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Where Are They Now? Marc Lappé and the Missing Data

May 19th, 2013

The recrudescence of silicone “science” made me wonder where some of the major players in the silicone litigation are today. Some of the plaintiffs’ expert witnesses were characters who gave the litigation “atmosphere.”

Marc Alan Lappé was an experimental pathologist, who testified frequently for plaintiffs in toxic exposure cases. He founded an organization, The Center for Ethics & Toxics (CETOS), to serve as platform for his advocacy activities. Lappé was a new-age scientist, and an author of popular books on toxic everything: Chemical Deception: The Toxic Threat to Health and the Environment, and Against the Grain: Biotechnology and the Corporate Takeover of Your Food. When the silicone-gel breast implant litigation went viral, or immunologic, Lappé was embraced by the silicone sisters and their lawyers as one of their leading immunology guys. Lappé, a revolutionary, obliged and produced another pop science classic: Marc Lappé, The Tao Of Immunology: A Revolutionary New Understanding Of Our Body’s Defenses (1997).

Lappé jumped in to the silicone litigation early. He supported autoimmune claims, as well as the dubious claim that polyurethane-covered breast implants caused or accelerated breast cancer. Livshits v. Natural Y Surgical Specialties, Inc., 1991 WL 261770 (S.D.N.Y. Nov. 27, 1991). In depositions and in trial testimony, Lappé was combative and evasive, but when he wanted to be clear, he could be clear enough:

“It’s my opinion that silicone directly or indirectly can precipitate an activated immune state in such women that can lead to an autoimmune condition.”

Lappé Dep. 44:19-22 (Aug. 21, 1995), in Roden v. Medical Engineering Corp., No. 94-02-103, in District Court of Wise County, Texas, 271st Judicial District.

Plaintiffs also offered Lappé as an ethicist, in what was an obvious attempt to turn personal injury cases into passion plays and to raise the emotional temperature of the court rooms. Plaintiffs were able to get away with such nonsense in some state court cases, but the federal judges generally would not abide expert witnesses on ethics. See, e.g., Switzer v. McGhan Medical Corp., CV 94-P-14229-S, Transcript at 96-98, N.D. Ala. (Jan. 4, 1996) (Pointer, J.) (noting that Lappé would not be permitted to testify that the defendant’s conduct was unethical or unconscionable). Ironically, Lappé would become ensnared by an article, the publication of which was surrounded in ethical controversy.

Although Lappé had some experience in experimental immunology, he had no background in silicone. Undaunted, he set about to publish a work of science fiction. Marc Lappé, “Silicone-reactive disorder: a new autoimmune disease caused by immunostimulation and superantigens,” 41 Medical Hypotheses 348 (1993). Lappé went on to find some researchers with whom he could join forces, and in 1993, he and his co-authors published an article based upon what was ostensibly bench research on silicone immunology. Alas, Lappé did not really know the other authors, who were pitching their immunological screening test to plaintiffs’ support groups and to plaintiffs’ lawyers. Lappé signed up as a co-author without knowing the authors’ marketing plan, and without ever having seen the underlying data and statistical analyses. Given his credentials as a bioethicist, the lapse was remarkable. Lappé learned only through his involvement as an expert witness that his coauthors had been warned by the Food and Drug Administration about unlawful marketing of their “test,” and that some of his co-authors were involved in litigation against Bristol-Myers Squibb. Although the article was clearly intended to support both the marketing of the test, the litigation that would have benefited his coauthors directly, as well as Lappé’s testimonial adventures, the article contained no conflict of interest disclosures. Laurence Wolf, Marc Lappé, Robert Peterson, and Edward Ezrailson, “Human immune response to polydimethylsiloxane (silicone): screening studies in a breast implant population,” 7 Faseb J. 1265 (1993).

Lappé was an advocate, but he was not stupid. The late Chuck Walsh took some of Lappé’s early depositions in the breast implant litigation, and pressed him on whether he had seen or had access to the underlying data. Lappé Dep. Roden at 94:4 -21 (Aug. 21, 1995). Lappé also acknowledged that he had been unaware that the data presented in the published paper was truncated from the data originally obtained in the study. Id. at 108:19 – 109:7. Lappé bristled, as well he should, at these challenges to his ethical bona fides. He apparently requested the underlying data on more than one occasion, but his colleagues would not share the data with him:

Question: I want to ask you, did you ever get the basic raw data?

