Court Opinion

ID: 3130631
Source: CourtListenerOpinion
Date Created: 2015-10-16 16:50:42.45238+00
Date Added: 2024-06-11T11:46:07.454205
License: Public Domain

COURT OF APPEALS
                        SECOND DISTRICT OF TEXAS
                             FORT WORTH

                              NO. 2-08-198-CV

ROSEMARY SMITH, BRADY SMITH,                                    APPELLANTS
AND DONNA HUBBARD,
INDIVIDUALLY AND AS PERSONAL
REPRESENTATIVE OF THE HEIRS
AND ESTATE OF DORMAN SMITH,
DECEASED

                                      V.

KELLY-MOORE PAINT COMPANY, INC.                                    APPELLEE

                                  ------------

          FROM THE 153RD DISTRICT COURT OF TARRANT COUNTY

                                  ------------

                                 OPINION

                                  ------------

      This is an appeal from a summary judgment in favor of appellee Kelly-

Moore Paint Company, Inc. in this asbestos exposure products liability case. 1

      1
        This court dismissed the Smiths’ appeal against Bondex International,
Inc. and RPM, Inc. in accordance with a joint motion by the Smiths, Bondex,
In a single issue, appellants Rosemary Smith, Brady Smith, and Donna Hubbard,

Individually and as Personal Representative of the Heirs and Estate of Dorman

Smith, Deceased (collectively, the Smiths), contend that the trial court erred by

granting a no-evidence summary judgment on the ground that the Smiths failed

to adduce sufficient evidence that Dorman had been exposed to chrysotile

asbestos in Kelly-Moore’s drywall joint compounds in a dose sufficient to have

been a substantial factor in causing his mesothelioma.

                               Background Facts

      Dorman began working in the construction business, specifically as a self-

employed drywaller finisher using joint compound, around 1955, and he

performed the same type of work through the mid 1980s. Doctors eventually

diagnosed him with mesothelioma in early 2005. As a result, the Smiths sued

several defendants, including Kelly-Moore, in Tarrant County, claiming that

exposure to the asbestos in those defendants’ joint compound products

proximately caused Dorman’s mesothelioma. Dorman died after filing suit, on

December 9, 2005.

      The case was transferred to the 11th District Court, the Texas

multidistrict litigation pretrial court. See Tex. Civ. Prac. & Rem. Code Ann.

and RPM. No. 02-08-00198-CV, 2009 WL 2356855, at *1 (Tex. App.—Fort
Worth July 30, 2009, no pet.).

                                       2
§ 90.010(a) (Vernon Supp. 2009); Tex. R. Jud. Admin. 13, reprinted in Tex.

Gov’t Code Ann. tit. 2, subtit. F app. (Vernon Supp. 2009). Before trial, Kelly-

Moore moved for both a no-evidence and traditional summary judgment,

contending that the Smiths had presented no evidence that Dorman’s exposure

to any of Kelly-Moore’s chrysotile asbestos-containing joint compound product

caused his mesothelioma, under the test set forth in the supreme court’s

opinion in Borg-Warner Corp. v. Flores, 232 S.W.3d 765 (Tex. 2007). 2 The

11th District Court granted Kelly-Moore’s no-evidence motion for summary

judgment and transferred the remaining claims back to the 153rd District Court

in Tarrant County for trial; however, the remaining claims against the other

defendants were either settled or dismissed, making the summary judgment

final. The Smiths then appealed the summary judgment ruling in favor of Kelly-

Moore.

      2
         Kelly-Moore challenged the Smiths’ evidence as to specific causation
only: whether Kelly-Moore’s asbestos-containing product caused Dorman’s
mesothelioma. They did not challenge the evidence as to general causation,
i.e., that Kelly-Moore’s asbestos-containing joint compound is capable of
causing mesothelioma in the general population. See Merrell Dow Pharm., Inc.
v. Havner, 953 S.W.2d 706, 714 (Tex. 1997), cert. denied, 523 U.S. 1119
(1998); Georgia Pac. Corp. v. Stephens, 239 S.W.3d 304, 308 (Tex.
App.—Houston [1st Dist.] 2007, pet. denied).

