NO. 2004 – 03964
No. 2004-42761



Plaintiffs file this consolidated response in opposition to Defendant Georgia-Pacific Corporation’s (“G-P’s”) motion to exclude general causation opinion testimony that “uncontaminated” chrysotile can cause mesothelioma. Plaintiffs will establish that the totality of the reliable medical and scientific evidence supports the conclusion that dust from products composed of chrysotile asbestos, with or without a tremolite component, can cause mesothelioma.

Table Of Contents


Chrysotile Asbestos Has Been Generally Accepted as a Cause of Mesothelioma.

Asbestos is divided into two main fiber types: “serpentines,” of which chrysotile is the only form commercially exploited; and “amphiboles,” a group that includes the commercial fibers amosite and crocidolite, and tremolite, a non-commercial form that occurs naturally in deposits of chrysotile ore and remains in products containing commercial chrysotile asbestos. Of the three commercial forms, chrysotile asbestos accounted for approximately 90 to 95 percent of all of the asbestos incorporated into products used in the United States.

Malignant mesothelioma is a rare form of cancer that is “nearly always attributable to asbestos exposure.”[1] Scientists in the relevant disciplines have concluded that, while amphibole fibers have greater carcinogenic potency on a fiber-by-fiber basis, both chrysotile and amphibole fibers are capable of causing mesothelioma in human beings.[2] These conclusions are based on generally accepted sources of scientific data, including epidemiological case-control and cohort studies, case studies, controlled animal experiments, and toxicological studies.[3] Dr. Arthur Frank, who began his career more than 30 years ago working with the pioneering asbestos researcher Dr. Irving Selikoff, explains that “while they recognize that there is controversy, groups of scientists that have looked at that issue . . . have universally concluded that chrysotile can cause mesothelioma. There are a few individuals who do not believe that. You know, there’s some people that still believe the world might be flat.”[4]

Indeed, virtually every group of scientists that has ever examined the question has found that reliable data show a causal relationship between chrysotile asbestos and mesothelioma. This scientific consensus has been reaffirmed in reports prepared by the 1997 Helsinki Conference,[5] the American Cancer Society,[6] the World Health Organization (“WHO”),[7] the World Trade Organization (“WTO”),[8] the Occupational Safety and Health Administration (“OSHA”),[9] the National Institute for Occupational Safety and Health (“NIOSH”),[10] the Environmental Protection Agency (“EPA”),[11] the Consumer Products Safety Commission (“CPSC”)[12] and the U.S. Department of Health and Human Services.[13]

G-P asks the Court to exclude this widely accepted scientific evidence of causation.[14] G-P’s argument rests on what is known as the “amphibole hypothesis” – the contention that amphiboles alone cause mesothelioma and that chrysotile asbestos is incapable of causing the disease. Proponents of the “amphibole hypothesis” discount any inconsistent data by assuming that mesothelioma cases in chrysotile-exposed populations are caused solely by tremolite “contamination”[15] or that such cases must be “spontaneous.”[16] The “amphibole hypothesis” has not been accepted by any neutral scientific panel or governmental agency.

Courts Have Consistently Admitted Scientific Evidence That Chrysotile Asbestos Causes Mesothelioma.

In the decade since Robinson[17] and Daubert[18] were decided, no court has ever accepted G-P’s argument. Although hundreds of mesothelioma cases have been tried throughout the country, G-P is unable to cite a single federal case excluding expert testimony that chrysotile causes mesothelioma. At least one state court has actually prohibited G-P from introducing expert testimony on the “amphibole hypothesis,” finding that it had not been generally accepted in the scientific community.[19]

Judge David Godbey, who was subsequently appointed to the federal bench by President George W. Bush, denied a motion to exclude expert testimony on chrysotile asbestos in 2001. After “having considered the extensive briefs and evidence filed by the parties, having heard oral argument, and having carefully considered the decision of the Texas Supreme Court in the cases of E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549 (Tex. 1995) and Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706 (Tex. 1996),” Judge Godbey concluded that the motion to exclude lacked merit.[20] Courts throughout Texas have reached the same conclusion.[21] One Texas court has made detailed findings of fact and conclusions of law regarding the “consistent and reliable epidemiological link” between chrysotile and mesothelioma.[22]

In effect, the Defendants seek to make Texas the only state in the country to forbid this scientific evidence. Given the widespread use of chrysotile, this wholesale exclusion of evidence would prevent most plaintiffs with mesothelioma from seeking any compensation. The Defendants have not identified any sound scientific or legal basis for such an unprecedented ruling.


Havner explicitly acknowledged the widely accepted “Bradford Hill” methodology for evaluating causal relationships.[23] The Bradford Hill methodology involves a number of considerations, including strength of association, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment and analogy.[24] The Bradford Hill considerations necessarily draw on a number of different data sets, including epidemiological case-control and cohort studies, case reports, animal studies, toxicological studies, tissue studies and other relevant biological and medical information.[25] As Sir Austin Bradford Hill himself observed, no single type of evidence can provide “indisputable evidence for or against the cause-and-effect hypothesis, and none can be required as a sine qua non.”[26]

G-P asks the Court to disregard entire categories of scientific data, including animal studies, in vitro cell studies and tissue studies. Even a brief review of the scientific literature indicates that scientists rely on all of these sources of data in mesothelioma research, and G-P has offered no reason for this Court to depart from accepted scientific standards. The Bradford Hill factors — the standard scientific method for assessing causality — necessarily involve consideration of such data.[27] In fact, the Court in Havner considered each of these types of data, although the unpublished studies at issue in Havner were found insufficient to create a fact issue on causation. By contrast, the studies of chrysotile asbestos have been published and widely analyzed and cited in the scientific and medical literature. In the context of mesothelioma research, all of these studies are reliable and relevant sources of data.

G-P also makes generalizations about epidemiological studies that are not necessarily relevant in the context of mesothelioma research. Because mesothelioma is extremely rare and strongly associated with asbestos, there is no way to calculate a definitive “background rate” that would occur absent asbestos exposure.[28] While a background incidence of mesothelioma has not been firmly established, “it is estimated that it occurs probably on the order of 1 case per million persons per year or less.”[29]

Because of its rarity, the increased incidence of mesothelioma is often not expressed in terms of “relative risk” but as a ratio with respect to total lung cancers or total deaths.[30] For the same reason, confidence intervals are not as readily calculated in studies of mesothelioma. Even with these inherent limitations, the epidemiological studies and other available data support the existence of a causal relationship. While “the number of mesothelioma cases from populations exposed only to chrysotile has been small, an association with chrysotile exposure has been definitively established.”[31]

Epidemiological Studies

Published epidemiological studies demonstrate significantly increased rates of mesothelioma, often more than double what was expected, in chrysotile-exposed populations.[32] The cohort of more than 17,000 insulators studied by Dr. Selikoff and Dr. Frank worked primarily with chrysotile and developed mesothelioma at a significantly higher rate than the general population.[33] Dr. Selikoff explained that the increase in mesothelioma and other asbestos-related diseases “cannot be ascribed to other than the one asbestos fiber that was in regular use in insulation materials during the 1930s – chrysotile.”[34] As Dr. Frank reiterated, “it was hard to imagine that . . . a few percent of amphibole . . . was the sole cause of the vast amount of mesothelioma we were seeing.”[35]

Studies of plasterers and dry wall workers, who were exposed to chrysotile-containing joint compound, have also documented significant increases in cases of mesothelioma.[36] One study of plasterers and cement masons reported 20 deaths from mesothelioma in a population of slightly more than 3,000 drywall plasterers.[37] Another study reported a Proportionate Mortality Ratio (PMR)[38] of 2.03 for mesothelioma deaths among plasterers.[39] While conducting a study to assess the increased risk of asbestos-related disease in construction occupations, researchers discovered that plasterers, compared to the general population, had more than twice the risk of dying from pleural and peritoneal cancers.[40] The increased relative risk of mesothelioma was also documented in a study of railroad workers exposed to chrysotile.[41] The author noted that “the consistent repeated development of a specific rare cancer such as mesothelioma in successive cohorts following prior exposure to commercial chrysotile asbestos illustrate the basic principle that the nature of the asbestos exposure was sufficient for the induction of the mesotheliomas.”[42]

In a 25-year longitudinal study covering 11,625 person-years of 515 male asbestos plant workers exposed to chrysotile-only asbestos in Chongqin, China, researchers found two cases of mesothelioma accounting for 1.5% of the total deaths. Using an expected rate of one mesothelioma in 1,000,000 person years, this finding documented a risk exceeding 170 times that of the non-exposed population. The authors found a third mesothelioma case in a child of a worker but did not include it because the child’s father was employed after the cohort started.[43] The amount of tremolite in the samples was described as “negligible.”

In a study of the mortality of 2,242 women in two chrysotile asbestos mining areas of the province of Quebec, seven “pleural cancers,” or mesotheliomas, were reported. The authors calculated a Standard Mortality Ratio (SMR)[44] of 7.63 at a 95% confidence interval of 3.06 to 15.73.[45] Researchers studied a group of 1,094 chrysotile production workers employed at the mine and mill in Balangero, Italy, finding two cases of mesothelioma — one confirmed pathologically and one based on radiographic findings and an examination of pleural fluid — among 427 deaths.[46] The presence of balangeroite, a fibrous silicate, may have enhanced the toxicity of the chrysotile asbestos.[47] No tremolite was detected in any of the chrysotile samples.[48]

The records of 51 Zimbabwean miners and millers who had been certified as having an occupational lung disease documented two cases of mesothelioma, one proven by biopsy and the other a probable mesothelioma based on radiographic findings.[49] The authors estimated that 7,000 Zimbabweans were engaged in the mining and milling operation. Among the chosen cohort of 27 miners with sufficient documentation, the authors discovered one mesothelioma case proven by pathology. Given the rarity of the disease and the size of the exposed population, the incidence of mesothelioma among these Zimbabwean miners significantly exceeded double that of the general population. Like the chrysotile ore mined in Balangero, Italy, no tremolite was detected in any of the samples, although some articles have suggested the presence of a small percentage of anthophyllite.

Among 5,932 male employees of a plastics research and development facility that used chrysotile asbestos, a study found an SMR of 3.73, with a 95% confidence interval of 1.21 to 8.70 for other respiratory deaths, all of which were attributable to the five deaths from pleural mesothelioma.[50] The actual SMR was probably higher, because a review of death certificates for the entire cohort revealed an additional four deaths from pleural mesothelioma as contributory causes during the observation period and a fifth death after the study had closed. In a study of workers employed in an asbestos textile, friction and packing manufacturing facility that utilized 99% chrysotile asbestos between 1940 and 1967, researchers observed 17 mesotheliomas, representing 4.3% of the deaths, a significantly elevated risk.[51]

Australian researchers recorded a significant number of mesothelioma cases in which the only detectable type of asbestos was chrysotile.[52] The results reflected a dose-response effect, with an increasing odds ratio (OR) at relatively low fiber concentration of less than 106 fibers per gram of dry lung tissue (log10 = 5.5-6; OR = 8.67).[53] In the German Federal State of Saxony-Anhalt, the authors reviewed 843 cases of “proven asbestos-accepted mesotheliomas” and concluded that 67 of the cases were attributable to chrysotile asbestos alone.[54]

These repeated findings cannot be explained by assuming exposure to tremolite or other amphiboles. As the National Academy of Sciences has observed, the “magnitude of the difference in reported risks is not likely to be explained by fiber or process differences alone.”[55] Moreover, if mesothelioma were “produced only by amphiboles, one would expect large differences in the mesothelioma lung cancer ratio between populations with pure chrysotile exposure and those with extensive amphibole exposure.”[56] Analyzing more than 40 epidemiological studies, the authors determined that “[t]he ratio of mesothelioma to lung cancer is seen in this analysis to be the same, within statistical uncertainty, for exposures to 100% chrysotile, 97%+ chrysotile, 100% amosite, and mixtures of chrysotile, amosite, and crocidolite. Only 100% crocidolite exposures appear to have a greater ratio, about two to four times above that of predominantly chrysotile exposures. …These data strongly suggest therefore that much of the mesothelioma risk in populations with predominantly chrysotile exposures is due to chrysotile.”[57]

The authors also compared studies of insulation workers exposed prior to 1935, when primarily chrysotile was used, compared with those exposed to more mixtures of chrysotile and amosite after 1935. The resulting analysis demonstrated that “the time course of mesothelioma risk is totally incompatible with an exposure pattern that begins only in the late 1930s. Indeed, the 95% confidence limits on three of the four data points do not intercept the distribution that would be expected, were amosite exposure responsible for mesothelioma in this population. Barring undiscovered exposures to amphiboles prior to 1935, these data present strong evidence that chrysotile is the substantial, indeed the dominant contributor to the mesothelioma risk experienced by this group of insulation workers.”[58]

