DON R. WILLETT, Justice.
In Borg-Warner Corp. v. Flores,
In 2002 Bostic was diagnosed with mesothelioma. He was 40 years old, and died of the disease in 2003. Mesothelioma is a rare cancer of a lining of the body's internal organs. There is no dispute that asbestos, when breathed into the lungs, can cause mesothelioma. Bostic's relatives, individually and on behalf of Bostic's estate (Plaintiffs), sued Georgia-Pacific and 39 other defendants, alleging that the defendants' products exposed Bostic to asbestos and caused his disease. Plaintiffs alleged causes of action for negligence and products liability. Plaintiffs claimed that as a
The case went to trial in 2006. The jury found Georgia-Pacific liable under negligence and marketing defect theories, and was asked to allocate causation among numerous entities. The jury assessed 25% of the causation to Knox Glass Company, a former employer who had settled with Bostic, and 75% to Georgia-Pacific.
The trial court signed an amended judgment awarding Plaintiffs approximately $6.8 million in compensatory damages and approximately $4.8 million in punitive damages. The court of appeals concluded that the evidence of causation was legally insufficient and rendered a take-nothing judgment.
The Plaintiffs contend the court of appeals erred in holding that the causation evidence was legally insufficient. In conducting a legal sufficiency review, the final test "must always be whether the evidence at trial would enable reasonable and fair-minded people to reach the verdict under review."
Flores concerned proof of causation in a case where Flores, a brake mechanic, allegedly suffering from asbestosis, sued Borg-Warner, a brake pad manufacturer. The jury found that Flores suffered from asbestos-related disease and apportioned to Borg-Warner 37% of the causation.
On further analysis, we held that "proof of mere frequency, regularity, and proximity is necessary but not sufficient, as it provides none of the quantitative information necessary to support causation under Texas law."
Plaintiffs urge that the standards established in Flores are not fully applicable because today's case is a mesothelioma case and Flores was an asbestosis case. They contend that a key factual distinction between the two diseases is that relatively minute quantities of asbestos can result in mesothelioma. In Flores, we noted that the development of asbestosis requires a heavy exposure to asbestos, while mesothelioma may result from low levels of exposure.
While Flores left open the prospect of treating asbestosis and mesothelioma cases differently, we decline to do so. We believe the Flores framework for reviewing the legal sufficiency of causation evidence lends itself to both types of cases. In particular, we hold that even in mesothelioma cases proof of "some exposure" or "any exposure" alone will not suffice to establish causation. While the experts in this case testified that small amounts of asbestos exposure can result in mesothelioma, that fact alone does not merit a different analysis. With both asbestosis and mesothelioma, the likelihood of contracting the disease increases with the dose. As to asbestosis, we noted in Flores that this disease "appears to be dose-related, so that the more one is exposed, the more likely the disease is to occur, and the higher the exposure the more severe the disease is likely to be."
If any exposure at all were sufficient to cause mesothelioma, everyone would suffer from it or at least be at risk of contracting the disease. In Flores we noted that one of the plaintiff's experts acknowledged that "everyone is exposed to asbestos in the ambient air" and that "it's very plentiful in the environment, if you're a typical urban dweller."
More fundamentally, if we were to adopt a less demanding standard for mesothelioma cases and accept that any exposure to asbestos is sufficient to establish liability, the result essentially would be not just strict liability but absolute liability against any company whose asbestos-containing product crossed paths with the plaintiff throughout his entire lifetime. However, "[w]e have recognized that `[e]xposure to asbestos, a known carcinogen, is never healthy but fortunately does not always
If an "any exposure" theory of liability is accepted for mesothelioma cases because science has been unable to establish a dose below which the risk of disease disappears, the same theory would arguably apply to all carcinogens. Dr. Lemen, Plaintiffs' epidemiologist and a former Assistant Surgeon General, testified that for all carcinogens the threshold at which the risk falls to zero is unknown.
The any exposure theory effectively accepts that a failure of science to determine the maximum safe dose of a toxin necessarily means that every exposure, regardless of amount, is a substantial factor in causing the plaintiff's illness. This approach negates the plaintiff's burden to prove causation by a preponderance of the evidence. As a federal district court reasoned in excluding the testimony of Dr. Hammar, Plaintiffs' expert on specific causation in today's case:
Further, there are cases where a plaintiff's exposure to asbestos can be tied to a defendant, but that exposure is minuscule as compared to the exposure resulting from other sources. Proof of any exposure at all from a defendant should not end the inquiry and result in automatic liability. The Restatement Third of Torts provides that "[w]hen an actor's negligent conduct constitutes only a trivial contribution to a causal set that is a factual cause of harm under § 27 [addressing multiple sufficient causes], the harm is not within the scope of the actor's liability."
The any exposure theory is also illogical in mesothelioma cases, where a small exposure can result in disease, because it posits that any exposure from a defendant above background levels should impose liability, while the background level of asbestos should be ignored. But the expert testimony in this case was undisputed that the background level varies considerably from location to location. We fail to see how the theory can, as a matter of logic, exclude higher than normal background levels as the cause of the plaintiff's disease, but accept that any exposure from an individual defendant, no matter how small, should be accepted as a cause in fact of the disease. Under the any exposure theory a background dose of 20 does not cause cancer, but a defendant's dose of 2 plus a background dose of 5 does.
Plaintiffs complain that the court of appeals erred in requiring them to prove but for causation in addition to substantial factor causation. The term "but for causation" may encompass several meanings. As we attempt to clarify, "but for" and "substantial factor" are overlapping concepts and, to the extent they embody different tests, application of those tests usually lead to the same result. But here we are concerned that the court of appeals' decision might be read to require satisfying a proof requirement that but for Bostic's exposure to Georgia-Pacific's products, he would not have contracted mesothelioma. We agree with Plaintiffs that language in the court of appeals' decision appears to require such proof. The court stated that "[b]oth producing and proximate cause contain the cause-in-fact element, which requires that the defendant's act be a substantial factor in bringing about the injury and without which the harm would not have occurred."
To a point, we agree with Georgia-Pacific that but for causation is a recognized standard for proof of producing cause, also known as causation in fact,
Nor is there anything unusual in our recognizing but for causation as the causation standard in tort cases. The Restatement Second of Torts in section 431 generally recognizes that an "actor's negligent conduct is a legal cause of harm to another if [] his conduct is a substantial factor in bringing about the harm."
The Restatement Third of Torts likewise embraces but for causation as the general causation standard in tort cases. Section 26 of the subtitle on Liability for Physical and Emotional Harm provides: "Tortious conduct must be a factual cause of harm for liability to be imposed. Conduct is a factual cause of harm when the harm would not have occurred absent the conduct."
However, we follow Flores and conclude that in products liability cases where the plaintiff was exposed to multiple sources of asbestos, substantial factor causation is the appropriate basic standard of causation without including as a separate requirement that the plaintiff meet a strict but for causation test. Due to the nature of the disease process, which can occur over decades and involve multiple sources of exposure, establishing which fibers from which defendant actually caused the disease is not always humanly possible. Even if the exposure from a particular defendant was by itself sufficient to cause the disease, in multiple-exposure cases the plaintiff may find it impossible to show that he would not have become ill but for the exposure from that defendant.
In Flores we recognized "the proof difficulties accompanying asbestos claims. The long latency period for asbestos-related diseases, coupled with the inability to trace precisely which fibers caused disease and from whose product they emanated, make this process inexact."
This language is inconsistent with a strict requirement of proving that but for the particular fibers traceable to the sued defendant, the plaintiff would not have become ill. In Flores we keyed on substantial factor causation, and did not require proof of but for causation. The absence of but for language in Flores was not inadvertent.