                                       3
            No-Evidence Summary Judgment Standard of Review

      After an adequate time for discovery, the party without the burden of

proof may, without presenting evidence, move for summary judgment on the

ground that there is no evidence to support an essential element of the

nonmovant’s claim or defense.      Tex. R. Civ. P. 166a(i).   The motion must

specifically state the elements for which there is no evidence.      Id.; Timpte

Indus., Inc. v. Gish, 286 S.W.3d 306, 310 (Tex. 2009). The trial court must

grant the motion unless the nonmovant produces summary judgment evidence

that raises a genuine issue of material fact. See Tex. R. Civ. P. 166a(i) & cmt.;

Hamilton v. Wilson, 249 S.W.3d 425, 426 (Tex. 2008).

      When reviewing a no-evidence summary judgment, we examine the entire

record in the light most favorable to the nonmovant, indulging every reasonable

inference and resolving any doubts against the motion. Sudan v. Sudan, 199
S.W.3d 291, 292 (Tex. 2006). We review a no-evidence summary judgment

for evidence that would enable reasonable and fair-minded jurors to differ in

their conclusions. Hamilton, 249 S.W.3d at 426 (citing City of Keller v. Wilson,

168 S.W.3d 802, 822 (Tex. 2005)).          We credit evidence favorable to the

nonmovant if reasonable jurors could, and we disregard evidence contrary to

the nonmovant unless reasonable jurors could not. Timpte Indus., Inc., 286
S.W.3d at 310 (quoting Mack Trucks, Inc. v. Tamez, 206 S.W.3d 572, 582

                                       4
(Tex. 2006)).   If the nonmovant brings forward more than a scintilla of

probative evidence that raises a genuine issue of material fact, then a no-

evidence summary judgment is not proper. Smith v. O’Donnell, 288 S.W.3d
417, 424 (Tex. 2009).

                     Issue on Appeal–Specific Causation

      The ground raised in Kelly-Moore’s no-evidence summary judgment

motion—and therefore the issue on appeal—is whether the Smiths produced

sufficient evidence that Dorman was exposed to chrysotile asbestos from Kelly-

Moore’s joint compound product at an exposure level or dose sufficient to have

been a substantial factor in his developing mesothelioma. According to Kelly-

Moore’s no-evidence summary judgment motion, the Smiths did not produce

any credible evidence of (1) the amount of chrysotile asbestos from Kelly-Moore

products to which Dorman had been exposed, (2) epidemiological studies of

similarly situated persons showing that exposure to chrysotile asbestos in any

amount would double the risk of developing mesothelioma, or (3) a minimum

threshold exposure to asbestos above which an increased risk of developing

mesothelioma occurs. Thus, Kelly-Moore contends that the Smiths did not

bring forward sufficient evidence of specific causation under the test set forth

by the Texas Supreme Court in Borg-Warner v. Flores and applied in a similar

fact scenario by the Houston Fourteenth Court of Appeals in Georgia Pacific

                                       5
Corp. v. Stephens. At oral argument, Kelly-Moore clarified that it was relying

on the distinction between chrysotile and other types of asbestos; 3 in other

words, Kelly-Moore contends that although the Smiths may have brought

forward at least some sufficient evidence that exposure to amphibole or other

types of asbestos in the amount to which Dorman was exposed leads to an

increased risk of mesothelioma, they brought forward no evidence that

exposure to only chrysotile asbestos would amount to such an increased risk.

Kelly-Moore further contends that there is no evidence in the record of a

minimum threshold of chrysotile above which a person is at increased risk of

developing mesothelioma.

