Rhyne et al v. United States Steel Corporation et al
Filing
249
ORDER that Defendant's motions to exclude the testimony of Plaintiff's experts (Docs. 182, 184, 186, 188, 190, 192, 195, 197, 203) are GRANTED in part and DENIED in part as stated herein. Plaintiff's evidentiary motions (Docs. 193, 198, 200) are GRANTED in part and DENIED in part as stated herein. Signed by District Judge Robert J. Conrad, Jr on 7/23/2020. (brl)
UNITED STATES DISTRICT COURT
WESTERN DISTRICT OF NORTH CAROLINA
CHARLOTTE DIVISION
3:18-cv-00197-RJC-DSC
BRUCE RHYNE and JANICE RHYNE,
Plaintiffs,
v.
UNITED STATES STEEL
CORPORATION, SAFETY-KLEEN
SYSTEMS, INC., and THE SAVOGRAN
COMPANY,
Defendants.
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ORDER
THIS MATTER comes before the Court on the parties’ motions under Daubert
and Federal Rule of Evidence 702 to exclude expert testimony and Plaintiffs’ motions
in limine to exclude certain evidence.
I.
BACKGROUND
This is a toxic tort action brought by Bruce Rhyne and his wife, Janice Rhyne,
arising out of Mr. Rhyne’s diagnosis with acute myeloid leukemia (“AML”). Plaintiffs
allege that Mr. Rhyne was diagnosed with AML as a result of his exposure to benzene
in various products manufactured by Defendants.
Nine of the twelve original
Defendants have been dismissed pursuant to settlement or court order. As for the
three remaining Defendants, Plaintiffs allege that Mr. Rhyne was exposed to benzene
from using (a) Liquid Wrench containing raffinate supplied by Defendant United
States Steel Corporation (“USS”), (b) 105 Solvent manufactured by Defendant SafetyKleen Systems, Inc., and (c) Kutzit manufactured by Defendant The Savogran
Case 3:18-cv-00197-RJC-DSC Document 249 Filed 07/23/20 Page 1 of 57
Company. Mr. Rhyne’s alleged exposure to Defendants’ benzene-containing products
occurred performing non-occupational work at home from approximately 1970 to
1975, during his high school internship at an auto mechanic shop from approximately
1974 to 1975, and during his employment with Duke Energy as a pipefitter and
maintenance mechanic from 1976 to 1998.1
Before the Court are Defendants’ motions to exclude the testimony of Plaintiffs’
causation and exposure experts, Plaintiffs’ motion to exclude the testimony of one
defense expert, and Plaintiffs’ motions in limine to exclude evidence of radiation
exposure and a genetic defect as alternative causes of Mr. Rhyne’s AML. The motions
have been fully briefed and are ripe for adjudication.2
II.
LEGAL FRAMEWORK
Rule 702 of the Federal Rules of Evidence governs the admissibility of expert
testimony. Rule 702 states:
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;
Although Mr. Rhyne’s employment with Duke Energy continued after 1998 to May
2015, he was employed as a maintenance supervisor during that time and had
limited, if any, exposure to benzene. (See Doc. No. 148-3, at 4–16.)
2 During the summary judgment hearing, the Court sought to schedule a several day
hearing on the anticipated motions under Daubert and Rule 702. (Doc. No. 179, at
80:17–25, 81:15–83:23.) Counsel for Plaintiffs then suggested that the motions be
decided on the papers, and counsel for Defendants did not make any objection thereto.
(Doc. No. 179, at 84:4–86:9.) Accordingly, the Court resolves the motions without
conducting a Daubert hearing.
1
2
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(b) the testimony is based on sufficient facts or data;
(c) the testimony is the product of reliable principles and methods; and
(d) the expert has reliably applied the principles and methods to the
facts of the case.
Fed. R. Evid. 702. “Courts have distilled the requirements of Rule 702 into two crucial
inquiries: 1) whether the proposed expert’s testimony is relevant; and 2) whether it
is reliable.” Yates v. Ford Motor Co., 113 F. Supp. 3d 841, 845 (E.D.N.C. 2015). “The
Supreme Court has made clear that it is the trial court’s duty to play a gatekeeping
function in deciding whether to admit expert testimony: ‘The trial judge must ensure
that any and all scientific testimony or evidence admitted is not only relevant, but
reliable.’” United States v. Crisp, 324 F.3d 261, 265 (4th Cir. 2003) (quoting Daubert
v. Merrell Dow Pharm., Inc., 509 U.S. 579, 589 (1993)).
In Daubert, the Supreme Court announced five factors that district courts may
consider in assessing the relevance and reliability of expert testimony. 509 U.S. at
593–94. Those factors are:
(1) whether the particular scientific theory “can be (and has been)
tested”; (2) whether the theory “has been subjected to peer review and
publication”; (3) the “known or potential rate of error”; (4) the “existence
and maintenance of standards controlling the technique’s operation”;
and (5) whether the technique has achieved “general acceptance” in the
relevant scientific or expert community.
Crisp, 324 F.3d at 266 (quoting Daubert, 509 U.S. at 593–94). The Daubert factors,
however, are neither definitive nor exhaustive. Kumho Tire Co. v. Carmichael, 526
U.S. 137, 150–51 (1999). “In determining whether proffered expert testimony is
reliable, the district court has broad discretion to consider whatever factors bearing
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on validity that the court finds to be useful; the particular factors will depend upon
the unique circumstances of the expert testimony involved.”
United States v.
Hammoud, 381 F.3d 316, 337 (4th Cir. 2004); see also Kumho Tire, 526 U.S. at 142
(“[T]he law grants a district court the same broad latitude when it decides how to
determine reliability as it enjoys in respect to its ultimate reliability determination.”).
“The inquiry to be undertaken by the district court is ‘a flexible one’ focusing on the
‘principles and methodology’ employed by the expert, not on the conclusions reached.”
Westberry v. Gislaved Gummi AB, 178 F.3d 257, 261 (4th Cir. 1999) (quoting
Daubert, 509 U.S. at 594–95). At the same time, “conclusions and methodology are
not entirely distinct from one another,” and “nothing 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.” GE v. Joiner, 522 U.S. 136, 146
(1997). In determining the admissibility of expert testimony, district courts “should
be conscious of two guiding, and sometimes competing, principles: (1) that Rule 702
was intended to liberalize the introduction of relevant expert evidence; and (2) that
due to the difficulty of evaluating their testimony, expert witnesses have the potential
to be both powerful and quite misleading.” Hammoud, 381 F.3d at 337 (quotation
marks omitted).
To succeed on their claims, Plaintiffs must prove both general causation and
specific causation. Dunn v. Sandoz Pharm. Corp., 275 F. Supp. 2d 672, 676 (M.D.N.C.
2003). General causation exists when exposure to an agent can cause the disease at
issue, and specific causation exists when exposure to the agent in fact caused the
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disease in a particular individual. Doe v. Ortho-Clinical Diagnostics, Inc., 440 F.
Supp. 2d 465, 471 (M.D.N.C. 2006). The Fourth Circuit has held that “[i]n order to
carry the burden of proving a plaintiff’s injury was caused by exposure to a specified
substance, the plaintiff must demonstrate the levels of exposure that are hazardous
to human beings generally as well as the plaintiff’s actual level of exposure.”
Westberry, 178 F.3d at 263 (quotation marks omitted). Typically, expert testimony
is necessary to prove general and specific causation. Zellars v. NexTech Northeast,
LLC, 895 F. Supp. 2d 734, 739 (E.D. Va. 2012), aff’d, 533 F. App’x 192 (4th Cir. July
17, 2013).
It is well recognized that epidemiology usually provides the best evidence of
general causation in toxic tort actions. Norris v. Baxter Healthcare Corp., 397 F.3d
878, 882 (10th Cir. 2005); Rider v. Sandoz Pharm. Corp., 295 F.3d 1194, 1198 (11th
Cir. 2002); In re Lipitor (Atorvastatin Calcium) Mktg., Sales Practices & Prods. Liab.
Litig., 174 F. Supp. 3d 911, 914 (D.S.C. 2016). “Epidemiology is the field of public
health and medicine that studies the incidence, distribution, and etiology of disease
in human populations.” Michael D. Green et al., Reference Guide on Epidemiology,
in Fed. Judicial Ctr., Reference Manual on Scientific Evidence 551 (3d ed. 2011)
[hereinafter Reference Guide on Epidemiology]. “Epidemiologic evidence identifies
agents that are associated with an increased risk of disease in groups of individuals,
quantifies the amount of excess disease that is associated with an agent, and provides
a profile of the type of individual who is likely to contract a disease after being exposed
to an agent.” Id. at 552.
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The ultimate question with which epidemiologists are concerned is whether a
causal relationship exists between an agent and a disease. Id. at 566. To establish
causation, epidemiological studies must first show an association between exposure
to an agent and the disease. Id.; accord In re Lipitor, 174 F. Supp. 3d at 914. An
association, however, is not equivalent to causation.
Reference Guide on
Epidemiology, at 552. “An association between exposure to an agent and disease
exists when they occur together more frequently than one would expect by chance.”
Id. at 566. Epidemiological studies commonly express the existence and strength of
an observed association between exposure and disease as “relative risk.” Id. A
relative risk equal to 1.0 indicates that there is no association between exposure to
the agent and the disease—the risk of disease in exposed individuals is the same as
the risk of disease in unexposed individuals. Id. at 567. A relative risk greater than
1.0 indicates a positive association between exposure to the agent and the disease—
the risk of disease in exposed individuals is greater than the risk of disease in
unexposed individuals. Id. And a relative risk less than 1.0 indicates a negative
association between exposure to the agent and the disease—the risk of disease in
exposed individuals is less than the risk of disease in unexposed individuals. Id.;
accord In re Lipitor, 174 F. Supp. 3d at 915.
An observed association in a study, however, may result from random error.
Reference Guide on Epidemiology, at 572. The two main techniques for assessing
random error are statistical significance and confidence intervals. Id. at 573. To
measure the statistical significance of a study, epidemiologists calculate a p-value.
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Id. at 576. “A p-value represents the probability that an observed positive association
could result from random error even if no association were in fact present.” Id. If the
observed p-value for a study falls below the preselected level, most commonly .05,
then the study is statistically significant—that is, the results are unlikely to be due
to random error. Id. at 573, 576–77. “A confidence interval provides both the relative
risk (or other risk measure) found in the study and a range (interval) within which
the risk likely would fall if the study were repeated numerous times.” Id. at 573. Put
differently, “[a] confidence interval is essentially a margin of error for the estimated
relative risk.” In re Lipitor, 174 F. Supp. 3d at 915 (quotation marks omitted). “If a
95% confidence interval is specified, the range encompasses the results we would
expect 95% of the time if samples for new studies were repeatedly drawn from the
population.” Reference Guide on Epidemiology, at 580. If the range of possible
results includes a relative risk of 1.0, the study is not statistically significant because
it includes a result which does not indicate an association. Id. at 581; accord In re
Lipitor, 174 F. Supp. 3d at 915.
