DOCKET NO. FBT-CV17-6066689-S
`
`ADAM M. BREAKELL,
`
`v.
`
`
`
`SUPERIOR COURT
`
`J.D. OF FAIRFIELD
`
`AT BRIDGEPORT
`
`3M CO. (f/k/a Minnesota Mining & Manufacturing
`Co.), et al.
`
`FEBRUARY 26, 2020
`
`DEFENDANT HONEYWELL INTERNATIONAL INC.’S
`DAUBERT/PORTER MOTION TO EXCLUDE DR. MOLINE AND DR. ZHANG’S
`CAUSATION OPINIONS AND REQUEST FOR EVIDENTIARY HEARING
`
`Defendant, Honeywell International Inc., f/k/a Allied Signal, as successor in interest to
`
`Allied Corporation, as successor in interest to The Bendix Corporation (“Honeywell”), moves
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`the Court to exclude Dr. Jacqueline Moline and Dr. David Zhang’s causation opinions.
`
`INTRODUCTION
`
`Honeywell challenges the testimony of Plaintiff’s medical experts, Dr. Jacqueline Moline
`
`and Dr. David Zhang. Plaintiff’s experts’ opinions are not based on any coherent, reproducible or
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`testable scientific methodology or principle for determining causation, much less on any
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`generally accepted methodology. Specifically, Plaintiff’s experts do not utilize the scientific
`
`method, or even published studies based on the scientific method, which test his opinion that
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`brake dust (the product at issue in this case) causes peritoneal mesothelioma (the disease at issue
`
`in this case). Instead, they are expected to offer testimony that exposure to dust from Bendix
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`brakes, regardless of how low the dose, was a contributing cause of Mr. Breakell’s peritoneal
`
`mesothelioma. They reach this opinion by asserting the fiction that if there were any identifiable
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`exposures to “asbestos” and mesothelioma was diagnosed, then ipso facto, those known
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`exposures were a cause of the disease. Under Connecticut law, Plaintiff’s experts’ causation
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`opinions should be excluded.
`
`I-1676482.1
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`

`

`Plaintiff’s experts’ theory, commonly referred to as the “cumulative exposure” theory,
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`relieves Dr. Moline and Dr. Zhang of any obligation to individually assess Mr. Breakell’s alleged
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`exposures or to even estimate his potential exposure to brake dust.1 Their theory avoids
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`consideration of the highly relevant dose-response analysis, the different potency among the
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`fiber types, as well as differences between processed chrysotile found in brake dust and raw
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`fiber. This theory is a litigation-driven hypothesis that is not based on any case-controlled data,
`
`testing, peer-reviewed literature, or scientific principle.
`
`One of the trial courts in New York City especially charged with handling asbestos
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`personal injury suits rejected Dr. Moline’s unscientific “cumulative exposure” theory of
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`causation. In re New York City Asbestos Litig. (Juni), 48 Misc. 3d 460, 11 N.Y.S.3d 416 (N.Y.
`
`Sup. Ct. 2015) (holding that Dr. Moline’s “opinion that every single exposure constitutes a
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`significant contributing factor because the exposures cumulatively cause the disease” was
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`…”irreconcilable with the well-recognized scientific requirement… that the amount, duration,
`
`and frequency of exposure be considered in assessing the sufficiency of an exposure in
`
`increasing the risk of developing a disease”), aff’d, 148 A.D.3d 233, 48 N.Y.S.3d 365 (N.Y.
`
`App. Div. 2017).2 This Court should likewise reject her testimony as it is not based on a proper,
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`generally accepted, and reliable scientific methodology.
`
`Similarly, the Supreme Court of New York for Nassau County excluded Dr. Zhang’s
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`“every exposure” or “cumulative exposure” causation opinion. Pistone v. American Biltrite, Inc.,
`
`et al., Order of Supreme Court of New York, April 19, 2018, at 23-25 (“While he opines that
`
`1 While Plaintiff’s experts use the terminology “cumulative exposure” rather than “each and every exposure,” the
`sum and substance of the “theories” are the same. See, e.g., Rockman v. Union Carbide Corp., 266 F. Supp. 3d 839
`(2017) (“Although Plaintiffs’ experts do not explicitly use the phrase “each and every exposure,” the theories are
`one and the same...”). Any suggestion that this is different from the “each and every exposure” opinion is a
`distinction without a difference.
`
`2 On November 27, 2018, New York’s highest court affirmed the decision of the appellate court.
`
`2
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`