Again, our approach did not break new ground. While but for causation is a core concept in tort law, it yields to the more general substantial factor causation in situations where proof of but for causation is not practically possible or such proof otherwise should not be required. A leading treatise has observed that the substantial factor approach "in the great majority of cases ... produces the same legal conclusion as the but-for test," but "was developed primarily for cases in which application of the but-for rule would allow each defendant to escape responsibility because the conduct of one or more others would have been sufficient to produce the
The Restatement Second of Torts likewise recognizes an alternative to strict but for causation in certain cases involving multiple causes of injury. While, as noted, section 431 and its comment a generally require but for causation, comment a further notes that this rule applies "[e]xcept as stated in § 432(2)." Section 432(2) addresses cases involving multiple causation: "If two forces are actively operating, one because of the actor's negligence, the other not because of any misconduct on his part, and each of itself is sufficient to bring about harm to another, the actor's negligence may be found to be a substantial factor in bringing it about."
Likewise, while the Restatement Third generally embraces but for causation in section 26,
And comment g posits the scenario closest to our case:
In short, we do not think the Restatements, in their attempts to synthesize many decades of tort law, would require the plaintiffs to meet a strict but for causation test in a case like today's case. More importantly, our controlling decision in Flores does not impose this requirement. Accordingly, we hold that Plaintiffs were required to establish substantial factor causation, but were not required to prove that but for Bostic's exposure to Georgia-Pacific's products, he would not have contracted mesothelioma. The court of appeals erred insofar as it stated otherwise.
We write further on the meaning of substantial factor causation in asbestos cases. First, we note that for all the refinements Flores places on the substantial causation standard, we also believe that some discretion must be ceded to the trier of fact in determining whether the plaintiff
We recognized a quantitative approach to causation in Merrell Dow Pharmaceuticals, Inc. v. Havner,
In Havner, the plaintiffs sued on behalf of a child born with birth defects allegedly caused by a drug, Bendectin, taken by the mother while she was pregnant. The Court held that the expert testimony, which relied in part on epidemiological studies, was legally insufficient to establish causation.
While recognizing that causation might be established through epidemiological studies showing more than a doubling of the risk, also described as a relative risk of more than 2.0,
Havner is a foundational part of our jurisprudence. We have never held that it applies universally to all tort cases where causation is an issue.
Despite differences between Havner and today's case, Havner's focus on proof of more than a doubling of risk, as established by scientifically reliable studies, is premised on fundamental principles of tort law that have application here. Havner's discussion of epidemiological studies was based on the tenet in our law that expert testimony on causation must be scientifically reliable. "If the expert's scientific testimony is not reliable, it is not evidence."
Havner also held that, notwithstanding competing policies of deterrence, risk-avoidance, or compensating innocent injured parties, "[o]ur legal system requires
In sum, Havner enunciated principles in toxic tort cases that (1) expert testimony of causation must be scientifically reliable, (2) the plaintiff must establish the elements of his claim by a preponderance of the evidence, and (3) where direct evidence of causation is lacking, scientifically reliable evidence in the form of epidemiological studies showing that the defendant's product more than doubled the plaintiff's risk of injury appropriately corresponds to the legal standard of proof by
Multiple-exposure cases raise the issues of how the finder of fact should consider exposure from sources other than the defendant, what proof might be required as to those other sources, and who has the burden of proof regarding those other sources. These are difficult questions.
We recognized in Havner, generally, that "if there are other plausible causes of the injury or condition that could be negated, the plaintiff must offer evidence excluding those causes with reasonable certainty."
However, when evidence is introduced of exposure from other defendants or other sources, proof of more than a doubling of the risk may not suffice to establish substantial factor causation. In the Restatement Second of Torts, and as quoted by our Court in Flores, substantial factor causation "denote[s] the fact that the defendant's conduct has such an effect in producing the harm as to lead reasonable men to regard it as a cause, using that word in the popular sense, in which there always lurks the idea of responsibility,
Suppose a plaintiff shows that his exposure to a defendant's product more than doubled his chances of contracting a disease, but the evidence at trial also established that another source of the toxin increased the chances by a factor of 10,000. In this circumstance, a trier of fact or a court reviewing the sufficiency of the evidence should be allowed to conclude that the defendant's product was not a substantial factor in causing the disease.
JUSTICE LEHRMANN presents a thorough and thought-provoking dissent, but we cannot agree with its ultimate conclusion that the evidence of causation was legally sufficient in this case. The dissent contends that Havner primarily focused on general causation. As noted above, Havner was concerned with general causation while today's case is not. But Havner was also concerned with specific causation. General causation is never the ultimate issue of causation tried to the finder of fact in a toxic tort case. The ultimate issue is always specific causation — whether the defendant's product caused the plaintiff's injury. General causation as established through epidemiological studies is relevant only insofar as it informs specific causation. In Havner, we held that where direct evidence of specific causation is unavailable, specific causation may be established through an alternative two-step process whereby the plaintiff establishes general causation through reliable studies, and then demonstrates that his circumstances are similar to the subjects of the studies.
The dissent suggests that our analysis is flawed because specific causation as explicated
The dissent argues that Havner is inapplicable to multiple-exposure cases. We are at a loss to understand why. If exposure from other sources were irrelevant when we decided Havner, we would not have stated that other causes of the disease should be excluded,
The dissent also suggests that we would require the application of Havner even in cases where the only conceivable source of exposure to a toxin is the defendant. If the plaintiff can establish with reliable expert testimony that (1) his exposure to a particular toxin is the only possible cause of his disease, and (2) the only possible source of that toxin is the defendant's product (or, in another of the dissent's hypotheticals, the products of two defendants whose combined doses established the required threshold dose to cause disease), this proof might amount to direct proof of causation and the alternative approach embraced in Havner might be unnecessary. These hypotheticals certainly do not apply to today's case, as discussed further below. Plaintiffs never claimed that Georgia-Pacific was the only source of Bostic's exposure or that combined exposures from multiple defendants were needed to cause his disease.
We conclude that in all asbestos cases involving multiple sources of exposure, including mesothelioma cases, the standards for proof of causation in fact are
• proof of "any exposure" to a defendant's product will not suffice and instead the plaintiff must establish the dose of asbestos fibers to which he was exposed by his exposure to the defendant's product;
• the dose must be quantified but need not be established with mathematical precision;
• the plaintiff must establish that the defendant's product was a substantial factor in causing the plaintiff's disease;
• the defendant's product is not a substantial factor in causing the plaintiff's disease if, in light of the evidence of the plaintiff's total exposure to asbestos or other toxins, reasonable persons would not regard the defendant's product as a cause of the disease;
• to establish substantial factor causation in the absence of direct evidence of causation, the plaintiff must prove with scientifically reliable expert testimony that the plaintiff's exposure to the defendant's product more than doubled the plaintiff's risk of contracting the disease.
Georgia-Pacific manufactured and sold asbestos-containing joint compound from 1965 to 1977. Bostic was born in 1962 and turned 15 in 1977. The joint compound was sold in a dry-mix form, to which water was added to make drywall "mud," and a pre-mixed form. The compound was used to smooth cracks and joints during drywall installation and repair. During the 1965-77 period, the compound contained chrysotile asbestos,
Bostic and his father Harold Bostic (Harold) testified by deposition at trial. Bostic's exposure to asbestos-containing Georgia-Pacific products occurred when, as a child and teenager, he assisted Harold in remodeling projects for friends and family. Plaintiffs contend that Bostic's exposure as a child is particularly significant since several experts agreed that children are especially vulnerable to exposure to asbestos and carcinogens in general. Bostic helped his father mix and sand drywall compound from the age of five. Plaintiffs contend that Bostic was also exposed to asbestos from exposure to Harold's clothing. Bostic lived with his father until his parents divorced in 1972, when he was 9, and he stayed with his father thereafter on weekends, holidays, and at times during the summer.
