Joann Schultz v. Akzo Nobel Paints, LLC , 721 F.3d 426 ( 2013 )

In the
United States Court of Appeals
For the Seventh Circuit
No. 12-1902
JOANN E VELYN S CHULTZ, Individually and as
Personal Representative of the Estate of
Donald Walter Schultz,
Plaintiff-Appellant,
v.
A KZO N OBEL P AINTS, LLC, et al.,
Defendants-Appellees.
Appeal from the United States District Court
for the Eastern District of Wisconsin.
No. 08-C-919—Rudolph T. Randa, Judge.
A RGUED O CTOBER 30, 2012—D ECIDED JUNE 26, 2013
Before B AUER, F LAUM, and W OOD , Circuit Judges.
W OOD , Circuit Judge. Between 1981 and 1989, Donald
Schultz worked as a painter for American Motors Corpora-
tion (which was acquired by Chrysler in 1987). Schultz’s
job was to paint equipment, floors, walls, ceilings, and
pipes at company plants. In November 2005 he was
diagnosed with acute myeloid leukemia (AML), a
2 No. 12-1902
disease that claimed his life in September 2006.
Joann Schultz, his wife, acting on her own behalf and
as the representative of her late husband’s estate, sued
Akzo Nobel Paints (formerly known as The Glidden
Company, but we will refer to it under its current
name, Akzo) and Durako Paint and Color Corp., alleging
that these companies produced or distributed the
paint Schultz used while working at Chrysler and that
benzene from these paints caused his AML. Schultz
offered reports from two experts to support his causa-
tion theory: Dr. Stewart, an industrial hygienist, who
reconstructed Schultz’s work with the paints in order
to quantify his benzene exposure; and Dr. Gore, an
oncologist, who testified that benzene is both generally
known to cause AML and specifically was a substantial
factor in the development of Schultz’s disease.
The district court granted Akzo’s motion for summary
judgment on the ground that Dr. Gore’s testimony was
scientifically unreliable; without that crucial evidence,
Schultz had no way of linking his disease to Akzo’s
paints. At the same time, the court granted Durako’s
motion for summary judgment. Schultz appeals both of
these rulings. Because we find that the district court
erred in excluding Dr. Gore’s testimony, we reverse the
grant of Akzo’s motion for summary judgment. We
affirm the judgment in favor of Durako, however,
because of a lack of evidence indicating that Schultz
was exposed to a Durako product.
No. 12-1902 3
I
Because this case turns for the most part on the rules
governing expert witnesses, we will not dwell on
Schultz’s experience with Akzo, details about his
medical history, or the source of the benzene, except
insofar as these points bear on the issue before us. We
turn instead directly to the two expert reports that
Schultz proffered in an effort to avoid summary judgment.
Dr. Stewart reconstructed Schultz’s quantitative expo-
sure to benzene using Monte Carlo Analysis, a risk assess-
ment model that accounts for variability and uncertainty
in risk factors such as the likely variation in Schultz’s
exposure to benzene during different periods and at
different plants. The U.S. Environmental Protection
Agency (EPA) has endorsed this methodology as a
reliable way to evaluate risk arising from environ-
mental exposure. EPA, Office of the Scientific Advisor,
Guiding Principles for Monte Carlo Analysis, http://www.
epa.gov/raf/publications/guiding-monte-carlo-analysis.htm
(last visited June 21, 2013) (noting “the EPA’s position
that such probabilistic analysis techniques as Monte
Carlo analysis, given adequate supporting data and
credible assumptions, can be viable statistical tools for
analyzing variability and uncertainty in risk assess-
ments.”). Dr. Stewart interviewed Schultz’s former co-
workers and reviewed their deposition testimony to
evaluate the extent of Schultz’s exposure to Akzo paint.
He then derived the chemical composition of the paints
from material safety data sheets that Akzo had produced.
He entered this data into the Monte Carlo model in order
4 No. 12-1902
to reconstruct Schultz’s total benzene exposure. After
twice revising his report to account for new information
about the amount of paint used each day and to correct
a typo in one of the numbers in the model, Dr. Stewart
concluded that Schultz had been exposed on the job to a
total of 24 parts-per-million years (ppm-years) of benzene.
