rosemary-smith-brady-smith-and-donna-hubbard-individually-and-as ( 2010 )

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
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FROM THE 153RD DISTRICT COURT OF TARRANT COUNTY
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OPINION
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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
21
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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