Harold testified that he performed drywall work on various projects during the relevant period. He testified that he used Georgia-Pacific drywall compounds "[l]ike 98% of the time." Bostic assisted Harold on projects during the 1967-77 time frame when Georgia-Pacific drywall compound contained asbestos. Harold testified that he and Bostic used Georgia-Pacific compound "[m]any, many, many times." He was able to recall specifically eight projects during the relevant period, although he thought there were other projects he simply could not recall. Of the specific projects he could recall, he specifically identified one where Georgia-Pacific compound was used, a job where he constructed a kit house for a friend. He could not
Bostic was exposed to asbestos from Knox Glass Company. Harold was employed at Knox Glass from 1962 until 1984. Bostic lived with his father until his parents divorced and sometimes stayed with his father after 1972 as noted above. He also lived with his father from ages 15 to 18. Bostic worked at Knox Glass in the summers of 1980, 1981, and 1982. While Plaintiffs point to Bostic's testimony that he spent only about three months during these summers in the "hot end" of the plant where asbestos was prevalent, he testified that he frequently worked 16 hours a day as "a relief hot end worker." Asbestos was used in products extensively at the plant, in cements, fireproofing, asbestos cloth, pumps, packing, valves, furnaces, and other products. Bostic's work included cutting asbestos cloth, cleaning up after asbestos pipe insulation was repaired, removing and replacing asbestos from machines, and wearing asbestos gloves. One of his main jobs was cutting asbestos cloth. He had no respiratory protection. He was exposed to asbestos from the Knox Glass plant due to his own employment and also from exposure to asbestos brought home on his father's clothes. Bostic and Harold participated in a study finding that 27% of workers at the plant had developed asbestos-related illnesses, although the duration of Bostic's employment at the plant was at the low end of the employees studied.
Bostic was exposed to asbestos while employed by another company, Palestine Contractors, in 1977 and 1978, and while working alone and with his father on automobiles with brake pads and other parts that contained asbestos. As an adult Bostic was also exposed to asbestos while doing remodeling work, where he was exposed to shingles, tiles, and other asbestos-containing building materials that were not manufactured by Georgia-Pacific. His primary employment, from 1984 until he stopped working due to his illness at the end of 2002, was as a correctional officer with the Texas Department of Criminal Justice (TDCJ). He did not claim exposure to asbestos from this employment.
Work history sheets provide certain details of Bostic's work history. These were based on information provided by Bostic and reviewed by Plaintiffs' experts. Bostic reported that he had used drywall compounds from seven different manufacturers.
Plaintiffs offered the testimony of several experts. Dr. Richard Lemen, an epidemiologist, testified about the history of research linking asbestos in its various forms to diseases including mesothelioma. Dr. William Longo, a material scientist, testified about the concentrations of asbestos that would be released into the air by workers performing typical drywall work. Dr. Arnold Brody, a pathologist, testified regarding asbestos, including the chrysotile variety used in the drywall compound, as a recognized cause of mesothelioma and other diseases. Dr. Samuel Hammar, a pathologist, was Plaintiffs' expert on specific causation.
Hammar testified that any asbestos exposure above background levels causes mesothelioma. He testified that he had not reviewed the deposition testimony of Bostic and Harold. He reviewed the work history sheets but conceded they did not indicate the duration or intensity of exposure. Hammar, Brody, and Lemen repeatedly testified that "each and every exposure" to asbestos was a cause of Bostic's
We conclude, under the principles stated above, that the causation evidence was legally insufficient to uphold the verdict. Proof of substantial factor causation requires some quantification of the dose resulting from Bostic's exposure to Georgia-Pacific's products. Plaintiffs did not establish even an approximate dose. Instead, the expert testimony was to the effect that any exposure was sufficient to establish causation, a theory we rejected in Flores. Plaintiffs' counsel reinforced this testimony in opening and closing argument by embracing the any exposure theory. In opening counsel argued:
In closing counsel argued:
Counsel invited the jury to find that any exposure was sufficient to impose liability and that aggregate and relative dose did not matter.
Rather than attempting to quantify the aggregate dose of asbestos attributable to Georgia-Pacific's products, Plaintiffs' experts expressly eschewed this approach in favor of the view that any exposure at all was sufficient to constitute a cause of the disease, even though Hammar, Brody, and Lemen conceded that all asbestos diseases are dose-related,
Not only did Flores reject the any exposure theory, but Plaintiffs' experts purported to rely on studies that contradicted or at least did not confirm a theory that each and every exposure should be treated as a substantial cause of the disease. For example, Brody, Lemen, and Hammar purported to rely on a repore
Hammar and Lemen testified that any exposure to asbestos should be treated as a cause of Bostic's mesothelioma. In reaching this conclusion they relied in part on publications in the Federal Register, including a 1977 report of the Consumer Product Safety Commission
So far as we can tell, none of the peer-reviewed scientific studies on which Plaintiffs' experts relied found a statistically significant link between mesothelioma and occasional exposure to joint compounds comparable to Bostic's exposure, namely the occasional exposure of a son helping his father on building renovation projects that were not the primary occupation of either father or son, and which included drywall work as well as other construction activities. For example, Lemen testified about one of his own published articles
Plaintiffs' experts did not show, through reliance on scientifically reliable evidence, that Bostic's exposure to asbestos from Georgia-Pacific's products more than doubled his risk of contracting mesothelioma.
Evidence was presented of another source of asbestos exposure, namely Bostic's employment at Knox Glass, where he was exposed to asbestos from numerous sources. Hammar testified that Bostic's exposure to asbestos from Knox Glass was minimal as compared to his exposure from construction, but this testimony was conclusory, as it was not based on any scientific studies or any scientific attempt to measure the relative exposures. An expert's testimony that brings no more than "his credentials and a subjective opinion" will not support a judgment.
The dissent would hold the causation evidence legally sufficient if an expert testified that exposure to a defendant's product was "significant." In bringing this suit Plaintiffs claimed exposure from 40 defendants, and the case as Plaintiffs tried it to the jury (1) relied on opening and closing arguments and on multiple experts who repeatedly testified
For these reasons, we conclude that the evidence of causation was legally insufficient to sustain the verdict in this case.
While we do not agree with all of the language of the court of appeals' decision, that court reached the correct result in reversing the trial court's judgment and rendering a take-nothing judgment. We affirm the court of appeals' judgment.
Justice GUZMAN filed a concurring opinion.
Justice LEHRMANN filed a dissenting opinion, in which Justice BOYD and Justice DEVINE joined.
Justice GUZMAN, concurring.
Over the last several decades, asbestos litigation has become ubiquitous in our federal and state courts. In Texas, the Court has decided a handful of seminal cases articulating a legal framework for toxic torts in the context of asbestos litigation. Here, though the Court correctly deems the evidence of causation legally insufficient, I write separately because my approach is more nuanced in that I believe proving an occasional exposure mesothelioma case with epidemiological studies is not an impossible task. I also write to note my belief that the asbestos litigation framework proposed by the dissent fails to adhere to our well-settled precedents as they relate to the preponderance of evidence standard. In short, I am concerned that both writings do not faithfully interpret the preponderance of the evidence standard that stands as the lodestar of civil liability in Texas. A plaintiff must always prove his toxic tort claim by this standard: Nothing less will suffice, but nothing more is required.
When we allowed scientific rather than direct proof for toxic torts in Havner, we interpreted the preponderance standard to mean that a plaintiff must prove he was exposed to a dose of the toxin that more than doubled his risk of injury. In Flores and here, the preponderance standard demands that if the plaintiff was exposed to toxins from multiple defendants, he must nonetheless prove he was exposed to a dose of the defendant's toxin that more
This matter requires us to apply the preponderance of the evidence standard to mesothelioma cases, and I fear that while the Court may demand too much, the dissent misconstrues our precedents to require too little. The Court holds here that the plaintiff's epidemiological studies were insufficient because they were not "the occasional exposure of a son helping his father on building renovation projects which were not the primary occupation of either father or son, and which included drywall work as well as other construction activities." 439 S.W.3d 332, 364. But we have only required substantially similar — not completely identical — epidemiological studies. Plaintiffs must resolve any differences between the studies and the plaintiff's pattern of exposure through reliable scientific evidence. Here, the plaintiff offered epidemiological studies of occupational exposure that were extrapolated to purportedly measure risk from occasional exposure. But the plaintiff never substantiated those extrapolations, yielding an analytical gap in his proof of causation. Nonetheless, I agree with the Court that the plaintiff failed to prove his approximate dose of exposure to the defendant's asbestos. Thus, I join the Court's opinion except for parts II.A.3 and II.B.
