“Undoubtedly, the most useful and conclusive type of evidence in a case such as this is epidemiological studies.”
How later courts described this case
- “Undoubtedly, the most useful and conclusive type of evidence in a case such as this is epidemiological studies.”
- The general causation standard concerns “whether a substance is capable of causing a particular injury or condition in the general population”
- “Dr. Jenkins offered no scientific support for his general theory that exposure to Toluene solution at any level would cause RADS.”
- regulatory “agencies’ threshold of proof is reasonably lower than that appropriate in tort law”
Written by the judges who cited it.
The opinion
REVISED JUNE 26, 2012
IN THE UNITED STATES COURT OF APPEALS
FOR THE FIFTH CIRCUIT United States Court of Appeals
Fifth Circuit
FILED
June 20, 2012
No. 11-50193 Lyle W. Cayce
Clerk
GREGORY SCOTT JOHNSON,
Plaintiff – Appellant,
v.
ARKEMA, INCORPORATED,
Defendant – Appellee.
Appeal from the United States District Court
for the Western District of Texas
Before REAVLEY, ELROD, and HAYNES, Circuit Judges.
PER CURIAM:
In this toxic tort case, we consider whether the district court erred in:
(1) excluding the opinions of Gregory Johnson’s expert witnesses on the element
of causation; and (2) granting summary judgment in favor of Arkema, Inc.
because Johnson was unable to prove causation without the opinions of his
excluded causation experts. We AFFIRM the district court’s judgment in all
respects except as to Johnson’s claims regarding his acute injuries, on which we
REVERSE and REMAND for further proceedings.
No. 11-50193
I.
Johnson worked as a machine repairman at Owens Illinois Inc.’s glass
bottling plant in Waco, Texas from May 1998 to the end of 2008. On two
separate occasions, first in early June 2007 and again on July 15, 2007, Johnson
was directed to perform work in close proximity to a device known as a C-4 Hood,
which was designed, manufactured, and installed by Arkema. C-4 Hoods are
utilized by Owens Illinois to apply a chemical known as Certincoat to the glass
bottles it produces as the bottles are transported along a conveyor belt.1
Certincoat is composed mostly of monobutyltin trichloride (MBTC), an
organometallic compound based on tin. Under the elevated temperatures of the
C-4 hoods, MBTC vaporizes and then decomposes when it contacts the glass
bottles on the conveyer belt. Hydrochloric acid (HCl) and tin oxide are
byproducts of MBTC. Arkema’s C-4 Hoods are designed to vacuum up and
capture any vapors that are not deposited on the glass bottles, thus preventing
the escape of MBTC, HCl and tin oxide into the workplace environment.
According to Johnson, the C-4 Hood he worked near on those two occasions in
the summer of 2007 failed to perform its proper preventative function, resulting
in his exposure to Certincoat and its chemical byproducts.
Specifically, Johnson alleges that within fifteen minutes of first
approaching the C-4 hood in early June 2007 he: (1) smelled a sweet, unique
chemical odor; (2) noticed chemical buildup on the conveyer belt; (3) developed
a sore throat; (4) felt burning and watery eyes; and (5) experienced chest pain
and breathing difficulty. Johnson nevertheless continued to work in these
conditions for approximately four to five hours and, thereafter, neither reported
the incident to his supervisor nor sought immediate medical attention. A few
days later, on June 9, 2007, Johnson’s family doctor diagnosed him with
1
Arkema is also the designer and manufacturer of Certincoat.
2
No. 11-50193
pneumonia. At his June 18, 2007 follow-up visit, Johnson reported that he “fe[lt]
a lot better” and his doctor concluded that he could return to work the following
day.
The next month, on July 15, 2007, Johnson was again instructed to work
near the C-4 Hood. While doing so for approximately two to three hours,
Johnson experienced the same symptoms that he felt during his first alleged
instance of Certincoat exposure. This time, however, Johnson reported the
incident to his supervisor and sought immediate medical attention at a local
emergency room.
On August 8, 2007, upon Johnson’s disclosure of the two exposure
incidents to his treating physician, Dr. Camille Hinojosa, Johnson was diagnosed
with chemical pneumonitis and advised to see a pulmonologist. According to
Johnson, his lung condition progressively worsened over the course of the years
following the exposure incidents, culminating in a diagnosis of severe restrictive
lung disease and pulmonary fibrosis.2
II.
On November 3, 2008, Johnson filed a personal injury lawsuit against
Arkema in the 60th Judicial District Court of Jefferson County, Texas, claiming
that Arkema’s C-4 Hood proximately caused his restrictive lung disease and
pulmonary fibrosis.3 Arkema removed the matter to the Eastern District of
Texas and, on April 30, 2009, this matter was transferred to the Western
District of Texas. In his complaint, Johnson raises theories of negligence and
strict liability based on Arkema’s design, manufacture, marketing, and
installation of its C-4 Hoods. Johnson seeks compensatory and punitive
2
Although Arkema disputes this diagnosis, the dispute is not material to the disposition
of this appeal.
3
Johnson’s brief defines pulmonary fibrosis as the “inflammation and progressive
fibrosis of the pulmonary alveolar walls”; it is “one of a family of related diseases called
interstitial lung diseases. All of these diseases can result in lung scarring.”
3
No. 11-50193
damages, including, but not limited to, compensation for past physical pain and
medical expenses.
Arkema filed motions to exclude the opinions of Dr. Richard Schlesinger,
Johnson’s expert toxicologist, and Dr. Charles Grodzin, Johnson’s expert
pulmonologist, under Federal Rule of Evidence 702 and the Supreme Court’s
decision in Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579 (1993). Arkema
also filed a motion for summary judgment, contending that Johnson was unable
to present scientifically reliable evidence establishing that exposure to the
chemicals in Certincoat can cause restrictive lung disease and pulmonary
fibrosis.
On December 16, 2010, the magistrate judge issued a report and
recommendation to the district court regarding Arkema’s Daubert motions. The
magistrate judge recommended: (1) excluding Dr. Schlesinger’s opinion, which
only addressed causation, as unreliable and irrelevant; and (2) limiting
Dr. Grodzin’s opinion so that he could only opine on the nature and extent—but
not the cause—of Johnson’s illness. The district court adopted the report and
recommendation and subsequently granted summary judgment in favor of
Arkema. The district court reasoned that summary judgment was appropriate
because—given the exclusion of Dr. Schlesinger’s opinion and the limitation of
Dr. Grodzin’s opinion—Johnson “ha[d] no evidence that any lung injury he
suffered [was] a result of his exposure to MBTC and/or HCl.” In so doing, the
district court rejected Johnson’s claim that the similar symptoms experienced
by his co-workers provided sufficient summary judgment evidence of causation:
The only thing presented with the summary judgment material
which was not presented to Magistrate Judge Manske is Plaintiff’s
evidence that other Owens employees suffered lung injuries similar
to his. However, an inspection of this evidence fails to reveal a
single employee who has suffered a permanent, or chronic, lung
injury after exposure to Arkema’s chemicals. While other employees
4
No. 11-50193
may have been exposed to the same chemicals, they suffered only
transitory symptoms which quickly resolved.
