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Judicial Gatekeeping Cures Claims That Viagra Can Cause Melonoma

January 24th, 2020

The phosphodiesterases 5 inhibitor medications (PDE5i) seem to arouse the litigation propensities of the lawsuit industry. The PDE5i medications (sildenafil, tadalafil, etc.) have multiple indications, but they are perhaps best known for their ability to induce penile erections, which in some situations can be a very useful outcome.

The launch of Viagra in 1998 was followed by litigation that claimed the drug caused heart attacks, and not the romantic kind. The only broken hearts, however, were those of the plaintiffs’ lawyers and their expert witnesses who saw their litigation claims excluded and dismissed.[1]

Then came claims that the PDE5i medications caused non-arteritic anterior ischemic optic neuropathy (“NAION”), based upon a dubious epidemiologic study by Dr. Gerald McGwin. This litigation demonstrated, if anything, that while love may be blind, erections need not be.[2] The NAION cases were consolidated in a multi-district litigation (MDL) in front of Judge Paul Magnuson, in the District of Minnesota. After considerable back and forth, Judge Manguson ultimately concluded that the McGwin study was untrustworthy, and the NAION claims were dismissed.[3]

In 2014, the American Medical Association’s internal medicine journal published an observational epidemiologic study of sildenafil (Viagra) use and melanoma.[4] The authors of the study interpreted their study modestly, concluding:

“[s]ildenafil use may be associated with an increased risk of developing melanoma. Although this study is insufficient to alter clinical recommendations, we support a need for continued investigation of this association.”

Although the Li study eschewed causal conclusions and new clinical recommendations in view of the need for more research into the issue, the litigation industry filed lawsuits, claiming causality.[5]

In the new natural order of things, as soon as the litigation industry cranks out more than a few complaints, an MDL results, and the PDE5i – melanoma claims were no exception. By spring 2016, plaintiffs’ counsel had collected ten cases, a minion, sufficient for an MDL.[6] The MDL plaintiffs named the manufacturers of sildenafil and tadalafil, two of the more widely prescribed PDEi5 medications, on behalf of putative victims.

While the MDL cases were winding their way through discovery and possible trials, additional studies and meta-analyses were published. None of the subsequent studies, including the systematic reviews and meta-analyses, concluded that there was a causal association. Most scientists who were publishing on the issue opined that systematic error (generally confounding) prevented a causal interpretation of the data.[7]

Many of the observational studies found statistically significantly increased relative risks about 1.1 to 1.2 (10 to 20%), typically with upper bounds of 95% confidence intervals less than 2.0. The only scientists who inferred general causation from the available evidence were those who had been recruited and retained by plaintiffs’ counsel. As plaintiffs’ expert witnesses, they contended that the Li study, and the several studies that became available afterwards, collectively showed that PDE5i drugs cause melanoma in humans.

Not surprisingly, given the absence of any non-litigation experts endorsing the causal conclusion, the defendants challenged plaintiffs’ proffered expert witnesses under Federal Rule of Evidence 702. Plaintiffs’ counsel also embraced judicial gatekeeping and challenged the defense experts. The MDL trial judge, the Hon. Richard Seeborg, held hearings with four days of viva voce testimony from four of plaintiffs’ expert witnesses (two on biological plausibility, and two on epidemiology), and three of the defense’s experts. Last week, Judge Seeborg ruled by granting in part, and denying in part, the parties’ motions.[8]

The Decision

The MDL trial judge’s opinion is noteworthy in many respects. First, Judge Richard Seeborg cited and applied Rule 702, a statute, and not dicta from case law that predates the most recent statutory version of the rule. As a legal process matter, this respect for judicial process and the difference in legal authority between statutory and common law was refreshing. Second, the judge framed the Rule 702 issue, in line with the statute, and Ninth Circuit precedent, as an inquiry whether expert witnesses deviated from the standard of care of how scientists “conduct their research and reach their conclusions.”[9]

Biological Plausibility

Plaintiffs proffered three expert witnesses on biological plausibility, Drs. Rizwan Haq, Anand Ganesan, and Gary Piazza. All were subject to motions to exclude under Rule 702. Judge Seeborg denied the defense motions against all three of plaintiffs’ plausibility witnesses.[10]

The MDL judge determined that biological plausibility is neither necessary nor sufficient for inferring causation in science or in the law. The defense argued that the plausibility witnesses relied upon animal and cell culture studies that were unrealistic models of the human experience.[11] The MDL court, however, found that the standard for opinions on biological plausibility is relatively forgiving, and that the testimony of all three of plaintiffs’ proffered witnesses was admissible.

The subjective nature of opinions about biological plausibility is widely recognized in medical science.[12] Plausibility determinations are typically “Just So” stories, offered in the absence of hard evidence that postulated mechanisms are actually involved in a real causal pathway in human beings.

Causal Association

The real issue in the MDL hearings was the conclusion reached by plaintiffs’ expert witnesses that the PDE5i medications cause melanoma. The MDL court did not have to determine whether epidemiologic studies were necessary for such a causal conclusion. Plaintiffs’ counsel had proffered three expert witnesses with more or less expertise in epidemiology: Drs. Rehana Ahmed-Saucedo, Sonal Singh, and Feng Liu-Smith. All of plaintiffs’ epidemiology witnesses, and certainly all of defendants’ experts, implicitly if not explicitly embraced the proposition that analytical epidemiology was necessary to determine whether PDE5i medications can cause melanoma.

