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Too Many Narratives – Historians in the Dock

July 13th, 2014

Historical Associates Inc. (HAI) is a commercial vendor for historical services, including litigation services. Understandably, this firm, like the academic historians who service the litigation industry, takes a broad view of the desirability of historian expert witness testimony.  An article in one of the HAI’s newsletters stakes out lawyer strategies in trying to prove historical facts.  Lawyers can present percipient witnesses, or they

“can present the story themselves, but in the end, arguments by advocates can raise questions of bias that obscure, rather than clarify, the historical facts at issue.”

Mike Reis and Dave Wiseman, “Introducing and interpreting facts-in-evidence: the historian’s role as expert witness,” HAIpoints 1 (Summer 2010)[1]. These commercial historians recommend that advocacy bias, so clear in lawyers’ narratives, be diffused or obscured by having a professional historian present the “story.”  They tout the research skills of historians: “Historians know how to find critical historical information.” And to be sure, historians, whether academic or for-hire may offer important bibliographic services, as well as help in translating, authenticating, and contextualizing documents.  But these historians from HAI want a role on center-stage, or at least in the witness box.  They tell us that:

“Historians synthesize information into well-documented, compelling stories.”

Ah yes, compelling stories, as in “the guiltless gust of a rattling good yarn[2].” The legal system should take a pass on such stories.

*     *     *     *     *     *

A recent law review article attempts to provide a less commercial defense of expert witness testimony.  See Alvaro Hasani, “Putting history on the stand: a closer look at the legitimacy of criticisms levied against historians who testify as expert witnesses,” 34 Whittier L. Rev. 343 (2013) [Hasani].  Hasani argues that historians strive to provide objective historical “interpretation,” by selecting reliable sources, and reliably reading and interpreting these sources to create a reliable “narrative.” Hasani at 355. Hasani points to some courts that have thrown up their hands and declared Daubert reliability factors inapplicable to non-scientific historian testimony. See, e.g., United States v. Paracha, No. 03 CR. 1 197(SHS), 2006 WL 12768, at *19 (S.D.N.Y. Jan. 3, 2006) (noting that Daubert is not designed for gatekeeping of a non-scientific, historian expert witness’s methodology); Saginaw Chippewa Indian Tribe of Michigan v. Granholm, 690 F. Supp. 2d 622, 634 (E.D. Mich. 2010) (noting that “[t]here is no way to ‘test’ whether the experts’ testimony concerning the historical understanding of the treaties is correct. Nor is it possible to establish an ‘error rate’ for historical experts.”).

Not all testifying historians agree, however, that their research and findings are non-scientific.  Here is how one plaintiffs’ expert witness characterized historical thinking:

“Q. Do you believe that historical thinking is a form of scientific thinking?

A. I do. I think that history is sometimes classed with the humanities, sometimes classed with the social sciences, but I think there is a good deal of historical research and writing that is a form of social science.”

Examination Before Trial of Gerald Markowitz, in Mendez v. American Optical, District Court for Tarrant County, Texas (342d Judicial District), at 44:13-20 (July 19, 2005). Professor Susan Haack, and others, have made a persuasive case that the epistemic warrants for claims of knowledge, whether denominated scientific or non-scientific, are not different in kind. If historian testimony is not about knowledge of the past, then it clearly has no role in a trial. Furthermore, Professor Markowitz is correct that sometimes historical opinions are scientific in the sense that they can be tested. If a labor historian asserts that workers are exploited and subjected to unsafe work conditions due to the very nature of capitalism and the profit motives, then that historian’s opinion will be substantially embarrassed by the widespread occupational disease in European and Asian communist regimes.

When Deborah Lipstadt described historian David Irving as a holocaust denier[3], Irving sued Lipstadt for defamation.  In defending against the claim, Lipstadt successfully carried the burden of proving the truth of her accusation.  The trial court’s judgment, quoted by Hasani, reads like a so-called Daubert exclusion of plaintiff Irving’s putative historical writing. Irving v. Penguin Books Ltd., No. 1996-1-1113, 2000 WL 362478, at ¶¶ 1.1, 13.140 (Q.B. Apr. 11, 2000)(finding that “Irving ha[d] misstated historical evidence; adopted positions which run counter to the weight of the evidence; given credence to unreliable evidence and disregarded or dismissed credible evidence.”).

The need for gatekeeping of historian testimony should be obvious.  Historian testimony is often narrative of historical fact that is not beyond the ken of an ordinary fact finder, once the predicate facts are placed into evidence.  Such narratives of historical fact present a serious threat to the integrity of fact finding by creating the conditions for delegation and deferring fact finding responsibility to the historian witness, with an abdication of responsibility by the fact finder. See Ronald J. Allen, “The Conceptual Challenge of Expert Evidence,” 14 Discusiones Filosóficas 41, 50-53 (2013).

Some historians clearly believe that they are empowered by the witness chair to preach or advocate. Allan M. Brandt, who has served as a party expert witness to give testimony on many occasions for plaintiffs in tobacco cases, unapologetically described the liberties he has taken thus:

“It seems to me now, after the hopes and disappointments of the courtroom battle, that we have a role to play in determining the future of the tobacco pandemic. If we occasionally cross the boundary between analysis and advocacy, so be it. The stakes are high, and there is much work yet to do.”

Allan M. Brandt, The Cigarette Century: The Rise, Fall, and Deadly Persistance of the Product That Defined American 505 (2007).

Hasani never comes to grips with the delegation problem or with Brandt’s attitude, which is quite prevalent in the product liability arena. The problem is more than merely “occasional.” The overreaching by historian witnesses reflects the nature of their discipline, the lack of necessity for their testimony, and the failure of courts to exercise their gatekeeping. The problem with Brandt’s excuse making is that neither analysis nor advocacy is needed or desired. Advocacy is the responsibility of counsel, as well as the kind of analysis involved in much of historian testimony.  For instance, when historians offer testimony about the so-called “state of the art,” they are drawing inferences from published and unpublished sources about what people knew or should have known, and about their motivations.  Although their bibliographic and historical researches can be helpful to the fact finder’s effort to understand who was writing what about the issue in times past, historians have no real expertise, beyond the lay fact finder, in discerning intentions, motivations, and belief states.

Hasani concludes that the prevalence of historian expert witness testimony is growing. Hasani at 364.  He cites, however, only four cases for the proposition, three of which pre-date Daubert.  The fourth is an native American rights case. Hasani at 364 n.139. There is little or no evidence that historian expert witness testimony is becoming more prevalent, although it continues in product liability where state of the art — who knew what, when — remains an issue in strict liability and negligence. Mack v. Stryker Corp., 893 F. Supp. 2d 976 (D. Minn. 2012), aff’d, 748 F.3d 845 (8th Cir. 2014). There remains a need for judicial vigilance in policing such state-of-the-art testimony.

[1] Mike Reis is the Vice President and Director of Litigation Research at History Associates Inc. Mr. Reis was received his bachelor’s degree from Loyola College, and his master’s degree from George Washington University, both in history. David Wiseman, an erstwhile trial attorney, conducts historical research for History Associates.

[2] Attributed to Anthony Burgess.

[3] Deborah E. Lipstadt, Denying the Holocaust: The Growing Assault on Truth and Memory 8 (1993).

 

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Twerski’s Defense of Daubert

July 6th, 2014

Professor Aaron D. Twerski teaches torts and products liability at the Brooklyn Law School.  Along with a graduating student, Lior Sapir, Twerski has published an article in which the authors mistakenly asseverate that “[t]his is not another article about Daubert.” Aaron D. Twerski & Lior Sapir, “Sufficiency of the Evidence Does Not Meet Daubert Standards: A Critique of the Green-Sanders Proposal,” 23 Widener L.J. 641, 641 (2014) [Twerski & Sapir].

A few other comments.

1. The title of the article.  True, true, and immaterial. As Professor David Bernstein has pointed out many times, Daubert is no longer the law; Federal Rule of Evidence 702, a statute, is the law.  Just as the original Rule 702 superseded Frye in 1975, a revised Rule 702, in 2000, superseded Daubert in 1975. See David E. Bernstein, “The Misbegotten Judicial Resistance to the Daubert Revolution,” 89 Notre Dame L. Rev. 27 (2013).

2. Twerski and Sapir have taken aim at a draft paper by Professors Green and Sanders, who also presented similar ideas at a workshop in March 2012, in Spain. The Green-Sanders manuscript is available on line. Michael D. Green & Joseph Sanders, “Admissibility Versus Sufficiency: Controlling the Quality of Expert Witness Testimony in the United States,” (March 5, 2012) <downloaded on March 25, 2012>. This article appears to have matured since spring 2012, but it has never progressed to parturition.  Professor Green’s website suggests a mutated version is in the works:  “The Daubert Sleight of Hand: Substituting Reliability, Methodology, and Reasoning for an Old Fashioned Sufficiency of the Evidence Test.”

Indeed, the draft paper is a worthwhile target. See “Admissibility versus Sufficiency of Expert Witness Evidence” (April 18, 2012).  Green and Sanders pursue a reductionist approach to Rule 702, which is unfaithful to the letter and spirit of the law.

3. In their critique of Green and Sanders, Twerski and Sapir get some issues wrong. First they insist upon talking about Daubert criteria.  The “criteria” were never really criteria, and as Bernstein’s scholarship establishes, it is time to move past Daubert.

4. Twerski and Sapir assert that Daubert imposes a substantial or heavy burden of proof upon the proponent of expert witness opinion testimony:

“The Daubert trilogy was intended to set a formidable standard for admissibility before one entered the thicket of evaluating whether it was sufficient to serve as grounds for recovery.”

Twerski & Sapir at 648.

Daubert instituted a “high threshold of reliability”.

Twerski & Sapir at 649.

“But, the message from the Daubert trilogy is unmistakable: a court must have a high degree of confidence in the integrity of scientific evidence before it qualifies for consideration in any formal test to be utilized in litigation.”

Twerski & Sapir at 650.

“The Daubert standard is anything but minimal.”

Twerski & Sapir at 651.

Twerski and Sapir never explain whence comes “high,” “formidable,” and “anything but minimal.” To be sure, the Supreme Court noted that “[s]ince Daubert . . . parties relying on expert evidence have had notice of the exacting standards of reliability such evidence must meet.” Weisgram v. Marley Co., 528 U.S. 440, 455 (2000) (emphasis added). An exacting standard, however, is not necessarily a heavy burden.  It may be that the exacting standard is infrequently satisfied because the necessary evidence and inferences, of sufficiency quality and validity, are often missing. The truth is that science is often in the no-man’s land of indeterminate, inconclusive, and incomplete. Nevertheless, Twerski and Sapir play into the hands of the reductionist Green-Sanders’ thesis by talking about what appears to be a [heavy] burden of proof and the “weight of evidence” needed to sustain the burden.

5. Twerski and Sapir obviously recognize that reliability is different from sufficiency, but they miss the multi-dimensional aspect of expert witness opinion testimony.  Consider their assertion that:

“[t]he Court of Appeals for the Eleventh Circuit in Joiner had not lost its senses when it relied on animal studies to prove that PCBs cause lung cancer. If the question was whether any evidence viewed in the light most favorable to plaintiff supported liability, the answer was probably yes.”

Twerski & Sapir at 649; see Joiner v. Gen. Electric Co., 78 F.3d 524, 532 (11th Cir. 1996) rev’d, 522 U.S. 136 (1997).

The imprecision in thinking about expert witness testimony obscures what happened in Joiner, and what must happen under the structure of the evidence statutes (or case law).  The Court of Appeals never relied upon animal studies; nor did the district court below.  Expert witnesses relied upon animal studies, and other studies, and then offered an opinion that these studies “prove” PCBs cause human lung cancer, and Mr. Joiner’s lung cancer in particular.  Those opinions, which the Eleventh Circuit would have taken at face value, would be sufficient to support submitting the case to jury.  Indeed, courts that evade the gatekeeping requirements of Rule 702 routinely tout the credentials of the expert witnesses, recite that they have used science in some sense, and that criticisms of their opinions “go to the weight not the admissibility” of the opinions.  These are, of course, evasions used to dodge Daubert and Rule 702. They are evasions because the science recited is at a very high level of abstraction (“I relied upon epidemiology”), because credentials are irrelevant, and because “weight not the admissibility” is a conclusion not a reason.

