PLAINTIFF’S RESPONSE TO DEFENDANT DAIMLER CHRYSLER CORPORATION’S
MOTION IN LIMINE TO STRIKE EXPERT TESTIMONY THAT
FRICTION PRODUCTS CAUSE MESOTHELIOMA
Plaintiff files this Response to Defendant Daimler Chrysler Corporation’s (“Chrysler’s”) Motion in Limine to Strike Expert Testimony that Friction Products Cause Mesothelioma, Asbestosis and Lung Cancer (“Motion in Limine”) and would respectfully show the Court as follows:
Table Of Contents
In Horton v. Harwick Chem. Corp. (1995), 73 Ohio St.3d 679, 653 N.E.2d 1196, the Ohio Supreme Court addressed the standards for proving causation in asbestos cases. In refusing to adopt a “mechanistic test regarding causation,” the Court recognized the existence of a “reasonable dispute as to what level of exposure can cause asbestos-related diseases. . . . Medical science suggests that very limited exposure to asbestos can cause mesothelioma, perhaps the worst of asbestos-related diseases.” Id. at 683-84. The Court specifically cited an article from the Journal of the American Medical Association, which explained:
[E]pidemiologists are recording cases of [mesothelioma] in persons who have worked with materials containing even small quantities of asbestos. . . . Brake-lining repair-persons, workers in chemical plants, refineries, powerhouses, and factories, and building maintenance personnel all are at risk.
Mesothelioma: Has Patient Had Contact With Even Small Amount of Asbestos? 257 JAMA 1569 (Mar. 27, 1987), attached as Exhibit 1 (emphasis added) (cited in Horton, 73 Ohio St.3d at 684). The view expressed in the Journal of the American Medical Association is shared by scientists throughout the world, based on an extensive body of scientific research regarding asbestos and mesothelioma. See, e.g., Huncharek, Brake Mechanics, Asbestos, and Disease Risk, Am. J. Forensic Med. & Pathology 11:236-240, 236 (1990), attached as Exhibit 2; Lemen, Asbestos in Brakes: Exposure and Risk of Disease, Am. J. Indus. Med. 45:229 (2004), attached as Exhibit 3; Environmental Protection Agency, Guidance for Preventing Asbestos Disease Among Auto Mechanics (June 1986), at 1, attached as Exhibit 4; World Trade Organization, European Communities – Measures Affecting Asbestos and Asbestos-Containing Products, Report of the Panel, Sept. 18, 2000 (“WTO Report”), excerpts attached as Exhibit 5, at ¶¶ 5.261, 5.263 (statements of independent scientific experts that “there is a risk of disease from the release of chrysotile fibres from friction products (as in brakes and clutches)” and that “[e]xposure to chrysotile asbestos through the manufacturing and downstream manipulation of friction products and textiles carries with it the risks associated with exposure to asbestos, most notably, lung cancer, asbestosis and mesothelioma.”); National Institute for Occupational Safety and Health Bulletin (“NIOSH Bulletin”), attached as Exhibit 6, at 1 (observing that “workers engaged in the maintenance and repair of automobile and truck brake linings are exposed to potentially hazardous levels of airborne asbestos dust.”).
Chrysler argues that this widely accepted scientific conclusion must be rejected, based on its interpretation of selected epidemiological studies. Chrysler has submitted an affidavit from Dr. Michael Goodman, a pediatrician and epidemiologist with very little experience in studying asbestos-related diseases. As discussed below, studies of brake mechanics suffer from inherent limitations and provide very little meaningful information. See, e.g., Huncharek, Changing Risk Groups for Malignant Mesothelioma, Cancer 69:2704-2711 (1992), attached as Exhibit 7 (summarizing problems in conducting epidemiological studies of brake mechanics). Dr. Goodman has essentially ignored these limitations and exaggerated the significance of the studies. Dr. Goodman’s analysis is not scientifically sound, nor does it provide a legal basis for excluding the Plaintiff’s expert testimony with respect to a disputed issue of fact.
Dr. Goodman’s affidavit was originally submitted in support of a similar motion in Chapin v. A&L Parts, Inc., before the Third Judicial Circuit Court in Michigan. That court, which has specialized in asbestos cases for more than a decade, recognized the numerous flaws in Dr. Goodman’s analysis and held that the plaintiff’s expert testimony had a reliable scientific basis. See Transcript of Daubert Hearing, Chapin v. A&L Parts, Inc., No. 03-324775-NP (Mich. Cir. Ct., Wayne County, Mich.) May 25, 2004, excerpts attached as Exhibit 8.