(This is equivalent to being exposed to 1 ppm of benzene
each year for 24 years.)
In order to show that this degree of exposure was, as a
scientific matter, a substantial factor in the development
of Schultz’s AML, Schultz presented Dr. Gore’s report.
Dr. Gore is both a practicing oncologist and a Professor
of Oncology at the Comprehensive Cancer Center
at Johns Hopkins University. He has been on the
Johns Hopkins Medical School faculty since 1990;
before that, he spent three years as a Senior Clinical
Fellow in Oncology at Johns Hopkins University
School of Medicine. He received a Master’s degree in
pharmacology and a M.D. from Yale University, and he
has published more than 75 articles, most relating to the
biology and treatment of leukemias, lymphomas, and
other diseases of the blood. Dr. Gore explained that as
part of his “day job” as a clinical oncologist, he diagnoses
and treats dozens of leukemia patients every year, many
with AML. Dr. Gore’s standard diagnostic practice is
to take an extensive history from each patient, reviewing
his occupation, family history, lifestyle, and other life
activities that may have led to exposures to chemicals
or environmental risk factors, in order to assess whether
any factors can be identified that might have con-
No. 12-1902 5
tributed to the patient’s disease. He has used this
process, called differential diagnosis, to assess the
causes contributing to the diseases of several hundred
AML patients. Dr. Gore explained that oncologists regu-
larly rely on differential diagnosis to identify causal
factors in order to treat patients, because a patient whose
leukemia was caused by exposure to a known chemical
is treated differently from one whose leukemia arose
from an unknown cause. Dr. Gore’s report concluded
that Schultz’s history of smoking and exposure to
benzene were both significant causes of Schultz’s AML.
In his deposition, Dr. Gore explained:
[W]orkers who had greater than eight to sixteen
per million years exposure to Benzene, are estimated
to be [sic] a six-fold increase of leukemia, compared
to people who don’t. And, if it is greater than sixteen
parts per million years, the relative risk was a
hundred-fold. So, either way with these estimates,
Mr. Schultz was well within these diagnosis
risk exposures. And, it’s my understanding that
Dr. Stewart was only estimating the risk from six
years of exposure. And, in fact, the gentleman worked
in these plants for considerably longer than that. So
minimally, we think he is exposed to a very toxic
and dangerous level within six years of exposure.
And, that’s ignoring the other years of painting
that he did.
At a different point, Dr. Gore testified that “[s]ix or less
parts per million year exposure, greater than fifteen
years, one can argue that they don’t seem to be at in-
6 No. 12-1902
creased risk epidemiologically. But, those with—it looks
like eleven parts per million years, do.” Finally, Dr. Gore
opined that Schultz’s smoking history probably also
contributed to his AML, but he found no evidence that
any other risk factor played a role. He explained that
“[t]he fact that Mr. Schultz’s cigarette smoking may
have contributed to his AML in no way undermines my
conclusion that his benzene exposure played a sub-
stantial role in the development of the disease.”
To refute Dr. Gore’s conclusion that Schultz’s AML was
caused in part by benzene exposure, Akzo introduced a
report of its own expert toxicologist, David Pyatt, who
concluded that benzene exposure was unlikely to have
contributed to Schultz’s AML. To support this conclu-
sion, Pyatt cited a study finding that only workers ex-
posed to greater than 40 ppm-years benzene were at
a higher risk for developing AML. Pyatt also stated that
the risk of developing AML decreases as time passes
following exposure to benzene. Based on this opinion,
Akzo argued that Schultz’s AML was not likely to
have been caused by exposure to benzene: his exposure
was less than 40 ppm-years, and there was a 15-year
latency period between Schultz’s exposure to benzene
and the time he developed AML.