Some of the issues obscured by the reductionist weight-of-the-evidence approach are the internal and external validity of the studies cited, whether the inferences drawn from the studies cited are valid and accurate, and whether the method of synthesizing  conclusion from disparate studies is appropriate. These various aspects of an evidentiary display cannot be reduced to a unidimensional “weight.” Consider how many observational studies suggested, some would say demonstrated, that beta carotene supplements reduced the risk of lung cancer, only to be pushed aside by one or two randomized clinical trials.

6. Twerski and Sapir illustrate the crucial point that gatekeeping judges must press beyond the conclusory opinions by exploring the legal controversy over Parlodel and post-partum strokes.  Twerski & Sapir at 652. Their exploration takes them into some of the same issues that confronted the Supreme Court in Joiner:  extrapolations or “leaps of faith” between different indications, different species, different study outcomes, between surrogate end points and the end point of interest, between very high to relatively low therapeutic doses. Twerski and Sapir correctly discern that these various issues cannot be simply subsumed under weight or sufficiency.

7. Professors Green and Sanders have published a brief reply, in which they continue their “weight of the evidence” reductionist argument. Michael D. Green & Joseph Sanders, “In Defense of Sufficiency: A Reply to Professor Twerski and Mr. Sapir,” 23 Widener L.J. 663 (2014). Green and Sanders restate their position that courts can, should, and do sweep all the nuances of evidence and inference validity into a single metric – weight and sufficiency – to adjudicate so-called Daubert challenges.  What Twerski and Sapir seem to have stumbled upon is that Green and Sanders are not engaged in a descriptive enterprise; they are prescribing a standard that abridges and distorts the law and best practice in order to ensure that dubious causal claims are submitted to the finder of fact.

Posted in Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Twerski’s Defense of Daubert

Zoloft MDL Excludes Proffered Testimony of Anick Bérard, Ph.D.

June 27th, 2014

Anick Bérard is a Canadian perinatal epidemiologist in the Université de Montréal.  Bérard was named by plaintiffs’ counsel in the Zoloft MDL to offer an opinion that selective serotonin reuptake inhibitor (SSRI) antidepressants as a class, and Zoloft (sertraline) specifically, cause a wide range of birth defects. Bérard previously testified against GSK about her claim that paroxetine, another SSRI antidepressant is a teratogen.

Pfizer challenged Bérard’s proffered testimony under Federal Rules of Evidence 104(a), 702, 703, and 403.  Today, the Zoloft MDL transferee court handed down its decision to exclude Dr. Bérard’s testimony at the time of trial.  In re Zoloft (Sertraline Hydrochloride) Prods. Liab. Litig., MDL 2342, Document 979 (June 27, 2014).  The MDL court acknowledged the need to consider the selectivity (“cherry picking”) of studies upon which Dr. Bérard relied, as well as her failure to consider multiple comparisons, ascertainment bias, confounding by indication, and lack of replication of specific findings across the different SSRI medications, and across studies. Interestingly, the MDL court recognized that Dr. Bérard’s critique of studies as “underpowered” was undone by her failure to consider available meta-analyses or to conduct one of her own. The MDL court seemed especially impressed by Dr. Bérard’s having published several papers that rejected a class effect of teratogenicity for all SSRIs, as recently as 2012, while failing to identify anything that was published subsequently that could explain her dramatic change in opinion for litigation.

Posted in Causation, Expert Witnesses, Meta-analysis, Rule 702, Scientific Misconduct | Comments Off on Zoloft MDL Excludes Proffered Testimony of Anick Bérard, Ph.D.

Substituting Risk for Specific Causation

June 15th, 2014

Specious, Speculative, Spurious, and Sophistical

Some legal writers assert that all evidence is ultimately “probable,” but that assertion appears to be true only to the extent that the evidentiary support for any claim can be mapped on scale from 0 to 1, much as probability is.  Probability thus finds its way into discussions of burdens of persuasion as requiring the claim to be shown more probably than not, and expert witness certitude as requiring “reasonable degree of scientific probability.”

There is a contrary emphasis in the law on “actual truth,” which is different from “mere probability.”  The rejection of probabilism can be seen in some civil cases, in which courts have emphasized the need for individualistic data and conclusions, beyond generalizations that might be made about groups that clearly encompass the individual at issue. For example, the Supreme Court has held that charging more for funding a woman’s pension than a man’s is discriminatory because not all women will outlive all men, or the men’s average life expectancy. City of Los Angeles Dep’t of Water and Power v. Manhart, 435 U.S. 702, 708 (1978) (“Even a true generalization about a class is an  insufficient reason for disqualifying an individual to whom the generalization does not apply.”). See also El v. Southeastern Pennsylvania Transportation Authority, 479 F.3d 232, 237 n.6 (3d Cir. 2007) (“The burden of persuasion … is the obligation to convince the factfinder at trial that a litigant’s necessary propositions of fact are indeed true.”).

Specific causation is the soft underbelly of the toxic tort world, in large measure because courts know that risk is not specific causation. In the context of risk of disease, which is usually based upon a probabilistic group assessment, courts occasionally distinguish between risk and specific causation. See “Probabilism Case Law” (Jan. 28, 2013) (collecting cases for and against probabilism).

In In re Fibreboard Corp., 893 F. 2d 706, 711-12 (5th Cir. 1990), the court rejected a class action approach to litigating asbestos personal injury claims because risk could not substitute for findings of individual causation:

“That procedure cannot focus upon such issues as individual causation, but ultimately must accept general causation as sufficient, contrary to Texas law. It is evident that these statistical estimates deal only with general causation, for ‘population-based probability estimates do not speak to a probability of causation in any one case; the estimate of relative risk is a property of the studied population, not of an individual’s case.’ This type of procedure does not allow proof that a particular defendant’s asbestos ‘really’ caused a particular plaintiff’s disease; the only ‘fact’ that can be proved is that in most cases the defendant’s asbestos would have been the cause.”

Id. at 711-12 (citing Steven Gold, “Causation in Toxic Torts: Burdens of Proof, Standards of Persuasion, and Statistical Evidence,” 96 Yale L.J. 376, 384, 390 (1986). See also Guinn v. AstraZeneca Pharms., 602 F.3d 1245, 1255 (11th Cir. 2010) (“An expert, however, cannot merely conclude that all risk factors for a disease are substantial contributing factors in its development. ‘The fact that exposure to [a substance] may be a risk factor for [a disease] does not make it an actual cause simply because [the disease] developed.’”) (internal citation omitted).

Specific causation is the soft underbelly of the toxic tort world, in large measure because courts know that risk is not specific causation. The analytical care of the Guinn case and others is often abandoned when it will stand in the way of compensation. The conflation of risk and (specific) causation is prevalent precisely because in many cases there is no scientific or medical way to discern what antecedent risks actually played a role in causing an individual’s disease.  Opinions about specific causation are thus frequently devoid of factual or logical support, and are propped up solely by hand waving about differential etiology and inference to the best explanation.

In the scientific world, most authors recognize that risk, even if real and above baseline, regardless of magnitude, does not support causal attribution in a specific case.[1]  Sir Richard Doll, who did so much to advance the world’s understanding of asbestosis as a cause of lung cancer, issued a caveat about the limits of specific causation inference. Richard Doll, “Proof of Causality: Deduction from Epidemiological Observation,” 45 Perspectives in Biology & Medicine 499, 500 (2002) (“That asbestos is a cause of lung cancer in this practical sense is incontrovertible, but we can never say that asbestos was responsible for the production of the disease in a particular patient, as there are many other etiologically significant agents to which the individual may have been exposed, and we can speak only of the extent to which the risk of the disease was increased by the extent of his or her exposure.”)

Similarly, Kenneth Rothman, a leading voice among epidemiologists, cautioned against conflating epidemiologic inferences about groups with inferences about causes in individuals. Kenneth Rothman, Epidemiology: An Introduction 44 (Oxford 2002) (“An elementary but essential principal that epidemiologists must keep in mind is that a person may be exposed to an agent and then develop disease without there being any causal connection between exposure and disease.”  … “In a courtroom, experts are asked to opine whether the disease of a given patient has been caused by a specific exposure.  This approach of assigning causation in a single person is radically different from the epidemiologic approach, which does not attempt to attribute causation in any individual instance.  Rather, the epidemiologic approach is to evaluate the proposition that the exposure is a cause of the disease in a theoretical sense, rather than in a specific person.”) (emphasis added).

The late David Freedman, who was the co-author of the chapters on statistics in all three editions of the Reference Manual on Scientific Evidence, was also a naysayer when it came to transmuting risk into cause:

“The scientific connection between specific causation and a relative risk of two is doubtful. *** Epidemiologic data cannot determine the probability of causation in any meaningful way because of individual differences.”

David Freedman & Philip Stark, “The Swine Flu Vaccine and Guillaine-Barré Syndrome:  A Case Study in Relative Risk and Specific Causation,” 64 Law & Contemporary Problems 49, 61 (2001) (arguing that proof of causation in a specific case, even starting with a relative risk of four, was “unconvincing”; citing Manko v. United States, 636 F. Supp. 1419, 1437 (W.D. Mo. 1986) (noting relative risk of 3.89–3.92 for GBS from swine-flu vaccine), aff’d in part, 830 F.2d 831 (8th Cir. 1987)).

Graham Colditz, who testified for plaintiffs in the hormone therapy litigation, similarly has taught that an increased risk of disease cannot be translated into the “but-for” standard of causation.  Graham A. Colditz, “From epidemiology to cancer prevention: implications for the 21st Century,” 18 Cancer Causes Control 117, 118 (2007) (“Knowledge that a factor is associated with increased risk of disease does not translate into the premise that a case of disease will be prevented if a specific individual eliminates exposure to that risk factor. Disease pathogenesis at the individual level is extremely complex.”)

Another epidemiologist, who wrote the chapter in the Federal Judicial Center’s Reference Manual on Scientific Evidence, on epidemiology, put the matter thus:

“However, the use of data from epidemiologic studies is not without its problems. Epidemiology answers questions about groups, whereas the court often requires information about individuals.”

Leon Gordis, Epidemiology 362 (5th ed. 2014) (emphasis in original).

=========================================================

In New Jersey, an expert witness’s opinion that lacks a factual foundation is termed a “net opinion.” Polzo v. County of Essex, 196 N.J. 569, 583 (2008) (explaining New Jersey law’s prohibition against “net opinions” and “speculative testimony”). Under federal law, Rule 702, such an opinion is simply called inadmissible.

Here is an interesting example of a “net opinion” from an expert witness, in the field of epidemiology, who has testified in many judicial proceedings:

 

                                                                                          November 12, 2008

George T. Brugess, Esq.
Hoey & Farina, Attorneys at Law
542 South Dearborn Street, Suite 200
Chicago, IL 60605

Ref: Oscar Brooks v. Ingram Barge and Jantran Inc.

* * * *

Because [the claimant] was employed 28 years, he falls into the greater than 20 years railroad employment category (see Table 3 of Garshick’s 2004 paper) which shows a significant risk for lung cancer that ranges from 1.24 to 1.50. This means that his diesel exposure was a significant factor in his contracting lung cancer. His extensive smoking was also a factor in his lung cancer, and diesel exposure combined with smoking is an explanation for the relatively early age, 61 years old, of his diagnosis.