At a minimum, a reasonable scientific dispute exists with respect to whether exposure to asbestos from friction products causes mesothelioma. When the scientific evidence is disputed, “[i]t is not the province of the judge to immediately foreclose the validity” of expert testimony on the issue. Horton, 73 Ohio St. 3d at 685. “The inquiry by the trial judge should be whether there is evidence of exposure and evidence tying that exposure to the disease. Whether that evidence is strong enough to prove causation is an issue for the jury.” Id. at 686. The Court reaffirmed this general approach to expert testimony in Miller v. Bike Athletic Co., explaining that “a trial court’s role in determining whether an expert’s testimony is admissible under Evid. R. 702(C) focuses on whether the opinion is based upon scientifically valid principles, not whether the expert’s conclusions are correct or whether the testimony satisfies the proponent’s burden of proof at trial.” Miller v. Bike Athletic Co. (1998), 80 Ohio St.3d 607, 613-14, 687 N.E.2d 735 (quoting Joiner v. Gen. Elec. Co. (11th Cir. 1996), 78 F.3d 524, 530).
In this case, the Plaintiff’s expert testimony is based on scientifically valid principles and published, peer-reviewed scientific literature. Chrysler has offered no plausible legal or scientific basis for excluding this testimony.
MEDICAL AND SCIENTIFIC BACKGROUND
Asbestos and mesothelioma
The risk of mesothelioma is a function of asbestos exposure, not job classification. The causal relationship between asbestos and mesothelioma is so strong that mesothelioma is regarded as a “signature” or “sentinel” disease for asbestos exposure: a disease so associated with a single cause “that the presence of the disease presumes that cause.” Hall v. Baxter Healthcare Corp. (D. Or. 1996), 947 F. Supp. 1387, 1402. A textbook on epidemiology explains the significance of such diseases:
Certain conditions, known as “sentinel” health events, are so closely associated with occupational exposures that the occurrence of any cases serves as an indication of an occupational hazard. Malignant mesothelioma (which is nearly always attributable to asbestos exposure) . . . fit[s] this description.
Research Methods in Occupational Epidemiology 248 (Checkoway, et al., eds. 2d ed. 2004), excerpts attached as Exhibit 9 (citations omitted). Significantly, when a “sentinel” or “signature” disease has been identified, epidemiologists regard case reports as “particularly informative…. In fact, recognition of even a small number of cases of the ‘sentinel’ diseases” such as “malignant mesothelioma, which is strongly related to asbestos exposure can sometimes be invoked as prima facie evidence of exposure to the putative causal agent.” Research Methods in Occupational Epidemiology, supra, Exh. 1 at 60. The 1960 study that is generally credited with establishing the link between asbestos and mesothelioma was in fact a series of case reports. See Wagner, et al., Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province, Brit. J. Indus. Med. 17:260-271 (1960), attached as Exhibit 10. Indeed, one of the epidemiological studies cited by Chrysler acknowledges that “[m]esothelioma is a rare cancer with one major etiologic exposure, therefore surveillance using each case as a sentinel event might seem more reasonable for this disease than for cancers with multifactorial causation.” Teschke et al., Mesothelioma Surveillance to Locate Sources of Exposure to Asbestos, 88 Canadian J. Public Health 163, 167 (May – June 1997).
It is generally accepted among scientists that “[a]n occupational history of brief or low-level exposure [to asbestos] should be considered sufficient for mesothelioma to be designated as occupationally related.” Consensus Report, Asbestos, Asbestosis, and Cancer: The Helsinki Criteria for Diagnosis and Attribution, Scand. J. Work Envtl. Health 23:311-316 (1997), attached as Exhibit 11, at 313; see also J. Am. Med. Ass’n., supra, at 1569 (“To date, there has been no threshold level defined for asbestos-induced mesothelioma.”). In a study of low-level asbestos exposures, including those in the motor vehicle repair industry, a group of French researchers calculated that at cumulative asbestos exposures between 0.5 and 0.99 fibers/cc-years, the relative risk of mesothelioma rises to 4.2 (2.0-8.8 95% CI). Iwatsubo, et al., Pleural Mesothelioma: Dose-Response Relation at Low Levels of Asbestos Exposure in a French Population-Based Case-Control Study, Am. J. Epidemiology 148:133-42 (1998), attached as Exhibit 12, at 139 (Table 5). At cumulative exposures between 1 and 9.9 fibers/cc-years, the relative risk is 5.2 (3.1-8.8 95% CI). Id.