“Once an association has been found between exposure to an agent and
development of a disease, researchers consider whether the association reflects a true
cause-effect relationship.” Reference Guide on Epidemiology, at 597. “Assessing
whether an association is causal requires an understanding of the strengths and
weaknesses of the study’s design and implementation, as well as a judgment about
how the study findings fit with other scientific knowledge.” Id. at 553. To determine
whether an association reflects a causal relationship, epidemiologists apply the
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factors set out by Sir Austin Bradford Hill in his 1965 article on providing
epidemiological evidence of causation: (1) temporal relationship, (2) strength of the
association, (3) dose-response relationship, (4) replication of the findings, (5)
biological plausibility, (6) consideration of alternative explanations, (7) cessation of
exposure, (8) specificity of the association, and (9) consistency with other knowledge.
Id. at 600; accord In re Lipitor, 174 F. Supp. 3d at 916. “Whether an established
association is causal is a matter of scientific judgment, and scientists appropriately
employing this method ‘may come to different judgments’ about whether a causal
inference is appropriate.” In re Lipitor, 174 F. Supp. 3d at 916 (quoting Milward v.
Acuity Specialty Prods. Grp., Inc., 639 F.3d 11, 18 (1st Cir. 2011)).
III.
DEFENDANTS’ MOTIONS3
As to general causation, Plaintiffs offer the expert testimony of Peter F.
Infante, an epidemiologist, and Robert Harrison, a medical doctor. As to specific
causation, Plaintiffs offer the expert testimony of Infante, Harrison, and Steven D.
Gore, a medical doctor. And as to Mr. Rhyne’s level of exposure to benzene, Plaintiffs
offer the expert testimony of Robert F. Herrick, an industrial hygienist. Defendants
have moved to exclude the testimony of all Plaintiffs’ experts.
A.
Safety Kleen’s Mineral Spirits Product
Before turning to the reliability and relevance of each expert’s opinion, it is
USS and Safety Kleen filed most of the Daubert motions presently before the Court.
As Savogran filed a notice stating it joined in all the motions filed by USS and Safety
Kleen, (Doc. Nos. 205, 235, 242), the Court refers to the motions as though they were
filed by all Defendants and addresses defendant-specific arguments where necessary.
3
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necessary to address an argument raised by Safety Kleen that is specific to its
product.
Safety Kleen’s 105 Solvent (“parts washer solvent” or “mineral spirits
solvent”) is mineral spirits based. Mineral spirits are petroleum-derived distillate
mixtures that contain benzene and other chemicals. (Doc. No. 196-9, ¶ 32.) In this
case, Plaintiffs’ general causation experts opine that exposure to benzene can cause
AML, and Plaintiffs’ specific causation experts opine that Mr. Rhyne’s exposure to
benzene in Defendants’ products—including Safety Kleen’s parts washer solvent—
caused his AML. Safety Kleen argues that, with respect to Plaintiffs’ claims as to
Safety Kleen, the causation question in this case is not whether exposure to benzene
can and did cause Mr. Rhyne’s AML, but whether exposure to mineral spirits can and
did cause Mr. Rhyne’s AML. According to Safety Kleen, the opinions of Plaintiffs’
causation experts are unreliable and irrelevant because they focus on benzene
instead of mineral spirits.
In making this argument, Safety Kleen relies on a
declaration of its expert David Pyatt, a toxicologist, and two cases: Henricksen v.
Conoco Phillips Co., 605 F. Supp. 2d 1142 (E.D. Wash. 2009) and Burst v. Shell Oil
Co., No. 14-109, 2015 U.S. Dist. LEXIS 77751 (E.D. La. June 16, 2015).
Henricksen was a former gasoline tanker truck driver who was diagnosed with
AML. 605 F. Supp. 2d at 1148. Henricksen and his wife alleged that his AML was
caused by his exposure to benzene in defendant’s gasoline. Id. The parties agreed
that defendant’s gasoline contained benzene and that the scientific literature
provided clear evidence of a causal relationship between certain levels of exposure to
benzene and benzene-containing solvents, on the one hand, and the development of
9
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AML, on the other. Id. at 1150. Plaintiffs’ theory was that low dose exposure to
benzene in gasoline can cause AML. Id. at 1170. Defendant argued that plaintiffs
could not establish that there was a sufficient level of benzene as an ingredient of
gasoline for exposure to gasoline to result in an increased risk of AML. Id. at 1148,
1151. Defendant’s experts opined that competitive inhibition between benzene and
the other compounds found in gasoline mitigate the potential carcinogenic properties
of the small amounts of benzene in gasoline.4 Id. at 1151.
The court identified the general causation question as whether exposure to the
benzene component of gasoline can cause AML. Id. at 1156. The court recognized
that, in addition to the numerous studies on the hazardous effects of benzene, there
were numerous studies on the hazardous effects of gasoline. Id. at 1170. The court
engaged in an in-depth review of the scientific literature on benzene and gasoline.
The court first concluded that the studies on which plaintiffs’ experts relied to support
their opinions that low dose exposure to benzene in gasoline can cause AML did not
reliably support such opinions. Id. at 1170–72 (discussing the reports and studies
that investigated the Tranguch gasoline spill and the Australian Institute of
Petroleum’s Health Watch reports). The court noted that the most relevant studies
cited by plaintiffs’ experts were those addressing occupational gasoline exposure and
the risk of AML. Id. at 1172. One case-control study5 found a statistically significant
In Henricksen, plaintiffs offered Infante as a general causation expert, and
defendant offered Pyatt as a causation expert. In this case, Plaintiffs and Defendants
also offer Infante and Pyatt, respectively, as causation experts.
5 A case-control study compares the rates of exposure in the group of individuals with
the disease to the rates of exposure in the group of individuals without the disease.
4
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association between the risk of AML and employment in automobile manufacturing,
as a gas station attendant, and in petroleum manufacturing. Id. at 1173. The study
did not find a statistically significant association between the risk of AML and
employment in automobile mechanics or employment as a truck, bus, or taxi driver.
Id. The study authors concluded that the associations between certain occupational
exposures to gasoline and the risk of AML remain unclear. Id.
The other study cited by plaintiffs’ experts that addressed occupational
gasoline exposure and AML studied the risk of AML within different occupations.
The only occupation that resulted in an increased risk of AML was “male petrol
station attendants and demonstrators.” Id. The authors hypothesized that exposure
to benzene from petrol had contributed to the excess risk of AML, but the court noted
that the study had been criticized by other scientists for various reasons—including
for the discovery that three of the ten reported AML cases observed among petrol
station attendants never worked as a petrol station attendant and three others only
did so for a short time. Id. Plaintiffs’ and defendant’s experts recognized that the
studies on gasoline station attendants yielded inconsistent results, and the largest
study on service station workers found no statistically significant increased risk of
AML among 19,000 gasoline attendants. Id.
The experts agreed that the most relevant studies were those on tanker truck
drivers or gasoline distribution workers. Id. Three major epidemiological studies
involving large cohorts of such workers had been conducted, and each showed no
Reference Guide on Epidemiology, at 557.
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statistically significant increased risk of AML among tanker truck drivers or gasoline
distribution workers. Id. at 1173–74.
The court excluded the testimony of plaintiffs’ general causation experts
because the studies on which they relied did not support their causation conclusions
“in the face of the overwhelming body of contradictory and inconsistent
epidemiological evidence.” Id. at 1175. The court explained that the studies relied
on by plaintiffs’ experts “make clear that the connection between gasoline or the
benzene component of gasoline and AML is at this point in time only a hypothesis in
need of further investigation” and, as a result, plaintiffs’ “experts can only reliably
attest to gasoline exposure as a theoretical or possible cause, not a probable cause of
Henricksen’s AML.” Id. at 1176.
In Burst,6 plaintiff alleged that her late husband’s regular exposure to benzene
in defendants’ gasoline during the years he worked as a gas station attendant and
mechanic caused his AML. 2015 U.S. Dist. LEXIS 77751, at *3. As in Henricksen,
plaintiff’s expert opined that low dose exposure to benzene in gasoline can cause AML
and that plaintiff’s late husband’s exposure to benzene in gasoline caused his AML.
Id.
The parties agreed that gasoline contains benzene and, at certain levels of
exposure, benzene can cause AML. Id. at *23–24. Defendants argued, however, that
there is no scientific basis for concluding that exposure to gasoline containing benzene
causes AML. Id. at *9. The court noted that “the data related to gasoline exposure
Plaintiff and defendants also offered Infante and Pyatt, respectively, as causation
experts in Burst.
6
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is far from consistent with the data related to benzene exposure.” Id. at *23. And
like defendant in Henricksen, defendants argued that the observed carcinogenic
effects of gasoline are different from those of benzene because of the small
concentration of benzene in gasoline and because of the competitive inhibition
between the components of gasoline. Id. at *25–26. The court thus concluded that
although the scientific literature on benzene was relevant to plaintiff’s expert’s
general causation opinion, it alone could not provide a reliable basis for such opinion.
Id. at *27.
The court then turned to the gasoline literature on which plaintiff’s expert
relied. The court concluded that the expert’s methodology was not reliable because
he relied on a number of studies that did not isolate exposure to gasoline or did not
provide exposure metrics; he relied on studies that did not exhibit statistically
significant results or did not indicate a positive association between gasoline exposure
and AML; he relied on studies that did not specifically examine AML; and he cherrypicked data from studies that did not otherwise support his conclusion, failed to
explain contrary results, reached conclusions that the authors of the study did not
make, and manipulated data without providing any evidence of his work. Id.
There are critical differences between Henricksen and Burst, on the one hand,
and this case, on the other. A significant basis for the courts’ decisions in both
Henricksen and Burst was that there was a body of scientific literature that
specifically investigated the association between exposure to gasoline and the risk of
AML that was inconsistent and failed to support a causal relationship between
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exposure to gasoline and the risk of AML. And in both cases, the defense experts
provided a scientific explanation as to why exposure to benzene in gasoline does not
cause an increased risk of AML despite the known causal relationship between
exposure to benzene and the risk of AML.
Here, there is no evidence of a contrary body of literature on mineral spirits
that is inconsistent with the literature on benzene generally. Safety Kleen relies on
a declaration of its expert, Pyatt, who states that “there have been over a dozen
studies where investigators have specifically evaluated mineral spirits (or similar
distillates) related to AML or leukemia risk” and “[t]hese studies are uniformly
negative regarding increased risk of leukemia, AML or related diseases.” (Doc. No.
196-9, ¶ 33.)
Pyatt cites eighteen different studies to support this statement,
seventeen of which are included in the record.7 (Doc. No. 196-10.)
The Court has extensively reviewed the seventeen studies and, contrary to
Pyatt’s declaration, they are not uniformly negative regarding exposure to mineral
spirits and an increased risk of AML. For example, Bouchardy et al. (2016) was a
case-referent study that presented an overview of cancer risk patterns by
socioeconomic status and occupation in Switzerland. Christine Bouchardy et al.,
Cancer Risk by Occupation and Socioeconomic Group Among Men—A Study by the
Association of Swiss Cancer Registries, 28 Scandinavian J. of Work, Env’t & Health
1 (2002).8 The authors found an excess of acute leukemia cases among foundry
Only the abstract of Poynter et al. (2016), the study cited at reference 168 of Pyatt’s
declaration, is included in the record. (See Doc. No. 196-10, at Ex. 10-J.)
8 See Doc. No. 196-10, at Ex. 10-d.
7
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workers, electricians, and science professionals.
Id. at 32.
