1.Is it a “clear abuse of discretion” for a court to consider all of the potentially relevant scientific evidence before ruling on its reliability and sufficiency?

2.Should a multidistrict litigation court be required to resolve challenges to expert testimony on a global basis, when the record does not contain all of the relevant scientific evidence?


In November 2004, the court charged with overseeing Texas asbestos multidistrict litigation (“MDL”) heard a global motion to strike expert testimony that asbestos from “friction products”[1] can cause asbestos-related diseases. After a lengthy hearing, the MDL court granted the motion in part and denied it in part, pending review of the expert testimony offered in individual cases.[2] Chrysler seeks a writ of mandamus ordering the MDL court to strike all case-specific expert testimony.[3] The evidence in the record supports the MDL court’s decision to consider case-specific expert testimony before ruling on its admissibility.

Overview of Asbestos-Related Diseases

Asbestos is a firmly established cause of several different diseases, including malignant mesothelioma, asbestosis and lung cancer.[4] Malignant mesothelioma, which is caused by exposure to asbestos, is literally a textbook example of a “signature” or “sentinel” disease:

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), silicosis, and adult lead poisoning, fit this description.[5]

To put it in more precise numerical terms, for men with pleural mesothelioma, the “attributable risk” with respect to asbestos exposure is nearly 90 percent.[6] Asbestosis is distinct from mesothelioma but is also a signature disease for asbestos exposure.[7] Lung cancer, which has multiple causes, is not a signature disease but is indisputably linked with occupational asbestos exposure.[8]

In 1997, a multidisciplinary panel of scientists meeting in Helsinki, Finland published a set of criteria for the diagnosis and attribution of asbestos-related diseases.[9] The Helsinki Criteria describe accepted methods for determining occupational exposure and evaluating the physical manifestations of asbestos-related disease.

Scientific Criteria for Evaluating Asbestos-Related Diseases

The Helsinki Criteria explain the use of “histological, immunohistochemical and ultrastructural markers for the diagnosis of mesothelioma.”[10] A “lung fiber count exceeding the background range for the laboratory in question or the presence of radiographic or pathological evidence of asbestos-related tissue injury (e.g., asbestosis or pleural plaques) or histopathologic evidence of abnormal asbestos content (e.g., asbestos bodies in histologic sections of lung) should be sufficient to relate a case of pleural mesothelioma to asbestos exposure on a probability basis.”[11]

At the hearing, Dr. Ronald Dodson testified about the analysis of asbestos fibers in tissue samples. Dr. Dodson is a professor of cell biology at the University of Texas Health Center at Tyler who has specialized in the study of asbestos-related diseases since 1977.[12] Over that period of time, he has published nearly 100 articles and several textbook chapters on asbestos-related diseases.[13] Dr. Dodson described the accepted methods used to analyze asbestos fibers and asbestos bodies in tissue samples and the “biological significance” of such analysis.[14] The MDL court subsequently found Dr. Dodson’s testimony “scientifically provable, measurable, peer-reviewed and credible.”[15]

Measuring Occupational Exposures to Asbestos

In evaluating exposure, the Helsinki Criteria recommend using “reliable work histories” to “identify persons who have a work history compatible with significant asbestos exposure.”[16] In addition, “[d]ust measurements can be used in the estimation of past fiber levels at typical workplaces and in the use of asbestos-containing materials. A cumulative fiber dose, as expressed in fiber-years per cubic centimeter [f/cc-years], is an important parameter of asbestos exposure.”[17]

During the relevant time frame, friction products contained up to 50 percent chrysotile asbestos.[18] Several studies have documented the levels of asbestos released by friction products, particularly during the grinding of new brake linings.[19] Tests conducted in New York demonstrated that the grinding of new brake linings produced asbestos “in quantities . . . capable of causing all three of the asbestos-related diseases.”[20] Significant asbestos exposure also occurs when dust is blown out of brake linings using compressed air, which was at one time a “very common practice.”[21] Asbestos exposures from work on friction products can exceed the maximum accepted levels on both a time-weighted average and a peak exposure basis.[22]

Outside the context of litigation, the automotive industry has reached similar conclusions. The head of Ford Motor Company’s Industrial Hygiene Section wrote in 1975 that “[f]or 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.”[23] Several years before, the director of the Friction Materials Standard Institute had cautioned the industry that “[w]hen 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.”[24]

Effects of Asbestos Exposure from Friction Products

It is generally accepted 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.”[25] This finding has been confirmed in several epidemiological studies, including a French study published in the American Journal of Epidemiology in 1998.[26] This study of low-level asbestos exposures, including those in the motor vehicle repair industry, calculated that at cumulative asbestos exposures between 0.5 and 0.99 fibers/cc-years,[27] the relative risk of mesothelioma rises to 4.2 (2.0-8.8 95% CI).[28] At cumulative exposures between 1 and 9.9 fibers/cc-years, the relative risk is 5.2 (3.1-8.8 95% CI).[29] A 1994 study grouped several occupational exposures, including brake lining work or repair, and reported a relative risk for mesothelioma of 10.7 at a 95% confidence interval.[30]

Despite the difficulties in “tracing a large, nonunionized group of workers” such as brake mechanics,[31] many scientists have concluded that exposure to asbestos from friction products can cause asbestos-related disease. A 1987 article in the Journal of the American Medical Association explained that mesothelioma occurs “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.”[32] More recently, members of a scientific panel convened by the World Trade Organization concluded 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.”[33]