The World Health Organization (WHO) reviewed the extensive epidemiological literature in 1998 and concluded that “[c]ommercial grades of chrysotile have been associated with an increased risk of pneumoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of exposed workers.”[59] The report further notes that although epidemiological studies have primarily involved the mining, milling and manufacturing sectors, “there is evidence, based on the historical pattern of disease associated with exposure to mixed fibre types in western countries, that risks are likely to be greater among workers in construction and possibly other user industries.”[60]

Dismissing these findings, G-P asserts incorrectly that “[w]ith respect to uncontaminated chrysotile, the WHO recognized that the question of a potential causal link to mesothelioma ‘has not been resolved.’” Motion at 20. G-P’s partial quotation does not accurately reflect the report. The quoted passage is actually referring to the unresolved nature of the “amphibole hypothesis”: “Since commercial chrysotile may contain fibrous tremolite, it has been hypothesized that the latter may contribute to the induction of mesotheliomas in some populations exposed primarily to chrysotile. The extent to which the observed excesses of mesothelioma might be attributed to the fibrous tremolite content has not been resolved.”[61] As discussed above, attributing the cases of mesothelioma solely to tremolite exposure is not a reasonable interpretation of the data.[62] The WHO concluded that “[e]xposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer and mesothelioma in a dose-dependent manner” and that no “threshold has been identified for carcinogenic risks.”[63]

Case Studies

In addition to cohort studies, case reports are highly significant with respect to mesothelioma. Epidemiologists classify mesothelioma as a “sentinel” disease, meaning that “the occurrence of any cases serves as an indication of an occupational hazard.”[64] For such diseases, “[c]ase series reports are particularly informative.”[65] In fact, the 1960 study that is generally credited with establishing the link between asbestos and mesothelioma was a series of case reports.[66] Outside the context of asbestos, scientists have relied on case reports to establish causal connections between SARS and the SARS virus, vinyl chloride and angiosarcoma, and pneumococcal bacteria and pneumonia.[67] Mesothelioma has been attributed to chrysotile exposure repeatedly in published, well-documented case studies.[68]

Experimental Data (In Vivo and In Vitro Studies)

Experiments are a key component of accepted scientific methodology.[69] While in vivo animal studies and in vitro cell studies “standing alone” may not establish causality,[70] such experiments provide highly relevant information about the biological effects of asbestos. Chrysotile is a proven carcinogen both in animals and humans. The experiments summarized below demonstrate that chrysotile causes mesothelioma in animal subjects and that chrysotile fibers, when placed in contact with the peritoneum or pleura, have the ability to cause malignant changes in mesothelial cells.

Animal toxicology studies are highly relevant to determining causation in humans. “Neoplasms of rodents and other animals are . . . fundamentally similar in nature, and there are many examples of chemicals that cause tumors in both humans and animals. It is a fundamental principle of the IARC Monograph evaluations that in the absence of adequate data on humans, it is biologically plausible and prudent to regard agents and mixtures for which there is sufficient evidence of carcinogenicity in experimental animals as . . . a carcinogenic risk to humans.”[71] Paul Kotin, former medical director for Johns-Manville, wrote that “ingestion by human beings of any amounts of a compound shown to be carcinogenic in test animals must be regarded as a threat to human health.”[72]

Experimental samples of chrysotile fibers have been shown in multiple long-term inhalation studies to cause fibrogenic and carcinogenic effects. Many of the relevant studies are summarized in Table 1, infra, and in Dr. Egilman’s affidavit. The observed effects of chrysotile include interstitial fibrosis and cancer of the lung and pleura. In most cases, there appears to be an association between fibrosis and tumors in the rat lung. Fibrogenic and carcinogenic effects have also been found in long-term animal studies (mainly in rats) using other modes of administration (e.g., intratracheal instillation and intrapleural or intraperitoneal injection). The results of early inhalation experiments were presented in Environmental Health Criteria 53. Fibrosis was observed in many species following inhalation of chrysotile, and in several studies there was progression of fibrosis following cessation of exposure.[73]

In experimental inhalation studies with different fiber types it has been an almost universal finding that fibers that are very fibrogenic are also carcinogenic. Davis & Cowie emphasized this by reporting on advanced fibrosis in 144 rats, aged 2.5 years or more, that had been exposed to a number of different asbestos types, including Rhodesian and Canadian chrysotile.[74] The 85 animals that had pulmonary tumours showed almost twice the level of advanced pulmonary fibrosis as the 59 animals that had not developed tumours. The studies summarized in Table 2, infra, show the results of intratracheal injection with chrysotile documenting fibrosis in sheep, rats and mice. At high doses (100 mg) of chrysotile administered via intratracheal instillation in sheep, fibrosis appeared to be more marked with chrysotile than with crocidolite.

Other injection studies, summarized in Table 3 and Table 4, infra, have demonstrated the carcinogenicity of chrysotile asbestos in laboratory animals. Animal studies using different routes of exposure confirm that both chrysotile and amphibole fibers are capable of inducing mesothelioma.[75] In experiments designed to compare different forms of asbestos, chrysotile asbestos is typically more likely to induce mesothelioma than other asbestos types.[76]

At the cellular level, multiple in vitro studies have confirmed that chrysotile fibers penetrate cells and induce abnormal chromosome formations.[77] Some of these abnormalities include the deletion of the P53 gene that controls cell growth.[78] Many of the key studies on the genotoxicity of chrysotile fibers are summarized in Table 5, infra.

As a rule, the studies have used asbestos samples prepared by the International Union Against Cancer (UICC). Analysis of these samples has confirmed that they do not contain tremolite, meaning that the “disease induced in animal models correlates with chrysotile-induced pathology and does not support an explanation based on the ‘amphibole hypothesis.’ Thus, chrysotile should be considered as having the biologic ability to produce cancers, including mesotheliomas, based on the extensive use of this material as standard reference material.”[79]

Tissue Studies

There is “ good evidence from lung burden studies . . . that chrysotile alone can cause mesothelioma.”[80] Studies of human tissue demonstrate that chrysotile fibers concentrate in the pleura, where most mesotheliomas develop.[81] Drs. Suzuki and Yuen published an analysis of tissue samples taken from the lungs and pleura of 151 malignant mesothelioma cases.[82] The authors broke the cases into three groups, one where they examined both lung and mesothelial tissues, one in which they looked only at lung tissue and one in which they limited their examination to mesothelial tissues. For approximately one quarter of the cases in each group, the only type of asbestos detected was chrysotile asbestos.[83]

Applying generally accepted scientific standards, the available data support the conclusion that chrysotile causes mesothelioma. As Dr. Frank explained, “[Y]ou don’t take one paper or one isolated finding and try to hang everything on that . . . [H]aving looked for 30 years at the subject of asbestos and its ability to produce disease, you look at the wide range of pieces of information and using things like the Bradford Hill criteria, . . . when you line that information all up, each individual piece by itself may not be sufficient to say conclusively that this is a causal link. But when you have all of these pieces of information from many different sources and that data is analyzed by scientific methodology of many types, by epidemiological studies, by animal studies, by cell culture studies, by pathologic studies, by measurement with electron microscopes of what’s in the material, and you put all of that together it is entirely, in my mind and to most scientists, a reasonable conclusion that chrysotile causes mesothelioma.”[84]


Plaintiffs Are Not Required to Provide “Conclusive Epidemiological Proof” of Causation.

The crux of G-P’s legal argument is that it is not possible “to conclude definitively” that “pure chrysotile” causes mesothelioma and that “conclusive epidemiological proof” of causation is required.[85] Texas law has never imposed such a burden of proof with respect to causation. Under Texas law, the plaintiff “must only prove the greater probability is that a defendant’s conduct was a cause” of injury.86 With respect to general causation in a toxic tort case, the plaintiff’s burden is to present legally sufficient evidence that “a substance is capable of causing a particular injury or condition in the general population.”[87] Causation evidence is “legally sufficient” under Havner if the evidence, as a whole, “rises to a level that would enable reasonable and fair-minded people to differ in their conclusions.”[88] As discussed above, “reasonable and fair-minded” people throughout the world have concluded that chrysotile asbestos is capable of causing mesothelioma.

Havner does not require “conclusive epidemiological proof.” Havner held that epidemiological studies “may be part of the evidence supporting causation in a toxic tort case.”89 Thus, epidemiology is a permissive, not a mandatory, source of proof. See Allison v. Fire Ins. Exch. 98 S.W.3d 227, 239(Tex. App.—Austin 2002, no pet.). In Havner, the Court emphasized the flexible nature of the inquiry, explaining that “a number of criteria must be considered,” and that the determination must be made “from all the evidence.”90

In Havner,the Texas Supreme Court evaluated the sufficiency of evidence to support a causal connection between the prescription drug Bendectin ingested by a pregnant mother and the limb reduction birth defect in her child. Bendectin litigation was not new; the Court noted a pattern of state and federal courts rejecting the expert evidence offered to support causation. Havner does not, as Defendants suggest, stand for the notion that only epidemiological evidence can support general causation.

The final draft of the new Restatement (Third) of Torts: Liability for Physical Harm observes that “most courts have appropriately declined to impose a threshold requirement that a plaintiff always must prove causation with epidemiologic evidence.”91 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.92

Federal courts have held in a variety of circumstances that epidemiological studies are not a prerequisite to the admission of expert causation testimony.[93]

The Havner Court unambiguously held that epidemiological studies showing less than a doubling of the risk may still be part of a plaintiff’s causation evidence: “We do not hold . . . that a relative risk of more than 2.0 is a litmus test[.] . . . Other factors must be considered. . . . Even if a particular study reports a low relative risk, there may in fact be a causal relationship.”[94] The Court went on to explain that “there are a number of reasons why reliance on a relative risk of 2.0 as a bright-line boundary would not be in accordance with sound scientific methodology in some cases.”[95] As the Court noted:

We 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. We emphasize, however, that evidence of causation from whatever source must be scientifically reliable.[96]

In Minnesota Mining and Manufacturing Co. v. Atterbury, the Texarkana Court of Appeals summarized Havner succinctly as follows:

Despite [defendant’s] allegations of set rules, the [Havner]court 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. Reliable epidemiological evidence with a relative risk lower than 2.0 should be considered because . . . it is relevant evidence. However, the Texas Supreme Court has stated that an epidemiological study with a relative risk of less than 2.0 must be supported by other credible, reliable evidence . . . [97]

In Texas Workers’ Compensation Ins. Fund v. Lopez, the court held that an epidemiological study that showed a relative risk factor under 2.0 was admissible and ultimately found the causation evidence in that case to be adequate.[98] Lopez involved a plaintiff who suffered chronic obstructive pulmonary disease from exposure to silica while working as a sandblaster. Although the epidemiological evidence showed an average risk of 1.87, the court explained: “[O]ur reading of Havner does not reveal a clear indication that a doubling of the risk is necessary . . .”[99] Accordingly, the Lopez court held that, despite a relative risk factor of less than 2.0, the cumulative scientific causation evidence “overwhelmingly” showed that exposure to silica caused the injury in question.[100]

Rather than imposing simplistic requirements, Havner calls for “[c]areful exploration and explication of what is reliable scientific methodology in a given context.”[101] Havner stressed that courts must make a determination of reliability from all the evidence. Courts should allow a party, plaintiff or defendant, to present the best available evidence, assuming it passes muster under Robinson, and only then should a court 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.[102]

The Available Epidemiological Evidence Supports a Finding of General Causation.

Even if this Court were to depart from Havner and examine the epidemiological studies in isolation, the available epidemiological data support the conclusion that chrysotile causes mesothelioma. As discussed above, epidemiological studies have found significantly high rates of meothelioma in insulators, construction workers, miners, millers and other populations exposed primarily to chrysotile. G-P has asked the Court to disregard these epidemiological studies because they do not isolate exposures to “pure chrysotile,” but G-P has offered no legal or scientific basis for ignoring these studies.