If the Court arrives at the correct result by potentially setting the evidentiary bar too high for future claimants, the dissent reaches an implausible conclusion by neglecting the preponderance standard as established by our precedents. Not requiring quantifiable evidence that a defendant's asbestos product more than doubled the risk of harm, as the dissent proposes, eases the required burden of proof to something subaltern to a preponderance of the evidence. While mesothelioma is a unique disease in that relatively limited exposure can induce illness, this does not change the burden of proof. It simply permits the plaintiff to present lesser dosage evidence (i.e., epidemiological studies for mesothelioma will show more than a doubling of the risk at a lower dose, and plaintiffs need only show exposure comparable to this dose). The pathological peculiarities of mesothelioma should not render a plaintiff's claim almost impossible to prove or almost impossible to lose. Therefore, I respectfully concur in the Court's judgment.
This Court's foundational case for proving causation in toxic torts matters is Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706, 708 (Tex.1997). Havner addressed litigation surrounding a drug for pregnant mothers that was alleged to have caused birth defects.
In the wake of Havner and Flores, then, a plaintiff employing epidemiological studies to prove causation must set forth reliable studies showing exposure to a dosage that more than doubles the risk of injury (general causation) and that the plaintiff's exposure to the defendant's toxin was comparable to or greater than the more than doubling of the risk dose in the studies (specific causation). The standard will be the same for both asbestosis and mesothelioma cases, though the epidemiological studies will likely vary considerably depending upon the ailment involved given that different exposure levels are associated with each illness.
I agree with the Court's ultimate conclusion that Bostic did not produce epidemiological studies that complied with Havner and failed to prove his approximate dose of exposure to Georgia-Pacific asbestos. Because I believe the Court's opinion may be interpreted to foreclose recovery in a mesothelioma case based on occasional exposure to asbestos, I expound on this issue.
I believe Georgia-Pacific advances the more cogent argument. All but one of the studies Bostic presented were not sufficiently analogous to his situation to meet Havner and Flores standards; for instance, these studies largely concerned occupational exposure, which measures a much different phenomenon than the occasional exposure Bostic experienced.
The Consumer Product Safety Commission (CPSC) report, however, is based on a much more similar pattern of exposure to that of Bostic.
Second, as was the case with the eponymous plaintiff in Flores, Bostic failed to prove his dose was comparable to or greater than the dose in the study. He vigorously contests this, citing the accommodating language of Flores regarding scientific proof. See 232 S.W.3d at 772-73. But even if Flores did not require numerically precise dosage, some reasonable approximation is required to satisfy causation. Bostic failed to marshal such an approximation because, as the Court's thorough analysis indicates, testimony only indicated one drywall job where Bostic's father recalled using Georgia-Pacific joint compound, and the father did not recall if Bostic was present during that job.
It bears noting that even though Bostic failed to prove his case, the preponderance standard does not present an insuperable hurdle for all occasional exposure mesothelioma cases. While the bulk of epidemiological studies appear to focus on occupational exposure, properly substantiated extrapolations can bridge the gap between those studies and the plaintiff who contracted mesothelioma from occasional exposure to asbestos. But such a plaintiff must provide a reliable scientific basis for the extrapolation and exposure to a dose of the defendant's toxin comparable to or greater than the extrapolated dose that more than doubled the risk of injury. Here, Bostic failed to do either.
The Court also seems to improperly apply its own articulated standard governing how closely-tailored an epidemiological study must be to a plaintiff's demonstrated exposure. Interestingly, the Court rightly notes that the exposure measured in the studies and stemming from the plaintiff's own experience need only be "substantially similar," not precisely congruent. 439 S.W.3d at 361 (quoting Garza, 347 S.W.3d at 266). Although the Court advances the proper standard, it seems to misapply it by dismissing all of Bostic's epidemiological studies because they were not "the occasional exposure of a son helping his father on building renovation projects which were not the primary occupation of either father or son, and which included drywall work as well as other construction activities." 439 S.W.3d at 361. As a practical matter, requiring this level of exactitude may imply that hardly any mesothelioma
Lastly, I cannot join Part II.A.3 of the Court's opinion because of the potential conflict between its articulation of substantial factor causation and the Texas comparative fault statute. The Court believes that substantial factor causation means that a defendant whose toxin more than doubled the plaintiff's risk of injury may not be liable if exposure to another defendant's toxin was at a factor 10,000 times more. 439 S.W.3d at 361. For simplicity's sake, assume a jury found a lesser such defendant 1% at fault and the greater defendant 99% at fault. Applying the Court's view of substantial factor causation to this scenario is problematic. If the Court's interpretation of substantial factor causation requires the defendant found 99% at fault to assume the remaining 1% liability, this runs afoul of the comparative fault statute — the purpose of which is to make each defendant liable for its percentage fault. And if the Court's interpretation requires the plaintiff to assume the remaining liability, this conflicts with our long-standing tradition that a plaintiff can recover the percentage attributable to the defendant after carrying his burden by a preponderance of the evidence. The Court's injection of an ostensibly common sense approach to causation unnecessarily skews the preponderance standard (just in the opposite direction that the dissent's common sense approach does, as addressed below). This deviation from the preponderance standard we have long adhered to is unwarranted, especially in a case where it does not apply.
If the Court impliedly requires too much of a mesothelioma plaintiff in requiring overly congruent epidemiological studies, the dissent errs in the opposite direction — significantly and errantly easing the burden of proof requirement to something below a preponderance of the evidence. First, it misapprehends Havner, suggesting that the case need not apply because Bostic has offered sufficient direct evidence, and therefore alternative methods of proving causation are unnecessary. I disagree. While Bostic introduced evidence of exposure to Georgia-Pacific products containing asbestos, the evidence
Second, the dissent overstates the scientific hurdles confronting a mesothelioma plaintiff attempting to prove Havner causation. While it contends that "no epidemiological study has established the threshold of exposure over which the risk of developing mesothelioma is doubled" for intermittent exposure, the epidemiological studies in the CPSC report cited previously may serve as a baseline for future mesothelioma plaintiffs with occasional exposure (provided that they substantiate the extrapolation and their approximate dose). 439 S.W.3d 332, 361 (Lehrmann, J., dissenting). In short, then, Havner permits a mesothelioma plaintiff to prove causation and recover in tort, and at least one scientific study may exist as a benchmark. Bostic merely failed to sufficiently relate the epidemiological studies in the CPSC report to his own case or submit proper evidence that his dose was comparable to or greater than that in the study. Thus, his failure to prove specific causation renders his claim unrecoverable.
More generally, I fear that the dissent's failure to pronounce a clear standard risks instilling confusion in our courts, where future asbestos litigation will inevitably occur. A plaintiff may recover by direct evidence of causation, or may attempt to prove alternative causation consonant with Havner's framework. Regardless of the litigation path trod, causation must be proved by a preponderance of the evidence. This standard is satisfied differently depending upon whether direct or Havner evidence is involved, but under either approach, the plaintiff faces the same burden of proof. We must not dilute the preponderance of the evidence standard that has stood as a hallmark of toxic tort litigation in order to make mesothelioma cases easier to prove. We have declined prior invitations from tort claimants to weaken the preponderance of the evidence standard as it relates to scientific proof of causation. See Havner, 953 S.W.2d at 730; Flores, 232 S.W.3d at 774. I join the Court in declining to do so today.
Accordingly, I join all but Parts II.A.3 and II.B of the Court's opinion and concur in the judgment.
Justice LEHRMANN, joined by Justice BOYD and Justice DEVINE, dissenting.
Throughout history, science has informed our society in important ways. Educated people once believed that the sun orbited the earth, until Nicolaus Copernicus used geometry and astronomy to
In this case, the Court ignores this advance in scientific research and holds that a jury's verdict must be set aside because the Bostics, the petitioners here, did not present evidence demonstrating a threshold of exposure to asbestos above which a person's risk of developing mesothelioma is doubled. To arrive at this holding, the Court conflates the alternative measure of proof we announced in Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706, 715 (Tex.1997), and the understanding of substantial-factor causation we approved in Flores, 232 S.W.3d at 770. This combination is both illogical and inequitable. The Bostics showed by direct, scientifically reliable evidence that Timothy Bostic's mesothelioma was caused by exposure to asbestos, and that he was exposed to Georgia-Pacific's asbestos-containing products in substantial quantities. Because the Court holds that this evidence was insufficient to sustain a jury verdict in their favor, I am compelled to respectfully dissent.