Answer: That was asked and answered as recently as three weeks ago. And the same answer applies today: No. I had asked for it. It was not give[n] to me. I have asked for it again. It’s not been given to me.

Lappé Dep. at 172:9-14 (Mar. 21, 1996), in Wolf v. Surgitek, Inc., No. 92-60186, 113th Judicial District, District Court of Harris County, Texas.

In early 1998, before Judge Pointer’s neutral expert witnesses delivered their reports in the multi-district proceedings, I traveled to Gualala, California, to take Lappé’s deposition in Page v. Bristol-Myers Squibb Co., No. JCCP-2754-03740, California Superior Court, County of San Diego (Jan. 19, 1998). I recall the little coastal town of Gualala well. The hotel, restaurant, and even the deposition room were infested with fruit flies, no doubt because pesticides were banned under Lappé’s influence. When I asked Lappé whether he had changed his views in any way, he gracefully backed away from his previous testimony:

“I believe that the current evidence, the weight of evidence suggests that the antibodies that are formed in women, perhaps in excess of their background levels for IGG antibody, may not have a specificity towards silicone itself as an antigen but may bind preferentially to silicone and therefore given nonspecific binding results such as those as the Emerald Labs detected in their plate bioassay. I think their evidence does not presently weigh in favor of considering silicone by itself as an antigen.”

Lappé Dep. Wolf at 100: 5-18. Later that year, 1998, Tim Pratt extracted further concessions from Lappé, in a Mississippi case. Lappé acknowledged that the MDL court’s neutral expert witnesses had done a “reasonably good job,” and that he agreed with them that there was not consistent evidence to support the claim that silicone caused autoimmune disease. Lappé Dep. at 26:1-9 (Dec. 17, 1998), in Brassell v. Medical Engineering Corp., Case No. 251-96-1074 CIV, Hinds County Circuit Court, Mississippi.

The litigation faded away, and so did Lappé. He died in 2005. Douglas Martin, “Marc Lappé, 62, Dies; Fought Against Chemical Perils,” N.Y. Times (May 21, 2005). Few other expert witnesses for silicone plaintiffs had the intellectual integrity to confess error. I hope he has found his missing data.

Posted in Expert Witnesses, Scientific Evidence, Underlying Data | Comments Off

Biopersistant Silicone

May 18th, 2013

From the late 1980’s until the late 1990’s, a cadre of public health zealots waged war against various silicone medical devices, but especially against silicone gel breast implants. Their charge was that silicone degraded in vivo to silica, and that it caused autoimmune disease. Their supposed method: weight of the evidence.

I recall sitting next to Professor Carl Cranor at a meeting in Washington, D.C. When the subject of silicone gel breast implants came up, he started trash talking the exonerative epidemiology. When I introduced myself and told him that I represented one of the defendants in that litigation, he got up and moved. Thankfully.

In 1999, the Institute of Medicine issued its consensus report that debunked the plaintiffs’ attempts to draw a causal connection between silicone and autoimmune disease. Stuart Bondurant, et al., Safety of Silicone Breast Implants (1999). The phrases “weight of the evidence” or “weight of evidence” are never mentioned in the report, over 500 pages long.

Recently, the silicone plaintiffs’ causal theory has resurfaced. There has been no new important evidence, but with the scientific community’s attention drawn elsewhere, some old zealots and some new have wandered back into the field to recycle the claims and hypotheses that consumed lawyers and scientists in the last century.

Last year saw a review by Yehuda Shoenfeld and his Israeli colleagues, who describe a “new” syndrome that manifests with various immune-system disturbances. These authors call their syndrome ASIA (autoimmune syndrome induced by adjuvant). M. Lidar, N. Agmon-Levin, P. Langevitz, and Y. Shoenfeld, “Silicone and scleroderma revisited,” 21 Lupus 121 (2012).

Shoenfeld, who has dabbled with this theory for 20 years, acknowledges that the epidemiologic studies fail to support the ASIA notion. Despite the lack of support from controlled, observational studies, these authors proceed to describe “the mechanisms by which silicone may mediate autoimmunity in general, as well as the evidence for causal associations with more specific autoimmune syndromes in general, and scleroderma in particular.” Id. at 121.