`

`chrysotile asbestos causes peritoneal mesothelioma, he has not provided any proper support for
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`that conclusion….While Dr. Zhang notes that it has not been determined that any dose no matter
`
`how low is safe, he cannot from that conclude that any amount can therefore be considered
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`causative.”), attached as Exhibit A.
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`Here, Plaintiff’s experts must base causation opinions on a scientifically valid
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`methodology. Neither relied on the scientific method to reach their opinions and provide no
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`reliable or testable basis for an opinion that Mr. Breakell’s exposure to any Defendants’ product
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`contributed to the development of his mesothelioma. This Court should reject the testimony
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`espoused by Drs. Moline and Zhang as inherently unreliable and contrary to established
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`principles for establishing causation. At a minimum, Honeywell requests the Court hold an
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`evidentiary hearing to receive and evaluate further evidence on this critical issue.
`
`I.
`
`MR. BREAKELL
`
`BACKGROUND FACTS
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`Mr. Breakell was diagnosed with peritoneal mesothelioma at the age of 41. Peritoneal
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`mesothelioma is a rare form of cancer affecting mesothelial cells in the lining of the abdomen.
`
`While both pleural and peritoneal mesothelioma arise from tissues that are of mesodermal origin,
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`there is growing evidence that malignant peritoneal mesothelioma differs from pleural
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`mesothelioma in that it has a distinct natural history, afflicts both sexes approximately equally
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`and both entities are clinically and pathologically distinct. 3 Unlike pleural mesothelioma, which
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`has been described as a signature disease for asbestos exposure, peritoneal mesothelioma is not a
`
`3 See e.g., Varghese, S, et al., “Activation of the Phosphoinositide-3-Kinase and Mammalian Target of Rapamycin
`Signaling Pathways Are Associated With Shortened Survival in Patients With Malignant Peritoneal Mesothelioma”
`Cancer January 2011; Singhi, AD, et al., “The prognostic significance of BAP1, NF2, and CDKN2A in malignant
`peritoneal mesothelioma,” Modern Pathology (2015); Dragon, Julie, et al., “Differential susceptibility of human
`pleural and peritoneal mesothelial cells to asbestos exposure,” Journal of Cellular Biochemistry 116:8(2015):1540,
`1548.
`
`3
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`

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`signal or sentinel tumor indicating asbestos exposure.4 While historically some peritoneal
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`mesotheliomas in men were related to heavy, prolonged exposures to commercial amphibole
`
`fiber, malignant peritoneal mesothelioma currently “is rarely associated with asbestos exposure;
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`in a large series, only 8% of patients reported exposure, and malignant pleural peritoneal
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`mesothelioma afflicts men and women equally – as anticipated when mesothelioma is not caused
`
`by occupational exposure.”5 In the minority of male peritoneal mesotheliomas that are asbestos-
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`related, the strong association of peritoneal mesothelioma with amphibole exposure (and the
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`absence of a demonstrated association with chrysotile exposure) is generally accepted throughout
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`the scientific and medical community. This general acceptance is demonstrated by the fact that
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`virtually every major pulmonary and pathology textbook that critically addresses this topic
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`describes the association of peritoneal mesothelioma as being with amphibole forms of asbestos
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`– not the type of asbestos used in brakes.6
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`Plaintiff alleges that he developed mesothelioma as a result of exposure from bystander
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`and take-home exposure to asbestos from Bendix brakes during his childhood and early teenage
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`years while accompanying his father to work at his excavation and construction companies.
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`Plaintiff testified to being in his father’s and other employees’ presence when they performed
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`repair and maintenance work on automobiles, light, medium and heavy duty trucks and
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`4 Indeed, it is not appropriate scientific methodology to treat the literature on pleural and peritoneal mesotheliomas
`as if the diseases were interchangeable. They are separate diseases. “The etiology, gender distribution, pathology,
`natural history, and treatment options for mesothelioma (MM) differ substantially depending on the site of origin.”
`Kindler, H., “Peritoneal Mesothelioma: The Site of Origin Matters,” American Society of Clinical Oncology
`Educational Book, Dizon, D. (Ed.), American Society of Clinical Oncology, Alexandria, VA, pp. 182-188, 2013.
`
`5 Carbone, Michele, et al., “Mesothelioma: scientific clues for prevention, diagnosis, and therapy,” CA Cancer J Clin
`2019:69:402, 421.
`
`6 See e.g., Pavilsko, E.N., et al., “Mesothelioma” In Pathology of Asbestos-Associated Diseases, Oury, T.D., et al.,
`(Eds.), New York, Springer, Verlag pp. 81, 121 (2014); Russi, N.B., “Malignancies of the Respiratory Tract and
`Pleura,” Textbook of Clinical and Environmental Medicine, Rosenstock, L., (Eds.), Elsevier Saunders: Philadelphia,
`pp. 727, 735 (2005).
`
`4
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`