Now assuming that diesel exposure truly causes lung cancer, what was the basis for this witness (David F. Goldsmith, PhD) to opine that diesel exposure was a “significant factor” in the claimant’s developing lung cancer?  None really.  There was no basis in the report, or in the scientific data, to transmute an exposure that yielded a risk ratio of 1.24 to 1.50 for lung cancer, in a similarly exposed population to diesel emissions, into a “significant factor.” The claimant’s cancer may have arisen from background, baseline risk.  The cancer may have arisen from the risk due to smoking, which would have been on the order of a 2,000% increase, or so.  The cancer may have arisen from the claimed carcinogenicity of diesel emissions, on the order of 25 to 50%, which was rather insubstantial compared with his smoking risk.  Potentially, the cancer arose from a combination of the risk from both diesel emissions and tobacco smoking. In the population of men who looked like Mr. Oscar Brooks, by far, the biggest reduction in incidence would be achieved by removing tobacco smoking.

There were no biomarkers that identified the claimant’s lung cancer as having been caused by diesel emissions.  The expert witness’s opinion was nothing more than an ipse dixit that equated a risk, and a rather small risk, with specific causation.  Notice how a 24% increased risk from diesel emissions was a “significant factor,” but the claimant’s smoking history was merely “a factor.”

Goldsmith’s report on specific causation was a net opinion that exemplifies what is wrong with a legal system that encourages and condones baseless expert witness testimony. In Agent Orange, Judge Weinstein pointed out that the traditional judicial antipathy to probabilism would mean no recovery in many chemical and medicinal exposure cases.  If the courts lowered their scruples to permit recovery on a naked statistical inference of greater than 50%, from relative risks greater than two, some cases might remain viable (but alas not the Agent Orange case itself). Judge Weinstein was, no doubt, put off by the ability of defendants, such as tobacco companies, to avoid liability because plaintiffs would never have more than evidence of risk.  In the face of relative risks often in excess of 30, with attributable risks in excess of 95%, this outcome was disturbing.

Judge Weinstein’s compromise was a pragmatic solution to the problem of adjudicating specific causation on the basis of risk evidence. Although as noted above, many scientists rejected any use of risk to support specific causation inferences, some scientists agreed with this practical solution.  Ironically, David Goldsmith, the author of the report in the Oscar Brooks case, supra, was one such writer who had embraced the relative risk cut off:

“A relative risk greater than 2.0 produces an attributable risk (sometimes called attributable risk percent10) or an attributable fraction that exceeds 50%.  An attributable risk greater than 50% also means that ‘it is more likely than not’, or, in other words, there is a greater than 50% probability that the exposure to the risk factor is associated with disease.”

David F. Goldsmith & Susan G. Rose, “Establishing Causation with Epidemiology,” in Tee L. Guidotti & Susan G. Rose, eds., Science on the Witness Stand:  Evaluating Scientific Evidence in Law, Adjudication, and Policy 57, 60 (OEM Press 2001).

In the Brooks case, Goldsmith did not have an increased risk even close to 2.0. The litigation industry ultimately would not accept anything other than full compensation for attributable risks greater than 0%.

[1] See, e.g., Sander Greenland, “Relation of the Probability of Causation to Relative Risk and Doubling Dose:  A Methodologic Error that Has Become a Social Problem,” 89 Am. J. Pub. Health 1166, 1168 (1999)(“[a]ll epidemiologic measures (such as rate ratios and rate fractions) reflect only the net impact of exposure on a population”); Joseph V. Rodricks & Susan H. Rieth, “Toxicological Risk Assessment in the Courtroom:  Are Available Methodologies Suitable for Evaluating Toxic Tort and Product Liability Claims?” 27 Regulatory Toxicol. & Pharmacol. 21, 24-25 (1998)(noting that a population risk applies to individuals only if all persons within the population are the same with respect to the influence of the risk on outcome); G. Friedman, Primer of Epidemiology 2 (2d ed. 1980)(epidemiologic studies address causes of disease in populations, not causation in individuals)

 

Posted in Causation, Expert Witnesses, Risk and Risk Factor, Rule 702 | Comments Off on Substituting Risk for Specific Causation

Hysterical Histortions

June 12th, 2014

Ramses Delafontaine is a young, aspiring historian. In his graduate thesis, Historicizing the Forensification of History: A Study of Historians as Expert Witnesses in Tobacco Litigation in the United States of America (Univ. Ghent 2013), discusses my commentary on Marxist historians, David Rosner and Gerald Markowitz, and suggests that I claim that lawyers without historical training or experience can do the job of historians.  Id. at 98-100.

Given their training and skills in documenting and recounting narratives, lawyers do, indeed, often do the job of historians, and they often do it very well. Of course, lawyers are often guided, inspired, and assisted by professional historians. Sometimes that guidance is necessary. Lawyers’ narratives, unlike historians’, are also subject to judicial control in the form of evidentiary rules about speculation, relevance, reliability, authentication, and trustworthiness.

Regurgitating Historical Evidence

American courts have thus appropriately limited the use of expert witnesses to present historical narratives in judicial proceedings.  See In re Fosamax Prods. Liab. Litig., 645 F. Supp. 2d 164, 192 (S.D.N.Y. 2009) (‘‘[A]n expert cannot be presented to the jury solely for the purpose of constructing a factual narrative based upon record evidence.’’) (internal citations omitted).[1] In Fosamax, Judge Keenan excluded Dr. Susan Parisian’s proffered narrative account of the development and approval of a bisphosphonate medication for osteoporosis in a case involving a claim of osteonecrosis of the jaw (“phossy jaw”).  Judge Keenan detailed the problems that arise from using expert witnesses to present partisan historical narratives:

“In detailing the factual basis for her opinions, Dr. Parisian’s report presents a narrative of select regulatory events through the summary or selective quotation from internal Merck documents, regulatory filings, and the deposition testimony of Merck employees.

The Court agrees with Merck that, to the extent such evidence is admissible, it should be presented to the jury directly. Dr. Parisian’s commentary on any documents and exhibits in evidence will be limited to explaining the regulatory context in which they were  created, defining any complex or specialized terminology, or drawing inferences that would not be apparent without the benefit of experience or specialized knowledge. She will not be permitted to merely read, selectively quote from, or ‘regurgitate’ the evidence.”

Id.[2]

Ramses Delafontaine is wrong, however, to opine that my rants against Rosner and Markowitz suggest that I have ruled out any role for historians in litigation.   Lisa K. Walker is an historian, who trained at the University of California, Berkeley.  In the welding fume litigation, plaintiffs’ counsel weaved a complex narrative of conspiracy allegations, based in large measure upon the absence of evidence. At the request of Metropolitan Life Insurance Company, Professor Walker researched the dates of publication for various editions of a booklet, Health Protection in Welding, which formed the basis for the plaintiffs’ speculations. Walker found and analyzed eight separate editions, and dated each by internal and external references.  Based upon her research, Walker submitted a declaration, which ultimately was immensely helpful to the resolution of the issues. See In re Welding Rod Prods. Liab. Litig., Case No. 1:03-CV-17000 (MDL Docket No. 1535) (N.D.Ohio Nov. 24, 2004; In re Welding Fume Prods. Liab. Litig., 2007 WL 1087605 (N.D. Ohio April 9, 2007)  (O’Malley, J.) (granting summary judgment in favor of Metropolitan Life Insurance Company).

Although Metropolitan Life should not have had to disprove the allegations, Walker’s research showed the plaintiffs’ historical speculation to be clearly wrong. Sometimes historians can and do contribute valuably to the resolution of legal issues, but the issues are usually more modest than the ones that social and labor historians want to see resolved in favor of their pet theories.

Delafontaine also has a website on the role of historians as expert witnesses in United States tobacco cases.  One of his theses is that “historians who have been involved as expert witnesses for the tobacco industry have been in it for the money and have sold their professional integrity as a historian and an academic.” Delafontaine’s approach is a bit one-sided in that he sees only defendants’ expert witnesses as being “in it for the money,” despite the substantial billings of plaintiffs’ expert witnesses, and their ideological biases. Somehow Delafontaine has missed how even the feel-good advocacy of anti-tobacco activists occasionally outruns its evidentiary headlights.  See, e.g., Michael Siegel, “Is the tobacco control movement misrepresenting the acute cardiovascular health effects of secondhand smoke exposure? An analysis of the scientific evidence and commentary on the implications for tobacco control and public health practice,” 4 Epidem. Persp. & Innov. 12 (2007).

[1] See also In re Prempro Prods. Liab. Litig., 554 F.Supp. 2d 871, 880, 886 (E.D.Ark.2008) (overturning a punitive damages award based on Dr. Parisian’s testimony in part because she ‘‘did not explain the documents, provide summaries, or tie them in to her proposed regulatory testimony’’ and ‘‘did not provide analysis, opinion, or expertise’’); Highland Capital Management, L.P. v. Schneider, 379 F.Supp. 2d 461, 469 (S.D.N.Y.2005)(‘‘[A]n expert cannot be presented to the jury solely for the purpose of constructing a factual narrative based upon record evidence.’’); In re Rezulin Products Liab. Litig., 309 F.Supp. 2d 531, 546 (S.D.N.Y.2004) (rejecting portion of expert report presenting history of Rezulin for no purpose but to ‘‘provid[e] an historical commentary of what happened,’’ along with subjective assessments of intent, motives, and states of mind); In re Diet Drugs Prods. Liab. Litig., MDL No. 1203, 2000 WL 876900, at *9 (E.D.Pa. June 20, 2000) (same); Taylor v. Evans, 1997 WL 154010, at *2 (S.D.N.Y. Apr.1, 1997) (rejecting portions of expert report on the ground that the testimony consisted of ‘‘a narrative of the case which a lay juror is equally capable of constructing’’).

[2] Dr. Parisian appears to be a serial narrative abuser, who has been repeatedly but not consistently excluded. See Scheinberg v. Merck & Co. 924 F.Supp. 2d 477, 497 (S.D.N.Y. 2013); Pritchett v. I-Flow Corp., 2012 WL 1059948, at *7 (D. Colo. Mar. 28, 2012); Miller v. Stryker Instruments, 2012 WL 1718825, at *10-12 (D. Ariz. Mar. 29, 2012) (excluding narrative testimony); Kaufman v. Pfizer Pharms., Inc., 2011 WL 7659333, at *6-10 (S.D. Fla. Aug. 4, 2011), reh’g denied, 2011 WL 10501233 (S.D. Fla. Aug. 10, 2011)(narrative testimony); Hines v. Wyeth, 2011 WL 2680842, at *7 (S.D.W. Va. July 8, 2011), reh’g granted in part, 2011 WL 2730908, at *2 (S.D.W. Va. July 13, 2011); In re Heparin Prods. Liab. Litig., 2011 WL 1059660, at *8 (N.D. Ohio March 21, 2011); Lopez v. I-Flow Inc., 2011 WL 1897548, at *9-10 (D. Ariz. Jan. 26, 2011) (narrative testimony); In re Trasylol Prods. Liab. Litig., 709 F.Supp.2d 1323, 1351 (S.D. Fla. 2010)(tendentious narrative testimony) (“Plainly stated, Dr. Parisian is an advocate, presented with the trappings of an expert but with no expectation or intention of abiding by the opinion constraints of Rule 702.”), reh’g denied, 2010 WL 2541892 (S.D. Fla. June 22, 2010); In re Gadolinium-Based Contrast Agents Prods. Liab. Litig., 2010 WL 1796334, at *13 (N.D. Ohio May 4, 2010); Bessemer v. Novartis Pharms. Corp., 2010 WL 2300222 (N.J. Super. Law Div. April 30, 2010); In re Prempro Prods. Liab. Litig., 554 F. Supp. 2d 871, 879-87 (E.D. Ark. 2008)(reversing judgment on grounds of erroneous admission of narrative testimony), aff’d  in relevant part, 586 F.3d 547, 571 (8th Cir. 2009). Occasionally, Dr. Parisian slips through the gate.  See, e.g., Block v. Woo Young Medical Co., 937 F.Supp.2d 1028, 1044-47 (2013)

Posted in Historian Testimony, Rule 702 | Comments Off on Hysterical Histortions

Goodman v Viljoen – Statistical Fallacies from Both Sides

June 8th, 2014

There was a deep irony to the Goodman[1] case.  If a drug company, in 1995, marketed antenatal corticosteroid (ACS) for the prevention of cerebral palsy (CP) in the United States, the government might well have prosecuted the company for misbranding.  The company might also be subject to a False Claims Act case as well. No clinical trial had found ACS efficacious for the prevention of CP at the significance level typically required by the FDA; no meta-analysis had found ACS statistically significantly better than placebo for this purpose.  In the Goodman case, however, failure to order a full course of ACS was malpractice with respect to the claimed causation of CP in the Goodman twins.

