                     IN THE SUPREME COURT OF TEXAS
                                                 444444444444
                                                   NO . 10-0775
                                                 444444444444


 SUSAN ELAINE BOSTIC , INDIVIDUALLY AND AS PERSONAL REPRESENTATIVE OF
   THE H EIRS AND ESTATE OF TIMOTHY SHAWN BOSTIC , D ECEASED ; H ELEN
           DONNAHOE; AND KYLE ANTHONY BOSTIC , PETITIONERS,
                                                        v.


                           GEORGIA-PACIFIC CORPORATION, RESPONDENT

                4444444444444444444444444444444444444444444444444444
                                   ON PETITION FOR REVIEW FROM THE
                            COURT OF APPEALS FOR THE FIFTH DISTRICT OF TEXAS
                4444444444444444444444444444444444444444444444444444


                                             Argued September 9, 2013


       JUSTICE WILLETT delivered the opinion of the Court, in which CHIEF JUSTICE HECHT ,
JUSTICE GREEN , JUSTICE JOHNSON , and JUSTICE BROWN joined, and in all but Parts II.A.3 and II.B
of which JUSTICE GUZMAN joined.

          JUSTICE GUZMAN filed a concurring opinion.

          JUSTICE LEHRMANN filed a dissenting opinion, in which JUSTICE BOYD and JUSTICE DEVINE
joined.


          In Borg-Warner Corp. v. Flores,1 we addressed standards imposed by Texas law for

establishing causation in asbestos-disease cases. Flores concerned a plaintiff suffering from

asbestosis. In today’s case, the plaintiffs sued for damages resulting from the suffering and death



          1
              232 S.W .3d 765 (Tex. 2007).
of a family member, Timothy Bostic (Bostic), who succumbed to mesothelioma. We hold that the

standard of substantial factor causation recognized in Flores applies to mesothelioma cases, and

write on the meaning of substantial factor causation in this context. We further hold that the

plaintiffs were not required to prove that but for Bostic’s exposure to Defendant Georgia-Pacific

Corporation’s asbestos-containing joint compound, Bostic would not have contracted mesothelioma.

In this regard, we disagree with language in the court of appeals’ decision. However, we agree with

that court that the plaintiffs failed to offer legally sufficient evidence of causation, and accordingly

affirm the court of appeals’ judgment.

                                           I. Background

       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

child and teenager Bostic had been exposed to asbestos while using Georgia-Pacific drywall joint

compound.

       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.

                                                   2
        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.2

                                                    II. Discussion

                               A. Proof of Causation in Mesothelioma Cases

        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.”3 “We must view the evidence in the light most favorable to the verdict and ‘must credit

favorable evidence if reasonable jurors could, and disregard contrary evidence unless reasonable

jurors could not.’”4

                                                       1. Flores

        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.5 We




        2
            320 S.W .3d 588, 590, 602.

        3
          Del Lago Partners, Inc. v. Smith, 307 S.W .3d 762, 770 (Tex. 2010) (quoting City of Keller v. Wilson, 168
S.W .3d 802, 827 (Tex. 2005)).

        4
            Id. (footnote omitted) (quoting City of Keller, 168 S.W .3d at 827).

        5
            Flores, 232 S.W .3d at 768.

                                                            3
concluded that the causation evidence was legally insufficient.6 We held, consistent with section 431

of the Restatement Second of Torts, that to establish causation in fact the plaintiff must prove that

the defendant’s product was a substantial factor in causing the disease, and that mere proof that the

plaintiff was exposed to “some” respirable fibers traceable to the defendant was insufficient.7 “The

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.”8 We held the evidence legally insufficient because the record revealed “nothing

about how much asbestos Flores might have inhaled.”9 We held that “while some respirable fibers

may be released upon grinding some brake pads, the sparse record here contains no evidence of the

approximate quantum of Borg-Warner fibers to which Flores was exposed, and whether this

sufficiently contributed to the aggregate dose of asbestos Flores inhaled, such that it could be

considered a substantial factor in causing his asbestosis.”10

        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



       6
           Id. at 774.

       7
           Id. at 766, 770.

       8
           Id. at 770 (quoting R ESTATEM EN T (S ECO N D ) O F T O RTS § 431 cmt. a (1965)).

       9
           Id. at 771.

       10
            Id. at 772.

                                                             4
causation under Texas law.”11 While the plaintiff was not required to establish causation with

“mathematical precision,” we required “[d]efendant-specific evidence relating to the approximate

dose to which the plaintiff was exposed, coupled with evidence that the dose was a substantial factor

in causing the asbestos-related disease.”12 In rejecting a standard that “some” exposure would

suffice, the Court recognized: “As one commentator notes, ‘[i]t is not adequate to simply establish

that ‘some’ exposure occurred. Because most chemically induced adverse health effects clearly

demonstrate ‘thresholds,’ there must be reasonable evidence that the exposure was of sufficient

magnitude to exceed the threshold before a likelihood of ‘causation’ can be inferred.”13

         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.14 Plaintiffs presented

evidence of this same distinction.15




         11
              Id.

         12
              Id. at 773.

         13
              Id.

         14
              Id. at 771.

         15
           For example, one of Plaintiffs’ experts, Dr. Brody, testified that “there’s no safe level for mesothelioma. In
other words, no one’s ever been able to show a level that will prevent everyone from getting mesothelioma. Now, you
can do that for asbestosis, and you can get pretty close probably for most lung cancer cases, but for mesothelioma, no
one’s ever shown a safe level.”

                                                           5
       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.”16 As to asbestos-related cancer, in Flores we discussed the California Supreme Court’s

decision in Rutherford v. Owens-Illinois, Inc.17 That case described how expert testimony was

presented from both sides establishing “that the plaintiffs’ asbestos-related disease was ‘dose-

related’—i.e., that the risk of developing asbestos-related cancer increased as the total occupational

dose of inhaled asbestos fibers increased.”18 And in today’s case, Plaintiffs’ experts consistently

testified that all asbestos-related diseases are dose-related.19 Plaintiffs’ experts Brody, Lemen, and

Hammar relied in part on the “Helsinki Conference” report,20 a report stating that “[m]esothelioma



       16
            232 S.W .3d at 771 (internal quotation marks omitted).

       17
            941 P.2d 1203 (Cal. 1997), discussed in Flores, 232 S.W .3d at 772–73.

       18
            Rutherford, 941 P.2d at 1209.

       19
            See infra note 96.

       20
            See infra notes 99–100 an accompanying text.

                                                           6
can occur in cases with low asbestos exposure. However, very low background environmental

exposures carry only an extremely low risk.”

