THE RISE OF THE UBER-EXPERT
One of the curious aspects of the First Circuit’s decision in Milward was the court’s willingness to tolerate a so-called weight of the evidence (WOE) assessment of a causal issue by toxicologist Martyn Smith, when much of the key evidence did not involve toxicology. In defending WOE, Professor Cranor argues that scientists (such as those in an International Agency for Research on Cancer (IARC) working group) evaluate evidence from different lines of research into a single, evaluative judgment of the likelihood of causation. The lines of evidence may involve animal toxicology, cell biology, epidemiology or other disciplines:
“In drawing conclusions from the data to a theory or explanation, it is necessary for scientists to evaluate the quality of different lines of evidence, to integrate them and to assess what conclusion the lines of evidence most likely supports and how well they do so in comparison with alternative explanations.”
See Carl F. Cranor, “Milward v. Acuity Specialty Products: Advances in General Causation Testimony in Toxic Tort Litigation,” PDF 3 Wake Forest J. L. & Policy 105, 117 (2013)[hereinafter cited as Cranor].
Presumably, the scientists will come to the table with the training, experience, and expertise appropriate to their discipline. The curious aspect of Cranor’s defense is that Martyn Smith’s expertise did not encompass many of the lines of research advanced, in particular, the epidemiologic. Of course, in the real world of science, the assessment of the “lines” of evidence is conducted by scientists from the different, relevant disciplines. In the make-believe world of courtroom science, the collaboration breaks down when a single expert witness, such as Smith, offers opinions outside his real expertise. Because the law is not particularly demanding with respect to the extent and scope of expertise, Smith was able to hold forth not only on animal experiments, but on human epidemiologic studies. The defense was able to show that Smith disregarded basic principles of epidemiology, but the First Circuit agreed with Cranor, that consideration of Smith’s disregard should be kicked down the road, to the jury for its consideration.
As a practical matter, in today’s world of highly specialized scientific disciplines, it is simply not possible for an expert witness to address evidence from all the fields needed to evaluate the multiple lines of evidence relevant to a causal issues. We should rightfully be skeptical of a single expert witness who claims the ability to weigh disparate lines of evidence to synthesize a judgment of causation. Of course, this is how science is practiced in a courtroom, not in a university.
REJECTION OF EVIDENCE HIERARCHY
Another salient feature of Cranor’s argument is his insistence that there is no hierarchy of evidence. Cranor’s argument is ambiguous between rejecting a hierarchy of disciplines or a hierarchy within epidemiology itself . Cranor never actually argues directly for a leveling of all types of epidemiologic studies, and as we will see, his one key citation (repeated three times) is for the hierarchy of disciplines: epidemiology, molecular biology, genetics, pathology, and the like.
Clearly there are instances of causation determined without epidemiology. The Henle-Koch postulates after all were developed to assess causation by infection biological organisms. And in some instances, very suggestive evidence of viral causes of cancer has been attained before confirming epidemiologic evidence. If there is a meaningful population attributable risk, however, epidemiology should be able to confirm the suspicions of virology or molecular biology.
Cranor repeatedly cites a meeting report of a workshop held in Washington, D.C., in 2003. See also Michael Green, Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence 549, 564 (3d ed. 2011) (citing same meeting report). Cranor’s citations and quotations misleadingly suggest that the report was an official function of the National Cancer Institute (NCI), and that the published report was an official pronouncement of the NCI. Neither suggestion is true.
Cranor praises the Circuit’s Milward decision for adopting his argument and citing the meeting report for his claim that there is no hierarchy of evidence:
“Citing National Cancer Institute scientists, [the Circuit] also added that “[t]here should be no such hierarchy” of evidence for carcinogenicity as between epidemiological and some other kinds of evidence.100 These scientists and many distinguished scientific committees would not require epidemiological studies to support claims that a substance can cause adverse effects in humans or place certain other a priori constraints on evidence.101”
Cranor at 119 (citing Milward, at 17, citing Michele Carbone, et al., Modern Criteria to Establish Human Cancer Etiology, 64 Cancer Research 5518, 5522 (2004)).
Given the emphasis that Cranor places upon the Carbone article, it is worth taking a close look. Carbone’s article was styled “Meeting Report.” See also Michelle Carbone, Jack Gruber, and May Wong, “Modern criteria to establish human cancer etiology,” 14 Semin. Cancer Biol. 397 (2004). The article was a report of a workshop, not an official NCI publication. The NCI hosted the meeting; the meeting was not sponsored by the NCI, and the published meeting report was not an official statement of the NCI. Notably, the report appeared in Cancer Research as a paid advertisement, not in the Journal of the National Cancer Institute as a scholarly article.
In assessing the citation, readers should consider the authors of the meeting report. Importantly, the discipline of epidemiology was not strongly represented; most of the chairpersons and scientists in attendance were pathologists, cell biologists, virologists, and toxicologists. The authors of the meeting report reflect the interests and focus of the scientists in attendance. The lead author was Michele Carbone, a pathologist at Loyola University Chicago. Some may recognize Carbone as one of the proponents of Simian Virus 40 as a cause of mesothelioma, a hypothesis that has not fared terribly well in the crucible of epidemiologic science. Other authors included:
George Klein, with the Microbiology and Tumor Biology Center, Karolinska Institute, in Stockholm,
Jack Gruber, a virologist with the Cancer Etiology Branch of the NCI, and
May Wong, a biochemist, with the NCI.