The study did not
investigate or make any conclusions regarding associations between exposure to
mineral spirits and the risk of AML. As another example, Pyatt cites Siemiatycki et
al. (1987), a case-referent study that examined the associations between exposure to
twelve different petroleum-derived liquids—including mineral spirits—and fourteen
different cancers. Jack Siemiatycki et al., Associations Between Several Sites of
Cancer and Twelve Petroleum-Derived Liquids, 13 Scandinavian J. of Work, Env’t &
Health 493 (1987).9 Neither AML nor even leukemia generally, however, were among
the cancers investigated, and Pyatt fails to connect or extrapolate the study’s findings
on associations between exposure to mineral spirits and the risk of other cancers to
the risk of AML. See Burst, 2015 U.S. Dist. LEXIS 77751, at *17 (“[S]tudies that do
not examine the precise disease at issue may not provide good grounds for an expert’s
opinion.”); Reference Guide on Epidemiology, at 605 n.169 (“When a party claims that
evidence of a causal relationship between an agent and one disease is relevant to
whether the agent caused another disease, courts have required the party to show
that the mechanisms involved in development of the disease are similar.”). The other
studies cited by Pyatt are likewise not relevant to the state of the literature regarding
the association between exposure to mineral spirits and the risk of AML because they
either do not assess exposure to mineral spirits or do not assess the risk of AML.
Further, the defense experts in Henricksen and Burst opined that exposure to
benzene in gasoline does not cause an increased risk of AML due to competitive
9
See Doc. No. 196-10, at Ex. 10-m.
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inhibition between the various components of gasoline that mitigates the
carcinogenic properties of benzene. Here, other than Pyatt’s conclusion regarding the
studies on mineral spirits, Safety Kleen has not provided any explanation for why
exposure to benzene in mineral spirits should be evaluated differently than exposure
to benzene in other solvents. Safety Kleen makes much about the fact that the World
Health Organization’s International Agency for Research on Cancer (“IARC”)
classifies benzene as a carcinogen but does not classify mineral spirits as a
carcinogen. Safety Kleen’s argument is not convincing.
IARC establishes working groups of independent scientists to evaluate the
carcinogenic risk of certain agents to humans and publishes in the form of
monographs reviews of the carcinogenicity data on those agents. In each monograph,
IARC categorizes the carcinogenicity of the agent into one of five categories. Group
1 includes agents that are carcinogenic to humans, and this category is used when
there is sufficient evidence of carcinogenicity in humans. Group 2A includes agents
that are probably carcinogenic to humans, and this category is used when there is
limited evidence of carcinogenicity in humans and sufficient evidence of
carcinogenicity in experimental animals. Group 2B includes agents that are possibly
carcinogenic to humans, and this category is generally used for agents for which there
is limited evidence in humans in the absence of sufficient evidence in experimental
animals. Group 3 includes agents that are not classifiable as to their carcinogenicity
in humans, and this category is used when the agent does not fall into any other
category. And Group 4 includes agents that are probably not carcinogenic to humans,
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and this category is used for agents for which there is evidence suggesting lack of
carcinogenicity in humans together with evidence suggesting lack of carcinogenicity
in experimental animals.
IARC, Some Organic Solvents, Resin Monomers and
Related Compounds, Pigments and Occupational Exposures in Paint Manufacture
and Painting, 47 Monographs on the Evaluation of Carcinogenic Risks to Humans
29–30 (1989).
IARC’s monograph on mineral spirits is from 1989 and it concluded that there
was inadequate evidence of the carcinogenicity of mineral spirits in humans and no
available data on the carcinogenicity of mineral spirits in experimental animals. Id.
at 72.
IARC thus classified mineral spirits as a Group 3 agent that was not
classifiable as to its carcinogenicity in humans. Id. IARC expressly states, however,
that benzene is excluded from its monograph on mineral spirits. Id. at 35. Moreover,
IARC’s 2018 monograph on benzene expressly recognizes the use of mineral spirits
as a potential source of benzene exposure. IARC, Benzene, 120 Monographs on the
Evaluation of Carcinogenic Risks to Humans 68 (2018).
In short, unlike Henricksen and Burst, there are not compelling reasons for
evaluating exposure to benzene in mineral spirits differently than exposure to
benzene in other solvents. The evidence shows that 99% of all occupational exposures
to benzene are not from technical grade benzene, but from solvents containing
benzene. (Doc. No. 196-5, at 173:4–8.) As a result, the scientific literature on benzene
primarily examines exposure to benzene as a component of other products rather
than exposure to technical grade benzene. (Doc. No. 196-5, at 153:2–18.) Herrick
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calculated Mr. Rhyne’s benzene exposure from his use of Safety Kleen’s mineral
spirits solvent (as well as the other Defendants’ products), and Plaintiffs’ experts’
causation opinions are based on Mr. Rhyne’s benzene exposure as calculated by
Herrick. (Doc. No. 194-3, at 131:9–15; Doc. No. 191-3, at 62:9–63:14.) Consistent
with Henricksen and Burst, the Court concludes that the general causation question
in this case is whether exposure to benzene in Defendants’ various products—
including Safety Kleen’s mineral spirits solvent—can cause AML. Unlike Henricksen
and Burst, the Court concludes that the scientific literature on the association
between exposure to benzene as a component of other solvents and the risk of AML
provides a reliable basis for Plaintiffs’ experts’ causation opinions. See Milward v.
Acuity Specialty Prods. Grp., Inc., 639 F.3d 11, 14–15 (1st Cir. 2011) (concluding that
plaintiffs’ general causation expert’s opinion that exposure to benzene causes acute
promyelocytic leukemia was reliable and relevant to plaintiffs’ claims that exposure
to benzene in defendants’ products caused Milward’s acute promyelocytic leukemia);
Campos v. Safety-Kleen Sys., Inc., 98 F. Supp. 3d 372, 378–79 (D.P.R. 2015)
(concluding that plaintiffs’ causation experts’ opinions that exposure to benzene
causes chronic myelogenous leukemia was admissible and rejecting Safety Kleen’s
argument that the experts considered the wrong substance because Safety Kleen’s
mineral spirits solvent is not benzene and the fact that it contains benzene does not
support the conclusion that it can cause chronic myelogenous leukemia); Wagoner v.
Exxon Mobil Corp., 813 F. Supp. 2d 771, 799 (E.D. La. 2011) (identifying the general
causation question as whether exposure to benzene can cause multiple myeloma
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where plaintiff alleged that exposure to benzene in defendants’ products, including a
mineral spirits product, caused the decedent’s development of multiple myeloma).
B.
Infante
Plaintiffs offer Infante to provide expert testimony on both general causation
and specific causation. Defendants argue that Infante’s opinion must be excluded
because it is unreliable. Defendants further argue that Infante is not qualified to
render an opinion on specific causation.
Infante’s expert report, dated October 2, 2017, states: “The historical literature
clearly demonstrates by 1971 . . . that exposure to benzene caused severe bone
marrow depression and most likely all forms of leukemia as well.” (Doc. No. 148-4,
at 24.) In October 2018, Infante gave a PowerPoint presentation to representatives
of the Norwegian government and numerous petrochemical companies. (Doc. No.
196-5, at 60:9–15, 61:6–13.) One of Infante’s PowerPoint slides stated that “only after
the Infante et al. 1977 study was benzene generally accepted as a cause of AML.”
(Doc. No. 186-3.) Defendants argue that the statement in Infante’s expert report is
inconsistent with the statement in his PowerPoint presentation and, as a result,
Infante’s opinion is unreliable.
Defendants’ argument is meritless. That a fact is clearly demonstrated by the
historical literature does not mean that the fact is generally accepted by the relevant
scientific community. During Infante’s deposition, defense counsel had Infante read
the statement in his report regarding the state of the historical literature in 1971.
(Doc. No. 196-5, at 57:16–58:2.)
Defense counsel then asked if it was Infante’s
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testimony that it was generally accepted by 1971 that benzene causes AML, to which
Infante replied: “No, it doesn’t say that.”
(Doc. No. 196-5, at 58:4–7.)
Infante
explained that in 1971, there were many people who thought exposure to benzene
caused all forms of leukemia. (Doc. No. 196-5, at 59:11–13.) But Infante repeatedly
stated that general acceptance means acceptance by everyone, and exposure to
benzene as a cause of AML was not generally accepted until after publication of
Infante et al. (1977).
(Doc. No. 196-5, at 66:5–14, 67:12–68:4.)
There is no
inconsistency between the statement in Infante’s report regarding the state of the
historical literature in 1971 and the statement in Infante’s PowerPoint presentation
that exposure to benzene was not generally accepted as a cause of AML until after
Infante et al. (1977).
Defendants also argue that Infante is not qualified to render an opinion on
specific causation. Infante is an epidemiologist; he is not a hematologist, oncologist,
toxicologist, or medical doctor. (Doc. No. 196-5, at 14:8–22.) As discussed above,
epidemiology focuses on the issue of general causation, not specific causation. In
opposition to Defendants’ argument, Plaintiffs restate Infante’s qualifications that
undoubtedly qualify him to render an opinion on general causation. For example,
Plaintiffs state that Infante has over forty-five years of experience researching the
toxicity and carcinogenicity of benzene and determining the cancer risk from
exposure to chemicals as a director with OSHA, has published over twenty-five
scientific articles related specifically to benzene exposure and the risk of leukemia
and other benzene-related diseases, and has served as an expert epidemiologist on an
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IARC working group. Plaintiffs make no effort, however, to tie those qualifications
to Infante’s offered opinion on specific causation. As the proponents of Infante’s
testimony, Plaintiffs bear the burden of proving that Infante is qualified to give the
offered opinions by a preponderance of proof. Cooper v. Smith & Nephew, Inc., 259
F.3d 194, 199 (4th Cir. 2001). Plaintiffs have not met their burden with respect to
Infante’s offered opinion on specific causation. See In re Viagra Prods. Liab. Litig.,
658 F. Supp. 2d 950, 960 (D. Minn. 2009) (concluding that an epidemiologist was not
qualified to give an opinion on specific causation).
Therefore, the Court grants
Defendants’ motions as to Infante’s specific causation opinion and excludes the same.
The Court denies Defendants’ motions as to Infante’s general causation opinion.
C.
Harrison
Defendants move to exclude Harrison’s expert testimony on both general
causation and specific causation.
1.
General Causation
With respect to general causation, Defendants argue that to support Harrison’s
opinion that exposure to low doses of benzene can cause AML, Harrison relies on two
studies that do not support his opinion: Kirkeleit et al. (2008) and Stenehjem et al.
(2015).
Kirkeleit et al. (2008) was a historical cohort study10 of Norway upstream
petroleum workers engaged in drilling and production of crude oil, natural gas, and
In general, a cohort study measures and compares the incidence of disease in the
group of individuals who were exposed to the agent and the group of individuals who
were not exposed to the agent. Reference Guide on Epidemiology, at 557.
10
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natural gas liquids. Kirkeleit et al., Increased Risk of Acute Myelogenous Leukemia
and Multiple Myeloma in a Historical Cohort of Upstream Petroleum Workers
Exposed to Crude Oil, 19 Cancer Causes Control 13 (2008).11 Benzene is a natural
component of crude oil and natural gas. Id. The study categorized petroleum workers
into five categories: (1) upstream operator offshore, (2) drilling and well maintenance
offshore, (3) catering offshore, (4) others offshore, and (5) petroleum workers onshore.