Dr. Michael Goodman, an expert witness for Chrysler, testified that his “re-analysis” indicated that the asbestos from friction products does not cause disease.[34] Dr. Goodman admitted during his deposition that this re-analysis was initially rejected for publication by the peer-reviewed journal Occupational and Environmental Medicine.[35] The re-analysis subsequently appeared in a publication called Risk Analysis. All but one of the authors of the article were employed by Exponent, a firm that performs consulting work for Chrysler.[36]

Dr. Goodman, who was trained as a pediatrician, has no significant expertise in studying asbestos-related diseases.[37] His interpretations of the available data are highly debatable.[38] Dr. Goodman’s affidavit conceded that only four of the studies on which he relied actually examined the association between mesothelioma and brake repair.[39] One of these (Hessel, et al. 2003) was the “re-analysis” discussed above, which was rejected by peer reviewers. Even for this smaller group of studies, he was unable to specify the criteria used to classify workers.[40]

Dr. Goodman relied on one study in which the average age of the participants was 38.[41] Dr. Goodman’s analysis also included studies that lacked sufficient statistical power to detect risk.[42] More broadly, any effort to make generalizations about mechanics as a class is vulnerable to misclassification errors. The inclusion of a wide range of different exposures in the same job classification dilutes the sample, which “would tend to bias the odds ratio toward one, i.e. no effect[.]”[43]

Analyzing Causation in Individual Cases

The Plaintiffs called Dr. Richard Lemen to discuss the relevant scientific literature. Before his retirement, Dr. Lemen spent more than 25 years conducting and supervising epidemiological research on asbestos and other occupational hazards for the National Institute on Occupational Safety and Health (NIOSH).[44] At the time of his retirement, he was Deputy Director of NIOSH and Assistant Surgeon General of the United States.[45] He has published extensively on asbestos-related diseases, including the monograph on the carcinogenic effects of asbestos adopted by the World Health Organization’s International Agency for Research on Cancer in 1976.[46]

As the MDL court observed, Dr. Lemen candidly acknowledged that he was not aware of “an epidemiological cohort study that says workers who work around friction products have a relative risk of two or greater to develop asbestos disease.”[47] Asked if that was “the end of the story,” Dr. Lemen explained:

The end of the story is if an individual is exposed and [develops] a disease that has been recognized in multiple epidemiological studies, as is the case of asbestos where we have ample evidence from epidemiology that asbestos causes various diseases including asbestosis, lung cancer, mesothelioma, then it is a matter of looking at the individual and the exposure to the individual . . . It is not the title of the occupation [but] the exposure within that occupation that determines the risk.[48]

Because the “general causation epidemiology” has “already been established,” the relevant question is “can brake mechanics who work with asbestos-containing friction products develop asbestos-related disease, and the answer is clearly, yes, if they are exposed to asbestos in sufficient amounts to cause disease.”[49] This question is “purely dependent upon whether the friction worker is exposed . . . .”[50]

Asbestos-related diseases are “dose-response” diseases, meaning that “the higher the exposure, the more the risk of developing disease.”[51] With respect to friction products, “it is the dose and it is the ability of the friction product to produce asbestos that can result in the disease.”[52] Workplace measurements have confirmed that friction products “release chrysotile fibers in an amount and size . . . capable of producing asbestos disease.”[53] If friction products “are manipulated, if they are used in the way that we have talked about, they are capable of releasing fibers of asbestos sufficient to cause asbestos-related disease.”[54]

At the conclusion of his direct testimony, Dr. Lemen summarized his analysis of the causation issue:

Q.Is it your opinion that we need to look at individual cases and individual exposures *** before a determination of causation can be made ***?

A.Well, I think the exposures vary from individual to individual. I think that you have to look at it from an individual by individual basis as to what the exposures were. The lack of the epidemiological studies showing overall statistical significance would point you to the direction of looking at the exposures, and as those exposures develop what are the results and can the disease be attributed to such exposures based upon sound scientific criteria such as the Helsinki Criteria or the American Thoracic [Society] Criteria or other criteria for diagnosing cases and disease.[55]

The court clarified the point further during Dr. Lemen’s cross-examination:

The Court:You just used two words, can and do. Let me ask you to break that out because the person that testified in Havner used the word “can.”[56]

The Witness:Yes, sir.

The Court:There is a difference between “can” and “did”?

The Witness:Yes, sir.

The Court:Are you saying “can” or are you saying “did” in every case?

The Witness:No. I don’t think you can say “did” in every case. I think you can say they “can” put an individual at an increased risk of developing disease. ***

The Court:To get you to “did,” that requires somebody to testify to specific causation which you are not doing here?

The Witness:That is correct.[57]

In light of the scientific evidence, the MDL court ultimately concluded that “[r]egrettably, . . . the court is unable to find that either a total granting or denial of the motion is possible on this record . . . .”[58] Because the studies of brake mechanics as a class did not “establish a causation link,” the court would have to examine the individual plaintiff’s occupational history and medical condition:

By way of example, if a plaintiff worked for forty years as a brake mechanic, and an autopsy showed chrysotile fibers in his lungs, there could well be a scientific basis for allowing such testimony to be considered by a jury.[59]

The MDL court therefore denied the motion in part, “ without prejudice to a determination, on a case-by-case basis, that the specific evidence offered on behalf of a plaintiff is legally insufficient to constitute admissible testimony.”[60]

Subsequent Findings on Chrysotile Asbestos

Several months later, after conducting a more comprehensive “general causation” hearing, the MDL court ruled that the Plaintiffs had made “a valid epidemiological case” that chrysotile asbestos is capable of causing mesothelioma.[61] The court relied on Dr. Lemen’s “credible and consistent” testimony regarding the relevant epidemiological studies, which demonstrated a “sound scientific basis” for the Plaintiffs’ general causation evidence.[62] The court also concluded that expert testimony on cell biology was “credible, consistent, generally accepted in the scientific literature, and is sufficient evidence, even without epidemiological evidence discussed above, for proof of general causation.”[63] As discussed above, chrysotile asbestos was the type used in Chrysler’s products.

