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Two Schools of Thought

May 25th, 2013

In litigation of claims of professional malpractice, the “two schools of thought doctrine” is a complete defense.  Jones v. Chidester, 531 Pa. 31, 40, 610 A.2d 964 (1992).

As explained by the Pennsylvania Supreme Court, physicians may defend against claims that they deviated from the standard of care, or of professional malpractice, by adverting to support for their treatment by a minority of professionals in their field:

“Where competent medical authority is divided, a physician will not be held responsible if in the exercise of his judgment he followed a course of treatment advocated by a considerable number of recognized and respected professionals in his given area of expertise.”

Id. at 40.  See also Fallon v. Loree, 525 N.Y.S.2d 93, 93 (N.Y. App. Div. 1988) (“one of several acceptable techniques”); Dailey, “The Two Schools of Thought and Informed Consent Doctrine in Pennsylvania,” 98 Dickenson L. Rev. 713 (1994); Douglas Brown, “Panacea or Pandora’ Box:  The Two Schools of Medical Thought Doctrine after Jones v. Chidester,” 44 J. Urban & Contemp. Law 223 (1993).

Perhaps the two schools doctrine is an interesting anomaly that harkens back to a legal epistemology founded in authority rather than evidence.  In the law of expert witnesses, the criterion for admissibility of opinion has shifted from “general acceptance” to epistemic warrant, but malpractice law still allows custom and practice to dictate the standard of care.  The two schools doctrine ameliorates the practice of basing standard of care on authoritative, non-evidence based practices and opinions.  If standards of care were truly evidence based, then there might still be situations in which the available evidence was inconclusive between two approaches to patient care.  In situations of inconclusive evidence between two approaches, the two schools doctrine would provide a defense.

Products Liability

In products liability cases, failure-to-warn theories are often predicated upon claims that defendants should have known of a risk of harm posed by their products.  Plaintiffs will cite past pronouncements made by authors as evidence that the harm was “known” to others, and thus the defendants should have known of the harm, and thus should have warned about the harm.  This species of claiming often takes place, however, without any analysis whether the past pronouncements were made with good and adequate scientific bases.

If products liability law persists in treating past, putative knowledge uncritically, then it should, at least, allow defendants to defend on the ground that there were contrary pronouncements made. Juries should be told that the existence of contrary pronouncements from a respectable minority of writers is a complete defense. The two schools of thought doctrine should thus be given wider play in tort law than just professional malpractice.  Products liability should honor the basic underlying principle of malpractice law that the opinions of even a respected minority of experts fully answers the claim of negligence. The existence of the contrary opinions should bar punitive damage claims altogether.

Consider what happens in the typical failure to warn case.  The plaintiff  goes trash picking through the dustbin of medical history to find some prescient writer who argued that the product in question causes disease.  Defendant points to other authors who disputed the relationship.  The court instructs the jury that they may find defendant negligent for failing to warn if they believe the plaintiffs’ evidence.  The jury makes its decision, thoroughly infected with hindsight bias.

This scenario is unsatisfactory and unduly restrictive.  Applying the two schools of thought doctrine, the court should instruct the jury to find for the plaintiff only if there was not a considerable number of recognized and respected professionals and  experts, who had opined that the product caused the specific injury in question.  The existence of such a minority should defeat claims for punitive damages as a matter of law.

United States v. Harkonen

On May 7, 2013, the Ninth Circuit of the United States Court of Appeals denied, Dr. Harkonen’s petition for rehearing in United States v. Harkonen.  No data or analyses were false or fabricated in the Harkonen case.  The government’s prosecution was predicated on a statistical orthodoxy that is opposed by a large number of recognized and respected statisticians.  This fact would have been a complete defense to a claim of professional negligence.  The two schools doctrine should completely bar a prosecution for fraud.

Remarkably, expert witnesses commonly testify to causal associations on lesser evidence than Dr. Harkonen relied upon in a press release for his judgment of causal efficacy, but the trial court believed the jury could infer scienter and falsity from conversations between an “orthodox” statistician and Dr. Harkonen about the propriety of drawing a casual inference from a given dataset.

Perhaps civil litigants should start counterclaiming for fraud when they receive expert witness reports.

Posted in Causation, Scientific Evidence | Comments Off on Two Schools of Thought

Asbestos Litigation Blues

May 22nd, 2013

Mr. Curtis  Geatz alleges that he has mesothelioma as a result of asbestos exposure, including exposure to crocidolite from having smoked Kent Micronite filtered cigarettes for nine months, in 1955-56. Geatz v. Benjamin Moore & Co., File No. 62CV124946, Minn. D. Ct. for Ramsey Cty. (2d Jud. Dist.).  See “Lorillard Executive Admits Asbestos Once Included in Kent Filters” (April 23, 2013) (misleadingly suggesting that testimony about filter content was something other than very old news).

Crocidolite is clearly the most potent cause of mesothelioma.  In a published cohort study of workers at Hollingsworth & Vose, a company that made the filters for the Kent cigarette, over 15 percent of all deaths were due to mesothelioma.  James Talcott, et al., “Asbestos-Associated Diseases in a Cohort of Cigarette-Filter Workers,” 321 New Engl. J. Med. 1220 (1989).

Despite the high potency of crocidolite in causing mesothelioma, the late Irving Selikoff  worked hard to advance his opinion that all asbestos fiber types were comparable.  Selikoff also propagandized the view that crocidolite was not widely used in the United States, although he and his colleagues documented the use of “blue” fiber at Johns-Manville factories in the United States. See “Selikoff and the Mystery of the Disappearing Amphiboles” (Dec. 10, 2010).

In Mr. Geatz’s case, Lorillard moved for summary judgment on grounds that crocidolite fibers in the cigarettes plaintiff smoked were not a substantial contributing factor of his mesothelioma. The trial court denied Lorillard’s motion, apparently on the strength of unidentified exhibits attached to an attorney affidavit (Tiffany Dickenson).