The Goodman case also occasioned a well-worn debate over the difference between scientific and legal evidence, inference, and standards of “proof.” The plaintiffs’ case rested upon a Cochrane review of ACS with respect to various outcomes. For CP, the Cochrane meta-analyzed only clinical trial data, and reported:

“a trend towards fewer children having cerebral palsy (RR 0.60, 95% CI 0.34 to 1.03, five studies, 904 children, age at follow up two to six years in four studies, and unknown in one study).”[2]

The defendant, Dr. Viljoen, appeared to argue that the Cochrane meta-analysis must be disregarded because it did not provide a showing of efficacy for ACS in preventing CP, at a significance probability less than 5 percent.  Here is the trial court’s characterization of Dr. Viljoen’s argument:

“[192] The argument that the Cochrane data concerning the effects of ACS on CP must be ignored because it fails to reach statistical significance rests on the flawed premise that legal causation requires the same standard of proof as medical/scientific causation. This is of course not the case; the two standards are in fact quite different. The law is clear that scientific certainty is not required to prove causation to the legal standard of proof on a balance of probabilities (See: Snell v. Farrell, [1990] 2 S.C.R. 311, at para. 34). Accordingly, the defendant’s argument in this regard must fail and for the purposes of this court, I accept the finding of the Cochrane analysis that ACS reduces the instance [sic] of CP by 40%.”

“Disregard” seems extreme for a meta-analysis that showed a 40% reduction in risk of a serious central nervous system disorder, with p = 0.065.  Perhaps Dr. Viljoen might have tempered his challenge some by arguing that the Cochrane analysis was insufficient.  One problem with Dr. Viljoen’s strident argument about statistical significance was that it overshadowed the more difficult, qualitative arguments about threats to validity in the Cochrane finding from loss to follow up in the aggregated trial data. These threats were probably stronger arguments against accepting the Cochrane “trend” as a causal conclusion. Indeed, the validity and the individual studies and the meta-analyses, along with questions about the accuracy of data, were not reflected in Bayesian analysis.

Another problem is that Dr. Viljoen’s strident assertion that p < 0.05 was absolutely necessary fed plaintiffs’ argument that the defendant was attempting to change the burden of proof for plaintiffs from greater than 50% to 95% or greater.  Given the defendant’s position, great care was required to prevent the trial court from committing the transposition fallacy.

Justice Walters rejected the suggestion that a meta-analysis with a p-value of 6.5% should be disregarded, but the court’s discussion skirts the question whether and how the Cochrane data can be sufficient to support a conclusion of ACS efficacy. Aside from citing a legal case, however, Justice Walters provided no basis for suggesting that the scientific standard of proof was different from the legal standard. From the trial court’s opinion, the parties or their expert witnesses appeared to conflate “confidence,” a technical term when used to describe intervals or random error around sample statistics, with “level of certainty” in the obtained result.

Justice Walters is certainly not the first judge to fall prey to the fallacious argument that the scientific burden of proof is 95%.[3]  The 95% is, of course, the coefficient of confidence for the confidence interval that is based upon a p-value of 5%. No other explanation for why 95% is a “scientific” standard of proof was offered in Goodman; nor is it likely that anyone could point to an authoritative source for the claim that scientists actually adjudge facts and theories by this 95 percent probability level.

Justice Walters’ confusion was led by the transposition fallacy, which confuses posterior and significance probabilities.  Here is a sampling from Her Honor’s opinion, first from Dr. Jon Barrett, one of the plaintiffs’ expert witnesses, an obstetrician and fetal maternal medicine specialist at Sunnybrook Hospital, in Toronto, Ontario:

“[85] Dr. Barrett’s opinion was not undermined during his lengthy cross-examination. He acknowledged that the scientific standard demands 95% certainty. He is, however, prepared to accept a lower degree of certainty. To him, 85 % is not merely a chance outcome.

                                                                                        * * *

[87] He acknowledged that scientific evidence in support of the use of corticosteroids has never shown statistical significance with respect to CP. However, he explained it is very close at 93.5%. He cautioned that if you use a black and white outlook and ignore the obvious trends, you will falsely come to the conclusion that there is no effect.”

Dr. Jon (Yoseph) Barrett is a well-respected physician, who specializes in high-risk pregnancies, but his characterization of a black-white outlook on significance testing as leading to a false conclusion of no effect was statistically doubtful.[4]  Dr. Barrett may have to make divinely inspired choices in surgery, but in a courtroom, expert witnesses are permitted to say that they just do not know. Failure to achieve statistical significance, with p < 0.05, does support a conclusion that there is no effect.

Professor Andrew Willan was plaintiffs’ testifying expert witness on statistics.  Here is how Justice Walters summarized Willan’s testimony:

“[125] Dr. Willan described different statistical approaches and in particular, the frequentist or classical approach and the Bayesian approach which differ in their respective definitions of probability. Simply, the classical approach allows you to test the hypothesis that there is no difference between the treatment and a placebo. Assuming that there is no difference, allows one to make statements about the probability that the results are not due to chance alone.

To reach statistical significance, a standard of 95% is required. A new treatment will not be adopted into practice unless there is less than a 5% chance that the results are due to chance alone (rather than due to true treatment effect).

[127] * * * The P value represents the frequentist term of probability. For the CP analysis [from the Cochrane meta-analysis], the P value is 0.065. From a statistical perspective, that means that there is a 6.5% chance that the differences that are being observed between the treatment arm versus the non-treatment arm are due to chance rather than the treatment, or conversely, a 93.5% chance that they are not.”

Justice Walters did not provide transcript references for these statements, but they are clear examples of the transposition fallacy. The court’s summary may have been unfair to Professor Willan, who seems to have taken care to avoid the transposition fallacy in his testimony:

“And I just want to draw your attention to the thing in parenthesis where it says, “P = 0.065.” So, basically that is the probability of observing data this extremely, this much in favor of ACS given, if, if in fact the no [sic, null] hypothesis was true. So, if, if the no hypothesis was true, that is there was no difference, then the probability of observing this data is only 6.5 percent.”

Notes of Testimony of Andrew Willan at 26 (April , 2010). In this quote, Professor Willan might have been more careful to point out that the significance probability of 6.5%  is a cumulative probability by describing the data observed “this extremely” and more. Nevertheless, Willan certainly made clear that the probability measure was based upon assuming the correctness of the null hypothesis. The trial court, alas, erred in stating the relevant statistical concepts.

And then there was the bizarre description by Justice Walters, of the Cochrane data, as embodying a near-uniform distribution represented by the Cochrane data:

“[190] * * * The Cochrane analysis found that ACS reduced the risk of CP (in its entirety) by 40%, 93.5% of the time.”

The trial court did not give the basis for this erroneous description of the Cochrane ACS/CP data.[5] To be sure, if the Cochrane result were true, then 40% reduction might be the expected value for all trials, but it would be a remarkable occurrence for 93.5% of the trials to obtain the same risk ratio as the one observed in the meta-analysis.

The defendant’s expert witness on statistical issues, Prof. Robert Platt, similarly testified that the significance probability reported by the Cochrane was dependent upon an assumption of the null hypothesis of no association:

“What statistical significance tells us, and I mentioned at the beginning that it refers to the probability of a chance finding could occur under the null-hypothesis of no effect. Essentially, it provides evidence in favour of there being an effect.  It doesn’t tell us anything about the magnitude of that effect.”

Notes of Testimony of Robert Platt at 11 (April 19, 2010)

Perhaps part of the confusion resulted from Prof. Willan’s sponsored Bayesian analysis, which led him to opine that the Cochrane data permitted him to state that there was a 91 to 97 percent probability of an effect, which might have appeared to the trial court to be saying the same thing as interpretation of the Cochrane’s p-value of 6.5%.  Indeed, Justice Walters may have had some assistance in this confusion from the defense statistical expert witness, Prof. Platt, who testified:

“From the inference perspective the p-value of 0.065 that we observe in the Cochrane review versus a 91 to 97 percent probability that there is an effect, those amount to the same thing.”

Notes of Testimony of Robert Platt at 50 (April 19, 2010).  Now the complement of the p-value, 93.5%, may have fallen within the range of posterior probabilities asserted by Professor Willan, but these probabilities are decidedly not the same thing.

Perhaps Prof. Platt was referring only to the numerical equivalence, but his language, “the same thing,” certainly could have bred misunderstanding.  The defense apparently attacked the reliability of the Bayesian analysis before trial, only to abandon the challenge by the time of trial.  At trial, defense expert witness Prof. Platt testified that he did not challenge Willan’s Bayesian analysis, or the computation of posterior probabilities.  Platt’s acquiescence in Willan’s Bayesian analysis is unfortunate because the parties never developed testimony exactly as to how Willan arrived at his posterior probabilities, and especially as to what prior probability he employed.

Professor Platt went on to qualify his understanding of Willan’s Bayesian analysis as providing a posterior probability that there is an effect, or in other words, that the “effect size” is greater than 1.0.  At trial, the parties spent a good deal of time showing that the Cochrane risk ratio of 0.6 represented the decreased risk for CP of administering a full course of ACS, and that this statistic could be presented as an increased CP risk ratio of 1.7, for not having administered a full course of ACS.  Platt and Willan appeared to agree that the posterior probability described the cumulative posterior probabilities for increased risks above 1.0.

“[T]he 91% is a probability that the effect is greater than 1.0, not that it is 1.7 relative risk.”

Notes of Testimony of Robert Platt at 51 (April 19, 2010); see also Notes of Testimony of Andrew Willan at 34 (April 9, 2010) (concluding that ACS reduces risk of CP, with a probability of 91 to 97 percent, depending upon whether random effects or fixed effect models are used).[6]

One point on which the parties’ expert witnesses did not agree was whether the failure of the Cochrane’s meta-analysis to achieve statistical significance was due solely to the sparse data aggregated from the randomized trials. Plaintiffs’ witnesses appeared to have testified that had the Cochrane been able to aggregate additional clinical trial data, the “effect size” would have remained constant, and the p-value would have shrunk, ultimately to below the level of 5 percent.  Prof. Platt, testifying for the defense, appropriately criticized this hand-waving excuse:

“Q. and the probability factor, the P value, was 0.065, which the previous witness had suggested is an increase in probability of our reliability on the underlying data.  Is it reasonable to assume that this data that a further increase in the sample size will achieve statistical significance?

A. No, that’s not a reasonable assumption….”

Notes of Testimony of Robert Platt at 29 (April 19, 2010).

Positions on Appeal

Dr. Viljoen continued to assert the need for significance on appeal. As appellant, he challenged the trial court’s finding that the Cochrane review concluded that there was a 40% risk reduction. See Goodman v. Viljoen, 2011 ONSC 821, at ¶192 (CanLII) (“I accept the finding of the Cochrane analysis that ACS reduces the instance of CP by 40%”). Dr. Viljoen correctly pointed out that the Cochrane review never reached such a conclusion. Appellant’s Factum, 2012 CCLTFactum 20936, ¶64.  It was the plaintiffs’ expert witnesses, not the Cochrane reviewers, who reached the conclusion of causality from the Cochrane data.

On appeal, Dr. Viljoen pressed the point that his expert witnesses described statistical significance in the Cochrane analysis would have been “a basic and universally accepted standard” for showing that ACS was efficacious in preventing CP or PVL. Id. at ¶40. The appellant’s brief then commits to the very error that Dr. Barrett complained would follow from a finding that did not have statistical significance; Dr. Viljoen maintained that the “trend” of reduced CP reduced CD rates from ACS administration “is the same as a chance occurrence.” Defendant (Appellant), 2012 CCLTFactum 20936, at ¶40; see also id. at ¶14(e) (arguing that the Cochrane result for ACS/CP “should be treated as pure chance given it was not a statistically significant difference”).