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`construction equipment. Neither Plaintiff’s father nor brother could estimate the number of times
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`that Plaintiff was present when brake jobs were performed at his father’s companies.
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`Plaintiff also testified to alleged exposure to asbestos from his work at Goshen Tractor
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`Co. as a mechanic’s helper in the summer of 1991 and part-time through January 1992. Plaintiff
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`performed mechanical work and assisted mechanics with mechanical work, brake replacements,
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`tune-ups and engine overhauls. Plaintiff also washed dirty tractors, cleaned the shop, and picked
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`up parts. The mechanics did one or two brake jobs per week, and Plaintiff thought he assisted on
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`about one half of the brake jobs.
`
`II.
`
`BRAKE DUST
`
`“Asbestos” does not refer to a manufactured product, but is a generic term for a diverse
`
`group of naturally occurring minerals with different physical and chemical properties and,
`
`therefore, disease-causing potential. Chapters 1, 5, Pathology of Asbestos-Associated Diseases
`
`(Oury, T., Roggli, V. et al. eds.), Springer-Verlag Berlin Heidelberg, 3d ed. 2014. There are two
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`major asbestos fiber types: amphibole and chrysotile. Id. at Chapter 1. Chrysotile was the only
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`type of asbestos used in Bendix brakes as a raw material.
`
`There are significant differences between brake dust and raw chrysotile asbestos.
`
`Plaintiff’s experts’ theory does not consider these differences. The manufacturing process used
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`to create brake pads involves applying significant heat and pressure to the raw chrysotile used as
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`an ingredient in the formulae for automotive brakes. In addition to being repeatedly heated (on at
`
`least one occasion to 400 degrees Fahrenheit for five hours), the chrysotile in brake pads was
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`subjected to pressures of approximately 1800 PSI and soaked in naphtha. These sorts of
`
`manipulations have been shown to “inactivate” chrysotile fibers, greatly reducing or eliminating
`
`their potential to cause cancer. See Valentine, R., et al. “Thermal Modification of Chrysotile
`
`5
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`

`

`Asbestos: Evidence for Decreased Cytotoxicity.” Environ. Health Perspectives, 51:357-368, 363
`
`(1983).
`
`The manipulation of new asbestos-containing friction products “generates residue
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`containing fibers that, to a great extent, remain bound to the matrix of the underlying brake
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`material,” and the data supports that such work does “not pose an important source of exposure
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`to respirable asbestos fibers.” Weir FW and LB Meraz, “Morphological characteristics of
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`asbestos fibers released during grinding and drilling of friction products,” App. Occup. Environ.
`
`Hyg. 15(12):1147-1149, 2001.
`
`Brake wear dust that remains after the braking process contains little, if any, chrysotile:
`
`Studies have shown that thermal treatment and mechanical
`manipulation of chrysotile alters both its surface and structure.
`Service conditions created on brake pads both heats and tears down
`the fiber. Chrysotile subjected to these severe conditions cannot,
`and does not, retain its natural properties. Chrysotile biological
`activity is thereby greatly reduced, and can become virtually nil
`hundreds of degrees below the olivine transformation temperature.
`Complete transformation of the mineral is not required to result in
`loss of activity. Exposure to brake wear debris, which has been
`created as the result of these forces, may be associated with little or
`no risk of asbestos disease. Blowouts and cleanups of wear debris,
`both visually dusty work practices, might constitute no asbestos
`hazard to workers.
`
`Langer, AM. Reduction of the biological potential of chrysotile asbestos arising from conditions
`
`of service on brake pads. Regulatory Toxicology and Pharmacology (2003) 38:71-77 at 76.
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`Recent animal inhalation studies concluded that brake dust does not cause any material
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`biologic reaction and certainly not the same biologic reactions in the lung or pleura as amphibole
`
`asbestos. Both 5-day and 28-day exposure studies demonstrated that brake dust caused no
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`material biologic damage to the lung or the pleura, i.e., results virtually identical to the results
`
`from inhaling normal air. On the other hand, amphibole fibers produced immediate and sustained
`
`6
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`