This appeal followed.
III.
The first issues we consider concern the district court’s evidentiary rulings
under Rule 702 and Daubert, which we review for abuse of discretion. Curtis v.
M&S Petroleum, Inc. 174 F.3d 661, 668 (5th Cir. 1999). “A trial court abuses its
discretion when its ruling is based on an erroneous view of the law or a clearly
erroneous assessment of the evidence.” Bocanegra v. Vicmar Servs., Inc., 320
F.3d 581, 584 (5th Cir. 2003). In conducting our review, “[w]e are mindful that
under Daubert and Fed. R. Evid. 702, a district court has broad discretion to
determine whether a body of evidence relied upon by an expert is sufficient to
support that expert’s opinion.” Knight v. Kirby Inland Marine Inc., 482 F.3d
347, 354 (5th Cir. 2007); see also Rider v. Sandoz Pharm. Corp., 295 F.3d 1194,
1197 (11th Cir. 2002) (“[J]udges have considerable leeway in both how to test the
reliability of evidence and determining whether such evidence is reliable.” (citing
Kumho Tire Co., Ltd. v. Carmichael, 526 U.S. 137, 151–53 (1999))).
The admissibility of expert testimony is governed by Federal Rule of
Evidence 702, which provides:
A witness who is qualified as an expert by knowledge, skill,
experience, training, or education may testify in the form of an
opinion or otherwise if:
(a) the expert’s scientific, technical, or other specialized knowledge
will help the trier of fact to understand the evidence or to determine
a fact in issue;
(b) the testimony is based on sufficient facts or data;
(c) the testimony is the product of reliable principles and methods;
and
5
No. 11-50193
(d) the expert has reliably applied the principles and methods to the
facts of the case.
Fed. R. Evid. 702.
In Daubert, the Supreme Court “explained that Rule 702 assigns to the
district judge a gatekeeping role to ensure that scientific testimony is both
reliable and relevant.” Curtis, 174 F.3d at 668 (citing Daubert, 509 U.S. at 597).
The reliability prong mandates that expert opinion “be grounded in the methods
and procedures of science and . . . be more than unsupported speculation or
subjective belief.” Id. (citing Daubert, 509 U.S. at 590); see also Moore v.
Ashland Chem., Inc., 151 F.3d 269, 276 (5th Cir. 1998) (en banc) (“[T]he party
seeking to have the district court admit expert testimony must demonstrate that
the expert’s findings and conclusions are based on the scientific method, and,
therefore, are reliable.”). The relevance prong requires the proponent to
demonstrate that the expert’s “reasoning or methodology can be properly applied
to the facts in issue.” Curtis, 174 F.3d at 668 (citing Daubert, 509 U.S. at
592–93).
Furthermore, courts consider the following non-exclusive list of factors
when conducting the reliability inquiry:
(1) whether the theory or technique has been tested; (2) whether the
theory or technique has been subjected to peer review and
publication; (3) the known or potential rate of error of the method
used and the existence and maintenance of standards controlling
the technique’s operation; and (4) whether the theory or method has
been generally accepted by the scientific community.
Id. at 668–69 (citing Daubert, 509 U.S. at 593–94). “The proponent need not
prove to the judge that the expert’s testimony is correct, but she must prove by
a preponderance of the evidence that the testimony is reliable.” Moore, 151 F.3d
at 276; see also Wells v. Smithkline Beecham Corp., 601 F.3d 375, 378 (5th Cir.
2010) (“Although there are ‘no certainties in science,’ the expert must present
6
No. 11-50193
conclusions ‘ground[ed] in the methods and procedures of science.’” (alteration
in original) (quoting Daubert, 509 U.S. at 590)).
A.
Johnson contends that the district court abused its discretion in excluding
Dr. Schlesinger’s expert opinion that MBTC and HCl4 can cause restrictive lung
disease and pulmonary fibrosis.5 The district court excluded Dr. Schlesinger’s
testimony after determining that: (1) Dr. Schlesinger could not cite to one
epidemiological or controlled study of humans indicating that exposure to MBTC
or HCl could cause restrictive lung disease and pulmonary fibrosis;
(2) Dr. Schlesinger relied, in part, on two animal studies that were highly
distinguishable from and not correlated to Johnson’s two instances of MBTC and
HCl exposure; and (3) the scientific literature is devoid of any data or peer-
reviewed articles indicating that exposure to MBTC or HCl will result in chronic
lung disease, and such a proposition is not generally accepted in the scientific
community. Johnson argues that the district court erred in so ruling because:
(1) MBTC and HCl are part of a toxicological class of chemicals labeled as
irritants that are known to potentially cause pulmonary fibrosis;
(2) Dr. Schlesinger based his opinion on reliable scientific data concerning MBTC
and HCl exposure—including animal studies, material safety data sheets, and
guidelines from regulatory and advisory bodies—that support his conclusions;
and (3) Dr. Schlesinger’s opinion is buttressed by the temporal connection
between Johnson’s exposure and illness. As set forth below, because we are
unable to conclude that the district court abused its broad discretion in
4
Although Certincoat also contains tin oxide, Dr. Schlesinger did not offer the opinion
that tin oxide can cause restrictive lung disease and pulmonary fibrosis.
5
Dr. Schlesinger has an extensive background in the field of inhalation toxicology and
is currently a professor in the Department of Biology and Health Sciences at Pace University.
In pursuing its Daubert motion, Arkema did not dispute Dr. Schlesinger’s qualifications as a
toxicologist.
7
No. 11-50193
performing its gatekeeping function under Daubert, we affirm the exclusion of
Dr. Schlesinger’s expert opinions.
1.
Johnson first claims that the district court erred in discounting
Dr. Schlesinger’s “class of chemicals” theory. Johnson asserts that
Dr. Schlesinger’s opinion is reliable because “MBTC and HCl are part of a group
of chemicals labeled by toxicologists as ‘strong irritants.’” According to Johnson,
this classification is significant because “[a]ll ‘strong irritants’ have the same
physiological effect when they contact biological tissue—production of
inflammation.” Moreover, numerous peer-reviewed studies of exposure to other
chemicals labeled as irritants—including chlorine, ammonia, and nitric acid
vapor—have reported lung scarring following acute exposure to those respective
irritants. Thus, although Dr. Schlesinger only relied on one MBTC and one HCl
study in forming his opinions, Johnson contends that Dr. Schlesinger’s
conclusions are reinforced by the more prevalent studies involving other
irritants.