Last month, an article was published online with a collection of case reports from the Netherlands. Jan Tervaert & R. M. Kappel, “Silicone implant incompatibility syndrome (SIIS):A frequent cause of ASIA (Shoenfeld’s syndrome),” 56 Immunologic Research (2013), published online, April 2013. The authors employ Shoenfeld’s criteria for ASIA, and postulate a causal relationship between silicone implants and the syndrome in 32 cases.

This month, the assault has stepped up. Yehuda Shoenfeld, “Video Q&A: what is ASIA? An interview with Yehuda Shoenfeld,” 11 BMC Medicine 118 (2013). The video of Dr. Shoenfeld is also available for those who may find it hard to believe that article has found its way into print.

Silicone. It never goes away.

Posted in Causation, Scientific Evidence | Comments Off

IARC and Cranor’s Apologetics for Flawed and Fallacious Science

May 13th, 2013

In his recent contribution to the Center for Progressive Reform’s symposium on the Milward case, Professor Cranor suggests that the International Agency for Research on Cancer (IARC) uses weight of the evidence (WOE) in its carcinogenicity determinations. 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 (2013)[hereinafter cited as Cranor] Cranor’s suggestion is demonstrably wrong.

The IARC process is described in several places, but the definitive presentation of the IARC’s goals and methods is set out in a document known as the “Preamble.” World Health Organization, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans — Preamble (2006) [cited herein as Preamble]. There is no mention of WOE in the Preamble.

The IARC process consists upon assessments of carcinogenicity of substances or exposure circumstances, and categorization into specified groups:

IARC Category	Verbal Description	IARC “Findings”
Group 1	[Known] Carcinogenic to humans	111
Group 2A	Probably carcinogenic to humans	65
Group 2B	Possibly carcinogenic to humans	274
Group 3	Not classifiable as to its carcinogenicity to humans	504
Group 4	Probably not carcinogenic to humans	1

The IARC operative definitions that a substance to a category are highly stylized and unique to IARC. The definitions do not coincide with ordinary language definitions or general scientific usage. Only one substance is categorized as “probably not carcinogenic to humans” is Caprolactam.

Alas, oxygen, nitrogen, carbon dioxide, sugar, table salt, water, and many other exposures we all experience, and even require, do not make it to “probably not carcinogenic.” This fact should clue in the casual reader that the IARC classifications are greatly influenced by the precautionary principle. There is nothing wrong with this influence, as long as we realize that IARC categorizations do not necessarily line up with scientific determinations.

Cranor attempts to exploit IARC classifications and their verbiage, but in doing so he misrepresents the IARC enterprise. For instance, his paper for the CPR symposium strongly suggests that a case involving a Group 2A carcinogen would necessarily satisfy the preponderance of evidence standard common in civil cases because the IARC denominates the substance or exposure circumstance as “probably carcinogenic to humans.” This suggestion is wrong because of the technical, non-ordinary language meanings given to “probably” and “known.” The IARC terminology involves a good bit of epistemic inflation. Consider first what it means for something to be “probably” a carcinogen:

“Group 2.

This category includes agents for which, at one extreme, the degree of evidence of carcinogenicity in humans is almost sufficient, as well as those for which, at the other extreme, there are no human data but for which there is evidence of carcinogenicity in experimental animals. Agents are assigned to either Group 2A (probably carcinogenic to humans) or Group 2B (possibly carcinogenic to humans) on the basis of epidemiological and experimental evidence of carcinogenicity and mechanistic and other relevant data. The terms probably carcinogenic and possibly carcinogenic have no quantitative significance and are used simply as descriptors of different levels of evidence of human carcinogenicity, with probably carcinogenic signifying a higher level of evidence than possibly carcinogenic.”

Preamble at 22, § 6(d). So probably does not mean “more likely than not,” and “possibly” means something even less than some unspecified level of probability. An IARC classification of 2A will not help a plaintiff reach the jury because it does not connote more likely than not.