Relying upon the Daubert decision from the United States, as well as Canadian cases, Dr. Viljoen framed one of his appellate issues as whether the trial court had “erred in relying upon scientific evidence that had not satisfied the benchmark of statistical significance”:

“101. Where a scientific effect is not shown to a level of statistical significance, it is not proven. No study has demonstrated a reduction in cerebral palsy with antenatal corticosteroids at a level of statistical significance.

102. The Trial Judge erred in law in accepting that antenatal corticosteroids reduce the risk of cerebral palsy based on Dr. Willan’s unpublished Bayesian probability analysis of the 48 cases of cerebral palsy reviewed by Cochrane—an analysis prepared for the specific purpose of overcoming the statistical limitations faced by the Plaintiffs on causation.”

Defendant (Appellant), 2012 CCLTFactum 20936. The use of the verb “proven” is problematic because it suggests a mathematical demonstration, which is never available for empirical propositions about the world, and especially not for the biological world.  The use of a mathematical standard begs the question whether the Cochrane data were sufficient to establish a scientific conclusion of the efficacy of ACS in preventing CP.

In opposing Dr. Viljoen’s appeal, the plaintiffs capitalized upon his assertion that science requires a very high level of posterior probability for establishing a causal claim, by simply agreeing with it. See Plaintiffs’ (Respondents’) Factum,  2012 CCLTFactum 20937, at ¶31 (“The scientific method requires statistical significance at a 95% level.”).  By accepting the idealized notion that science somehow requires 95% certainty (as opposed to 95% confidence levels as a test for assessing random error), the plaintiffs made the defendant’s legal position untenable.

In order to keep the appellate court thinking that the defendant was imposing an extra-legal, higher burden of proof upon plaintiffs, the plaintiffs went so far as to misrepresent the testimony of their own expert witness, Professor Willan, as having committed the transposition fallacy:

“49. Dr. Willan provided the frequentist explanation of the Cochrane analysis on CP:

a. The risk ratio (RR) is .060 which means that there is a 40% risk reduction in cerebral palsy where there has been administration of antenatal corticosteroids;

b. The upper limit of the confidence interval (CI) barely crosses 1 so it just barely fails to meet the rigid test of statistical significance;

c. The p value represents the frequentist term of probability;

d. In this case the p value is .065;

e. From a statistical perspective that means that there is a 6.5% chance that the difference observed in CP rates is due to chance alone;

f. Conversely there is a 93.5% chance that the result (the 40% reduction in CP) is due to a true treatment effect of ACS.”

2012 CCLTFactum 20937, at ¶49 (citing Evidence of Dr. Willan, Respondents’ Compendium, Tab 4, pgs. 43-52).

Although Justice Doherty dissented from the affirmance of the trial court’s judgment, he succumbed to the parties’ misrepresentations about scientific certainty, and their prevalent commission of the transposition fallacy. Goodman v. Viljoen, 2012 ONCA 896 (CanLII) at ¶36 (“Scientists will draw a cause and effect relationship only when a result follows at least 95 per cent of the time. The results reported in the Cochrane analysis fell just below that standard.”), leave appeal den’d, Supreme Court of Canada No. 35230 (July 11, 2013).

The statistical errors on both sides redounded to the benefit of the plaintiffs.

[1] Goodman v. Viljoen, 2011 ONSC 821 (CanLII), aff’d, 2012 ONCA 896 (CanLII), leave appeal den’d, Supreme Court of Canada No. 35230 (July 11, 2013).

[2] Devender Roberts & Stuart R Dalziel “Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth,” Cochrane Database of Systematic Reviews, at 8, Issue 3. Art. No. CD004454 (2006).

[3] See, e.g., In re Ephedra Prods. Liab. Litig., 393 F.Supp. 2d 181, 191, 193 (S.D.N.Y. 2005) (fallaciously arguing that the use of a critical value of less than 5% of significance probability increased the “more likely than not” burden of proof upon a civil litigant.  Id. at 188, 193.  See also Michael O. Finkelstein, Basic Concepts of Probability and Statistics in the Law 65 (2009) (criticizing the Ephedra decision for confusing posterior probability with significance probability).

[4] I do not have the complete transcript of Dr. Barrett’s testimony, but the following excerpt from April 9, 2010, at page 100, suggests that he helped lead Justice Walters into error: “When you say statistical significance, if you say that something is statistically significance, it means you’re, for the scientific notation, 95 percent sure. That’s the standard we use, 95 percent sure that that result could not have happened by chance. There’s still a 5 percent chance it could. It doesn’t mean for sure, but 95 percent you’re sure that the result you’ve got didn’t happen by chance.”

[5] On appeal, the dissenting judge erroneously accepted Justice Walters’ description of the Cochrane review as having supposedly reported a 40% reduction in CP incidence, 93.5% of the time, from use of ACS. Goodman v. Viljoen, 2012 ONCA 896 (CanLII) at ¶36, leave appeal den’d, Supreme Court of Canada No. 35230 (July 11, 2013).

[6] The Bayesian analysis did not cure the attributability problem with respect to specific causation.

 

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Goodman v Viljoen – Statistical Fallacies from Both Sides

Recrudescence of Traumatic Cancer Claims

June 4th, 2014

In 1991, Peter Huber, discussing traumatic cancer claims, wrote:

“After years of floundering in the junk science morass of traumatic cancer, judges slowly abandoned sequence-of-events logic, turned away from the sympathetic speculations of family doctors, and struggled on to the higher and firmer ground of epidemiology and medical science.  Eventually, the change of heart among appellate judges was communicated back down to trial judges and worker’s compensation boards, and traumatic cancer went into almost complete remission.”

Peter W. Huber, Galileo’s Revenge: Junk Science in the Courtroom 55-56 (1991).

With the advent of Daubert and meaningful gatekeeping of expert witness opinion testimony, the traumatic cancer claims did recede. For a while. Plaintiffs’ counsel, and stalwart opponent of epistemic standards for scientific claims in court, Kenneth Chesebro attacked Huber’s précis of the traumatic cancer law and science. Kenneth J. Chesebro, “Galileo’s Retort: Peter Huber’s Junk Scholarship,” 42 Am. Univ. L. Rev. 1637 (1993). Defenses of the dubious science continue to appear, although mostly in non-peer-reviewed publications.[1]

One of the more disturbing implications of the West Virginia Supreme Court’s decision in Harris v. CSX Transportation, Inc., 232 W.Va. 617, 753 S.E.2d 275 (2013), was the Court’s reliance upon its own, recent approval of traumatic cancer claims.  The Harris Court cited, with approval, a 2002 traumatic cancer case, State ex rel. Wiseman v. Henning, 212 W.Va. 128, 569 S.E.2d 204 (2002).  The Wiseman case involved a specious claim that a traumatic rib injury caused multiple myeloma, a claim at odds with scientific method and observation.  The West Virginia Supreme Court blinked at the challenge to the physician expert witness who advanced the causal claim in Wiseman; and in Harris, the Court made clear that blinking is what trial courts should do when confronted with methodological challenges to far-fetched causal opinions.

A couple of years ago, the New York Times ran an article about traumatic cancer. C. Claiborne Ray, “Injury and Insult” (Nov. 5, 2012), responding to the question “Is it possible for cancer to develop as a result of an injury?” Here is how Times science reporter responded:

A. “It’s a common myth that injuries can cause cancer,” the American Cancer Society says on its Web site. Until the 1920s, some doctors believed trauma did cause cancer, “despite the failure of injury to cause cancer in experimental animals.” But most medical authorities, including the cancer society and the National Cancer Institute, see no such link. The more likely explanation, the society suggests, is that a visit to the doctor for an injury could lead to finding an existing cancer.

Other possibilities are that scar tissue from an old trauma could look like a cancerous lesion and that an injured breast or limb would be more closely watched for cancer to develop.

Ms. Ray went on to note a published study, in which would-be myth-busters presented observational data purportedly showing a relationship between physical injury and subsequent breast cancer.  The paper cited by Ms. Ray was a report on a small case-control study done by investigators at the Department of Geography, Lancaster University. See Jan Rigby, et al., “Can physical trauma cause breast cancer?” 11 Eur. J. Cancer. Prev. 307 (2002). The study consisted of 67 breast cancer cases and 134 controls, matched on age, family history, age of menarche, parity, age at first birth, and menopausal status.

Not surprisingly, considering its small size, the Rigby study reported no statistically significant differences for several factors known to be associated with breast cancer: social class, education, residence, smoking and alcohol consumption.  Although lacking power to detect differences of known risk factors, this study turned up a large, statistically significant association between physical trauma and breast cancer:

“Women with breast carcinoma were more likely to report physical trauma to the breast in the previous 5 years than were the controls (odds ratio (OR) 3.3, 95% confidence interval (CI) 1.3-10.8, P < 0.0001).”

* * * * *

“More likely to [self-]report” hardly implies causation, but the authors jumped not only to a causal explanation but to a causal conclusion:

* * * * *

“In conclusion, recall bias is an unlikely explanation for these results in view of the nature and severity of physical trauma. Models of epithelial cell generation indicate that a causal link between physical trauma and cancer is plausible. A latent interval between cancer onset and presentation of under 5 years is also plausible. The most likely explanation of the findings is that physical trauma can cause breast cancer.”

Rigby at 307.

The Rigby study is a valuable demonstration of how malleable researchers can be in discovering plausible explanations for their data.  The authors fail to discuss the natural history of breast carcinoma, such as tumor doubling time, which would make their five-year window decidedly implausible.  The Rigby paper also demonstrates how strident researchers can be in claiming that they have produced a study that has eliminated bias in observational research, when they have barely scratched the surface of bias or confounding. Magical thinking is not the exclusive domain of lawyers.

Until reading the Harris and Wiseman cases, I had thought that the legal system had graduated from the “mythology” of traumatic cancer cases.[2]  To be sure, in the past, any number of physicians have supported traumatic cancer claims, in print and in the courtroom.[3] Some authors attempted to put some rational limits on the extent of the traumatic cancer claims.[4] By 1947, at least, the trauma theory was criticized in leading texts.[5]  In 1974, the Mayo Clinic published a review that emphasized the lack of experimental evidence to support the claim that uncomplicated trauma causes cancer.[6] The law review literature attempted to make sense of the compensation-frenzied courts, without much success.[7]

Many cases from most jurisdictions have approved traumatic cancer claims.  Some are set out below. Some courts heroically resisted the pro-compensation Zeitgeist, usually on case-specific evidentiary issues.[8]

In New York, judges seem to be well aware that post hoc ergo propter hoc is a fallacy.  Cassano v. Hagstrom, 5 N.Y.2d 643, 159 N.E.2d 348, 187 N.Y.S.2d 1 (1959) (affirming dismissal of case based because of plaintiffs’ attempt to use fallacious reasoning in the form of  “post hoc ergo propter hoc”); Holzberg v. Flower & Fifth Ave. Hosps., 39 AD 2d 526 (N.Y. 1st Dep’t 1972). Still, the New York courts struggled with traumatic cancer claims, and appeared to oscillate wildly without clear guidance on whether or to what extent the courts could reject specious claiming supported by speculative or unreliable expert witness opinion testimony.[9] Given the current hostility to gatekeeping of expert witness opinion, a recrudescence of traumatic cancer claims is likely.

