Schultz v. Akzo Nobel Paints, LLC

Decision Date26 June 2013
Docket NumberNo. 12–1902.,12–1902.
Citation721 F.3d 426
PartiesJoann Evelyn SCHULTZ, Individually and as Personal Representative of the Estate of Donald Walter Schultz, Plaintiff–Appellant, v. AKZO NOBEL PAINTS, LLC, et al., Defendants–Appellees.
CourtU.S. Court of Appeals — Seventh Circuit

OPINION TEXT STARTS HERE

Steve B. Jensen (argued), Attorney, Scott R. Frieling, Attorney, Allen Stewart, P.C., Dallas, TX, Steven R. Penn, Attorney, Penn Rakauski, Racine, WI, for PlaintiffAppellant.

Mark W. Rattan (argued), Attorney, Litchfield Cavo, Brookfield, WI, Ryan G. Braithwaite (argued), Attorney, Crivello Carlson, S.C., Milwaukee, WI, for DefendantsAppellees.

Eric G. Laskar, Attorney, Hollingsworth, Washington, DC, for Amicus Curiae.

Before BAUER, FLAUM, and WOOD, Circuit Judges.

WOOD, Circuit Judge.

Between 1981 and 1989, Donald Schultz worked as a painter for American Motors Corporation (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 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 causation 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.

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 exposure to benzene using Monte Carlo Analysis, a risk assessment 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 environmental 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 assessments.”). Dr. Stewart interviewed Schultz's former coworkers 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 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 contributed 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 regularly 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 increased 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 substantial 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 conclusion, Pyatt cited a study finding that only workers exposed 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 assertions. 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 China,” which was introduced as an exhibit to his deposition. In the Chinese study, which involved more than 30 cases, leukemogenic effects were observed at exposures well below 40 ppm-years. The authors concluded 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 exposure 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.”...

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