        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.”21 In today’s case, one of Plaintiffs’ experts,

Dr. Brody, confirmed that “[w]e all have some asbestos” in our lungs. He then explained that

background levels are sufficiently low that they do not cause disease,22 and that “multiples of fibers

many times over” were required to cause mesothelioma.23 Acceptance of an any exposure theory


        21
             232 S.W .3d at 767.

        22
             Brody testified:

        W ell, so when we’re talking about background, we’re talking about what we all have. And it’s just
        a fact of modern society as materials that contain asbestos break down or if you live in an area where
        there’s naturally occurring asbestos, that asbestos will accumulate in the lung to some level, which
        does not produce disease. That’s not a level that anyone can measure disease.

        23
             Brody testified:

        Q: Can one fiber of chrysotile [asbestos] or one fiber of amosite [asbestos] cause mesothelioma?

        A: No.

        Q: Okay, Do you have to have more than one?

        A: Yeah, of course. I mean a single fiber can cause a genetic error, but I told you that that’s not
        enough to cause disease.

        Q: Okay. You have to have more than one, some number greater than one to actually cause these
        mutations that actually . . . cause the uncontrolled cell growth that you talked about?

        A: Oh, yes, you have to have many—

        Q: Okay.



                                                          7
would contradict the testimony of plaintiffs’ own expert, ignore the importance of dose in

determining a causative link, and impose liability even where, for all the jury can tell, the plaintiff

might have become ill from his exposure to background levels of asbestos or for some other reason.24

         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 result in disease.’”25 And we have never embraced the concept of industry-wide liability

on grounds that proof of causation might be difficult. Instead, we have rejected such thinking and

held firm to the principle that liability in tort must be based on proof of causation by a preponderance

of the evidence. In a mesothelioma case, we rejected theories of collective liability—alternative

liability, concert of action, enterprise liability, and market share liability—and held instead: “A

fundamental principle of traditional products liability law is that the plaintiff must prove that the

defendants supplied the product that caused the injury.”26 Merrell Dow Pharmaceuticals, Inc. v.

Havner, another toxic tort case, further explains:



         A: — multiples of fibers many times over to get those kinds of changes.

         24
           See Baker v. Chevron USA, Inc., 680 F. Supp. 2d 865, 878 n.9 (S.D. Ohio 2010) (“[S]ince benzene is
ubiquitous, causation under the one-hit theory could not be established because it would be just as likely that ambient
benzene was the cause of Plaintiffs’ illnesses.”), aff’d, 533 F. App’x 509 (6th Cir. 2013).

         25
              Flores, 232 S.W .3d at 770–71.

         26
              Gaulding v. Celotex Corp., 772 S.W .2d 66, 68 (Tex. 1989).

                                                           8
       Others have argued that liability should not be allocated only on the basis of reliable
       proof of fault because legal rules should have the goals of “risk spreading, deterrence,
       allocating costs to the cheapest cost-avoider, and encouraging socially favored
       activities,” and because “consumers of American justice want people compensated.”
       It has been contended that “[f]or some cases that very well may mean creating a
       compensatory mechanism even in the absence of clear scientific proof of cause and
       effect” . . . . We expressly reject these views. Our legal system requires that
       claimants prove their cases by a preponderance of the evidence. . . . As Judge Posner
       has said, “[l]aw lags science; it does not lead it.”27

       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.28

       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


       27
            953 S.W .2d 706, 728 (Tex. 1997) (citations omitted).

       28
            Lemen testified:

       Q: And isn’t it true that this principle that we don’t know of any safe level of exposure is true for any
       carcinogen?

       A: At the present time, we aren’t able to identify the carcinogenic compounds, what is safe and what
       is not safe. And that is true pretty much across the board for things that cause cancer.

       Q: So for anything on this list of carcinogens that we’ll talk about later, your answer is true that if it
       is on the list of carcinogens, it’s not just asbestos, it’s the entire list that you would say we know of no
       safe level of exposure to it, correct?

       A: Basically that’s correct.

       Q: Even if it’s used even today day-in and day-out in industrial and consumer products?

       A: That’s correct. . . .

                                                            9
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:

       Rule 702 and Daubert recognize above all else that to be useful to a jury an expert’s
       opinion must be based on sufficient facts and data. The every exposure theory is
       based on the opposite: a lack of facts and data. . . . It seeks to avoid not only the rules
       of evidence but more importantly the burden of proof. . . . Dr. Hammar wants to be
       allowed to tell a jury that all of the plaintiff’s possible exposures to asbestos during
       his entire life were contributing causes of the plaintiff’s cancer, and, therefore,
       sufficient to support a finding of legal liability as to the manufacturer of each
       asbestos containing product, without regard to dosage or how long ago the exposure
       occurred. Just because we cannot rule anything out does not mean we can rule
       everything in.29

       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.”30 In Flores we held the

causation evidence legally insufficient because the record revealed “nothing about how much

asbestos Flores might have inhaled” but also because Flores did not “introduce evidence regarding

what percentage of that indeterminate amount may have originated in Borg-Warner products.”31 And



       29
            Smith v. Ford Motor Co., 2013 W L 214378, at *2–3 (D. Utah Jan. 18, 2013) (emphasis in original).

       30
            R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY   FO R   P H YSIC AL AN D E M O TIO N AL H ARM § 36 (2010).

       31
            232 S.W .3d at 771–72.

                                                                    10
in Havner we held 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.”32 That

statement requires some explication in cases involving multiple exposures to the same toxin, as we

discuss below, but here it properly stands for the proposition that, even in mesothelioma cases,

liability cannot be imposed on every conceivable defendant whose product exposed the plaintiff to

some unquantified amount of asbestos, without proof of something more. “The recent, increasingly

strict exposure cases . . . reflect a welcome realization by state courts that holding defendants liable

for causing asbestos-related disease when their products were responsible for only de minimis

exposure to asbestos, and other parties were responsible for far greater exposure, is not just . . . .”33

        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.




        32
             Havner, 953 S.W .2d at 720.

       33
             David E. Bernstein, Getting to Causation in Toxic Tort Cases, 74 B RO O K . L. R EV . 51, 59 (2008).

                                                            11
         For these reasons, we extend the reasoning and holdings of Flores to mesothelioma cases,

including our rejection of the “any exposure” theory of liability, with the clarifications discussed

below.

                                                2. But For Causation

         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.”34 It stated, “‘In asbestos

cases, then, we must determine whether the asbestos in the defendant’s product was a substantial

factor in bringing about the plaintiff’s injuries,’ and without which the injuries would not have

occurred.”35 In doing so, the court of appeals quoted from Flores but appended but for language to

the end of its sentence. The court expressly disagreed with Plaintiffs’ assertion that Flores did not



         34
          320 S.W .3d at 596 (quoting Metro Allied Ins. Agency, Inc. v. Lin, 304 S.W .3d 830, 835 (Tex. 2009) (internal
quotation marks omitted)).