                    Specific Causation in Asbestos Cases

      In Borg-Warner v. Flores, an automobile mechanic sued Borg-Warner and

others claiming that the dust generated by the grinding of asbestos-containing

brake pads caused his asbestosis. 232 S.W.3d at 766.      In reviewing the

intermediate appellate court’s determination that Flores had brought forward

      3
         There are six different types of asbestos; chrysotile is the most
abundant type of asbestos fiber and is a serpentine fiber consisting of “pliable
curly fibrils which resemble scrolled tubes.” Borg-Warner, 232 S.W.3d at 766
n.4 (citing Lee S. Siegel, Note, As the Asbestos Crumbles: A Look at New
Evidentiary Issues in Asbestos Related Property Damage Litigation, 20 Hofstra
L. Rev. 1139, 1149 (1992)). The remaining five types are generally referred
to as amphiboles.

                                       6
legally sufficient evidence of causation at trial, the supreme court considered

the appropriate causation standard to be applied in cases in which a plaintiff

“claim[s] to be injured by an asbestos-containing product.” Id. at 768–69. The

court held that in such cases, “we must determine whether the asbestos in the

defendant’s product was a substantial factor in bringing about the plaintiff’s

injuries.” Id. at 770. Because “exposure to asbestos, a known carcinogen, is

never healthy but fortunately does not always result in disease,” a plaintiff must

prove more than exposure to an asbestos-containing product to prove that a

particular product was a substantial factor in bringing about his or her

injuries. Id. at 770–71. To prove “substantial factor causation,” a plaintiff

must show both frequent, regular, and proximate exposure to the product and

reasonable quantitative evidence that the exposure increased the risk of

developing the asbestos-related injury. Id. at 769–72; Georgia Pac. Corp. v.

Stephens, 239 S.W.3d 304, 312 (Tex. App.—Houston [1st Dist.] 2007, pet.

denied); see also Lohrmann v. Pittsburgh Corning Corp., 782 F.2d 1156, 1162

(4th Cir. 1986). Epidemiological studies showing at least a doubling of the risk

of disease upon exposure to asbestos have evidentiary significance only if “the

injured person can show that ‘the exposure or dose levels were comparable to

or greater than those in the studies.’”     Borg-Warner, 232 S.W.3d at 771

(quoting Havner, 953 S.W.2d at 720–21). According to Borg-Warner, then, to

                                        7
prove specific causation in an asbestos exposure case, there must be some

evidence of an aggregate dose of exposure to the plaintiff that was a

substantial factor in causing the asbestos-related disease; in other words, there

must be some evidence that the dose to which the plaintiff was exposed

exceeds a minimum dose, or “threshold,” at which an increased risk of

developing the injury has been shown.       See Borg-Warner, 232 S.W.3d at

770–73; Stephens, 239 S.W.3d at 312, 321.

      The Fourteenth Court of Appeals applied the Borg-Warner “substantial

factor causation” test in a suit brought by a commercial painter who alleged

that his mesothelioma was caused by exposure to Georgia Pacific’s joint

compound, which contained only chrysotile asbestos. Stephens, 239 S.W.3d

at 306. In Stephens, a jury trial case, the plaintiff not only failed to provide

legally sufficient evidence of frequent, regular, and proximate exposure to

Georgia Pacific’s product, but he also failed to show a minimum dose at which

an increased risk of mesothelioma from chrysotile-only asbestos exposure

would occur. Id. at 321. Stephens’s experts testified instead that there is no

minimum level of exposure to chrysotile asbestos below which an increased risk

of injury does not occur, despite acknowledging that asbestos fibers are present

in the ambient air we breathe, especially in urban areas; in other words, the

experts testified that any exposure to chrysotile asbestos increases the risk of

                                       8
injury. Id. at 314–15. The court of appeals held that Borg-Warner requires

proof of more than “any exposure” as a minimum level to which the aggregate

dose can be compared; otherwise, there is no way to determine whether the

product was a substantial factor in causing the plaintiff’s mesothelioma as

opposed to it being attributable to asbestos exposure in the ambient air. Id. at

321; see Temple-Inland Forest Prods. Corp. v. Carter, 993 S.W.2d 88, 95 (Tex.

1999).