In this case we consider the legal sufficiency of the Bostics' evidence on causation. Accordingly, a detailed review of that evidence is warranted. I begin by examining the testimony of the Bostics' expert witnesses on the nature and pathology of mesothelioma. Because Dr. Brody was the first expert to testify, I set forth his testimony more fully and then note the opinions with which other expert witnesses agreed. Next, I proceed to the testimony of Timothy Bostic and his father, Harold, who recounted Timothy's exposure to Georgia-Pacific's products. Finally, I conclude with the expert testimony of Dr. Longo, who determined Timothy's approximate level of asbestos exposure resulting from those products.
Dr. Arnold Brody is an experimental pathologist, which means that he studies diseases and their causes. At trial, Dr. Brody explained that the only known environmental cause of mesothelioma in North America is asbestos. He testified that scientists agree that smoking plays no role. Dr. Richard Lemen, an epidemiologist, concurred with Dr. Brody, adding that the only other known cause is radiation treatment for certain types of cancer. There was no testimony at trial that Timothy was ever treated with radiation.
Dr. Brody went on to explain that, though all people inhale some asbestos, accumulation at such "background" levels "does not produce disease." However, when a person is exposed to asbestos in amounts above background levels, every exposure "is contributing and making it more likely" that the individual will develop mesothelioma in the future. Dr. Brody explained that, though scientists have successfully established a threshold level below which exposure to asbestos does not cause asbestosis, scientists have been unable to establish a similar threshold with respect to mesothelioma. Dr. Lemen
Dr. Brody also emphasized that individuals have different levels of susceptibility to mesothelioma depending on particular genetic factors, as with all carcinogens. Dr. Lemen elaborated on this point, stating that "[t]here are other factors besides the exposure ... individual characteristics, genetic make up of individuals, some individuals are more susceptible to developing disease than others." Dr. Lemen also noted that epidemiologists have not yet identified the factors that make one person more susceptible than another. Both doctors agreed, however, that children were especially vulnerable to the harmful effects of asbestos.
Using images from an electron microscope, Dr. Brody explained how a person develops mesothelioma, which is a type of cancer that afflicts the pleura, the thin membrane covering the lung. While lung cancer and asbestosis develop inside the lung, mesothelial cells are located outside the lung, which means that the asbestos fibers, once inhaled, must travel through lung tissue in order to cause mesothelioma. The fibers migrate through the lung tissue when they are picked up by macrophages and other types of cells. These cells then make their way into the "fluid flow of the lung," which includes blood vessels and lymphatic tissue. This pathway carries the asbestos-laden cells out of the lung and into the pleura, where mesothelial cells are located. Asbestos fibers are deposited in the pleura and, once deposited, can cause genetic errors in mesothelial cells. Dr. Brody explained that "if a person has cancer, what you know is that the original cell that got that first error divided and passed on the error to the offspring." This same cell "a year or two years later" can be "hit again with another fiber," which causes the cell to "accumulate[ ] a second error." Eventually, a cell is exposed to a sufficient number of asbestos fibers and accumulates a sufficient number of genetic errors that cell growth becomes uncontrolled. Considering this process "from a molecular biology point of view," Dr. Samuel Hammar, another pathologist, confirmed that "a very brief exposure could be a critical exposure in the development of a single cancer cell."
Dr. Lemen testified that, when a person is exposed to the asbestos fibers of multiple manufacturers, there is no way for a scientist to determine who manufactured the fibers that actually migrated through the lung and triggered the genetic errors that resulted in mesothelioma. Dr. Hammar agreed. Even if a person is exposed to a large quantity of asbestos from product A, and a small quantity of asbestos from product B, it could be the product B fibers that traveled through the lung and into the pleura, causing the tumor to develop. For that reason, Dr. Lemen opined that it is impossible, in a mesothelioma case, for a scientist to determine which product or manufacturer was responsible on a cellular level for the person's condition.
Trial testimony revealed that Timothy Bostic was exposed to asbestos from more than one manufacturer's products. However, his earliest exposures were to Georgia-Pacific's joint compound. From the time he was five years old, Timothy helped his father, Harold, complete sheetrock work on residential construction projects.
Timothy was also exposed to asbestos from the Knox Glass Company, which employed him for three summers and his father for twenty-two years. When Timothy was younger, he was exposed to fibers that were carried home on his father's clothes. However, Timothy's parents divorced when he was nine years old, reducing the amount of time he spent at home with Harold. When Timothy was older, he joined his father as a temporary employee of the company, where he worked for three summers. Timothy estimated that, during his time at the company, he worked for approximately three months, total, at the "hot end" of the plant, where asbestos was the most prevalent. The rest of the time, Timothy swept floors, cleaned, packed cartons, inspected bottles, cut asbestos cloth, and performed other tasks.
Finally, Timothy was exposed to asbestos from Palestine Contractors, where he worked for two summers. Timothy was employed as a welder's helper, and his job was to assist the principal welder with pipeline repairs, a task that included removing gaskets from the pipes. Some of the pipes Timothy encountered had been insulated with asbestos, exposing him to the fibers.
In order to shed light on the approximate quantity of asbestos Timothy inhaled, the plaintiffs called Dr. William Longo. Dr. Longo is a materials scientist, which means that he studies products like ceramics, metals, polymers, and bio-materials to determine their properties and the contexts in which they can be safely and effectively used. At trial, Dr. Longo testified about Timothy's exposure to Georgia-Pacific's products, which occurred during the period Timothy assisted his father with residential construction projects. Relying on his own calculations and a study performed by the Environmental Protection Agency, Dr. Longo estimated that a twenty-five pound bag of Georgia-Pacific joint compound contains an average of 11.4 quadrillion asbestos fibers. He also detailed the average concentrations of asbestos released when a person performed tasks related to the use of joint compound. In the experiment he conducted, before performing any sample tasks, Dr. Longo measured a background level of .0002 asbestos fibers per cubic centimeter in the room that would serve as the site for his study. After dry joint compound was sanded on the walls, the doctor measured an average concentration of 4.97 fibers of asbestos per cubic centimeter of air. When dust generated by the sanding was being cleaned up, Dr. Longo measured an average concentration of 4.7 fibers of asbestos per cubic centimeter of air. Dr. Longo noted that the precise quantity of asbestos released depends on many factors. But, after reviewing Timothy Bostic's work history, Dr. Longo testified that Timothy's exposure to Georgia-Pacific's product was "significant." When asked to clarify, Dr. Longo confirmed that he meant Timothy had been exposed to Georgia-Pacific's asbestos
In toxic tort cases, we determine whether a plaintiff has proven causation by addressing three areas of inquiry: (1) General Causation: Does the toxin in question have the capacity to cause the type of injury sustained by the plaintiff? And if so, what dose, or amount of exposure, is required? (2) Specific Causation: Was the plaintiff's injury actually caused by the toxin? (3) Substantial-Factor Causation: When multiple manufacturers contribute to a plaintiff's exposure, was the toxin produced by the defendant a substantial factor in causing the plaintiff's injury? See David E. Bernstein, Getting to Causation in Toxic Tort Cases, 74 BROOK. L.REV. 51, 52, 55 (2008). In this part, I explain why the alternative standard of proof we announced in Havner is only useful for resolving the first two causation questions, and is not useful for resolving the third causation question: whether exposure to one of several defendants' products was a substantial cause of the plaintiff's harm. I argue that the Court improperly applies Havner to answer all three causation questions, and effectively renders Havner the exclusive measure of proof in all toxic tort cases. This ignores our affirmation that a plaintiff is always free to prove his case by "direct, scientifically reliable proof of causation." Havner, 953 S.W.2d at 715. By disregarding this avenue of proof, the Court turns substantial-factor causation on its head, requiring a toxic tort plaintiff to prove that exposure to a particular defendant's product was, by itself, the cause of his injury. Because this contravenes well-established principles of tort law, I disagree with the Court's opinion.