Id. at 14. Upstream operator offshore workers had the most extensive contact with
products containing benzene, and the study found a statistically significant increased
risk of AML among those workers. Id. at 17. The authors concluded that “[g]iven the
established association between benzene exposure and hematologic neoplasms,
benzene exposure probably caused the observed risk of [AML.]” Id. Safety Kleen
criticizes Harrison’s reliance on the study because the authors recognized the lack of
good exposure estimates as a major limitation and acknowledged “it is unclear at
which level of exposure benzene poses an increased risk of developing hematologic
neoplasms.”
Id.
Still, the authors concluded that the benzene exposure levels
reported in crude oil assays and the low benzene content of crude oil
indicate that the atmospheric exposure from the crude or condensate
has been well below the exposure levels that most studies have reported
to be necessary for inducing hematologic neoplasms. This increased risk
thus implies that the exposure levels have been higher than published
for this industry, or that the increased risk for these neoplasms can be
found at lower levels of exposure than previously assumed. In support
of the latter interpretation a few studies have reported an association
between a mean benzene exposure around, and even below, 1 ppm and
increased risk of [AML] . . . .
11
See Doc. No. 194-6.
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Id. at 19 (emphasis added). The study thus lends support for Harrison’s opinion that
benzene exposure at lower doses can cause AML, notwithstanding that the study did
not definitively conclude that an increased risk of AML can be found at lower levels
of exposure. See Knight v. Kirby Inland Marine Inc., 482 F.3d 347, 354 (5th Cir.
2007) (“We also understand that in epidemiology hardly any study is ever conclusive,
and we do not suggest that an expert must back his or her opinion with published
studies that unequivocally support his or her conclusion.”); Yates, 113 F. Supp. 3d at
851 (“[T]he general level of hazardous exposure need not be expressly established by
a particular scientific study, so long as the expert is able to establish that he uses a
scientifically reliable method to extrapolate the results from scientific literature.”).
Stenehjem et al. (2015) was another historical cohort study of Norwegian
upstream petroleum workers. J.S. Stenehjem et al., Benzene Exposure and Risk of
Lymphohaematopoietic Cancers in 25,000 Offshore Oil Industry Workers, 112 British
J. of Cancer 1603 (2015).12 The study found an association between cumulative lowlevel benzene exposure and the risk of AML; however, the result was not statistically
significant. Id. at 1607–08. Safety Kleen contends that because the result was not
statistically significant, the study does not provide a reliable basis for Harrison’s
opinion, citing cases from other jurisdictions. But the Fourth Circuit has expressly
“decline[d] to establish a bright-line rule requiring experts to rely only on evidence
that is statistically significant or else have their opinions excluded.” In re Lipitor
(Atorvastatin Calcium) Mktg., Sales Practices & Prods. Liab. Litig., 892 F.3d 624, 642
12
See Doc. No. 194-9.
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(4th Cir. 2018).
Therefore, the Court concludes that Kirkeleit et al. (2008) and Stenehjem et al.
(2015) provide a reliable basis for Harrison’s opinion that exposure to lower doses of
benzene can cause AML.
2.
Specific Causation
Defendants argue that Harrison’s specific causation opinion must be excluded
because he failed to perform a reliable differential diagnosis.
“[D]ifferential diagnosis is a standard scientific technique of identifying the
cause of a medical problem . . . 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.” Cooper, 259 F.3d at 200 (quotation marks omitted) (omission in original).
“This technique has widespread acceptance in the medical community, has been
subject to peer review, and does not frequently lead to incorrect results.” Westberry,
178 F.3d at 262 (quotation marks omitted). Thus, the Fourth Circuit has held that
“a reliable differential diagnosis provides a valid foundation for an expert opinion.”
Id. at 263.
Defendants argue that Harrison’s differential diagnosis is unreliable because
he failed to rule out radiation exposure, a genetic defect, and obesity as alternative
causes of Mr. Rhyne’s AML.
“A differential diagnosis that fails to take serious
account of other potential causes may be so lacking that it cannot provide a reliable
basis for an opinion on causation.” Id. at 265. “Thus, if an expert utterly fails to
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consider alternative causes or fails to offer an explanation for why the proffered
alternative cause was not the sole cause, a district court is justified in excluding the
expert’s testimony.”
Cooper, 259 F.3d at 202.
“However, [a] medical expert’s
causation conclusion should not be excluded because he or she has failed to rule out
every possible alternative cause of a plaintiff’s illness.” Westberry, 178 F.3d at 265
(quotation marks omitted) (alteration in original). “In such cases, the alternative
causes suggested by a defendant normally affect the weight that the jury should give
the expert’s testimony and not the admissibility of that testimony.” Cooper, 259 F.3d
at 202.
The parties do not dispute that Mr. Rhyne was exposed to radiation during his
employment with Duke Energy, and the experts agree that radiation exposure at
certain levels is a risk factor for AML. Defense experts Pyatt and Debra Kaden, a
toxicologist, testified that Mr. Rhyne’s radiation exposure was insufficient to cause
his AML. (Doc. No. 199-9, at 115:2–22; Doc. No. 199-10, at 88:1–17.) And Defendants
expressly concede that they do not posit that radiation caused Mr. Rhyne’s AML.
(Doc. No. 207, at 5.) Accordingly, radiation exposure is not a plausible alternative
cause of Mr. Rhyne’s AML. See Kannankeril v. Terminix Int’l, 128 F.3d 802, 808 (3d
Cir. 1997) (stating that defendant may attack plaintiff’s expert’s differential
diagnosis by pointing to “a plausible cause of the plaintiff’s illness other than the
defendant’s actions”).
Nevertheless, Harrison adequately ruled out radiation exposure as an
alternative cause of Mr. Rhyne’s AML.
Harrison understood that Mr. Rhyne’s
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dosimetry measurements indicate that Mr. Rhyne’s cumulative radiation exposure
over his lifetime was 0.5 REM,13 and Harrison testified that 0.5 REM is insufficient
to cause AML. (Doc. No. 194-3, at 44:3–7.) Defendants take issue with Harrison’s
assumption that Mr. Rhyne’s radiation exposure was 0.5 REM, but Defendants do
not contend that Mr. Rhyne’s radiation exposure was greater than 0.5 REM.
Moreover, Harrison testified that radiation exposure is only significant to AML at 5
REMs or above. (Doc. No. 194-3, at 146:8–22.) Therefore, Harrison adequately ruled
out radiation exposure as the sole cause of Mr. Rhyne’s AML. Cooper, 259 F.3d at
202 (stating that “if an expert utterly fails to consider alternative causes or fails to
offer an explanation for why the proffered alternative cause was not the sole cause, a
district court is justified in excluding the expert’s testimony”).
Defendants also argue that Harrison failed to rule out that Mr. Rhyne’s AML
was familial. Mr. Rhyne’s sister was diagnosed with AML, and the experts agree that
AML can have a familial or genetic link. There are a number of genetic or heritable
mutations that are commonly found in familial AML, and the presence of these
mutations can be determined by genetic analysis. (Doc. No. 194-3, at 36:7–11.)
Harrison testified that in order to determine whether Mr. Rhyne’s AML is familial,
Harrison would need to see genetic testing confirming the presence of one or more of
the genetic defects commonly found in familial AML. (Doc. No. 194-3, at 39:4–12.)
Mr. Rhyne did not have these tests done because of the critical condition he was in
when he first presented with AML. (Doc. No. 191-3, at 41:9–19.) As a result, Harrison
13
REM stands for roentgen equivalent man and is a unit of radiation dosage.
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could not conclusively rule out familial AML. Harrison explained, however, that
familial AML is rare, accounting for only about 4% of all AML cases. (Doc. No. 1943, at 36:5–6.) In addition, the average age of persons who present with familial AML
is in the thirties, and it is unusual for familial AML to present in someone in their
fifties or sixties. (Doc. No. 194-3, at 37:1–5.) Mr. Rhyne was diagnosed with AML at
age 59. Therefore, the Court concludes that Harrison considered the possibility that
Mr. Rhyne’s AML is familial, and his inability to conclusively rule out familial AML
does not render his causation opinion unreliable, but instead goes to the weight that
the jury should give the opinion.
Cooper, 259 F.3d at 202 (stating that “the
alternative causes suggested by a defendant normally affect the weight that the jury
should give the expert’s testimony and not the admissibility of that testimony”).
Last, Defendants argue that Harrison failed to rule out obesity as an
alternative cause of Mr. Rhyne’s AML. There is scientific literature suggesting that
obesity is a risk factor for AML, and Mr. Rhyne was obese at the time of diagnosis.
Harrison’s expert report incorrectly states that Mr. Rhyne was not obese. (Doc. No.
148-6, at 12.) But during his deposition, Harrison testified that if Mr. Rhyne were
obese, then obesity is a possible contributing factor to his AML. (Doc. No. 194-3, at
145:3–9.) Harrison also explained that even if Mr. Rhyne were obese, cancer can be
multifactorial and exposure to benzene was still a substantial contributing factor to
the development of Mr. Rhyne’s AML.
(Doc. No. 194-3, at 196:15–25.)
Thus,
Harrison’s mistaken belief that Mr. Rhyne was not obese does not render his
differential diagnosis unreliable and can be attacked on cross-examination. See
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Bresler v. Wilmington Tr. Co., 855 F.3d 178, 195 (4th Cir. 2017) (stating that
“questions regarding the factual underpinnings of the [expert’s] opinion affect the
weight and credibility of the [witness’s] assessment, not its admissibility” (quotation
marks omitted)); United States v. Moreland, 437 F.3d 424, 431 (4th Cir. 2006) (“The
court need not determine that the proffered expert testimony is irrefutable or
certainly correct. As with all other admissible evidence, expert testimony is subject
to testing by ‘vigorous cross-examination, presentation of contrary evidence, and
careful instruction on the burden of proof.’” (citation omitted) (quoting Daubert, 509
U.S. at 596)).
*
*
*
Therefore, the Court concludes that Harrison’s causation opinions are both
reliable and relevant. The Court denies Defendants’ motions to exclude Harrison’s
expert testimony.
D.
Gore
Plaintiffs offer Gore to provide expert testimony on specific causation.
Defendants make three arguments as to why Gore’s testimony should be excluded:
(1) he failed to perform a reliable differential diagnosis, (2) he should not be permitted
to rely on Herrick’s exposure calculations, and (3) his opinion that a damaged
hematopoietic, or blood-forming, stem cell may stay quiescent for many years or even
decades before it proliferates and causes leukemia is not based on a reliable method.
1.
Differential Diagnosis
Defendants contend that Gore’s differential diagnosis is unreliable because he
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failed to rule out radiation exposure, a genetic defect, and obesity as alternative
causes of Mr. Rhyne’s AML.
As discussed above, defense experts Pyatt and Kaden testified that Mr.
Rhyne’s radiation exposure was insufficient to cause his AML, (Doc. No. 199-9, at
115:2–22; Doc. No. 199-10, at 88:1–17), and Defendants concede that they do not posit
that radiation caused Mr. Rhyne’s AML. Thus, radiation exposure is not a plausible
alternative cause of Mr. Rhyne’s AML. See Kannankeril, 128 F.3d at 808 (stating
that defendant may attack plaintiff’s expert’s differential diagnosis by pointing to “a
plausible cause of the plaintiff’s illness other than the defendant’s actions”).