Exposure to asbestos from friction products
Friction products contained between 30 and 50 percent asbestos. Motion in Limine at 19. Although no safe threshold has been established with respect to mesothelioma, the maximum permissible exposure level is 0.1 fibers/cc, on an eight-hour time-weighted average (TWA). Tests conducted by government regulators and the manufacturers themselves have documented that mechanics are exposed to significant levels of asbestos during operations such as grinding, beveling and “blow-out.” See, e.g., Roberts & Zumwalde, NIOSH, Assessment of Asbestos Exposure to Mechanics Performing Brake Service Operations (April 27, 1981), attached as Exhibit 13, at 24 (finding exposures of up to 0.28 f/cc TWA for brake mechanics); Hickish & Knight, Exposure to Asbestos During Brake Maintenance, Ann. Occup. Hygiene 13:17-21 (1970), attached as Exhibit 14, at 18-19 (reporting TWA of up to 1.75 f/cc for work on truck brakes and up to 0.68 f/cc for work on car brakes); Kauppinen & Korhonen, Exposure to Asbestos During Brake Maintenance of Automotive Vehicles by Different Methods, Am. Indus. Hyg. Ass’n J., 48:499-504, 501 (1987), attached as Exhibit 15 (grinding of new brake linings results in “heavy exposure.”); Huncharek, Brake Mechanics, Asbestos, and Disease Risk, Am. J. Forensic Med. & Pathology 11:236-240 (1990), supra, at 237 (use of compressed air jet “liberates large quantities of asbestos dust into the surrounding environment.”); Environmental Protection Agency, Guidance for Preventing Asbestos Disease Among Auto Mechanics, supra, at 1 (“Millions of asbestos fibers can be released during brake and clutch servicing. Grinding and beveling friction products can cause even higher exposures.”); Letter from Paul E. Toth, April 23, 1975, attached as Exhibit 16 (“For the most part, whenever air hoses were used to clean dust out of the brake drums, we found exposures in excess of limits established in the OSHA standards on asbestos dust.”).
Tests conducted by researchers at the Mount Sinai School of Medicine in the 1970s found that average peak asbestos air concentrations for fibers longer than 5 μm were 10.5 f/ml for “blow-out” of automobile drum brake assemblies; 3.75 f/ml for grinding of used truck brake linings, and 37.3 f/ml for bevelling of new truck brake linings. See NIOSH Bulletin, supra, at 1. These levels of fibers longer than 5 μm were recorded even though the majority of the fibers were shorter than 5 μm. See id. NIOSH researchers concluded that “enough asbestos is preserved to produce significant exposures during certain brake servicing procedures.” Id.
Scientific consensus on friction products and mesothelioma
Given the level of asbestos exposure from friction products, and the extensive evidence that asbestos exposures cause mesothelioma and other asbestos-related diseases, independent scientists throughout the world have concluded that friction products cause disease. Dr. Arthur Musk, an independent expert consulted by the World Trade Organization in 2000, stated that “[i]t is my opinion that there is a risk of disease from the release of chrysotile fibres from friction products (as in brakes and clutches)… In general the risk will be dependent on the degree of exposure…” WTO Report 5.263. Dr. Peter Infante, former Director of the OSHA Office of Standards Review, explained in the same report that “[e]xposure to chrysotile asbestos through the manufacturing and downstream manipulation of friction products and textiles carries with it the risks associated with exposure to asbestos, most notably, lung cancer, asbestosis and mesothelioma.” Id. at 5.261.
The WTO also consulted with Dr. Douglas Henderson, one of the world’s leading experts on mesothelioma, who testified that the Australian Mesothelioma Registry has documented extraordinarily high rates of mesothelioma among workers exposed to asbestos from friction products. Chrysler attacks Dr. Henderson with a misleading citation to “the report of the World Trade Organization.” Motion at 15-16. The passage quoted by Chrysler is nothing but a summary of the arguments made by Canada’s representative. After consulting with the independent scientific experts, the Panel explicitly rejected Canada’s arguments, explaining that the “statistical data . . . confirmed the impact of chrysotile on mechanics exposed to that material in a car brake maintenance context.” WTO Report, supra, at 8.192 (emphasis added). The Panel further noted the “limits” of the Woitowitz study, on which both Chrysler and the Canadian government have placed inordinate weight. Id. The Panel concluded that the opinions of its independent scientific advisors “confirm the health risk associated with exposure to chrysotile in its various uses” and that the scientific evidence supported a finding that chrysotile posed a risk of causing “mesothelioma in the occupational sectors downstream of production and processing . . . .” Id. at 8.194.