In their motions to exclude Ahmed-Saucedo, Singh, and Liu-Smith, the defense pointed out that, although many of the studies yielded statistically significant estimates of melanoma risk, none of the available studies adequately accounted for systematic bias in the form of confounding. Although the plaintiffs’ plausibility expert witnesses advanced “Just-So” stories about PDE5i and melanoma, the available studies showed an almost identical increased risk of basal cell carcinoma of the skin, which would be explained by confounding, but not by plaintiffs’ postulated mechanisms.[13]

The MDL court acknowledged that whether epidemiologic studies “adequately considered” confounding was “central” to the Rule 702 inquiry. Without any substantial analysis, however, the court gave its own ipse dixit that the existence vel non of confounding was an issue for cross-examination and the jury’s resolution.[14] Whether there was a reasonably valid association between PDE5i and melanoma was a jury question. This judicial refusal to engage with the issue of confounding was one of the disappointing aspects of the decision.

The MDL court was less forgiving when it came to the plaintiffs’ epidemiology expert witnesses’ assessment of the association as causal. All the parties’ epidemiology witnesses invoked Sir Austin Bradford Hill’s viewpoints or factors for judging whether associations were causal.[15] Although they embraced Hill’s viewpoints on causation, the plaintiffs’ epidemiologic expert witnesses had a much more difficult time faithfully applying them to the evidence at hand. The MDL court concluded that the plaintiffs’ witnesses deviated from their own professional standard of care in their analysis of the data.[16]

Hill’s first enumerated factor was “strength of association,” which is typically expressed epidemiologically as a risk ratio or a risk difference. The MDL court noted that the extant epidemiologic studies generally showed relative risks around 1.2 for PDE5i and melanoma, which was “undeniably” not a strong association.[17]

The plaintiffs’ epidemiology witnesses were at sea on how to explain away the lack of strength in the putative association. Dr. Ahmed-Saucedo retreated into an emphasis on how all or most of the studies found some increased risk, but the MDL court correctly found that this ruse was merely a conflation of strength with consistency of the observed associations. Dr. Ahmed-Saucedo’s dismissal of the importance of a dose-response relationship, another Hill factor, as unimportant sealed her fate. The MDL court found that her Bradford Hill analysis was “unduly results-driven,” and that her proffered testimony was not admissible.[18] Similarly, the MDL court found that Dr. Feng Liu-Smith similarly conflated strength of association with consistency, which error was too great a professional deviation from the standard of care.[19]

Dr. Sonal Singh fared no better after he contradicted his own prior testimony that there is an order of importance to the Hill factors, with “strength of association,” at or near the top. In the face of a set of studies, none of which showed a strong association, Dr. Singh abandoned his own interpretative principle to suit the litigation needs of the case. His analysis placed the greatest weight on the Li study, which had the highest risk ratio, but he failed to advance any persuasive reason for his emphasis on one of the smallest studies available. The MDL court found that Dr. Singh’s claim to have weighed strength of association heavily, despite the obvious absence of strong associations, puzzling and too great an analytical gap to abide.[20]

Judge Seeborg thus concluded that while the plaintiffs’ expert witness could opine that there was an association, which was arguably plausible, they could not, under Rule 702, contend that the association was causal. In attempting to advance an argument that the association met Bradford Hill’s factors for causality, the plaintiffs’ witnesses had ignored, misrepresented, or confused one of the most important factors, strength of the association, in a way that revealed their analyses to be result driven and unfaithful to the methodology they claimed to have followed. Judge Seeborg emphasized a feature of the revised Rule 702, which often is ignored by his fellow federal judges:[21]

“Under the amendment, as under Daubert, when an expert purports to apply principles and methods in accordance with professional standards, and yet reaches a conclusion that other experts in the field would not reach, the trial court may fairly suspect that the principles and methods have not been faithfully applied. See Lust v. Merrell Dow Pharmaceuticals, Inc., 89 F.3d 594, 598 (9th Cir. 1996). The amendment specifically provides that the trial court must scrutinize not only the principles and methods used by the expert, but also whether those principles and methods have been properly applied to the facts of the case.”

Given that the plaintiffs’ witnesses purported to apply a generally accepted methodology, Judge Seeborg was left to question why they would conclude causality when no one else in their field had done so.[22] The epidemiologic issue had been around for several years, and addressed not just in observational studies, but systematically reviewed and meta-analyzed. The absence of published causal conclusions was not just an absence of evidence, but evidence of absence of expert support for how plaintiffs’ expert witnesses applied the Bradford Hill factors.

Reliance Upon Studies That Did Not Conclude Causation Existed

Parties challenging causal claims will sometimes point to the absence of a causal conclusion in the publication of individual epidemiologic studies that are the main basis for the causal claim. In the PDE5i-melanoma cases, the defense advanced this argument unsuccessfully. The MDL court rejected the defense argument, based upon the absence of any comprehensive review of all the pertinent evidence for or against causality in an individual study; the study authors are mostly concerned with conveying the results of their own study.[23] The authors may have a short discussion of other study results as the rationale for their own study, but such discussions are often limited in scope and purpose. Judge Seeborg, in this latest round of PDE5i litigation, thus did not fault plaintiffs’ witnesses’ reliance upon epidemiologic or mechanistic studies, which individually did not assert causal conclusions; rather it was the absence of causal conclusions in systematic reviews, meta-analyses, narrative reviews, regulatory agency pronouncements, or clinical guidelines that ultimately raised the fatal inference that the plaintiffs’ witnesses were not faithfully deploying a generally accepted methodology.