Mr. Geatz’ claim is not implausible on its face, but the trial court’s refusal of Lorillard’s motion for summary judgment is a conclusory black box.  It may be right or wrong, but it fails to describe the defendant’s evidence or arguments as to why potent crocidolite in the Kent filter could not have been a substantial factor, or the plaintiffs’ evidence as to why the jury should be allowed to say otherwise.  Lorillard may have argued that the fibers did not leave the filter, or that the exposure would have been too low, even to the extremely potent crocidolite fiber.  Apparently there was no threshold issue of admissibility of each side’s expert witnesses, but still, the scientific issues, the plaintiffs, and the defendants deserve some explanation of the court’s decision.

Posted in Causation | Comments Off on Asbestos Litigation Blues

As They WOE, So No Recovery Have the Reeps

May 22nd, 2013

Late last year, Justice York excluded Dr. Shira Kramer’s WOE-ful opinion that gasoline fumes from an alleged fuel-line leak caused Sean Reep to be born with cerebral palsy.  Reeps v. BMW of North America, LLC, 2012 NY Slip Op 33030(U), N.Y.S.Ct., Index No. 100725/08 (New York Cty. Dec. 21, 2012) (York, J.).  Kramer’s opinion was a parody of science, pieced together from case reports, animal studies, and epidemiologic studies that looked at exposures utterly unlike that of Mrs. Reep’s exposure.

Justice York saw through the charade.  The animal studies were largely exonerative. The case reports were of birth defects quite different from those sustained by Sean Reeps.  The epidemiologic studies were of different chemicals or chemicals at levels very different from those experienced by Mrs. Reeps. Plaintiffs’ expert witnesses ignored established principles of teratology in claiming late-term birth defects to have been causally related to early term exposures. Plaintiffs’ expert witnesses gave a convincing presentation of how not to do science, and why judicial gatekeeping is necessary.  See “New York Breathes Life into Frye Standard – Reeps v. BMW” (Mar. 5, 2013).

Justice York clearly articulated that the “plaintiff’s burden to prove the methodology applied to reach the conclusions will not be rejected by specialists in the field.”  Reeps, slip op. at 11.  The trial court recognized that under the New York state version of Frye, the court must determine whether plaintiffs’ expert witnesses are faithfully applying a methodology, such as the Bradford Hill criteria, or whether they are they are “pay[ing] lip service to them while pursuing a completely different enterprise.”  Id.  Justice York recognized that the court must examine a proffered opinion to determine whether it “properly relates existing data, studies or literature to the plaintiff’s situation, or whether, instead, it is connected to existing data only by the ipse dixit of the expert.” Id. (internal quotations omitted).

Plaintiffs were unhappy with Justice York’s decision, and their counsel moved for reconsideration, positing only 15 supposed errors or misunderstandings in the opinion. On May 10, the trial court denied the motion for reconsideration and further explicated the scientific deficiencies of plaintiffs’ witnesses’ opinions.

The trial court was unimpressed:

“In general, attorney for plaintiffs misrepresents the substance of this court’s Decision. The court did not prefer conclusions of defendants’ experts to that of plaintiffs – disagreement among experts is to be expected, since causation analysis involves professional judgment in interpreting data and literature. An expert opinion is precluded when it is reached in violation of generally accepted scientific principles. The court determined that Drs. Kramer and Frazier did not follow generally accepted scientific methodology.”

Reeps, 2013 NY Slip Op 31055(U) at 2 (Opinion on Motions to Reargue, to Renew, and for Oral Hearing) (May 10, 2013).

The court noted that the plaintiffs’ witnesses’ novel claim that low-level gasoline vapor inhalation causes birth defects, a claim that had escaped the attention of all other scientists and regulatory agencies, cried out for judicial intervention.  Id. at 3.

The court also rebuffed the claim that plaintiffs’ witnesses, Shira Kramer and Linda Frazier, had followed the Bradford Hill guidelines:

 “These guidelines are employed only after a study finds an association to determine whether that association reflects a true causal relationship.”

Id. at 5 (quoting Federal Judicial Center, National Research Council, Reference Manual on Scientific Evidence at 598-599 (3d ed. 2011)) (emphasis in the original). Kramer and Frazier never got off the dime with the Bradford Hill guidelines.

In considering the plaintiffs’ motions, the trial court also had occasion to revisit the assertion that “weight of the evidence” (WOE) substituted for, or counted as, a scientific basis for a conclusion of causality:

“The metaphorical use of the term is, if nothing else, ‘a colorful way to say the body of evidence we have examined and judged using a method we have not described but could be more or less inferred from a careful between-the-lines reading of our paper’.”

Id. at 5 (quoting Douglas Weed, “Weight of Evidence: A Review of Concept and Methods,” 25 Risk Analysis 1545, 1546-47 (2005).

Unmoved by the sophistical hand waving, the court emphasized that Kramer and Frazier had confused “suggestive” evidence with “conclusions,” and they had misrepresented the meaning and significance of threshold limit values.  All in all, a convincing demonstration of the need for, and the judicial competence to carry out, gatekeeping of expert witness opinion testimony.

Posted in Causation, Expert Witnesses, Frye, Scientific Evidence | Comments Off on As They WOE, So No Recovery Have the Reeps

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.

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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.” 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.

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Cranor’s Defense of Milward at the CPR’s Celebration

Reconstructing Professor Sanders on Expert Witness Gatekeeping

May 5th, 2013

Last week, I addressed two papers from a symposium organized by the litigation industry to applaud the First Circuit’s decision in Milward v. Acuity Products Group, Inc., 639 F.3d 11 (1st Cir. 2011), cert. denied, 132 S.Ct. 1002 (2012).  Professor Joseph Sanders also contributed to the symposium, in a paper that is a bit more measured, scholarly, and disinterested than the other papers in the group.  Joseph Sanders, “Milward v. Acuity Specialty Products Group: Constructing and Deconstructing Sciences and Law in Judicial Opinion,” 3 Wake Forest J. L & Policy 141 (2013).  PDF  Still, the industry sponsor, the so-called Center for Progressive Reform, has reasons to be satisfied with the result.

Sanders argues that the Milward opinion is important because it highlights what he characterizes as a “rhetorical conflict that has been ongoing, often below the surface, since the United States Supreme Court’s 1993 opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc.”  Id. at 142.  The argument is overly kind to the judiciary.  There has not been so much as a rhetorical conflict as a reactionary revolt against evidence-based decision making in the federal courts.  Milward simply represents the highwater mark of this revolt against law and science.  See, e.g., David Bernstein on the Daubert Counterrevolution (April 19, 2013).