Our review of Supreme Court and this circuit’s case law confirms that, in
forming a reliable opinion regarding the effects of exposure to a particular
chemical, an expert may extrapolate data from studies of similar chemicals. See
Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997) (“Trained experts commonly
extrapolate from existing data.”); Moore, 151 F.3d at 278–79. However, “[t]o
support a conclusion based on such reasoning, the extrapolation or leap from one
chemical to another must be reasonable and scientifically valid.” Moore, 151
F.3d at 279. Thus, courts are free to reject a theory based on extrapolation when
“there is simply too great an analytical gap between the data and the opinion
proffered.” Joiner, 522 U.S. at 146.
We applied the foregoing principles in our decision in Wells, 601 F.3d at
380. In that case, three experts relied on a study of a class of drugs known as
8
No. 11-50193
“dopamine agonists” in support of their conclusion that a specific drug within the
class, Requip, could have potentially caused the appellant’s compulsive gambling
problem.6 Id. We held that the district court did not abuse its discretion in
excluding the experts, in part, because they failed to bridge the analytical gap
between the generalized nature of the class-wide dopamine agonist study and
the specific characteristics of Requip, “a drug that functions differently than
other dopamine agonists.” Id.; cf. Knight, 482 F.3d at 350, 352–53 (exclusion of
expert who relied on studies of organic solvents was not an abuse of discretion,
in part, because of the expert’s failure to address how exposure to benzene, the
specific organic solvent at issue, could be correlated to those studies involving
exposure to other organic solvents in addition to benzene).
We also view the Tenth Circuit’s Rider decision as particularly instructive
in this case. 295 F.3d at 1200–02. In Rider, the experts relied on evidence that
drugs in a class known as “ergot alkaloids” caused vasoconstriction to support
the proposition that a specific drug within the class, bromocriptine, did so as
well. Id. at 1200–01. The Rider court first reiterated that, in Joiner, the
Supreme Court:
established the important test of analytical “fit” between the
methodology used and the conclusions drawn. . . . The [C]ourt
reasoned that just because a methodology is acceptable for some
purposes, it may not be acceptable for others, and a court may not
admit evidence when there is “simply too great an analytical gap
between the data and the opinion proffered.”
Id. at 1197 (quoting Joiner, 522 U.S. at 146). The court then affirmed the
exclusion of the experts because ergot alkaloids have diverse chemical
compositions and the experts failed to demonstrate that bromocriptine “should
have the same effects as other drugs in that class.” Id. at 1201–02.
6
A dopamine agonist is a drug “that stimulates the dopamine receptors in the brain to
alleviate symptoms of Parkinson’s [Disease].” Id. at 377.
9
No. 11-50193
In this case, we conclude that the district court did not abuse its discretion
in excluding Dr. Schlesinger’s “class of chemicals” theory. Dr. Schlesinger
opined that MBTC and HCl can cause pulmonary fibrosis because they are part
of a class of chemicals labeled as irritants:
It is generally accepted in the field of toxicology that both HCl
and MBTC belong to a class of chemicals known as irritants.
Toxicologically, all irritants have the same effect when they contact
biological tissue, namely production of inflamation.
...
It is an accepted fact that acute inhalation of irritants can result in
chronic diseases, including restrictive lung disease and pulmonary
fibrosis.
...
While all irritants produce inflammation, as described above,
respiratory irritants are different in their specific chemical structure.
These differences relate to toxic potency (the exposure concentration
needed to produce damage) and solubility (which affects the area of
the lung an inhaled irritant would be expected to reach). Exhibit A
#6. However, while chemicals within a class may differ in toxic
potency and solubility, the mechanism of toxicity is the same, as
described above. Therefore, if exposure to an irritant is of sufficient
concentration to cause inflammation, there are no other differences
among irritants in the same class in terms of capability to cause a
particular lung injury.
(Emphasis added). Dr. Schlesinger did not go further, however, and explain
how, based on any of the specific properties and toxicities of similar irritants
when compared with those of MBTC and HCl, Johnson’s exposure to MBTC and
HCl was at a sufficient concentration level to cause restrictive lung disease and
pulmonary fibrosis.7 See Moore, 151 F.3d at 278–79 (“Dr. Jenkins made no
attempt to explain his conclusion by asserting that the Toluene solution [to
7
Instead, Dr. Schlesinger’s opinion that the concentration levels of MBTC and HCl were
sufficient to cause lung damage was based on other scientific evidence deemed unreliable by
the district court, discussed infra at III.2–3.
10
No. 11-50193
which plaintiff was exposed] had properties similar to another chemical exposure
to which [reactive airway dysfunction syndrome, or (RADS)] had been
scientifically linked.”); see also Mitchell v. Gencorp. Inc., 165 F.3d 778, 782 (10th
Cir. 1999) (although the “record contain[ed] some testimony about the
similarities between benzene and [d]efendant’s products,” there was no
“additional testimony explaining exactly what these similarities [were] and how
the similarities cause[d] the human body to respond to [d]efendant’s chemicals
in a manner similar to benzene”). Put differently, save for highlighting their
shared classifications as irritants, Dr. Schlesinger did not attempt to explain any
direct correlation or “fit” between the chemicals in Certincoat and the known
scientific data concerning exposure to, for example, chlorine, ammonia, or nitric
acid vapor. Accordingly, given the diverse chemical structures and toxicities of
irritants, which Dr. Schlesinger acknowledged,8 we hold that the district court
did not abuse its discretion in concluding that Dr. Schlesinger’s “class of
chemicals” theory presented “too great an analytical gap between the data and
the opinion proffered.”9 Joiner, 522 U.S. at 146.
2.
Johnson next asserts that reliable and relevant scientific data concerning
exposure to HCl supports Dr. Schlesinger’s conclusion that HCl causes scarring
to lung tissue. Johnson first points to the material safety data sheet (MSDS)
issued by Airgas, Inc., a company wholly unrelated to Arkema, which warns that
8
One of the articles Dr. Schlesinger submitted with his report also implicitly addressed
the diverse characteristics of irritants, providing that “[t]he health effects of an acute exposure
to an irritant gas or vapor are dependent on the physiochemical properties of that particular
gas or vapor, as well as specific host factors.” (Emphasis added).
9
This outcome may have been different had Dr. Schlesinger presented other reliable
scientific evidence to support his causation opinion. For instance, if Dr. Schlesinger had other
reliable evidence demonstrating that the concentration levels of MBTC and HCl were
sufficiently high to impair respiratory function, then the analytical leap found in his “class of
chemicals” theory could potentially have been reduced to a mere step, rendering
Dr. Schlesinger’s opinion reliable.
11
No. 11-50193
HCl can be “severely corrosive to the respiratory system.” The district court
found the warning irrelevant and unreliable because: (1) “the Airgas MSDS does
not state that exposure to HCl can cause severe restrictive lung disease and
pulmonary fibrosis”; and (2) “most importantly,” Johnson did not provide “any
science behind the MSDS,” such as “the duration or concentration of exposure
needed to produce the noted effects” or the scientific literature “relied upon by
Airgas for the statements contained in the MSDS.”