The defense argument that pointed to the individual epidemiologic studies themselves derives some legal credibility from the Supreme Court’s opinion in General Electric Co. v. Joiner, 522 U.S. 136 (1997). In Joiner, the SCOTUS took plaintiffs’ expert witnesses to task for drawing stronger conclusions than were offered in the papers upon which they relied. Chief Justice Rehnquist gave considerable weight to the consideration that the plaintiffs’ expert witnesses relied upon studies, the authors of which explicitly refused to interpret as supporting a conclusion of human disease causation.[24]

Joiner’s criticisms of the reliance upon studies that do not themselves reach causal conclusions have gained a foothold in the case law interpreting Rule 702. The Fifth Circuit, for example, has declared:[25]

“It is axiomatic that causation testimony is inadmissible if an expert relies upon studies or publications, the authors of which were themselves unwilling to conclude that causation had been proven.”

This aspect of Joiner may properly limit the over-interpretation or misinterpretation of an individual study, which seems fine.[26] The Joiner case may, however, perpetuate an authority-based view of science to the detriment of requiring good and sufficient reasons to support the testifying expert witnesses’ opinions.  The problem with Joiner’s suggestion that expert witness opinion should not be admissible if it disagrees with the study authors’ discussion section is that sometimes study authors grossly over-interpret their data.  When it comes to scientific studies written by “political scientists” (scientists who see their work as advancing a political cause or agenda), then the discussion section often becomes a fertile source of unreliable, speculative opinions that should not be given credence in Rule 104(a) contexts, and certainly should not be admissible in trials. In other words, the misuse of non-rigorous comments in published articles can cut both ways.

There have been, and will continue to be, occasions in which published studies contain data, relevant and important to the causation issue, but which studies also contain speculative, personal opinions expressed in the Introduction and Discussion sections.  The parties’ expert witnesses may disagree with those opinions, but such disagreements hardly reflect poorly upon the testifying witnesses.  Neither side’s expert witnesses should be judged by those out-of-court opinions.  Perhaps the hearsay discussion section may be considered under Rule 104(a), which suspends the application of the Rules of Evidence, but it should hardly be a dispositive factor, other than raising questions for the reviewing court.

In exercising their gatekeeping function, trial judges should exercise care in how they assess expert witnesses’ reliance upon study data and analyses, when they disagree with the hearsay authors’ conclusions or discussions.  Given how many journals cater to advocacy scientists, and how variable the quality of peer review is, testifying expert witnesses should, in some instances,  have the expertise to interpret the data without substantial reliance upon, or reference to, the interpretative comments in the published literature.

Judge Seeborg sensibly seems to have distinguished between the absence of causal conclusions in individual epidemiologic studies and the absence of causal conclusions in any reputable medical literature.[27] He refused to be ensnared in the Joiner argument because:[28]

“Epidemiology studies typically only expressly address whether an association exists between agents such as sildenafil and tadalafil and outcomes like melanoma progression. As explained in In re Roundup Prod. Liab. Litig., 390 F. Supp. 3d 1102, 1116 (N.D. Cal. 2018), ‘[w]hether the agents cause the outcomes, however, ordinarily cannot be proven by epidemiological studies alone; an evaluation of causation requires epidemiologists to exercise judgment about the import of those studies and to consider them in context’.”

This new MDL opinion, relying upon the Advisory Committee Notes to Rule 702, is thus a more felicitous statement of the goals of gatekeeping.

Confidence Intervals

As welcome as some aspects of Judge Seeborg’s opinion are, the decision is not without mistakes. The district judge, like so many of his judicial colleagues, trips over the proper interpretation of a confidence interval:[29]

“When reviewing the results of a study it is important to consider the confidence interval, which, in simple terms, is the ‘margin of error’. For example, a given study could calculate a relative risk of 1.4 (a 40 percent increased risk of adverse events), but show a 95 percent ‘confidence interval’ of .8 to 1.9. That confidence interval means there is 95 percent chance that the true value—the actual relative risk—is between .8 and 1.9.”

This statement is inescapably wrong. The 95 percent probability attaches to the capturing of the true parameter – the actual relative risk – in the long run of repeated confidence intervals that result from repeated sampling of the same sample size, in the same manner, from the same population. In Judge Seeborg’s example, the next sample might give a relative risk point estimate 1.9, and that new estimate will have a confidence interval that may run from just below 1.0 to over 3. A third sample might turn up a relative risk estimate of 0.8, with a confidence interval that runs from say 0.3 to 1.4. Neither the second nor the third sample would be reasonably incompatible with the first. A more accurate assessment of the true parameter is that it will be somewhere between 0.3 and 3, a considerably broader range for the 95 percent.

Judge Seeborg’s error is sadly all too common. Whenever I see the error, I wonder whence it came. Often the error is in briefs of both plaintiffs’ and defense counsel. In this case, I did not see the erroneous assertion about confidence intervals made in plaintiffs’ or defendants’ briefs.

[1]  Brumley  v. Pfizer, Inc., 200 F.R.D. 596 (S.D. Tex. 2001) (excluding plaintiffs’ expert witness who claimed that Viagra caused heart attack); Selig v. Pfizer, Inc., 185 Misc. 2d 600 (N.Y. Cty. S. Ct. 2000) (excluding plaintiff’s expert witness), aff’d, 290 A.D. 2d 319, 735 N.Y.S. 2d 549 (2002).