Sanders invokes the ghost of Derrida and his black brush of deconstruction to suggest that the Daubert process is nothing more than the unraveling of the scientific enterprise, with the goal of showing that it is arbitrary and subjective.  Sanders at 143-44.  According to Sanders, radical deconstruction pushes towards a leveling of “distinctions between fact and faction … more akin to poetry and music than to evidence and argument.” Id. at 145 (citing Stephan Fuchs & Steven Ward, “What Is Deconstruction and Where and When Does It Take Place? Making Facts in Science, Building Cases in Law,” 59 Am. Soc. Rev. 481, 482-83 (1994)).

Lawyers sometimes realize the cost of radical deconstruction is a nihilism that undermines their own credibility and their ability to claim or defend factual assertions.  Sometimes, of course, lawyers ignore these considerations and talk out of both sides of their mouths. In re Welding Fume Prods. Liab. Litig., No. 1:03-CV-17000, MDL 1535, 2006 WL 4507859, *33 (N.D. Ohio 2006) (“According to plaintiffs, the rate of PD [Parkinson’s disease] mortality is so poor a proxy for measuring the rate of overall PD incidence, that the Coggon study proves nothing. In the next breath, however, plaintiffs set forth an unpublished statistical analysis (by Dr. Wells) of PD mortality data collected by the National Center for Health Statistics, arguing it proves that welders, as a group, suffer earlier onset of PD than the general population.77 Of course, the devil is in the details, discussion of which is beyond the scope of this opinion (and perhaps beyond the scope of understanding of the average juror),78 but this example shows how hard it is to tease out whether the limitations of a given study make it unreliable under Daubert.”).

Sanders gives a nod to Sheila Jasanoff, whom he quotes with apparent approval:

“[t]he adversarial structure of litigation is particularly conducive to the deconstruction of scientific facts, since it provides both the incentive (winning the lawsuit) and the formal means (cross-examination) for challenging the contingencies in their opponents’ scientific arguments.”

Sanders at 147 (quoting Shelia Jasanoff, “What Judges Should Know About the Sociology of Science,” 32 Jurimetrics J. 345, 348 (1992)).

With his acknowledgment that adversarial litigation of scientific issues involves  “deconstruction,” or just good, old-fashioned rhetorical excess, Sanders points to the Daubert trilogy as the Supreme Court’s measured response to the problem.

Sanders is, however, not entirely happy about the judiciary’s attempt to rein in the rhetorical excesses of adversarial litigation of scientific issues. Daubert barely scratched the surface of the scientific validity and reliability issues in the Bendectin record, but Sanders asserts that Chief Justice Rehnquist went too far in looking under the hood of the lemon that Joiner’s expert witnesses were trying to sell:

“perhaps Chief Justice Rehnquist erred in the other direction in Joiner when he systematically reviewed the animal studies and four separate epidemiological studies cited by the plaintiff as supporting the position that exposure to PCBs either caused or ‘promoted’66 the plaintiff’s lung cancer.67”

Sanders at 154.  Horrors!  A systematic review!! Perish the thought.

Sanders seems to fault the Chief Justice’s approach of picking off “one-by-one” the studies relied upon by Joiner’s expert witnesses as a deconstructive exercise.  Id. at 154 – 55.  As Sanders notes, the Court’s opinion delved into the internal and external validity of the four cited epidemiologic studies to recognize that the:

“studies did not support the plaintiff’s position because the authors of the study said there was no evidence of a relationship, the relationship was not statistically significant, the substance to which the subjects were exposed was not the same as that to which Mr. Joiner was exposed, and the subjects were simultaneously exposed to other carcinogens.70”

Id. at 155.  To be fair, not all of these were dispositive considerations, but they represent a summary of a district court’s extensive consideration of the scientific record.

Channeling Susan Haack, Sanders argues that the one-by-one approach (which Professor Green pejoratively called a “Balkanized” approach, and Sanders calls “atomistic”) ignores that a wall is made up of constituent bricks.  Sanders might have done better to study a more accomplished philosopher-scientist:

“[O]n fait la science avec des faits comme une maison avec des pierres; mais une accumulation de faits n’est pas plus une science qu’un tas de pierres n’est une maison.”

Jules Henri Poincaré, La Science et l’Hypothèse (1905) (chapter 9, Les Hypothèses en Physique)(“Science is built up with facts, as a house is with stones. But a collection of facts is no more a science than a heap of stones is a house.”).  Poincaré’s metaphor is more powerful and descriptive than Sander’s because it acknowledges that interlocking pieces of evidence may cohere as a building, or they may be no more than a pile of rubble.  Deeper analysis is required. Poorly constructed walls revert to the pile of bricks from which they came.  Furthermore, the mason must look at the individual bricks to see whether they are cracked, crumbling, or crooked before building a wall that must endure. We want a wall that will endure at least long enough to stand on, or put a roof on. Much more is required than simply invoking “mosaics,” “walls from bricks,” or “crossword puzzles” to transmute a pile of studies into a “warranted” claim to knowledge. Litigants, either plaintiff or defendant, should not be allowed to pick out isolated findings in a variety of studies, and throw them together as if that were science.  This is precisely the rhetorical excess against which Rule 702, with its requirement of “knowledge,” should protect judges, juries, and litigants.

Indeed, as Sanders eventually concedes, the Joiner Court noted the appropriateness of considering the four relied-upon epidemiologic studies, individually or collectively:

“We further hold that, because it was within the District Court’s discretion to conclude that the studies upon which the experts relied were not sufficient, whether individually or in combination, to support their conclusions that Joiner’s exposure to PCB’s contributed to his cancer, the District Court did not abuse its discretion in excluding their testimony.71”

General Elec. Co. v. Joiner, 522 U.S. 136, 146-47 (1997).