Havner was decided in the context of the extensive litigation surrounding the manufacture of Bendectin, a prescription medication that was marketed and sold in the United States and abroad for the treatment of nausea during pregnancy. Id. at 708. In that case, we considered whether the plaintiff had adduced evidence sufficient to support a jury verdict that the plaintiff's ingestion of Bendectin had caused her daughter's birth defects. Id. In our analysis, we distinguished between general and specific causation. Id. at 714. While these labels are flexible, in the context of a toxic tort case they correspond to causation questions (1) and (2). See id.; see also Bernstein, 74 BROOK. L.REV. at 52. We explained, "[g]eneral causation is whether a substance is capable of causing a particular injury or condition in the general population, while specific causation is whether a substance caused a particular individual's injury." Havner, 953 S.W.2d at 714.
As the Court acknowledges today, the principal dispute in Havner concerned general causation, that is, whether scientists had determined that a pregnant woman's ingestion of Bendectin could cause birth defects in her child. Id. at 708. Our opinion noted that more than thirty studies had been conducted in an effort to resolve that question, and that experts had not arrived at a consensus. Id. However, because we recognized the proof problems associated with toxic torts, we held that "[i]n the absence of direct, scientifically reliable proof of causation, claimants may attempt to demonstrate that exposure to the substance at issue increases the risk of their particular injury." Id. at 715. More specifically, we held that when epidemiological studies show that the risk of injury in a population exposed to a certain dose of a particular toxin is more than double the
With respect to question (2), specific causation, we held that "a claimant must do more than simply introduce into evidence epidemiological studies that show a substantially elevated risk." Id. at 720. The claimant must also show "that he or she is similar to those in the studies." Id. This demonstration includes among other considerations "proof that the injured person was exposed to the same substance, that the exposure or dose levels were comparable to or greater than those in the studies, that the exposure occurred before the onset of injury, and that the timing of the onset of injury was consistent with that experienced by those in the study." Id.
Havner did not address causation question (3), which considers whether, when multiple sources contribute to a plaintiff's exposure, the plaintiff's exposure to the defendant's product was a substantial factor in causing his injury. This stands to reason because, in that case, the plaintiff had only been exposed to Bendectin from one source. Id. at 708. For that reason, proof that the plaintiff's daughter's birth defects had been caused by Bendectin was equivalent to proof that her birth defects had been caused by Merrell Dow. The facts did not require us to consider whether the plaintiff's exposure to the defendant's product was substantial; there were no other sources of exposure. The framework we approved in Havner, then, did not contemplate a factual scenario involving multiple manufacturers. As a result, that alternative measure of proof should only be used to resolve causation questions (1) and (2).
Rather than recognize the fundamental differences between Havner and the case at bar, the Court applies a version of our Havner framework to causation questions (1), (2), and (3). There are three problems with the Court's approach. First, though I agree that in the absence of direct, scientifically reliable proof of causation Havner may be applied to resolve causation questions (1) and (2), the Court's opinion today suggests that Havner is the exclusive measure of proof with respect to those questions in every toxic tort case. We spoke plainly in Havner when we stated that proof of causation by epidemiological studies is an alternative measure: a plaintiff may always establish general and specific causation by "direct, scientifically reliable proof" as the Bostics did here. Id. at 715. Under the Court's formulation, however, a mesothelioma plaintiff with intermittent exposure is unable to recover even when he has been exposed to the products of only one manufacturer of asbestos. This is because, with respect to plaintiffs with intermittent exposure, the Court has been made aware of no epidemiological study that has established the threshold of exposure over which the risk of developing mesothelioma is doubled.
Second, the Court mistakes testimony that Timothy was exposed to "significant" levels of asbestos as dose-related evidence that might only be relevant to the epidemiological approach outlined in Havner. Because the Bostics were unable to produce an epidemiological study establishing a threshold of exposure over which risk is doubled for individuals who are exposed only intermittently, the Court dismisses as insufficient the evidence of Timothy's exposure to asbestos. However, evidence of the approximate quantum of fibers Timothy ingested is also relevant to plaintiffs who opt to prove causation by direct, scientifically
The same is true in this case. Though the Bostics did not produce an autopsy demonstrating the concentration of asbestos fibers in Timothy's lungs, they did produce the testimony of reliable expert witnesses who stated that Timothy's ingestion of asbestos exceeded the level over which that toxic substance can cause mesothelioma. When the Court is confronted with this evidence, it only considers its probative value in relation to the method of proof by epidemiological study we explained in Havner. But the Court also should have considered whether the Bostics proved their case in the traditional way, by "direct, scientifically reliable proof of causation." Havner, 953 S.W.2d at 715. As I demonstrate in the forthcoming sections, the Bostics accomplished this task.
Finally, and most problematically, the Court implements Havner to resolve causation question (3). This makes little sense in light of the fact that Havner contemplated the degree of increased risk a plaintiff must demonstrate in order to prove that a certain toxin caused her injury in the absence of direct proof. Id. But causation question (3) has nothing whatsoever to do with whether a toxin caused a plaintiff's injury: that inquiry is resolved by causation questions (1) and (2). Rather, causation question (3) contemplates whether the actions of a specific defendant were significant enough to be denominated a substantial factor in bringing about the plaintiff's disease. See Bernstein, 74 BROOK. L. REV. at 55. The first two questions contemplate risk, and resort to Havner is appropriate. The third question contemplates substantiality, and Havner has no place.
In order to apply that case's framework to a causation question that was not presented by its facts, the Court must alter the standard in a subtle, but significant way. According to the Court, multiple-exposure toxic tort plaintiffs must now produce "scientifically reliable proof that the plaintiff's exposure to the defendant's product more than doubled his risk of contracting the disease." Ante at 350 (emphasis added). This is a marked departure from our precedent. The Court now holds that in multiple-exposure cases a plaintiff must isolate his exposure to each defendant's product and show that exposure to that particular defendant's product, alone, more than doubled his risk. This transforms a substantial-factor inquiry into a singular-factor inquiry. Rather than require a plaintiff to prove that exposure to each defendant's product was, relative to his exposure from other sources, a substantial
This extension of Havner not only imposes an illogical burden on plaintiffs, but also departs from Flores, in which we first approved substantial-factor causation in the multiple-exposure toxic tort context. After today, the law in these types of cases will be that exposure to a single defendant's product is a "substantial factor" in bringing about a plaintiff's injury only when that exposure would have been sufficient, by itself, to more than double the plaintiff's risk of developing a particular disease. But imagine a case in which a plaintiff demonstrates that she has been exposed to a certain toxin, from two different sources, that was certainly the cause of her disease. In other words, the plaintiff proves causation questions (1) and (2), but question (3) remains disputed. Now also imagine that the plaintiff's expert witness testifies that the plaintiff's exposure to Company A's toxin is 75% responsible for her illness, while the plaintiff's exposure to Company B's toxin is 25% responsible for her illness. However, on cross-examination, the expert admits that neither exposure, by itself, would more than double the plaintiff's risk of developing the disease. He also concludes that the plaintiff's illness is not overdetermined. Under the paradigm the Court urges, a jury would not be entitled to conclude that the plaintiff's exposure to the toxin produced by Company A was a substantial factor in bringing about her injury, even though the plaintiff's expert testified that it bore 75% of the responsibility for causing that injury, because the plaintiff's exposure to that toxin was not sufficient, by itself, to cause the plaintiff's illness.