In his deposition, Dr. Gore responded to Pyatt’s asser-
tions. He explained that the hypothesis of a 40 ppm-
year threshold originated in a study based on just nine
cases of leukemia, only six of which were AML. Dr. Gore
pointed to a larger study, Hayes et al., “Benzene and the
Dose-Related Incidence of Hematologic Neoplasms in
No. 12-1902 7
China,” which was introduced as an exhibit to his dep-
osition. In the Chinese study, which involved more
than 30 cases, leukemogenic effects were observed at
exposures well below 40 ppm-years. The authors con-
cluded that “[r]isks . . . are elevated at average benzene-
exposure levels of less than 10 ppm and show a
tendency, although not a strong one, to rise with
increasing levels of exposure.” He mentioned other
literature as well that was consistent with the
Chinese study.
In addition to this specific testimony supporting a
threshold of approximately 10 ppm-years (well below
the 24 ppm-years to which Shultz was exposed), at one
point in his deposition Dr. Gore was asked whether
there was an acknowledged threshold level below which
one could say with scientific certainty that benzene ex-
posure would not cause AML. Dr. Gore essentially said
no. He explained “it is my belief that there is no
threshold risk of safe exposure to Benzene. Biologically,
it doesn’t make sense that there would be a threshold.
Because, Benzene is a genotoxic agent. Any molecules
of Benzene interacting with your DNA can cause damage
to DNA.” But in any event, he said, “forty ppm-years, . . .
is way out of the mainstream industrial epidemiologic
literature to my reading.” And he identified a lower
limit below which he was prepared to find that a person’s
risk of contracting AML would no longer be enhanced.
First, he noted that the risk of contracting AML from
benzene exposure decreases with time following expo-
sure. Second, he pointed out that according to the
studies he relied on, someone who was exposed to less
8 No. 12-1902
than 6 ppm-years would no longer be at an elevated
risk for AML after a 15-year latency period. On the
other hand, Dr. Gore noted that these studies also
show that people exposed to more than 10 ppm-years
still face approximately an eight-times greater risk of
developing AML than those in the general population,
even after a 15-year latency period.
In granting Akzo’s motion for summary judgment, the
district court seized on the portion of Dr. Gore’s testi-
mony in which he discussed the “no threshold” idea,
and on that basis, it found the entirety of Dr. Gore’s
opinion to be scientifically unreliable because it thought
that the “no threshold” theory is “merely a hypothesis.”
The district court also faulted Dr. Gore for failing to
rule out other potential causes of Schultz’s AML, particu-
larly his history of smoking.
II
We review de novo whether a district court properly
followed the framework for determining the admissi-
bility of expert testimony under Rule 702 of the Federal
Rules of Evidence, which largely codified Daubert v.
Merrell Dow Pharm., Inc., 509 U.S. 579 (1993). United States
v. Brumley, 217 F.3d 905, 911 (7th Cir. 2000). If the court
properly applied the rule, we review its decision to
admit or exclude expert testimony only for an abuse of
discretion. Id. The ultimate decision to grant summary
judgment is subject to de novo review. Myers v. Illinois
Cent. R.R. Co., 629 F.3d 639, 641 (7th Cir. 2010). Here, as
we have already observed, these issues collapse into one:
No. 12-1902 9
if the district court correctly excluded Dr. Gore’s testi-
mony, then Akzo was entitled to prevail as a matter of
law; if it did not, then it was error to grant summary
judgment and Schultz is entitled to a trial.
Rule 702 permits a qualified expert witness to offer
an opinion if the following criteria are met:
(a) the expert’s scientific, technical, or other special-
ized knowledge will help the trier of fact to under-
stand the evidence or to determine a fact in issue;
(b) the testimony is based on sufficient facts or data;
(c) the testimony is the product of reliable principles
and methods; and
(d) the expert has reliably applied the principles and
methods to the facts of the case.
F ED. R. E VID. 702. As Daubert explained, the reliability
of the expert’s principles and methods can be examined
by looking at factors such as (1) whether the scientific
theory or technique can be (and has been) tested;
(2) whether the theory or technique has been subjected
to peer review and publication; (3) whether a particular
technique has a known potential rate of error; and
(4) whether the theory or technique is generally accepted
in the relevant scientific community. Daubert, 509 U.S. at
593-94. (This assumes that we are speaking of a
scientific expert, such as the ones in this case; experiential
experts are also permissible, see Kumho Tire Co. v.