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`damage to both lungs and pleura of exposed animals. Id. 7 Plaintiff’s experts fail to consider these
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`important factors, among others, in forming their causation opinions in this case.
`
`III.
`
`BACKGROUND LEVELS OF ASBESTOS
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`Asbestos is ubiquitous in the air we breathe, the food we eat, and the water we drink. For
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`instance, the U.S. EPA standard for safe drinking water sets the “asbestos” limit at or below 7
`
`million fibers of asbestos (longer than 10 microns) in a liter. See 40 CFR § 141.51. The
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`National Research Council reported that among the general population in this country the typical
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`lifetime exposure to asbestos is expected to be about 100 million fibers. Comm. on Non-
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`Occupational Health Risks of Asbestiform Fibers, et al., Asbestiform Fibers Non-Occupational
`
`Health Risk, at 62 (Nat’l Acad. Press 1984). Similarly, the ATSDR calculated the range of
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`lifetime exposures to asbestos in the general population from non-occupational sources (i.e. from
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`the ambient air) to be 0.002 to 0.4 f/cc years. Toxicol. Profile for Asbestos, at 151, U.S. Dept.
`
`HHS, Public Health Srv, ATSDR (Sept. 2001). There is no scientific evidence that background
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`exposures to chrysotile asbestos cause or contribute to the development of mesothelioma. Dr.
`
`Moline and Dr. Zhang agree that background levels of asbestos do not increase the risk of
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`developing mesothelioma. Breakell v. 3M Co. (f/k/a Minnesota Mining & Manufacturing Co.), et
`
`al., Deposition of Dr. Zhang, November 18, 2019, at 133, attached as Exhibit B; Byer v. 3M Co.,
`
`et al., Deposition of Dr. Moline, January 8, 2015, at 63-69, attached as Exhibit C. There is no
`
`scientific evidence that Mr. Breakell’s cumulative dose of asbestos, including his potential dose
`
`7 Bernstein, D., et al, “Evaluation of the deposition, translocation and pathological response of brake dust with and
`without added chrysotile in comparison to crocidolite asbestos following short-term inhalation: Interim results,”
`Toxicol Appl Pharmacol 276:28-46 (2014); Bernstein D, et al., “Evaluation of the fate and pathological response in
`the lung and pleura of brake dust alone and in combination with added chrysotile compared to crocidolite asbestos
`following short-term inhalation exposure,” Toxicol Appl Pharmacol 283:20-34 (2015); Bernstein, D., et al,
`“Evaluation of the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to
`chrysotile or crocidolite asbestos in a 28-day quantitative inhalation toxicology study,” Toxicol Appl Pharmacol
`351:74-92 (2018).
`
`7
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`