Professor Sanders might have raised a justiciable argument against the gatekeeping process in Joiner if he had shown, or if he had adverted to other analyses, that the four relied-upon studies collectively meshed to overcome each other’s clear inadequacies.  The silence of Sanders, and other critics, on this score is telling.  Was Rabbi Teitelbaum (one of the Joiners’ expert witnesses) simply insightful or prescient in reading the early returns on PCBs and lung cancer?  What has happened subsequently?  Has the IARC embraced PCBs as a known cause of lung cancer?  Have well-conducted studies and meta-analyses vindicated Teitelbaum’s claims, or have they further confirmed that the gatekeeping in Joiner successfully excluded witnesses who were advancing pathologically weak, specious claims, by pushing and squeezing data until they fit into a pre-determined causal conclusions.

The complaints about judicial “deconstruction” are unfair and empty without looking at these details.  It behooves evidence scholars who want to write in this area to roll up their sleeves and look at the evidence that was in front of the courts, and to learn something about science.  Of course, scientists did not stop exploring the PCB/lung cancer hypothesis after Joiner was decided.  See, e.g, Avima Ruder, Misty Hein, Nancy Nilsen, et al., “Mortality among Workers Exposed to Polychlorinated Biphenyls (PCBs) in an Electrical Capacitor Manufacturing Plant in Indiana: An Update,” 114 Envt’l Health Perspect. 18 (2006) (study by National Institute for Occupational Safety and Health, showing reduced rates of respiratory cancer among PCB-exposed workers, with age-standardized risk ratio of 0.85, and a 95% confidence interval, 0.6 to 1.1)

Stevens’ partial dissent in Joiner of course invested deeply in the mosaic theory, which we now know was the brainchild of plaintiffs’ counsel, Barry Nace. Michael D. Green, “Pessimism about Milward,” 3 Wake Forest J. L & Policy 41, 63 (2013) (reporting that Barry Nace acknowledged having “fed” this rhetorical device to expert witness Alan Done to support arguments for manufacturing certainty in the face of an emerging body of exonerative evidence).  Justice Stevens also cited the EPA as employing “weight of the evidence,” which simply makes the point that WOE is a precautionary approach to scientific evidence, not one for serious causal determinations.  Justice Stevens, and Professor Sanders, might have done better to have looked at what the FDA requires for health claims.  See, e.g., FDA, Guidance for industry evidence-based review system for the scientific evaluation of health claims (2009) (articulating an evidence-based approach). Justice Stevens’ argument fundamentally misconstrues the scientific enterprise of determining causation of health outcomes by reducing it to a precautionary enterprise of regulating possible harms.  Professor Sanders is unclear whether he is restating Justice Stevens’ view, or his own, when he writes:

“Chief Justice Rehnquist was wrong to show the flaws of individual bricks, because it is the wall as a whole that makes up the plaintiff’s case.74”

Sanders at 157 (citing Stevens’ opinion in Joiner, 522 U.S. 136, 153n.5  (1997).  If this is Professor Sanders’ view, it is profoundly wrong.  Looking at the individual bricks is necessary to determine whether it can support the plaintiff’s case.  Of course, to the extent it was Justice Stevens’ view, it was a dissent, not a holding, and it was superseded by a statute when Rule 702 was revised in 2000.

 

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Milward’s Singular Embrace of Comment C

May 4th, 2013

Professor Michael D. Green is one of the Reporters for the American Law Institute’s Restatement (Third) of Torts: Liability for Physical and Emotional Harm.   Green has been an important interlocutor in the on-going debate and discussion over standards for expert witness opinions.  Although many of his opinions are questionable, his writing is clear, and his positions, transparent.  The seduction of Professor Green and the Wake Forest School of Law by one of the litigation-industry’s organizations, the Center for Progressive Reform, is unfortunate, but the resulting symposium gave Professor Green an opportunity to speak and write about the justly controversial comment c.   Restatement (Third) of Torts: Liability for Physical and Emotional Harm § 28, cmt. c (2010).

Mock Pessimism Over Milward

Professor Green professes to be pessimistic about the Milward decision, but his only real ground for pessimism is that Milward will not be followed.  Michael D. Green, “Pessimism about Milward,” 3 Wake Forest J. L & Policy 41 (2013).  Green describes the First Circuit’s decision in Milward as “fresh,” “virtually unique and sophisticated,” and “satisfying.” Id. at 41, 43, and 50.  Green describes his own reaction to the decision in terms approaching ecstasy:  “delighted,” “favorable,” and “elation.”  Id. at 42, 42, and 43.

Green interprets Milward to embrace four comment c propositions:

  1. “Recognizing that judgment and interpretation are required in assessments of causation.52
  2. Endorsing explicitly and taking seriously weight of the evidence methodology,53 against the great majority of federal courts that had, since Joiner, employed a Balkanized approach to assessing different pieces of evidence bearing on causation.54
  3. Appreciating that because no algorithm exists to constrain the inferential process, scientists may reasonably reach contrary conclusions.55
  4. Not only stating, but taking seriously, the proposition that epidemiology demonstrating the connection between plaintiff’s disease and defendant’s harm is not required for an expert to testify on causation.56 Many courts had stated that idea, but very few had found non-epidemiologic evidence that satisfied them.57”

Id. at 50-51.

Green’s points suggest that comment c was designed to reinject a radical subjectivism into scientific judgments allowed to pass for expert witness opinions in American courts.  None of the points is persuasive.  Point (1) is vacuous.  Saying that judgment is necessary does not imply that anything goes or that we will permit the expert witness to be the judge of whether his opinion rises to the level of scientific knowledge.  The required judgment involves an exacting attention to the role of random error, bias, or confounding in producing an apparent association, as well as to the validity of the data, methods, and analyses used to interpret observational or experimental studies.  The required judgment involves an appreciation that not all studies are equally weighty, or equally worthy of consideration for use in reaching causal knowledge.  Some inferences are fatally weak or wrong; some analyses or re-analyses of data are incorrect.  Not all judgments can be blessed by anointing some of them “subjective.”

Point (2) illustrates how far the Restatement process has wondered into the radical terrain of abandoning gatekeeping altogether.  The approach that Green pejoratively calls “Balkanized” is a careful look at what expert witnesses have relied upon to assess whether their conclusions or claims follow from their relied upon sources.  This is the approach used by International Agency for Research on Cancer (IARC) working groups, whose method Green seems to endorse.  Id. at 59.  IARC working groups discuss and debate their inclusionary and exclusionary criteria for studies to be considered, and the validity of each study and its analyses, before they get to an assessment of the entire evidentiary display.  (And several of the IARC working groups have been by no means free of the conscious bias and advocacy that Green sees in party-selected expert witnesses.)  Elsewhere, Green refers to the approach of most federal courts as “corpuscular.”  Id. at 51. Clearly, expert witnesses want to say things in court that do not, so to speak, add up, but Green appears to want to give them all a pass.