We conclude that the district court did not abuse its discretion in
disregarding the Airgas MSDS. Dr. Schlesinger failed to come forth with any
scientific data to support the MSDS’s warning. He also acknowledged that there
is scant scientific evidence of a “cause-and-effect relationship between
hydrochloric acid and restrictive lung disease.” Under such circumstances, the
Airgas MSDS, standing alone, need not have been accorded any weight. See
Moore, 151 F.3d at 278 (stating that the district court did not abuse its discretion
in finding a MSDS unreliable in part because the expert “did not know what
tests Dow [Corning] had conducted in generating the MSDS”).
Johnson next cites a 1993 study of HCl’s effect on nine baboons who were
exposed “for fifteen minutes to three concentrations (500 ppm, 5,000 ppm, and
10,000 ppm) of HCl for a one year period.”10 The study found that one of the nine
baboons developed fibrosis after being exposed to a 10,000 ppm concentration of
HCl. It ultimately concluded that HCl inhalation did not result in “the
development of impaired respiratory/pulmonary function, except at the highest
concentration.” Although Johnson was only exposed to a ten to fifty ppm
concentration of HCl, Johnson claims that the baboon study is reliable and
relevant because: (1) Johnson was exposed to HCl for a much longer time period
than the baboon who developed fibrosis; (2) baboons are considered to be an
10
The acronym “ppm” stands for “parts per million.”
12
No. 11-50193
animal species that is a surrogate of man; and (3) the study shows that HCl is
capable of causing fibrosis.
We have previously recognized the “‘very limited usefulness of animal
studies when confronted with questions of toxicity.’” Allen v. Pa. Eng’g Corp.,
102 F.3d 194, 197 (5th Cir. 1996) (quoting Brock v. Merrell Dow Pharm., 874
F.2d 307, 313 (5th Cir. 1989)). Accordingly, “studies of the effects of chemicals
on animals must be carefully qualified in order to have explanatory potential for
human beings.”11 Id. Here, the district court found the baboon study unreliable
and irrelevant because Dr. Schlesinger did not even attempt to show that there
was a “correlation between the duration and length of the baboon exposure and
Mr. Johnson’s exposure.” Likewise, Dr. Schlesinger admitted that the
respiratory tracts of humans are “pretty unique,” further diminishing the
significance of the baboon study. Finally, Johnson’s reliance upon the baboon
study was weakened by the fact that there are no other studies of baboons or
other animals that corroborate the baboon study’s conclusions. See id. In light
of Allen’s “careful qualification” requirement, we conclude that the district court
did not abuse its discretion in rejecting the baboon study. See also Joiner, 522
U.S. at 144–45 (finding that the court did not abuse its discretion in rejecting the
experts’ reliance on animal studies—which involved the injection of “massive
doses” of certain chemicals into infant mice—because the “studies were so
dissimilar to the facts presented in th[e] litigation”); cf. Gulf S. Insulation v. U.S.
Consumer Prod. Safety Comm’n, 701 F.2d 1137, 1146 (5th Cir. 1983) (finding a
rat study inconclusive because of the small number of rats tested, the high
11
In Allen, we concluded that a study’s finding that ethylene oxide (EtO) caused cancer
in rats provided “at best speculative support” for the conclusion that EtO could cause cancer
in humans because a different study of mice produced no such results. Id. In explaining our
conclusion, we adopted the following logic of the appellee’s expert: “Thus, the lack of capacity
for the F-344 rat to predict how even the mouse model responds necessarily undercuts
confidence that the rat will predict accurately how other species including humans will respond
[to EtO exposure].” Id.
13
No. 11-50193
dosages given to the rats, and difficulty in extrapolating those results to
humans).
Finally, Johnson contends that he was exposed to amounts of HCl that
were between two and ten times the permissible exposure levels set by the
Occupational Safety and Health Administration (OSHA) and the National
Institute for Occupational Safety and Health (NIOSH). Johnson also references
the Acute Exposure Guideline Levels set by the National Research Council
(NRC), which provide that Johnson could have been exposed to a “disabling” and
possibly “lethal” dose of HCl.
In Allen, we addressed the significance of guidelines promulgated by
regulatory and advisory bodies:
Regulatory and advisory bodies such as IARC, OSHA and EPA
utilize a “weight of the evidence” method to assess the
carcinogenicity of various substances in human beings and suggest
or make prophylactic rules governing human exposure. This
methodology results from the preventive perspective that the
agencies adopt in order to reduce public exposure to harmful
substances. The agencies’ threshold of proof is reasonably lower
than that appropriate in tort law, which “traditionally make[s] more
particularized inquiries into cause and effect” and requires a
plaintiff to prove “that it is more likely than not that another
individual has caused him or her harm.”
Allen, 102 F.3d at 198 (emphasis added) (quoting Wright v. Willamette
Industries, Inc., 91 F.3d 1105, 1107 (8th Cir.1996)). Thus, Allen demonstrates
that chemical guidelines are not necessarily reliable in all toxic tort cases. It
may be appropriate first to consult the underlying basis for their proscriptions
before an expert’s reliance on them can pass Daubert muster.
As with the Airgas MSDS, however, Johnson once again does not provide
any scientific data or literature to explain how or why the various exposure
limits and guidelines were established for HCl. Similarly, Johnson does not
argue that the guidelines and exposure limits exist to protect people from
14
No. 11-50193
developing severe restrictive lung disease and pulmonary fibrosis. Thus, we
conclude that the OSHA, NIOSH, and NRC guidelines and exposure limits,
standing alone, are insufficient to demonstrate abuse of discretion on the part
of the district court. See also id. at 195–96 (“[U]nder the circumstances of this
case, the fact that EtO has been classified as a carcinogen by agencies
responsible for public health regulations is not probative of the question whether
Allen’s brain cancer was caused by EtO exposure.”).
In sum, the Airgas MSDS, baboon study, and OSHA, NIOSH, and NRC
guidelines do not sufficiently support Johnson’s theory that HCl is known to
cause scarring to lung tissue.12 The district court did not abuse its discretion in
dismissing this data as irrelevant and unreliable under Daubert.
3.
Johnson also argues that reliable and relevant scientific data concerning
exposure to MBTC supports Dr. Schlesinger’s conclusion that MBTC causes
scarring to lung tissue. Johnson first references Arkema’s MSDS, which
explains that MBTC “CAUSES RESPIRATORY TRACT IRRITATION” and that:
Inhalation and skin contact are expected to be the primary routes
of occupational exposure to this material. Based on single exposure
animal tests, it is considered to be slightly toxic if swallowed and
corrosive to eyes and skin. If swallowed, this material may cause
severe internal injury, characterized by pain in the mouth, throat
and stomach, vomiting and breathing difficulties.