  Application of Substantial Factor Causation Test in Mesothelioma Cases

        The Smiths first contend that the “substantial factor causation” test

announced by the supreme court in Borg-Warner and applied by the Fourteenth

Court of Appeals in Stephens is not applicable in every asbestos exposure

case.    Specifically, they contend that “Borg-Warner . . . did not create an

absolute requirement in every asbestos case that [a] plaintiff produce

quantitative evidence of ‘dose’ to each defendant’s product, as a condition

precedent to a finding of liability.”   They point out the difference between

mesothelioma and asbestosis, which is the disease at issue in Borg-Warner.

Asbestosis is a dose-related disease that is typically the result of either “long-

term, high-level exposure to asbestos” or “relatively brief but extremely heavy

exposure.” Borg-Warner, 232 S.W.3d at 771. It “appears to be dose-related,

‘so that the more one is exposed, the more likely the disease is to occur, and

                                        9
the higher the exposure the more severe the disease is likely to be.’”        Id.

(quoting 3 David L. Faigman et al., Modern Scientific Evidence: The Law and

Science of Expert Testimony § 28.22, at 447 (2007)). In addition, there are

over 100 causes of asbestosis. Id. at 766. On the other hand, the Smiths

presented evidence that mesothelioma is a signature disease, meaning that it

does not typically occur in the absence of asbestos exposure. See C.R. at

1706 (citing P. Boffetta, Health Effects of Asbestos Exposure in Humans: a

Quantitative Assessment, Med Lav 89(6):471–80 (1998) (“Because of the

rarity of the disease and the specificity of the causal association, all cases

occurring   among   asbestos    exposed    workers   are   attributed   to   this

exposure.”)). In addition, it is generally accepted that a person can develop

mesothelioma from only low levels of asbestos exposure. Borg-Warner, 232
S.W.3d at 771 (citing 3 Faigman, supra). The Smiths contend that the nature

of mesothelioma thus distinguishes this case from Borg-Warner so that the

requirements of showing a total and threshold dose are not necessary.

      Although it appears from both scientific literature and case law that the

causative connection between mesothelioma and asbestos exposure is much

more solidly linked than in cases of asbestosis and asbestos exposure, such

that asbestos exposure in any amount other than general background levels

                                      10
would appear to be causative of mesothelioma, 4 we cannot read Borg-Warner,

and the test announced therein, so narrowly as to apply only to asbestosis or

asbestos-exposure cases other than mesothelioma. The supreme court quite

clearly states that the test it announces is the standard to be applied in cases

in which a plaintiff “claim[s] to be injured by an asbestos-containing product.”

Id. at 768–69. The court did not distinguish among different diseases caused

by asbestos exposure, nor among different types of asbestos.          Thus, we

conclude and hold—as we must, being bound by supreme court precedent—that

a plaintiff in a mesothelioma suit that he or she claims is caused by an

asbestos-containing product must prove the elements set forth in Borg-Warner’s

“substantial factor causation test”: specifically, an aggregate dose of exposure

from the defendant’s product and a minimum threshold dose above which an

increased risk of developing mesothelioma occurs. See Stephens, 239 S.W.3d
4
         Other jurisdictions have recognized the need for taking into account
the nature of the plaintiff’s asbestos related disease in determining causation.
See, e.g., Purcell v. Asbestos Corp., 959 P.2d 89, 94 (Or. Ct. App. 1998)
(declining to adopt the Lohrmann test but noting that “even the jurisdictions
that follow the frequency, regularity, and proximity test apply it less rigidly
when dealing with mesothelioma, because it can be caused by very minor
exposures”), opinion modified on nondispositive grounds, 963 P.2d 729 (1998);
Wehmeir v. UNR Indus., Inc., 572 N.E.2d 320, 337 (Ill. App. Ct. 1991) (stating
that in applying the Lohrmann factors, each case will stand on its facts and
pointing out the difference in exposure levels needed to cause mesothelioma
and asbestosis).

