
9 that unless you actually did side-by-side
10 comparisons, which we didnt do obviously.
11 What problems are posed by the fact
12 that I, the reader, cannot interpret the inter-lab
13 variations, if any, between how Dr. Case does
14 things in his lab versus Dr. Churg in the way they
15 do things in their lab, and then when they try to
16 mesh them together into one result?
17 A Well, I think those are the things that I
18 went over with Mr. Schachter that I know both of
19 the investigators and I know they do things a
20 little different and include things a little
21 different.
22 Q From the 97 paper Dr. Case, Dr. McDonald
23 — in fairness, do the authors concede that
24 because of the inevitable uncertainty of things,
25 including the absence of controls, questions of
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1 risk and causation cannot be addressed?
2 A Thats what they say.
3 Q If they cant do it, can the reader
4 reasonably do it anyway?
5 A No, sir.
6 Q Okay. I want to talk about the Suzuki and
7 Yuen paper from the analysis, if any, that went in
8 at the ATSDR that was discussed earlier, the
9 Berman & Crump analysis.
10 MR. LEONE: Object to the form. It
11 confuses the ATSDR and the Berman & Crump
12 analysis.
13 THE COURT: Dont confuse them.
14 Please proceed.
15 QUESTIONS BY MR. SIMON:
16 Q My question was, I believe, a little
17 different than it was characterized in
18 cross-examination and if not I want to be clear.
19 My question is not did they discuss it. It is,
20 did they ultimately include it in their risk
21 calculation?
22 A I dont know that they did.
23 Q They do discuss it and I want to talk
24 about that for a minute. At 315 it says: During
25 this discussion one panelist reviewed a
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1 publication, Suzuki and Yuen, that was mentioned
2 in the workshop. One that had to do with legal
3 cases. The panelist had several criticisms of the
4 study. First, he indicated samples were analyzed
5 using a nonstandard technique. He questioned
6 other things. The panelist suspected that the
7 chrysotile reportedly found in the study might be
8 the result from specimen contamination. Finally,
9 the panelist noted that a more rigorous study,
10 Boutin, of asbestos fibers found in parietal
11 pleura found a mixture of fibers. Based on these
12 concerns, the panelist concluded the publication
13 of concern is seriously flawed and it is
14 recommended should be excluded from the EPAs
15 analysis.
16 Now, I want you to just assume thats
17 what happened. That study then got excluded from
18 the risk calculation. If thats true, is that the
19 kind of rigorous examination that when you have
20 served on panels you have found to be appropriate
21 in simply excluding a study altogether?
22 A Well, I guess the indication there that is
23 troubling is a pick-and-choose mode.
24 Q What do you mean by that?
25 A Well, you like one article and it found
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1 amphiboles and the other article found chrysotile,
2 and there was a critique of the methodology
3 intently without what I saw was the documentation
4 of that critique. I have read the Suzuki paper.
5 Q You were read this reference, Report on
6 the Expert Panel on Health Effects of Asbestos in
7 Synthetic Vitreous Fibers, the Influence of Fiber
8 Length by the Eastern Research Group. Do you
9 recall that?
10 A Yes.
11 Q In which this portion was discussed,
12 Cancer Effects of Short Fibers: Given findings
13 from epidemiologic studies, laboratory animal
14 studies, and in vitro genotoxicity studies
15 combined with the lungs ability to clear short
16 fibers, the panelists agreed that there is a
17 strong weight of evidence that asbestos and SVF –
18 what is that?
19 A Vitreous fibers.
20 Q — shorter than 5 microns are unlikely to
21 cause cancer in humans.
22 Now, which epidemiological study looks
23 at people exposed only to short fibers? Which one
24 do they mean?
25 A I dont know that study.
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1 Q Yeah. On Page 32: One panelist indicated
2 that no studies have evaluated cancer outcomes
3 associated with fibers shorter than 5 microns
4 because no occupational cohort is exposed
5 exclusively to such fibers.
6 Did they just do it anyway?
7 A They cant find the reference it appears
8 from what they admitted.
9 MR. LEONE: Under optional
10 completeness, the next sentence indicates: For
11 insight into the carcinogenicity of the short
12 fiber, they reviewed findings reported for two
13 occupational cohorts — they reviewed findings
14 reported for two occupational cohorts. They were
15 exposed predominantly, though not exclusively, to
16 short asbestiform fibers.
17 QUESTIONS BY MR. SIMON:
18 Q Lets just take that. Let me see if I
19 understand. If you have, according to the
20 authors, a mix of exposures, some long and some
21 short, it is appropriate now to make
22 epidemiological conclusions anyway, correct?
23 A Seems so.
24 Q If you have mixed fiber exposures, is it
25 not appropriate then to make epidemiological
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1 conclusions about the predominant fiber?
2 MR. LEONE: Object. No foundation.
3 The witness already testified he is not qualified
4 to give epidemiological opinions.
5 THE COURT: Overruled.
6 A (By the witness) Would you rephrase,
7 please?