Nevertheless, Gore testified that Mr. Rhyne’s position at Duke Energy was not a highrisk radiation occupation, and it would be very unlikely that radiation exposure
caused Mr. Rhyne’s AML. (Doc. No. 191-3, at 17:25–18:12.) The Court thus concludes
that Gore considered radiation exposure as an alternative cause of Mr. Rhyne’s AML
and offered an adequate explanation as to why it was not the sole cause. See Cooper,
259 F.3d at 202 (stating that “if an expert utterly fails to consider alternative causes
or fails to offer an explanation for why the proffered alternative cause was not the
sole cause, a district court is justified in excluding the expert’s testimony”).
As discussed with respect to Harrison’s differential diagnosis, the genetic tests
necessary to determine the presence of genetic defects commonly found in familial
AML were not done for Mr. Rhyne due to his critical condition. This does not render
Gore’s opinion unreliable, but instead affects its weight. Smith v. Wyeth-Ayerst Labs.
Co., 278 F. Supp. 2d 684, 692 (W.D.N.C. 2003) (stating that “differential diagnosis
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doesn’t require plaintiff to rule out every other cause, only to offer an explanation and
take account of the other potential causes”).
With respect to Mr. Rhyne’s obesity, Gore considered it as an alternative cause
of Mr. Rhyne’s AML. Gore recognized that “[t]he aggregate data suggests that obesity
may increase the risk of AML by a factor of approximately 1.5” and that Mr. Rhyne’s
“obesity may be considered a contributing factor.” (Doc. No. 148-8, at 11.) But that
obesity may have been a contributing factor to Mr. Rhyne’s AML does not render
exposure to benzene a non-substantial contributing factor to Mr. Rhyne’s AML. (Doc.
No. 148-8, at 19.) Therefore, the Court concludes that Gore performed a reliable
differential diagnosis.
2.
Reliance on Herrick’s Exposure Calculations
Defendants also contend that Gore should not be permitted to rely on Herrick’s
exposure calculations because Gore’s report relied on exposure calculations
performed by a different expert whom Plaintiffs have since withdrawn, and Gore did
not amend his report to indicate that he intended to rely on Herrick’s exposure
calculations. Defendants argue that without Herrick’s exposure calculations, Gore
cannot reliably “rule in” exposure to benzene as a cause of Mr. Rhyne’s AML.
Federal Rule of Civil Procedure 26(a)(2) requires the parties to disclose the
identity of any expert witness whom may be used at trial. Such disclosure must be
accompanied by a written report prepared by the witness that contains “a complete
statement of all opinions the witness will express and the basis and reasons for them,”
“the facts or data considered by the witness in forming them,” “any exhibits that will
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be used to summarize or support them,” “the witness’s qualifications,” “a list of all
other cases in which, during the previous 4 years, the witness testified as an expert
at trial or by deposition,” and “a statement of the compensation to be paid for the
study and testimony in the case.” Fed. R. Civ. P. 26(a)(2)(B). “Rule 26(e)(1) requires
a party to supplement its experts’ reports and deposition testimony when the party
learns of new information.” S. States Rack & Fixture, Inc. v. Sherwin-Williams Co.,
318 F.3d 592, 595–96 (4th Cir. 2003).
“If a party fails to provide information or identify a witness as required by Rule
26(a) or (e), the party is not allowed to use that information or witness to supply
evidence on a motion, at a hearing, or at a trial, unless the failure was substantially
justified or is harmless.” Fed. R. Civ. P. 37(c)(1). “District courts are accorded broad
discretion in determining whether a nondisclosure or untimely disclosure of evidence
is substantially justified or harmless.” Bresler, 855 F.3d at 190 (quotation marks
omitted). In making this determination, district courts consider the following factors:
“(1) the surprise to the party against whom the evidence would be offered; (2) the
ability of that party to cure the surprise; (3) the extent to which allowing the evidence
would disrupt the trial; (4) the importance of the evidence; and (5) the nondisclosing
party’s explanation for its failure to disclose the evidence.” S. States, 318 F.3d at 597.
“The first four factors listed above relate primarily to the harmlessness exception,
while the last factor, addressing the party’s explanation for its nondisclosure, relates
mainly to the substantial justification exception.” Bresler, 855 F.3d at 190.
The Court concludes that Plaintiffs’ failure to supplement Gore’s report to
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indicate that he was relying on Herrick’s exposure calculations was harmless. With
respect to the first factor, any surprise from Plaintiffs’ failure to supplement Gore’s
report was minimal. This case was originally filed in Pennsylvania state court. While
the case was proceeding in Pennsylvania, Plaintiffs provided the expert reports of
Infante, Harrison, Gore, and Stephen Petty, an industrial hygienist who calculated
Mr. Rhyne’s level of exposure to benzene. After the Pennsylvania court dismissed the
case based on forum non conveniens, Plaintiffs refiled it in this Court. Plaintiffs’
deadline to provide reports from their expert witnesses in this case was August 29,
2019. (Doc. No. 110.) Plaintiffs re-served the reports of Infante, Harrison, and Gore,
but did not re-serve Petty’s report. Instead, Plaintiffs provided the report of Herrick
and designated him as their exposure expert. Thus, Defendants were aware at least
as of September 2019 that Plaintiffs were relying on Herrick, rather than Petty, to
establish Mr. Rhyne’s level of exposure to benzene. Moreover, during his November
4, 2019 deposition, Gore testified that he was relying on Herrick’s exposure
calculations. (Doc. No. 191-3, at 46:1–5.)
Turning to the second factor, Defendants were able to cure any purported
surprise. Defendants were put on notice that Plaintiffs were relying on Herrick as
their exposure expert at least two months before Gore’s deposition and approximately
one year before the trial is scheduled to begin in September 2020. See Bresler, 855
F.3d at 194 (concluding that plaintiff’s untimely disclosure did not affect defendant’s
ability to conduct its defense in any material respect where defendant had access to
the untimely disclosed information two months before trial).
And importantly,
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Herrick’s calculation of Mr. Rhyne’s exposure level was significantly less than Petty’s
calculation, thereby minimizing the prejudicial effect of any purported surprise.
Further, there is nothing in the record to suggest that allowing Gore’s testimony in
reliance on Herrick’s calculations would disrupt the trial in any way. Thus, the
second and third factors also strongly weigh in favor of finding that the nondisclosure
was harmless.
The fourth and fifth factors weigh in favor of Defendants. The evidence is
important to Plaintiffs’ ability to prove specific causation, and Plaintiffs have not
offered any justification for the nondisclosure. Nevertheless, given the minimal
surprise caused by the nondisclosure, Defendants’ ample ability to cure any surprise,
and that allowing the evidence would not disrupt the trial, the Court concludes that
Plaintiffs’ failure to supplement Gore’s report to indicate he was relying on Herrick’s
exposure calculations was harmless, and Gore may rely on Herrick’s calculations at
trial.
See id. (concluding that the district court did not abuse its discretion in
admitting plaintiff’s untimely expert evidence where the first three factors supported
a finding that the untimely disclosure was harmless even though the last two factors
weighed in favor of exclusion).
3.
Quiescent Stem Cell Opinion
Defendants also move to exclude Gore’s opinion that a damaged hematopoietic,
or blood-forming, stem cell may stay quiescent for many years or even decades before
it proliferates and causes leukemia. Defendants argue that Gore’s quiescent stem
cell opinion is not based on a reliable method. Relying on a declaration of Pyatt,
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Defendants argue that numerous epidemiological studies establish that only those
benzene exposures that occurred within ten to fifteen years of diagnosis cause or
contribute to AML. (Doc. No. 182-9, ¶¶ 7–15.) Gore, however, failed to cite any
scientific literature in support of his opinion that a damaged hematopoietic stem cell
may stay quiescent for many years or even decades before it proliferates and causes
leukemia. And according to Pyatt’s declaration, the studies that have addressed the
length of time that stem cells remain quiescent do not support Gore’s opinion.14 (Doc.
No. 182-9, ¶¶ 25–34.)
In their opposition to Defendants’ motion to exclude Gore’s testimony,
Plaintiffs do not address Gore’s quiescent stem cell opinion or Defendants’ arguments
for the exclusion thereof. Although Gore’s opinion may very well be correct, “nothing
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.”
GE, 522 U.S. at 146. That is essentially what Plaintiffs ask this Court to do. Gore
does not cite any scientific literature or data to support his quiescent stem cell
opinion, and Plaintiffs make no effort to show or argue that the opinion is the product
of a reliable methodology. While Gore testified during his deposition approximately
eight months ago that there are a “gazillion” articles that support his quiescent stem
cell opinion, (Doc. No. 191-3, at 58:9–59:2), Plaintiffs did not have Gore submit a
supplemental report with citations to any supporting articles or other data.
None of the studies cited by Pyatt regarding Gore’s quiescent stem cell opinion are
included in the record.
14
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Plaintiffs bear the burden of proving that Gore’s opinion is reliable by a
preponderance of proof.
In the face of literature contrary to Gore’s opinion, an
absence of any literature or data supporting Gore’s opinion, and Plaintiffs’ failure to
make any effort to show or argue that Gore’s opinion is reliable, the Court is
constrained to conclude that Plaintiffs have not met that burden with respect to
Gore’s quiescent stem cell opinion. Therefore, the Court excludes Gore’s opinion that
a damaged hematopoietic stem cell may stay quiescent for many years or even
decades before it proliferates and causes leukemia.
E.
Herrick15
Herrick first calculated Mr. Rhyne’s daily average benzene exposure from each
product. Herrick then used Mr. Rhyne’s daily average benzene exposures to calculate
Mr. Rhyne’s cumulative benzene exposure from each product. Herrick opines that
the medium range of Mr. Rhyne’s cumulative benzene exposure was 12.96 to 26.57
parts per million-years (“ppm-years”)16 with a midrange value of 17.53 ppm-years.
(Doc. No. 132-8.)
In support of their motions to exclude Herrick’s testimony,
Defendants raise arguments that are specific to Herrick’s exposure calculations for
their respective products, as well as an argument that is not specific to any product
or calculation. The Court addresses Defendants’ product-specific arguments first and
In response to Defendants’ motions to exclude Herrick’s expert testimony, Plaintiffs
filed a declaration of Herrick. (Doc. No. 226-1.) Defendants argue that Herrick’s
declaration is an improper and untimely supplemental expert report. The Court need
not decide the propriety of Herrick’s declaration because the Court concludes that
Herrick’s testimony is admissible without considering Herrick’s declaration.
16 Cumulative exposure is expressed in ppm-years and is the product of Mr. Rhyne’s
average daily exposure to benzene and the number of years of exposure to benzene.
15
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then turns to the general argument.
1.
Safety Kleen’s Product-Specific Arguments
i.
Herrick’s Use of ART
To calculate Mr. Rhyne’s exposure to benzene from Safety Kleen’s parts washer
solvent, Herrick used the Advanced REACH Tool (“ART”). Safety Kleen argues that
ART is not a reliable tool for conducting an individual retrospective exposure
assessment. The Court disagrees.