[2]  “Love is Blind but What About Judicial Gatekeeping of Expert Witnesses? – Viagra Part I” (July 7, 2012); “Viagra, Part II — MDL Court Sees The Light – Bad Data Trump Nuances of Statistical Inference” (July 8, 2012).

[3]  In re Viagra Prods. Liab. Litig., 572 F.Supp. 2d 1071 (D. Minn. 2008), 658 F. Supp. 2d 936 (D. Minn. 2009), and 658 F. Supp. 2d 950 (D. Minn. 2009).

[4]  Wen-Qing Li, Abrar A. Qureshi, Kathleen C. Robinson, and Jiali Han, “Sildenafil use and increased risk of incident melanoma in US men: a prospective cohort study,” 174 J. Am. Med. Ass’n Intern. Med. 964 (2014).

[5]  See, e.g., Herrara v. Pfizer Inc., Complaint in 3:15-cv-04888 (N.D. Calif. Oct. 23, 2015); Diana Novak Jones, “Viagra Increases Risk Of Developing Melanoma, Suit Says,” Law360 (Oct. 26, 2015).

[6]  See In re Viagra (Sildenafil Citrate) Prods. Liab. Litig., 176 F. Supp. 3d 1377, 1378 (J.P.M.L. 2016).

[7]  See, e.g., Jenny Z. Wang, Stephanie Le , Claire Alexanian, Sucharita Boddu, Alexander Merleev, Alina Marusina, and Emanual Maverakis, “No Causal Link between Phosphodiesterase Type 5 Inhibition and Melanoma,” 37 World J. Men’s Health 313 (2019) (“There is currently no evidence to suggest that PDE5 inhibition in patients causes increased risk for melanoma. The few observational studies that demonstrated a positive association between PDE5 inhibitor use and melanoma often failed to account for major confounders. Nonetheless, the substantial evidence implicating PDE5 inhibition in the cyclic guanosine monophosphate (cGMP)-mediated melanoma pathway warrants further investigation in the clinical setting.”); Xinming Han, Yan Han, Yongsheng Zheng, Qiang Sun, Tao Ma, Li Dai, Junyi Zhang, and Lianji Xu, “Use of phosphodiesterase type 5 inhibitors and risk of melanoma: a meta-analysis of observational studies,” 11 OncoTargets & Therapy 711 (2018).

[8]  In re Viagra (Sildenafil Citrate) and Cialis (Tadalafil) Prods. Liab. Litig., Case No. 16-md-02691-RS, Order Granting in Part and Denying in Part Motions to Exclude Expert Testimony (N.D. Calif. Jan. 13, 2020) [cited as Opinion].

[9]  Opinion at 8 (“determin[ing] whether the analysis undergirding the experts’ testimony falls within the range of accepted standards governing how scientists conduct their research and reach their conclusions”), citing Daubert v. Merrell Dow Pharm., Inc. (Daubert II), 43 F.3d 1311, 1317 (9th Cir. 1995).

[10]  Opinion at 11.

[11]  Opinion at 11-13.

[12]  See Kenneth J. Rothman, Sander Greenland, and Timothy L. Lash, “Introduction,” chap. 1, in Kenneth J. Rothman, et al., eds., Modern Epidemiology at 29 (3d ed. 2008) (“no approach can transform plausibility into an objective causal criterion).

[13]  Opinion at 15-16.

[14]  Opinion at 16-17.

[15]  See Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295 (1965); see also “Woodside & Davis on the Bradford Hill Considerations” (April 23, 2013).

[16]  Opinion at 17 – 21.

[17]  Opinion at 18. The MDL court cited In re Silicone Gel Breast Implants Prod. Liab. Litig., 318 F. Supp. 2d 879, 893 (C.D. Cal. 2004), for the proposition that relative risks greater than 2.0 permit the inference that the agent under study “was more likely than not responsible for a particular individual’s disease.”

[18]  Opinion at 18.

[19]  Opinion at 20.

[20]  Opinion at 19.

[21]  Opinion at 21, quoting from Rule 702, Advisory Committee Notes (emphasis in Judge Seeborg’s opinion).

[22]  Opinion at 21.

[23]  See “Follow the Data, Not the Discussion” (May 2, 2010).

[24]  Joiner, 522 U.S. at 145-46 (noting that the PCB studies at issue did not support expert witnesses’ conclusion that PCB exposure caused cancer because the study authors, who conducted the research, were not willing to endorse a conclusion of causation).

[25]  Huss v. Gayden, 571 F.3d 442  (5th Cir. 2009) (citing Vargas v. Lee, 317 F.3d 498, 501-01 (5th Cir. 2003) (noting that studies that did not themselves embrace causal conclusions undermined the reliability of the plaintiffs’ expert witness’s testimony that trauma caused fibromyalgia); see also McClain v. Metabolife Internat’l, Inc., 401 F.3d 1233, 1247-48 (11th Cir. 2005) (expert witnesses’ reliance upon studies that did not reach causal conclusions about ephedrine supported the challenge to the reliability of their proffered opinions); Happel v. Walmart, 602 F.3d 820, 826 (7th Cir. 2010) (observing that “is axiomatic that causation testimony is inadmissible if an expert relies upon studies or publications, the authors of which were themselves unwilling to conclude that causation had been proven”).

[26]  In re Accutane Prods. Liab. Litig., 511 F. Supp. 2d 1288, 1291 (M.D. Fla. 2007) (“When an expert relies on the studies of others, he must not exceed the limitations the authors themselves place on the study. That is, he must not draw overreaching conclusions.) (internal citations omitted).