Point (3) is, at best, a half truth.  Is Green claiming that reasonable scientists always disagree?  His statement of the point suggests epistemiologic nihilism. Although there are no clear algorithms, the field of science is littered with abandoned and unsuccessful theories from which we can learn when to be skeptical or dismissive of claims and conclusions.  Certainly there are times when reasonable experts will disagree, but there are also times when experts on one side or the other, or both, are overinterpreting or misinterpreting the available evidence.  The judicial system has the option and the obligation to withhold judgments when faced with sparse or inconsistent data.  In many instances, litigation arises because the scientific issues are controversial and unsettled, and the only reasonable position is to look for more evidence, or to look more carefully at the extant evidence.

Point (4) is similarly overblown and misguided.  Green states his point as though epidemiology will never be required.  Here Green’s sympathies betray any sense of fidelity to law or science.  Of course, there may be instances in which epidemiologic evidence will not be necessary, but it is also clear that sometimes only epidemiologic methods can establish the causal claim with any meaningful degree of epistemic warrant.

ANECDOTES TO LIVE BY

Anthony Robbins’ Howler

Professor Green delightfully shares two important anecdotes.  Both are revealing of the process that led up to comment c, and to Milward.

The first anecdote involves the 2002 meeting of the American Law Institute.  Apparently someone thought to invite Dr. Anthony Robbins as a guest. (Green does not tell us who performed this subversive act.)  Robbins is a member of SKAPP, the organization started with plaintiffs’ counsel’s slush fund money diverted from MDL 926, the silicone-gel breast implant litigation.

Robbins rose at the meeting to chastise the ALI for not knowing what it was talking about:

“clear, in my opinion, misstatements of . . . science” or reflected a misunderstanding of scientific principles that “leaves everyone in doubt as to whether you know what you are talking about . . . .”

Id. at 44 (quoting from 79th Annual Meeting, 2002 A.L.I. PROC. at 294).  Pretty harsh, except that Professor Green proceeds to show that it was Robbins who had no idea of what he was talking about.

Robbins asserted that the requirement of a relative risk of greater than two was scientifically incorrect. From Green’s telling of the story, it is difficult to understand whether Robbins was complaining about the use of relative risks (greater than two) for inferring general or specific causation.  If the former, there is some truth to his point, but Robbins would be wrong as to the latter.  Many scientists have opined that relative risks provide information about attributable fractions, which in turn permit inferences about individual cases.  See, e.g., Troyen A. Brennan, “Can Epidemiologists Give Us Some Specific Advice?” 1 Courts, Health Science & the Law 397, 398 (1991) (“This indeterminancy complicates any case in which epidemiological evidence forms the basis for causation, especially when attributable fractions are lower than 50%.  In such cases, it is more probable than not that the individual has her illness as a result of unknown causes, rather than as a result of exposure to hazardous substance.”).  Others have criticized the inference, but usually on the basis that the inference requires that the risk be stochastically distributed in the population under consideration, and we often do not know whether this assumption is true.  Of course, the alternative is that we must stand mute in the face of even very large relative risks and established general causation.  See, e.g., McTear v. Imperial Tobacco Ltd., [2005] CSOH 69, at ¶ 6.180 (Nimmo Smith, L.J.) (“epidemiological evidence cannot be used to make statements about individual causation… . Epidemiology cannot provide information on the likelihood that an exposure produced an individual’s condition.  The population attributable risk is a measure for populations only and does not imply a likelihood of disease occurrence within an individual, contingent upon that individual’s exposure.”).

Robbins second point was truly a howler, one that suggests his animus against gatekeeping may grow out of a concern that he would never pass a basic test of statistical competency.  According to Green, Robbins claimed that “increasing the number of subjects in an epidemiology study can identify small effects with ‘an almost indisputable causal role’.” Id. at 45 (quoting Robbins).  Ironically, lawyer and law professor Green was left to take Robbins to school, to educate him on the differences between sampling error, bias, and confounding.  Green does not get the story completely right because he draws an artificial line between observational epidemiology and experimental clinical trials, and incorrectly implies that bias and confounding are problems only in observational studies.  Id. at 45 n. 24.  Although randomization is undertaken in clinical trials to control for bias and confounding, it is not true that this strategy always works or always works completely.  Still, here we have a lawyer delivering the comeuppance to the scolding scientist.  Sometimes scientists really have no good basis to support their claims, and it is the responsibility of the courts to say so.  Green’s handling of Robbins’ errant views is actually a wonderful demonstration of gatekeeping in action.  What is lovely about it is that the claims and their rebuttal were documented and reported, rather than being swept away in the fog of a jury verdict.

Professor Green’s account of Robbins’ foolery should be troubling because, despite Robbins’ manifest errors, and his more covert biases, we learn that Robbins’ remarks had “a profound impact” on the ALI’s deliberations. Courts that are tempted by the facile answers of comment c should find this impact profoundly disturbing.

Alan Done’s Weight of the Evidence (WOE) or Mosaic Methodology

Professor Green relays an anecdote that bears repeating, many times.  In the Bendectin litigation, plaintiffs’ expert witness, Alan Done testified that Bendectin caused birth defects in children of mothers who ingested the anti-nausea medication during pregnancy.  Done had a relatively easy time spinning his speculative web in the first Bendectin trial because there was only one epidemiologic study, which qualitatively was not very good.  In his second outing, Done was confronted by the defense with an emerging body of exonerative epidemiologic research. In response, he deployed his “mosaic theory” of evidence, of different pieces or lines of evidence that singularly do not show much, but together paint a conclusive picture of the causal pattern. Id. at 61 (describing Done’s use of structure-activity, in vitro animal studies, in vivo animal studies, and his own [idiosyncratic] interpretation of the epidemiologic studies).  Done called his pattern a “mosaic,” which Green correctly sees is none other than “weight of the evidence.”  Id. at 62.