As a practical matter, there is no such thing as a “pure chrysotile exposure.” Occupational exposures are almost never “pure,” a fact readily acknowledged by epidemiologists, industrial hygienists and physicians. In one of the deposition excerpts attached to G-P’s motion, Dr. Arnold Brody attempts to explain that abstract questions regarding “pure exposures” are “academic” and “almost even moot.”[103] Dr. Bruce Case, who will testify in support of G-P’s motion, agrees that “[p]ure chrysotile exposure rarely, if ever, occurs.”[104] In “the real world of workers exposed to products, for all intents and purposes, there are no ‘pure chrysotile’ exposures.”[105] G-P argues, illogically, that the Plaintiffs must produce studies of these non-existent “pure chrysotile exposures.”[106] This Court should examine scientific research as it is conducted in the real world rather than addressing questions framed by a “cadre of lawyers.”[107]

If G-P’s argument were accepted, Plaintiffs would be required to produce separate epidemiological studies of the exact formulations of each Defendant’s product. This type of argument was squarely rejected in Jarrell v. Park Cities Carpet & Upholstery Cleaning, Inc.[108] In Jarrell, the Dallas Court of Appeals held that the trial court abused its discretion by holding that “no studies are valid unless they deal specifically” with the products at issue.[109] The court held that studies of a product’s “chemical components” were admissible to prove causation, even though the studies did not involve the specific product formulations at issue.[110]

G-P’s argument also disregards well-established legal principles of causation. The final draft of the new Restatement recognizes that “[i]n some cases, a person may be exposed to two or more toxic agents, each of which is known to be capable of causing (general causation) the person’s disease.”[111] In asbestos cases involving such “multiple exposures,” courts have generally held that “each actor’s asbestos products to which the person was exposed” may be considered “a factual cause of the person’s disease.”[112] The Restatement describes this “asbestos rule” as “a means for adapting proof requirements to the available scientific knowledge.”[113]

Texas courts have applied these principles for many years. In Click v. Owens-Corning Fiberglas Corp., the Houston Court of Appeals acknowledged that “[i]t is difficult to determine exactly which exposure to asbestos is the cause of an asbestos-related cancer” but held that “some evidence existed that appellees supplied the products that caused or contributed to George Click’s death.”[114] In Borel v. Fibreboard Paper Products Corp., the Fifth Circuit applied Texas law and held that the evidence was sufficient to support a finding of causation even though “it is impossible, as a practical matter, to determine with absolute certainty which particular exposure to asbestos dust resulted in injury to Borel.”[115]

These principles are not unique to asbestos cases. Texas courts have long recognized that there may be more than one cause of a single injury.[116] There may be more than one proximate cause of an injury, and “[a]ll persons who contributed to the injury are liable.”[117] As the Dallas Court of Appeals has explained, “The plaintiff need not exclude all possibilities; it is sufficient to prove that the greater probability is that the defendant’s conduct, alone or in contribution with others, was the cause of the harm.”[118] In the asbestos context, the correct question is not whether each Defendant’s product caused harm by itself but whether exposure to a Defendant’s product, alone or in combination with other exposures, caused harm.

It has been suggested that this Court’s letter opinion regarding friction products[119] requires a Plaintiff to show which specific products or fibers caused his or her disease. Plaintiffs respectfully submit that any such interpretation of this Court’s opinion is in error because it would require proof of what is in fact unprovable. As discussed above, courts in Texas and other jurisdictions have long recognized that it is not possible to prove which particular asbestos fibers caused a given disease. The new Restatement addresses this issue in its discussion of “multiple sufficient casual sets”:

In some cases, tortious conduct by one actor is insufficient, even with other background causes, to cause the plaintiff’s harm. Nevertheless, when combined with conduct by other persons, the conduct overdetermines the harm, i.e., is more than sufficient to cause the harm. This circumstance thus creates the multiple sufficient causal set situation addressed in this comment. The fact that an actor’s conduct requires other conduct to be sufficient to cause another’s harm does not obviate the applicability of this Section.[120]

The reporter’s note explains that “[c]ourts have not required plaintiffs to prove the unprovable: which asbestos exposures were the actual cause of plaintiff’s disease.”[121] In the context of multiple exposures to a toxic substance over time, it is neither feasible nor necessary to identify each and every exposure as a “but for” cause. Tortfeasors whose independent acts combine to produce a single, indivisible injury are each liable for the victim’s entire injury.[122] G-P’s unreasonable focus on “pure chrysotile” is ultimately moot, since there is no reason to believe that any of the Defendants’ products were composed of “pure chrysotile.” For example, tests of G-P’s joint compound and Garlock gaskets have detected tremolite.[123] These results are entirely consistent with other published tests showing tremolite in commercial and industrial joint compounds,[124] as well as tissue studies showing tremolite in the lungs of workers exposed to finished chrysotile products.[125] The tremolite remains in finished chrysotile products.[126] In “the real world of workers exposed to products, for all intents and purposes, there are no ‘pure chrysotile’ exposures.”[127] Given these facts about asbestos exposure, researchers have concluded that “it is important to look at combined exposures, to chrysotile and amphiboles, because exposure to a small amount of amphibole added to chrysotile causes a disproportionate mesothelioma risk.”[128]

Dr. Egilman explains this principle with the following analogy: “[P]lacing a lit match alone on a wooden desk may create a risk of fire, but placing a lit match on a gasoline-soaked rag on the same desk transforms that risk into a flame. Evaluating the risk of the match alone is not a measure of the true risk when the lit match is always placed on a gasoline-soaked rag which is always present on the desk.”[129] By the same reasoning, the combined effects of chrysotile and amphibole exposure cannot be accurately measured in isolation. Moreover, to the extent that researchers have been able to examine chrysotile exposures separately to any significant degree, the results are consistent with the conclusion that chrysotile causes mesothelioma.[130]

The Totality of the Reliable Scientific Data Supports a Finding of General Causation.

Although the epidemiological evidence supports a finding of general causation, such evidence should not be considered in isolation. Citing the widely accepted “Bradford Hill” factors, the Court in Havner explained that conclusions about causation should not be reached “until a number of criteria have been considered.”[131] The Court also cautioned that “[c]areful exploration and explication of what is reliable scientific methodology in a given context is necessary.”[132] For example, “isolated case reports” may not provide significant information in the context of birth defects.[133] By contrast, in the context of rare “sentinel diseases” such as mesothelioma, “[c]ase series reports are particularly informative.”[134] The scientific acceptance of mesothelioma as a “sentinel” or “signature” disease has shaped court decisions in asbestos cases. The Restatement (Third) of Torts 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.”[135]

Strength and consistency of association. The “strength of association” reflects the power of a given study and may refer to human, animal or microbiologic studies.[136] Studies of workers exposed to chrysotile asbestos have demonstrated the occurrence of mesothelioma at rates more than double what would be expected.[137] The association of chrysotile and mesothelioma is also consistent, observed in different occupational and environmental settings and repeated in controlled experiments. As discussed above, mesothelioma has been connected with chrysotile exposure in extensive, published case studies.[138] Given the rarity of mesothelioma and its strong association with asbestos, such a consistent association is very unlikely to be random. In discussing “consistency of association,” Sir Austin Bradford Hill reasoned that a causal relationship was more likely if an association has been “repeatedly observed by different persons, in different places, circumstances and times . . . .”[139]

Experiment. In vivo animal studies and in vitro cell studies are also highly significant in the context of mesothelioma research. While such studies are not “conclusive” proof of a causal relationship,[140] they have established key facts about the biological effects of all types of asbestos. The published studies have demonstrated the ability of chrysotile and other forms of asbestos to induce mesothelioma and illustrated the mechanisms by which chrysotile fibers penetrate the cells and produce chromosomal aberrations.[141] To return to Bradford Hill’s words, such experimental data can often provide “1the strongest support for the causation hypothesis.”[142]


The experimental data also confirm that the causal connection between chrysotile asbestos and mesothelioma is “biologically plausible.”[143] By contrast, G-P’s arguments based on the iron content of chrysotile lack biological plausibility.[144] The health effects of asbestos fibers are a function of morphology rather than chemical composition.[145] Many researchers contend that the potency of crocidolite asbestos is related to its thin diameter. While chrysotile asbestos has a different morphology, chrysotile fibers have a tendency to cleave longitudinally, creating extremely thin fibrils.[146]

G-P also asserts that chrysotile cannot cause malignancy because it is has less “bio-persistence,” meaning that it is cleared from the lungs more readily than other forms of asbestos.[147] This argument overlooks the fact that chrysotile is an undisputed cause of lung cancer, indicating that it does have carcinogenic effects irrespective of its bio-persistence. G-P’s own expert witness, Dr. John Craighead, has conceded that with regard to both lung cancer and mesothelioma, the damage inflicted by asbestos fibers probably occurs “within minutes, hours, days, weeks at most after the inhalation . . . .”[148] Moreover, as discussed above, chrysotile fibers are typically “cleared” into the pleura, where most mesotheliomas develop.[149]

Coherence. In explaining the importance of “coherence,” Bradford Hill observed that “the cause-and-effect interpretation of our data should not seriously conflict with the generally known facts of the natural history and biology of the disease.”[150] G-P does not dispute that chrysotile, in common with other forms of asbestos, causes both asbestosis and lung cancer. Moreover, G-P does not dispute that the amphibole forms of asbestos cause mesothelioma. Given the comparable carcinogenic effects of chrysotile and amphibole fibers with respect to lung cancer, it is less likely that they have entirely different effects with respect to mesothelioma. The “amphibole hypothesis” is thus at odds with the known facts about the natural history and biology of mesothelioma and lung cancer.

Analogy. The causal connection between chrysotile asbestos and mesothelioma is supported by analogy. Havner explicitly recognized the role of analogy in scientific reasoning, quoting the following example: “With the effects of thalidomide and rubella before us we would surely be ready to accept slighter but similar evidence with another drug or another viral disease in pregnancy.”[151] By the same reasoning, the established causal connection between asbestos and mesothelioma logically supports the finding that chrysotile, a type of asbestos, causes mesothelioma. The convergent effects of chrysotile and amphibole fibers with respect to lung cancer further support the conclusion that both fiber types can cause mesothelioma.

G-P asks the Court to depart from both Havner and the Bradford Hill methodology by holding that reasoning by analogy is improper.[152] To support this argument, G-P asserts that Plaintiffs’ experts “ultimately disavow” the use of analogy.[153] G-P is mischaracterizing the expert testimony. For example, G-P cites a deposition in which Dr. Brody agreed that “scientific evidence that amosite asbestos causes mesothelioma in humans is not by itself proof that chrysotile asbestos causes mesothelioma in humans.”[154] No one has ever maintained that evidence regarding amosite or crocidiolite is “by itself” proof that chrysotile asbestos causes mesothelioma. As Dr. Frank explained in his deposition for this proceeding, “if all I knew was that amosite causes mesothelioma, I would be loath[] to say that chrysotile does it, but that’s not the state of our knowledge. I was relying on the totality of what was known . . . .”[155]

The totality of the scientific evidence regarding asbestos and mesothelioma supports the finding that chrysotile is capable of causing mesothelioma in the general population. The observed epidemiological and experimental data indicate a strong, consistent, coherent and plausible causal relationship. Expert testimony on this causal relationship is scientifically reliable and therefore admissible.

The Expert Testimony on Causation Is Reliable and Admissible Under the Standards Adopted in Robinson.

Courts “should allow a party, plaintiff or defendant, to present the best available evidence, assuming it passes muster under Robinson . . . .”[156] The expert testimony in this case certainly “passes muster” under the standards adopted in Robinson. The essence of a Robinson/Daubert analysis is to ascertain how the scientific evidence is received “outside the confines of the courtroom.”[157] An expert’s testimony should be supported by “a well-considered consensus of at least a substantial segment of the scientific, technical, or specialized community to which he belongs.”[158] Expert testimony should be admitted if the experts can “point to some objective source — a learned treatise, the policy statement of a professional association, a published article in a reputable scientific journal or the like — to show that they have followed the scientific method, as it is practiced by (at least) a recognized minority of scientists in their field.”[159] The Plaintiffs’ causation testimony is squarely based on scientific methods accepted and applied “outside the courtroom.”

“Non-judicial” applications

Building on the analysis in Daubert, Robinson explicitly held that courts should examine “non-judicial” applications of the scientific methodology at issue.[160] In Havner, for example, the court explicitly cited federal regulations in evaluating the reliability of scientific evidence.[161] In Curtis v. M&S Petroleum, Inc.,[162] the Fifth Circuit held that the “OSHA standard on benzene” as well as other scientific publications provided “generous support” for the expert’s “general causation theory” and that the trial court had abused its discretion in excluding the expert testimony on causation under Daubert.[163] In Snyder Oil Corp. v. Samedan Oil Corp.,[164] the Fifth Circuit held that official reports of federal agencies are “inherently more reliable than are private reports.”[165] Reports by regulatory agencies provide an important benchmark for gauging scientific reliability.

Despite the case law, G-P argues that the Court may not consider the opinions of regulatory agencies because they do not follow “the standards that govern in a court of law.”[166] This argument turns Robinson on its head. A properly conducted Robinson analysis should focus on how scientific evidence is treated outside a “court of law.” See Kerr-McGee Corp. v. Helton, 133 S.W.3d 245, 262 (Tex. 2004) (Hecht, J., concurring) (“Reliability does not mean one thing outside the courtroom and something less inside.”). In accordance with Robinson and Havner, this Court can and should examine how the scientific evidence is accepted and applied outside the courtroom by government agencies, scientific organizations and the asbestos products industry as a whole.