In each of these rulings, the MDL court has determined that its rulings on expert testimony must be based on the totality of the relevant scientific evidence. With respect to friction products, the court has held that individual Plaintiffs must proffer scientifically reliable evidence of causation. Chrysler has not identified any factual or legal basis for overturning that decision.


The MDL Court Did Not Abuse Its Discretion By Deciding to Consider the Totality of the Relevant Scientific Evidence.

A.Trial Courts Have Broad Discretion in Deciding How to Evaluate Expert Testimony.

The trial court is “the evidentiary gatekeeper” with primary responsibility for determining the reliability of expert testimony.[64] The court “enjoys wide latitude in determining whether expert testimony is admissible.”[65] The court “must have the same kind of latitude in deciding how to test an expert’s reliability, and to decide whether or when special briefing or other proceedings are needed to investigate reliability, as it enjoys when it decides whether or not that expert’s relevant testimony is reliable. . . .That [abuse of discretion] standard applies as much to the trial court’s decisions about how to determine reliability as to its ultimate conclusion.”[66]

The “factors a trial court will find helpful in determining whether the underlying theories and techniques of the proffered evidence are scientifically reliable will differ with each particular case,”[67] and “[c]areful exploration and explication of what is reliable scientific methodology in a given context is necessary.”[68] As the Third Circuit observed several years ago, the scientific evidence regarding friction products “creates an issue that could well go either way as to whether Plaintiffs satisfy the Daubert gatekeeping standard.”[69]

B.Chrysler Must Establish a Clear Abuse of Discretion.

In order to warrant mandamus relief, Chrysler must show “that the trial court clearly abused its discretion” and that it has “no adequate remedy by appeal.”[70] As this Court explained in Prudential, in some cases an error is “was clear enough, and correction simple enough,” that mandamus review is appropriate.[71] Chrysler has not made such a showing in this case.

Chrysler argues that one of this Court’s comments on the MDL rules “presumes that parties do not have an adequate remedy by appeal.”[72] This Court has never adopted a “presumption” that parties in an MDL lack an adequate remedy by appeal. Mandamus may or may not be appropriate in an MDL proceeding, or in any other type of proceeding, depending “on the circumstances presented.”[73] As the party seeking mandamus, Chrysler must provide this Court “with a sufficient record to establish [its] right to mandamus relief.”[74]

Under the standards described in Prudential, the availability of mandamus review depends on the nature of the alleged error and the scope of the record. If the trial court is presented with the question of whether “2 + 2 = 4,” a wrong answer can readily be corrected by mandamus. If the trial court is presented with the question of whether “2 + x + y = 4,” the correctness of the answer depends on variables that have not yet been defined. Chrysler essentially asked the MDL court to consider one aspect of the causation evidence, and the court concluded that more information was necessary to determine whether the “totality of the evidence” created a fact issue as to causation. As the court observed in In re Dow Corning Corp.,[75] cited on page 32 of Chrysler’s brief, general causation is “only part of the liability equation.”[76]

C.The MDL Court Did Not Find that the Evidence of General Causation Was Insufficient.

The cornerstone of Chrysler’s argument is the contention that the MDL court “made an express finding that plaintiffs did not demonstrate general causation.”[77] The court made no such finding, express or otherwise. The court found that the epidemiological studies of mechanics as a class did not “establish a causation link” but that other evidence could provide a reliable scientific basis for causation testimony.[78] The court concluded that, on the record before it, it was not possible to grant or deny the motion to strike in its entirety.[79]

Chrysler’s argument rests on an incorrect use of the term “general causation.” As defined by this Court in Havner, the concept of “general causation” involves whether “a substance is capable of causing a particular injury or condition in the general population.”[80] The concept of “specific causation” involves whether “a substance caused a particular individual’s injury.”[81]

In this case, the substance at issue is asbestos, more precisely chrysotile asbestos.[82] None of the parties disputed that exposure to chrysotile asbestos is capable of causing asbestos-related diseases.[83] After a more comprehensive hearing, the MDL court expressly found that the Plaintiff had made “a valid epidemiological case” that chrysotile asbestos is capable of causing mesothelioma.[84] The question is whether exposure to asbestos from friction products caused or contributed to disease in particular plaintiffs. That question necessarily requires an examination of the medical and scientific evidence with respect to those plaintiffs.

Chrysler cites a number of cases, virtually all of which involve threshold questions about whether the substance at issue is even capable of causing disease. In Hall v. Baxter Healthcare Corp., 947 F.Supp. 1387 (1996) (D. Or. 1996), cited on pages 33 and 39-40 of Chrysler’s Brief, the court explained that “the issue before me in this Daubert hearing is silicone gel’s ability to cause disease in women with breast implants. Courts, however, have recognized two levels of causation: general causation (i.e., whether silicone gel can cause disease in anyone) and specific causation (i.e., whether silicone gel breast implants caused disease in this plaintiff).”[85] When a toxic substance is used in different products, studies of the relevant “chemical components” may provide “reliable causation evidence” under Havner.[86]

In Hall, the court found no scientifically reliable evidence that connective tissue disease was “silicone-induced” or that “silicone ‘more likely than not’ causes disease . . . in women.”[87] The court specifically distinguished asbestos cases, noting that silicone was not associated with any “‘signature’ disorder to suggest . . . that the cause is silicone exposure.”[88] The court explained that “[a] signature disease is one so associated with a particular cause that the presence of the disease presumes that cause. For example, malignant mesothelioma is a signature disease for asbestos causation.”[89] In denying one of Chrysler’s previous Daubert motions, a Michigan court made a similar observation:

This case does not present a situation like the one that was presented to me in the breast implant litigation regarding whether the science supported the plaintiffs’ claims that breast implants caused injury to the auto-immune system. The science with respect to asbestos and causation of mesothelioma has existed for years.[90]

Chrysler does not cite a single case involving general causation with respect to asbestos. This is not accidental. In a comment developed in consultation with the National Academy of Sciences, the final draft of the new Restatement (Third) of Torts: Liability for Physical Harm explains that “[w]hen the connection between an agent and a disease is strong and well documented, general-causation issues fade into the background. Thus, in asbestos cases, the general-causation question does not arise with regard to mesothelioma, asbestosis and lung cancer because the causal connection between asbestos and those diseases is quite well-established.”[91]

In Pittsburgh Corning Corp. v. Walters,[92] the only reported case that has discussed Havner in the context of mesothelioma, the court explained that the causation questions identified in Havner “do not arise. In other words, there is no dispute here that Douglas Walters’ condition was caused by inhalation of asbestos fibers.”[93] In this case, there was likewise no dispute that mesothelioma is caused by inhalation of asbestos fibers:

The Court:If you have mesothelioma, you probably got it from asbestos? *** From some kind of asbestos?

The Witness:That is correct. Yes, sir.

The Court:That’s not disputed, is it?

Mr. Thackston:No, Your Honor.[94]

The Court:Nobody disputes that. What you’re trying to do it establish the reverse, that in a particular plaintiff they got mesothelioma from the products of, in part at least, using the legal causation standard given to us by the Supreme Court, by the products of these defendants . . . .[95]

As Dr. Lemen explained, the answer to this question depends on the nature and extent of the plaintiff’s exposure.[96] During Dr. Goodman’s testimony, counsel for the Plaintiffs observed that “[a]s an epidemiologist, you don’t know the permutations of exposure that exist out there.”[97] Dr. Goodman responded, “I see the point.”[98] Questioned about mechanics who may have higher exposures, Dr. Goodman replied “I don’t know what to say to that. It’s a hypothetical. I don’t even know those guys exist[] . . . .”[99]

Rather than addressing individual facts, Chrysler’s attorney simply hypothesized that every Plaintiff in the MDL did “a couple of these brake jobs a week.”[100] To its credit, the MDL court did not rely on such vague generalizations. The court decided that it was necessary to conduct “a case-by-case review of the occupational history of each Plaintiff, together with a review of the pathology, to determine whether there is a scientific basis to admit any evidence of causation as to any Defendant’s product [and] any particular Plaintiff.”[101]

D.The Plaintiffs Are Entitled to Present All Relevant and Reliable Causation Evidence.

Chrysler contends that “[i]t is well-settled Texas law that when epidemiology fails to establish general causation, plaintiffs cannot offer ‘other evidence’ . . . .”[102] This cannot be “well-settled Texas law,” since no Texas court has ever made such a ruling. In Havner, this Court explained that “[w]e need not decide in this case whether epidemiological evidence with a relative risk less than 2.0, coupled with other credible and reliable evidence, may be legally sufficient to support causation.”[103] The Court emphasized that “evidence of causation from whatever source must be scientifically reliable. Post hoc, speculative testimony will not suffice.”[104] The MDL court has not admitted any “[p]ost hoc, speculative testimony.” The court has held that the Plaintiffs may offer scientifically reliable evidence in individual cases.

As discussed above, reliable epidemiological evidence does establish general causation with respect to chrysotile asbestos, the substance at issue. More specific evidence is necessary to establish causation in individual cases. Chrysler asserts that “[c]ausation in toxic tort cases requires epidemiology and Havner requires that relevant studies show a doubling of the risk of disease among the relevant population.”[105] Neither Havner nor any other Texas case has held that “[c]ausation in toxic tort cases requires epidemiology,” and the majority of courts have rejected such a dogmatic position.[106]

Indeed, many of the cases cited in Chrysler’s brief expressly reject this argument. In 3M v. Atterbury,[107] which Chrysler cites several times, the court explained in no uncertain terms that “[d]espite 3M’s allegations of set rules, [Havner] refused to set any strict rules regarding what types of evidence would be sufficient or not sufficient to support a finding of causation. There is no requirement in a toxic tort case that a party must have reliable epidemiological evidence of a relative risk of 2.0 or greater.”[108]

In Pick v. American Medical Systems, Inc.,[109] cited on page 32 of Chrysler’s brief, the court was equally emphatic: “As noted, AMS takes the position that epidemiological evidence is required by the Fifth Circuit before a hypothesis can be considered scientifically valid in a court of law, citing Brock, supra. This Court disagrees. In Brock, the court stated that epidemiological proof was ‘the most useful and conclusive type of evidence’ but specifically stated that [it was] not holding that it is a ‘necessary element in all toxic tort cases.’ Brock, 874 F.2d at 313. . . .Other courts have more clearly stated that epidemiological evidence is not essential for an expert opinion to be admissible in a case such as this: ‘As long as the basic methodology employed to reach such a conclusion is sound, such as use of tissue samples, standard tests, and patient examination, products liability law does not preclude recovery.’”[110]

This Court has certainly never adopted Chrysler’s approach. In Havner, this Court held that epidemiological studies “may be part of the evidence supporting causation in a toxic tort case.”[111] The Court recognized that in other cases, “there will be objective criteria by which it can be determined with reasonable certainty that a particular individual’s injury was caused by exposure to a given substance.”[112] The Court emphasized that “evidence of causation from whatever source must be scientifically reliable”[113] In this case, the MDL court denied the motion with respect to causation testimony that was “scientifically provable, measurable, peer-reviewed and credible.”[114]