12
Johnson also notes that Arkema’s own expert acknowledged that HCl, if inhaled, may
cause “acute lung injury or chronic persistent pulmonary function abnormalities,” including
“upper airway edema and burns, hypoxia, stridor, pneumonitis and tracheobronchitis.” This
admission does not indicate, however, the duration or concentration of HCl exposure that is
necessary to cause such ailments. Furthermore, the expert’s admission does not demonstrate
that HCl can cause severe restrictive lung disease or pulmonary fibrosis. Finally, assuming
it exists, Johnson does not provide any of the underlying data Arkema’s expert may have relied
on in forming an opinion regarding the potential dangers associated with HCl exposure. The
district court acted within its discretion in discounting this admission as it relates to
Dr. Schlesinger’s opinions.
15
No. 11-50193
Johnson relies on our decision in Curtis, 174 F.3d at 669, for the proposition that
Arkema’s MSDS constitutes scientifically reliable evidence supporting
Dr. Schlesinger’s causation opinion.13
Johnson’s reliance on Curtis is unavailing. In Curtis, we merely found
that a MSDS was reliable because it was consistent with a wealth of other
reliable information (including a detailed Supreme Court discussion) regarding
the potential hazards associated with benzene exposure.14 Id. at 669–70. There
is, however, nothing in Curtis indicating that material safety data sheets
constitute per se reliable support for an expert’s opinion. To the contrary, in
exercising its discretion as a gatekeeper, a court may refrain from treating a
MSDS as reliable until it is presented with scientific evidence justifying the
relevant statements found within the MSDS. See Moore, 151 F.3d at 278
(district court did not abuse its discretion in finding a MSDS unreliable in part
because the expert “did not know what tests Dow had conducted in generating
the MSDS”).
Moreover, the district court did not abuse its discretion in rejecting the
only evidence underlying Arkema’s MSDS, namely, one unpublished study
performed by Arkema in 1988 concerning MBTC’s effect on rats. The study was
designed to assess the toxic effects of MBTC when administered by inhalation
to rats for six hours per day, five days per week, for four weeks at target
concentrations of one, ten, and thirty milligrams per cubic meter. The study did
not make any conclusions regarding restrictive lung disease and pulmonary
13
Johnson also offers a temporal proximity argument, stating that Johnson’s initial
symptoms after his exposure to Certincoat were in accord with the warnings in Arkema’s
MSDS. This temporal proximity issue is addressed in III.4, infra.
14
We also note that the MSDS did not play an important role in Curtis as the defendant
“d[id] not seriously challenge” the expert’s conclusion that “exposure to benzene at levels of
200-300 ppm would cause the injuries suffered by Plaintiffs.” Id. at 670. Instead, the primary
dispute was over a matter wholly unrelated to the MSDS: whether the expert had shown that
the plaintiffs were actually exposed to 200-300 ppm levels of benzene. Id. at 670–72.
16
No. 11-50193
fibrosis, and instead only found that exposure to MBTC had a discernable effect
on the lung tissue of rats.15 The district court determined that the rat study was
irrelevant and unreliable because Dr. Schlesinger admitted that “there is no
correlation between the durations of exposure” experienced by the rats, on the
one hand, and Johnson, on the other. Based on Allen’s requirement that animal
studies be “carefully qualified in order to have explanatory potential for human
beings,” we conclude that the district court did not abuse its discretion in
discounting this rat study.16 Allen, 102 F.3d at 197. It follows that the district
court did not abuse its discretion in discounting Arkema’s MSDS because its
warnings were founded on the rat study.
Johnson also raises the fact that he was exposed to a concentration level
of MBTC that was between 100 and 500 times OSHA’s permissible MBTC
exposure limit of .1 milligrams per cubic meter. The district court was
unpersuaded by the sheer magnitude of, according to OSHA’s exposure limit,
Johnson’s over-exposure to MBTC. It found the maximum exposure limit
misleading because OSHA set the .1 milligram per cubic meter threshold for all
15
Specifically, the study concluded that:
Grossly, the incidence of lung discoloration was increased in exposed males and
females. Microscopically, amorphous material, (perhaps the test material or
monobutyltin dihydroxy chloride, the hydrolysis product of monobutyltin
trichloride) and alveolar edema were evident in the lungs of exposed males and
females. Other lung changes which occurred with increased incidence and
severity in the exposed groups included peribronchial lymphoid cell
accumulation and perivascular lymphoid cell infiltrate, extravasated erthrocytes
(males only), and accumulation of alveolar macrophanges. Dose related
responses were shown only by alveolar edema in both sexes and by alveolar
erthrocytes in males only.
16
Johnson was exposed to between ten and fifty milligrams per cubic meter of MBTC.
Johnson was, therefore, exposed to amounts of MBTC that were similar in concentration but
not duration to the amounts of MBTC involved in the rat study. Nevertheless, Dr. Schlesinger
could not adequately explain, as required by Allen, why MBTC’s effect on the rats provides a
reliable scientific basis for the conclusion that MBTC can cause restrictive lung disease and
pulmonary fibrosis in human beings.
17
No. 11-50193
organotins, not just MBTC. Critically, Dr. Schlesinger conceded that this
threshold for organotin exposure was “clear[ly]” not set based on data relating
specifically to MBTC. Instead, according to Dr. Schlesinger, the OSHA threshold
would be “based on whichever [organotin] they had the most data on in terms of
inhalation.” Dr. Schlesinger also conceded that some organotin compounds are
more toxic than others. Given Dr. Schlesinger’s concessions, we conclude that
the district court did not abuse its discretion in refusing to treat the OSHA
exposure limit as reliable scientific evidence. See Allen, 102 F.3d at 198
(regulatory “agencies’ threshold of proof is reasonably lower than that
appropriate in tort law”).
Accordingly, we hold that Arkema’s MSDS, the rat study, and OSHA’s
guidelines do not sufficiently support Johnson’s theory that MBTC is known to
cause scarring to lung tissue. The district court did not abuse his discretion in
dismissing this data as irrelevant and unreliable under Daubert.
4.
Finally, Johnson contends that the strong temporal connection between
Johnson’s exposure to Certincoat and subsequent lung injury supports
Dr. Schlesinger’s causation conclusion. Johnson states that he “has never
smoked and, prior to July 2007, had never suffered a lung injury, never been
diagnosed with asthma, never been exposed to a dangerous level of any other
toxic chemical, and had no history of lung disease or breathing difficulties.”
Moreover, “Johnson had worked in the same plant for over nine years without
incident prior to the installation of Arkema’s new chemical hoods in June 2007.”
In Curtis, we explained that “temporal connection standing alone is
entitled to little weight in determining causation.” Curtis, 174 F.3d at 670.
“However, a temporal connection is entitled to greater weight when there is an
established scientific connection between exposure and illness or other
circumstantial evidence supporting the causal link.” Id.