         35
              Id. (quoting Flores, 232 S.W .3d at 770).

                                                          12
require proof of but for causation.36 It then concluded that the testimony of Dr. Hammar was

wanting because “he could not opine that Timothy would not have developed mesothelioma absent

exposure to Georgia-Pacific asbestos-containing joint compound.”37

         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,38 applicable to this products liability

case.39 We have often recognized but for causation, alone or in combination with substantial factor

causation, as the standard for establishing causation in fact.40 Indeed, “to say of a cause of an injury




         36
           Id. (“[Plaintiffs] assert that Flores does not require ‘but-for’ causation in proving specific causation and that
Flores requires only that [Plaintiffs] prove Timothy’s exposure to Georgia-Pacific asbestos-containing joint compound
was a ‘substantial factor’ in contributing to his risk of mesothelioma. W e disagree.”).

         37
              Id.

         38
            See Transcon. Ins. Co. v. Crump, 330 S.W .3d 211, 223 (Tex. 2010) (recognizing that “the producing cause
inquiry is conceptually identical to that of cause in fact”).

         39
             Producing cause is the level of causation applicable to products liability cases. See, e.g., Rourke v. Garza,
530 S.W .2d 794, 801 (Tex. 1975). Plaintiffs sued under theories of negligence and products liability, the latter being
based on a marketing defect theory. However, Plaintiffs concede that but for causation was required under their
negligence theory of liability because the jury was instructed that proximate cause, a necessary element of negligence
liability, required proof of but for causation. The jury was instructed that proximate cause “means that cause which, in
a natural and continuous sequence, produces an event, and without which cause such event would not have occurred.”
See City of Fort Worth v. Zimlich, 29 S.W .3d 62, 71 (Tex. 2000) (“Since neither party objected to this instruction, we
are bound to review the evidence in light of this definition.”).

         40
            E.g., Crump, 330 S.W .3d at 222–23 (“Cause in fact is established when the act or omission was a substantial
factor in bringing about the injuries, and without it, the harm would not have occurred.”) (quoting IHS Cedars Treatment
Ctr. v. Mason, 143 S.W .3d 794, 799 (Tex. 2004)); Marathon Corp. v. Pitzner, 106 S.W .3d 724, 727 (Tex. 2003) (“The
test for cause in fact, or ‘but for causation,’ is whether the act or omission was a substantial factor in causing the injury
‘without which the harm would not have occurred.’”); Union Pump Co. v. Allbritton, 898 S.W .2d 773, 775 (Tex. 1995)
(“Cause in fact means that the defendant’s act or omission was a substantial factor in bringing about the injury which
would not otherwise have occurred.”); Gen. Motors Corp. v. Saenz, 873 S.W .2d 353, 357 (Tex. 1993) (holding that to
establish causation in fact element common to both negligence and products liability causes of action, “plaintiffs must
show that but for GM’s omission the accident would not have occurred”).

                                                             13
that it is one ‘but for which the injury would not have happened’ is to repeat something already

included in the usual and ordinary meaning of the word ‘cause.’”41

         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.”42 Comment a to this section makes clear that, as a general proposition,

substantial factor causation incorporates the concept of but for causation: “In order to be a legal

cause of another’s harm, it is not enough that the harm would not have occurred had the actor not

been negligent. Except as stated in § 432(2), this is necessary, but it is not of itself sufficient.”43

Hence, the comment indicates that but for causation is generally a component of substantial factor

causation.

         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



         41
          Tex. Indem. Ins. Co. v. Staggs, 134 S.W .2d 1026, 1030 (Tex. 1940) (quoting Tex. & Pac. Ry. v. Short, 62
S.W .2d 995, 999 (Tex. App.— Eastland 1933, writ ref’d)).

         42
           R ESTATEM EN T (S ECO N D ) OF T O RTS § 431 (1965). This provision addresses negligence liability, and as noted
today’s case is, for our purposes, a products liability case. See supra note 39. However, the element of causation in fact
is the same under the two theories of liability. To recover under a negligence theory, the plaintiff must establish
proximate causation, while recovery under a products liability theory requires proof of producing causation. Proximate
cause and producing cause share the common element of causation in fact, with proximate cause including the additional
element of foreseeability. See Crump, 330 S.W .3d at 222–23; Flores, 232 S.W .3d at 770; Union Pump, 898 S.W .2d
at 775; Saenz, 873 S.W .2d at 356; see also R ESTATEM EN T (T HIRD ) O F T O RTS : P RO D UCTS L IA BILITY § 15 (1998)
(“W hether a product defect caused harm to persons or property is determined by the prevailing rules and principles
governing causation in tort.”); R ESTATEM EN T (S ECO N D ) O F T O RTS § 431 cmt. e (1965) (“Although the rules stated in this
Section are stated in terms of the actor’s negligent conduct, they are equally applicable where the conduct is intended
to cause harm, or where it is such as to result in strict liability.”).

         43
              R ESTATEM EN T (S ECON D ) O F T O RTS § 431 cmt. a (1965).

                                                              14
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.”44 The

Restatement Third not only embraces but for causation, but includes some criticism of the substantial

factor test.45

        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.”46 Along similar

lines, the Virginia Supreme Court recently observed that “if the traditional but-for definition of

proximate cause was invoked, the injured party would virtually never be able to recover for damages




        44
             R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY   FO R   P H YSIC AL AN D E M O TIO N AL H ARM § 26 (2010).

        45
             See id.§ 26 cmt. j.

        46
             232 S.W .3d at 772.

                                                                     15
arising from mesothelioma in the context of multiple exposures . . . .”47 Further, in Flores we quoted

from Rutherford:

        Plaintiffs cannot be expected to prove the scientifically unknown details of
        carcinogenesis, or trace the unknowable path of a given asbestos fiber. . . . Instead,
        we can bridge this gap in the humanly knowable by holding that plaintiffs may prove
        causation in asbestos-related cancer cases 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 dose of asbestos
        the plaintiff or decedent inhaled or ingested, and hence to the risk of developing
        asbestos-related cancer, without the need to demonstrate that fibers from the
        defendant’s particular product were the ones, or among the ones, that actually
        produced the malignant growth.48

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




        47
             Boomer v. Ford Motor Co.,736 S.E.2d 724, 729 (Va. 2013).

       48
             941 P.2d at 1219 (footnote omitted) (emphasis in original), quoted in Flores, 232 S.W .3d at 772–73.

