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Austin v. Kerr-McGee Refining Corp.6/29/2000
can be treated interchangeably. The Austins have not indicated whether Tietelbaum's theory can be or has been tested and have not directed us to any location in the record where other scientists espouse this theory.
The Austins cite the testimony of Kerr-McGee's toxicology expert, Dr. Gary Krieger, who testified that benzene can affect the pluripotential stem cell. However, Krieger testified that benzene can attack at a variety of places and that benzene-related leukemias have been recognized at slightly more differentiated cell levels. He testified that while benzene affects the pluripotential stem cell, it has never been shown to cause the lesion called the Philadelphia Chromosome, which he opined is what causes CML. Furthermore, to refute Kerr-McGee's theory that benzene does not cause the development of the Philadelphia Chromosome, the Austins point only to Fialkow's paper, in which Fialkow merely suggests that the initial hit or mutation occurs before the Philadelphia Chromosome develops. The Austins give no further explanation regarding the possibility that the Philadelphia Chromosome may cause CML independently of other possible causes.
The Austins also contend that the epidemiological studies' authors' grouping choices demonstrate that the different leukemia cell-types are so closely related in terms of how and why they develop that they can be treated interchangeably. They cite Dr. Otto Wong's epidemiological study, in which Wong stated that based on the conclusion that transformation events occur at an early multipotent stem cell level, it was appropriate to combine lymphoma and leukemia in some of his analyses. But Wong's opinion is not so one-sided. Despite the similarity between lymphoma and leukemia that Wong recognized in his study, Wong testified at the Robinson/Havner hearing that leukemia consists of different types of diseases that have different patterns and different etiological agents. Simply because the authors group their findings under broad headings like "lymphatic and hematopoietic cancers" does not mean that the authors believe all leukemias are derived from the same source. In one study, the author, recognizing that very few studies reviewed medical records or histologic data to ensure correct categorization of diseases, expressed a need for more accurate categorization. Travis, supra, at 92.
Additionally, we find persuasive the rulings on a similar issue in two cases tried in the federal courts. In the cases of Mitchell v. Gencorp Inc., 165 F.3d 778 (10th Cir. 1999), and Chambers v. Exxon Corp., 81 F.Supp.2d 661 (M.D. La. 2000), the plaintiffs sought to establish that the exposure of the deceased worker to benzene or chemicals defined as benzene derivatives caused him to contract CML. In both cases the courts excluded the plaintiffs' scientific evidence because it was not shown to be reliable. Although the scientific studies relied on in those cases are not the same as those relied on in our case, they all suffer from the same defects, inadequacies, and inconclusiveness. In those cases the courts found that the experts' estimates and conclusions were little more than guesswork, and that the experts' assurances that the methodology and supporting data were reliable would not suffice. In fact, in Chambers the court pointed out that while no study found a statistically significant association between CML and exposure to benzene, to the contrary, there were several scientifically-significant studies that demonstrated no association between benzene exposure and the development of CML. Chambers, 81 F.Supp.2d at 664-65.
The Austins concede that there is insufficient reliable data to establish an association between exposure to benzene and CML. In
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