As the WTO Panel observed, epidemiological studies involving brake mechanics offer very limited information. Few epidemiological studies have actually focused on brake mechanics, because of inherent problems in “tracing a large, nonunionized group of workers.” Huncharek, Changing Risk Groups for Malignant Mesothelioma, supra, at 2704. Although Chrysler seeks to inflate the number, Dr. Goodman admits in his affidavit that only four studies have ever specifically examined brake repair: a study authored by Spirtas et al.; an article by Hessel et al. (a “re-analysis” of the Spirtas data co-authored by Dr. Goodman); the study authored by Woitowitz and Rodelsperger; and the study authored by Teschke et al. See Affidavit of Dr. Michael Goodman (“Goodman Affidavit”) at 22. The Spirtas study does not actually calculate a relative risk for brake installation or repair. See Spirtas, et al., Malignant Mesothelioma: Attributable Risk of Asbestos Exposure, Occup. & Envtl. Med. 51:804-811 (1994).
The “re-analysis” of the Spirtas data, co-authored by Drs. Hessel and Goodman, was rejected for publication by the journal Occupational and Environmental Medicine, although Dr. Goodman fails to disclose that fact in his affidavit. See Deposition of Dr. Michael Goodman, excerpts attached as Exhibit 17, at 57-60. As discussed above, the significant limitations of the Woitowitz study were addressed in the WTO Report. The authors of the Teschke study acknowledge that “[m]esothelioma is a rare cancer with one major etiologic exposure, therefore surveillance using each case as a sentinel event might seem more reasonable for this disease than for cancers with multifactorial causation.” Teschke et al., Mesothelioma Surveillance to Locate Sources of Exposure to Asbestos, 88 Canadian J. Public Health 163, 167 (1997).
In light of the extensive body of scientific evidence that low-level asbestos exposure causes mesothelioma, these limited epidemiological studies should not be given undue weight in evaluating causation. Professor Sander Greenland, co-author of the standard textbook Modern Epidemiology, has explained the “logical fallacy of treating absence of evidence as evidence of absence” and notes that such an approach “has been recognized as a fallacy for over forty years.” Greenland, The Need for Critical Appraisal of Expert Testimony in Epidemiology and Statistics, 39 Wake Forest L. Rev. 2004 291, (2004), attached as Exhibit 18, at 298.
Outside the context of litigation, scientists do not rely solely on epidemiological studies in determining causal relationships. Professor Greenland has explained that it is never possible to determine causal relationships “from epidemiologic data alone.” Id. at 293. Particularly with respect to cancer, it is a “misconception” that causation can be determined “solely from the relative risk.” Greenland, Relation of Probability of Causation to Relative Risk and Doubling Dose: A Methodologic Error That Has Become a Social Problem, Am. J. Pub. Health 89:1166-1169 (1999), attached as Exhibit 19, at 1166. The correct way to assess causation “is by positing a specific biologic model for the disease process.” Id. at 1167; see also Savitz, Interpreting Epidemiologic Evidence: Strategies for Study Design and Analysis 294 (2003) (“[A] comprehensive evaluation of health risks or benefits ought never be based solely on epidemiologic information. Other biomedical disciplines, including toxicology, genetics, and pathology have relevance to human health.”) (emphasis added).
With respect to mesothelioma, scientists have generally accepted the biological model: exposure to asbestos fibers, even at low levels, causes mesothelioma. Consequently, scientists in the relevant disciplines have concluded that “[a]n occupational history of brief or low-level exposure [to asbestos] should be considered sufficient for mesothelioma to be designated as occupationally related.” Consensus Report, Asbestos, Asbestosis, and Cancer: The Helsinki Criteria for Diagnosis and Attribution, supra, at 313. In the legal context, whether the evidence of exposure is sufficient to show causation is a question for the jury. Horton, 73 Ohio St. 3d at 686.
ARGUMENTS AND AUTHORITIES
Ohio Law Does Not Require Epidemiological Studies to Prove Causation.
While epidemiological studies can be “‘powerful evidence of causation,’ their absence ‘is not fatal to a plaintiff’s case.’” Valentine v. PPG Indus., Inc. (Pickaway App.), 158 Ohio App. 3d 615, 2004-Ohio-4521, 821 N.E.2d 580, at ¶39, appeal allowed, No. 2004-1619, 104 Ohio St.3d 1438, 2004-Ohio-7033, 819 N.E.2d 1122 (quoting Rider v. Sandoz Pharm. Corp. (11th Cir. 2002), 295 F.3d 1194, 1198). Ohio courts have not used epidemiological studies as a “litmus test” for proving causation. Such a litmus test would conflict with the approach taken by the supreme court in Horton, rejecting a standard that “stacks the deck against plaintiffs by foreclosing all but one avenue of proof of causation.” Horton, 73 Ohio St. 3d at 686.