18
No. 11-50193
Our foregoing discussion indicates that there is neither an established
scientific connection between exposure to Certincoat and subsequent lung
disease nor sufficient circumstantial evidence to indicate a causal link between
the same. Therefore, under Curtis, the district court acted well within its
discretion in according little weight to the temporal connection theory alleged by
Johnson.
5.
In conclusion, we hold that the district court did not abuse its discretion
in excluding Dr. Schlesinger’s expert opinion under Daubert. Dr. Schlesinger
could not cite to one epidemiological or controlled study of humans indicating
that exposure to MBTC or HCl could cause restrictive lung disease and
pulmonary fibrosis. See Allen, 102 F.3d at 197 (“Undoubtedly, the most useful
and conclusive type of evidence in a case such as this is epidemiological
studies.”). Also, Dr. Schlesinger neither extrapolated from existing data
concerning chemicals similar to those in Certincoat nor correlated existing
animal studies to Johnson’s two exposure episodes. Instead, he relied on blanket
statements from presumably credible sources—such as material safety data
sheets and advisory guidelines—but failed to present the scientific evidence
upon which those statements were founded. Cf. Joiner, 522 U.S. at 146
(“[N]othing in either Daubert or the Federal Rules of Evidence requires a district
court to admit opinion evidence that is connected to existing data only by the
ipse dixit of the expert.”). Finally, Dr. Schlesinger did not offer evidence that his
theory has been generally accepted by the scientific community. The district
court’s exclusion of Dr. Schlesinger’s expert opinion is affirmed.
B.
Johnson next contests the district court’s limitation of Dr. Grodzin’s
opinion, which prevented Dr. Grodzin from expressing his conclusion that MBTC
19
No. 11-50193
and HCl17 caused Johnson’s lung disease.18 In reaching his causation conclusion,
Dr. Grodzin’s research and analysis essentially mirrored Dr. Schlesinger’s save
for one key distinction: Dr. Grodzin performed a “differential diagnosis” of
Johnson. Accordingly, we need only consider whether, given the existence of
Dr. Grodzin’s differential diagnosis, the district court’s exclusion of Dr. Grodzin’s
opinion constitutes the abuse of discretion.19
As the Fourth Circuit has observed:
A reliable differential diagnosis typically, though not invariably, is
performed after “physical examinations, the taking of medical
histories, and the review of clinical tests, including laboratory tests,”
and generally is accomplished by determining the possible causes
for the patient’s symptoms and then eliminating each of these
potential causes until reaching one that cannot be ruled out or
determining which of those that cannot be excluded is the most
likely.
Westberry v. Gislaved Gummi AB, 178 F.3d 257, 262 (4th Cir. 1999) (quoting
Kannankeril v. Terminix Int’l, Inc., 128 F.3d 802, 807 (3d Cir. 1997)). Many
17
Like Dr. Schlesinger, Dr. Grodzin’s opinion did not address whether tin oxide caused
Johnson’s lung disease.
18
Dr. Grodzin currently serves as the Medical Director for the Denton Medical Services
Pulmonary Rehabilitation Center. Arkema does not challenge Dr. Grodzin’s credentials.
We also note that Johnson sought to admit Dr. Grodzin as an expert so that Dr. Grodzin
could offer his medical diagnosis that Johnson suffers from “interstitial lung disease resulting
in a severe restrictive condition, and pulmonary fibrosis.” The district court ruled that this
portion of Dr. Grodzin’s opinion satisfied Daubert’s requirements and was, therefore,
admissible. Johnson’s appeal only relates to the district court’s exclusion of Dr. Grodzin’s
opinion regarding the cause of Johnson’s lung disease.
19
At the Daubert hearing, Johnson informed the magistrate judge that Dr. Grodzin’s
opinion was derivative of Dr. Schlesinger’s opinion with the exception of Dr. Grodzin’s
differential diagnosis analysis. Accordingly, we need not restate our conclusions in III.A.,
supra, here.
Dr. Grodzin also considered scientific evidence indicating that a prescription drug called
Bleomycin can cause pulmonary fibrosis and argued that this evidence supported a similar
finding with regard to MBTC and HCl. This theory fails for the reasons stated in III.A.1.,
supra.
20
No. 11-50193
courts have found that a properly performed differential diagnosis can yield a
reliable expert opinion. See id. at 262–63.
However, the results of a differential diagnosis are far from reliable per se.
In Moore, for example, after conducting a differential diagnosis, the expert
diagnosed the plaintiff with RADS. Moore, 151 F.3d at 273; See also id. at
288–90 (Dennis, J., dissenting) (noting that the expert had conducted a
differential diagnosis of the plaintiff). The expert also concluded that the
plaintiff’s RADS was caused by certain chemicals to which the plaintiff was
exposed based on his analysis of MSDS warnings, his examination and testing
of the plaintiff, and the close temporal proximity between the plaintiff’s exposure
and subsequent injury. Id. Despite the expert’s differential diagnosis, we held
that the district judge did not abuse its discretion in excluding the expert’s
causation testimony because he failed to present reliable scientific support
showing that the chemicals at issue could actually cause RADS. Id. at 278–79.
Furthermore, Moore illustrates that an expert may not rely on a
differential diagnosis to circumvent the requirement of general causation. See
id. at 278 (“Dr. Jenkins offered no scientific support for his general theory that
exposure to Toluene solution at any level would cause RADS.”); see also Curtis,
174 F.3d at 669–70; Goebel v. Denver & Rio Grande W. R.R. Co., 346 F.3d 987,
999 (10th Cir. 2003) (A district court “can admit a differential diagnosis that it
concludes is reliable if general causation has been established”). As we explained
in Knight:
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. Evidence concerning specific causation in toxic
tort cases is admissible only as a follow-up to admissible
general-causation evidence. Thus, there is a two-step process in
examining the admissibility of causation evidence in toxic tort cases.
First, the district court must determine whether there is general
21
No. 11-50193
causation. Second, if it concludes that there is admissible
general-causation evidence, the district court must determine
whether there is admissible specific-causation evidence.
Knight, 482 F.3d at 351 (internal quotation marks and citations omitted). Thus,
before courts can admit an expert’s differential diagnosis, which, by its nature,
only addresses the issue of specific causation, the expert must first demonstrate
that the chemical at issue is actually capable of harming individuals in the
general population, thereby satisfying the general causation standard. See id.
Here, like in Moore, Dr. Grodzin’s differential diagnosis is based on the
presumption that MBTC and HCl are actually capable of causing restrictive lung
disease and pulmonary fibrosis in the general population. Dr. Grodzin has not
presented any reliable or relevant scientific evidence to bolster this presumption.