A European regulation titled Registration, Evaluation, Authorization and
Restriction of Chemicals (“REACH”) requires manufacturers and importers of
chemical substances to conduct quantitative occupational exposure studies for
identified and selected exposure scenarios. ART was developed to assist companies
in complying with REACH. (Doc. No. 148-3, at 18.) It simulates exposure to various
substances from different activities that users create through exposure scenarios by
selecting predetermined options regarding the product being used and circumstances
of use. (Doc. No. 201-3, at 86:11–17.) ART has two components: (1) a mechanistic
model based on physicochemical properties such as the product, vapor pressure, size
of the room, and type of use, and (2) calibration data of 2,500 to 3,000 real-world
measurements of exposure that are characteristic of the scenario being modeled.
(Doc. No. 201-3, at 87:10–16, 101:17–21, 102:22–103:12.)
In LeBlanc et al. (2018), cited in Herrick’s report, the authors compared ART’s
benzene exposure predictions from using a mineral spirits parts washer solvent to
real-world measurements and found that ART’s exposure estimates were closer to the
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real-world measurements than other modeling approaches. (Doc. No. 204-8; Doc. No.
201-3, at 162:13–21, 165:1–13.) In addition, Herrick brought three recently published
articles to his deposition that compared different models’ predictions against realworld exposure measurements that further support the superiority of ART over other
models. (Doc. No. 201-3, at 89:18–91:17.) While ART may have been developed to
assess exposures under REACH, that does not mean ART is an unreliable tool for
modeling individual retrospective exposure assessments.
There is scientific
literature supporting the reliability of ART’s individual exposure estimates and,
therefore, the Court concludes that Herrick’s methodology of using ART to calculate
Mr. Rhyne’s benzene exposure from use of Safety Kleen’s parts washer solvent was
reliable. See Milward v. Acuity Specialty Prods. Grp., Inc., 969 F. Supp. 2d 101, 108
(D. Mass. 2013) (concluding that expert’s exposure assessment was admissible where
expert used ART to calculate plaintiff’s benzene exposure from using paint that
contained mineral spirits), aff’d, 2016 U.S. App. LEXIS 7470 (1st Cir. Apr. 25, 2016).
ii.
Herrick’s Estimate of the Benzene Concentration in the
Parts Washer Solvent
In modeling Mr. Rhyne’s exposure to benzene from using Safety Kleen’s parts
washer solvent, Herrick estimated that the concentration of benzene in the solvent
was 58 ppm. Safety Kleen argues that in estimating the benzene concentration was
58 ppm, Herrick ignored relevant and reliable real-world data on the benzene
concentration of mineral spirits, thus rendering his calculations unreliable.
Safety Kleen operated a recycling center in Lexington, South Carolina, which
collected samples of its parts washer solvent for testing. Composite testing data
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indicates that from May 1992 through June 1993, the average concentration of
benzene in samples of parts washer solvent from the Lexington facility was 32.1 ppm
with a maximum of 64.3 ppm and a minimum of 11.6 ppm. (Doc. No. 206.) Additional
composite testing data indicates that the average concentration of benzene in samples
of parts washer solvent from the Lexington facility was 22.5 ppm in the first quarter
of 1994, 19.5 ppm in the second quarter of 1994, and 15.6 ppm in the fourth quarter
of 1994.17 (Doc. No. 201-6.) Safety Kleen argues that Herrick’s use of 58 ppm benzene
in the face of that data was unreliable.
The evidence tends to show that Mr. Rhyne used the parts washer solvent from
the mid-1970s through 1998.
The benzene concentration in mineral spirits has
decreased over the years as the hazardous effects of benzene became known and
accepted and governmental agencies started regulating the benzene content of
products. (See Doc. No. 201-3, at 329:11–21.) The benzene concentration in mineral
spirits was thus higher in the 1970s and 1980s than it was in the 1990s. (Doc. No.
148-3, at 24–25.) Accordingly, the concentration of benzene in Safety Kleen’s mineral
spirits solvent in the early 1990s is not representative of the solvent’s benzene
concentration in the 1970s and 1980s. Moreover, the benzene in the parts washer
solvent decays over time, (Doc. No. 201-3, at 218:9–15), thus suggesting that the
benzene concentration in the samples at the time they were tested was less than the
concentration to which users were exposed.
Further, Herrick’s use of 58 ppm was not based on mere speculation, as Safety
17
There is no data for the third quarter of 1994.
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Kleen contends. The purpose of the parts washer is to recirculate the solvent so that
it is used repeatedly.
(Doc. No. 201-3, at 218:20–24.)
As a result, based on
information from Safety Kleen on how often the parts washer solvent was replaced
with fresh solvent, Herrick estimated that the parts washer only contained fresh
solvent about every two weeks. (Doc. No. 201-3, at 323:16–22.) As the benzene in the
solvent decays over time, the benzene concentration in the solvent on any given day
was somewhere between the original benzene concentration when the solvent was
first replaced and the benzene concentration as time passed. (Doc. No. 201-3, at
323:23–324:2.) Herrick did not have specific information or data on the original
benzene concentration in the parts washer solvent. (Doc. No. 201-3, at 324:14–19,
325:5–8.) Herrick cited to scientific literature suggesting that until at least 2000, the
benzene content of fresh mineral spirits ranged from 100 ppm to 1,000 ppm, and other
literature reported ranges from 1,000 ppm to 10,000 ppm. (Doc. No. 148-3, at 24–25;
Doc. No. 201-3, at 325:9–14, 326:9–13.) Herrick thus recognized that there was not a
consensus as to the starting concentration of benzene in mineral spirits and
estimated that the average benzene concentration of the solvent used by Mr. Rhyne
was 58 ppm.
(Doc. No. 201-3, at 325:9–18.)
He explained that 58 ppm was a
reasonable value based on the historical literature and the rate at which Safety Kleen
changed out the solvent, and that 58 ppm was a conservative value that was likely
on the low end. (Doc. No. 201-3, at 217:5–10, 218:8–24, 323:16–324:23, 325:4–18,
326:9–22.) In addition, by using a concentration of 58 ppm, Herrick was able to
validate ART’s predictions using the results of Fedoruk et al. (2003), which took real-
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world exposure measurements from use of a mineral spirits solvent containing 58
ppm benzene. (Doc. No. 201-3, at 323:9–15.)
Therefore, the Court concludes that Herrick’s estimate that the parts washer
solvent contained 58 ppm benzene was not based on mere speculation, and Safety
Kleen’s challenges to the accuracy of that factual underpinning go to the weight that
the jury should give Herrick’s opinion. See Bresler, 855 F.3d at 195 (stating that
“questions regarding the factual underpinnings of the [expert’s] opinion affect the
weight and credibility of the [witness’s] assessment, not its admissibility” (quotation
marks omitted)); Manpower, Inc. v. Ins. Co. of Pa., 732 F.3d 796, 808 (7th Cir. 2013)
(“The reliability of data and assumptions used in applying a methodology is tested by
the adversarial process and determined by the jury; the court’s role is generally
limited to assessing the reliability of the methodology—the framework—of the
expert’s analysis.”).
iii.
Herrick’s Inclusion of Far Field Exposures
Safety Kleen also argues that Herrick’s exposure assessment is unreliable
because his calculation of Mr. Rhyne’s exposure from using Safety Kleen’s parts
washer solvent includes exposures from other products being used around Mr. Rhyne.
ART allows one to measure exposure in the near field, which includes sources
within approximately three feet of the user, and the far field, which are secondary
sources of exposure outside the near field. (Doc. No. 201-3, at 133:11–134:4, 228:9–
12.) In modeling Mr. Rhyne’s exposure from his use of Safety Kleen’s parts washer
solvent, Herrick included near field and far field sources of exposure. (Doc. No. 201-
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3, at 342:8–13.) The far field sources of exposure were other sources of benzene
exposure in general, and one cannot tell from ART’s results how much exposure is
from the near field and how much is from the far field. (Doc. No. 201-3, at 238:22–
25, 343:3–8.) As a result, Herrick’s assessment of Mr. Rhyne’s benzene exposure from
using Safety Kleen’s parts washer solvent includes exposure from other sources for
which Safety Kleen is not responsible. Safety Kleen contends that this renders
Herrick’s exposure assessment unreliable.
The Court disagrees. The inclusion of secondary sources of exposure is a
question as to the factual underpinnings of Herrick’s opinion, and it is for the jury to
determine the soundness of those factual underpinnings and the weight to be given
to his resulting conclusions. See Milward, 969 F. Supp. 2d at 108 (stating that
“questions about the proper [ART] input parameters are questions about the factual
underpinnings of the opinion, which are matters going to weight rather than
admissibility”).
2.
USS’s Product-Specific Arguments
Plaintiffs contend that Mr. Rhyne was exposed to benzene from raffinate, a
chemical byproduct of USS’s coking operations that was captured and sold. USS’s
raffinate contained a minimum of 5% benzene. USS sold raffinate to non-party
Radiator Specialty Company (“Radiator”) from 1960 through 1978 in bulk sales. In
turn, Radiator designed, manufactured, labeled, and sold a product called Liquid
Wrench that contained raffinate. USS last sold raffinate to Radiator in April 1978.
USS argues that as a result, Herrick’s estimate that Mr. Rhyne used the raffinate
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formula of Liquid Wrench until January 1979 is mere speculation.
USS’s argument is without merit. Although USS last sold raffinate to Radiator
in April 1978, it does not follow that the raffinate formula of Liquid Wrench ceased
to exist in the marketplace at that time. Herrick explained that he estimated that
Mr. Rhyne used Liquid Wrench that contained raffinate until January 1979 because
he was trying to account for the fact that there was a certain amount of the raffinatecontaining Liquid Wrench in the marketplace that continued to be used after USS
last sold raffinate to Radiator in April 1978. (Doc. No. 201-3, at 166:15–167:6.)
Herrick’s estimate was not based on mere speculation, and USS’s challenges to the
correctness of that estimate and Herrick’s conclusions based thereon are for the jury.
See United States v. Cavely, 318 F.3d 987, 997–98 (10th Cir. 2003) (stating that
questions as to the validity of the assumptions underlying the expert’s opinion go to
weight and not admissibility); Acosta v. Vinoskey, 310 F. Supp. 3d 662, 673 (W.D. Va.
2018) (stating that “arguments about the factual basis of an expert’s opinion normally
go to its weight and not its admissibility”).
3.
Savogran’s Product-Specific Arguments
Savogran argues that Herrick’s exposure calculations are based on mere
speculation and that Herrick failed to use a reliable methodology.
i.
Exposure from Using Kutzit at Home
Herrick relied on Mr. Rhyne’s deposition testimony for information about Mr.
Rhyne’s product use. From 1970 to 1975, Mr. Rhyne used Kutzit at home while
working with his dad on the family cars. (Doc. No. 214-2, at 316:14–317:19, 328:14.)
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Specifically, Mr. Rhyne used Kutzit to cut and scrape off gaskets. (Doc. No. 214-2, at
316:21–317:8, 317:16–17.) To calculate Mr. Rhyne’s exposure to benzene from using
Kutzit at home, Herrick estimated that Mr. Rhyne worked on the family cars one day
per month for six to seven hours. (Doc. No. 148-3, at 31.) Mr. Rhyne testified that he
did not use Kutzit every time he worked on cars with his dad. (Doc. No. 214-2, at
330:16–18.) Herrick thus estimated that Mr. Rhyne used Kutzit one day in every
three days that he worked on cars.