                                      11
at 312, 320–21; see also Lubbock County, Tex. v. Trammel’s Lubbock Bail

Bonds, 80 S.W.3d 580, 585 (Tex. 2002) (noting that once the supreme court

announces a proposition of law, that proposition is binding precedent and may

not be modified or abrogated by a court of appeals).

      Thus, in this case, we must determine whether there is any evidence that

would raise a genuine fact issue as to (1) the total dose of chrysotile asbestos

from Kelly-Moore products to which Dorman was exposed and (2) whether that

dose exceeds a minimum threshold dose above which an increased risk of

developing mesothelioma occurs.

          Dorman’s Total Exposure to Kelly-Moore Joint Compound

Lay Witness Testimony

      The Smiths attached excerpts from Dorman’s deposition to their summary

judgment response, in which he testified that as a drywall finisher, he “always”

worked with joint compounds. He personally mixed, sanded, and swept the

dust generated by the joint compound during mixing and sanding. He also

breathed in a significant amount of that dust during those activities. During the

mixing process, the dust would come right back up in his face and he would

                                       12
breathe it. 5 Dorman said he “looked like Frosty the Snowman after finishing a

job.”

        Dorman testified that he did thousands of drywall jobs over his career.

Over that career, he used all the brands of joint compound “about the same.” 6

According to Dorman, when he used Kelly-Moore product, he breathed in the

dust the same as he would when he did jobs using other products. Dorman did

not know when he first started using Kelly-Moore joint compound, but he

stopped using it in the mid to late 1970s, after Kelly-Moore had removed

asbestos from its products.

        Dorman’s son Brady Smith worked with him from the late 1960s to the

1970s. He testified in his deposition that when he worked with his father, they

only used Kelly-Moore ready mixed product (so the only dust would be

generated from sanding and sweeping). According to Brady, they used Kelly-

Moore product on a “pretty regular basis,” but the amount could vary, and they

used it a little less than others because of the price.

        5
        Dorman used both quick and non quick set joint compound (one
creates dust when mixing, and the other is premixed so the only dust is from
sanding and sweeping). But in the beginning of his career, he “always mixed
it.”
        6
       When asked which product he used the most, Dorman answered, “All
of them,” and “[w]hatever was closest for me to get, that’s what I bought.”

                                       13
      According to Brady, he and his father spent the majority of their time

working in residential tract homes and apartment buildings; they spent about

10 percent of their work time on commercial projects. Brady estimated they

spent 10 percent of the work week sanding—and fifteen percent mixing and

sweeping—joint compound.      An average house they worked in would be a

three-bedroom, two-bath with about 1400 to 1800 square feet; the average

size of the bedrooms was about 10 x 10, the average size of the bathrooms 6

x 6, and the average size of the dining and living areas about 15 x 12. The

apartments they worked in were about 800 to 900 square feet with 10 x 10

bedrooms and 20 x 20 kitchen/living/dining combination areas.

Expert Testimony

      Dr. Ronald Dodson performed a tissue burden analysis on Dorman’s lung

tissue after he died. The Smiths provided deposition excerpts in which Dr.

Dodson testified that he found silica, talc, glass, and chrysotile fibers in

Dorman’s lung tissue. He could not tell when any of the chrysotile fibers were

deposited into the lung tissue. All of the chrysotile fibers he observed were

longer than what he would expect to find in the lungs of the general population,

i.e., those who had only had background exposure, and not occupational

exposure, to asbestos.

                                      14
      The Smiths also attached deposition excerpts from a defendant’s expert,

Patricia Hall, a certified industrial hygienist, in which she estimated that as a

“worst-case estimate,” Dorman had a total exposure to asbestos-containing

joint compounds of six years, 7 working with joint compound at least fifty

percent of the day, amounting to a total exposure of 9-15 fibers/cc year over

the course of his career. However, Hall disputed that this amount of exposure

correlates to any increased risk of mesothelioma if all of that exposure was to

chrysotile asbestos only.