In this respect, Ohio is in accord with the vast majority of states. The final draft of the new Restatement (Third) of Torts: Liability for Physical Harm, which includes a section on toxic substances developed in consultation with the National Academy of Sciences, observes that “most courts have appropriately declined to impose a threshold requirement that a plaintiff always must prove causation with epidemiologic evidence.” Restatement (Third) of Torts: Liability for Physical Harm (hereinafter “Restatement (Third)”) §28, cmt. c (Final Draft No. 1, April 6, 2005). As the Fourth Circuit has explained:
[W]e do not read Daubert as restricting expert testimony to opinions that are based solely upon epidemiological data. Daubert merely requires that the expert testimony be both relevant and reliable; and Daubert clearly vests the district courts with discretion to determine the admissibility of expert testimony. Under the Daubert standard, epidemiological studies are not necessarily required to prove causation, as long as the methodology employed by the expert in reaching his or her conclusion is sound.
Benedi v. McNeil-P.P.C., Inc., 66 F.3d 1378, 1384 (4th Cir. 1995).
With respect to friction products, appellate courts have held that the available evidence creates a fact issue with respect to causation. For example, the New Jersey Supreme Court recognized that “whether the dust from brake products can cause mesothelioma” is a “factual dispute” that the jury should resolve:
…the trial revolved around a factual dispute over whether the dust from brake products can cause mesothelioma. In sum, plaintiff’s expert … testified in support of the propositions that garage mechanics are at risk of contracting the disease, that chrysotile asbestos can cause mesothelioma in humans, and that brake dust contains chrysotile. Defense experts, on the other hand, expressed the view that processed chrysotile does not cause mesothelioma and that used-brake dust contains chrysotile only in amounts under established safety standards. Confronted with that disagreement, the trial court should have permitted the jury to resolve the disputed issue of fact in respect of the dangers of the asbestos product involved in this case.
Becker v. Baron Bros., Coliseum Auto Parts, Inc. (1994), 138 N.J. 145, 158-59, 649 A.2d 613 (emphasis added). More recently, in Borg-Warner Corp. v. Flores, 153 S.W.3d 209 (Tex. App. 2004), the court affirmed a verdict against a brake manufacturer in an asbestosis case, based on expert testimony that “asbestosis can be caused by the inhalation of dust emitted from brake pads containing asbestos . . . .” Id. at 215 n.2. The court observed that “[i]n the context of asbestos-related claims, if there is sufficient evidence that the defendant supplied any of the asbestos to which the plaintiff was exposed, then the plaintiff has met the burden of proof.” Id. at 213.
As discussed above, scientists do not rely solely on epidemiological studies in assessing causation, particularly when the epidemiological studies have significant limitations. See Savitz, Interpreting Epidemiologic Evidence: Strategies for Study Design and Analysis 294 (2003) (“[A] comprehensive evaluation of health risks or benefits ought never be based solely on epidemiologic information. Other biomedical disciplines, including toxicology, genetics, and pathology have relevance to human health.”). Professor Greenland has explained that the likelihood of causation can never “be computed from epidemiologic data alone.” Greenland, supra, at 293.
Moreover, there is no scientific or legal basis for Chrysler’s assertion that a relative risk of 2.0 provides a “bright line” for determining causation. See, e.g., Sander Greenland, Relation of Probability of Causation to Relative Risk and Doubling Dose: A Methodologic Error That Has Become a Social Problem, supra, at 1166-67 (refuting the “misconception” that causation can be determined “solely from the relative risk” and explaining that a relative risk of 2.0 is not a prerequisite to finding a causal relationship). In rejecting a defendant’s argument that “unless [the substance at issue] is shown to create a relative risk greater than 2.0, [the expert’s] testimony is inadmissible,” one federal district court credited testimony that “the magnitude of relative risk is a continuum and a threshold of 2.0 is an arbitrary cut-off . . . .” Miller v. Pfizer, Inc. (D. Kan. 2002), 196 F. Supp. 2d 1062, 1079, aff’d, (10th Cir.), 356 F.3d 1326, cert. denied, (2004), 125 S. Ct. 40, 160 L. Ed. 2d 201. The New Jersey Supreme Court held that “a relative risk of 2.0 is not so much a password to a finding of causation as one piece of evidence, among others, for the court to consider in determining whether the expert has employed a sound methodology in reaching his or her conclusion.” Landrigan v. Celotex Corp. (N.J. 1992), 605 A.2d 1079, 1087.
Epidemiological Studies of Friction Products Have Limited Significance.