                                                          16
conduct of one or more others would have been sufficient to produce the same result.”49 Likewise,

Rutherford reasoned that “[t]he substantial factor standard generally produces the same results as

does the ‘but for’ rule of causation,” but the substantial factor test “has been embraced as a clearer

rule of causation—one which subsumes the ‘but for’ test while reaching beyond it to satisfactorily

address other situations, such as those involving independent or concurrent causes in fact.”50 This

problem arises in toxic tort cases such as Flores, Boomer, Rutherford, and today’s case, where the

plaintiff has suffered exposure from multiple sources.

       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.”51 Section 432(2) recognizes a scenario

where the actor’s conduct is not, strictly speaking, a but for cause, because another force would have

caused the harm anyway.




       49
            W . P AGE K EETO N   ET AL .,   P RO SSER AN D K EETO N   O N TH E   L AW   OF   T O RTS § 41 (5th ed. 1984).

       50
            941 P.2d at 1214.

       51
            R ESTATEM EN T (S ECON D ) O F T O RTS § 432(2) (1965).

                                                                 17
          Likewise, while the Restatement Third generally embraces but for causation in section 26,52

as noted above, it elsewhere still recognizes substantial factor causation in some products liability

cases53 and in a sense recognizes the converse of substantial factor causation, by providing in

section 36 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, the harm is not within the scope of the actor’s

liability.”54 So while not requiring substantial factor causation in section 26, which sets out the

general causation standard, it recognizes in the negative that a trivial contribution to causation will

not suffice. This rule hardly represents a sea change, as section 433(a) of the Restatement and

Restatement Second have long stated that, in making a substantial factor determination, an important

consideration is “the number of other factors which contribute in producing the harm and the extent

of the effect which they have in producing it.”55 Further, while section 26 moves away from the

substantial factor standard, comment j to that section explains its particular usefulness in certain

multiple-causation cases.56




          52
               R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY   FO R   P H YSIC AL AN D E M O TIO N AL H ARM § 26 (2010).

         53
            See R ESTATEM ENT (T H IR D ) O F T O RTS : P RO D U CTS L IABILITY § 16(a) (1998) (“W hen a product is defective
at the time of commercial sale or other distribution and the defect is a substantial factor in increasing the plaintiff’s harm
beyond that which would have resulted from other causes, the product seller is subject to liability for the increased
harm.”).

          54
               R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY   FO R   P H YSIC AL AN D E M O TIO N AL H ARM § 36 (2010).

          55
               R ESTATEM EN T (S ECON D ) O F T O RTS § 433(a) (1965); R ESTATEM EN T O F T ORTS § 433(a) (1934).

          56
            R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY FOR P H Y SIC AL AND E M OTIO N AL H ARM § 26 cmt. j (2010) (stating
that the “primary function” of the substantial-factor test “was to permit the factfinder to decide that factual cause existed
when there were multiple sufficient causes— each of two separate causal chains sufficient to bring about the plaintiff’s
harm, thereby rendering neither a but-for cause”).

                                                                       18
        Moreover, the Restatement Third, like the earlier Restatements, does not require strict but

for causation in a toxic tort multiple-exposure case like today’s case. Section 26 generally requires

but for causation, by stating that “[c]onduct is a factual cause of harm when the harm would not have

occurred absent the conduct.” However, section 26 ends by stating that “[t]ortious conduct may also

be a factual cause of harm under section 27.” Section 27 addresses cases of multiple causation and

states: “If multiple acts occur, each of which under § 26 alone would have been a factual cause of

the physical harm at the same time in the absence of the other act(s), each act is regarded as a factual

cause of the harm.”57 Read in a vacuum, sections 26 and 27 might appear to require strict but for

causation for each defendant in a multiple-exposure case where the exposures did not occur “at the

same time,” the position we understand Georgia-Pacific to take. These sections are fraught with

complexities and what if scenarios, set out in many comments and illustrations. Comment f to

section 27 states:

        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. . . . 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.58

And comment g posits the scenario closest to our case:

        [T]he situation addressed in Comment f has occurred most frequently in cases in
        which persons have been exposed to multiple doses of a toxic agent. When a person
        contracts a disease such as cancer, and sues multiple actors claiming that each
        provided some dose of a toxic substance that caused the disease, the question of the

        57
             Id. § 27.

        58
             Id. § 27 cmt. f.

                                                  19
         causal role of each defendant’s toxic substance arises. Assuming that there is some
         threshold dose sufficient to cause the disease, the person may have been exposed to
         doses in excess of the threshold before contracting the disease. Thus, some or all of
         the person’s exposures may not have been but-for causes of the disease.
         Nevertheless, each of the exposures prior to the person’s contracting the disease . .
         . is a factual cause of the person’s disease under the rule in this Section.59

         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.

        3. Further Analysis, under Havner, of Substantial Causation in Asbestos Cases

         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 met that

standard. One respected treatise has opined that it is “neither possible nor desirable to reduce

[substantial factor] to any lower terms.”60




         59
              Id. § 27 cmt. g.

         60
            W . P AGE K EETO N ET AL., P RO SSER AN D K EETO N O N TH E L AW O F T O RTS § 41 (5th ed. 1984); see also id. §
41, at n.30 (“Hart and Honoré . . . object strongly to the phrase as undefinable. So, Green suggests is ‘reasonable,’ but
that does not prevent its use to pose an issue for the jury.”).

                                                            20
         We recognized a quantitative approach to causation in Merrell Dow Pharmaceuticals, Inc.

v. Havner,61 and Georgia-Pacific urges use of that approach in today’s case. Havner provides useful

insights that should be integrated with our analysis here.

         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.62 We recognized that epidemiological studies showing that the population exposed to a

toxin faced more than double the risk of injury facing the unexposed or general population could be

used to establish causation.63

         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 2.0,64 we

recognized that this requirement was not a “litmus test” or “bright-line boundary” and that a single

study would not suffice to establish legal causation.65 We discussed several other indicia of scientific

validity. A claimant must show that his circumstances are similar to the group analyzed in the

study.66 We observed that scientific studies also consider the “significance level” or “confidence


         61
              953 S.W .2d 706 (Tex. 1997).

         62
              Id. at 708, 730.

         63
              Id. at 717–18.

         64
           See id. at 718; see also id. at 721 (“For the result to indicate a doubling of the risk, the relative risk must be
greater than 2.0.”).