      The Smiths further presented an affidavit and deposition testimony from

Dr. William Longo, who performed fiber release studies measuring the effects

of mixing, sanding, and sweeping up the dust from various joint compounds in

a laboratory setting. The dry powder Kelly-Moore product he tested contained

8% chrysotile. 8 Dr. Longo measured Kelly-Moore joint compound as emitting

an average of 1.2 fibers/cc for mixing, 1.6 fibers/cc for sanding, and 1.3

fibers/cc for sweeping. Thus, in a job in which Dorman mixed, sanded, and

      7
       Hall’s opinion was in the context of determining what Dorman’s
exposure to Sherwin Williams’s products might have been.
      8
       In answering the Smiths’ interrogatories, Kelly-Moore provided a chart
showing that its dry powder joint compounds contained between 0 and 8.3
percent chrysotile asbestos. But Dr. Longo points out in his affidavit that he
never tested a Kelly-Moore joint compound that contained zero or “a wide
range” of chrysotile.

                                       15
swept Kelly-Moore joint compound, he would have been exposed to an average

of 4.1 fibers/cc, which exceeds the 1976 OSHA recommended limit of 2

fibers/cc (this permissible exposure level (PEL) was further reduced by OSHA

in the 1990s to .1 fiber/cc for all asbestos fiber types). Dr. Longo also opined

that a real world exposure would have been higher because a person working

on a typical dry wall finishing project would use around 25 bags of mix and

sand an entire room as opposed to five linear feet sanded in Dr. Longo’s tests.

Conclusion

        Considering this evidence in the light most favorable to the Smiths, there

is at least a fact question as to how often Dorman used (and was therefore

exposed to) Kelly-Moore joint compound as opposed to other companies’ joint

compounds; because he testified that he used it “about the same” as any other,

it is possible to roughly estimate his total use of Kelly-Moore product as a

fraction of the total estimated use divided by the number of products he

allegedly used. Based on these facts, the Smiths at least raised a genuine issue

of material fact as to the aggregate dose of Kelly-Moore asbestos-containing

joint   compound     (and   total   asbestos   fibers)   to   which   Dorman   was

exposed. Accordingly, we conclude and hold that the Smiths raised a genuine

issue of material fact as to the Lohrmann factors (frequency, regularity, and

proximity). We must next determine whether they raised a genuine issue of

                                         16
material fact as to whether the total dose of chrysotile asbestos to which

Dorman was exposed exceeds a minimum dose above which mesothelioma

does not occur. See Borg-Warner, 232 S.W.3d at 770–73; Stephens, 239
S.W.3d at 312, 321.

    No Evidence of Minimum Dose of Chrysotile at Which Increased Risk
                   of Developing Mesothelioma Occurs

      Dr. Arnold Brody, a research scientist in lung biology and lung pathology,

averred in an affidavit that “[a]ll of the asbestos varieties have been shown to

cause genetic errors[,] and fibers less than five microns can bind DNA and thus

contribute to the development of genetic damage. . . . Exposure to asbestos

fibers of all types and lengths should be considered in assessing a person’s risk

of developing mesothelioma.”     However, he did not opine as to how much

asbestos Dorman had been exposed to or what a minimum exposure at which

a person’s risk of mesothelioma increases might be. Thus, his opinion only

goes to general causation. See Havner, 953 S.W.2d at 714; Stephens, 239
S.W.3d at 308.

      Another of the Smiths’ experts, Dr. John Maddox, who is board certified

in anatomical and clinical pathology and hematology, concluded that Dorman

breathed substantial amounts of dust from the products of each of the

defendants and that these exposures were a substantial contributing factor in

                                       17
the development of his mesothelioma. According to Dr. Maddox, “[b]ecause

asbestos dust is so strongly associated with mesothelioma, proof of significant

exposure to asbestos dust is proof of specific causation.” Dr. Maddox opined

that it is generally accepted in the scientific community that there is no

minimum level of exposure to asbestos “above background levels” below which

adverse effects do not occur. In fact, he stated that “[a]ttempts to define any

such a minimum level of exposure above background levels of asbestos have

been dismissed as ‘logical nonsense.’” 9 He estimated a mean background level

at .0003 to .0004 fibers/cc, which is well below Dorman’s estimated total

exposure. See, supra, Conclusion.