(Doc. No. 148-3, at 31.)
Based on those
estimations, Herrick used ART to determine that Mr. Rhyne’s daily average exposure
to benzene over each year from using Kutzit at home was 0.04 ppm. (Doc. No. 148-3,
at 31.)
Savogran argues that Herrick’s exposure assessment is based on mere
speculation because Mr. Rhyne never testified that he worked on family cars one day
per month or that he used Kutzit one in every three days at home. While Mr. Rhyne
did not testify to such concrete data on how frequently he used Kutzit, Herrick’s
estimates are not based on mere speculation. Mr. Rhyne testified that he and his dad
worked on cars sometimes during the week after his dad got off from work and
sometimes on the weekend. (Doc. No. 214-2, at 330:9–13.) Based on that testimony,
Herrick’s estimate that Mr. Rhyne worked on cars one day per month is conservative.
As to how often he used Kutzit while working on cars, Mr. Rhyne testified that he did
not use Kutzit every time, but that he used Kutzit when he had to cut and scrape off
gaskets. (Doc. No. 214-2, at 317:16–17, 319:15–18.) Based on the type of work Mr.
Rhyne used Kutzit for, Herrick conservatively estimated that Mr. Rhyne used Kutzit
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one-third of the time that he worked on cars. (Doc. No. 148-3, at 19; Doc. No. 201-3,
at 347:12–25, 348:23–349:16.) Thus, while Herrick’s estimates are not based on exact
data on how often Mr. Rhyne used Kutzit at home, Herrick’s estimates are not based
on mere speculation. To require expert testimony to be based on exact information
as to how frequently plaintiff used a product fifty years ago, as Savogran suggests,
would effectively prohibit a plaintiff from ever recovering in a latent disease case.
Herrick’s estimates as to how often Mr. Rhyne used Kutzit at home are not based on
mere speculation, and Savogran’s challenges to the accuracy of those estimates go to
the weight that the jury should give to Herrick’s opinion. See Bresler, 855 F.3d at
195 (stating that “questions regarding the factual underpinnings of the [expert’s]
opinion affect the weight and credibility of the [witness’s] assessment, not its
admissibility” (quotation marks omitted)).
Like Safety Kleen, Savogran also argues that ART is not a reliable tool for
conducting an individual retrospective exposure assessment. As discussed above, the
Court rejects that argument and concludes that Herrick’s methodology of using ART
to calculate Mr. Rhyne’s benzene exposure from using Kutzit at home is reliable.
ii.
Exposure from Using Kutzit at Setzer’s
During his junior and senior years of high school (1974 and 1975), Mr. Rhyne
worked at Setzer’s Buick and Pontiac, an auto mechanic shop. (Doc. No. 214-2, at
584:13–16.) In his work at Setzer’s, Mr. Rhyne used Kutzit to cut and scrape off
gaskets.
(Doc. No. 214-2, at 663:12–16.)
To calculate Mr. Rhyne’s exposure to
benzene from using Kutzit at Setzer’s in 1974, Herrick estimated that Mr. Rhyne
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used a formulation of Kutzit that contained up to 56% benzene. (Doc. No. 148-3, at
17–18, 34.) But to calculate Mr. Rhyne’s exposure in 1975, Herrick estimated that
Mr. Rhyne used a formulation of Kutzit that contained approximately 0.025 to 0.5%
benzene. (Doc. No. 148-3, at 34.) To determine exposure from Mr. Rhyne’s use of
Kutzit, Herrick relied on Young et al. (1978), which collected air samples for five
sequential five-minute periods when a formula containing 52% benzene was used for
paint stripping. (Doc. No. 148-3, at 18, 34; Doc. No. 204-5.) The concentration of
benzene in the air samples ranged from 73 ppm to 225 ppm for an average of 130 ppm
over the 25-minute period. (Doc. No. 148-3, at 34; Doc. No. 204-5.) Accordingly, to
calculate Mr. Rhyne’s benzene exposure from using the benzene formulation of Kutzit
in 1974, Herrick used 130 ppm as Mr. Rhyne’s benzene exposure from using Kutzit
for a one-hour period. (Doc. No. 148-3, at 34.) To calculate Mr. Rhyne’s benzene
exposure from using the toluene formulation of Kutzit in 1975, Herrick reduced the
130 ppm value in proportion to his estimate that the toluene formulation of Kutzit
contained 0.025 to 0.5% benzene, yielding an average benzene exposure of 0.65 ppm
over a one-hour period. (Doc. No. 148-3, at 34.) Herrick then estimated that Mr.
Rhyne used Kutzit for one hour per day, one day per week, during the 9-month school
year. (Doc. No. 148-3, at 34.) Herrick’s estimations yielded a daily average exposure
of 2.44 ppm in 1974 and 0.01 ppm in 1975. (Doc. No. 148-3, at 34.) But because Mr.
Rhyne testified that some days he would work on gaskets (and use Kutzit) and other
days he would clean bolting or carburetors (and not use Kutzit), Herrick divided those
estimates in half, yielding an average daily exposure of 1.22 ppm in 1974 and 0.005
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ppm in 1975. (Doc. No. 148-3, at 34.)
Savogran first argues that Herrick’s estimate that Mr. Rhyne used a Kutzit
formulation in 1974 that contained up to 56% benzene is baseless because Herrick
had no information as to which formulation of Kutzit Mr. Rhyne used in 1974.
The evidence suggests that sometime around the end of 1973 and the beginning
of 1974, Savogran developed a new formulation of Kutzit in which benzene was
removed as an ingredient and replaced with toluene, thereby reducing but not
eliminating the benzene content of Kutzit. There is conflicting information, however,
as to when benzene was removed as an ingredient of Kutzit. (Doc. No. 148-3, at 17–
18.) Savogran inventory records indicate that the benzene formulation of Kutzit was
used until February 28, 1974. (Doc. No. 148-3, at 17.) Herrick thus estimated that
the benzene formulation of Kutzit existed in the marketplace and was used until it
was depleted at the end of 1974. (Doc. No. 201-3, at 359:21–362:1.) Herrick’s estimate
is not based on mere speculation and the accuracy thereof is for the jury.
Next, Savogran argues that Herrick’s methodology of using the exposure levels
reported in Young et al. (1978) to calculate Mr. Rhyne’s exposure from using Kutzit
is unreliable because (1) Herrick states that the authors used a Kutzit formula but
nothing in the study indicates a Kutzit product or formula was used, (2) the authors
conducted the paint stripping in a two-car garage measuring approximately eight feet
by twenty-one feet by twenty feet and there is no reason to believe that Mr. Rhyne’s
workspace at Setzer’s was “anywhere close” to a two-car garage, and (3) the authors
only collected air samples for five sequential five-minute periods.
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Savogran’s arguments are meritless. Although there is nothing in the study to
indicate that a Kutzit formula was used, the study used a solvent containing 52%
benzene, and Herrick estimated that the Kutzit formulation used by Mr. Rhyne
contained up to 56% benzene. As a result, the reported air sample levels provide a
reliable basis for Herrick’s estimate as to Mr. Rhyne’s exposure from using Kutzit in
1974, and Herrick’s methodology of reducing that value in proportion to the lesser
benzene content of the toluene formulation of Kutzit to estimate Mr. Rhyne’s
exposure from using Kutzit in 1975 was reliable. Turning to Savogran’s second point,
that there is no information as to the exact size and ventilation of Mr. Rhyne’s
workspace at Setzer’s does not render Herrick’s use of the reported exposure levels
from Young unreliable. Such a challenge goes to the weight that the jury should give
Herrick’s opinion. The same is true of Savogran’s criticism that the authors only
collected five air samples.
Last, Savogran argues that Herrick’s exposure assessment is based on mere
speculation because Mr. Rhyne never testified that his use of Kutzit averaged out to
one hour per day, one day per week. In so arguing, Savogran seeks to impose a
standard of exactness and overlooks a critical step in Herrick’s methodology.
Herrick’s starting estimate that Mr. Rhyne used Kutzit one hour per day, one day per
week is based on Mr. Rhyne’s testimony that he worked at Setzer’s one day per week
and on the days that he cleaned gaskets, he used Kutzit for one hour. (Doc. No. 2142, at 584:17–19, 661:22–662:3.) Mr. Rhyne also testified, however, that some days he
would clean gaskets and thus use Kutzit, and other days he would clean bolting or
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carburetors for which he did not use Kutzit. (Doc. No. 214-2, at 661:10–21.) To
account for the fact that Mr. Rhyne did not clean gaskets each day he went to Setzer’s,
Herrick divided his exposure calculations in half. (Doc. No. 148-3, at 34.) In so doing,
Herrick effectively changed his estimate as to how often Mr. Rhyne used Kutzit from
one hour per day, one day per week to one hour per day, one day every other week.
Therefore, the Court concludes that Herrick’s assessment of Mr. Rhyne’s benzene
exposure from using Kutzit at Setzer’s is based on a reliable methodology.
iii.
Exposure from Using Kutzit at Duke Energy
Savogran challenges Herrick’s reliance on Young et al. (1978) to calculate Mr.
Rhyne’s benzene exposure from using Kutzit at Duke Energy.
For the reasons
discussed above, the Court concludes that Young et al. (1978) provides a reliable basis
for Herrick’s exposure calculations.
Savogran also argues that Herrick’s assessment of Mr. Rhyne’s exposure to
benzene from using Kutzit at Duke Energy is based on speculation because there is
no evidentiary support for Herrick’s assumption that Mr. Rhyne used Kutzit at Duke
Energy from 1985 to 1998.
Mr. Rhyne testified that his use of Kutzit during his employment with Duke
Energy was limited to his time as a maintenance mechanic. (Doc. No. 214-2, at 323:2–
9.) Mr. Rhyne further testified that he became a maintenance mechanic in 1985 and
continued as a maintenance mechanic until 1998 when he became a maintenance
supervisor.
(Doc. No. 214-2, at 323:14–16, 426:9–16.)
Accordingly, there is
evidentiary support for Herrick’s estimate that Mr. Rhyne used Kutzit at Duke
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Energy from 1985 to 1998, and Herrick’s assessment of Mr. Rhyne’s benzene exposure
from using Kutzit at Duke Energy is based on a reliable methodology.
4.
Defendants’ General Argument for Exclusion
All Defendants argue that Herrick’s exposure assessment is unreliable because
he excluded exposures from certain products for which there was sufficient evidence
and included exposures from certain products for which there was insufficient
evidence. Specifically, Defendants contend that Herrick excluded exposures from Mr.
Rhyne’s use of Tap Magic and Spotcheck even though Mr. Rhyne testified to using
those products, and included exposures from Mr. Rhyne’s use of CRC 3-36 even
though there was insufficient evidence that the CRC Industries product used by Mr.
Rhyne was CRC 3-36.
Defendants’ argument is not persuasive. Herrick explained that he did not
calculate Mr. Rhyne’s benzene exposure from Tap Magic because although an April
1992 approved chemical list for Duke Energy’s McGuire facility included a Tap Magic
product, several Material Safety Data Sheets18 for Tap Magic products report a
composition of petroleum distillates ranging from 40 to 75%. (Doc. No. 148-3, at 30.)
As the record does not indicate which of those Tap Magic products Mr. Rhyne used,
Herrick did not estimate Mr. Rhyne’s benzene exposure from his use of Tap Magic.