         65
              Id. at 718–19, 727.

         66
              Id. at 720.

                                                             21
level,” that the generally accepted confidence level is 95%,67 and that statistical significance also

requires a “confidence interval” that does not include the number 1.68 We noted that “[t]here are

many other factors to consider in evaluating the reliability of a scientific study including, but

certainly not limited to, the sample size of the study, the power of the study, confounding variables,

and whether there was selection bias.”69 We also noted that courts must be “especially skeptical of

scientific evidence that has not been published or subjected to peer review,”70 and that “[a] related

factor . . . is whether the study was prepared only for litigation.”71

         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.72 It offers an alternative method of

establishing causation “[i]n the absence of direct, scientifically reliable proof of causation.”73 To

some extent Havner’s discussion of the use of scientific studies addressed whether those studies




         67
              Id. at 723–24.

         68
              Id. at 723.

         69
              Id. at 724.

         70
           Id. at 727 (internal quotation marks omitted); see also E.I. du Pont de Nemours & Co. v. Robinson, 923
S.W .2d 549, 557 (Tex. 1995) (holding that one factor in deciding reliability of expert testimony is “whether the theory
has been subjected to peer review and/or publication”).

         71
              Havner, 953 S.W .2d at 726.

         72
           For example, we noted in Flores that epidemiological studies discussed in Havner “are not necessary to prove
causation” though properly designed studies can serve as part of the evidence establishing causation. Flores, 232 S.W .3d
at 772.

         73
              Havner, 953 S.W .2d at 715.

                                                           22
supported general causation—the issue of whether Bendectin was capable of causing birth defects.74

Epidemiological studies by their nature address general causation by analyzing a cohort of

individuals,75 rather than specific causation—the jury issue of whether the defendant’s product

caused the specific injury in issue,76 but these studies are sometimes used effectively by experts to

help establish specific causation, as Havner recognized.77 In today’s case, general causation is not

an issue. Georgia-Pacific does not dispute, for purposes of this appeal, that exposure to asbestos

fibers can cause mesothelioma.78

         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




         74
             Id. (“The Havners rely to a considerable extent on epidemiological studies for proof of general causation.”);
see also Merck & Co. v. Garza, 347 S.W .3d 256, 265 (Tex. 2011) (“Havner holds . . . that when parties attempt to prove
general causation using epidemiological evidence, a threshold requirement of reliability is that the evidence demonstrate
a statistically significant doubling of the risk.”).

         75
           See Havner, 953 S.W .2d at 715 (“Epidemiological studies examine existing populations to attempt to
determine if there is an association between a disease or condition and a factor suspected of causing that disease or
condition.”).

         76
           Id. at 714 (“General 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.”).

         77
              Id. at 715.

         78
            Some of the Georgia-Pacific drywall compound to which Bostic was allegedly exposed contained chrysotile
asbestos fibers. Plaintiffs’ experts testified that the prevailing scientific consensus is that chrysotile fibers can cause
mesothelioma. W hile Georgia-Pacific contends that a scientific debate continues as to whether inhalation of chrysotile
fibers causes mesothelioma, it states in its principal brief that it is not challenging “the assumption that exposure to
chrysotile can cause mesothelioma.”

                                                            23
the expert’s scientific testimony is not reliable, it is not evidence.”79 We discussed our decision in

E.I. du Pont de Nemours and Co. v. Robinson,80 where we analyzed the issue of expert reliability.81

As recognized in Robinson, “In addition to being relevant, the underlying scientific technique or

principle must be reliable. Scientific evidence which is not grounded in the methods and procedures

of science is no more than subjective belief or unsupported speculation. Unreliable evidence is of

no assistance to the trier of fact and is therefore inadmissible under Rule 702.”82

       Havner also held that, notwithstanding competing policies of deterrence, risk-avoidance, or

compensating innocent injured parties, “[o]ur legal system requires that claimants prove their cases

by a preponderance of the evidence,” and we rejected all rationales for adopting a lesser burden of

proof.83 In concluding that studies showing more than a doubling of the risk may be supportive of

legal causation, provided that other indicia of reliability are met, we explained that this standard

corresponds to the legal requirement that the plaintiff prove his case by a preponderance of the

evidence:

               Recognizing that epidemiological studies cannot establish the actual cause of
       an individual’s injury or condition, a difficult question for the courts is how a
       plaintiff faced with this conundrum can raise a fact issue on causation and meet the
       “more likely than not” burden of proof.
                                              ***



       79
            Id. at 713.

       80
            923 S.W .2d 549 (Tex. 1995).

       81
            Havner, 953 S.W .2d at 712, 714.

       82
            Robinson, 923 S.W .2d at 557 (citation, internal quotation marks omitted).

       83
            953 S.W .2d at 728.

                                                          24
               Other courts have likewise found that the requirement of a more than 50%
       probability means that epidemiological evidence must show that the risk of an injury
       or condition in the exposed population was more than double the risk in the
       unexposed or control population.
                                                 ***
               Although we recognize that there is not a precise fit between science and legal
       burdens of proof, we are persuaded that properly designed and executed
       epidemiological studies may be part of the evidence supporting causation in a toxic
       tort case and that there is a rational basis for relating the requirement that there be
       more than a “doubling of the risk” to our no evidence standard of review and to the
       more likely than not burden of proof.
               Assume that a condition naturally occurs in six out of 1,000 people even
       when they are not exposed to a certain drug. If studies of people who did take the
       drug show that nine out of 1,000 contracted the disease, it is still more likely than not
       that causes other than the drug were responsible for any given occurrence of the
       disease . . . . However, if more than twelve out of 1,000 who take the drug contract
       the disease, then it may be statistically more likely than not that a given individual’s
       disease was caused by the drug.
               This is an oversimplification of statistical evidence relating to general
       causation . . . but it illustrates the thinking behind the doubling of the risk
       requirement.
                                                 ***
       [T]he law must balance the need to compensate those who have been injured by the
       wrongful actions of another with the concept deeply imbedded in our jurisprudence
       that a defendant cannot be found liable for an injury unless the preponderance of the
       evidence supports cause in fact. The use of scientifically reliable epidemiological
       studies and the requirement of more than a doubling of the risk strikes a balance
       between the needs of our legal system and the limits of science.84

       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


       84
            Id. at 715–18 (citations omitted) (emphasis in original).

                                                           25
a preponderance of the evidence. These principles should apply to asbestos cases. As to the

availability of scientific studies, asbestos-related disease has been researched for many decades and

the population of potentially affected persons numbers in the millions. Dr. Lemen, one of Plaintiffs’

experts, testified that many millions of people have been exposed to chrysotile asbestos from

manmade sources, that a scientific consensus that asbestos causes serious illness has existed since

1930, that a statistically significant link between asbestos and mesothelioma was shown in 1963, and

that by 1965 over a thousand publications discussed asbestos disease. We observed over 15 years

ago that “[a]sbestos litigation, particularly asbestos products cases, has achieved maturity.”85 We

therefore conclude that in the absence of direct proof of causation, establishing causation in fact

against a defendant in an asbestos-related disease case requires scientifically reliable proof that the

plaintiff’s exposure to the defendant’s product more than doubled his risk of contracting the disease.

A more than doubling of the risk must be shown through reliable expert testimony that is based on

epidemiological studies or similarly reliable scientific testimony.

