IN THE UNITED STATES COURT OF APPEALS

FOR THE FIFTH CIRCUIT

No. 11-50193

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.

United States Court of Appeals

Fifth Circuit

F I L E D

June 20, 2012

Lyle W. Cayce

Clerk

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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

 Arkema is also the designer and manufacturer of Certincoat. 1

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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 60 Judicial District Court of Jefferson County, Texas, claiming th

that Arkema’s C-4 Hood proximately caused his restrictive lung disease and

pulmonary fibrosis. Arkema removed the matter to the Eastern District of 3

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

Although Arkema disputes this diagnosis, the dispute is not material to the 2

disposition of this appeal.

Johnson’s brief defines pulmonary fibrosis as the “inflammation and progressive 3

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.” 

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installation of its C-4 Hoods. Johnson seeks compensatory and punitive

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

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injury after exposure to Arkema’s chemicals. While other employees

may have been exposed to the same chemicals, they suffered only

transitory symptoms which quickly resolved.

This appeal followed. 

III.

The firstissues 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

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(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

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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 HCl can cause restrictive lung 4

disease and pulmonary fibrosis. The district court excluded Dr. Schlesinger’s 5

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 peerreviewed 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

Although Certincoat also contains tin oxide, Dr. Schlesinger did not offer the opinion 4

that tin oxide can cause restrictive lung disease and pulmonary fibrosis. 

Dr. Schlesinger has an extensive background in the field of inhalation toxicology and 5

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.

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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

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“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. Id. We held that the district court did not abuse its discretion in 6

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. 

A dopamine agonist is a drug “that stimulates the dopamine receptors in the brain to 6

alleviate symptoms of Parkinson’s [Disease].” Id. at 377. 

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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. See Moore, 151 F.3d at 278–79 (“Dr. Jenkins made no 7

attempt to explain his conclusion by asserting that the Toluene solution [to

Instead, Dr. Schlesinger’s opinion that the concentration levels of MBTC and HCl

7

were sufficientto cause lung damage was based on other scientific evidence deemed unreliable

by the district court, discussed infra at III.2–3.

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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, we hold that the district court 8

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.” Joiner, 522 U.S. at 146. 9

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

One of the articles Dr. Schlesinger submitted with his report also implicitly addressed

8

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). 

This outcome may have been different had Dr. Schlesinger presented other reliable 9

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. 

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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.” The study found that one of the nine 10

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

 The acronym “ppm” stands for “parts per million.” 

10

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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.” Id. Here, the district court found the baboon study unreliable 11

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

In Allen, we concluded that a study’s finding that ethylene oxide (EtO) caused cancer 11

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.

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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

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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. The district court did not abuse its discretion in 12

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 thatMBTC “CAUSES RESPIRATORY TRACTIRRITATION” 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.

Johnson also notes that Arkema’s own expert acknowledged that HCl, if inhaled, may 12

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. 

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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. Id. at 669–70. There 14

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

Johnson also offers a temporal proximity argument, stating that Johnson’s initial 13

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. 

We also note that the MSDS did not play an important role in Curtis as the defendant 14

“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. 

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fibrosis, and instead only found that exposure to MBTC had a discernable effect

on the lung tissue of rats. The district court determined that the rat study was 15

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. Allen, 102 F.3d at 197. It follows that the district 16

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

 Specifically, the study concluded that:

15

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 elveolar edema in both sexes and by

alveolar erthrocytes in males only. 

Johnson was exposed to between ten and fifty milligrams per cubic meter of MBTC. 16

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. 

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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.

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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 conclusionthatMBTC

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and HCl caused Johnson’s lung disease. In reaching his causation conclusion, 17 18

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 ofDr. 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 clinicaltests,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

Like Dr. Schlesinger, Dr. Grodzin’s opinion did not address whether tin oxide caused 17

Johnson’s lung disease. 

Dr. Grodzin currently serves as the Medical Director for the Denton Medical Services 18

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. 

 At the Daubert hearing, Johnson informed the magistrate judge that Dr. Grodzin’s 19

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.

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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

ofthe 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

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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

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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

In one sentence and without reference to any authority, Johnson also argues that 20

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”). 

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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 2–3hours 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. 247 S.W.3d 662 (Tex. 2007). The court 21

first explained that “[t]he general rule has long been that expert testimony is

 We have previously summarized the Morgan decision as follows: 21

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). 

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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. Id. at 667. The court found that such evidence 22

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

 The decedent’s treatment and medical expenses included:

22

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. 

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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

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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 causallink.” 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

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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.

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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

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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. 

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