Opinions Approving Causation in Traumatic Cancer Cases

California

Santa Ana Sugar Co. v. Industrial Accid. Comm’n, 170 P. 630, 630 (Cal. Dist. Ct. App. 1917)

Colorado

Canon Reliance Coal Co. v. Indus. Comm’n, 72 Colo. 477, 211 P. 868, 869-70 (1922) (cancer caused by being hit on cheek with a lump of coal)

Georgia

National Dairy Prods. Corp. v. Durham, 154 S.E.2d 752, 753-54 (Ga. Ct. App. 1967)

Kentucky

Louisville Ry v. Steubing’s Adm’r, 136 S.W. 634, 634 (Ky. Ct. App. 1911)

Louisiana

Reed v. Mullin Wood Co., 274 So. 2d 845, 846-47 (La. Ct. App. 1972), cert. denied, 275 So. 2d 729, 791 (La. 1973);

Thompson v. New Orleans Ry. & Light Co., 83 So. 19, 20 (La. 1919)

Michigan

Wilson v. Doehler-Jarvis Div. of Nat’l Lead Co., 353 Mich. 363, 91 N.W.2d 538, 539-40 (1958) (blow to lip caused cancer)

Mooney v. Copper Range RR, 27 N.W.2d 603, 604 (Mich. 1947)

Minnesota

Daly v. Bergstedt, 267 Minn. 244, 126 N.W.2d 242, 247–48 (1964) (affirming jury finding of causation between traumatic leg fracture and breast cancer; six physicians testified against causation; one stated cancer “could” result from trauma; imagining that scientific and legal standards of causation differ)

Pittman v. Pillsbury Flour Mills, Inc., 48 N.W.2d 735, 736 (Minn. 1951)

Hertz v. Watab Pulp & Paper Co., 237 N.W. 610, 611 (Minn. 1931)

Austin v. Red Wing Sewer Pipe Co., 163 Minn. 397, 204 N.W. 323, 323-24 (Minn. 1925) (cancer developed one year after worker was hit in the face with coal)

Gaetz v. City of Melrose, 193 N.W. 691, 692 (Minn. 1923)

Missouri

Vitale v. Duerbeck, 338 Mo. 536, 92 S.W.2d 691, 695 (1936)

New Hampshire

Jewell v. Grand Trunk Ry, 55 N.H. 84 (1874) (reversing traumatic cancer verdict on other grounds)

New Mexico

White v. Valley Land Co., P.2d 707, 708-10 (N.M. 1957)

Ohio

Hanna v. Aetna Ins., 24 Ohio Misc. 27, 52 Ohio Op. 2d 316, 259 N.E.2d 177, 177-79 (Ohio Mun. Ct. Dayton 1970)(breast lump found three months after car accident)

Glenn v. National Supply, 129 N.E.2d 189, 190-91 (Ohio Ct. App. 1954)

Oregon

Devine v. Southern Pacific Co., 207 Or. 261, 295 P.2d 201 (1956) (holding that physician’s testimony as to “probable” causation between shoulder fracture and lung cancer was sufficient; jury verdict for plaintiff reversed on other grounds).

Pennsylvania

Baker v. DeRosa, 413 Pa. 164, 196 A.2d 387, 389–90 (Pa. 1964)

Menarde v. Philadelphia Transp. Co., 376 Pa. 497, 103 A.2d 681, 684(1954) (the fact that breast cancer was found in the same place as the injury-caused bruise helped establish causation);

Southern S.S. Co. v. Norton, 41 F. Supp. 103 (E.D. Pa. 1940) (trauma to skull and lower back held to have caused lung cancer)

Tennessee

Koehring-Southern & Am. Mut. Ins. Co. v. Burnette, 464 S.W.2d 820, 821 (Tenn. 1970)

Boyd v. Young, 193 Tenn. 272, 246 S.W.2d 10, 10 (Tenn. 1951)

Rhode Island

Valente v. Bourne Mills, 77 R.I. 274, 278-79, 75 A.2d 191, 193-94 (1950) (adopting house of cards position in which any rational inference suffices even if not supported by expert medical opinion)

Emma v. A.D. Julliard & Co., 75 R.I. 94, 63 A.2d 786, 787-89 (R.I. 1949)(plaintiff had malignant tumor removed from her breast seven weeks after being hit with a can of juice)

Texas

Traders & General Insur. Co. v. Turner, 149 S.W.2d 593, 597-98 (Tex. Civ. App. 1941) (testicular cancer)

Virginia

Ellis v. Commonwealth Dep’t of Highways, 28 S.E.2d 730, 731-32, 735 (Va. 1944) (accepting post-hoc reasoning “[f]acts prevail over possibilities or probabilities”)

Winchester Milling Corp. v. Sencindiver, 138 S.E. 479, 480-81 (Va. 1927)

[1] See, e.g., Melvin A. Shiffman, Can Trauma Cause or Accelerate the Growth of Cancer? Forensic Examiner 6 (Fall 2004).

[2] See Manasco v. Insurance Co. of State of Pennsylvania, 89 S.W.3d 239 (Tex. App. Texarkana 2002) (affirming denial of benefits to worker who claimed head injury caused brain tumor; citing to epidemiological studies that failed to show an association between trauma and brain tumors).

[3] See, e.g., George R. Parsons, “Sufficiency of Proof in Traumatic Cancer Cases,” 2 Tort & Med. Year Book 335 (1962); Stoll & Crissey, “Epithelioma from Single Trauma,” 62 N.Y. St. J. Med. 496 (Feb. 15, 1962); Wilhelm C. Hueper, Trauma and Cancer (1959); Arden R. Hedge, “Can a Single Injury Cause Cancer?” 90 Calif. Med. 55 (1959); R. Crane, “The Relationship of a Single Act of Trauma to Subsequent Malignancy,” in Alan R. Moritz & David S. Helberg, eds., Trauma and Disease 147 (1959); Shields Warren, M.D., “Minimal criteria required to prove causation of traumatic or occupational neoplasms,” Ann. Surgery 585 (1943); Bishop, “Cancer, Trauma, and Compensation,” 32 So. Med. J. 302 (1939); Knox, “Trauma and Malignant Tumors, 26 Am. J. Surg. 66, 69-70 (1934); William B. Coley & Norman L. Higinbotham, “Injury as a causative factor in the development of malignant tumors,” 98 Ann. Surg. 991 (1933); Wainwright, “Single Trauma, Carcinoma and Workman’s Compensation,” 5 Am. J. Surg. 433 (1928); Alson R. Kilgore & Curtis E. Smith, “Industrial liability for cancer,” 25 Calif. & Western Med. 70 (1926); Charles Phelps, “The relation of trauma to cancer formation,” 51 Ann. Surgery 609 (1910).

[4] James Ewing, “Modern Attitudes Toward Traumatic Cancer,” 19 Arch. Path. 690, 692 (1935); James Ewing, “The Relation of Trauma to Malignant Tumors,” Am. J. Surg. 30, 31-34 (Feb. 1926).

[5] See, e.g., James A. Tobey, Public Health Law 321 (3ed 1947) (“Although there is little, if any, scientific evidence to prove conclusively that malignant growths such as carcinoma, sarcoma, and other forms of cancer are ever caused by single blows, wounds, injuries, or other forms of trauma, the courts have awarded damages in a number of instances to persons who have developed cancers following single injuries.”) (internal citations omitted).

[6] George R. Monkman, Gregg Orwoll & John C. Ivins, “Trauma and Oncogenesis,” 49 Mayo Clinic Proc. 157 (1974).

[7] The trauma theory of carcinogenesis was discussed and questioned in several law review articles.  See, e.g., Orrin E. Tilevitz, “Judicial Attitudes Towards Legal and Scientific Proof of Cancer Causation,” 3 Colum. J. Envt’l L. 344 (1977); Donald J. Ladanyi, “Impact Trauma As ‘Legal Cause’ of Cancer,” 20 Cleveland State L. Rev. 409 (1971); Theodore Dyke, “Traumatic Cancer?” 15 Clev.-Marshall L. Rev. 472 (1966); Jerry G. Elliott, “Traumatic cancer and ‘an old misunderstanding between doctors and lawyers’,” 13 U. Kan. L. Rev. 79 (1964); Comment, Sufficiency of Proof in Traumatic Cancer: A Medico-Legal Quandary, 16 Ark. L. Rev. 243 (1962); Comment, “Sufficiency of Proof in Traumatic Cancer Cases,” 46 Cornell L.Q. 581 (1961); Adelson, Injury and Cancer, 5 Western Res. L. Rev. 150 (1954).

[8] State Compensation Ins. Fund v. Kindig, 445 P.2d 72 (Colo. 1968) (head injury held not to have caused leukemia 68 days later); Slack v. C.L. Percival Co., 198 Iowa 54, 199 N.W. 323, 326 (1924) (anticipating Daubert by rejecting expert witness opinion that was “wholly in the realm of conjecture, speculation, and surmise”); Ortner v. Zenith Carburetor Co., 207 Mich. 610, 175 N .W. 122 (1919) (holding that 30 months was too long for a claim that accident that crushed worker’s fingers caused blood poisoning and penile cancer); Stordahl v. Rush Implement Co., 417 P.2d 95 (Mont. 1966) (rejecting traumatic causation of malignant tumor); Tonkovich v. Dep’t of Lab. & Indus., 31 Wash. 2d 220, 195 P.2d 638 (1948) (injury to foot held not to have caused abdominal cancer)

[9] See Dennison v. Wing, 279 App. Div. 494, 110 N.Y.S.2d 811, 813 (1952) (rejecting cancer claim when latency was two months on grounds that cancer took longer to develop); Sikora v. Apex Beverage Corp., 282 App. Div. 193, 196-97 (1953) (reversing judgment for plaintiff based upon jury’s finding that slip and fall accelerated breast cancer based upon lack of evidentiary support), aff’d, 306 N.Y. 917, 119 N.E.2d 601 (1954); Frankenheim v. B. Altman & Co., 13 Misc. 2d 1079, 1080-81, 177 N.Y.S.2d 2 (Bronx Cty. S.Ct. 1958) (granting motion to set aside verdict for plaintiff based upon traumatic cancer claim on grounds of insufficient evidence), app. dism’d, 8 App. Div. 2d 809 (First Dep’t 1959). But see McGrath v. Irving, 24 App. Div. 2d 236, 265 N.Y.S.2d 376 (1965) (affirming jury verdict based upon claim that plaintiff’s swallowing glass in car accident caused or accelerated development of laryngeal cancer); Mattfield v. Ward Baking Co., 14 App. Div. 2d 942, 221 N.Y.S.2d 224, 224 (1st Dep’t 1961) (affirming award for traumatic cancer based upon the “usual” conflicting expert witness testimony) Mattfield v. Ward Baking Co., 14 App. Div. 2d 942, 942 (1961) (affirming workman’s compensation award for “aggravation” of cancer, which resulted after “the usual conflict of medical opinion”); Pezzolanti v. Green Bus Lines, 114 App. Div. 2d 553, 553-54, 494 N.Y.S.2d 168, 169 (1985) (affirming workman’s compensation award for disability to wrist, which resulted from “trauma” of hitting pothole, which in turn injured asymptomatic wrist destabilized by pre-existing cancer).

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Recrudescence of Traumatic Cancer Claims

Intellectual Due Process in West Virginia and Beyond

June 1st, 2014

Harris v. CSX Transportation

I have borrowed and modified the phrase “Intellectual Due Process” from earlier writers because of its obvious implications for the presentation, interpretation, synthesis, and evaluation of scientific evidence in court. See Scott Brewer, “Scientific Expert Testimony and Intellectual Due Process,” 107 Yale L. J. 1535 (1998). The major reason courts write opinions is to explain and justify their decisions to litigants, present and future, and to a wider audience of lawyers, scholars, and the general public. Judicial opinions involving scientific evidence, whether in legislation, regulation, or litigation must satisfy the societal need to explain and justify the acceptance and rejection of scientific claims. Despite a great deal of hand waving that law and science are somehow different, in the end, when courts describe their acceptance or rejection of scientific claims, they are addressing the same epistemic warrant that scientists themselves employ. Even a cursory review of the judicial output reveals an unsatisfactory state of affairs in which many courts mangle scientific and statistical evidence and inference.  There is much that is needed to correct the problem.