       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.”86 We think this statement in Havner is correct but cannot be applied without

       85
            In re Ethyl Corp., 975 S.W .2d 606, 610 (Tex. 1998).

       86
            953 S.W .2d at 720.

                                                         26
qualification to cases involving multiple sources of exposure to the same toxin. We think the

plaintiff should be required to establish more than a doubling of the risk attributable to the

defendant’s product, for the reasons discussed, but do not think it necessary or fair to require a

plaintiff to track down every possible source of asbestos exposure and disprove that those other

exposures caused the disease. Strict application of Havner’s requirement of ruling out all other

possible causes of disease would in effect re-introduce a strict but for requirement, which for reasons

already discussed is not appropriate in a multiple-exposure case like today’s case. Our law accepts

that in cases of multiple exposure multiple defendants may be held liable for causing the plaintiff’s

disease. And in multiple-exposure cases few if any plaintiffs could ever establish which particular

fibers from which particular defendant caused the disease, and we do not believe the plaintiff should

be required to quantify the exposure from every other conceivable source, occurring perhaps over

a period of decades.

       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, 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




                                                  27
occurred.”87 The law should retain this concept. Along the same lines, the Restatement Third

recognizes that a defendant’s trivial contribution to multiple causes will not result in liability.88

        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




       87
            Flores, 232 S.W .3d at 770 (quoting R ESTATEM EN T (S ECO N D ) OF T O RTS § 431 cmt. a (1965)).

       88
            R ESTATEM EN T (T H IR D ) O F T O RTS : L IA BILITY   FO R   P H YSIC AL AN D E M O TIO N AL H ARM § 36 (2010).

                                                                    28
studies, and then demonstrates that his circumstances are similar to the subjects of the studies.89 By

meeting these requirements, the plaintiff shows that his exposure to the defendant’s product more

than doubled his individual risk and thereby establishes specific causation. Havner is, therefore,

relevant to our analysis today. Its recognition that every plaintiff must prove his case by a

preponderance of the evidence has application here.

         The dissent suggests that our analysis is flawed because specific causation as explicated in

Havner is different from substantial factor causation. We disagree. “Substantial factor” is a term

we use to describe the level of proof required to establish specific causation, which is always an

element of the plaintiff’s case.

         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,90 a requirement we

actually relax in today’s case because of the special difficulties encountered in multiple-exposure

cases, as discussed above. But we think Havner’s requirement of proof of a more than doubling of

         89
             See Havner, 953 S.W .2d at 715 (“[I]n many toxic tort cases . . . there will be no reliable evidence of specific
causation. In 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. The finder of fact is asked to infer that
because the risk is demonstrably greater in the general population due to exposure to the substance, the claimant’s injury
was more likely than not caused by that substance. Such a theory . . . is based on a policy determination that when the
incidence of a disease or injury is sufficiently elevated due to exposure to a substance, someone who was exposed to that
substance and exhibits the disease or injury can raise a fact question on causation.”); id. at 720 (“To raise a fact issue
on causation and thus to survive legal sufficiency review, a claimant must do more than simply introduce into evidence
epidemiological studies that show a substantially elevated risk. A claimant must show that he or she is similar to those
in the studies.”); see also Merck, 347 S.W .3d at 265 (“Havner holds . . . that when parties attempt to prove general
causation using epidemiological evidence, a threshold requirement of reliability is that the evidence demonstrate a
statistically significant doubling of the risk. In addition, Havner requires that a plaintiff show ‘that he or she is similar
to [the subjects] in the studies . . . .’”).

         90
              953 S.W .2d at 720.

                                                             29
the risk is particularly useful in multiple-exposure cases where the alternative is to abdicate resort

to scientifically reliable proof and accept that any exposure will suffice.

        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.91 Plaintiffs tried the case in exactly the

opposite manner, by insisting that any exposure to asbestos beyond background exposure should be

treated as a cause of Bostic’s disease. Further, in the real world of complex environments and

complex organisms, we think that science is often limited to establishing probabilities. Havner’s


       91
            On the latter point, the following exchange occurred at oral argument:

        Q: [Y]ou argue, as I understand it, that if there hadn’t been any other exposure, the exposure to
        Georgia-Pacific product was enough.

        A: Correct, Your Honor, which is what—

        Q: So you’re not making the argument that even though it wasn’t enough, if you add it in with
        everything else, that would have been enough.

        A: No. W e are not at all, and I want to be very clear on that . . . .



                                                            30
recognition that science must sometimes resort to probabilistic approaches is hardly a valid criticism

of that decision. We assume the dissent has no quarrel with quantum mechanics. Establishing the

direct proof posited in the dissent’s hypotheticals might prove far more difficult than the method of

proof sanctioned in Havner. Excluding the universe of all other possible causes, which we do not

require, might prove more daunting than what we do require. And even in a single-exposure case,

we think that proof of dose would be required, because as Flores noted, “One of toxicology’s central

tenets is that the dose makes the poison.”92 As explained below, dose was not established in this

case.

                                                 4. Recapitulation

        We conclude that in all asbestos cases involving multiple sources of exposure, including

mesothelioma cases, the standards for proof of causation in fact are the same. In reviewing the legal

sufficiency of the evidence:

•       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;




        92
             Flores, 232 S.W .3d at 770 (internal quotation marks omitted).

                                                          31
•        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.

                                     B. Proof of Causation in This Case

         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,93 the most common form of asbestos used

commercially. Asbestos fibers can become airborne when dry compound is sanded, mixed, or swept

as part of normal drywall work.

         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



         93
            As noted above, see supra note 78, Georgia-Pacific does not dispute for purposes of this appeal that exposure
to chrysotile asbestos fibers can cause mesothelioma. “Chrysotile asbestos is the most abundant type of asbestos fiber
and is a serpentine fiber consisting of ‘pliable curly fibrils which resemble scrolled tubes.’” Flores, 232 S.W .3d at 766
n.4.

                                                           32
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 recall whether Bostic was present

when drywall work was done on this project. Bostic could not recall with certainty ever using

Georgia-Pacific drywall products during the relevant 1967–77 period.

       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

                                                33
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.



                                                 34
       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 disease.94 Longo conceded that his studies did not attempt to “mimic any one

       94
            For example, Hammar testified:

       Q: And is it fair to say then that to a reasonable degree of medical probability, that if somebody has
       mesothelioma that each and every exposure to asbestos that that person had would be a significant
       contributing factor to the development of mesothelioma?

       A: I believe so, at least potentially a contributing factor, yes.
                                                          ***
       Q: And did each and every exposure that Timothy Bostic had to Georgia Pacific joint compounds and
       wallboard materials increase his risk of mesothelioma?