[27]  See Rutigliano v. Valley Bus. Forms, 929 F. Supp. 779, 785 (D.N.J. 1996), aff’d, 118 F.3d 1577 (3d Cir. 1997) (“law warns against use of medical literature to draw conclusions not drawn in the literature itself …. Reliance upon medical literature for conclusions not drawn therein is not an accepted scientific methodology.”).

[28]  Opinion at 14

[29]  Opinion at 4 – 5.

Posted in Causation, Confounding, Expert Witnesses, Meta-analysis, Rule 702, Scientific Evidence | Comments Off on Judicial Gatekeeping Cures Claims That Viagra Can Cause Melonoma

Science Bench Book for Judges

July 13th, 2019

On July 1st of this year, the National Judicial College and the Justice Speakers Institute, LLC released an online publication of the Science Bench Book for Judges [Bench Book]. The Bench Book sets out to cover much of the substantive material already covered by the Federal Judicial Center’s Reference Manual:

Acknowledgments

Table of Contents

  1. Introduction: Why This Bench Book?
  2. What is Science?
  3. Scientific Evidence
  4. Introduction to Research Terminology and Concepts
  5. Pre-Trial Civil
  6. Pre-trial Criminal
  7. Trial
  8. Juvenile Court
  9. The Expert Witness
  10. Evidence-Based Sentencing
  11. Post Sentencing Supervision
  12. Civil Post Trial Proceedings
  13. Conclusion: Judges—The Gatekeepers of Scientific Evidence

Appendix 1 – Frye/Daubert—State-by-State

Appendix 2 – Sample Orders for Criminal Discovery

Appendix 3 – Biographies

The Bench Book gives some good advice in very general terms about the need to consider study validity,[1] and to approach scientific evidence with care and “healthy skepticism.”[2] When the Bench Book attempts to instruct on what it represents the scientific method of hypothesis testing, the good advice unravels:

“A scientific hypothesis simply cannot be proved. Statisticians attempt to solve this dilemma by adopting an alternate [sic] hypothesis – the null hypothesis. The null hypothesis is the opposite of the scientific hypothesis. It assumes that the scientific hypothesis is not true. The researcher conducts a statistical analysis of the study data to see if the null hypothesis can be rejected. If the null hypothesis is found to be untrue, the data support the scientific hypothesis as true.”[3]

Even in experimental settings, a statistical analysis of the data do not lead to a conclusion that the null hypothesis is untrue, as opposed to not reasonably compatible with the study’s data. In observational studies, the statistical analysis must acknowledge whether and to what extent the study has excluded bias and confounding. When the Bench Book turns to speak of statistical significance, more trouble ensues:

“The goal of an experiment, or observational study, is to achieve results that are statistically significant; that is, not occurring by chance.”[4]

In the world of result-oriented science, and scientific advocacy, it is perhaps true that scientists seek to achieve statistically significant results. Still, it seems crass to come right out and say so, as opposed to saying that the scientists are querying the data to see whether they are compatible with the null hypothesis. This first pass at statistical significance is only mildly astray compared with the Bench Book’s more serious attempts to define statistical significance and confidence intervals:

“4.10 Statistical Significance

The research field agrees that study outcomes must demonstrate they are not the result of random chance. Leaving room for an error of .05, the study must achieve a 95% level of confidence that the results were the product of the study. This is denoted as p ≤ 05. (or .01 or .1).”[5]

and

“The confidence interval is also a way to gauge the reliability of an estimate. The confidence interval predicts the parameters within which a sample value will fall. It looks at the distance from the mean a value will fall, and is measured by using standard deviations. For example, if all values fall within 2 standard deviations from the mean, about 95% of the values will be within that range.”[6]

Of course, the interval speaks to the precision of the estimate, not its reliability, but that is a small point. These definitions are virtually guaranteed to confuse judges into conflating statistical significance and the coefficient of confidence with the legal burden of proof probability.

The Bench Book runs into problems in interpreting legal decisions, which would seem softer grist for the judicial mill. The authors present dictum from the Daubert decision as though it were a holding:[7]

“As noted in Daubert, ‘[t]he focus, of course, must be solely on principles and methodology, not on the conclusions they generate’.”

The authors fail to mention that this dictum was abandoned in Joiner, and that it is specifically rejected by statute, in the 2000 revision to the Federal Rule of Evidence 702.

Early in the Bench Book, it authors present a subsection entitled “The Myth of Scientific Objectivity,” which they might have borrowed from Feyerabend or Derrida. The heading appears misleading because the text contradicts it:

“Scientists often develop emotional attachments to their work—it can be difficult to abandon an idea. Regardless of bias, the strongest intellectual argument, based on accepted scientific hypotheses, will always prevail, but the road to that conclusion may be fraught with scholarly cul-de-sacs.”[8]

In a similar vein, the authors misleadingly tell readers that “the forefront of science is rarely encountered in court,” and so “much of the science mentioned there shall be considered established….”[9] Of course, the reality is that many causal claims presented in court have already been rejected or held to be indeterminate by the scientific community. And just when readers may think themselves safe from the goblins of nihilism, the authors launch into a theory of naïve probabilism that science is just placing subjective probabilities upon data, based upon preconceived biases and beliefs:

“All of these biases and beliefs play into the process of weighing data, a critical aspect of science. Placing weight on a result is the process of assigning a probability to an outcome. Everything in the universe can be expressed in probabilities.”[10]

So help the expert witness who honestly (and correctly) testifies that the causal claim or its rejection cannot be expressed as a probability statement!