Outside the courtroom, regulatory agencies throughout the world have relied on the body of scientific evidence linking chrysotile asbestos and mesothelioma. In 2000, the World Trade Organization gathered an independent panel of scientists to assess the health effects of chrysotile asbestos, in order to determine whether Canada should be permitted to export chrysotile.[167] The assembled scientists agreed that chrysotile asbestos caused mesothelioma.[168] The WTO Panel concluded that chrysotile products posed a health risk to “downstream” users, “in particular as regards lung cancer and mesothelioma.”[169]

Governmental agencies in the United States have reached the same conclusion:

  • In 1977, the Consumer Product Safety Commission (CPSC) banned an entire class of joint compounds containing chrysotile asbestos, finding that the products posed an “unreasonable risk of injury to the public.”[170] Specifically, the Commission found that the products posed the risk of causing both lung cancer and mesothelioma.[171]


  • In 1986, after reviewing 55,000 pages of epidemiological studies, scientific articles and voluminous testimony “concerning the toxicity and carcinogenicity of different asbestos fiber types,” the Occupational Safety and Health Organization (“OSHA”) determined that “all fiber types, alone or in combination, have been observed in studies to induce lung cancer, mesothelioma, and asbestosis in exposed workers.”[172]
  • In 1989, the EPA acknowledged that “some evidence exists indicating that amphiboles may be more potent in inducing mesothelioma than chrysotile” but relied on the “volume of data showing the carcinogenic potency of all fiber types.” The EPA relied on both the epidemiological studies and “numerous animal studies [that] have demonstrated that chrysotile is at least as potent as amphiboles in inducing both mesothelioma and lung cancer by inhalation, as well as by injection or implantation.”[173] The Texas Department of Health has adopted the EPA’s asbestos standard.[174] The EPA reviewed the scientific literature on chrysotile again in 1999 and 2000 and found nothing “that persuasively contradicted the risk assessment approach” with respect to chrysotile asbestos.[175]
  • In 1990, the New York State Asbestos Advisory Board concluded that “the claim that various types of asbestos differ in their hazard is particularly insidious. It is put forth by the manufacturers of Canadian asbestos (chrysotile asbestos), the type of asbestos most widely used in New York and throughout the United States. The central claim here is that the Canadian product, termed ‘chrysotile asbestos’ is relatively harmless. However, that claim is not based on fact, and it is not supported by the results of epidemiological and toxicological studies conducted in the United States and overseas. These studies show that all types of asbestos, including Canadian asbestos, are fully capable of producing the full spectrum of asbestos-related diseases including . . . mesothelioma . . . .”[176]
  • In 1994, OSHA again reviewed the scientific evidence and reaffirmed its original conclusion that chrysotile asbestos presented a significant mesothelioma risk to exposed workers.[177]
  • In 1997, the U.S. Department of Health and Human Services stated that “both epidemiologic evidence and experimental confirmation indicate that chrysotile, amosite, and crocidolite asbestos are causative agents for mesothelioma.”[178]
  • In 1998, the NIOSH Atlas of Respiratory Disease Mortality reiterated that “[a]mphibole fiber types, especially crocidolite, appear to be the most potent inducers of malignant mesothelioma. However, chrysotile exposure can also cause this disease [Ross and McDonald 1995]. Therefore, all occupational groups exposed to asbestos are at risk of developing asbestos-related pleural malignancy.”[179]

A “well-considered consensus” among scientists

An expert’s testimony should be supported by “a well-considered consensus of at least a substantial segment of the scientific, technical, or specialized community to which he belongs.”[180] The opinions of the Plaintiffs’ experts are supported by a broad consensus of scientists throughout the world:

  • In 1997, an interdisciplinary group of epidemiologists, pathologists, industrial hygienists and other experts on asbestos-related disease gathered in Helsinki, Finland. The consensus among the scientists was that both chrysotile and amphibole fibers are capable of causing mesothelioma in human beings.[181]


  • In 1998, the World Health Organization’s International Progamme on Chemical Safety (IPCS) published an exhaustive report on chrysotile asbestos. After analyzing data from more than 400 scientific articles, the IPCS concluded that “[c]ommercial grades of chrysotile have been associated with an increased risk of pneumoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of exposed workers.”[182] The report analyzed all of the available scientific data, including epidemiological studies, tissue studies, and repeated in vivo and in vitro experiments. The data demonstrated that “[e]xposure to chrysotile asbestos poses increased risks for asbestosis, lung cancer and mesothelioma in a dose-dependent manner” and that no “threshold has been identified for carcinogenic risks.”[183] The original IPCS report on asbestos in 1986 explained that “[e]pidemiologic studies, mainly on occupational groups, have established that all types of asbestos fibers are associated with…primary malignant tumors of the pleura….”[184]
  • The International Agency for Research on Cancer (IARC) published a monograph in 1979 reporting that “[a] types of commerical asbestos fibres that have been tested are carcinogenic in mice, rats, hamsters and rabbits, producing mesotheliomas and lung carcinomas after inhalation, and after intrapleural, intratrachael and intraperitoneal administration.”[185] The IARC, which is generally considered the leading scientific authority on carcinogenic substances, follows a rigorous and comprehensive review process. The original IARC Monograph on asbestos was developed by the world’s leading authorities on asbestos research, including Dr. Irving Selikoff and Dr. J.C. Wagner.[186]
  • In 2004, the American Cancer Society’s revised guide to mesothelioma stated that “[a]mphiboles (particularly crocidolite) are considered to be the most carcinogenic . . . However, even the more commonly used chrysotile fibers are associated with malignant mesotheliomas and should be considered dangerous as well.”[187]
  • Over the past several decades, medical textbooks and scientific publications have consistently reflected the “well-considered consensus” that all forms of asbestos, including chrysotile, cause mesothelioma.[188]

These findings are consistent with decades of published, peer-reviewed scientific literature. Publication and peer review provide the strongest indicators of scientific reliability.[189] As discussed above, the methods and conclusions of the Plaintiffs’ causation experts have been subjected to scrutiny in scientific journals for many years. The testimony of the Plaintiffs’ experts is no different from the views expressed in their scientific publications. This “readiness to publish” has been called the “ultimate test of the integrity of an expert witness in the scientific arena.”[190]

The U.S.-Canada Mesothelioma Panel

The U.S.-Canada Mesothelioma Panel is a group of physicians specializing in the diagnosis of mesothelioma. Because mesothelioma is an unusual cancer, physicians generally refer suspected cases to the Panel for evaluation and diagnosis. By its nature, the Panel comprises the most qualified specialists and mesothelioma. Current and former members of the Panel have consistently concluded that chrysotile exposure causes mesothelioma. Dr. Roggli, a member of the Panel, has stated that chrysotile is “certainly . . . capable of producing mesothelioma in humans.”[191] Dr. Hector Battifora has stated that “[t]he vast majority of epidemiologists, pathologists, etc., whose opinions I rely on to form my opinion, is that indeed chrysotile is capable of producing mesothelioma in humans.”[192] Dr. Samuel Hammar, another member of the Panel who will testify on behalf of Owens-Illinois in this proceeding, agrees that there is “overwhelming evidence that chrysotile asbestos causes mesothelioma.”[193]

Dr. Philip Cagle, a member of the Panel, has agreed that “chrysotile can cause mesothelioma.”[194] Finally, Dr. Andrew Churg, another member of the Panel has testified that chrysotile exposure was a concurrent cause of mesothelioma in an insulator and that “both of these types of asbestos, amphiboles and chrysotile, are producing this tumor.”[195] Dr. Churg stated unequivocally that “[c]hrysotile can cause mesothelioma.”[196] In 2002, Dr. Churg reiterated his view that chrysotile causes mesothelioma.[197] Dr. Churg added that “I don’t make an issue of whether there’s tremolite or not tremolite. . . . If we consider chrysotile joint compounds, they may have tremolite; but, as I said before, it’s irrelevant because, with all that we know about chrysotile disease, tremolite doesn’t matter.”[198]

Experts for Plaintiffs and Defendants agree that chrysotile causes mesothelioma

With few exceptions, expert witnesses for Defendants in asbestos litigation have conceded that chrysotile causes mesothelioma. Dr. Cagle and Dr. Churg, whose opinions on chrysotile are discussed above, testify on behalf of asbestos Defendants. Dr. James Crapo and Dr. Allen Gibbs, who will testify for the Defendants in this proceeding, have also admitted that chrysotile can cause mesothelioma.[199] Dr. Battifora and Dr. Hammar, whose opinions on chrysotile are also discussed above, generally testify on behalf of Plaintiffs in asbestos litigation. For purposes of this proceeding, the relevant point is that reputable scientists acknowledge the causal relationship whether they are testifying on behalf of Plaintiffs or Defendants. Their opinions on this issue are shaped not by litigation strategy but by scientific analysis.

Industry acceptance

The court should also examine whether the relevant industry relies on the scientific evidence at issue. If “the industry would rely on expert analysis” similar to that offered by the witness, then it is “reliable for purposes of the trial.”[200] Outside the litigation context, asbestos product manufacturers have readily acknowledged that chrysotile asbestos can cause mesothelioma. Garlock, Inc. has published a Material Safety Data Sheet (“MSDS”) stating that inhalation of chrysotile asbestos fibers “can cause the well-known long term effects of asbestosis, lung cancer and mesothelioma.”[201] The MSDS for Union Carbide’s Calidria asbestos likewise identifies chrysotile asbestos as a known carcinogen and states that exposure to chrysotile asbestos “has caused damage to lungs (asbestosis), lung cancer and mesothelioma of the pleura and peritoneum.”[202] Mesothelioma is also named as a hazard of chrysotile asbestos products manufactured by other companies, including Energy Services Group,[203] John Crane,[204] Anchor Packing Co.,[205] Dresser-Rand Co.[206] and Durabla Manufacturing Co.[207]

It is true that an MSDS “standing alone” is not sufficient to prove causation.[208] But an MSDS combined with published scientific literature is “generous support” for expert testimony on general causation.[209] An MSDS is based on “all of the information regarding health and environmental hazards,” and “the manufacturer is required to research the best peer-reviewed scientific literature to form these material safety data sheets.”[210] The numerous statements made by asbestos product manufacturers demonstrate the widespread “non-judicial” application and acceptance of the opinions of the Plaintiffs’ experts.

Disagreement Among Experts Is Not a Valid Basis for Excluding Evidence.

It is true that not all scientists agree with the consensus view that chrysotile causes mesothelioma, but that disagreement does not render Plaintiffs’ expert testimony inadmissible. As one court has observed:

Daubert neither requires nor empowers trial courts to determine which of several competing scientific theories has the best provenance. It demands only that the proponent of the evidence show that the expert’s conclusion has been arrived at in a scientifically sound and methodologically reliable fashion.[211]

G-P suggests that expert testimony should be excluded if it is a subject of debate among scientists.[212] This reflects the profoundly mistaken view that “‘science’ presents an ‘objective’ method of establishing that, in all cases, reasonable minds cannot differ on the issue of factual causation. Such a view is incorrect.”[213] As the new draft of the Restatement explains, although “one scientist or group of scientists comes to one conclusion about factual causation, they recognize that another group that comes to a contrary conclusion might still be ‘reasonable.’ These scientists’ views reflect their scientific experience outside the courtroom.”[214] Thus “reasonable scientists can come to differing conclusions on whether a body of epidemiologic data justifies an inference of causation.”[215]

All scientific studies have limitations, and all are subject to criticism. Indeed, the studies cited by the Defendants have serious methodological shortcomings, and the interpretations offered by the Defendants’ experts are themselves open to debate. In fact, reasonable scientists can differ not only in their interpretation of the individual epidemiological studies. No epidemiological study, by itself, is conclusive. It must be interpreted in light of its methodology and underlying factual predicates. Moreover, extrapolating data from one study and comparing it to other populations is extremely difficult. As noted by the Committee on Nonoccupational Health Risks of Asbestiform Fibers[216]:

Comparisons of risk estimates from various studies are further limited by variations due to incomplete tracing of the cohort; misclassification of cause of death; use of inappropriate comparison groups; and more aggressive efforts to ascertain disease (or deaths) in the cohort than in the comparison group. . . . Some of the observed variation in risk may be due to differences in the effects of fibers of different types or dimensions and the use of these fibers in processes in which other contaminants are present. However, the magnitude of the difference in reported risks is not likely to be explained by fiber or process differences alone. Thus, on the basis of epidemiological data, it is not possible to determine the role of fiber type and fiber size in the risk of lung cancer and mesothelioma or to attribute greater or lesser risk to some types of asbestos fibers for lung cancer and mesothelioma.