After this second trial was won with the jury, but lost on post-trial motions, plaintiffs’ counsel, Barry Nace, pressed the mosaic theory as a legitimate scientific strategy to demonstrate causation, and the appellate court accepted the strategem:

“Like the pieces of a mosaic, the individual studies showed little or nothing when viewed separately from one another, but they combined to produce a whole that was greater than the sum of its parts: a foundation for Dr. Done’s opinion that Bendectin caused appellant’s birth defects. The evidence also established that Dr. Done’s methodology was generally accepted in the field of teratology, and his qualifications as an expert have not been challenged.103”

Id. at 61(citing Oxendine v. Merrell Dow Pharm., Inc., 506 A.2d 1100, 1110 (D.C. 1986).  Green then drops his bombshell:  the philosopher of science who developed the “mosaic theory” (WOE) was the plaintiffs’ lawyer, Barry Nace. According to Green, Nace declared the mosaic idea “Damn brilliant, and I was the one who thought of it and fed it to Alan [Done].”  Id. at 63.

Green attempts to reassure himself that Milward does not mean that Done could use his WOE approach to testify today that Bendectin causes human birth defects.  Id. at 63.  Alas, he provides no meaningful solution to protect against future bogus cases.  Green fails to come to grips with the obvious truth that Done was wrong ab initio.  He was wrong before he was exposed for his perjurious testimony.  See id. at 62 n. 107, and he was wrong before there was a “solid body” of exonerative epidemiology.  His method never had the epistemic warrant he claimed for it, and the only thing that changed over time was a greater recognition of his character for veracity, and the emergence of evidence that collectively supported the null hypothesis of no association.  The defense, however, never had the burden to show that Done’s methodology was unreliable or invalid, and we should look to the more discerning scientists who saw through the smokescreen from the beginning.

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I Don’t See Any Method At All

May 2nd, 2013

Kurtz: Did they say why, Willard, why they want to terminate my command?
Willard: I was sent on a classified mission, sir.
Kurtz: It’s no longer classified, is it? Did they tell you?
Willard: They told me that you had gone totally insane, and that your methods were unsound.
Kurtz: Are my methods unsound?
Willard: I don’t see any method at all, sir.
Kurtz: I expected someone like you. What did you expect? Are you an assassin?
Willard: I’m a soldier.
Kurtz: You’re neither. You’re an errand boy, sent by grocery clerks, to collect a bill.

* * * * * * * * * * * * * * * *

The Royal Society, the National Academies of Science, the Nobel Laureates have nothing on the organized plaintiffs’ bar.  Consider the genius and the accomplishments of these men and women.  They have discovered and built a perpetual motion machine — the asbestos litigation.  They have learned how to violate the law of non-contradiction with impunity (e.g., industry is evil, and (litigation) industry is good).  In the realm of the sciences, especially as applied in the courtroom, they have demonstrated the falsity of one of core beliefs: ex nihilo nihil fit.  We have a lot to learn from the plaintiffs’ bar.

WOE to Corporate America

Steve Baughman Jensen is a plaintiffs’ lawyer and he justifiably gloats over his success as lead counsel in Milward v. Acuity Products Group, Inc., 639 F.3d 11 (1st Cir. 2011), cert. denied, 132 S.Ct. 1002 (2012).  In a recent article for the litigation industry’s scholarly journal, Jensen touts Milward as Ariadne’s thread, which will take plaintiffs out of the mazes and traps set for them by the benighted law of expert witnesses.  Steve Baughman Jensen, “Reframing the Daubert Issue in Toxic Tort Cases,” 49 Trial 46 (Feb. 2013).  Jensen alleged that his client worked with solvents that contained varying amounts of  benzene, which caused him to develop Acute Promyelocytic Leukemia (APL), a subtype of Acute Myeloid Leukemia (AML).  The district court excluded plaintiffs’ expert witnesses’ causation opinions; the First Circuit reversed.  Jensen crows about his accomplished feat.

Weight of the Evidence (WOE) — Let Them Drink Ripple

Jensen, with help from philosopher of popular science Carl Cranor and toxicologist Martyn Smith persuaded the appellate court that a “weight of the evidence” (WOE) analysis necessarily involves scientific judgment. (Millward, 639 F.3d at 18), and that this “use of judgment in the weight of the evidence methodology is similar to that in differential diagnosis, which we have repeatedly found to be a reliable method of medical diagnosis.” Id. (internal citations omitted).

Is this what judicial gatekeeping of scientific expert opinion has come to?  Phrenology, homeopathy, aroma therapy, and reflexology involve medical judgment, of sorts, and so they too are now reliable methodologies.  Ripple makes red wine, and so does Chateau Margaux.  Chateau Margaux is based upon judgment in oenology, and so is Ripple.  That only one of these products will stand the test of time is irrelevant; both are the product of oenological judgment.  It’s all a question of the weight you would assign the differing qualities of Ripple and a premier cru bordeaux.

Jensen never defines WOE; the closest he comes to describing WOE is to tell us that it essentially involves a delegation to expert witnesses to validate their own subjective weighing of the evidence. As in the King of Hearts, Jensen rejoices that the inmates are now running the asylum.

Too Much of Nothing

Jensen complains about a “divide and conquer” strategy by which defendants take individual studies, one at a time, pronounce them inadequate to support a judgment of causality, and then claim that the aggregate evidence fails to support causality as well.  Surely sometimes that approach is misguided; yet sometimes the evidentiary display collectively represents “too much of nothing.”  In some litigations, there are hundreds of studies, which despite their numbers, still fail to support causation.  In General Electric v. Joiner, the Supreme Court discerned that the studies relied upon were largely irrelevant or inconclusive, and that taken alone or together, the cited studies failed to support plaintiffs’ claim of causality.  In the silicone-gel breast implant litigation, the plaintiffs’ steering committee submitted banker boxes of studies and argument to the court’s appointed expert witnesses, in an attempt to manufacture causation.  The committee, however, took its time and saw that the evidence taken individually or collectively did not amount to a scientific peppercorn.