      According to Dr. Maddox, “[t]he overwhelming world scientific consensus

is that dust from all three commercial types of asbestos - amosite, crocidolite

and chrysotile - are all capable of causing diffuse mesothelioma.” However, the

literature upon which Dr. Maddox relied is inconclusive regarding the effect of

exposure to only chrysotile fibers; while studies have shown increased risks of

mesothelioma in chrysotile miners and millers and in people living in chrysotile

mining areas, researchers have hypothesized that this may be because the

      9
       Dr. Maddox opined that “while there is no known safe level of
exposure to asbestos that will protect against mesothelioma, it is generally
accepted that there is such a threshold for asbestosis.”

                                      18
chrysotile was mixed with other types of fibers. 10 Additionally, the studies

showing an increased incidence of mesothelioma in these populations did not

attempt to extrapolate any minimum dose of chrysotile to which these

populations were exposed. Most of the studies agree that amphibole fibers are

considered   more    potent   than   chrysotile   fibers   in   terms   of   causing

mesothelioma.11 Moreover, at least one study notes that mesothelioma is rare,

even among populations exposed only to chrysotile. 12

      10
        And one study noted, “In some studies . . . workers exposed to only
chrysotile asbestos have shown no increased risk of lung cancer . . . . As a
consequence, researchers have implicated not chrysotile per se but a
contaminant amphibole fiber as the specific cause of lung cancer . . . and
malignant mesothelioma.”
      11
          One study found the risk of mesothelioma to be 1:100:500 for
chrysotile, amosite, and crocidolite, respectively. Patricia Hall stated in her
deposition testimony that her “understanding of the literature is that chrysotile
asbestos is not associated with an increased risk of mesothelioma unless the
dose, the cumulative dose, is so massive as to be able to cause asbestosis. So
we’re looking at high numbers. . . . There are . . . some numbers that are
presented in the literature that the . . . dose of chrysotile to produce asbestosis
is in the range of 100 to 200 fiber years. So it takes a sufficient dose in order
to be able to cause asbestosis with just a chrysotile exposure. It takes a
significant dose.” Dr. Dodson acknowledged in his deposition that some
scientists believe that amphiboles and chrysotile are equally potent, but others
believe amphiboles are more potent than chrysotile. He agreed that it would be
reasonable to say that most scientists and researchers would opine and do
opine in the peer-reviewed literature that amphiboles are more potent than
chrysotile.
      12
         Another study indicates that environmental exposure to abestos is
also associated with mesothelioma.

                                        19
      Dr. Maddox cited OSHA regulations for the proposition that chrysotile is

capable of causing mesothelioma. Current OSHA PELs for all fiber types are .1

fiber/cc; Dorman’s estimated exposure clearly exceeded those levels. However,

even the comments to the OSHA guidelines acknowledge that chrysotile studies

are inconclusive as to what level of chrysotile creates an elevated risk of

mesothelioma but nevertheless conclude that the PEL for chrysotile should be

the same as for all other fiber types because asbestos is so dangerous and

clearly has adverse effects. 13

      To support his opinion that Dorman’s exposure to chrysotile was a

substantial factor in causing his mesothelioma, Dr. Maddox points specifically

to a study that found a proportionate mortality ratio of 2.03 for mesothelioma

deaths among plasterers in England. According to Dr. Maddox, the plasterers

were “individuals who used joint compounds that contained chrysotile

asbestos.” But the copy of the study attached to his affidavit does not mention

the nature of the work done by the plasterers, nor does it differentiate among

      13
         The regulations note that “although there is some evidence linking
chrysotile to a lower mesothelioma rate than some amphibole fiber types, OSHA
believes that there is insufficient evidence to show that chrysotile does not
present a significant mesothelioma risk to exposed employees.” 29 C.F.R. Part
1910, Occupational Exposure to Asbestos: Final Rule (Aug. 10, 1994).
Exposure above the OSHA levels cannot be used as evidence of negligence per
se, however. See McClure v. Denham, 162 S.W.3d 346, 353 (Tex. App.—Fort
Worth 2005, no pet.).