In the context of friction products, epidemiological studies should be interpreted with even more caution. Very few of the studies have examined a meaningful sample size because of the inherent difficulty in “tracing a large, nonunionized group of workers.” Huncharek, Changing Risk Groups for Malignant Mesothelioma, supra, at 2704. Several of the studies cited in Dr. Goodman’s list do not even have sufficient data to reach a conclusion. See Goodman Affidavit at ¶ 24. Reliance on such studies is a well-recognized fallacy, in which “uncritical authors or unsophisticated readers of a report . . . misinterpret the failure to obtain ‘statistical significance’ as being evidence of negativity.” Hernberg, “Negative” Results in Cohort Studies – How To Recognize Fallacies, Scand. J. Work Envtl. Health 7:121-126 (1981), attached as Exhibit 20, at 122. A true “negative” study must fulfill three criteria: “(i) it must be large; (ii) it must be sensitive; (iii) it must have well-documented exposure data.” Id. at 121. Even a study that seems to have a large sample size may be insufficiently large “if the disease under study is rare in relation to the cohort size and follow-up time . . . Such a study is in fact small, although its number of person-years may seem very impressive and may thereby cause confusion.” Id. at 122.
Even with larger sample sizes, studies of brake mechanics cannot accurately quantify the exposures. Huncharek, Changing Risk Groups for Malignant Mesothelioma, supra, at 2704. The studies cited by Dr. Goodman rely largely on job classifications, a method that typically results in “random misclassification of exposure status.” Teta, et al., Mesothelioma in Connecticut, 1959-1977, J. Occup. Med, 25: 749-755 (1983), at 754. Several of the studies, such as the Agudo study, rely on interviews with friends or relatives of deceased subjects, increasing the likelihood of misclassification. “Random misclassification,” also known as “nondifferential misclassification,” results in dilution of the sample, meaning that “the effect estimate will be pulled toward its null value. Hence, a study can never be taken as an indication that the exposure is lacking effect if the exposure assessment has been inflicted with nondifferential misclassification.” Ahlbom, et al., Interpretation of “Negative” Studies in Occupational Epidemiology, Scand. J. Work Envtl. Health 16:153-57 (1990), attached as Exhibit 21, at 154 (emphasis added). Given these limitations, Dr. Goodman’s excessive reliance on these studies is inappropriate. As Professor Greenland has explained, “[i]f one is more concerned with explaining associations scientifically, rather than with mechanical statistical analysis, evidence about validity can be more important than statistical results.” Greenland, The Need for Critical Appraisal of Expert Testimony in Epidemiology and Statistics, supra, at 302.
Even assuming that the epidemiological studies have some probative value, Dr. Goodman’s interpretation of these studies does not support the exclusion of different opinions. The Court should “present legitimate conflicting views of experts for the jury’s consideration.” Miller v. Bike Athletic, 80 Ohio St.3d at 613-14 (quoting Joiner, 78 F.3d at 530); see also Jahn v. Equine Services, PSC (6th Cir. 2000), 233 F.3d 382, 391 (holding that the trial court erred in discounting testimony of Plaintiffs’ experts because it was contradicted by defense expert and explaining that “comparing two pieces of evidence and determining which is more credible should be left for the finder of fact and should not be considered when ruling on Rule 702 admissibility”); see also Kennedy v. Collagen Corp. (9th Cir. 1998), 161 F.3d 1226, 1229 (trial court improperly “failed to distinguish between the threshold question of admissibility of expert testimony and the persuasive weight to be accorded such testimony by a jury”); Cartwright v. Home Depot U.S.A., Inc. (M.D. Fla. 1996), 936 F.Supp. 900, 902 (“the gatekeeping responsibility of the trial courts is not to weigh or choose between conflicting scientific opinions”).
Reliable Scientific Evidence Supports the Conclusion that Exposure to Asbestos from Friction Products Causes Mesothelioma.
Asbestos is an undisputed cause of mesothelioma, and the medical and scientific evidence indicates that asbestos from friction products can cause or contribute to the development of mesothelioma. As discussed above, exposure studies have documented medically significant exposures occur during the installation and repair of friction products, particularly grinding, beveling and “blow-out.” See, e.g., Roberts & Zumwalde, supra; Hickish & Knight, supra; Environmental Protection Agency, Guidance for Preventing Asbestos Disease Among Auto Mechanics, supra; NIOSH Bulletin, supra.
Outside the context of litigation, the friction products industry has consistently acknowledged the potentially harmful exposure to asbestos from these products. See, e.g., Letter from Paul E. Toth, April 23, 1975, supra (“For the most part, whenever air hoses were used to clean dust out of the brake drums, we found exposures in excess of limits established in the OSHA standards on asbestos dust.”); Letter from E.W. Drislane, Executive Director of the Friction Materials Standard Institute (“FMSI”), Nov. 28, 1972, attached as Exhibit 22, at 1 (“When customers of yours drill linings, chamber linings, cut linings, or grind linings, they may very well raise the asbestos concentrations in the atmosphere to above the OSHA standard.”); FMSI Friction Materials Work Practices Guide, October 1978, attached as Exhibit 23, at 3 (“Potentially hazardous airborne concentrations of asbestos dust can be created by improper cleaning and handling of worn brake and clutch assemblies, uncontrolled machining operations and poor housekeeping.”).