Carmichael, 526 U.S. 137 (1999), but a somewhat dif-
ferent threshold inquiry is necessary for them.)
10 No. 12-1902
Although this places the judge in the role of gatekeeper
for expert testimony, the key to the gate is not the
ultimate correctness of the expert’s conclusions. Instead,
it is the soundness and care with which the expert
arrived at her opinion: the inquiry must “focus . . . solely
on principles and methodology, not on the conclusions
they generate.” Daubert, 509 U.S. at 595. So long as the
principles and methodology reflect reliable scientific
practice, “[v]igorous cross-examination, presentation
of contrary evidence, and careful instruction on the
burden of proof are the traditional and appropriate
means of attacking shaky but admissible evidence.” Id.
at 596. As we have noted before,
the question . . . whether the expert is credible or
whether his or her theories are correct given the
circumstances of a particular case is a factual one
that is left for the jury to determine after opposing
counsel has been provided the opportunity to cross-
examine the expert regarding his conclusions and
the facts on which they are based. It is not the
trial court’s role to decide whether an expert’s
opinion is correct. The trial court is limited to deter-
mining whether expert testimony is pertinent to
an issue in the case and whether the methodology
underlying that testimony is sound.
Smith v. Ford Motor Co., 215 F.3d 713, 719 (7th Cir. 2000)
(internal citations omitted); see also Ortiz v. City of Chicago,
656 F.3d 523, 536 (7th Cir. 2011). When a district court
excludes an expert’s testimony, it “must provide more
than just conclusory statements about admissibility to
No. 12-1902 11
show that it properly performed its gatekeeping function.”
Oritz, 656 F.3d at 536 (internal quotations omitted).
Two statements in Dr. Gore’s testimony require dis-
cussion: (1) Even after a 15-year latency period, a person
exposed to 11 ppm-years of benzene or more would be
at an eight-times greater risk for developing AML, and
thus (because Dr. Stewart ascertained that Schultz had
been exposed to more than double that amount) this
meant that Schultz’s benzene exposure was a significant
risk factor; and (2) With carcinogens like benzene,
which cause permanent DNA mutations, it is theoretically
possible that any amount of exposure could damage
the DNA in a human cell. It is important to understand
the difference between these two statements. The first
says, in essence, that scientific studies confirm the danger
of exposure to more than 10 ppm-years of benzene. The
second says that no one is sure whether 10 ppm-years
is the floor for risk, or 5 ppm-years, or 1 ppm-year, or
nothing. There is nothing inconsistent between these two
assertions. The latter may have been an unnecessary
observation in Schultz’s case, since his exposure was
24 ppm-years, but there is no rule requiring the exclu-
sion of expert testimony just because the expert digresses
into a collateral issue to explain where the frontier
of research lies. Our system relies on cross-examination
to alert the jury to the difference between good data
and speculation. Akzo’s counsel was also free to argue,
based on its own expert’s submission, that 11 ppm-
years was too low, and that risk does not arise until the
40 ppm-year level is reached.
12 No. 12-1902
In striking Dr. Gore’s findings because the “basic
thrust” of his opinion was that “the amount of benzene
exposure is irrelevant,” the district court overlooked
Dr. Gore’s unambiguous conclusion that Schultz had
been exposed to a level of benzene that has been shown
in studies to be a “very toxic and dangerous level.” Had
Dr. Stewart calculated that Schultz’s exposure was only
5 ppm-years, we would have a different case, in which
the district court’s concern about an ill-defined floor for
safety would have been justified. But we do not. Far
from limiting his testimony to the proposition that the
amount of exposure may be “irrelevant,” Dr. Gore
focused specifically on the amount of benzene to which
Schultz had been exposed and related this amount to the
scientific literature. He stated that, given a 15-year
latency period, exposures of less than 6 ppm-years are
unlikely to cause AML, but exposures of 11-ppm years or
more put one at an eight-times greater risk of AML (as
compared to the general population). Had Schultz been
exposed to less than 6 ppm-years, Akzo would have
been entitled to point out to the district court that
Schultz’s own expert was unwilling to point to benzene
exposure as a likely cause of Schultz’s AML. In short,
Dr. Gore not only identified 11 ppm-years as a level
that has been proven to be toxic, but he also suggested
that 6 ppm-years might be a lower limit given current
knowledge (while as a careful scientist reserving the
possibility that even less exposure might be dangerous).