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`from Bendix brake dust, exceeded the cumulative background range.
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`APPLICABLE STANDARD FOR ADMISSIBILITY
`
`In determining the admissibility of an expert’s opinion evidence, the Court’s analysis is
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`guided by the Connecticut Code of Evidence § 7-2 and the principles articulated in Daubert v.
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`Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), which the Supreme Court of
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`Connecticut has adopted as the relevant standard. See State v. Porter, 241 Conn. at 61. Plaintiff
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`bears the burden of proving the admissibility of his experts’ testimony. In determining whether
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`plaintiffs meet their burden of establishing the admissibility of expert evidence, the trial judge
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`must determine whether the testimony has “a reliable basis in the knowledge and experience of
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`[the relevant] discipline.” Daubert v. Merrell Dow Pharmaceuticals, Inc. (Daubert I), 509 U.S.
`
`579, 592 (1993). In performing its duty as “gatekeeper,” the trial court must determine whether
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`or not the underlying proposed expert testimony is scientifically valid, amounts to “scientific
`
`knowledge,” constitutes “good science,” and is “derived by the scientific method.” Daubert v.
`
`Merrell Dow Pharmaceuticals, Inc. (Daubert II), 43 F.3d 1311, 1316 (9th Cir. 1995). In addition
`
`to meeting the Daubert standard, any proffered expert opinion must “assist the trier of fact in
`
`understanding the evidence or in determining a fact in issue.”
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`To determine whether the evidence will assist the trier of fact, there must be “a
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`preliminary assessment of whether the reasoning or methodology underlying the testimony is
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`scientifically valid and of whether that reasoning or methodology properly can be applied to the
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`facts in issue.” Daubert, 509 U.S. at 592-93. Although general acceptance of a theory or
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`methodology is not required, the expert’s testimony must indicate that his theory is both reliable
`
`and relevant. See id. at 597; CONN. CODE OF EVID. §7-2, commentary.
`
`A theory is only reliable if it is “scientific knowledge rooted ‘in the methods and
`
`procedures of science.’” Porter, 241 Conn. at 64 (quoting Daubert, 509 U.S. at 590). Daubert
`
`8
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`

`

`held that courts should consider five criteria when determining the admissibility of expert
`
`testimony: (1) whether the proffered knowledge can be or has been tested; (2) whether the theory
`
`or technique has been subjected to peer review and publication; (3) the known or potential rate of
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`error; (4) the existence and maintenance of standards controlling the technique’s operation; and
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`(5) whether the theory or technique has gained general acceptance in the relevant scientific
`
`community. See Daubert I, 509 U.S. at 592- 94. A trial court should make findings on each of
`
`the relevant factors concerning whether expert testimony is scientifically reliable in order to
`
`properly exercise its discretion. See Kumho Tire Co., Ltd. v. Carmichael, 526 U.S. 137, 159
`
`(1999) (Scalia, J., concurring) (“[I]n a particular case[,] the failure to apply one or another of [the
`
`Daubert factors] may be unreasonable, and hence an abuse of discretion.”).
`
`The rationale behind the Daubert standard is to ensure that an expert employs in the
`
`courtroom the same level of intellectual rigor that characterizes the practice of an expert in the
`
`relevant field. See Kumho Tire Co., 526 U.S. at 152. Its overarching subject is the scientific
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`validity— and thus the evidentiary relevance and reliability —of the principles that underlie a
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`proposed submission. The focus must be solely on principles and methodology, not on the
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`conclusions that they generate. See Daubert I, 509 U.S. at 594-95.
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`This Court should evaluate whether the causation opinions that Dr. Moline and Dr. Zhang
`
`reach in this case are based on a scientific and reliable methodology as a prerequisite to allowing
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`the jury to consider the weight of competing expert testimony.
`
`9
`
`