To support the contention that amphiboles are the sole cause of mesothelioma, G-P relies on the affidavit of Dr. Timothy Lash and his interpretation of various epidemiological studies. In one section of his affidavit, Dr. Lash reviews epidemiologic studies comparing cohorts exposed to chrysotile asbestos with similar cohorts exposed to amphibole asbestos and concludes that mesothelioma only occurs in the cohorts exposed to amphiboles.[217] A closer examination of the studies he cites to support that contention, however, reveals that he has failed to consider all of the relevant data.

For example, Dr. Lash refers to Acheson’s study of gas mask filter workers in England during the Second World War.[218] One cohort of workers made filters with chrysotile and one cohort of workers with crocidolite. While, on the surface, this would appear to be an ideal opportunity to compare the relative potency of the different fiber types by examining the health effects in each population, substantial differences in exposure circumstances render such a comparison impractical. What Dr. Lash fails to mention is that the chrysotile gas mask operation was only active for about ten years, from 1936 until the end of the war. The factory making crocidolite filters, on the other hand, was active for about 30 years, from the 1930s until 1969. Moreover, the chrysotile filters were made by machine and the crocidolite filters were made by hand. As the authors of the paper conceded, “in addition to the known differences in types of asbestos fibre in use in the two factories, there may also have been unknown differences in dose and duration of exposure.”[219]

Another study cited by Dr. Lash is the Hughes study of two New Orleans asbestos cement manufacturing plants.[220] Chrysotile asbestos was the primary fiber used in both plants but in Plant 1 small amounts of amosite and crocidolite, intermittently, were used. In Plant 2, crocidolite was steadily used in pipe production. The study uncovered ten mesothelioma cases, 2 in Plant 1 and 8 in Plant 2. Dr. Lash is quick to point out that the two mesothelioma cases in Plant 1 with low amphibole content worked for less than a year and thus, their mesotheliomas may be the result of employment outside of the cement factory. Dr. Lash, however, fails to mention that one of the eight mesothelioma cases in Plant 2 occurred in a long-term worker (42 years) whose job assignment was confined to the shingle production area where only chrysotile asbestos was used.

As further support for his opinion that chrysotile is incapable of causing mesothelioma, Dr. Lash comments that no cases of mesothelioma have been reported among miners of South African chrysotile.[221] In formulating this conclusion, Dr. Lash, however, ignores a study by Dr. Rees that concludes that “findings in South Africa may need to be generalized to other settings with caution.”[222] Dr. Rees noted that:

One explanation for the absence of exclusively chrysotile cases is that production and use of the material in South Africa was so limited that the small number of exposed individuals has resulted in a paucity of cases.

According to asbestos production data presented in the paper, crocidolite and amosite were mined in South Africa since 1940. Chrysotile production, on the other hand, did not begin until 1960. Moreover, according to mine officials, during the 1980s and 1990s, the chrysotile fiber levels in the mine were consistently below 1 fiber per ml.[223] In addition, there were between 12,000 to 14,000 crocidolite miners were employed in the 1970s and 7,000 amosite miners, there were only 1,000 to 2,000 chrysotile miners employed at any one time. Given the relatively small population of chrysotile miners, the limited production of chrysotile, the long latency period for the induction of mesothelioma, and the moderate to low level exposure in the South African chrysotile mine, it is not surprising that no cases of mesothelioma have not yet appeared.[224]

Finally, Dr. Rees and his colleagues recognized that their findings in South Africa were not universal:

A number of recently published studies of almost exclusively chrysotile-exposed workers have shown high risks of mesothelioma. Raffn and colleagues [1993] reported on 269 men heavily exposed to asbestos and almost exclusively to chrysotile. The relative risk for mesothelioma was 22.73 for workers who had been employed at the facility for 20 or more years.[225]

Raffn’s finding of a more than 20-fold increased risk of mesothelioma in chrysotile exposed textile workers is not an anomaly. In a recent presentation at the Global Asbestos Congress held in Tokyo, Japan in November of 2004, Mamo and Costa addressed the issue of whether exposure to chrysotile asbestos alone, without contamination from amphibole asbestos causes mesothelioma and other asbestos diseases.[226] Their study of 1,653 Italian textile plant workers who were exposed to only chrysotile asbestos revealed a statistically significant 30-fold increased risk of dying from pleural mesothelioma among males (SMR=3322) and a 132-fold increase in females (SMR=13248).

Another study cited by Dr. Lash for the proposition that studies of cohorts exposed to chrysotile asbestos have observed no cases of mesothelioma is the McDonald study of a friction product plant in Connecticut.[227] Dr. Lash reports that there was “no mention of mesothelioma on the death certificate of any of 1228 male decedents or 112 female decedents.[228] Dr. Lash fails to mention, however, that in a subsequent study of the Connecticut tumor registry three cases of mesothelioma were identified in individuals who worked at the plant studied by McDonald.[229] Dr. Lash’s omission is particularly surprising since Teta specifically states:

Two of the three cases in employees at the asbestos plant were included by McDonald and Fry in their recently reported cohort study, which was based on death certificate information and employee records. The diagnosis of mesothelioma, however, was not ascertained since no mention of this disease as made on either death certificate. The third person, a male who was employed during the period 1921 to 1932, was not included in McDonald and Fry’s cohort which was defined as persons employed in the period 1937 to 1959 only.[230]

In addition to failing to mention these three cases of mesothelioma that occurred in a plant exclusively using chrysotile asbestos, Dr. Lash ignored several other studies of cohorts of chrysotile-exposed workers that have documented cases of mesothelioma. For example, in 1966, Dr. O’Donnell reported five cases of mesothelioma in workers at a textile plant that used chrysotile almost exclusively.[231] From this data, the authors concluded:

Selikoff et al found 10 mesotheliomas among American insulation workers – 4 in the pleura and 6 in the peritoneum. . . . The same investigators thought Chrysotile type asbestos fibers used primarily in the American asbestos industry to be carcinogenic, as well as the Crocidolite type asbestos referred to in the South African and British literature. We concur with the above opinion. The plant involved in this study used the Chrysotile type of asbestos fiber almost exclusively. The neoplastic hazard results from exposure to asbestos in general rather than to any one particular type fiber.[232]

Dr. Lash also failed to consider Dr. Enterline’s evaluation of the mortality experience of 1074 retired workers from a large United States products company.[233] Dr. Enterline reported that six cases of mesothelioma occurred in workers whose primary type of asbestos exposure was chrysotile.

In the final segment of his affidavit, Dr. Lash contends that those studies of chrysotile exposed cohorts that have reported cases of mesothelioma should not be interpreted to show a causal relationship because they are confounded by exposure to amphibole asbestos. Reasonable scientists could certainly disagree about the interpretation of these studies. For example, Dr. Lash reviewed Dr. Dement’s study of South Carolina asbestos textile workers that revealed two deaths from long-term workers primarily employed in spinning operations.[234] First, Dr. Lash contends that some crocidolite was used in small quantities at the plant from the 1950s to 1975. What he does not disclose is that the total quantity of crocidolite used was approximately 2,000 pounds compared to 6 to 8 million pounds per year of chrysotile. He further failed to disclose that the limited amount of crocidolite used in the plant was never carded, spun or twisted.[235]

Dr. Lash then contends that studies of the lungs of some of the plant workers with asbestosis and lung cancer revealed the presence of tremolite asbestos.[236] Dr. Lash fails to disclose that the lengths and aspect ratios of chrysotile fibers, but not amphibole fibers, were greater in the lungs of the asbestos workers when compared to controls, leading the researchers to conclude that the prevalence of asbestosis and lung cancer in this population resulted from exposure to the chrysotile asbestos.[237]

These disagreements among scientists are not a valid basis for excluding evidence. If scientists applying accepted methodologies can reach different conclusions, conflicts in the evidence should be resolved by the jury. As the Ninth Circuit explained in Kennedy v. Collagen Corp.:

Judges in jury trials should not exclude expert testimony simply because they disagree with the conclusions of the expert. The Daubert duty is to judge the reasoning used in forming an expert conclusion. The test is whether or not the reasoning is scientific and will assist the jury. If it satisfies these two requirements, then it is a matter for the finder of fact to decide what weight to accord the expert’s testimony. In arriving at a conclusion, the fact finder may be confronted with opposing experts, additional tests, experiments, and publications, all of which may increase or lessen the value of the expert’s testimony. But their presence should not preclude the admission of the expert’s testimony — they go to the weight, not the admissibility.[238]

The Texas Supreme Court has explained that the court’s role “is not to determine whether an expert’s conclusions are correct but only whether the analysis used to reach them is reliable.”[239] If an expert’s methodology meets the minimum threshold of scientific reliability, the jury should be allowed to determine its ultimate merit. Conflicts in expert testimony, like other factual disputes, are left to the jury when the evidence as a whole “rises to a level that would enable reasonable and fair-minded people to differ in their conclusions.”[240] Reasonable and fair-minded people can and do differ on whether chrysotile exposure causes mesothelioma, creating a fact issue with respect to causation.


These are not “junk science” cases. These cases involve generally accepted scientific opinions based on well-established methodologies. The relevant studies have been reviewed in scientific journals over a period of decades, and the data has led many scientists and public agencies, independent of any litigation, to conclude that chrysotile asbestos is capable of causing mesothelioma. Plaintiffs’ general causation testimony is reliable, admissible and legally sufficient.

WHEREFORE, PREMISES CONSIDERED, Plaintiffs respectfully requests that the Court deny G-P’s motion in all respects. Plaintiffs further request all other relief to which they may be entitled.