       A: Yes.
                                                        ***
       Q: And is that consistent with your opinion that each and every exposure to asbestos is a contributing
       factor?

       A: Yes.
                                                        ***
       Q: And do you agree that each and every exposure that he had to asbestos, regardless of the source to
       the extent he had an exposure, that those were significant and contributing factors in the development

                                                        35
person’s actual exposure to asbestos,” so he made no attempt to measure Bostic’s actual aggregate

dose assignable to Georgia-Pacific or any other source.95

         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:




         of his mesothelioma?

         A: Yes.

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.”

        95
           Longo’s experiments measured the intensity of exposure a worker might encounter while performing various
drywall tasks. He did not attempt to establish Bostic’s actual aggregate dose. W e think Georgia-Pacific’s expert, Dr.
W illiam Dyson, correctly explained the difference between intensity of exposure and dose:

         [A]ll diseases, including those associated with asbestos, follow a dose-response relationship. And a
         dose is the multiplication product of the exposure intensity times the exposure duration. Those are the
         two components of dose. So measuring the airborne concentration in fibers per cubic centimeter or
         a million particles per cubic foot is a measure of the intensity of the exposure or the level of exposure
         in the air. Then you take the duration of that exposure, and those two components give you dose.

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 R EFEREN CE M ANU AL O N S CIEN TIFIC E VID ENCE 633, 638 n.12 (Fed. Jud. Ctr. 3d ed.
2011) (“Dose is a function of both concentration and duration.”).

                                                            36
         [W]e have the burden of proof. . . . And we assume that burden and will prove this
         case to you by meeting that burden of proof. To prove our case that it is more likely
         true than not true that Georgia-Pacific sold an asbestos product, that Timothy Bostic
         was exposed to this asbestos product, and that he died as a result of the exposure to
         this and other asbestos products.

In closing counsel argued:

         The first part of this [jury] question is proximate cause, and that’s what I want to talk
         to you about first. . . . And in this case, you have seen that Timothy Bostic did have
         more than just one exposure to asbestos. And at no point in this trial have we ever
         said that one of those exposures you could just pull out and forget about it. You’re
         [] not going to hear us say that. You didn’t hear our experts say that. Each and every
         exposure is a contributing factor to the disease. That’s just the science. But when
         more than one exposure comes together to cause a disease, they’re all responsible.
         You can’t just separate one out.

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,96 Brody conceded that everyone has

         96
              Hammar testified:

         Q: Now, Doctor, that leads me to the next question, which is: Are asbestos-related diseases what we
         call dose-related diseases?

         A: Yes.

         Q: W hat does that mean?

         A: That means that the cumulative dose, at least up to the point at least in cancer where the first cell
         developed, were all causative or potentially causative of disease. And that basically means that the
         more asbestos exposure you have the greater the risk of developing asbestos-related disease.

He agreed “if you were to look at it from a probability point of view” that “higher levels may contribute more to the

                                                           37
some asbestos in his lungs, but at levels too low to cause disease,97 and Lemen conceded that “the

only way to adequately study subjects and their risk of developing disease is to study the exposure

they have.” We agree with the Pennsylvania Supreme Court that an expert opinion embracing the

any exposure theory while recognizing that the disease is dose-related “is in irreconcilable conflict

with itself. Simply put, one cannot simultaneously maintain that a single fiber among millions is

substantially causative, while also conceding that a disease is dose responsive.”98

         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 report99 of the “Helsinki Conference” on asbestos disease which states that while

mesothelioma can occur in cases of low exposure, “very low background environmental exposures

carry only an extremely low risk.”100 Brody also relied on an article by Philip Landrigan and others

finding it “widely accepted that asbestos fibers, including chrysotile fibers, increase the existing risk


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.”

         97
              See supra note 22.

         98
              Betz v. Pneumo Abex, LLC, 44 A.3d 27, 56 (Pa. 2012).

        99
            Consensus Report, Asbestos, Asbestosis, and Cancer: the Helsinki Criteria for Diagnosis and Attribution,
23 S CAN D IN AVIA N J. W O RK , E N V ’T & H EALTH 311 (1997).

         100
               Id. at 313.

                                                          38
of developing lung cancer in proportion to the cumulative exposure that occurred up to a time 10

years prior to evaluation.”101 Brody repeatedly testified that minimal exposure to asbestos does not

cause mesothelioma.102

        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 Commission103 (CPSC) proposing

to ban asbestos-containing patching compounds. This report was not itself a peer-reviewed

epidemiological study, although it cited a number of studies. It concluded, based in part on

theoretical arguments, that “[a] ‘no effect’ level theoretically may exist, but it has not been

demonstrated. Therefore, there is no known threshold below which exposure to respirable free-form

asbestos would be considered safe.”104 Lemen also discussed 1972 OSHA regulations concerning

asbestos exposure standards. This publication recognized “controversy as to the validity of the

measuring techniques” and “controversies concerning the relative toxicity of various kinds of

asbestos,” but concluded that in view of the risk of not acting “it is essential that the exposure be

regulated now, on the basis of the best evidence available now, even though it may not be as good

as scientifically desirable.”105 These publications are not scientific studies, and while a federal


        101
              Philip J. Landrigan et al., The Hazards of Chrysotile Asbestos: A Critical Review, 37 I N D U S . H EALTH 271,
273 (1999).

        102
              See supra notes 22–23.

        103
              Respirable Free-Form Asbestos, 42 Fed. Reg. 38782 (July 29, 1977).

        104
              Id. at 38786.

        105
              Standard for Exposure to Asbestos Dust, 37 Fed. Reg. 11318, 11318 (June 7, 1972).

                                                             39
agency may be authorized to ban a product based on the lack of proof of its safety,106 a “fundamental

principle” of Texas products liability law “is that the plaintiff must prove that the defendants

supplied the product which caused the injury.”107 Because “[o]ur legal system requires that claimants

prove their cases by a preponderance of the evidence,” our law “lags science; it does not lead it.”108

Like the CPSC, Lemen could not state that “there is not a safe level” of asbestos. Instead, his

testimony was that “we don’t know really how much exposure it takes to cause mesothelioma,” and

that “one of the reasons we recommend banning of asbestos, all types of asbestos, is because that

level is so low that we have not been able to measure that level.” As noted above, Lemen testified

that for all carcinogens, the threshold at which the risk of disease falls to zero is unknown. Brody

similarly testified that “no one’s ever been able to show a level that will prevent everyone from

getting mesothelioma.” Assuming this testimony is factually correct, the failure of science to isolate

a safe level of exposure does not prove specific causation in today’s case, but the any exposure

theory in effect asks the Court to do so. As noted above, one court, in refusing to admit Hammar’s

any exposure testimony, observed that “Dr. Hammar wants to be allowed to tell a jury that all of the

plaintiff’s possible exposures to asbestos during his entire life were contributing causes of the

plaintiff’s cancer, and, therefore, sufficient to support a finding of legal liability . . . . Just because




         106
             For example, the FDA “may make regulatory decisions . . . based on postmarketing evidence that gives rise
to only a suspicion of causation.” Matrixx Initiatives, Inc. v. Siracusano, 131 S. Ct. 1309, 1320 (2011). Hence, “efforts
to invoke . . . regulatory standards are also ineffectual in terms of substantial-factor causation, since the most these can
do is suggest that there is underlying risk from the defendants’ products . . . .” Betz, 44 A.3d at 55.