`

`ARGUMENT
`
`I.
`
`PLAINTIFFS’ EXPERTS’ OPINIONS ARE NOT BASED ON SCIENTIFICALLY
`DEFENSIBLE METHODOLOGIES AND ARE UNRELIABLE
`
`A.
`
`Dr. Moline
`
`Dr. Moline opines generally that Mr. Breakell developed “mesothelioma as a result of his
`
`cumulative exposure to asbestos.” Breakell v. 3M Co., et al., Deposition of Dr. Moline,
`
`December 19, 2019, at 65, attached as Exhibit D; see also December 3, 2019 Report of Dr.
`
`Moline, at 14, attached as Exhibit E. Dr. Moline subscribes to the theory that because Mr.
`
`Breakell has a history of asbestos exposure and developed a malignant mesothelioma, his
`
`mesothelioma was necessarily caused by the asbestos exposures. Etheridge v. Brenntag North
`
`America, Inc., et al., Deposition of Dr. Moline, February 21, 2018, at 210-211 (“My
`
`understanding of it is that if the product contains asbestos and there’s the exposure, then you can
`
`attribute it.”), attached as Exhibit F.
`
`While Dr. Moline testifies that she now adheres to the “cumulative exposure” opinion,
`
`i.e., that all exposures above background contribute to the cumulative dose that in turn causes
`
`one’s mesothelioma, Dr. Moline opined for years that each and every fiber of asbestos a person
`
`breathes can cause a mesothelioma. Byer v. 3M Co., et al., Deposition of Dr. Moline, January 8,
`
`2015, at 141-143, attached as Exhibit C; Herford v. AT&T Corp., et al, Deposition of Dr.
`
`Moline, September 5, 2017, at 222-228, attached as Exhibit G. This is a distinction without a
`
`difference. In fact, Dr. Moline has testified that the difference between the “cumulative
`
`exposure” theory and the “each and every exposure” theory is a “semantic issue.” Colvin v.
`
`ACandS, Inc., et al., Deposition of Dr. Moline, March 28, 2014, at 145-148, attached as Exhibit
`
`H.
`
`10
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`

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`Further, Dr. Moline opines that only “significant exposures” should be considered
`
`contributing factors in the development of a person’s mesothelioma. She distinguishes significant
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`exposures as exposures that are “non-trivial.” December 3, 2019 Report of Dr. Moline, at 24
`
`(“[E]ach non-trivial exposure to asbestos should be considered a contributing factor in the
`
`development of the malignant mesothelioma or lung cancer.”), attached as Exhibit E; Breakell v.
`
`3M Co., et al., Deposition of Dr. Moline, December 19, 2019, at 59 (“There can be trivial
`
`exposures that would not contribute [to a person developing mesothelioma].”), attached as
`
`Exhibit D. Dr. Moline defines a “significant” exposure or a “non-trivial” exposure to asbestos as
`
`an exposure to asbestos above the background range. Breakell v. 3M Co., et al., Deposition of
`
`Dr. Moline, December 19, 2019, at 184, attached as Exhibit D. However, she concedes that she
`
`cannot quantify the difference between a trivial exposure and a significant exposure.
`
`Q. Okay. Do you have an opinion in terms of a fiber per cc
`amount that delineates trivial from non-trivial?
`
`…
`
`A: There is no specific amount, no.
`
`Id. at 184. Therefore, any distinction between “significant” and “trivial” exposures is arbitrary
`
`and allows Dr. Moline to conclude that every exposure above background, no matter how brief,
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`contributed to a person’s mesothelioma.
`
`This opinion is convenient since she concedes that she is unable to testify as to which, if
`
`any, particular exposure from a product that a person experienced actually caused his
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`mesothelioma. See Breakell v. 3M Co., et al., Deposition of Dr. Moline, December 19, 2019, at
`
`58-59 (calling it an “unanswerable question” as to which exposure causes a person’s
`
`mesothelioma), attached as Exhibit D; Whelan v. AO Smith Corp., et al., Deposition of Dr.
`
`Moline, December 23, 2013, at 49-50 (“He had multiple exposures over his life and you can’t
`
`11
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`