Chrysler asserts that all of the potentially harmful asbestos in its products is transformed to “forsterite” during use. First, this argument is irrelevant to exposures that occur during installation, when the asbestos is in its original state. Moreover, independent testing has confirmed that even after “thermal degradation” of friction products, “enough asbestos is preserved to produce significant exposures during certain brake servicing procedures.” NIOSH Bulletin, supra, at 1. In a NIOSH survey of brake repair facilities, 30 percent of the fibers released were identified as chrysotile asbestos, compared with 20 percent forsterite, leading the researchers to conclude that brake servicing posed a “potential health hazard.” Roberts & Zumwalde, supra, at 26 (“While the fiber exposures reported do not represent 100% asbestos fiber, a potential health hazard still exists since at least 30% of the fibers are asbestos.”).
Chrysler also maintains that the asbestos fibers found in brake dust are too small to cause disease, but this contention is inaccurate. “Any assumption that short fibers, less than 5 μm in length, are not hazardous cannot be justified based on the available science.” Lemen, supra, at 230. The threshold of 5 μm is used for regulatory purposes, primarily because the phase contrast microscope can only fibers greater than 5 um in length. Id. In an analysis of lung and mesothelial tissues from 168 patients with mesothelioma, researchers found that the majority of asbestos fibers found in the mesothelial tissues were shorter than 5 μm, supporting the conclusion that these relatively “short” fibers are carcinogenic. Suzuki & Yuen, Asbestos Fibers Contributing to the Induction of Human Malignant Mesothelioma, Ann. N.Y. Acad. Sci., 982:160-176 (2002), attached as Exhibit 24, at 173; see also Dodson, et al., Asbestos Fiber Length as Related to Potential Pathogenicity: A Critical Review, Am. J. Indus. Med. 44:291-297 (2003), attached as Exhibit 25 (reviewing data indicating that fibers shorter than 5 μm contribute to disease).
Because mesothelioma is a “sentinel” disease, reports of mesothelioma among brake mechanics are “particularly informative.” Research Methods in Occupational Epidemiology, supra, at 60. A number of published reports have documented mesothelioma in workers whose only known asbestos exposure was through friction products. In 1982, researchers described “a diffuse pleural mesothelioma in a man whose sole exposure to asbestos was to the chrysotile form during brake maintenance and repair.” Langer & McCaughey, Mesothelioma in a Brake Repair Worker, Lancet (1982), attached as Exhibit 26. Autopsy specimens of the lung were examined, and electron diffraction analysis confirmed the structures found in the lung to be that of chrysotile asbestos. Ten percent of those fibers were longer than 10 μm. Id.; see also Hansen, Mortality of Auto Mechanics, Scand. J. Work and Envtl. Health 15:43-46, 45 (1989), attached as Exhibit 27 (“Asbestos exposure is known to occur during the replacement of brake linings, and the single case of pleural mesothelioma is an indication that the exposure has not been negligible.”); Huncharek et al., Pleural Mesothelioma in a Brake Mechanic, Brit. J. Indus. Med, 46:69-71 (1989), attached as Exhibit 28 (describing mesothelioma in man whose only asbestos exposure was from clutch and brake products); Huncharek, Chrysotile Asbestos Exposure and Mesothelioma, Brit. J. Indus. Med. 44:287-288 (1987), attached as Exhibit 29 (reporting mesothelioma in friction product workers; analysis of lung tissue specimens revealed 51 million to 266 million asbestos fibers per gram of wet tissue, 99% of which were chrysotile asbestos); Report of Occupational Disease Fatalities, Alberta, Canada (2001), attached as Exhibit 30 (“58-year old heavy duty mechanic developed malignant pleural mesothelioma as a result of a 26 year exposure to asbestos from brake linings and clutches”); Report of Occupational Disease Fatalities, Alberta, Canada (2002), attached as Exhibit 31 (“71-year old heavy duty mechanic died from malignant mesothelioma resulting from exposure to asbestos between 1959-1972”); McDonald et al., Epidemiology of Primary Malignant Mesothelial Tumors in Canada, Cancer, 914-918, 916-18 (1970), attached as Exhibit 32 (reporting mesothelioma in two workers who installed brake linings and observing that “[m]en employed in asbestos textile manufacture, the installation of brake linings, or as insulators were responsible for most of the excess of cases over controls”).