A category I finding is usually described as a “known” carcinogen, but the reality is that there may still be a good deal of epistemic uncertainty over the classification:

“Group 1: The agent is carcinogenic to humans.

This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent acts through a relevant mechanism of carcinogenicity.”

Preamble at 22, § 6(d).

Again, the precautionary nature of the categorization should be obvious. Knowledge of carcinogenicity is equated to sufficient evidence, which leaves open whether there is a body of contradictory evidence. The IARC’s definition of “sufficiency” does place some limits on what may affirmatively count as “sufficient” evidence:

“Sufficient evidence of carcinogenicity: The Working Group considers that a causal relationship has been established between exposure to the agent and human cancer. That is, a positive relationship has been observed between the exposure and cancer in studies in which chance, bias and confounding could be ruled out with reasonable confidence. A statement that there is sufficient evidence is followed by a separate sentence that identifies the target organ(s) or tissue(s) where an increased risk of cancer was observed in humans. Identification of a specific target organ or tissue does not preclude the possibility that the agent may cause cancer at other sites.”

Preamble (2006), at 19, § 6(a). This definition hardly helps Cranor in his attempt to defend bad science. Scientists may reasonably disagree over what is sufficient evidence, but the IARC requires, at a minimum, that “chance, bias and confounding could be ruled out with reasonable confidence.” Id. Ruling out chance, of course, introduces considerations of statistical significance, multiple comparisons, and the like. Ruling out bias and confounding with confidence is an essential part of the IARC categorization process, just as it is an essential part of the scientific process. Reviewing the relied upon studies for whether they ruled out chance, bias, and confounding, was precisely what the Supreme Court did in General Electric v. Joiner, and what the current statute, Federal Rule of Evidence 702, now requires. Failing to review the extant epidemiologic studies for their ability to rule out chance, bias, and confounding is exactly what the district court judge did in Milward.

IARC and Conflicts of Interest – Nemo iudex in causa sua

Holding out the IARC process as exemplifying scientific method involves other controversial aspects of the process. IARC’s classifications are determined by “working groups” that review the available scientific literature on an agent’s carcinogenicity. Members of these of groups are selected in part because they have “have published significant research related to the carcinogenicity of the agents being reviewed… .” Preamble at 5. See also Vincent Cogliano, Robert A. Baan, Kurt Straif, et al., “The science and practice of carcinogen identification and evaluation,” 112 Envt’l Health Persp. 1269, 1273 (2004).

While the IARC tries hard to avoid apparent financial conflicts of interest, its approach to selecting voting members of the working groups invites a more pervasive, more corrupting influence: working group members must vote on the validity of their own research. The prestige of their own research will thus be directly affected by the group’s vote, as well as by the analysis in the resulting IARC monograph. Many writers have criticized this approach. See, e.g., Paolo Boffetta, Joseph McLaughlin, Carlo La Vecchia, Robert Tarone, Loren Lipworth, and William Blot, “A further plea for adherence to the principles underlying science in general and the epidemiologic enterprise in particular,” 38 Internat’l J. Epidemiol. 678 (2009); Michael Hauptmann & Cecile Ronckers, “A further plea for adherence to the principles underlying science in general and the epidemiologic enterprise in particular,” 39 Internat’l J. Epidemiol. 1677 (2010).

Notably absent from Cranor’s defense of using bad science and incomplete evidence is his disregard of systematic reviews and meta-analysis. Although “agency” science is a weak shadow of the real thing, even federal agencies have come to see the importance of using principles of systematic reviews in their assessments of science for policy purposes. See, e.g., FDA, Guidance for industry evidence-based review system for the scientific evaluation of health claims (2009). Currently underway at the National Toxicology Program’s Office of Health Assessment and Translation (OHAT) is an effort to implement systematic review methodology in the Program’s assessments of potential human health hazards. That the NTP is only now articulating an OHAT Evaluation Process, incorporating principles of systematic review, suggests that something less rigorous has been used previously. See Federal Register Notice , 78 Fed. Reg. 37 (Feb. 25, 2013).

No one should be fooled by Cranor’s attempt to pass off precautionary judgments as scientific determinations of causality.

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Cranor’s Defense of Milward at the CPR’s Celebration

May 12th, 2013

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,” and it was questionably republished in a second journal. See 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.

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