`

`separate out these exposures and say it was -- it was only this one or it was only that one. It’s a
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`cumulative exposure that counts towards the development of mesothelioma.), attached as
`
`Exhibit I; Byer v. 3M Co., et al., Deposition of Dr. Moline, January 8, 2015, at 98 (Q: So you
`
`cannot say which ones did cause it and you cannot say which ones did not cause it, correct?; A:
`
`Neither I nor the scientific community. That’s why we go on cumulative exposure.”), attached
`
`as Exhibit C.
`
`Q. In other words, you are here, as I understand your testimony,
`your testimony is if someone is claiming exposure during the
`course of his work life to numerous asbestos-containing products,
`let’s say 20 or 30, you are saying that it is the cumulative exposure
`of everything that caused the disease and you are not parsing it out
`and saying one product was responsible and one product was not
`responsible, is that fair to say?
`
`A. That is fair to say.
`
`Q. So, you are not giving product specific opinions, you are just
`saying that the cumulative exposure of the entire history is
`responsible for the disease, that is fair to say?
`
`A. That is an oversimplification. Because, it is impossible to
`separate out and to specifically identify. But, yes, with what we
`know now, it is the cumulative exposure, rather than each with
`other further ones.
`
`In Re: NYC Asbestos Litigation, Trial Testimony of Dr. Moline, August 12, 2011, at 2821,
`
`attached as Exhibit J. To render a causation opinion in a mesothelioma case, Dr. Moline needs
`
`to know nothing more than that the plaintiff was exposed to asbestos above background and
`
`developed the disease (assuming an appropriate latency period). This is no methodology at all.
`
`The flaws of this unscientific “method” are clear. The theory actually contradicts Dr.
`
`Moline’s admissions that mesothelioma is a dose-response disease and that the risk of
`
`developing mesothelioma gets smaller as the dose gets smaller, and that amosite and crocidolite
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`(both forms of amphibole asbestos) are more potent carcinogens than chrysotile fibers. See
`
`12
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`

`

`Breakell v. 3M Co., et al., Deposition of Dr. Moline, December 19, 2019, at 59-60, attached as
`
`Exhibit D; Wirick v. A.O. Smith Water Products Co., et al, Deposition of Dr. Moline, August 30,
`
`2017, at 89, attached as Exhibit K. Under her “methodology,” these factors are irrelevant.
`
`Without accounting for dose and fiber type, Dr. Moline’s causation opinion is nothing but
`
`unsubstantiated personal (not scientific) opinions.
`
`B.
`
`Dr. Zhang
`
`Similarly, Dr. Zhang opines that “Mr. Breakell’s malignant mesothelioma is related to
`
`significant levels of asbestos exposure and the cumulative exposure of each asbestos-containing
`
`product significantly contributed to the development of his peritoneal malignant mesothelioma,
`
`epithelioid type.” November 14, 2019 Report of Dr. Zhang at 42, attached as Exhibit L. To reach
`
`his causation opinion, Dr. Zhang requires only a diagnosis of mesothelioma.
`
`Q. In your opinion, the diagnosis of mesothelioma establishes the
`causation of the disease, which is asbestos exposure; correct?
`
`A. It is a signal of the exposure. Yes.
`
`Breakell v. 3M Co. (f/k/a Minnesota Mining & Manufacturing Co.), et al., Deposition of Dr.
`
`Zhang, December 2, 2019, at 362, attached as Exhibit M. His “methodology” improperly
`
`reverses the burden of proof. He assumes the cause of the disease based on the diagnosis and
`
`then searches for the exposures.
`
`Q. My understanding from your prior testimony is that if an
`individual presents to you with mesothelioma, it is your opinion
`that the mesothelioma was caused by asbestos exposure unless
`proven otherwise. Is that still your testimony today?
`
`A. That is correct.
`
`Id. at 361-62.
`
`Dr. Zhang opines that each and every exposure to asbestos that Mr. Breakell experienced
`
`was a substantial contributing cause in the development of his mesothelioma because he is
`
`13
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`