  1. Research Methods in Occupational Epidemiology 248 (Checkoway, et al., eds. 2d ed. 2004), attached as Exhibit 1 to Plaintiffs’ Exhibits in Support of Response to Georgia Pacific’s Motion to Exclude (hereinafter Plaintiffs’ exhibits are simply referred to as “Ex. __”).
  2. See, e.g., Pathology of Asbestos-associated Diseases 108 (Roggli, et al., eds., 2nd ed. 2004), Ex. 2 (“[I]t is clear that sufficient exposure to chrysotile may result in the development of mesothelioma . . . .”); Harrington, The Carcinogenicity of Chrysotile Asbestos, in The Third Wave of Asbestos Disease: Exposure to Asbestos in Place (Landrigan & Kazemi, eds. 1991) 465, Ex. 3, at 470 (“[C]hrysotile asbestos is carcinogenic in humans, especially for the induction of lung cancer and mesothelioma in exposed populations . . . .”; Li et al., Cohort Studies on Cancer Mortality Among Workers Exposed Only to Chrysotile Asbestos: A Meta-Analysis, Biomedical & Envtl. Sci. 17:459-68 (2004), Ex. 4 (reporting, based on meta-analysis of multiple epidemiological studies, that exposure to chrysotile fibers alone increased risk of mesothelioma); Pathology of Occupational Lung Disease 351 (Churg & Green eds., 2nd ed. 1998), Ex. 5 (“These observations leave no doubt that enough exposure to chrysotile ore can produce mesothelioma in man.”); Selikoff & Lee, Asbestos and Disease 280 (1978), Ex. 6; Landrigan, et al., The Hazards of Chrysotile Asbestos: A Critical Review, Indus. Health 37:271-280 (1999), Ex. 6A (reviewing 40 studies of workers exposed to asbestos and concluding that “[c]linical and epidemiologic studies have established beyond all reasonable doubt that chrysotile asbestos causes cancer of the lung” and “malignant mesothelioma of the pleura and peritoneum . . . .”).
  3. See Affidavit of David S. Egilman, M.D. (“Egilman Aff.”), Ex. 7, at ¶ 14; Deposition of Dr. Arthur Frank (“Frank Depo.”), Ex. 8, at 32-33, 119-20.
  4. Frank Depo. at 103.
  5. Consensus Report, Asbestos, Asbestosis, and Cancer: The Helsinki Criteria for Diagnosis and Attribution, Scand. J. Work Envtl. Health 23:311, 313 (1997) (“Helsinki Criteria”), Ex. 9;
  6. American Cancer Society, Detailed Guide: Malignant Mesothelioma (Dec. 21, 2004), Ex. 10 (“Amphiboles (particularly crocidolite) are considered to be the most carcinogenic . . . However, even the more commonly used chrysotile fibers are associated with malignant mesotheliomas.”).
  7. World Health Organization, Environmental Health Criteria 203: Chrysotile Asbestos (1998) (“EHC 203”), Ex. 11, at ¶ 1.6 (“Commercial grades of chrysotile have been associated with an increased risk of pneumoconiosis, lung cancer and mesothelioma in numerous epidemiological studies of exposed workers.”).
  8. World Trade Organization, European Communities – Measures Affecting Asbestos and Asbestos-Containing Products, Report of the Panel (Sept. 18, 2000) (“WTO Report”), Ex. 12.
  9. OSHA, Occupational Exposure to Asbestos, Tremolite, Anthophylite, and Actinolite; Final Rules, excerpts attached as Ex. 13 (noting that “all fiber types, alone or in combination, have been observed in studies to induce lung cancer, mesothelioma, and asbestosis in exposed workers.”).
  10. NIOSH, Atlas of Respiratory Disease Mortality, United States: 1982-1993 (1998), Ex. 14 (“Amphibole fiber types, especially crocidolite, appear to be the most potent inducers of malignant mesothelioma. However, chrysotile exposure can also cause this disease [Ross and McDonald 1995]. Therefore, all occupational groups exposed to asbestos are at risk of developing asbestos-related pleural malignancy.”).
  11. EPA, Asbestos: Manufacture, Importation, Processing and Distribution in Commerce Prohibitions; Final Rule, (July 12, 1989), Ex. 15A.; EPA, Asbestos Worker Protection, Final Rule (Nov. 15, 2000), Ex. 15B.
  12. 16 C.F.R.§ 1304.5, Ex. 16.
  13. U.S. Dep’t of Heath and Human Services, Asbestos Bibliography (Sept. 1997), Ex. 17, at 86 (“[B]oth epidemiologic evidence and experimental confirmation indicate that chrysotile, amosite, and crocidolite asbestos are causative agents for mesothelioma”).
  14. See “Defendant Georgia-Pacific Corporation’s Motion Pursuant to E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549 (Tex. 1995), to Exclude General Causation Opinion Testimony That Uncontaminated Chrysotile, As Used in Georgia-Pacific’s Joint Compound, Can Cause Mesothelioma” (hereinafter “Motion”).
  15. Although tremolite is often described as a “contaminant,” the term is not entirely accurate. Tremolite occurs naturally throughout deposits of chrysotile ore and is normally found in products containing commercial chrysotile. See, e.g., Fischbein, et al., Drywall Construction and Asbestos Exposure, Am. Indus. Hyg. J. 40:402-407 (1979), Ex. 18.
  16. See Motion at 11-12, 30.
  17. E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549 (Tex. 1995).
  18. Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579 (1993).
  19. Decision and Order, In re Eighth Judicial District Asbestos Litigation, Index No. 2001-9946 (Supreme Court of New York, Eighth Judicial District, June 8, 2004), Ex. 19, at 7.
  20. Order, Plummer v. AC&S, Inc., Cause No. 00-07604 (160th Judicial Dist., Dallas County, Tex. Aug. 27, 2001), Ex. 20.
  21. See, e.g., Order, Rollins v. AC&S, Inc., Cause No. CC-01-01169-A (County Court at Law No. 1, Dallas County, Tex. March 17, 2003), Ex. 21; Order, Breaux v. AC&S, Inc., Cause No. 08271-1 (162nd Judicial Dist., Dallas County, Tex. July 25, 2001), Ex. 22; Order, Steenbergen v. AC&S, Inc., Cause No. 00962 (71st Judicial Dist., Harrison County, Tex. Sept. 6, 2001), Ex. 23; Order, Royer v. AC&S, Inc., Cause No. 14293*RM00 (149th Judicial Dist., Brazoria County, Tex. June 11, 2002), Ex. 24; Letter ruling, Cipov v. AC&S, Inc., Cause No. 153-189827-01 (153rd Judicial District, Tarrant County, Tex., April 2, 2002), Ex. 25; Letter ruling, Sheldon v. Bondex Int’l, Inc., No. 153-200794-03 (153rd Judicial District, Tarrant County, Tex., Nov. 3, 2004), Ex. 26; Order, Poore v. Alcoa, Inc., Cause No. 14221*JG00 (239th Judicial Dist., Brazoria County, Tex. Aug. 4, 2004), Ex. 27; Order, Schiller v. Garlock, Inc., Cause No. 02-C-220 (5th Judicial Dist., Cass County, Tex. Nov. 18, 2003), Ex. 28.
  22. In 2002, Judge John Dietz of Travis County found that: 1.Government and public health authorities, independent of any judicial proceedings and after extensive review of medical and scientific studies and testimony, have concluded that exposure to chrysotile asbestos causes mesothelioma in humans. 2.Medical and scientific experts in the field of asbestos disease, including pathologists and epidemiologists, have concluded that exposure to chrysotile asbestos causes mesothelioma in humans. 3.Peer reviewed studies published in recognized scientific and medical journals have concluded that exposure to chrysotile asbestos causes mesothelioma in humans. 4.A causal link between exposure to chrysotile asbestos and mesothelioma has been demonstrated through reliable scientific and medical methodology, including pathology and tissue burden studies. The use of pathology and tissue burden studies in this context is generally accepted by the medical community and is routinely utilized by pathologists during the course of medical practice independent of judicial proceedings. 5.A consistent and reliable epidemiological link has been established between exposure to chrysotile asbestos and mesothelioma in humans. Findings of Fact and Conclusions of Law, Miller v. Kellogg-Brown & Root, Inc., Cause No. GN2O 1185 (261st Judicial District, Travis County, Texas, Dec. 2, 2002), Ex. 29.
  23. See Havner, 953 S.W.2d at 718 n.2
  24. Id.
  25. See Egilman Aff. ¶¶ 15-26; Frank Depo. at 32-33, 119-20.
  26. Egilman Aff. ¶ 15.
  27. See Havner, 953 S.W.2d at 718 n.2
  28. Affidavit of Dr. Richard Lemen (“Lemen Aff.”), Ex. 30, at 5.
  29. Id.
  30. See EHC 203, supra.
  31. U.S. Dep’t of Heath and Human Services, Asbestos Bibliography (Sept. 1997), supra, at 86.
  32. See Egilman Aff. ¶ 28 (Table 1), ¶ 38 (Tables 3-4).
  33. Id. at 45, 47-48.
  34. Letter from Irving J. Selikoff, M.D. (July 31, 1973), Ex. 31.
  35. Frank Depo. at 47-48.
  36. See Stern, et al., Mortality Among Unionized Construction Plasterers and Cement Masons, Am. J. Indus. Med. 39:373-388 (2001), Ex. 32; Hodgson, et al., Mesothelioma Mortality in Britain: Patterns by Birth Cohort and Occupation, Ann. Occup. Hyg. 41(Suppl. 1):129-133 (1997), Ex. 33.
  37. Stern, supra.
  38. A “Proportionate Mortality Ratio” measures the proportion of deaths attributable to a particular cause in an occupational as compared with the reference population.
  39. Hodgson, supra.
  40. See Coggon, et al., Differences in Occupational Mortality from Pleural Cancer, Peritoneal Cancer, and Asbestosis, Occup. & Envtl. Med. 52:775-777 (1995) (PMR of 2.07 for pleural cancers and a PMR of 2.65 for peritoneal cancers), Ex. 34.
  41. Mancuso, Relative Risk of Mesothelioma Among Railroad Machinists Exposed to Chrysotile, Am. J. Indus. Med. 13:639-657 (1988), Ex. 35.
  42. Id. at 655.
  43. Yano, et al., Cancer Mortality Among Workers Exposed to Amphibole-Free Chrysotile Asbestos, Am. J. Epidemiology 154:538-43 (2001), Ex. 36; see also Egilman Aff. n.12.
  44. Because mesothelioma is invariably fatal, a relative risk and SMR can be used “almost interchangeably.” Egilman Aff. n. 26.
  45. Camus, et al., Nonoccupational Exposure to Chrysotile Asbestos and The Risk of Lung Cancer, New England J. Med. 338(22):1565-1571 (1998), Ex. 37.
  46. Piolatto, et al., An Update of Cancer Mortality Among Chrysotile Asbestos Miners in Balangero, Northern Italy, Br. J. Indus. Med. 47:810-814 (1990), Ex. 38
  47. Lemen Aff. at 6.
  48. Id.
  49. Cullen & Baloyi, Chrysotile Asbestos and Health in Zimbabwe: I. Analysis of Miners and Millers Compensated for Asbestos-related Diseases Since Independence (1980), Am. J. Indus. Med. 19:161-169 (1991), Ex. 39.
  50. Dell & Teta, Mortality Among Workers at a Plastics Manufacturing and Research and Development Facility: 1946-1988, Am. J. Indus. Med. 28:373-384 (1995), Ex. 40.
  51. Lemen Aff. at 8.
  52. Rogers, et al., Relationship Between Lung Asbestos Fiber Type and Concentration and Relative Risk of Mesothelioma, Cancer 67:1912-1920 (1991), Ex. 41.
  53. See id.; Lemen Aff. at 6.
  54. Strum, et al., Use of Asbestos, Health Risks and Induced Occupational Diseases in the Former East Germany, Toxicol Lett. 72:317-24 (1994), Ex. 42.
  55. Asbestiform Fibers: Nonoccupational Health Risks, Committee on Nonoccupational Health Risks of Asbestiform Fibers, Board on Toxicology and Environmental Health Hazards, Commission on Life Sciences, National Research Council, The National Academy of Sciences, (1984) at 134-35 (available at
  56. Landrigan, et al., supra, at 275.
  57. Id.; see also Nicholson, Comparative Dose-Response Relationships of Asbestos Fiber Types: Magnitudes and Uncertainties, Ann N.Y. Acad. Sci 643:74-84 (1991) Ex. 43.
  58. Id. at 276. Other researchers have since indicated that limited amounts of amphibole asbestos were used prior to 1935, but such use would still not account for the observed disease patterns.
  59. EHC 203, supra, at ¶ 1.6.
  60. Id. (emphasis added).
  61. Id.
  62. See, e.g., Frank Depo. at 47-48 (discussing Selikoff studies of insulators exposed primarily to chrysotile and explaining that “it was hard to imagine that . . . a few percent of amphibole . . . was the sole cause of the vast amount of mesothelioma we were seeing.”).
  63. EHC 203, supra, at ¶ 10.
  64. Research Methods in Occupational Epidemiology 248, supra.