Instead, Dr. Grodzin essentially relied on the same scientific evidence and
reached the same conclusions as Dr. Schlesinger. As we have explained, the
district court did not abuse its discretion in excluding Dr. Schlesinger’s opinion,
thus negating Dr. Schlesinger’s ability to satisfy the general causation
requirement. Consequently, the fact that Dr. Grodzin conducted a differential
diagnosis does not save his opinion from the same fate as Dr. Schlesinger’s
opinion. Cf. Curtis, 174 F.3d at 670 (“[S]cientific knowledge of the harmful level
of exposure to a chemical, plus knowledge that the plaintiff was exposed to such
quantities, are minimal facts necessary to sustain the plaintiffs’ burden in a
toxic tort case.” (emphasis added) (quoting Allen, 102 F.3d at 199)). The district
court did not abuse its discretion in excluding Dr. Grodzin’s causation opinion
because, irrespective of the differential diagnosis, Dr. Grodzin is unable to
satisfy the general causation requirement.
IV.
After excluding the causation opinions of Dr. Schlesinger and Dr. Grodzin,
the district court granted Arkema’s motion for summary judgment because
22
No. 11-50193
Johnson could not “prove the causation necessary to support a claim under Texas
law.” Johnson alleges that the district court erred in granting Arkema’s motion
for summary judgment because: (1) there is a strong temporal connection
supporting causation; (2) the symptoms experienced by other Owens Illinois’
employees provide additional circumstantial evidence of causation; and
(3) Arkema’s expert pulmonologist conceded that tin oxide is known to cause
scarring of the lung tissues.20
This court reviews a summary judgment de novo, applying the same
standard as the district court. Trinity Universal Ins. Co. v. Emp’rs. Mut. Cas.
Co., 592 F.3d 687, 690 (5th Cir. 2010). “Summary judgment should be affirmed
if, viewing the evidence in the light most favorable to the non-moving party,
there is no genuine dispute as to any material fact and the movant is entitled to
judgment as a matter of law.” Access Mediquip L.L.C. v. UnitedHealthcare Ins.
Co., 662 F.3d 376, 378 (5th Cir. 2011) (citations and internal quotation marks
omitted). Summary judgment must be entered “against a party who fails to
make a showing sufficient to establish the existence of an element essential to
that party’s case, and on which that party will bear the burden of proof at trial.”
Celotex Corp. v. Catrett, 477 U.S. 317, 322 (1986).
A.
Johnson first argues that the strong temporal connection between his
exposure to Certincoat and the onset of his symptoms offsets the need to present
expert testimony to establish causation. Johnson relies on the Supreme Court
20
In one sentence and without reference to any authority, Johnson also argues that
summary judgment was inappropriate because “[s]ix treating physicians in Waco would see
Johnson for his lung injury; all six physicians found that Johnson suffers from a lung condition
caused by an acute exposure to chemical vapors from Arkema’s hood.” Assuming this
argument is not waived, Johnson’s causation theory is nevertheless precluded by the general
causation requirement. See Knight, 482 F.3d at 351 (The general causation standard concerns
“whether a substance is capable of causing a particular injury or condition in the general
population”).
23
No. 11-50193
of Texas’s decision in Morgan v. Compugraphic Corporation, which held that
“[g]enerally, lay testimony establishing a sequence of events which provides a
strong, logically traceable connection between the event and the condition is
sufficient proof of causation.” 675 S.W.2d 729, 733 (Tex. 1984). Johnson argues
that such a sequence exists in this case because “Johnson (1) had never smoked
or had any history of asthma or lung disease prior to exposure, (2) worked within
2–3 feet of Arkema’s machine that was leaking chemical fumes, (3) was exposed
to chemical fumes at a level far above the OSHA limit, (4) could see, smell and
feel the chemical burning his throat and lungs, (5) suffered classic symptoms of
exposure to the chemical, (6) was administered oxygen and transported to the
emergency room after 2–3 hours of constant exposure, and (7) despite continuous
medical treatment to reduce lung inflammation, suffered permanent scarring to
his lung tissue.”
In its 2007 decision in Guevara v. Ferrer, the Texas Supreme Court
summarized the meaning of Morgan.21 247 S.W.3d 662 (Tex. 2007). The court
first explained that “[t]he general rule has long been that expert testimony is
21
We have previously summarized the Morgan decision as follows:
In Morgan, the plaintiff suffered from frequent skin rashes and problems with
her digestive and nervous systems, which she alleged were caused by her
exposure to chemical fumes from a leaking typesetting machine at her
workplace. The plaintiff testified that (1) she had always been in good health
prior to the installation of the typesetting machine near her desk, (2) she worked
with her face two inches from a typesetting machine that was leaking chemical
fumes, (3) soon thereafter she experienced problems with breathing and
swelling, and (4) after four or five days of constant exposure, she experienced
watery eyes, blurred vision, headaches, and swollen breathing passages. The
Texas Supreme Court held that this evidence established “a sequence of events
from which the trier of fact may properly infer, without the aid of expert medical
testimony, that the release of chemical fumes from the typesetting machine
caused [the plaintiff] to suffer injury.”
Hamburger v. State Farm Mut. Auto. Ins. Co., 361 F.3d 875, 884–85 (5th Cir. 2004) (citations
omitted).
24
No. 11-50193
necessary to establish causation as to medical conditions outside the common
knowledge and experience of jurors.” Id. at 665. The court reiterated, however,
that “non-expert evidence alone is sufficient to support a finding of causation in
limited circumstances where both the occurrence and conditions complained of
are such that the general experience and common sense of laypersons are
sufficient to evaluate the conditions and whether they were probably caused by
the occurrence.” Id. at 668–69. Such is generally the case when the lay
testimony “establish[es] a sequence of events which provides a strong, logically
traceable connection between the event and the condition.” Id. at 666 (quoting
Morgan, 675 S.W.2d at 733).
In the underlying dispute in Guevara, the plaintiff had presented evidence
at trial of: (1) the decedent’s condition before an automobile accident; (2) the
accident itself; and (3) the decedent’s post-accident condition, including his
numerous medical treatments.22 Id. at 667. The court found that such evidence
could establish that the accident caused “basic physical conditions which (1) are
within the common knowledge and experience of laypersons, (2) did not exist
before the accident, (3) appeared after and close in time to the accident, and
(4) are within the common knowledge and experience of laypersons, caused by
automobile accidents.” Id. The court nevertheless reversed because the evidence
22
The decedent’s treatment and medical expenses included:
among other expenses, the cost of (1) at least two abdominal surgeries; (2) three
separate confinements in health care facilities, one of which was for over three
months; (3) a great variety and quantity of various pharmaceutical supplies,
medicines, and drugs; (4) numerous varied laboratory procedures; (5) extensive
treatments for respiratory failure and therapy; (6) physical therapy of various
kinds; (7) treatments for kidney failure; and (8) a great assortment and quantity
of “central supply” and miscellaneous medical charges.
Id. at 669.