Moreover, this Court has explained that “[c]areful exploration and explication of what is reliable scientific methodology in a given context is necessary.”[115] The Court specifically disavowed any “bright-line boundary” or “litmus test.”[116] Courts “should be cautious about adopting specific ‘scientific’ principles, taken out of context, to formulate bright-line legal rules or conclude that reasonable minds cannot differ about factual causation.”[117]

Chrysler’s argument, which relies primarily on cases involving breast implants and Bendectin, does not address accepted scientific methodology in the context of asbestos-related disease. In one of the breast implant cases cited by Chrysler, the court explains that “[w]hile epidemiological evidence is not a necessary element in every toxic tort case, it is certainly a very important element, especially when there is no evidence of the biological mechanism which links the product to the complained-of condition.”[118] In this case, by contrast, the MDL court heard extensive evidence of the “biological mechanism” linking asbestos exposure and disease.

Indeed, after conducting a more comprehensive hearing, the MDL court observed that the biological evidence was “credible, consistent, generally accepted in the scientific literature, and is sufficient evidence, even without epidemiological evidence discussed above, for proof of general causation.”[119] In this proceeding, the court determined that additional case-specific evidence could provide a reliable scientific basis for causation testimony as to individual Plaintiffs. In light of this finding and the other evidence presented, the court’s decision to deny Chrysler’s motion in part was certainly not a “clear abuse of discretion.”


A.General and Specific Causation Do Not Require Separate Proof.

In Havner, this Court explained that “[s]ometimes, causation in toxic tort cases is discussed in terms of general and specific causation.”[120] Based on this observation, Chrysler maintains that it is an abuse of discretion to consider “‘other evidence’ without the requisite proof of general causation. Without proof of general causation, the admittance of ‘other evidence’ is erroneous under Texas law.”[121] Chrysler cites many cases discussing general and specific causation, but not one of them holds that it is improper for a court to consider all of the potentially relevant evidence before determining the admissibility of expert testimony. None of the cases involve scientific issues that are even analogous to the issues in this case.

Chrysler relies heavily on partial quotations from Coastal Tankships, U.S.A., Inc. v. Anderson[122] but ignores much of the court’s analysis in that case. Coastal Tankships does not stand for the proposition that a court must categorically refuse to consider evidence of specific causation without a preliminary showing of general causation. On the contrary, the court of appeals engaged in a very thorough examination of the specific evidence at issue before ultimately deciding that it was inadmissible.

More precisely, the court found that the differential diagnosis attributing the plaintiff’s bronchiolitis obliterans organizing pneumonia (BOOP) to naphtha exposure was not admissible in the absence of “any literature connecting BOOP to naphtha exposure.”[123] It was undisputed that BOOP had several potential causes and was usually idiopathic, meaning that its cause was unknown.[124] The court held that by its nature, a differential diagnosis is only relevant “if it is proven that a chemical generally causes a particular illness (general causation).”[125]

The court did not hold that separate proof of general causation is a prerequisite to the introduction of case-specific evidence. In fact, the court explains that “depending on the circumstances and the proof available to a plaintiff, similar evidence, if properly adapted, may possibly be used to prove both general and specific causation.”[126] In fact, the court quotes an article discussing causation analysis of “unique injuries,” such as mesothelioma.[127] The full text of the quoted passage explains:

Asbestos, the subject of the first great toxic tort case, is atypical because it causes ‘signature’ diseases. Asbestosis and mesothelioma are diseases so strongly related to asbestos exposure that there is little doubt that a person with these illnesses who has been exposed to asbestos contracted them because of the exposure.[128]

In his concurrence, Justice Brister emphatically and correctly rejected any suggestion that Texas law requires separate proof of general and specific causation: “Havner notes only that plaintiffs ‘sometimes’ offer general causation evidence when they cannot present reliable evidence of specific causation.”[129] Justice Brister’s concurrence also recognizes that “the term ‘toxic torts’ covers a lot of ground – from asbestos and breast implants to refinery explosions, vaccinations, and food poisoning. There is a logical appeal to requiring every plaintiff to prove that an alleged causation chain can actually occur. But if asbestos fibers are directly found in a plaintiff’s lungs, or thirty people eating at the same restaurant get sick at once, I hesitate to hold that each of them must prove ‘general causation’ simply because their tort implicates a toxin.”[130]

As the recent draft of the Restatement (Third) of Torts explained, “courts often address ‘exposure,’ ‘general causation,’ and ‘specific causation.’ Nevertheless, these items are not ‘elements’ of a plaintiff’s cause of action, and in some cases may not require separate proof. So long as the plaintiff introduces admissible and sufficient evidence of factual causation the burden of production is satisfied. . . . These categories function as devices to organize a court’s analysis, not as formal elements of the cause of action.”[131]

The plaintiff’s burden is to present evidence of causation that, “as a whole, ‘rises to a level that would enable reasonable and fair-minded people to differ in their conclusions.’”[132] In determining whether a plaintiff has met this burden, a trial court is required to consider “all the evidence” and “determine from a totality of the evidence, considering all factors affecting the reliability of particular studies, whether there is legally sufficient evidence to support a judgment.”[133] That is precisely what the MDL court is seeking to do in this litigation. The MDL court’s decision to consider “the totality of the evidence” is an exercise of its duty, not an abuse of its discretion.

B.The Record in This Case Does Not Provide a Basis for Resolving the Admissibility of Causation Testimony on a Global Basis.