                                      20
asbestos fibers.   Because there is insufficient information to compare the

exposure or dose levels of the plasterers to Dorman’s, this study cannot be

relied on as statistically significant in determining specific causation of

Dorman’s mesothelioma. See Borg-Warner, 232 S.W.3d at 771–72.

      The Smiths rely on several specific studies in their reply brief, arguing that

they provide at least a scintilla of evidence as to the minimum threshold value

required by Borg-Warner. The Selikoff studies measured the potential amount

of fibers to which a worker using joint compound in the same manner as

Dorman would have been exposed, but those studies did not “attempt to

correlate the exposures to any incidence of mesothelioma or asbestos-related

disease among the study subjects.” See Stephens, 239 S.W.3d at 317. And

a study by Iwatsubo showing a four-fold increase of mesothelioma at an

exposure level of .5 fibers/cc, and a study by Rodelsperger showing a 7.9 odds

ratio of an increased risk of mesothelioma at cumulative exposures between 0.0

and .15 fibers/cc year, both fail to provide the minimum dose evidence required

under Borg-Warner: neither study differentiates among fiber types.

      Dr. Maddox further relies on the results of “molecular biological studies,

animal experiments, epidemiological studies, case reports, and asbestos tissue

burden studies.”     Specifically, he notes that in one study, “151 human

malignant diffuse mesothelioma cases were identified and characterized by

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high-resolution analytical electron microscopy.     Chrysotile alone, with no

amphiboles, was found in the lungs in over 23% of the cases. In those cases

where the mesothelioma only was examined, 77% contained only chrysotile.”

Although this example clearly shows that chrysotile is capable of causing

mesothelioma, as evidenced by its presence in the decedents’ lung tissue, there

is no indication in the literature as to the approximate dose of chrysotile that

the studied decedents were exposed to. Thus, this study cannot be relied on

to show specific causation as to Dorman. See Borg-Warner, 232 S.W.3d at

771–72.    Moreover, there is no evidence of any attempt to correlate the

dosages in the animal studies to an approximate exposure level in humans, and

none of the epidemiological studies show a minimum threshold of chrysotile

exposure from which to measure whether Dorman had an elevated risk of

mesothelioma.

      It appears well-established in the scientific literature presented by the

Smiths that there is a threshold dose above which a person has an elevated risk

of developing asbestosis from chrysotile-only exposure. But that same evidence

does not support a minimum threshold dose for chrysotile only exposure that

would increase one’s risk of developing mesothelioma. Some of these same

studies upon which Dr. Maddox relies are the ones examined and found lacking

in Stephens. See 239 S.W.3d at 316. Thus, even though the Smiths raised

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a fact issue as to the Lohrmann factors (whereas evidence as to those factors

was lacking in Stephens), the Smiths’ evidence ultimately suffers the same

defect as the plaintiff’s in Stephens: “[w]ithout . . . scientific evidence of the

minimum exposure level leading to an increased risk of development of

mesothelioma” from exposure to chrysotile-only asbestos, such as that

contained in Kelly-Moore’s joint compound, Dr. Maddox’s opinion lacks “the

factual and scientific foundation required by Borg-Warner” and, thus, is

insufficient to raise a fact issue as to specific causation.    Id. at 321.   We

therefore must overrule the Smiths’ sole issue.

                                   Conclusion

      Having overruled the Smiths’ sole issue, we affirm the trial court’s

judgment.

                                            TERRIE LIVINGSTON
                                            JUSTICE

PANEL: LIVINGSTON, MCCOY, and MEIER, JJ.

DELIVERED: February 25, 2010

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