There was no need for him to do more for purposes of
Rule 702.
In finding Dr. Gore’s testimony unreliable, the dis-
trict court also emphasized that Dr. Gore’s conclusion
No. 12-1902 13
diverged from a different study in the record in which
the authors found that benzene has carcinogenic effects
only at exposures greater than 40 ppm-years. But
the competing study appears to rely on the identical
methodology—observing AML rates in populations ex-
posed to benzene over time—as the studies that Dr. Gore
cited in support of his opinion that greater than 10 ppm-
years exposure increases the risk of AML, even after
15 years. Indeed, as we noted earlier, Dr. Gore explained
that the study finding a 40 ppm-year threshold was
conducted with an extremely small sample size (only six
cases of AML), unlike (for example) the Chinese study
he submitted, which found that more than 10 ppm-
years’ exposure was a significant risk factor based on
observations of more than 30 cases of AML. Rule 702
did not require, or even permit, the district court to
choose between those two studies at the gatekeeping
stage. Both experts were entitled to present their views,
and the merits and demerits of each study can be
explored at trial.
The district court also suggested that Dr. Gore’s opin-
ion was unreliable because he failed to rule out other
potential causes of Schultz’s AML, including Schultz’s
weight and smoking history. While the district court’s
decision rather curiously says nothing about the legal
standard for Schultz’s toxic tort claim, we presume
that Wisconsin law applies. (The court was exercising
diversity jurisdiction on the ground that some of the
events took place in Wisconsin, and the default rule is
to apply the law of the state where the district court
sits unless the parties contend otherwise, which they
14 No. 12-1902
have not done here.) In Wisconsin, a strict products
liability action requires a plaintiff to show that the
product “was a cause (a substantial factor) of the plain-
tiff’s injuries or damages.” Zielinski v. A.P. Green Indus.,
Inc., 661 N.W.2d 491, 494 (Wis. Ct. App. 2003) (quoting
Cook v. Gran-Aire, Inc., 513 N.W.2d 652, 654 (Wis. Ct. App.
1994)). In order to show that a toxin is “a cause” or “a
substantial factor,” Schultz was not required to demonstrate
that benzene exposure was the sole cause of his disease, so
long as he showed that benzene contributed sub-
stantially to the disease’s development or significantly
increased his risk of developing AML.
Furthermore, the district court was mistaken if it
thought that Dr. Gore had ignored other possible causes
altogether. The method of differential diagnosis on
which Dr. Gore relied to assess the development of
Schultz’s AML routinely identifies multiple causal fac-
tors. We have recognized this method of differential
diagnosis and differential etiology as a generally
accepted means for evaluating the cause of a plaintiff’s
injury. Myers, 629 F.3d at 644 (“[I]n a differential
etiology, the doctor rules in all the potential causes of a
patient’s ailment and then by systematically ruling out
causes that would not apply to the patient, the physician
arrives at what is the likely cause of the ailment. There is
nothing controversial about that methodology. The ques-
tion of whether it is reliable under Daubert is made on a
case-by-case basis, focused on which potential causes
should be ‘ruled in’ and which should be ‘ruled out.’ ”)
(internal citations omitted).