One proposal would be to require that the parties file proposed findings of facts in connection with Rule 702 gatekeeping challenges.  Courts should file detailed findings of facts that underlie their decisions to admit or to exclude expert witness opinion testimony.  Another proposal would require courts to cite properly the scientific studies that they discuss in reaching a legal conclusion about sufficiency or admissibility.  These are small steps, but ones that would help reduce the gross inaccuracies and the glib generalizations, while increasing the opportunity for public scrutiny and criticism.

We do not think anything is amiss with special courts for tax, patent, family law, national security, equity, or commercial matters.  There is an even greater need for scientific skill, knowledge, and aptitude in a specialized science court.  The time has come for special courts to hear cases involving scientific claims in health effects and other litigation.

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A decision of the West Virginia Supreme Court, late last year, illustrates the need for substantial reform of how claiming based upon “scientific evidence” is permitted and evaluated in court.  Mrs. Harris sued the railroad for the wrongful death of her husband, who died of multiple myeloma. Mr. Harris had been exposed, in his railroad workplace, to diesel exhaust, which Mrs. Harris claimed caused his cancer. See Harris v. CSX Transportation, Inc., 232 W.Va. 617, 753 S.E.2d 275 (2013). The trial court excluded Mrs. Harris’s expert witnesses. Harris v. CSX Transportation, Inc., No. 12-1135, 2012 WL 8899119 (Cir. Ct. Marshall Cty., W.Va. Aug. 21, 2012).

1. The West Virginia Supreme Court reversed the trial court’s exclusion of witnesses on the basis of an asymmetrical standard of review, which would allow de novo review of trial court decisions to exclude expert witness opinions, but which would privilege trial court decisions to admit opinions by limiting appellate review to abuse of discretion. This asymmetry was, of course, the same dodge that the Third and Eleventh Circuits had used to keep the “gates open,” regardless of validity or reliability concerns, and the same dodge that the Supreme Court shut down in General Electric v. Joiner. A single judge dissented in Harris, Justice Loughry, who took the majority to task for twisting facts and law to get to a desired result.

2. The Harris Court cited a federal court case for dicta that “Rule 702 reflects an attempt to liberalize the rules governing the admissibility of expert testimony.” See Harris, 753 S.E.2d at 279 (citing and quoting from Weisgram v. Marley Co., 169 F.3d 514, 523 (8th Cir.1999). Remarkably, the Harris Court omitted reference to the United States Supreme Court’s unanimous affirmance of Weisgram, which saw Justice Ginsburg write that “[s]ince Daubert, moreover, parties relying on expert evidence have had notice of the exacting standards of reliability such evidence must meet.” Weisgram v. Marley Co., 528 U.S. 440, 442 (2000).  The Harris Court’s lack of scholarship is telling.

3. Meta-analysis appeared to play a role in the case, but the judicial decisions in Harris fail to describe the proffered evidence. The majority in Harris noted that one of plaintiff’s expert witnesses, Dr. Infante, relied upon a meta-analysis referred to as “Sonoda 2001.” Harris, 753 S.E.2d at 309. Neither the Court nor the dissent cited the published meta-analysis in a way that would help an interested reader in finding the paper.  One could imagine the hue and cry if courts cited judicial cases or statutes by short-hand names without providing enough information to access the relied upon source.  In this case, a PubMed search reveals the source so perhaps the error is harmless. Tomoko Sonoda, Yoshie Nagata, Mitsuru Mori, Tadao Ishida & Kohzoh Imai, “Meta-analysis of multiple myeloma and benzene exposure,” 11. J. Epidemiol. 249 (2001).  Still, the time has come for courts to describe and report the scientific evidence with the same care and detail that they would use in a car collision case.

4. A quick read shows that the Sonoda meta-analysis supports the dissent’s assessment:

“‘Dr. Infante testified on direct examination that Sonoda 2001 considered 8 case-control studies specific to engine exhaust and stated it concluded that diesel and non-diesel engine exhaust causes multiple myeloma.’ Yet, as the trial court found, ‘[o]n cross examination Dr. Infante acknowledged that none of the 8 papers included in the Sonoda meta-analysis mention diesel exhaust’.”

Harris, 753 S.E.2d at 309.  The dissent would have been considerably more powerful had it actually adverted to the language of Sonoda 2001:

“These results suggested that benzene exposure itself was not likely to be a risk factor of MM [multiple myeloma]. It is thought that several harmful chemical agents in engine exhaust, other than benzene, could be etiologically related to the risk of MM. Further case-control studies on MM are needed to obtain more information about detailed occupational exposure to toxic substances.”

Sonoda at 249 (2001) (emphasis added).  Contrary to Infante’s asseveration, Sonoda and colleagues never concluded that diesel exhaust causes multiple myeloma.  The state of scholarship and “intellectual due process” makes it impossible to tell whether or not Dr. Infante was telling the truth or the Harris Court badly misunderstood the record. Either way, something must give.

The dissent went on to note that Dr. Infante conducted his own meta-analysis, which included studies that did not mention diesel exhaust. Harris, 753 S.E.2d at 309.  The railroad complained that some of the studies were small and had limited power, but that is exactly why a meta-analysis would be appropriate.  The more disturbing complaints were that the meta-analysis left out important studies, and that it included irrelevant studies of benzene exposure and myeloma, which raised insuperable problems of external validity.

5. A half empty glass that is always full.  According to the Harris Court, the West Virginia shadow of Rule 702 is a rule of “admissibility rather than exclusion.” Harris, 753 S.E.2d at 279 (citing and quoting from In re Flood Litig. Coal River Watershed, 222 W.Va. 574, 581, 668 S.E.2d 203, 210 (2008), which in turn quoted a federal case, Arcoren v. United States, 929 F.2d 1235, 1239 (8th Cir. 1991), decided before the Supreme Court decided Daubert.)  This is just silly hand waving and blatant partisanship.  A rule that sets out criteria or bases for admissibility also demarcates the inadmissible.

6. Cherry Picking. Dr. Infante was permitted by the Harris Court to aggregate data from studies that did not observe diesel exposure, while he failed to include, or he deliberately excluded data from, a large, powerful, exonerative study conducted by scientists from the National Cancer Institute, the International Agency for Research on Cancer (IARC), and the Karolinska Institute. See Paolo Boffetta, Mustafa Dosemeci, Gloria Gridley, Heather Bath, Tahere Moradi and Debra Silverman, “Occupational exposure to diesel engine emissions and risk of cancer in Swedish men and women,” 12 Cancer Causes Control 365 (2001). Dr. Infante inexplicably excluded this study, which found a risk ratio for men exposed to diesel exhaust that was below one, 0.98, with a very narrow 95% confidence interval, 0.92-1.05. Boffetta at 368, Table 2.

7. The West Virginia articulated an incohorent definition of “reliable,” designed to give itself the ability to reject gatekeeping completely. Citing its earlier decision in Flood, the Court offered its own ipse dixit:

“The assessment of whether scientifically-based expert testimony is “reliable,” as that term is used in [Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), and Wilt v. Buracker, 191 W.Va. 39, 443 S.E.2d 196 (1993)], does not mean an assessment of whether the testimony is persuasive, convincing, or well-founded. Rather, assessing ‘reliability’ is a shorthand term of art for assessing whether the testimony is to a reasonable degree based on the use of knowledge and procedures that have been arrived at using the methods of science — rather than being based on irrational and intuitive feelings, guesses, or speculation. If the former is the case, then the jury may (or may not, in its sole discretion) ‘rely upon’ the testimony. In re Flood Litig., 222 W.Va. at 582 n. 5, 668 S.E.2d at 211 n. 5.”

Harris, 753 S.E.2d at 279-80. Surely, this is circular or vacuous or both. Opinions not “well-founded” will be ones that are based upon guesses or speculation.  Opinions arrived at by the “methods of science” will be ones that have an epistemic warrant that will survive a claim that they are not “well-founded.”

8. The Harris Court evidenced its hostility to scientific evidence by dredging up one of its own decisions involving a multiple myeloma causation claim, State ex rel. Wiseman v. Henning, 212 W.Va. 128, 569 S.E.2d 204 (2002).  Wiseman involved a specious claim that a traumatic rib injury caused multiple myeloma, a claim at odds with scientific method and observation:

“Some research has suggested that people in some jobs may have an increased risk of developing multiple myeloma because they are exposed to certain chemicals. But the International Agency for Research on Cancer (IARC) states that the evidence is limited overall. It has been suggested that people may have an increased risk if they work in the petrol or oil industry, farming, wood working, the leather industry, painting and decorating, hairdressing, rubber manufacturing or fire fighting. But there is no evidence to prove that any of these occupations carry an increased risk of myeloma.”

Cancer Research UK, “Myeloma risks and causes” (last visited May 28, 2014). Even the most non-progressive jurisdictions have generally eradicated specious claiming for trauma-induced cancers, but West Virginia has carved out a place second to none in its race to the bottom.

9. WOE.  Not surprisingly, the Harris Court relied heavily on the First Circuit’s “weight of the evidence” end-run around the notion of epistemic warrant for scientific claims, citing Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11 (1st Cir.2011), cert. denied sub nom., U.S. Steel Corp. v. Milward, ___ U.S. ___, 2012 WL 33303 (2012). The Harris Court went on to conflate and confuse WOE with Bradford Hill, and cited a recent New York case that confidently saw through WOE hand waving, while ignoring its devasting critique of expert witnesses’ attempts to pass off WOE for scientific, epistemic warrant.  Reeps ex rel. Reeps v. BMW of N. Am., LLC, No. 100725/08,

2013 WL 2362566, at *3, 2012 N.Y. Misc. LEXIS 5788; 2012 NY Slip Op 33030U  (N.Y. Sup. Ct. May 10, 2013).

10.  Link.  Dr. Infante links a lot, even when his sources do not:

“Dr. Infante testified that the International Agency for Research on Cancer issued Technical Publication Number 42 in 2009, and that the publication stated that diesel exhaust exposures have been linked to multiple myeloma and leukemia.”

Harris, 753 S.E.2d at 294. The Harris Court neglected to give the title of the publication, which tells a different story.  Identification of research needs to resolve the carcinogenicity of high-priority IARC carcinogens. The dissent was willing to go behind the conclusory and false characterization that Dr. Infante and plaintiff gave to this publication.  Harris, 753 S.E.2d at 309. The trial court’s finding (and the dissent’s assertion) that the IARC Technical Publication 42 intended to express a research agenda, not to make a causation statement, seems unassailable.  Furthermore, it appears to be precisely the sort of specious claim that a court should keep from a jury.  The cited IARC source actually notes that the then current IARC classification of diesel exhaust was of inadequate evidence for human carcinogenicity, with a focus on lung cancer, and barely a mention of multiple myeloma.

11.  The Benzene Connection. Plaintiffs’ expert witnesses, including Dr. Infante, argued that benzene was a component of diesel exhaust, and benzene caused multiple myeloma.  This move ignored not only the lack of evidence to implicate benzene in the causation of multiple myeloma, but it also ignored the large quantitative differences between the benzene occupational exposure studies and the very small amounts of benzene in diesel exhaust.  The Harris Court held that the trial court acted improperly by inquiring into and finding the following facts, which were “exclusively” for the jury:

  • “There is substantially more benzene in cigarette smoke than diesel exhaust.
  • Benzene is present only in trivial doses in diesel exhaust.
  • The hypothesis that diesel exhaust causes multiple myeloma is confounded by the fact that cigarette smoking does not.”

The Harris majority further chastised the trial court for adverting to the ten or so studies that failed to find a statistically significant association between benzene exposure and multiple myeloma.  Harris, 753 S.E.2d at 305-06.  This inquiry directly calls into question, however, Dr. Infante’s methodology.

If these facts, found by the trial court, were reasonably established, then Dr. Infante’s argument was less than bogus, and a major underpinning for inclusion of benzene studies in his meta-analysis was refuted.  These are precisely the sort of foundational facts that must be part of an inquiry into the methodological grounds of an expert witness’s opinion.