The court’s decision to exercise its “gatekeeper” function in individual cases does not, as Chrysler suggests, “vitiate the purpose of the MDL scheme.”[134] The MDL is a procedural device designed to “ensure the expeditious resolution of each case and the just and efficient conduct of the litigation as a whole.”[135] Such procedural devices may not be construed to enlarge or diminish any substantive rights:

Although a goal of our system is to resolve lawsuits with ‘great expedition and dispatch and at the least expense,’ the supreme objective of the courts is ‘to obtain a just, fair, equitable and impartial adjudication of the rights of litigants under established principles of substantive law.’ This means that ‘convenience and economy must yield to a paramount concern for a fair and impartial trial’ And basic to the right to a fair trial – indeed, basic to the very essence of the adversarial process – is that each party have the opportunity to adequately and vigorously present any material claims and defenses.[136]

In the context of asbestos litigation, this Court has cautioned that the “systemic urge to aggregate litigation must not be allowed to trump our dedication to individual justice, and we must take care that each individual plaintiff’s – and defendant’s – cause not be lost in the shadow of a towering mass litigation.”[137]

Dividing the causation question into “general” and “specific” components does not solve the problem. In Southwestern Refining Co., Inc. v. Bernal,[138] Justice Baker explained, in a concurrence joined by Justice Hecht, that the practice of “splitting causation into general and specific components” forced juries to “evaluate discrete issues out of context and without knowledge of all the evidence.”[139] Quoting a case involving Agent Orange, the concurrence explained that “[t]he relevant question … is not whether Agent Orange has the capacity to cause harm, the generic causation issue, but whether it did cause harm and to whom. That determination is highly individualistic, and depends upon the characteristics of individual plaintiffs (e.g. state of health, lifestyle) and the nature of their exposure to Agent Orange.”[140]

As the court observed in Coastal Tankships, “rulings on the reliability of proffered expert testimony are necessarily case specific.”[141] This is especially true in this context, where accepted scientific criteria call for an examination of each individual’s type of illness, history of exposure and physical manifestations of disease. The MDL court has decided to consider such evidence on its merits, and Chrysler has offered no reason to disturb that decision.


Chrysler has shown no abuse of the MDL court’s broad discretion in evaluating the reliability and admissibility of expert testimony on causation. The petition for writ of mandamus should be denied.