8 QUESTIONS BY MR. SIMON:
9 Q Sure. I am just asking if you think it is
10 scientifically consistent to say, I can make
11 epidemiological conclusions about fiber length,
12 especially short fibers, based on mixed fiber
13 exposures. But it is improper to make conclusions
14 about the role of the predominant fiber, say,
15 chrysotile in a mixed fiber exposure?
16 A Doesnt seem logical.
17 Q Here at Page 316 — excuse me. At 41, Dr.
18 Case said: There is a strong weight of evidence
19 that asbestos and SVF shorter than 5 microns do
20 not cause cancer in humans, and no further
21 research is needed on this matter.
22 Do you find that scientific
23 proposition to be so summarily proven that it is
24 true?
25 A I am afraid I take a different position
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1 than my colleague, Dr. Case, on that conclusion.
2 Q To what extent do you believe that injects
3 intellectual bias into the outcome?
4 A Well, it is pretty strong if it says we
5 dont know need to do any more concerning the
6 issue.
7 Q Are you aware that there are dramatic
8 differences in potency on a one-to-one fiber basis
9 between amphibole and chrysotile for lung cancer?
10 A There are differences.
11 Q Do you consider those to be dramatic
12 differences?
13 A I consider them to be some measurable
14 difference depending on your favorite number.
15 But, yes, there are differences.
16 Q Generally speaking, would you expect that
17 those differences for mesothelioma should be
18 dramatically wider than they are for lung cancer
19 for any particular reason?
20 A Well, the same mechanistic aspects, I
21 guess, would be in place for reducing cancer of
22 the lung as for the lining of mesothelial cells or
23 the peritoneum cells.
24 Q Do we have any reason to believe that the
25 way the fiber causes cancer in the lung should be
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1 altogether different than the way it would cause
2 cancer in the mesothelium?
3 A Dr. Brody, he has done considerable work
4 on the mechanistic aspect. He indicated the other
5 day that the same type of mechanism should apply.
6 Q I just wanted to ask you again about the
7 role of history as a means of assessing whether or
8 not a mesothelioma is asbestos-related and, if so,
9 to what?
10 MR. SCHACHTER: Objection. Asked and
11 answered. He just wants to ask him again.
12 MR. SIMON: Actually my frame of
13 reference raises something that occurred in cross.
14 THE COURT: I will allow this to put
15 it in context. Then get to a new subject.
16 QUESTIONS BY MR. SIMON:
17 Q Where I wanted to ask you about this was
18 the questions on cross-examination that say –
19 that went to the subject of, well, if you look at
20 asbestos fibers in tissue, say if its chrysotile,
21 you may not be able to tell in and of itself how
22 recent the exposure versus how distant the
23 exposure. Remember that question?
24 A Basically.
25 Q Here was my question in that respect. If
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1 you have tissue burden analysis and you can find
2 demonstrable, significant amounts of chrysotile
3 fiber and you can correlate it to a history of
4 significant exposure to chrysotile, what, if
5 anything, does that tell you, at least reasonably,
6 scientifically, probably about whether all of that
7 chrysotile is just brand new exposure or a
8 reference of some previous exposure?
9 A If you had the documented history and you
10 found it, I assume most people would buy into that
11 being a link.
12 Q That is all I have. Thank you.
13 THE COURT: Mr. Leone?
14 RECROSS-EXAMINATION
15 QUESTIONS BY MR. LEONE:
16 Q Dr. Dodson, is it true that you are not
17 aware of the epidemiologic modeling and regression
18 techniques that would allow a scientist to
19 evaluate the effects of fiber types in a mixed
20 exposure situation?
21 A I have seen some of that data, but I am
22 not — I am not professed to have expertise in
23 that. No, sir.
24 Q It is also true that you are not familiar
25 with the epidemiologic and modeling regression
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1 techniques that might allow a scientist to
2 separate the effects of different fiber sizes in a
3 mixed exposure situation?
4 A I think the same answer would be
5 applicable. Yes, sir.
6 Q Thank you.
7 THE COURT: Mr. Schachter?
8 MR. SCHACHTER: No thank you.
9 MR. SIMON: No, Your Honor. Thank
10 you.
11 THE COURT: May this witness be
12 excused? You are excused. Thank you for coming.
13
14 (PROCEEDINGS CONCLUDED FOR THE DAY)
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1 THE STATE OF TEXAS:
2 COUNTY OF HARRIS:
3 I, Terri W. Anderson, Official Court
4 Reporter, 11th District Court, Harris County,
5 Texas, certify that the above and foregoing
6 contains a true and correct transcription of all
7 portions of evidence and other proceedings
8 requested in writing by counsel for the parties to
9 be included in this volume of the Reporters
10 Record, in the above-styled and numbered cause,
11 all of which occurred in open court or in
12 chambers, where indicated and were reported by me.
13 WITNESS MY OFFICIAL HAND this _____
14 day of July, 2005.
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19 __________________________
Terri W. Anderson
20 Texas CSR #877
Official Court Reporter
21 11th District Court
Houston, Harris County, Tx.
22 301 Fannin, Suite 212
Houston, Texas 77002
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