12.  The Harris Court confused “proving causation” with “showing a methodology that provides an epistemic warrant for concluding.” Harris, 753 S.E.2d at 300. The Harris Court asserted that the trial court exceeded its gatekeeping function by inquiring into whether Mrs. Harris’s expert witnesses “proved” causation. Harris, 753 S.E.2d at 300. Speaking of “proof of” or “proving” causation is an affectation of lawyers, who refer to their evidence as their “proofs.”  Epidemiologic articles and meta-analyses do not end with quod erat demonstrandum. Beyond the curious diction, there is a further issue in the majority’s suggestion that the trial court set the bar too high in declaring that the plaintiff failed to “prove” causation.  Even if we were to accept the continuous nature of strength of evidence for a causal conclusion, Dr. Infante and the other plaintiff’s witnesses, would be fairly low on the curve, and their lowly position must of necessity speak to the merits of the defense motion to exclude under Rule 702.

13. Purely Matters for Jury. The Harris Court criticized the trial court for conducting a “mini-trial,” which set out to “resolve issues that were purely matters for jury consideration.” Harris, 753 S.E.2d at 305. In holding that the matters addressed in the pre-trial hearing were “exclusively grist for the jury and which had no relevancy to the limited role the trial court had under the facts of this case,” the Harris Court displayed a profound disregard for what facts would be relevant for a challenge to the plaintiff’s expert witnesses’ methodology. Many of the facts found by the trial court were directly relevant to “general acceptance,” validity (internal and external) of studies relied upon, and reliability of reasoning and inferences drawn. Aside from the lack of general acceptance and peer review of the plaintiff’s claimed causal relationship, the proffered testimony was filled with gaps and lacunae, which are very much at issue in methodological challenges to an opinion of causality.

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The Harris case has taken its place next to Milward in the litigation industry’s arsenal of arguments for abandoning meaningful judicial supervision and gatekeeping of expert witness opinion testimony.  See Andrew S. Lipton, “Proving Toxic Harm: Getting Past Slice and Dice Tactics,” 45 McGeorge L. Rev. 707, 731 (2014) (plaintiffs’ bar cheerleading for the Harris decision as “a lengthy and thoughtful analysis”, and for the Milward case as roadmap to evade meaningful judicial oversight).  Not all was perfect with the trial court’s opinion.  The defense seemed to have misled the court by asserting that “a difference between a case group and control group is not statistically significant then there is no difference at all.”  See Respondent’s Brief at 5, Harris v. CSX Transportation, Inc., 2013 WL 4747999 (filed (Feb. 4, 2013) (citing  App. 169, 228-230 (Shields) as having explained that the p-values greater than 0.05 do not support a causal association).

This is hardly true, and indeed, the lack of statistical significance does not lead to a claim that the null hypothesis of no association between exposure and outcome is correct.  The defense, however, did not have a burden of showing the null to be correct; only that there was no reliable method deployed to reject the null in favor an alternative that the risk ratio for myeloma was raised among workers exposed to diesel exhaust.

Still, the trial court did seem to understand the importance of replication, in studies free of bias and confounding. Courts generally will have to do better at delineating what are “positive” and “negative” studies, with citations to the data and the papers, so that judicial opinions provide a satisfactory statement of reasons for judicial decisions.

Posted in Causation, Expert Witnesses, Meta-analysis, Rule 702, Scientific Evidence | Comments Off on Intellectual Due Process in West Virginia and Beyond

Biostatistics and FDA Regulation: The Convergence of Science and Law

May 29th, 2014

On May 20, 2014, the Food and Drug Law Institute (FDLI), the Drug Information Association (DIA), and the Harvard Law School’s Petrie-Flom Center for Health Law Policy, Biotechnology, and Bioethics, in collaboration with the Harvard School of Public Health Department of Biostatistics and Harvard Catalyst | The Harvard Clinical and Translational Science Center, presented a symposium on“Biostatistics and FDA Regulation: The Convergence of Science and Law.”

The symposium might just as well have been described as the collision of science and law.

The Symposium agenda addressed several cutting-edge issues on statistical evidence in the law, criminal, civil, and regulatory. Names of presenters are hyperlinked to presentations slides that are available.

I. Coleen Klasmeier, of Sidley Austin LLP, introduced and moderated the first section, “Introduction to Statistics and Regulatory Law,” which focused on current biostatistical issues in regulation of drugs, devices, and foods by the Food and Drug Administration (FDA). Qi Jiang, Executive Director of Amgen, Robert T. O’Neill, retired from the FDA, and now Statistical Advisor in CDER, and Jerald S. Schindler, of Merck Research Laboratories, presented.

II. Qi Jiang moderated and introduced the second section on safety issues, and the difficulties presented by meta-analysis and other statistical assessments of safety outcomes in clinical trials and in marketing of drugs and devices. Lee-Jen Wei, of the Harvard School of Public Health, Geoffrey M. Levitt, an Associate General Counsel of Pfizer, Inc., and Janet Wittes, of the Statistics Collaborative, presented.

III. Aaron Katz, of Ropes & Gray LLP, introduced the third section, on “Statistical Disputes in Life Sciences Litigation,” which addressed recent developments in expert witness gatekeeping, the Avandia litigation, and the role of statistics in two recent cases, Matrixx, Inc. v. Siracusano, and United States v. Harkonen.  Anand Agneshwar, of Arnold & Porter LLP, Lee-Jen Wei, Christina L. Diaz, Assistant General Counsel of GlaxoSmithKline, and Nathan A. Schachtman presented.

IV. Christopher Robertson, a law professor now visiting at Harvard Law School, moderated a talk by Robert O’Neill on “Emerging Issues,” at the FDA.

V. Dr. Wittes moderated a roundtable discussion on “Can We Handle the Truth,” which explored developments in First Amendment and media issues involved in regulation and litigation. Anand Agneshwar, and Freddy A. Jimenez, Assistant General Counsel, Johnson & Johnson, presented.

Posted in Meta-analysis, Rule 702, statistical evidence | Comments Off on Biostatistics and FDA Regulation: The Convergence of Science and Law

The Outer Limits (and Beyond?) of Ex Parte Advocacy of Federal Judges

May 23rd, 2014

As every trial lawyer knows, people sometimes reveal important facts in curious ways, incorporated in their own biased narrative of events.  Recently, I heard a recorded lecture about expert witnesses, by a plaintiffs’ lawyer, who revealed a damning fact about a judge.  The lawyer clearly thought that this fact was commendatory, but in fact revealed another effort of scientific advocates and zealots to subvert the neutrality of federal judges.  See In re School Asbestos Litigation, 977 F.2d 764 (3d Cir. 1992) (describing effort by plaintiffs’ lawyers and the late Dr. Irving Selikoff to corrupt state and federal judges with one-sided ex parte presentations of their views at the so-called Third-Wave Conference).

Anthony Z. Roisman is the Managing Partner of the National Legal Scholars Law Firm.  This firm has a roster of affiliated law professors who serve as consultants for plaintiffs in environmental and tort cases. (Some other participants in this law firm include Jay M. Feinman, Lucinda M. Finley, Neil Vidmar, and Richard W. Wright.) Roisman has been active in various plaintiff organizations, including serving as the head of the ATLA Section on Toxic, Environmental & Pharmaceutical Torts (STEP). 

Roisman lectures frequently for the American Law Institute on expert witness issues. Recently, I was listening to an mp3 recording of one of Roisman’s lectures on expert witnesses in environmental litigation.  Given Roisman’s practice and politics, I was not surprised to hear him praise Judge Rothstein’s opinion that refused to exclude plaintiffs’ expert witnesses’ causation opinions in the PPA litigation.  See In re Phenylpropanolamine Prod. Liab. Litig., 289 F. 2d 1230 (2003).  What stunned me, however, was his statement that Judge Rothstein issued her opinion “fresh from a seminar at the Tellus Institute,” which he described as “organization set up by scientist trying to bring common sense to interpretation of science.”

Post hoc; ergo propter hoc?

Judge Rothstein’s PPA decision stands as a landmark of judicial gullibility.  Judge Rothstein conducted hearings and entertaining extensive briefings on the reliability of plaintiffs’ expert witnesses’ opinions, which were based largely upon one epidemiologic study, known as the “Yale Hemorrhagic Stroke Project (HSP).”  In the end, publication in a prestigious peer-reviewed journal proved to be a proxy for independent review: “The prestigious NEJM published the HSP results, further substantiating that the research bears the indicia of good science.” Id. at 1239 (citing Daubert II for the proposition that peer review shows the research meets the minimal criteria for good science). The admissibility challenges were refused.

Ultimately, the HSP study received much more careful analysis before juries, which uniformly returned verdicts for the defense. After one of the early defense verdicts, plaintiffs’ counsel challenged the defendant’s reliance upon underlying data in the HSP, which went behind the peer-reviewed publication, and which showed that the peer review failed to prevent serious errors.  The trial court rejected the plaintiffs’ request for a new trial, and spoke to the significance of challenging the superficial significance of peer review of the key study relied upon by plaintiffs in the PPA litigation:

“I mean, you could almost say that there was some unethical activity with that Yale Study.  It’s real close.  I mean, I — I am very, very concerned at the integrity of those researchers.”

“Yale gets — Yale gets a big black eye on this.”

O’Neill v. Novartis AG, California Superior Court, Los Angeles Cty., Transcript of Oral Argument on Post-Trial Motions, at 46 -47 (March 18, 2004) (Hon. Anthony J. Mohr)

Roisman’s endorsement of the PPA decision may have been purely result-oriented jurisprudence, but what of his enthusiasm for the “learning” that Judge Rothstein received at the Tellus Institute.  Tell us, what is this Tellus Institute?

In 2003, roughly contemporaneously with Judge Rothstein’s PPA decision, SKAPP published a jeremiad against the Daubert decision, with support from none other than the Tellus Group. See Daubert: The Most Influential Supreme Court Ruling You’ve Never Heard Of;  A Publication of the Project on Scientific Knowledge and Public Policy, coordinated by the Tellus Institute (2003). The Tellus Institute website tells us very little specific detail about the Institute’s projects, other than stating some vague and pious goals.  The alignment, however, of the Tellus Institute with David Michael’s SKAPP, which was created with plaintiffs’ lawyers’ funding, certainly seems like a dubious indicator of neutrality and scientific commitment.  See “Skapp a Lot” (April 30, 2010).

We might get a better idea of the organization from the Tellus membership.

Richard Clapp and David Ozonoff are both regular testifiers for plaintiffs in so-called toxic tort and environmental litigation. In an article published about the time of the PPA decision, Clapp and Ozonoff acknowledged having benefited from discussions with colleagues at the Tellus Institute.  See Richard W. Clapp & David Ozonoff, “Environment and Health: Vital Intersection or Contested Territory?” 30 Am. J. L. & Med. 189, 189 (2004) (“This Article also benefited from discussions with colleagues in the project on Scientific Knowledge and Public Policy at Tellus Institute, in Boston, Massachusetts.”).

In the infamous case of Selikoff and Motley and their effort to subvert the neutrality of Judge James M. Kelly in the school district asbestos litigation, the conspiracy was detected in time for a successful recusal effort. In re School Asbestos Litigation, 977 F.2d 764 (3d Cir. 1992).  Unfortunately, in the PPA litigation, there was no disclosure of the efforts by the advocacy group, Tellus Institute, to undermine the neutrality of a federal judge. 

Outside observers will draw their own inferences about whether Tellus was an “honest broker” of scientific advice to Judge Rothstein. One piece of evidence may be SKAPP’s website, which contains a page about Richard Clapp’s courtroom advocacy in the PPA litigation. Additional evidence comes from Clapp’s leadership role in Physicians for Social Responsibility, and his own characterization of himself as a healthcare professional advocate. Clapp, a member of Tellus, was an expert witness for plaintiffs in PPA cases.

Was Clapp present at the Tellus Institute meeting attended by Judge Rothstein? History will judge whether the Tellus Institute participated in corrupting the administration of justice.

Posted in Conflicts of Interest, Expert Witnesses, Rule 702 | Comments Off on The Outer Limits (and Beyond?) of Ex Parte Advocacy of Federal Judges

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