Let Ignorance Rule

One of Jensen’s clever attempts to beguile the judiciary involves the transmutation of scientific inference into personal credibility.  “Second-guessing an expert’s application of scientific judgment necessarily requires assessing that expert’s credibility, which is the jury’s role.” Jensen, 49 Trial at 49.  Jensen attempts to reduce the “battle of experts” to a credibility contest and thus outside the purview of judicial gatekeeping.  His argument conflates credibility with methodology and its application. Because the expert witness will predictably opine that he applied the methodology faithfully, Jensen asserts that the court is barred from examining the correctness of the expert witness’s self-validation.

But scientific inference is scientific because it does not depend upon the person drawing it.  The inference may be weak, strong, erroneous, valid, or invalid.  How we characterize the inference will turn on the data and their analysis, not on the witness’s say so.

Jensen cites comment c, to Section 28 of Restatement (Third) of Torts, as supporting his reactionary arguments for abandoning judicial gatekeeping of expert witness opinion testimony.  “Juries, not judges, should determine the validity of two competing expert opinions, both of which typically fall within the realm of reasonable science.” Jensen, 49 Trial at 51 (emphasis added).  The law, however, requires trial courts to assess the validity vel non of would-be testifying expert witnesses:

“[A] trial judge, acting as ‘gatekeeper’, must ‘ensure that any and all scientific testimony or evidence admitted is not only relevant, but reliable’.  This requirement will sometimes ask judges to make subtle and sophisticated determinations about scientific methodology and its relation to the conclusions an expert witness seeks to offer— particularly when a case arises in an area where the science itself is tentative or uncertain, or where testimony about general risk levels in human beings or animals is offered to prove individual causation.”

General Elec. Co. v. Joiner, 522 U.S. 136, 147–49 (1997) (Breyer, J., concurring) (citations omitted).  Not only is Jensen’s argument contrary to the law, the argument is based upon a cynical understanding that juries will usually have little time, experience, or aptitude for assessing  validity issues, and that delegating validity issues to juries ensures that the legal system will not be able to root out pathologically weak evidence and inferences. The resolution of validity issues will be hidden behind the secretive walls of the jury room, rather than in the open sight of reasoned, published opinions, subject to public and scholarly commentary.   See, e.g., In re Welding Fume Prods. Liab. Litig., No. 1:03-CV-17000, MDL 1535, 2006 WL 4507859, *33 n.78 (N.D. Ohio 2006).  (“even the smartest and most attentive juror will be challenged by the parties’ assertions of observation bias, selection bias, information bias, sampling error, confounding, low statistical power, insufficient odds ratio, excessive confidence intervals, miscalculation, design flaws, and other alleged shortcomings of all of the epidemiological studies.”)

Martyn Smith

Jensen extols the achievements of Dr. Martyn Smith, his expert witness who was excluded by the trial court in Milward.  A disinterested reader might mistakenly think that Smith was among the leading benzene researchers in the world, but a little Googling would turn up that Milward was not his first litigation citation.  Smith has been pulled over for outrunning his expert-witness headlights in several other litigations, including:

  • Jacoby v. Rite Aid, Phila. Cty. Ct. Common Pleas (Order of April 27, 2012; Opinion of April 12, 2012) (excluding Smith as an expert witness on the toxicity of Fix-o-Dent)
  • In re Baycol Prods. Litig., 495 F. Supp.2d 977 (D. Minn. 2007)
  • In re Rezulin Prods. Liab. Litig., MDL 1348, 441 F.Supp.2d 567 (S.D.N.Y. 2006)(“silent injury”)

None of these other cases involved benzene, but they all involved speculative opinions.

The Milward Symposium

Jensen took another victory lap at the Milward Symposium Organized By Plaintiffs’ Counsel and Witnesses.  The presentations from this symposium have now appeared in print:  Wake Forest Publishes the Litigation Industry’s Views on Milward.  See Steve Baughman Jensen, “Sometimes Doubt Doesn’t Sell:  A Plaintiffs’ Lawyer’s Perspective on Milward v. Acuity Products,” 3 Wake Forest J. L. & Policy 177 (2013).  Jensen’s contribution was mostly a shrill ad hominem against corporations, as well as their lawyers and scientists who complicitly support an alleged campaign to manufacture doubt.

Perhaps someday the law journal’s faculty advisors and editors will feel some embarrassment over the lack of balance and scholarship in Jensen’s contribution to the symposium.  Corporations are bad; get it?  They manufacture doubt about the litigation industry’s enterprise.  Don’t pay attention to massive litigation fraud, such as faux silicosis, faux asbestosis, faux fen-phen heart disease, faux product identification, etc.  See Larry Husten, “79-Year-Old Cardiologist Sentenced To 6 Years In Prison For Fen-Phen Fraud,” Forbes (Mar. 27, 2013).   Forget that ATLA/AAJ is one of the most powerful rent-seeking lobbies in the United States.  Litigants have a constitutional right to extrapolate as they please.  If a substance causes one disease at a very high dose, then it causes every ailment known to mankind at moderate or low doses.  Specific disease entails general disease, etc.  What you balk?  You must be a doubt mongerer.

Jensen assures us that many scientists support and agree with Martyn Smith, both in his methodology and in his conclusions.  Jensen’s articles are sketchy on details, and of course, the devil is in the details.  See Amended Amicus Curiae Brief of the Council for Education and Research on Toxins et al., In Support of Appellants, in Milward.  This Council seems to fly under the internet radar, but I suspect that its membership and that of the Center for Progressive Reform overlaps somewhat.

Jensen’s article is just one of several published in the Wake Forest Journal of Law & Policy.  Let’s hope the remaining articles have more substance to them.

Posted in Causation, Expert Witnesses, Rule 702 | Comments Off on I Don’t See Any Method At All

Further Musings on U.S. v. Harkonen

April 15th, 2013

Epistemic Crimes

In U.S. v. Harkonen, the government prosecuted a physician, company CEO, for issuing a press release that stated a clinical trial “demonstrated” benefit when the government believed that the clinical trial was inconclusive.  No doubt the government was intent upon punishing what it thought was off-label promotion in the same press release, but the jury acquitted on the charge of misbranding, and convicted on the wire fraud count.  The trial court denied post-trial motions, and recently, the United States Court of Appeals, for the Ninth Circuit, affirmed, in an unpublished per curiam opinion.  United States v. Harkonen, No. 11-10209, No. 11-10242, 2013 WL 782354, 2013 U.S. App. LEXIS 4472 (9th Cir. March 4, 2013).