This is in stark contrast to the position taken by the Restatement with respect to substantial-factor causation. In explaining its stance, the Restatement envisions a car, owned by Paul, parked at a scenic overlook. RESTATEMENT (THIRD) OF TORTS: PHYS. & EMOT. HARM § 27 cmt. f, illus. 3 (2010). It then suggests that Able, Baker, and Charlie negligently lean against the car, which results in the vehicle's "plummeting
In an attempt to justify its graft of a modified version of the test we developed in Havner onto the model of substantial-factor causation Flores approved, the Court criticizes what it perceives to be its only alternative. Specifically, the Court enumerates the many shortcomings of the "any exposure" theory of causation, which would permit a plaintiff to prove causation by showing any exposure to a defendant's product. The puzzling aspect of the Court's insistence that we should not adopt this position is that no one urges the Court to do so. At oral argument, the Bostics' attorney stated: "I want to be very clear... because Georgia-Pacific has stated repeatedly that we're after the[ ] any exposure test or [argue that] a single fiber can cause [mesothelioma]. That is not the standard that Borg-Warner adopted nor is it the standard we're proposing." So far as I can tell, this misunderstanding has arisen from a misreading of the expert testimony. At trial, several expert witnesses stated that every exposure to asbestos contributes to the causation of mesothelioma insofar as an increased quantity of asbestos concentrated in the lungs heightens a person's risk of developing the disease. Dr. Brody, for example, affirmed that "each and every exposure that a person has to asbestos contributes to their risk for developing disease." The doctor then clarified, "What that means is every time a person is exposed ... some proportion of those fibers will concentrate in the lung and some of those fibers will reach that site where the disease develops. There's no way to exclude any of them.... So everything the person's exposed to is contributing and making it more likely that the person gets disease." Other experts provided similar explanations. I agree with the Court that evidence that the plaintiff was exposed to any quantity of the defendant's asbestos, without more, is insufficient by itself to prove the causal link between a particular defendant's product and the plaintiff's injury. But this is not a controversial stance — no one argues that it should.
Still, the Court attempts to bolster its position by arguing that "[i]f any exposure at all were sufficient to cause mesothelioma, everyone would suffer from it or at least be at risk of contracting the disease." Ante at 339. This statement misunderstands the expert testimony regarding the nature of mesothelioma. As the expert witnesses testified at trial, mesothelioma is caused by asbestos fibers that migrate through the lung and cause genetic errors in mesothelial cells. When the exposure is only at background levels, "we tend to keep up and it's not a problem. As you start being exposed ... in other settings where it's above background, then it's more difficult." And even when a person's
Though both the Court and the concurrence disregard scientific consensus that very low levels of exposure to asbestos cause mesothelioma, the concurrence does so in a way that forecloses the avenue of "direct, scientifically reliable proof of causation" that our opinion in Havner preserved. 953 S.W.2d at 715. The concurrence states that the Bostics were required to resort to proof by epidemiological studies because they were unable to "tie a specific manufacturer's asbestos fiber to [Timothy's] ailment." Ante at 366. This statement is troubling for two reasons. For one, it reveals that the concurrence shares the Court's misunderstanding of the nature of mesothelioma. The expert testimony at trial flatly forecloses the notion that a single asbestos fiber could generate a sufficient number of genetic errors in a cell to cause a person to develop that disease. More problematically, however, the concurrence's statement suggests that a plaintiff must identify the particular fibers that contributed to the development of his mesothelioma should he opt to prove causation by direct, scientifically reliable evidence. This replaces substantial-factor causation with the equivalent of but-for causation, insofar as it requires a plaintiff to identify the fibers without which he would not have developed mesothelioma. Taken at its word, the concurrence obligates a plaintiff to chart the progress of his disease on a molecular level as it actually occurred. This would amount to conclusive evidence of a defendant's liability. In this manner, the concurrence advocates that the standard of proof be altered.
The concurrence also insists that the Bostics' evidence with respect to Timothy's exposure lacked specificity. As I recount in further detail in the next part, Dr. Longo concluded that Timothy was exposed to chrysotile asbestos in "significant" quantities, that is, at levels ten to twenty times the average background level. In light of the fact that exposure to very low levels of asbestos can cause mesothelioma, that Timothy did develop the disease, and that asbestos is the only known environmental cause of mesothelioma, I fail to see how the evidence the Bostics adduced was inadequate to prove causation by a preponderance of the evidence.
Having outlined the available avenues by which a plaintiff may prove causation in a toxic tort case, I turn to the facts at hand. I consider whether the Bostics have proven (1) that asbestos has the capacity to cause mesothelioma, and in what quantity, (2) that asbestos caused Timothy's mesothelioma, and (3) that Timothy's exposure to asbestos from Georgia-Pacific's product was a substantial factor in causing his mesothelioma. As I determine whether there is more than a scintilla of evidence to support the jury's findings, I consider "whether the evidence at trial would enable reasonable and fair-minded jurors to reach the verdict." Whirlpool Corp. v. Camacho, 298 S.W.3d 631, 638 (Tex.2009). This examination, which hinges on the reliability of expert testimony, encompasses the entire record. Id.
In toxic tort cases, we have indicated that general causation may be proved in two ways. Under Havner, a plaintiff may produce epidemiological studies that establish a threshold of exposure to a toxin over which a person's risk of sustaining injury is more than doubled. 953 S.W.2d at 715-18. From this evidence, jurors may infer that the toxin probably causes the injury in persons who are exposed to quantities at or above the threshold. Id. at 715. However, Havner has never been the exclusive measure of proof. Id. The plaintiff is always free to establish causation in the traditional way, by "direct, scientifically reliable proof." Id.
In the case at bar, multiple expert witnesses testified that chrysotile asbestos, which is the kind of asbestos Georgia-Pacific included in its products, causes mesothelioma. Dr. Lemen detailed the history of scientific research with respect to this important question, and concluded that the research supported an opinion that mesothelioma is caused by this type of asbestos, even when a person is exposed to only very low doses of the toxin. Dr. Hammar agreed and noted that the National Institute for Occupational Safety and Health, the Environmental Protection Agency, the American Industrial Hygiene Association, the International Agency for Research on Cancer, and the World Health Organization all affirm that chrysotile asbestos causes mesothelioma. As I recounted in Part I, Dr. Brody detailed the biological process by which asbestos fibers migrate through the lung, into the pleura, and cause genetic errors in mesothelial cells. He affirmed that chrysotile fibers were capable of causing these errors, even in very small quantities. This evidence is compelling. Taken together, it would have enabled reasonable jurors to conclude that asbestos from Georgia-Pacific's products can cause mesothelioma.
As with general causation, there are two methods by which a plaintiff may prove specific causation. Pursuant to Havner, a plaintiff may produce evidence that he was exposed to a dose of the toxin that brings him in line with epidemiological studies showing that his risk of injury was more than doubled. 953 S.W.2d at 720. As noted above, "[t]his would include proof that the injured person was exposed to the same substance, that the exposure or dose levels were comparable to or greater than those in the studies, that the exposure occurred before the onset of injury, and that the timing of the onset of injury was
In the case at bar, Dr. Hammar testified that chrysotile asbestos caused Timothy's mesothelioma. Dr. Hammar based his opinion on his own experience. TEX. R. EVID. 702. He explained that he had "personally diagnosed cases of mesothelioma in individuals with low exposures to chrysotile asbestos." In considering Timothy's level of exposure, Dr. Hammar reviewed Timothy's pathology materials, medical records, and work history. Dr. Hammar then testified that he had concluded that Timothy was "exposed at high enough levels ... in doing this drywall work, in mixing[,] sanding[,] and cleaning up of drywall materials" that asbestos exposure was, to a reasonable medical certainty, the cause of his mesothelioma. Dr. Longo affirmed this conclusion by testifying that Timothy had been exposed to chrysotile asbestos in "significant" quantities, that is, at levels ten to twenty times the average background level. This exposure is greater than the very low levels of exposure sufficient to cause mesothelioma. Dr. Longo based his conclusion on Timothy's and Harold's testimony, as well as experiments he had conducted to determine how much asbestos is released during the installation of drywall.