Although I have not read all of the Bench Book closely, there appears to be no meaningful discussion of Rule 703, or of the need to access underlying data to ensure that the proffered scientific opinion under scrutiny has used appropriate methodologies at every step in its development. Even a 412 text cannot address every issue, but this one does little to help the judicial reader find more in-depth help on statistical and scientific methodological issues that arise in occupational and environmental disease claims, and in pharmaceutical products litigation.

The organizations involved in this Bench Book appear to be honest brokers of remedial education for judges. The writing of this Bench Book was funded by the State Justice Institute (SJI) Which is a creation of federal legislation enacted with the laudatory goal of improving the quality of judging in state courts.[11] Despite its provenance in federal legislation, the SJI is a a private, nonprofit corporation, governed by 11 directors appointed by the President, and confirmed by the Senate. A majority of the directors (six) are state court judges, one state court administrator, and four members of the public (no more than two from any one political party). The function of the SJI is to award grants to improve judging in state courts.

The National Judicial College (NJC) originated in the early 1960s, from the efforts of the American Bar Association, American Judicature Society and the Institute of Judicial Administration, to provide education for judges. In 1977, the NJC became a Nevada not-for-profit (501)(c)(3) educational corporation, which its campus at the University of Nevada, Reno, where judges could go for training and recreational activities.

The Justice Speakers Institute appears to be a for-profit company that provides educational resources for judge. A Press Release touts the Bench Book and follow-on webinars. Caveat emptor.

The rationale for this Bench Book is open to question. Unlike the Reference Manual for Scientific Evidence, which was co-produced by the Federal Judicial Center and the National Academies of Science, the Bench Book’s authors are lawyers and judges, without any subject-matter expertise. Unlike the Reference Manual, the Bench Book’s chapters have no scientist or statistician authors, and it shows. Remarkably, the Bench Book does not appear to cite to the Reference Manual or the Manual on Complex Litigation, at any point in its discussion of the federal law of expert witnesses or of scientific or statistical method. Perhaps taxpayers would have been spared substantial expense if state judges were simply encouraged to read the Reference Manual.

[1]  Bench Book at 190.

[2]  Bench Book at 174 (“Given the large amount of statistical information contained in expert reports, as well as in the daily lives of the general society, the ability to be a competent consumer of scientific reports is challenging. Effective critical review of scientific information requires vigilance, and some healthy skepticism.”).

[3]  Bench Book at 137; see also id. at 162.

[4]  Bench Book at 148.

[5]  Bench Book at 160.

[6]  Bench Book at 152.

[7]  Bench Book at 233, quoting Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579, 595 (1993).

[8]  Bench Book at 10.

[9]  Id. at 10.

[10]  Id. at 10.

[11] See State Justice Institute Act of 1984 (42 U.S.C. ch. 113, 42 U.S.C. § 10701 et seq.).

Posted in Causation, Evidence, Expert Witness Discovery, Expert Witnesses, Frye, Reference Manual on Scientific Evidence, Rule 702, Rule 703, Scientific Evidence, statistical evidence | Comments Off on Science Bench Book for Judges

Creators of ToxicDocs Show Off Their Biases

June 7th, 2019

Columbia Magazine’s most recent issue includes a laudatory story about David Rosner, a professor of history in Columbia University.1 The “story” focuses on Rosner’s website, ToxicDocs, which has become his and Gerald Markowitz’s clearing house for what they assert are industry’s misdeeds in the realm of public health.

What the magazine’s story chooses not to discuss is the provenance of the ToxicDocs website in Rosner and Markowitz’s long collaboration with the lawsuit industry in a variety of litigation endeavors. And what you will not find on ToxicDocs are documents of the many misdeeds of the sponsoring lawsuit industry’s misdeeds, such as unlawful and unethical screenings, evidentiary frauds, specious claiming, and misleading and incompetent medical advice to its clients. Nor will you find much in the way of context for the manufacturing industry’s documents.

Media coverage of ToxicDocs from last year provides some further insight into the provenance of the website.2 According one account, Rosner and Markowitz (collectively Rosnowitz) bristled when they were attacked for their litigation work by historian Philip Scranton, a professor in Rutgers University. Scranton showed that Rosnowitz were guilty of a variety of professional sins, from “overgeneralization and failure to corroborate” to “selectively appropriat[ing] information.” Although the radical left came to Rosnowitz’s defense by labeling Scranton a “hired gun,” that charge range rather hollow when Scranton was a well-regarded historian, and Rosnowitz were long-term hired guns for the lawsuit industry.3

And so these leftist historians felt the need to defend their long-term collaboration with the lawsuit industry by putting what they believed were incriminating documents on line at their website, ToxicDocs.4 The problem, however, with Rosnowitz’s response to the Scranton critique is that their website suffers from all the undue selectivity, lack of context, and bias, which afflict their courtroom work, and which validated Scranton’s report. Most important, the reader will not find anything on ToxicDocs that challenges the misdeeds of the lawsuit industry, which has employed them for so many years.

In February 2018, the Journal of Public Health Policy (vol. 39, no. 1) published a series of editorials lauding ToxicDocs.5 Remarkably, not a single paper by Rosnowitz, and their associates, Robert Proctor, David Wegman, or Anthony Robbins mentioned their service to the lawsuit industry or the extent of their income from that service. Sheldon Whitehouse wrote an editorial, in which he disclosed his having served as Rhode Island’s Attorney General, but failed to disclose that he had worked in lockstep with the plaintiffs’ firm, Motley Rice, and that he had hired Rosnowitz, in Rhode Island’s lawsuit against major paint manufacturers. For those observers who are in a moral panic over “industry” conflicts of interest, please note the conflicts of lawsuit industrial complex.