  1. “Friction product” is a generic term for products such as brakes and clutches used in automobiles, trucks, tractors, airplanes and other vehicles. Chrysler’s counsel brought a brake shoe into the courtroom but acknowledged that it was only “one of the products that is at issue.” RR Vol. I at 21.
  2. Relator’s App. Tab A.
  3. See Relator’s Brief on the Merits in Support of Its Petition for Writ of Mandamus (“Br.”) at 42.
  4. RR Vol. III at 51-52.
  5. Research Methods in Occupational Epidemiology 248 (Checkoway, et al., eds. 2d ed. 2004), R. Tab B, P. Ex. 23.
  6. See, e.g., Spirtas, et al., Malignant Mesothelioma: Attributable Risk of Asbestos Exposure, Occup. & Envtl. Med. 51:804-11 (1994).
  7. RR Vol. III at 71-73.
  8. See RR Vol. I at 257-58.
  9. Consensus Report, Asbestos, Asbestosis, and Cancer: The Helsinki Criteria for Diagnosis and Attribution, Scand. J. Work Envtl. Health 23:311-316 (1997) (hereinafter “Helsinki Criteria”), R. Tab B, P. Ex.
  10. Id. at 313.
  11. Id.
  12. See RR Vol. II at 7-9.
  13. Id. at 13-14.
  14. See, e.g., RR Vol. II at 27-28, 43-44.
  15. Relator’s App. Tab A.
  16. Helsinki Criteria at 311.
  17. Id. The term “fibers/cc-years” simply refers to the occupational exposure level multiplied by the number of working years. For example, a person with an occupational exposure of 0.1 fibers/cc who worked for 10 years would be exposed to 1 f/cc-year.
  18. See R. Tab A at 9.
  19. Chrysler’s brief argues that all of the asbestos in friction products is destroyed or thermally transformed into a substance called Forsterite. Br. at 1. This is irrelevant to exposures during the installation of new brake linings, in which the asbestos is unaltered. Moreover, workplace measurements indicate that asbestos fibers remain in used brakes. See RR Vol. III at 40-41.
  20. RR Vol. III at 56; R. Tab B, P. Ex. 37 (Kauppinen & Korhonen, Exposure to Asbestos During Brake Maintenance of Automotive Vehicles by Different Methods, Am. Indus. Hyg. Ass’n J., 48:499-504 (1987)) at 501 (grinding of new brake linings results in “heavy exposure.”).
  21. RR Vol. III at 55; see also R. Tab B, P. Ex. 7 (Huncharek, Brake Mechanics, Asbestos, and Disease Risk, Am. J. Forensic Med. & Pathology 11:236-240 (1990)) at 237 (use of compressed air jet “liberates large quantities of asbestos dust into the surrounding environment.”).
  22. See RR Vol. III at 70-71; R. Tab B, P. Ex. 33 (Roberts & Zumwalde, NIOSH, Assessment of Asbestos Exposure to Mechanics Performing Brake Service Operations (April 27, 1981)) (finding exposures of up to 0.28 f/cc TWA for brake mechanics); P. Ex. 34 (Hickish & Knight, Exposure to Asbestos During Brake Maintenance, Ann. Occup. Hygiene 13:17-21 (1970)) (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).
  23. R. Tab B, P. Ex. 39; see also P. Ex. 41-45.
  24. R. Tab B, P. Ex. 44.
  25. Helsinki Criteria at 313.
  26. R. Tab B, P. Ex. 4 (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)).
  27. The term “fibers/cc-years” simply refers to the occupational exposure level multiplied by the number of working years. For example, a person with an occupational exposure of 0.1 fibers/cc who worked for 10 years would be exposed to 1 fiber/cc-year.
  28. Id. at Table 5.
  29. Id.
  30. See RR Vol. I at 200-01 (discussing Spirtas, et al., Malignant Mesothelioma: Attributable Risk of Asbestos Exposure, Occup. & Envtl. Med. 51:804-11(1994)).
  31. Huncharek, Changing Risk Groups for Malignant Mesothelioma, Cancer 69:2704-2711 (1992).
  32. Mesothelioma: Has Patient Had Contact With Even Small Amount of Asbestos? 257 JAMA 1569 (Mar. 27, 1987) (emphasis added).
  33. World Trade Organization, European Communities – Measures Affecting Asbestos and Asbestos-Containing Products, Report of the Panel, Sept. 18, 2000) at ¶¶ 5.261.
  34. RR Vol. I at 202-03.
  35. Deposition of Dr. Michael Goodman, R. Tab B, P. Ex. 15, at 57-60.
  36. See RR Vol. I at 191, 195-96.
  37. RR Vol. I at 186-89, 203-04.
  38. See Transcript of Daubert Hearing, Chapin v. A&L Parts, Inc., No. 03-324775-NP (Mich. Cir. Ct., Wayne County, Mich.) May 25, 2004, R. Tab B, Ex. 1 (observing that Dr. Goodman’s analysis was “subject to attack”).
  39. R. Tab A, D. Ex. A (Affidavit of Dr. Michael Goodman) at ¶ 22.
  40. RR Vol. I at 213.
  41. RR Vol. I at 214. Given that the typical latency for mesothelioma is 30 years, and that very few 8-year-olds are occupationally exposed to asbestos, such a study is not likely to yield meaningful information on asbestos-related diseases. See id. at 214-15.
  42. RR Vol. I at 241, 244, 254-57, 294-95.
  43. RR Vol. I at 238; see also RR Vol. I at 295-98.
  44. RR Vol. III at 7-14.
  45. Id. at 17.
  46. Id. at 10-11.
  47. RR Vol. III at 33.
  48. Id.
  49. Id. at 34-39.
  50. Id. at 40.
  51. Id. at 34-35; see also RR Vol. III at 42-43.
  52. Id. at 50-51.
  53. Id. at 70.
  54. Id. at 71.
  55. RR Vol. III at 84-85.
  56. The court was likely referring to page 729 of the Havner opinion, in which this Court observed that “testimony to the effect that a substance ‘could’ or ‘can’ cause a disease or disorder is not evidence that in reasonable probability it does.” Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706, 729 (Tex. 1996).
  57. RR Vol. III at 185-86.
  58. Relator’s App. Tab A.
  59. Id.
  60. Id.
  61. Ruling dated June 30, 2005, attached as Tab 1, at 6.
  62. Id. at 5-6.
  63. Id. at 10. The court acknowledged that this ruling was “markedly different” from the ruling on friction products, explaining that “[d]ifferent evidentiary records can and should lead to different rulings . . . .” Id.
  64. General Motors Corp. v. Sanchez 997 S.W.2d 584, 590 (Tex. 1999) (citing E.I. du Pont de Nemours and Co., Inc. v. Robinson, 923 S.W.2d 549, 556 (Tex. 1995).
  65. Keo v. Vu, 76 S.W.3d 725, 730 (Tex. App. – Houston [1st Dist.] 2002, pet. denied).
  66. Piro v. Sarofim, 80 S.W.3d 717, 720 (Tex. App. – Houston [1st Dist.] 2002, no pet.) (emphasis in original) (quoting Kumho Tire Co. v. Carmichael, 526 U.S. 137, 152-53 (1999)).
  67. Robinson, 923 S.W.2d at 557.
  68. Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706, 719 (Tex. 1996).