The testimony of Drs. Hammar and Longo was in keeping with the testimony of Dr. Lemen, who explained that individuals who work with joint compound are susceptible to mesothelioma. Dr. Lemen clarified that his conclusion was not limited to those with occupational exposure. He explained that his opinion was based on a study conducted by Dr. Selikoff, who found mesothelioma in drywallers who had "three months or less of exposure to asbestos." Dr. Lemen also testified that if a patient has a history of asbestos exposure above background levels, and no history of therapeutic radiation, then the "accepted" cause of his mesothelioma is asbestos. See also 3 DAVID L. FAIGMAN ET AL., MODERN SCIENTIFIC EVIDENCE: THE LAW AND SCIENCE OF EXPERT TESTIMONY § 26:24 (2013-14) ("It is generally accepted that any pulmonary asbestos concentration that is substantially above background is an indication of causation."). Taken together, the testimony of these expert witnesses would have enabled reasonable jurors to conclude that exposure to chrysotile asbestos caused Timothy Bostic's mesothelioma.
This final inquiry required the Bostics to show that Timothy's exposure to Georgia-Pacific's chrysotile asbestos was a substantial factor in causing his mesothelioma. As I explained in Part II, Havner may not be applied to resolve this question.
In Flores, we explained that "[t]he word `substantial' is used to denote the fact that the defendant's conduct has such an effect in producing the harm as to lead reasonable men to regard it as a cause, using that word in the popular sense, in which there always lurks the idea of responsibility, rather than in the so-called `philosophic sense,' which includes every one of the great number of events without which any happening would not have occurred." 232 S.W.3d at 770 (citation and internal quotation marks omitted). We clarified further that a plaintiff may satisfy the dictates of substantial-factor causation "`by demonstrating that the plaintiff's exposure to defendant's asbestos-containing product in reasonable medical probability was a substantial factor in contributing to the aggregate
For this reason, plaintiffs are not required to calculate dose in absolute terms. When it comes to the question of whether a plaintiff's exposure to a defendant's product in a multiple-exposure case was substantial, the relevant quantification is relative quantification: a plaintiff can prove causation by showing that her exposure to a certain defendant's product was sufficiently significant, in relative terms, that it should be considered a substantial factor in causing his injury. This is not the first time we have indicated that this consideration might be important. In Flores, we held that the plaintiff had failed to quantify his exposure to the defendant's product with sufficient particularity in part because this lack of evidence made us unable to determine whether that exposure "sufficiently contributed to the aggregate dose of asbestos Flores inhaled, such that it could be considered a substantial factor in causing his asbestosis." Id. at 772.
As the Court notes, consideration of a plaintiff's aggregate dose is in keeping with all three volumes of the Restatement of Torts. Both the first and second volumes recognize that an important consideration in determining whether a factor is so causative as to be considered substantial is "the number of other factors which contribute in producing the harm and the extent of the effect which they have in producing it." RESTATEMENT (SECOND) OF TORTS § 433(a) (1965); RESTATEMENT (FIRST) OF TORTS § 433(a) (1934). The third volume advises that "[w]hen an actor's negligent conduct constitutes only a trivial contribution to a causal set that is a factual cause of harm ... the harm is not within the scope of the actor's liability." RESTATEMENT (THIRD) OF TORTS: PHYS. & EMOT. HARM § 36 (2010).
In multiple-exposure cases, once a plaintiff proves causation questions (1) and (2), the only question that remains is whether the plaintiff's exposure to a defendant's product was substantial enough to be regarded as a cause "in the popular sense, in which there always lurks the idea of responsibility." Flores, 232 S.W.3d at 770. A jury is well-suited to make this determination. As the Court admits, "some discretion must be ceded to the trier of fact in determining whether the plaintiff met that standard. One respected treatise has opined that it is `neither possible nor desirable to reduce [substantial factor] to any lower terms.'" Ante at 347 (quoting W. PAGE KEETON, ET AL., PROSSER AND KEETON ON THE LAW OF TORTS § 41 (5th ed.1984)). As part of this determination, jurors may consider whether the plaintiff proved that a certain defendant's product was independently sufficient to cause his illness, either by resort to Havner or by "direct, scientifically reliable proof." Havner, 953 S.W.2d at 715. Jurors should consider this as one factor among many, as it may be more fitting to denominate an exposure substantial when it is independently sufficient to cause the plaintiff's disease. However, in contrast to the Court, I maintain that this consideration is relevant, rather than prerequisite.
The Bostics also produced evidence as to the approximate quantum of time Timothy was exposed to each source of asbestos: Timothy worked with his father throughout his childhood on residential construction projects. When he was only a boy, Timothy mixed dry joint compound, sanded it on the walls "[a]s far up as he could reach," and swept the dust generated by sanding. Expert witnesses consistently maintained that exposure to asbestos during childhood can be particularly detrimental. Timothy also worked at the Knox Glass plant for three summers, where his ingestion of asbestos may have been more severe in one part of the plant than in another. In addition, Timothy was exposed to fibers that his father carried home on his clothing from the plant. Because Timothy did not live with Harold full-time, this exposure was sporadic. Finally, Timothy worked at Palestine Contractors for two summers, where he encountered asbestos on an intermittent basis.
The Bostics also produced evidence that Timothy's exposure to Georgia-Pacific's products was independently sufficient to cause his mesothelioma. Dr. Hammar testified that Timothy was exposed to sufficiently high levels of asbestos that his exposure was, to a reasonable medical certainty, the cause of his mesothelioma. Dr. Longo agreed, testifying that Timothy had been exposed to Georgia-Pacific's asbestos at levels ten to twenty times the average background levels. This exposure is greater than the very low levels of exposure sufficient to cause mesothelioma.
And though the evidence the Bostics put forward with respect to Timothy's exposure is hardly exact, we do not require a plaintiff to reduce the quantity of exposure "to mathematical precision." Flores, 232 S.W.3d at 773. I would hold that the evidence the Bostics presented in this case was sufficiently specific to enable a jury to determine that Timothy's exposure to Georgia-Pacific's asbestos was a substantial factor in causing his illness.
By requiring every plaintiff to produce epidemiological studies demonstrating that exposure to every defendant's product independently more than doubled his risk of developing a disease, the Court renders Havner a hindrance rather than a help. In this case, the Bostics produced scientifically reliable evidence that asbestos causes mesothelioma, that it caused Timothy's development of that disease, and that Timothy's exposure to Georgia-Pacific's asbestos-containing products was substantial in relation to his exposure to other asbestos sources. Because they adduced this evidence in the traditional way, they had no need to resort to the alternative measure we approved in Havner. By elevating this standard to the exclusive measure of proof, the Court effectively forecloses recovery for mesothelioma plaintiffs with intermittent exposure to asbestos until researchers develop epidemiological studies demonstrating a doubling of the risk in that population. The Court also forecloses recovery for mesothelioma
Brody agreed that "each and every exposure that a person has to asbestos contributes to their risk for developing disease," and that "you have to consider that each and every one of those exposures played a role in the development of the disease." He agreed that "each and every one of the asbestos fibers that a person inhales into their lungs has to be considered a cause" of his mesothelioma. Lemen agreed that "each and every exposure that somebody has ... increase[s] their risk of developing mesothelioma." He agreed that "any exposure" and "each exposure" to asbestos "caused [Bostic's] mesothelioma."
Dyson further explained that "dose is a two-component factor. It's the intensity of exposure, which are the measurements that Dr. Longo provides us here but also the duration of exposure." See also Bernard D. Goldstein & Mary Sue Henifin, Reference Guide on Toxicology, in REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 633, 638 n. 12 (Fed.Jud.Ctr.3d ed.2011) ("Dose is a function of both concentration and duration.").
He agreed "if you were to look at it from a probability point of view" that "higher levels may contribute more to the development of the disease than exposures at much lower levels.... I would give you that at least from a probability point of view, the more exposure to asbestos that you have from any given exposure, the more likely that that exposure is to contribute to the development of that mesothelioma." Brody similarly agreed that "[a]ll these [asbestos] diseases are so-called dose response diseases. That means the more you're exposed to, the more likely you are to get [the] disease." He later testified that because Bostic worked only nine months at the Knox Glass plant his risk of disease would be less than the risk of employees who had worked at the plant for 20 years. Lemen agreed "that asbestos-related diseases were dose-response diseases." He stated: "I think the jury should understand that the higher the exposure, the more the risk increases."
Id. at 718.
Id. at 19.
Id.