The basis of the citation to Carbone’s meeting report is an informal discussion session that took place at the meeting. Those in attendance broke out into two groups, one chaired by Brook Mossman, a pathologist, and the other group chaired by Dr. Harald zur Hausen, a famous virologist who discovered the causal relationship between human papilloma virus and cervical cancer.
The meeting report included a narrative of how the two groups responded to twelve questions. Cranor’s citation to this article is based upon one sentence in Carbone’s report, about one of twelve questions:
“6. What is the hierarchy of state-of-the-art approaches needed for confirmation criteria, and which bioassays are critical for decisions: epidemiology, animal testing, cell culture, genomics, and so forth?
There should be no such hierarchy. Epidemiology, animal, tissue culture and molecular pathology should be seen as integrating evidences in the determination of human carcinogenicity.”
Carbone at 5522. Considering the fuller context of the meeting and this report, there is nothing particularly surprising about this statement. It is not clear that the full question and answer even remotely supports the weight that Cranor places upon it. Clearly, Cranor’s quotations are unduly selective. For instance, Cranor does not discuss the disagreement among those in attendance over criteria for different carcinogens:
“2. Should the criteria be the same for different agents (viruses, chemicals, physical agents, promoting agents versus initiating DNA-damaging agents)?
There were different opinions. Group 1 debated this issue and concluded that the current listing of criteria should remain the same because we lack sufficient evidence to develop a separate classification. Group 2 strongly supported the view that it is useful to separate the biological or infectious agents from chemical and physical carcinogens due to their frequently entirely different mode of action.”
Carbone at 5521.
Perhaps Cranor did not think a legal audience would be interested in the emphasis given to epidemiology. The authors of the meeting report noted that the importance to epidemiology for general causation, but its limitations for determining specific causation:
“Concerning the respective roles of epidemiology and molecular pathology, it was noted that epidemiology allows the determination of the overall effect of a given carcinogen in the human population (e.g., hepatitis B virus and hepatocellular carcinoma) but cannot prove causality in the individual tumor patient.”
Carbone at 5518. The report did not state that epidemiology was not necessary for confirmation of carcinogenicity in the species of interest (humans). The meeting report emphasized the need to integrate the findings of epidemiology and of molecular biology; it did not urge that epidemiology be ignored or disregarded:
“A general consensus was often reached on several topics such as the need to integrate molecular pathology and epidemiology for a more accurate and rapid identification of human carcinogens.”
Carbone at 5518.
“Ideally, before labeling an agent as a human carcinogen, it is important to have epidemiological, experimental animals, and mechanistic evidences (molecular pathology). Not all of the evidence is always available, and, at times, it may be prudent to identify a human carcinogen earlier rather than later.”
Carbone at 5519 (emphasis added). Unlike Cranor, the authors of the meeting report distinguish between instance when they are acting on a scientific determination of causation, and a precautionary assessment that proceeds prudentially “as if” causation is determined.
Against this fuller context, Cranor’s characterization of the meeting report, and his limited citations and quotations can be seen to be misleading:
“The First Circuit wisely followed the Etiology Branch of the National Cancer Institute, which sponsored a workshop on cancer causation that concluded ‘there should be no . . . hierarchy’ among epidemiology, animal testing, cell culture, genomics, and so forth.164”
Cranor at 129. The suggestion that the informal workshop statement represented the views of the Etiology Branch is bogus. Not content to misrepresent twice, Cranor comes back for yet a third misleading citation to this report:
“A further conclusion, already noted, is that scientific experts in court should be permitted to rely upon all scientifically relevant evidence in nondeductive arguments to draw conclusions about causation.209 “There should be no such hierarchy” of evidence, as the Milward court put it, following scientists conducting a workshop at the National Cancer Institute.210 This decision stands as an important corrective to the views of some other appellate and district courts concerning the scientific foundation for expert testimony in toxic tort cases.”
Cranor at 135 (emphasis in original) (citing Carbone for a third time). To see how misleading is Cranor’s suggestion that scientists should be permitted upon all scientific relevant evidence, consider the meeting report’s careful admonition about the lack of validity of some animal models and mechanistic research:
“Moreover, carcinogens and anticarcinogens can have different effects in different situations. As shown by the example of addition of β-carotene in the diet, β-carotene has chemopreventive effects in many experimental systems, yet it appears to have increased the incidence of lung cancer in heavy smokers. Animal experiments can be very useful in predicting the carcinogenicity of a given chemical. However, there are significant differences in susceptibility among species and within organs in the same species, and differences in the metabolic pathway of a given chemical among human and animals could lead to error.”
Carbone at 5521. Obviously relevance is conditioned upon validity, a relationship that is ignored, suppressed, and dismissed in Cranor’s article.
The devil, or the WOE, comes from with ignoring the details.