(Doc. No. 148-3, at 30; Doc. No. 201-3, at 51:20–52:2.) The same is true of Spotcheck.
A Material Safety Data Sheet is a document produced in compliance with the
hazard communication standard and is used by manufacturers and industry readers
as a means of communicating information to users of the product. (Doc. No. 201-3, at
308:10–18.)
18
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Although Spotcheck was on the April 1992 approved chemical list, Herrick was
unable to obtain a Material Safety Data Sheet for Spotcheck from the relevant time
period, and the record did not otherwise indicate the composition of the product. (Doc.
No. 148-3, at 30–31; Doc. No. 201-3, at 52:3–22, 53:15–21.) Accordingly, Herrick did
not estimate Mr. Rhyne’s benzene exposure from his use of Spotcheck. (Doc. No. 1483, at 31; Doc. No. 201-3, at 52:14–18.)
While the Court ultimately granted summary judgment in favor of former
Defendant CRC Industries, Inc. because there was insufficient evidence that the CRC
Industries product used by Mr. Rhyne was CRC 3-36, Herrick’s inclusion of that
product as a source of benzene exposure goes to the weight of Herrick’s opinion, rather
than its admissibility. See Bresler, 855 F.3d at 195 (stating that “questions regarding
the factual underpinnings of the [expert’s] opinion affect the weight and credibility of
the [witness’s] assessment, not its admissibility” (quotation marks omitted)).
*
*
*
Therefore, the Court concludes that Herrick’s exposure assessment is based on
sufficient data and the product of a reliable methodology.
The Court denies
Defendants’ motions to exclude Herrick’s testimony.
F.
Petty
Defendants move to exclude the expert testimony of Petty, whom Plaintiffs
offered as their exposure expert when the case was pending in Pennsylvania state
court. Plaintiffs did not file a response to Defendants’ motion, but as previously
discussed, Plaintiffs did not identify Petty as an expert when they refiled this case in
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this Court. Moreover, Plaintiffs concede that “Petty has been withdrawn as an expert
and his calculations have no bearing on this case now.”
(Doc. No. 218, at 23.)
Therefore, the Court grants Defendants’ motion to exclude Petty’s expert testimony.
IV.
PLAINTIFFS’ MOTIONS
Plaintiffs move to exclude certain testimony of defense expert John W.
Spencer. Plaintiffs also move to exclude evidence of radiation exposure and a genetic
defect as alternative causes of AML.
A.
Motion to Exclude Spencer’s Expert Testimony
Mr. Rhyne testified that during his employment with Duke Energy, he used
Liquid Wrench to cool hot couplings and pipe. (Doc. No. 209-1, at 268:1–3.) Put
differently, Mr. Rhyne testified that he used Liquid Wrench as a metal coolant. In
his expert report, Spencer opines that it is unlikely that Mr. Rhyne used Liquid
Wrench as he described. (Doc. No. 193-2, at 39.) Plaintiffs move to exclude that
opinion, arguing it is an impermissible attack on Mr. Rhyne’s credibility. The Court
agrees.
“The assessment of a witness’s credibility . . . is usually within the jury’s
exclusive purview. Thus, in the absence of unusual circumstances, Rule 702 renders
inadmissible expert testimony on issues of witness credibility.” United States v.
Lespier, 725 F.3d 437, 449 (4th Cir. 2013) (quotation marks and citation omitted). In
opining that it is unlikely Mr. Rhyne used Liquid Wrench as he testified to using it,
Spencer plainly calls into question Mr. Rhyne’s credibility. Exclusion of his opinion
is appropriate on that basis alone.
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The Court further concludes that Spencer’s opinion is not the product of
reliable methods. The basis for Spencer’s opinion that Mr. Rhyne likely did not use
Liquid Wrench as a metal coolant is (1) using Liquid Wrench in that manner may
have caused a fire, and (2) there were more suitable products for such use that were
available to Mr. Rhyne. (Doc. No. 193-2, at 39.) Even if Spencer’s opinion concerned
a matter appropriate for expert testimony, his opinion is not reliable—“there is
simply too great an analytical gap between the data and the opinion proffered.” Doe,
440 F. Supp. 2d at 471. That using Liquid Wrench as a metal coolant may have
caused a fire and that there were more suitable products for such use that were
available to Mr. Rhyne reliably support a conclusion that Mr. Rhyne should not have
used Liquid Wrench as a metal coolant, but those facts do not reliably support
Spencer’s offered opinion that Mr. Rhyne did not in fact use Liquid Wrench as a metal
coolant.
Therefore, the Court grants Plaintiffs’ motion and excludes Spencer’s
opinion that it is unlikely that Mr. Rhyne used Liquid Wrench as he described.
B.
Motion to Exclude Evidence of Radiation Exposure as an Alternative
Cause
Plaintiffs move to exclude evidence that radiation exposure can cause AML or
that radiation exposure caused Mr. Rhyne’s AML. As discussed above, Mr. Rhyne
was exposed to radiation during his employment with Duke Energy, and the experts
agree that, at certain levels, radiation exposure is a risk factor for AML.
But
Plaintiffs’ specific causation experts ruled out radiation exposure as an alternative
cause of Mr. Rhyne’s AML, and defense experts Pyatt and Kaden testified that Mr.
Rhyne’s radiation exposure was insufficient to cause his AML. And while Defendants
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concede that they do not offer radiation exposure as an alternative cause of Mr.
Rhyne’s AML, Defendants nonetheless contend that Mr. Rhyne’s radiation exposure
is relevant to the reliability of, and weight that should be given to, Plaintiffs’ specific
causation experts’ opinions that exposure to benzene caused his AML. The Court
disagrees.
Relevant evidence—that which has a tendency to make a fact of consequence
more or less probable than it would be without the evidence—is generally admissible.
Fed. R. Evid. 401–402.
Courts may exclude relevant evidence, however, if its
probative value is substantially outweighed by the danger of unfair prejudice,
confusing the issues, misleading the jury, undue delay, wasting time, or needlessly
presenting cumulative evidence. Fed. R. Evid. 403.
Plaintiffs’ and Defendants’ experts agree that Mr. Rhyne’s radiation exposure
was insufficient to have caused his AML, and Plaintiffs’ specific causation experts
considered and ruled out Mr. Rhyne’s radiation exposure as an alternative cause.
While “[t]he alternative causes suggested by a defendant affect the weight that the
jury should give the expert’s testimony,” Westberry, 178 F.3d at 265, Defendants do
not suggest that radiation exposure was an alternative cause of Mr. Rhyne’s AML.
For this reason, evidence of radiation exposure as an alternative cause of AML in
general and Mr. Rhyne’s AML is not relevant. In addition, allowing evidence of Mr.
Rhyne’s radiation exposure and radiation exposure generally as a cause of AML
would likely confuse the issues, mislead the jury, and cause undue delay. Therefore,
the Court concludes that evidence of radiation exposure as a cause of AML or that
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radiation exposure caused Mr. Rhyne’s AML is irrelevant. The Court alternatively
concludes that the probative value of such evidence is substantially outweighed by
the danger of confusing the issues, misleading the jury, and causing undue delay.
The Court grants Plaintiffs’ motion to exclude evidence that radiation exposure can
cause AML or that radiation exposure caused Mr. Rhyne’s AML.
C.
Motion to Exclude Evidence of a Genetic Defect as an Alternative Cause
Plaintiffs move to exclude evidence of Mr. Rhyne’s sister’s AML and evidence
that a genetic defect can cause AML or that a genetic defect caused Mr. Rhyne’s AML.
The basis for Plaintiffs’ motion is essentially the same as that for their motion to
exclude evidence of radiation exposure as an alternative cause—that no defense
expert has opined that Mr. Rhyne’s AML was familial.
While the experts agree that Mr. Rhyne’s radiation exposure was insufficient
to cause his AML, the genetic tests necessary to confirm the presence of genetic
defects commonly found in familial AML were not done. As a result, although the
Court has concluded that Plaintiffs’ specific causation experts adequately considered
the possibility that Mr. Rhyne’s AML was familial such that their differential
diagnoses were reliable, no expert could definitively rule out that Mr. Rhyne’s AML
was familial. And as discussed above, the inability of Plaintiffs’ specific causation
experts to conclusively rule out familial AML goes to the weight that the jury should
give those opinions.
Cooper, 259 F.3d at 202 (stating that “the alternative causes
suggested by a defendant normally affect the weight that the jury should give the
expert’s testimony and not the admissibility of that testimony”).
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Evidence of Mr. Rhyne’s sister’s AML and the lack of genetic tests confirming
or refuting the existence of genetic defects commonly found in familial AML is thus
relevant to whether Mr. Rhyne’s AML was familial—a fact that, unlike Mr. Rhyne’s
radiation exposure, is still of consequence to determining this action. Of course,
Plaintiffs will be permitted to rebut this evidence with evidence that familial AML is
rare and normally presents in patients much younger than Mr. Rhyne. It will then
be left to the jury to consider and weigh this evidence as to the cause of Mr. Rhyne’s
AML.
Therefore, the Court denies Plaintiffs’ motion to exclude evidence of Mr.
Rhyne’s sister’s AML and evidence of a genetic defect as a cause of AML generally or
Mr. Rhyne’s AML.
V.
CONCLUSION
IT IS THEREFORE ORDERED that:
1.
Defendants’ motions to exclude the testimony of Plaintiffs’ experts are
GRANTED in part and DENIED in part.
a.
USS’s and Safety Kleen’s motions to exclude Infante’s expert
testimony, (Doc. Nos. 186, 195), are GRANTED as to Infante’s
offered opinion on specific causation, and such opinion is
excluded. The motions are DENIED in all other respects.
b.
USS’s and Safety Kleen’s motions to exclude Harrison’s expert
testimony, (Doc. Nos. 188, 192), are DENIED.
c.
USS’s motion to exclude Gore’s expert testimony, (Doc. No. 182),
is GRANTED as to Gore’s quiescent stem cell opinion, and such
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opinion is excluded. The motion is DENIED in all other respects.
d.
Safety Kleen’s motion to exclude Gore’s expert testimony, (Doc.
No. 190), is DENIED.
e.
USS and Safety Kleen’s joint motion to exclude Herrick’s expert
testimony, (Doc. No. 197), and Savogran’s motion to exclude
Herrick’s expert testimony, (Doc. No. 203), are DENIED.
f.
USS and Safety Kleen’s joint motion to exclude Petty’s expert
testimony, (Doc. No. 184), is GRANTED, and Petty will not be
permitted to testify at trial.
2.
Plaintiffs’ evidentiary motions are GRANTED in part and DENIED in
part.
a.
Plaintiffs’ motion to exclude Spencer’s expert testimony, (Doc. No.
193), is GRANTED, and Spencer’s opinion that it is unlikely Mr.
Rhyne used Liquid Wrench as he described is excluded.
b.
Plaintiffs’ motion to exclude evidence of radiation exposure as an
alternative cause, (Doc. No. 198), is GRANTED, and the Court
excludes evidence that radiation exposure can cause AML or
caused Mr. Rhyne’s AML.
c.
Plaintiffs’ motion to exclude evidence of Mr. Rhyne’s sister’s AML
and a genetic defect as an alternative cause, (Doc. No. 200), is
DENIED.
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Signed: July 23, 2020
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