1 Carla Cantor, “ToxicDocs Exposes Industry Misdeeds” Columbia Magazine (Summer 2019).

2 Tik Root, “In ToxicDocs.org, a Treasure Trove of Industry Secrets,” Undark (Jan. 10, 2018).

3 See, e.g., Jon Wiener, “Cancer, Chemicals and History: Companies try to discredit the experts,” The Nation (Jan. 20, 2005).

4 See “ToxicHistorians Sponsor ToxicDocs” (Feb. 1, 2018); “David Rosner’s Document Repository” (July 23, 2017).

5 Anthony Robbins & Phyllis Freeman, “ToxicDocs (www.ToxicDocs.org) goes live: A giant step toward leveling the playing field for efforts to combat toxic exposures,” 39 J. Pub. Health Policy 1 (2018); David Rosner, Gerald Markowitz, and Merlin Chowkwanyun, “ToxicDocs (www.ToxicDocs.org): from history buried in stacks of paper to open, searchable archives online,” 39 J. Pub. Health Policy 4 (2018); Stéphane Horel, “Browsing a corporation’s mind,” 39 J. Pub. Health Policy 12 (2018); Christer Hogstedt & David H. Wegman, “ToxicDocs and the fight against biased public health science worldwide,” 39 J. Pub. Health Policy 15 (2018); Joch McCulloch, “Archival sources on asbestos and silicosis in Southern Africa and Australia,” 39 J. Pub. Health Policy 18 (2018); Sheldon Whitehouse, “ToxicDocs: using the US legal system to confront industries’ systematic counterattacks against public health,” 39 J. Pub. Health Policy 22 (2018); Robert N. Proctor, “God is watching: history in the age of near-infinite digital archives,” 39 J. Pub. Health Policy 24 (2018); Elena N. Naumova, “The value of not being lost in our digital world,” 39 J. Pub. Health Policy 27 (2018); Nicholas Freudenberg, “ToxicDocs: a new resource for assessing the impact of corporate practices on health,” 39 J. Pub. Health Policy 30 (2018).

Posted in Conflicts of Interest, Expert Witnesses, Historian Testimony | Comments Off on Creators of ToxicDocs Show Off Their Biases

Specious Claiming in Multi-District Litigation

May 2nd, 2019

In a recent article in an American Bar Association newsletter, Paul Rheingold notes with some concern that, in the last two years or so, there has been a rash of dismissals of entire multi-district litigations (MDLs) based upon plaintiffs’ failure to produce expert witnesses who can survive Rule 702 gatekeeping.[1]  Paul D. Rheingold, “Multidistrict Litigation Mass Terminations for Failure to Prove Causation,” A.B.A. Mass Tort Litig. Newsletter (April 24, 2019) [cited as Rheingold]. According to Rheingold, judges historically involved in the MDL processing of products liability cases did not grant summary judgments across the board. In other words, federal judges felt that if plaintiffs’ lawyers aggregated a sufficient number of cases, then their judicial responsibility was to push settlements or to remand the cases to the transferor courts for trial.

Missing from Rheingold’s account is the prevalent judicial view, in the early going of MDL of products cases, which held that judges lacked the authority to consider Rule 702 motions for all cases in the MDL. Gatekeeping motions were considered extreme and best avoided by pushing them off to the transferor courts upon remand. In MDL 926, involving silicone gel breast implants, the late Judge Sam Pointer, who was a member of the Rules Advisory Committee, expressed the view that Rule 702 gatekeeping was a trial court function, for the trial judge who received the case on remand from the MDL.[2] Judge Pointer’s view was a commonplace in the 1990s. As mass tort litigation moved into MDL “camps,” judges more frequently adopted a managerial rather than a judicial role, and exerted great pressure on the parties, and the defense in particular, to settle cases. These judges frequently expressed their view that the two sides so stridently disagreed on causation that the truth must be somewhere in between, and even with “a little causation,” the defendants should offer a little compensation. These litigation managers thus eschewed dispositive motion practice, or gave it short shrift.

Rheingold cites five recent MDL terminations based upon “Daubert failure,” and he acknowledges other MDLs collapsed because of federal pre-emption issues (Eliquis, Incretins, and possibly Fosamax), and that other fatally weak causal MDL claims settled for nominal compensation (NuvaRing). He omits other MDLs, such as In re Silica, in which an entire MDL collapsed because of prevalent fraud in the screening and diagnosing of silicosis claimants by plaintiffs’ counsel and their expert witnesses.[3] Also absent from his reckoning is the collapse of MDL cases against Celebrex[4] and Viagra[5].

Rheingold does concede that the recent across-the-board dismissals of MDLs were due to very weak causal claims.[6] He softens his judgment by suggesting that the weaknesses were apparent “at least in retrospect,” but the weaknesses were clearly discernible before litigation by the refusal of regulatory agencies, such as the FDA, to accept the litigation-driven causal claims. Rheingold also tries to assuage fellow plaintiffs’ counsel by suggesting that plaintiffs’ lawyers somehow fell prey to the pressure to file cases because of internet advertising and the encouragement of records collection and analysis firms. This attribution of naiveté to Plaintiffs’ Steering Committee (PSC) members does not ring true given the wealth and resources of lawyers on PSCs. Furthermore, the suggestion that PSC member may be newcomers to the MDL playing fields does not hold water given that most of the lawyers involved are “repeat players,” with substantial experience and financial incentives to sort out invalid expert witness opinions.[7]

Rheingold offers the wise counsel that plaintiffs’ lawyers “should take [their] time and investigate for [themselves] the potential proof available for causation and adequacy of labeling.” If history is any guide, his advice will not be followed.