  65. Id. at 60.
  66. See Wagner, et al., Diffuse Pleural Mesothelioma and Asbestos Exposure in the North Western Cape Province, Brit. J. Indus. Med. 17:260-271 (1960), Ex. 45.
  67. See Frank Depo. at 38-39, 43.
  68. See Dement, et al., supra;Teta, et al., Mesothelioma in Connecticut, 1955-1977, J. Occup. Med. 25:749-756 (1983), Ex. 46; Konetzke, et al., Asbestos-Induced Mesotheliomas – Results of a Retrospective Study, Proc. Int’l Symposium on the Prevention of Occupational Cancer, Helsinki, Finland (1981), Ex. 47; Vianna & Polan, Non-Occupational Exposure to Asbestos and Malignant Mesothelioma in Females, Lancet 1061-1063 (May 20, 1978), Ex. 48; McDonald, et al., Epidemiology of Primary Malignant Mesothelial Tumors in Canada, Cancer, 26:914-919 (1970), Ex. 49; Kagan & Jacobson, Lymphoid and Plasma Cell Malignancies: Asbestos-related Disorders of Long Latency, Am. J. Clin. Path. 80:14-20 (1983), Ex. 50; Huncharek, et al., Pleural Mesothelioma in a Brake Mechanic, Brit. J. Indus. Med. 46:69-71 (1989), Ex. 51; Greenberg & Davies, Mesothelioma Register 1967-68, Brit. J. Indus. Med. 31:91-104 (1974), Ex. 52; Lieben & Pistawka, Mesothelioma and Asbestos Exposure, Arch. Environ. Health 14:559-566 (1967), Ex. 53; Wolf, et al., Malignant Mesothelioma With Occupational and Environmental Asbestos Exposure in an Illinois Community Hospital, Arch. Intern. Med. 147:2145-2149 (1987), Ex. 54.
  69. See, e.g., Havner, 953 S.W.2d at 718 n.2.
  70. See id. at 728-31.
  71. Egilman Aff. ¶ 23 (quoting Wilbourn, et al., Response of Experimental Animals to Human Carcinogens: An Analysis Based on the IARC Monographs Programme, Carcinogeesis 7:1853-63 (1986) and Rice, et al., Tumors of the Nervous System in Carcinogenic Hazard Identification, Toxicological Path. 28:202-214 (2000)).
  72. Egilman Aff. ¶ 23.
  73. See, e.g., Wagner, et al., The Effects of the Inhalation of Asbestos in Rats, Br. J. Cancer 29:252-269 (1974), Ex. 55; see also Table 1.
  74. Davis & Cowie, The Relationship Between Fibrosis and Cancer in Experimental Animals Exposed to Asbestos and Other Fibers, Envtl. Health Perspectives 88:305-309 (1990).
  75. See Egilman Aff. ¶ 51; Libbus & Craighead, Chromosomal Translocations with Specific Breakpoints in Asbestos-induced Rat Mesotheliomas, Cancer Research 48:6455-6461 (1988), Ex. 56; Minardi & Maltoni, Results of Recent Experimental Research on the Carcinogenicity of Natural and Modified Asbestos, Ann. N.Y. Acad. Sci. 534:754-761 (1991), Ex. 57.
  76. See Bolton, et al., Variations in the Carcinogenicity of Mineral Fibres, Ann. Occup. Hyg. 26:569-582 (1982), Ex. 58; Wagner & Berry, Mesothelioma in Rats Following Inoculation with Asbestos, Br. J. Cancer 23:567-581 (1969), Ex. 59.
  77. See Levresse, et al., Analysis of Cell Cycle Disruptions in Cultures of Rat Pleural Mesothelial Cells Exposed to Asbestos Fibers, Am. J. Respir. Cell Mol. Biol. 17:660-671 (1997), Ex. 60; Jaurand, et al., Chromosomal Changes Induced by Chrysotile Fibres or Benzo-3,4-pyrene in Rat Pleural Mesothelial Cells, Mutation Research 169:141-148 (1986), Ex. 61.
  78. Lemen Aff. at 10.
  79. See Frank, et al., Carcinogenic Implications of the Lack of Tremolite in UICC Reference Chrysotile, Am. J. Ind. Med. 34: 314-317 (1998), Ex. 62; see also Kohyama, et al., Mineral Phases and Some Reexamined Characteristics of the International Union Against Cancer Standard Asbestos Samples, Am. J. Indus. Med. 30:515-528 (1996), Ex.63.
  80. Malignant Mesothelioma (Henderson, et al., eds. 1992) 230, Ex. 64.
  81. See Suzuki and Kohyama, Translocation of Inhaled Asbestos Fibers from the Lung to Other Tissues, Am. J. Indus. Med. 19:701-704 (1991), Ex. 65; Kohyama & Suzuki, Analysis of Asbestos Fibers in Lung Parenchyma, Pleural Plaques, and Mesothelioma Tissues of North American Insulation Workers, Ann. N.Y. Acad. Sci. 643:27-52 (1991), Ex. 66; Sebastien, et al., Asbestos Retention in Human Respiratory Tissues: Comparative Measurements in Lung Parenchyma and in Parietal Pleura, IARC Sci. Pub. 30:237-246 (1980), Ex. 67.
  82. Suzuki & Yuen, Asbestos Tissue Burden Study on Human Malignant Mesothelioma, Indus. Health 39:150-160 (2001), Ex. 68.
  83. Id.
  84. Frank Depo. at 119-20.
  85. Motion at 11, 35.
  86. El Chico Corp. v. Poole, 732 S.W.2d 306, 313 (Tex. 1987).
  87. Havner, 953 S.W.2d at 714 (emphasis added).
  88. Id. at 711.
  89. 953 S.W.2d at 717 (emphasis added).
  90. Id. at 718-20.
  91. Restatement (Third) of Torts §28, cmt. c (Final Draft No. 1, April 6, 2005) (hereinafter “Restatement (Third)”.
  92. Benedi v. McNeil-P.P.C., Inc., 66 F.3d 1378, 1384 (4th Cir. 1995).
  93. See, e.g., Kennedy v. Collagen Corp., 161 F.3d 1126, 1228-30 (9th Cir. 1998); Baker v. Dalkon Shield Claimants Trust, 156 F.3d 248, 252-53 (1st Cir. 1998); Zuchowicz v. United States, 140 F.3d 281, 386-87 (2d Cir. 1998); Heller v. Shaw Indus., Inc., 167 F.3d 146, 154-57 (3d Cir. 1999); Kannankeril v. Terminex Int’l, Inc., 128 F.3d 802, 807-09 (3d Cir. 1997); Westberry v. Gislaved Gummi AB, 178 F.3d 257, 262-63 (4th Cir. 1999); Glaser v. Thompson Med. Co., 32 F.3d 969, 978 (6th Cir. 1994); Hopkins v. Dow Corning Corp., 33 F.3d 1116, 1125 (9th Cir. 1994); Ambrosini v. Labarraque, 101 F.3d 129, 139 (D.C. Cir. 1996).
  94. 953 S.W.2d at 718.
  95. Id. at 719.
  96. Id.
  97. 978 S.W.2d 183, 188 (Tex. App. — Texarkana 1998, pet. denied) (emphasis added).
  98. 21 S.W.3d 358, 365 (Tex. App. — San Antonio 2000, pet. denied).
  99. Id. at 365.
  100. Id.
  101. 953 S.W.2d at 719.
  102. Id. at 720 (emphasis added).
  103. Deposition of Dr. Arnold Brody, July 28, 2004, Attachment F6 to G-P Motion, at 214.
  104. Case, Biological Indicators of Chrysotile Exposure, Ann. Occup. Hyg., 38:503-518 (1994), Ex. 69.
  105. Doll & Peto, Report to the British Health and Safety Commission (1985), Ex. 70, at 15-17.
  106. See, e.g., Motion at 11, 28.
  107. Havner, 953 S.W.2d at 727.
  108. 53 S.W.3d 901 (Tex. App. — Dallas 2001, pet. denied).
  109. Id. at 903.
  110. Id. at 902.
  111. Restatement (Third), supra, § 28, cmt. c.
  112. Id.
  113. Id.
  114. 899 S.W.2d 376, 377 (Tex. App. — Houston [14th Dist.] 1995, no writ); see also Quigley Co., Inc. v. Calderon, 2003 WL 77256 (Tex. App. – El Paso 2003, pet. denied) (not designated for publication) (“Absolute certainty is not required, nor must the plaintiff exclude every other possibility. . . . If there is sufficient evidence presented by Appellees showing that Appellant supplied any of the asbestos to which Appellees were exposed, then Appellees have adequately met their burden of proof.”); Fibreboard Corp. v. Pool, 813 S.W.2d 658, 685 (Tex. App. – Texarkana 1991, writ denied), cert. denied, 508 U.S. 909 (1993) (jury can apportion fault among asbestos product manufacturers even though “asbestos fibers found in the lungs cannot be traced to a specific product.”); Celotex Corp. v. Tate, 797 S.W.2d 197, 204 (Tex. App. – Corpus Christi 1990, writ dism’d).
  115. 493 F.2d 1076, 1094 (5th Cir. 1974).
  116. See, e.g., Sysco Food Services, Inc. v. Trapnell, 890 S.W.2d 796 (Tex. 1994) (holding that fact issue existed on causation based on expert testimony that sulfites from defendant’s products, in combination with sulfites from other sources, contributed to injury); Havner v. E-Z Mart Stores, Inc., 825 S.W.2d 456, 459 (Tex. 1992) (“The act or omission need not be the sole cause.”); Wilson v. Brister, 982 S.W.2d 42, 44 (Tex. App. — Houston [1st Dist.] 1998, pet. denied) (“More than one action may be the proximate cause of the same injury.”).
  117. El Chico Corp. v. Poole, 732 S.W.2d 306, 313 (Tex. 1987).
  118. Berly v. D & L Sec. Serv. and Investigations, Inc., 876 S.W.2d 179, 182 (Tex. App. — Dallas 1994, writ denied) (emphasis added).
  119. Letter opinion (Jan. 10, 2005).
  120. Restatement (Third), supra, § 27, cmt. f.
  121. Id., reporter’s note to cmt. g; see also id. at § 28, cmt. l (noting that all of the asbestos products to which a plaintiff is exposed, rather than a single defendant’s product, are considered a cause of harm).
  122. The classic Texas case in this area is Landers v. East Tex. Salt Water Disposal Co., 248 S.W.2d 731 (1952), in which one defendant’s oil pipeline and another defendant’s salt water disposal line ruptured at about the same time, releasing oil and salt water into plaintiff’s lake. The Texas Supreme Court found the injury an “indivisible” one and held both defendants jointly and severally liable even though it could not be said that the damage would not have happened “but for” either source of pollution. As discussed above, this “indivisible injury” rule has been consistently applied to asbestos cases in Texas. See, e.g., Celotex Corp. v. Tate, 797 S.W.2d at 204 (“Thus, when a defendant has in fact caused harm to the plaintiff, he may not escape liability merely because the harm he has inflicted has combined with similar harm inflicted by other wrongdoers.”). Courts throughout the country have reached the same conclusion. See, e.g., Mavroudis v. Pittsburgh-Corning Corp., 935 P.2d 684, 689 (Wash. App. 1997) (holding that a defendant cannot avoid liability “solely on the ground that the plaintiff probably would have suffered the same disease from inhaling fibers originating from the products of other suppliers” ); Spaur v. Owens-Corning Fiberglas Corp., 510 N.W.2d 854, 861 (Iowa 1994) (“We hold that it is not necessary and indeed may be impossible to establish exactly how much one party’s asbestos product contributed to the resulting injury.”); Eagle-Picher Ind., Inc. v. Balbos, 604 A.2d 445, 459 (Md. 1992); Koichan v. Owens-Corning Fiberglas Corp., 610 N.E.2d 683, 689 (Ill. Ct. App. 1993); Hollingsworth & Vose Co. v. Connor, 764 A.2d 318, 331-32 (Md. Ct. Spec. App. 2000) (approving an instruction stating: “Where a plaintiff has proved a disease resulting from exposure to asbestos products of different identified manufacturers or suppliers, no manufacturer or supplier has a defense solely on the ground that the plaintiff would probably have suffered the same disease from inhaling or ingesting fibers originating from the products of others”).
  123. See Reports of Dr. William Longo, Ex. 71 and Ex. 72; Report of MVA Scientific Consultants, Ex. 73.
  124. See, e.g., Fischbein, et al., supra (discussing four joint compounds containing between 2% and 12% tremolite in addition to chrysotile).
  125. See Deposition of Victor Roggli, M.D., King v. Allied-Signal, Inc., et al., No. 24242C-03, Newport News, Va. (Jan. 18, 2001), Ex. 74, at 63-64; Egilman Aff. ¶¶ 62-63.
  126. See Letter from Victor Roggli, M.D., to I.A. Feingold, M.D., (April 6, 2001), Ex. 75.
  127. Doll & Peto, supra.
  128. Egilman Aff. ¶ 64.
  129. Id. at ¶ 65.
  130. See Li, supra, (reporting, based on meta-analysis of multiple epidemiological studies, that exposure to chrysotile fibers alone increased risk of mesothelioma); Yano, supra, at 542 (“[W]e found no evidence in support of the amphibole contaminant hypothesis. To the contrary, a strong potential for chrysotile asbestos alone to cause lung cancer and mesothelioma was suggested.”); Frank, supra (explaining that based on the absence of tremolite from chrysotile samples used in biomedical research, “chrysotile should be considered as having the biologic ability to produce cancers, including mesotheliomas.”); Frank Depo. at 60.