`

`unable to exclude any particular exposure as the cause. Id. at 361-362 (testifying that the only
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`“exposure” he can exclude is one that does not involve asbestos).
`
`Q. Dr. Zhang, is there any exposure to asbestos associated with
`any product in this case that you exclude as a cause or a substantial
`contributing factor to the development of Mr. Breakell’s
`mesothelioma?
`…
`A. Yes, if any products do not have asbestos in there, that should
`be excluded.
`
`Id. Rather, he opines that “every single exposure” that one experiences is “significant” and
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`contributes to one’s disease. Even an exposure that makes up “less than one percent [of Mr.
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`Breakell’s cumulative dose], still significant.” Breakell v. 3M Co. (f/k/a Minnesota Mining &
`
`Manufacturing Co.), et al., Deposition of Dr. Zhang, November 18, 2019, at 80, attached as
`
`Exhibit B. His opinion is convenient as he does not know what percentage of Mr. Breakell’s
`
`cumulative dose of asbestos was associated with dust related to Bendix brakes. Id. at 79. In fact,
`
`he cannot say whether Mr. Breakell’s potential exposure from Bendix brakes was one one-
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`hundredth of a percent of his cumulative dose. Id at 80. To him, the percentage is “not even
`
`relevant.” Id. at 79-80.
`
`The arbitrariness of his opinion is illuminated by the fact that despite not knowing what
`
`level of exposure Mr. Breakell experienced related to Bendix brakes, he nonetheless opines that
`
`the level would be “significant.” Id at 63. Dr. Zhang relies on Dr. Compton to determine the
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`amount of exposure Mr. Breakell experienced related to Bendix brake dust. Id. at 61. However,
`
`he concedes that Dr. Compton did not provide any estimate as to Mr. Breakell’s cumulative
`
`lifetime dose of asbestos or a dose of asbestos from Bendix brakes, specifically. Id. at 76-77. He
`
`ultimately admits that the dose is not necessary for him to reach a causation opinion. Id. at 77.
`
`14
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`

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`Further, Dr. Zhang believes there is no scientific evidence that cumulative exposures to
`
`asbestos within the range of ambient increase the risk of developing mesothelioma. Id. at 132-33.
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`However, without any information as to Mr. Breakell’s exposure dose from ambient air or from
`
`Bendix brakes, he is unable to determine whether his exposure from Bendix brakes was within
`
`the range of ambient air exposures. Id. at 133.
`
`II.
`
`PLAINTIFF’S EXPERTS’ CAUSATION OPINIONS FAIL ALL OF THE
`DAUBERT FACTORS.
`
`Plaintiff’s experts’ opinions are nothing more than the impermissible ipse dixit of
`
`professional witnesses. They show no meaningful understanding of Mr. Breakell’s alleged
`
`exposures to asbestos, particularly with respect to any specific products for which Defendants
`
`may be responsible. Plaintiff’s experts’ approach to causation is certainly convenient, but
`
`abdicates responsibility for engaging in the real inquiry at hand, both scientific (determination of
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`general and specific causation) and legal (“meaningful contribution” causation analysis),
`
`discussed in more detail below. Their causation theory is nothing more than a manufactured
`
`litigation position, an improper attempt to evade evidentiary burdens and the contrary body of
`
`scientific literature. This type of speculative testimony fails all of the Daubert factors and should
`
`not reach a jury in this Court.
`
`A.
`
`The theory cannot be tested or proven true or false.
`
`“[I]n order to qualify as ‘scientific knowledge,’ an inference or assertion must be derived
`
`by the scientific method.” Daubert, 509 U.S. at 590. “Scientific methodology today is based on
`
`generating hypotheses and testing them to see if they can be falsified; indeed, this methodology
`
`is what distinguishes science from other fields of human inquiry.” Id. at 593 (quotation and
`
`citation omitted).
`
`The medical and scientific community does not know the exact cause or mechanisms of
`
`15
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`

`

`cancer at the cellular level. As a result, it is not possible to know which, if any, of the fibers to
`
`which an individual is exposed are the causative fibers. There is no way to track those fibers to a
`
`specific defendant’s product. Consequently, given the current state of scientific knowledge, on
`
`the level of molecular biology, the cumulative exposure theory can be neither falsified nor
`
`validated. It remains an unproven hypothesis. See Butler, 310 Ga. App. at 38, 712 S.E.2d at 549
`
`(finding that plaintiff’s expert failed the first element of the Daubert scientific test because he
`
`testified that the any exposure theory “is not practically testable and has not been tested.”).
`
`Essentially, Plaintiff’s experts’ causation theory assumes what it wants to prove. It
`
`ignores the substantial differences between brake dust and chrysotile that are established in the
`
`scientific literature. And the theory does not allow the expert to exclude as causative any above-
`
`background exposure within an appropriate latency period.
`
`It is contrary to scientific methodology and common sense to presume that the presence
`
`of a disease is sufficient to prove its cause. See McClain v. Metabolife International, Inc. 401
`
`F.3d 1233 (11th Cir. 2005); Porter v. Whitehall L