No. 12-1902 15
In Myers, we found an expert’s testimony unreliable
because it “did not rule in any causes of Myers’s ailment,
nor did [it] rule out anything.” Id. When asked about a
prior back surgery that may have contributed to Myers’s
back problems, Myers’s physician responded, “I don’t
really think that it makes a hell of a lot of difference one
way or the other . . . Now, if you are interested in causation,
then from your standpoint, it’s important.” Id. at 645 (em-
phasis in original). This made clear that the physician had
not considered potential causes of Myers’s injury at all.
(This may be a good illustration of the difference in
perspective between doctors and lawyers: doctors
normally want to treat the patient’s ailment, no matter
how it may have come about, while lawyers must dig
further into causation.) Myers illustrates the situation
contemplated by the Committee Notes to Rule 702, pro-
viding that a court may consider “[w]hether the expert
has adequately accounted for obvious alternative ex-
planations.” FED. R. E VID . 702 (2000) Committee Note.
That consideration should show why a particular alter-
native explanation is not, in the expert’s view, the sole
cause of the disease. See Heller v. Shaw Indus., Inc., 167 F.3d
146, 156 (3d Cir. 1999). Beyond that, while Myers and the
Committee Notes suggest that a reliable expert should
consider alternative causes, they do not require an
expert to rule out every alternative cause.
Unlike the expert in Myers, Dr. Gore considered
which alternative causes should be ruled in, and which
could be ruled out. He “determined that [Schultz’s]
smoking history may have contributed, but [he] found no
evidence that any other risk factor played a role.” He
16 No. 12-1902
further “ruled out, to a reasonable degree of medical
certainty, that any other known risk factors for AML
contributed to Mr. Schultz’s disease.” In fact, Dr. Gore’s
report thoroughly addressed the possibility of alterna-
tive causes, explaining that:
[N]o case of cancer truly has only a single cause.
Because cancer development is a complex, multi-
stage process where many factors work together to
contribute to the ultimate emergence of a full blown
malignancy, each of those factors . . . must properly
be considered a cause of the ultimate cancer and a
substantial factor in bringing it about. . . . Thus, criti-
cally for the purposes of a specific causation
analysis, the mere fact that genetics and/or other
environmental risk factors . . . have been identified
as probable causes of a particular case of cancer in
no way refutes the possibility that chemical ex-
posures being investigated have also played a sub-
stantial contributing role at one or more stages of
the development of that person’s cancer.
In his deposition, Dr. Gore elaborated on the reasons
why he concluded that exposure to benzene was a sig-
nificant cause for Schultz, despite the history of cigarette
smoking: “[T]obacco is one of the strongest causative
factors . . . [but] it’s not as strong on a risk basis, per se,
as Benzene. . . . As a matter of fact, the Benzene in the
smoke is one of the things that is thought, potentially,
to contribute to the development of leukemia. . . .”
Daubert counseled that courts should focus “solely on
principles and methodology, not on the conclusions that
No. 12-1902 17
they generate.” 509 U.S. at 595. Because Dr. Gore’s testi-
mony does not suffer from either of the deficiencies
that the district court attributed to it, the court erred by
excluding it. Moreover, with Dr. Gore’s contribution
restored to the case, we conclude that Schultz has pre-
sented enough to defeat Akzo’s motion for summary
judgment.
III
Durako is another matter. The only evidence in the
record even hinting that Schultz was exposed to Durako
products is a document provided by Chrysler entitled
“Possible Paint Related Products Active at Kenosha
Plants 1985-89” in which one Durako product is men-
tioned. This document was not authenticated; there
appears to be no foundation in the record about who
created it or why; and it does not indicate when, how
much, or how often the Durako product was used. This
falls short, as a matter of law, for the purpose of demon-
strating that Schultz used any amount of Durako paint
during the course of his work for Chrysler. There-
fore, Schultz cannot support a products liability claim
against Durako. Zielinski, 661 N.W.2d at 494.
IV
For these reasons, we R EVERSE the district court’s deci-
sion granting Akzo’s motion for summary judgment,
and we A FFIRM the district court’s decision granting
Durako’s motion for summary judgment. The case is
18 No. 12-1902
R EMANDED to the district court for further proceedings
consistent with this opinion.
6-26-13