25
No. 11-50193
was legally insufficient to support a finding that the automobile accident caused
all of the medical expenses awarded by the jury:
Non-expert evidence of circumstances surrounding the accident and
Arturo’s complaints is sufficient to allow a layperson of common
knowledge and experience to determine that Arturo’s immediate
post-accident condition which resulted in his being transported to an
emergency room and examined in the emergency room were causally
related to the accident. Thus, the evidence is legally sufficient to
support a finding that some of his medical expenses were causally
related to the accident. On the other hand, the evidence is not
legally sufficient to prove what the conditions were that generated
all the medical expenses or that the accident caused all of the
conditions and the expenses for their treatment.
Id. at 669–70 (emphasis added). It remanded the case to the court of appeals for
determination of appropriate remittiturs or, if necessary, a new trial. Id. at 670.
Here, Johnson’s alleged chronic injuries, the severe restrictive lung disease
and pulmonary fibrosis, did not develop shortly after the Certincoat exposure
incidents but instead manifested in the years following the incidents. In light
of Guevara, we conclude that this significant gap in time renders the fact-finder
unable to evaluate the cause of Johnson’s chronic lung disease based solely on
its common sense and general experience. We, therefore, agree with the district
court’s conclusion that Johnson needs the assistance of experts to prove that his
Certincoat exposure caused his chronic injuries.
On the other hand, Johnson’s acute injuries—which immediately followed
his exposure to Certincoat and precipitated an emergency room visit and at least
two other doctors’ office visits during the summer of 2007—are within those
limited circumstances where expert opinion is unnecessary. See id. at 669–70;
see also Ballard v. Bunge N. Am Inc., 338 F. App’x 447, 448 (5th Cir. 2009)
(Owen, J., concurring) (joined by Haynes, J.) (unpublished). Accordingly, the
district court erred in granting summary judgment to Arkema regarding
26
No. 11-50193
Johnson’s alleged acute injuries. We therefore reverse and remand, in part, for
further proceedings concerning Johnson’s alleged acute injuries.
B.
Johnson next argues that “the lower court erred in failing to address the
fact that a number of other Owens Illinois employees suffered similar
respiratory distress and lung injury as Johnson following similar acute
exposures to Arkema’s chemicals while working within a few feet of Arkema’s
hoods.” Relying on Curtis, 174 F.3d at 669, Johnson argues that the symptoms
of his co-workers provide other circumstantial evidence to corroborate his
temporal proximity theory.
Johnson’s reliance on our Curtis decision is misplaced. With regard to the
reliability of an expert’s causation opinion under Daubert, the Curtis court found
that “a temporal connection is entitled to greater weight when there is an
established scientific connection between exposure and illness or other
circumstantial evidence supporting the causal link.” Id. at 670 (emphasis added).
However, the issue here does not require analysis of our Daubert jurisprudence;
rather, the question is whether, under Texas law, Johnson can satisfy the
element of causation without the assistance of an expert. Johnson has not cited
any Texas case law indicating that evidence of similar injuries to others
dispenses with the need for expert testimony in this toxic tort case. Accordingly,
Johnson’s reliance on his co-worker’s alleged injuries does not support reversal
of the district court’s summary judgment.
C.
Finally, Johnson posits that summary judgment was inappropriate
because Arkema’s expert pulmonologist, Dr. Aris, testified that tin oxide can
“cause lung injury and fibrosis.” According to Johnson, Dr. Aris also referenced
two human case studies indicating that “tin oxide is capable of and does cause
the type of lung injury suffered by Johnson.” Johnson further notes that other
27
No. 11-50193
human and animal studies of tin oxide show that it is capable of causing
interstitial lung disease.
Even assuming that this evidence suffices to demonstrate that tin oxide
is capable of causing restrictive lung disease, thus satisfying general causation,
the evidence falls short of satisfying the requirement of specific causation. As
discussed in III.B., supra, specific causation concerns whether “a substance
caused a particular individual’s injury.” Knight, 482 F.3d at 351. Johnson does
not offer any evidence that the actual amounts of tin oxide to which he was
exposed were of a sufficient concentration level to cause his restrictive lung
disease and pulmonary fibrosis. See also Curtis, 174 F.3d at 670 (“[S]cientific
knowledge of the harmful level of exposure to a chemical, plus knowledge that
the plaintiff was exposed to such quantities, are minimal facts necessary to
sustain the plaintiffs’ burden in a toxic tort case.” (emphasis added) (quoting
Allen, 102 F.3d at 199)). Thus, summary judgment was appropriate on this
issue.
V.
For the foregoing reasons, we AFFIRM the district court’s judgment in all
respects except as to Johnson’s claims regarding his acute injuries, on which we
REVERSE and REMAND for further proceedings.
28
No. 11-50193
REAVLEY, Circuit Judge, concurring:
I agree that the summary judgment should be reversed, but I disagree
with the ruling to deny the trier of fact the testimony of these highly qualified
expert witnesses. There are fact issues, primarily the extent of exposure of
the plaintiff to the chemical vapors and the diagnosis of his ailment. There
may be a disagreement between the experts about what, if anything, it would
take for inhalation of these vapors to damage the lungs to the extent of
progressive disease. If that bears on the decision of the diagnosis and is in
question, the trier of fact needs the assistance of these experts.
It is simply incredible to me to decide that Dr. Schlesinger is an
unreliable source for any scientific question in this case. And the same is true
of the other expert witnesses appearing in this record. But certainly Dr.
Schlesinger is an eminent authority on respiratory toxicology and the study of
the adverse effects of exposure to inhaled chemicals. Relying on the diagnosis
made by Dr. Grodzin that the patient suffers from restrictive lung disease,
Dr. Schlesinger explains the path of physiological response of the lungs
inhaling these damaging vapors. And no one will deny that MBTC and
hydrochloric acid, if inhaled to some extent, will damage the lungs. The
majority in this opinion accept that testimony for “acute injuries,” but decide
not to allow proof of any relation to progressive disease.
The district court excluded the testimony of Dr. Schlesinger because he
could not cite fully tested and peer reviewed studies proving that hydrochloric
acid can cause restrictive lung disease. That significant damage may be done
is merely factual information. The possible extent of damage from breathing
these chemicals may be at issue and will require the testimony of fully
qualified and experienced experts, of which Dr. Schlesinger is surely one.
There are no studies to meet the requirement of the district court, and that is
not surprising. How would that study be designed and conducted, by
29
No. 11-50193
obtaining a large population of people to breathe this chemical vapor or that
vapor in this volume or that volume, then to have their lung function tested
and maybe biopsied? Where would so many persons be found to be subjected
to this?
Studies that the district court required may prove helpful in
determining the reliability of a particular scientific “theory or technique,”
Daubert v. Merrell Dow Pharmaceuticals, Inc., 113 S. Ct. 2786 (1993), but
that is no checklist and reliability may depend on “the nature of the issue, the
expert’s particular expertise, and the subject of his testimony.” Kumho Tire
Company v. Carmichael, 119 S. Ct. 1167, 1175 (1999). The trial court erred
in excluding testimony that is possibly relevant and clearly reliable.
30