As discussed above, the Australian Mesothelioma Registry confirmed excessive rates of mesothelioma among mechanics. Chrysler argues that the overall rate of mesothelioma in Australia is high, but vehicle mechanics have an increased risk of mesothelioma even when compared to other occupations in Australia. For a vehicle mechanic in Australia, the overall lifetime mesothelioma risk is calculated to be 0.7%, significantly higher than the background lifetime risk of mesothelioma in Australia, which is 0.007%. See Lemen, supra, at 234. It is highly unlikely that this substantial increase is due solely to chance. See id.
Plaintiff’s experts have concluded, based on reliable, generally accepted scientific principles, that exposure to asbestos from friction products contributes to the development of mesothelioma. Such expert testimony is admissible, whether or not the court agrees with the expert’s conclusion. See Miller v. Bike Athletic, 80 Ohio St.3d at 613-14 (“a trial court should not reject one expert opinion for another simply because it believes one theory over the other…. a trial court’s role in determining whether an expert’s testimony is admissible under Evid. R. 702(C) focuses on whether the opinion is based upon scientifically valid principles, not whether the expert’s conclusions are correct or whether the testimony satisfies the proponent’s burden of proof at trial”).
In sum, reliable scientific evidence supports a finding that exposure to asbestos from friction products contributes to the development of mesothelioma. Whether that exposure was a substantial factor in causing the Decedent’s mesothelioma must be left to the jury to determine. Horton, 73 Ohio St. 3d at 686 (“The inquiry by the trial judge should be whether there is evidence of exposure and evidence tying that exposure to the disease. Whether that evidence is strong enough to prove causation is an issue for the jury.”); see also Fraysure v. A Best Prod. Co., Cuyahoga App. No. 83017, 2003-Ohio-6882, at ¶¶8-9 (finding sufficient evidence of causation where decedent used valve packing containing chrysotile asbestos “extensively throughout the 1970s” and plaintiff’s experts testified that decedent’s work produced asbestos dust that exceeded OSHA standards, and that chrysotile asbestos was an established cause of mesothelioma); Blansett v. BP Exploration & Oil Inc., Allen App. No. 1-2000-40, 2002-Ohio-4757, at ¶58 (“In order to be injured, the party must, obviously, have been exposed to enough of the substance to cause harm. What amount causes harm is a question of fact for the jury to determine.”).
The Defendants have offered no sound legal or scientific basis for excluding Plaintiff’s expert testimony on causation. Plaintiff respectfully requests that the motion in limine regarding be denied in its entirety.
- ↑ This Response addresses the arguments pertinent to mesothelioma. Because the Plaintiff is not seeking compensation for asbestosis or lung cancer, any portions of Daimler Chrysler Corporation’s motion involving those diseases are irrelevant and will not be addressed in this Response.
- ↑ See Hurtado v. Purdue Pharma Co. (N.Y. Sup. Ct. 2005), 6 Misc. 3d 1015(A), ___ N.Y.S.2d ___, 2005 WL 192351, at *6 (contrasting injuries alleged in that case to “‘signature diseases’ like asbestosis or mesothelioma, which only come from asbestos contact”); In re Seventh Judicial Dist. Asbestos Litig. (N.Y. Sup. Ct. 2002), 191 Misc.2d 625, 631, 744 N.Y.S.2d 304 (“Although there may be other causes of lung cancer, mesothelioma has been described as the ‘….signature disease for asbestos exposure’ and may result from a relatively low level of exposure.”); Abadie v. Metro. Life Ins. Co. (La. App. 2001), 804 So.2d 11, 15 (noting that plaintiff “suffered from mesothelioma, a fatal signature disease related to asbestos exposure”).
- ↑ Hickish and Knight cautioned that their averages may have been too low, because “[o]ur environmental studies have not included maintenance procedures which involve the filing or grinding of brake lining material, and we would envisage that these would give rise to considerably increased air contamination by chrysotile asbestos . . . ” Hickisk & Knight, supra, at 21.
- ↑ Mr. Toth headed Ford Motor Company’s Industrial Hygiene Section.
- ↑ See also Cloud v. Pfizer Inc. (D. Ariz. 2001), 198 F. Supp. 2d 1118, 1134 (“the Court considers the 2.0 threshold as a factor, not the dispositive factor, in determining the reliability of [an expert’s] testimony on general causation”); McDaniel v. CSX Transp., Inc. (Tenn 1997), 955 S.W.2d 257, 264 (relative risk above 2.0 “is certainly relevant but we reject the contention that it should be adopted as matter of law”).