A Gedanken Experiment

An expert witness writes a report that X, a drug therapy, causes Y, a benefit in survival, for a disease, Z.

The expert witness sent his report by email, and regular mail, to counsel, who then served it upon his adversary.  The report set out some of the support for the opinion, as follows.

The expert witness relied upon a randomized clinical trial, conducted with one primary and nine secondary endpoints.  The multiple endpoints were chosen because of uncertainty of how the anticipated benefit would manifest.  Mortality (survival), although obviously a very important endpoint, was not made primary endpoint because the scientists who conducted the trial did not anticipate sufficient deaths over the course of the trials to see a statistically significant benefit.

This clinical trial had surprising results. Although the trial did not show a difference on the primary endpoint, a composite defined in terms of various pulmonary functional changes or death, the trial did “demonstrate,” according to the witness, a survival benefit.  Indeed, the survival benefit was clinically significant.  Patients randomized to therapy experienced a 40% decrease in mortality, compared to those randomized to placebo. (p = 0.084).  The expert witness pointed out, in his report, that the survival benefit was even stronger in a subgroup of the clinical trial, which consisted of the patients who had mild- to moderate-disease at the time of randomization.  For this subgroup, the decrease in mortality was even more dramatic, 70%, p = 0.004.  The witness’s report did not clearly label this subgroup as “post-hoc,” although a discerning reader might well have assessed it as such.

The expert witness was not relying upon only one clinical trial.  His report identified an earlier trial, published in a leading clinical medical journal, which reported benefit from the drug, p < 0.001.  This trial was extended, with continuing strong evidence of differential survival.  In terms of survival at five years, the earlier trial showed survival in the therapy group at 77.8%, compared to 16.7% in the control groups, p = 0.009.

The expert witness’s report did not explicitly reference clinical experience, or the in vitro and in vivo mechanistic evidence that the therapy, X, plays a role in inhibiting processes that are clearly involved in producing the disease, Z.  The expert witness could have written a stronger expert witness report with these references, but did not expect that this level of completeness was required.  The expert witness did note that he would marshal the data in more detail at a later time. The expert witness further relied upon the assessment of the principal investigator of the later clinical, who had written that the benefit against mortality of X was “compelling,” and that the finding was “a major breakthrough.”  The principal investigator of the trial noted that X was “the first treatment ever to show any meaningful clinical impact in this disease in rigorous clinical trials, and these results would indicate that [X] should be used early in the course of this disease in order to realize the most favorable long-term survival benefit.”  The report went on to note, accurately, that there are no FDA-approved therapies for Z.

Adversary counsel, receiving this report, moved pursuant to Federal Rules of Evidence 702 and 703, to exclude the expert witness’s report and his opinions.  The motion to exclude was made in advance of the deposition, and without a preliminary motion for more detail about the supporting data.  In particular, the motion to exclude claimed that the expert witness was unjustified in concluding that a benefit had been “demonstrated,” as opposed to being merely suggested.

What would be the challenger’s chances of success on the Rule 702 motion?  The outcome, Y, was not “statistically significant” at the conventional two-tail 5% (but would have been on a one-tail test).  The subgroup that sported a p-value of 0.004 was not clearly marked as a post-hoc subgroup, although the challenger could discern that it was likely exploratory, and challenged it as uncorrected for multiple testing.  The challenger, however, did not attempt to offer a modified p-value that took into account of multiple testing.  The essence of this challenge was that the expert witness’s statement that a benefit had been “demonstrated” was not supported by sufficient evidence, and that the low p-value of 0.004 was not truly “significant” because the result emerged from an analysis that was not pre-planned.

My hunch, based upon published judicial opinions on both state and federal Rule 702 motions, is that many judges would allow the challenged expert witness to testify.  There would be the usual judicial hand waving about the challenge’s going to the weight not the admissibility of the expert witness’s opinion.  Perhaps an occasional judge might order additional discovery.  I believe that most judges would not find that this expert witness had engaged in pathologically bad science such that the party proponent should be denied its expert witness.

Transmuting Disputed Causal Inferences Into Criminal Fraud

Instead of moving to exclude the expert witness’s opinion, why not turn the report over to the U.S. Attorney’s office to prosecute for wire or mail fraud?  Even if a trial court were to brand the opinion “inadmissible,” that outcome would hardly suggest that the opinion was the kind of speech that could qualify as fraudulent under federal wire or mail fraud statutes. Branding a scientist as a fraudfeasor, however, was exactly the result reached in U.S. v. Harkonen, where the Ninth Circuit upheld a wire fraud conviction of a physician whose written statements would likely have been admissible in most federal courtrooms, under Federal Rule 702.  As much as I would like to see more stringent gatekeeping of expert witness opinions, there is something unseemly about the government’s efforts here to criminalize scientific opinions with which it disagrees.

Dr. Harkonen has petitioned the Ninth Circuit for reconsideration, in a brief filed by attorneys, Mark Haddad and colleagues, of Sidley Austin.  Petition for Rehearing En Banc (filed 29, 2013).  The case raises important First Amendment and due process issues, which were addressed by the party and amici briefs before the Panel.

The case also raises the specter of prosecutions of scientists for speech in various contexts, including grant applications and reports, under the False Claims Act, for witness perjury for testimony in judicial, administrative, or legislative proceedings, or for wire or mail fraud for manuscript submissions to journals. On April 8th, Professor Robert Makuch, of Yale University, Professor Timothy Lash, of Emory University, and I filed an amicus brief, which addresses the government’s controversial branding statements “false as a matter of statistics.” The government has gone from one extreme of painting, broad brush, that statistical significance is not important or necessary (in Matrixx Initiatives Inc. v. Siracusano), to the other extreme that statistical significance is so important that a scientist who his opinion on causality on evidence the government believes is not statistically significant has committed fraud (in Harkonen).  Both extreme positions are untenable.

Posted in Causation, Rule 702, statistical evidence | Comments Off on Further Musings on U.S. v. Harkonen

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