  69. In re Federal-Mogul Global, Inc., 300 F.3d 368, 390 (3rd Cir. 2002).
  70. In re Prudential Ins. Co. of America, 148 S.W.3d 124, 135-36 (Tex. 2004).
  71. Id. at 137.
  72. Br. at 14.
  73. Prudential, 148 S.W.3d at 147.
  74. Walker v. Packer, 827 S.W.2d 833, 837 (Tex. 1992).
  75. 211 B.R. 545 (E.D. Mich. 1997).
  76. Id. at 594.
  77. Br. at 40.
  78. R. Tab C.
  79. Relator’s App. Tab A.
  80. Havner, 953 S.W.2d at 714.
  81. Id.
  82. Chrysler’s counsel referred to the chrysotile asbestos used in friction products as “modified short chrysotile, which I call MSC.” RR Vol. I at 20. Chrysler has never offered any sound scientific basis for this terminology, and a defendant may not render scientific evidence inadmissible merely by applying a new name to the chemical or substance at issue. Jarrell v. Park Cities Carpet and Upholstery Cleaning, Inc., 53 S.W.3d 901, 903 (Tex. App. – Dallas 2001, pet. denied). Accepting such arguments would “reduce[] the Robinson/Havner analysis to a matter of semantics, not science.” Id. The Plaintiffs refer to the substance at issue by the generally accepted terms “chrysotile asbestos” or simply “chrysotile.”
  83. Dr. Goodman testified that he was “undecided” as to whether chrysotile asbestos causes mesothelioma but agreed that other scientists had reached that conclusion and that “their opinion has merit.” RR Vol. I at 258.
  84. Ruling dated June 30, 2005, attached as Tab 1, at 6.
  85. Id. at 1412-13 (emphasis added); see also Pick v. American Medical Systems, Inc., 958 F.Supp. 1151, 1164 (E.D.La. 1997) (cited on page 32 of Chrysler’s brief) (“General causation deals with whether the substance at issue, i.e. silicone, can cause diseases or disorders in people in general. Specific causation focuses upon whether the substance, i.e. silicone, was in fact the cause of the ailments or symptoms in the particular patient.”).
  86. Jarrell, 53 S.W.3d at 902.
  87. Id. at 1402-05.
  88. Id. at 1402.
  89. Id. at 1402 n.33 (emphasis added).
  90. Transcript of Daubert Hearing, Chapin v. A&L Parts, Inc., No. 03-324775-NP (Mich. Cir. Ct., Wayne County, Mich.) May 25, 2004, R. Tab B, Ex. 1.
  91. Restatement (Third) of Torts §28 cmt. c (Final Draft No. 1, April 6, 2005) (hereinafter “Restatement (Third)”); see also Faigman, et Al., 3 Modern Scientific Evidence § 40-1.1 (1999) (“In spite of the asbestos litigation’s enormous size, cases involving the admissibility of scientific evidence have been relatively rare. In part, this is due to the fact that some asbestos-related injuries, e.g. mesothelioma, are ‘signature diseases.’ That is, they are uniquely related to asbestos exposure and are rarely observed in individuals not exposed.”).
  92. 1 S.W.3d 759 (Tex. App. – Corpus Christi 1999, pet. denied).
  93. Id. at 775 & n.11.
  94. Mr. Thackston was lead counsel for Chrysler.
  95. RR Vol. III at 75-76 (emphasis added).
  96. See id. at 34-40.
  97. RR Vol. I at 230.
  98. Id.
  99. RR Vol. I at 230.
  100. RR Vol. I at 22.
  101. R. Tab A.
  102. Br. at 5.
  103. 953 S.W.2d at 719.
  104. Id.
  105. Br. at 12.
  106. See Restatement (Third) § 28 cmt. c (“[M]ost courts have appropriately declined to impose a threshold requirement that a plaintiff always must prove causation with epidemiologic evidence.”); see also Benedi v. McNeil-P.P.C., Inc., 66 F.3d 1378, 1384 (4th Cir. 1995) (“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.”).
  107. 978 S.W.2d 183 (Tex. App. – Texarkana 1998, pet. denied).
  108. Id. at 198 (emphasis added).
  109. 958 F.Supp. 1151 (E.D. La. 1997); see also In re Meridia Products Liability Litig., 328 F.Supp.2d 791, 801 (N.D. Ohio 2004) (cited at p. 9 of Chrysler’s brief) (reviewing case law and concluding that “[u]ltimately, no court has held that epidemiological evidence is necessary to establish general causation when other methods of proof are available.”).
  110. Id. at 1158 (emphasis in original) (citations omitted). In addition to misstating the holding in Brock, Chrysler incorrectly asserts that the MDL court’s decision was “erroneous under Fifth Circuit authority.” Br. at 38. A Texas state court’s ruling can never be “erroneous under Fifth Circuit authority” for the simple reason that Texas state courts are not bound by Fifth Circuit authority. Penrod Drilling Corp. v. Williams, 868 S.W.2d 294, 296 (Tex. 1993). The MDL court is bound by this Court’s precedents, none of which have adopted Chrysler’s position.
  111. 953 S.W.2d at 719 (emphasis added).
  112. Id. at 715.
  113. Id. at 719 (emphasis added).
  114. Relator’s App. Tab A.
  115. Id. at 719.
  116. Id. at 718-19.
  117. Restatement (Third) § 28 cmt. c.
  118. Kelley v. American Heyer-Schulte Corp., 957 F.Supp. 873, 875 (W.D. Tex.1997) (emphasis added).
  119. Id. at 10. The court acknowledged that this ruling was “markedly different” from the ruling on friction products, explaining that “[d]ifferent evidentiary records can and should lead to different rulings . . . .” Id.
  120. 953 S.W.2d at 714.
  121. Br. at 37.
  122. 87 S.W.3d 591 (Tex. App. – Houston [1st Dist.] 2002, pet. denied).
  123. Id. at 597.
  124. Id. at 596.
  125. Id. at 609.
  126. Id. at 603 n.21 (emphasis added).
  127. See id. at 603 n.19 (quoting Joseph Sanders & Julie Machal-Fulks, The Admissibility of Differential Diagnosis Testimony to Prove Causation in Toxic Tort Cases: the Interplay of Adjective and Substantive Law, 64 Law and Contemporary Problems 107, 110-11 (2001)).
  128. Sanders, supra, at 110.
  129. 87 S.W.3d at 616 (Brister, J., concurring).
  130. Id. at 617.
  131. Restatement (Third) § 28 cmt. c.
  132. Havner, 953 S.W.2d at 711.
  133. Id. at 720.
  134. Br. at 7.
  135. Tex. R. Jud. Admin. 13.6(c).
  136. Henry Schein, Inc. v. Stromboe, 102 S.W.3d 675, 693 (Tex. 2002) (citations omitted).
  137. In re Ethyl Corp., 975 S.W.2d 606, 613 (Tex. 1998) (addressing consolidation of asbestos trials).
  138. 22 S.W.3d 425 (Tex. 2000).
  139. Id. at 440 (Baker, J., concurring).
  140. Id. (quoting In re Agent Orange Prod. Liab. Litig., 818 F.2d 145, 164-65 (2nd Cir. 1987)).
  141. 87 S.W.3d at 599 n.14.