  131. 953 S.W.2d at 718. The Bradford Hill methodology, and its application to the causal relationship between chrysotile asbestos and mesothelioma, is discussed in greater detail in Dr. Egilman’s affidavit, Dr. Lemen’s affidavit and in Dr. Lemen’s 2004 article on the subject. See Egilman Aff. ¶¶ 15-26; Lemen Aff. at 3-12; Lemen, Chrysotile Asbestos as a Cause of Mesothelioma: Application of the Hill Causation Model, Int’l J. Occup. Envtl. Health 10:233-239 (2004), infra.
  132. Id. at 719.
  133. Id. at 720.
  134. Research Methods in Occupational Epidemiology, supra.
  135. Restatement (Third) of Torts §28, cmt. c; Faigman, et al., 3Modern 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.”); see also In Re Joint Eastern & Southern Dist. Asbestos Lit., 52 F.3d 1124, 1130 (2nd Cir. 1995) (referring to “a mesothelioma-like signature disease arising only when a person of that age is exposed to asbestos.”).
  136. See Egilman Aff. ¶16.
  137. See id. at ¶ 28, Table 1.
  138. See Teta, et al., supra; Konetzke, et al., supra; Vianna & Polan, supra; McDonald, et al., supra; Kagan & Jacobson, supra; Huncharek, et al., supra; Greenberg & Davies, supra; Lieben & Pistawka, supra; Wolf, et al., supra.
  139. Havner, 953 S.W.2d at 718 n.2.
  140. See id. at 728-31.
  141. See Levresse, et al., supra; Jaurand, et al., supra.
  142. 953 S.W.2d at 718 n.2.
  143. Id.
  144. See Motion at 8.
  145. Lemen Aff. at 14.
  146. See id.
  147. Motion at 7-8.
  148. Deposition of John Edward Craighead, M.D., Lansford v. Able Supply Co., No. 26658, Shelby County, Tex. (Oct. 3, 2002), Ex. 76, at 80.
  149. See Suzuki & Kohyama, supra; Sebastien, et al., supra
  150. Havner, 953 S.W.2d at 718 n.2.
  151. Id.; see also Texas Workers’ Comp. Ins. Fund v. Lopez, 21 S.W.3d 358, 365 (Tex. App. — San Antonio 2000, pet. denied) (rejecting Daubert challenge and explaining that studies of gold miners were relevant to assessing the effects of silica particles on sandblaster’s lungs).
  152. See Motion at 38-39.
  153. Motion at 21.
  154. Brody Deposition, Attachment F1 to Motion, at 29-30 (emphasis added).
  155. Frank Depo. at 47.
  156. Havner, 953 S.W.2d at 720.
  157. 923 S.W.2d at 726.
  158. Volkswagen of America, Inc. v. Ramirez, __ S.W.3d __, 2004 WL 3019227 (Tex. 2004) (Hecht, J., concurring).
  159. Daubert v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1318-19 (9th Cir. 1995).
  160. 923 S.W.2d at 557.
  161. See Havner, 953 S.W.2d at 720 (citing 21 C.F.R. § 314.126); see also Texas Workers’ Comp. Ins. Fund v. Lopez, 21 S.W.3d 358, 366 (Tex. App. — San Antonio 2000, pet. denied) (explaining that federal regulators’ reliance on scientific evidence weighed in favor of admissibility under Robinson).
  162. 174 F.3d 661 (5th Cir. 1999).
  163. Id. at 669-72.
  164. 208 F.3d 521 (5th Cir. 2000).
  165. Id. at 527.
  166. Motion at 39. Nonetheless, G-P relies on a draft report prepared by consultants for the EPA. See Motion at 13-14. While this report has been frequently offered into evidence by defendants in asbestos litigation, neither the EPA nor any other neutral body has ever accepted or endorsed the views expressed in it. Indeed, there is no evidence that this deeply flawed report has been applied or accepted in any “non-judicial” setting.
  167. See Egilman Aff. ¶¶ 95-96.
  168. See, e.g., WTO Report at ¶ 5.267 (statement of Dr. Peter Infante that “[s]everal high quality epidemiological studies of workers exposed to chrysotile asbestos demonstrate an elevated risk of death from lung cancer, asbestosis and mesothelioma.”).
  169. Id. at ¶ 8.194.
  170. 16 C.F.R.§ 1304.5, supra.
  171. Id.
  172. OSHA, Occupational Exposure to Asbestos, Tremolite, Anthophylite, and Actinolite; Final Rules, supra.
  173. EPA, Asbestos: Manufacture, Importation, Processing and Distribution in Commerce Prohibitions; Final Rule, supra.
  174. 25 Tex. Admin. Code § 295.33.
  175. EPA, Asbestos Worker Protection, Final Rule (Nov. 15, 2000), supra.
  176. Second Annual Report, State of New York, Asbestos Advisory Board (Feb. 1990), Ex. 77.
  177. OSHA, Occupational Exposure to Asbestos; Final Rule, supra.
  178. U.S. Dep’t of Heath and Human Services, Asbestos Bibliography (Sept. 1997), supra, at 86.
  179. NIOSH, Atlas of Respiratory Disease Mortality, United States: 1982-1993, supra.
  180. Volkswagen of America, Inc. v. Ramirez, __ S.W.3d __, 2004 WL 3019227 (Tex. 2004) (Hecht, J., concurring).
  181. See Helsinki Criteria, supra; Lemen Aff. at 4.
  182. EHC 203, supra.
  183. Id. at ¶ 10.
  184. IPCS, Environmental Health Criteria 53, Ex. 78.
  185. IARC Monograph (Sept. 1979), Ex. 79.
  186. See Lemen Aff. at 4-5. Dr. Lemen was himself a member of the group asked to develop the IARC Monograph.
  187. American Cancer Society, supra.
  188. See, e.g., Pathology of Occupational Lung Disease, supra (“These observations leave no doubt that enough exposure to chrysotile ore can produce mesothelioma in man.”); Selikoff & Lee, Asbestos and Disease supra; Landrigan, et al., supra (“Clinical and epidemiologic studies have established beyond all reasonable doubt that chrysotile asbestos causes cancer of the lung” and “malignant mesothelioma of the pleura and peritoneum . . . .”); Malignant Mesothelioma 230, supra (discussing evidence that “chrysotile alone can cause mesothelioma.”); Lemen, Chrysotile Asbestos as a Cause of Mesothelioma: Application of the Hill Causation Model, Int’l J. Occup. Envtl. Health 10:233-239 (2004), Ex. 80. (“These findings along with the results of the experimental studies leave no doubt that the scientific evidence supports the carcinogenicity of chrysotile alone in the induction of mesothelioma.”); Smith & Wright, Chrysotile Asbestos Is the Main Cause of Pleural Mesothelioma, Am. J. Indus. Med. 30:252-66 (1996) (“Chrysotile asbestos is a potent cause of pleural mesothelioma.”), Ex. 81.
  189. See Robinson, 923 S.W.2d at 555-57; Havner, 953 S.W.2d at 726; see also Lopez, 21 S.W.3d at 365 (“Unlike the epidemiological study criticized in Havner, the studies referenced by Lopez have been published.”).
  190. Havner, 953 S.W.2d at 727; see also Ruiz-Troche v. Pepsi Cola of Puerto Rico Bottling Co., 161 F.3d 77, 85 (1st Cir. 1998) (publication and peer review “serve as an independent indicia of the reliability” of the expert’s opinions).
  191. Deposition of Victor Roggli, M.D., King v. Allied-Signal, Inc., et al., supra, at 58.
  192. Deposition of Hector Battifora, M.D., Darnold v. Able Supply Co., No. 98-10-04083E, 404th Judicial Dist., Cameron County, TX (July 19, 2001), Ex. 82, at 56-57.
  193. Deposition of Samuel P. Hammar, M.D., Turley v. AC&S, Inc. (March 22, 2001), Ex. 83, at 50-51.
  194. Testimony of Philip Cagle, M.D., Biales v. Pittshburgh Corning, 89-47734, 11th Jud. Dist. Ct., Harris Cty., Tex. (July 23, 1996), Ex. 84, at 11.
  195. Testimony of Dr. Andrew Churg, Anderson v. Fibreboard, et al., No. 85-2-00438-0, Kitsap County, Wash. (March 13, 1987), Ex. 85, at 11-14.
  196. Id. at 24; see also Testimony of Dr. Andrew Churg, Abate, et al., v. AC&S, Inc., et al., No. 89236704, Baltimore, Md. (May 21, 1992), Ex. 86, at 17023 (agreeing that “all forms of asbestos fibers can cause mesothelioma.”).
  197. See Deposition of Dr. Andrew M. Churg, Brauch v. Bondex Int’l, Inc., et al., No. BC-258-492 (Superior Ct. Los Angeles, Calif. March 27, 2002), Ex. 87.
  198. Id. at 18-25.
  199. See Deposition of James Crapo, M.D., Hicks v. AC&S, Inc. (Aug. 10, 2001), Ex. 88 at 66-67; Testimony of Dr. Allen Gibbs, Kelly-Moore v. Union Carbide Corp., Brazoria Cty., Tex. (Oct. 11, 2004), Ex. 89, at 173.
  200. Kerr-McGee Corp. v. Helton, 133 S.W.3d 245, 262 (Tex. 2004) (Hecht, J., concurring)
  201. Garlock MSDS, Ex. 90, at 2 (emphasis added).
  202. Union Carbide MSDS, Ex. 91, at 2-4 (emphasis added).
  203. Energy Services Group MSDS, Ex. 92.
  204. John Crane MSDS, Ex. 93.
  205. Anchor Packing Co. MSDS, Ex. 94.
  206. Dresser-Rand Co. MSDS, Ex. 95.
  207. Durabla Manufacturing Co. MSDS, Ex. 96.
  208. See Coastal Tankships, U.S.A., Inc. v. Anderson, 87 S.W.3d 591, 611 (Tex. App. — Houston [1st Dist.] 2002, pet. denied).
  209. Curtis v. M&S Petroleum Inc., 174 F.3d 661, 669 (5th Cir. 1999)
  210. Id.
  211. Ruiz-Troche, 161 F.3d at 85.
  212. See Motion at 32 n.26.
  213. Restatement (Third), supra, §28, cmt. c.
  214. Id.
  215. Id.
  216. Asbestiform Fibers: Nonoccupational Health Risks, supra, at 134-35.
  217. Affidavit of Dr. Timothy Lash (“Lash Aff.”), Attachment B to G-P Motion, at 12.
  218. Acheson, Mortality of Two Groups of Women Who Manufactured Gas Masks from Chrysotile and Crocidolite Asbestos: A 40-year Follow-up, Brit. J. indus. med. 39:344-348 (1982), Ex. 97.
  219. Dr. Lash also cites the Jones investigation of the gas mask facilities in Nottoway, England, but the authors of that presentation specifically declined to make any comparison by fiber type because of the limited number of workers in the chrysotile factory. See Jones, The Consequences of Exposure to Asbestos Dust in a Wartime Gas Mask Factory, Biological effects of mineral fibers, 637-53 (IARC 1980), Ex. 98.
  220. Hughes, Mortality of Workers Employed in Two Asbestos Cement Manufacturing Plants, Brit. J. Indus. Med. 44:161-174 (1987), Ex. 99.
  221. Lash Aff. at 11.
  222. Rees, Case-Control Study of Mesothelioma in South Africa, Am. J. Indus. Med. 35:213-222 (1999), Ex. 100.
  223. Rees, Asbestos Lung Fibre Concentrations in South African Chrysotile Mine Workers, Ann. occup. Hyg., 45(6):473-477 (2001), Ex. 101, at 476.
  224. It should be noted that Dr. Rees did not systematically study the South African chrysotile miners to determine whether any of them had, in fact, been diagnosed with mesothelioma. Instead, the mesothelioma cases in his study were randomly collected over a 16-month period, from late 1988 through early 1990, from various hospitals throughout South Africa.
  225. Rees, Case-Control Study of Mesothelioma in South Africa, supra, at 221.
  226. Abstract, Mamo and Costa, Mortality Experience in a Historical Cohort of Chrysotile Asbestos Textile Workers, Global Asbestos Congress, Epidemiology and Public Health (2004), Ex. 102. (available at
  227. McDonald, Dust Exposure and Mortality in an American Chrysotile Asbestos Friction Products Plant, Br. J. Indus. Med. 41:151-157 (1984), Ex. 103.
  228. Lash Aff. at 12.
  229. Teta, supra.
  230. Id. at 755.
  231. O’Donnell, Asbestos, an Extrinsic Factor in the Pathogenesis of Bronchogenic Carcinoma and Mesothelioma, Cancer 19:1143-1148 (1966), Ex. 104.
  232. Id. at 1147-48.
  233. Enterline, Asbestos and Cancer: A Cohort Followed up to Death, Brit. j. indus. med. 44:396-401 (1987), Ex. 105.
  234. Dement, Follow-Up Study of Chrysotile Asbestos Textile Workers: Cohort Mortality and Case-Control Analyses, Am. J. Indus. Med. 26:431-447 (1994), Ex. 106.
  235. Id. at 433.
  236. Dr. Lash cites Green, Exposure and Mineralogical Correlates of Pulmonary Fibrosis in Chrysotile Asbestos Workers, Occup. envtl. Med. 54(8):549-59 (1997), Ex. 107.
  237. See id.
  238. 161 F.3d 1126, 1230-31 (9th Cir. 1998); see also Ambrosini v. Labarraque, 101 F.3d 129,138-139 (D.C. Cir. 1996) (“[T]here is nothing in Daubert to suggest that judges become scientific experts, much less evaluators of the persuasiveness of an expert’s conclusion”); Globetti v. Sandoz Pharm. Corp., 111 F. Supp., 2d 1174, 1176 (N.D. Ala. 2000) (fact finder, not judge, is to decide whether opinion is correct or worthy of credence); Cartwright v. Home Depot U.S.A., Inc., 936 F.Supp. 900, 902 (M.D. Fla. 1996) (the “gatekeeping responsibility of the trial courts is not to weigh or choose between conflicting scientific opinions.”).
  239. Gammill v. Jack Williams Chevrolet, Inc., 972 S.W.2d 713, 718 (Tex. 1998).
  240. Havner, 953 S.W.2d at 711.