         107
               Gaulding v. Celotex Corp., 772 S.W .2d 66, 68 (Tex. 1989).

         108
               Havner, 953 S.W .2d at 728.

                                                            40
we cannot rule anything out does not mean we can rule everything in.”109 Stated another way, the

inability of science to establish a maximum safe dose does not mean that science cannot establish

a statistically significant link between a dose and the disease. It seems to us that all other things

being equal, the more toxic the substance, the easier it should be to establish a Havner-compliant

statistical link.

        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 articles110 which relied on a study of a Chinese asbestos

plant where workers were employed at the plant, presumably full-time, for an average of over two

decades.111 While, as Lemen reported, the study of the Chinese plant met standards we recognized

in Havner (a relative risk of 4.29, with a confidence level of 95% and a confidence interval of 2.17

to 8.46), the cohort studied consisted of individuals whose circumstances were very different from

those of Bostic. Lemen also discussed a study by Frank Stern and others112 of union plasterers and


        109
              Smith v. Ford Motor Co., 2013 W L 214378, at *3 (D. Utah Jan. 18, 2013).

        110
            Richard A. Lemem, Chrysotile Asbestos as a Cause of Mesothelioma: Application of the Hill Causation
Model, 10 I N T ’L J. O CCU PATIO N AL & E N VTL . H EALTH 233, 235 (2004).

        111
              Eiji Yano et al., Cancer Mortality Among Workers Exposed to Amphibole-Free Chrysotile Asbestos, 154
A M J. E PID EM IO LO GY 538 (2001).

        112
                Frank Stern et al., Mortality Among Unionized Construction Plasterers and Cement Masons, 39 A M . J.
I N D U S . M ED . 373 (2001).

                                                         41
cement masons where the authors made reference to another study of drywall construction which

found asbestos fiber concentrations “similar to those measured in the work environment of asbestos

insulation workers who”113 in yet another study by Irving Selikoff and others114 “had a seven-fold

increased risk of cancer of the lung and of the pleura.”115 However, the Stern and Selikoff studies

were of workers employed in the trades studied, not persons like Bostic who performed occasional

drywall work outside of their primary employment. Further, the Stern study found that the

correlation between employment in the trades studied and mesothelioma was “not statistically

significant,”116 despite special efforts by the authors to manually review death certificates “to obtain

a more accurate assessment of mesothelioma-related deaths in this cohort.”117 In Havner, we held

that the plaintiff “must show that he or she is similar to those in the studies. This 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 . . . and that the timing of the onset of injury

was consistent with that experienced by those in the study.”118                  Without such a showing,

“epidemiological studies are without evidentiary significance.”119 While the exposure of those in


        113
              Id. at 383.

        114
          Irving J. Selikoff et al., Mortality Experience of Insulation Workers in the United States and Canada,
1943–1976, 330 A N N ALS N.Y. A CAD . S CIS . 91 (1979).

        115
              Stern, supra note 112, at 383.

        116
              Id. at 376.

        117
              Id. at 381.

        118
              953 S.W .2d at 720.

        119
              Flores, 232 S.W .3d at 771.

                                                      42
the study need not exactly match the plaintiff’s exposure, “the conditions of the study should be

substantially similar to the claimant’s circumstances,”120 a requirement that was not met.

         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.121 The testimony may also

have been based on an incorrect assumption that Bostic’s primary occupation was in construction,

because the work history sheets Hammar reviewed made no mention of Bostic’s employment with

the TDCJ.122 “[C]ourts must look beyond the bare opinions of qualified experts and independently

evaluate the foundational data underlying an expert’s opinion in order to determine whether the




         120
               Merck, 347 S.W .3d at 266.

         121
               Havner, 953 S.W .2d at 712.

         122
            Hammar testified, incorrectly, that from his review of the work history sheets Bostic “actually worked in
construction primarily” and “it looked to me like his primary occupational exposure itself was actually in the construction
industry.” “W e are not required . . . to ignore fatal gaps in an expert’s analysis or assertions that are simply incorrect.”
Volkswagen of Am., Inc. v. Ramirez, 159 S.W .3d 897, 912 (Tex. 2004).

                                                             43
expert’s opinion is reliable.”123 If the testimony is not reliable, it is not evidence.124 Further, another

of Plaintiffs’ experts, Dr. Brody, testified that if, as was the case, Bostic worked nine months at the

Knox Glass plant and had amosite asbestos in his lungs, that exposure “substantially contributed to

his mesothelioma.” Without any meaningful and scientific attempt to quantify the exposures from

the two sources, the testimony was legally insufficient, for there was no meaningful way for the jury

to conclude that Bostic’s exposure to Georgia-Pacific’s products was a substantial factor in causing

his disease, nor was there any basis for the jury to apportion liability between these two sources of

asbestos. In Flores we found the evidence of causation legally insufficient not only because of the

plaintiff’s failure to establish his aggregate dose but also his failure to “introduce evidence regarding

what percentage of that indeterminate amount may have originated with [Defendant] Borg-Warner’s

products” as opposed to “other brands of brake pads.”125

        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 testified126 that any exposure to asbestos should

be considered a cause of Bostic’s disease, (2) failed to quantify, even approximately, the aggregate

dose, (3) failed to quantify, even approximately, the dose attributable to Georgia-Pacific, and


        123
              Merck, 347 S.W .3d at 262.

        124
              Havner, 953 S.W .2d at 713.

        125
              232 S.W .3d at 772.

        126
              See supra note 94.

                                                    44
(4) failed to show that the dose fairly assignable to Georgia-Pacific more than doubled Bostic’s

chances of contracting mesothelioma. The evidence was sufficient only if proof of some exposure

is sufficient to establish causation. It is not. The essential teaching of Flores is that dose matters,

and this requirement applies to mesothelioma cases.

        For these reasons, we conclude that the evidence of causation was legally insufficient to

sustain the verdict in this case.

                                          III. Conclusion

        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.




                                                       _____________________________________
                                                       Don R. Willett
                                                       Justice


OPINION DELIVERED: July 11, 2014




                                                  45