[1] Rheingold cites five MDLs that were “Daubert failures” in the recent times: (1) In re Lipitor (Atorvastatin Calcium) Marketing, Sales Practices & Prods. Liab.  Litig. (MDL 2502), 892 F.3d 624 (4th Cir. 2018) (affirming Rule 702 dismissal of claims that atorvastatin use caused diabetes); (2) In re Mirena IUD Products Liab. Litig. (Mirena II, MDL 2767), 713 F. App’x 11 (2d Cir. 2017) (excluding expert witnesses’ opinion testimony that the intrauterine device caused embedment and perforation); (3) In re Mirena Ius Levonorgestrel-Related Prods. Liab. Litig., (Mirena II), 341 F. Supp. 3d 213 (S.D.N.Y. 2018) (affirming Rule 702 dismissal of claims that product caused pseudotumor cerebri); (4) In re Zoloft (Sertraline Hydrochloride) Prods. Liab. Litig., 858 F.3d 787 (3d Cir. 2017) (affirming MDL trial court’s Rule 702 exclusions of opinions that Zoloft is teratogenic); (5) Jones v. SmithKline Beecham, 652 F. App’x 848 (11th Cir. 2016) (affirming MDL court’s Rule 702 exclusions of expert witness opinions that denture adhesive creams caused metal deficiencies).

[2]  Not only was Judge Pointer a member of the Rules committee, he was the principal author of the 1993 Amendments to the Federal Rules of Civil Procedure, as well as the editor-in-chief of the Federal Judicial Center’s Manual for Complex. At an ALI-ABA conference in 1997, Judge Pointer complained about the burden of gatekeeping. 3 Federal Discovery News 1 (Aug. 1997). He further opined that, under Rule 104(a), he could “look to decisions from the Southern District of New York and Eastern District of New York, where the same expert’s opinion has been offered and ruled upon by those judges. Their rulings are hearsay, but hearsay is acceptable. So I may use their rulings as a basis for my decision on whether to allow it or not.” Id. at 4. Even after Judge Jack Weinstein excluded plaintiffs’ expert witnesses’ causal opinions in the silicone litigation, however, Judge Pointer avoided having to make an MDL-wide decision with the scope of one of the leading judges from the Southern and Eastern Districts of New York. See In re Breast Implant Cases, 942 F. Supp. 958 (E. & S.D.N.Y. 1996). Judge Pointer repeated his anti-Daubert views three years later at a symposium on expert witness opinion testimony. See Sam C. Pointer, Jr., “Response to Edward J. Imwinkelried, the Taxonomy of Testimony Post-Kumho: Refocusing on the Bottom Lines of Reliability and Necessity,” 30 Cumberland L. Rev. 235 (2000).

[3]  In re Silica Products Liab. Litig., MDL No. 1553, 398 F. Supp. 2d 563 (S.D. Tex. 2005).

[4]  In re Bextra & Celebrex Marketing Sales Practices & Prod. Liab. Litig., 524 F. Supp. 2d 1166 (N.D. Calif. 2007) (excluding virtually all relevant expert witness testimony proffered to support claims that ordinary dosages of these COX-2 inhibitors caused cardiovascular events).

[5]  In re Viagra Products Liab. Litig., 572 F. Supp. 2d 1071 (D. Minn. 2008) (addressing claims that sildenafil causes vision loss from non-arteritic anterior ischemic optic neuropathy (NAION)).

[6]  Rheingold (“Examining these five mass terminations, at least in retrospect[,] it is apparent that they were very weak on causation.”)

[7] See Elizabeth Chamblee Burch & Margaret S. Williams, “Repeat Players in Multidistrict Litigation: The Social Network,” 102 Cornell L. Rev. 1445 (2017); Margaret S. Williams, Emery G. Lee III & Catherine R. Borden, “Repeat Players in Federal Multidistrict Litigation,” 5 J. Tort L. 141, 149–60 (2014).

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Specious Claiming in Multi-District Litigation

Expert Witnesses Who Don’t Mean What They Say

March 24th, 2019

’Then you should say what you mean’, the March Hare went on.
‘I do’, Alice hastily replied; ‘at least–at least I mean what I say–that’s the same thing, you know’.
‘Not the same thing a bit!’ said the Hatter. ‘You might just as well say that “I see what I eat” is the same thing as “I eat what I see!”’

Lewis Carroll, Alice’s Adventures in Wonderland, Chapter VII (1865)

Anick Bérard is an epidemiologist at the Université de Montréal. Most of her publications involve birth outcomes and maternal medication use, but Dr. Bérard’s advocacy also involves social media (Facebook, YouTube) and expert witnessing in litigation against the pharmaceutical industry.

When the FDA issued its alert about cardiac malformations in children born to women who took Paxil (paroxetine) in their first trimesters of pregnancy, the agency characterized its assessment of the “early results of new studies for Paxil” as “suggesting that the drug increases the risk for birth defects, particularly heart defects, when women take it during the first three months of pregnancy.”1 The agency also disclaimed any conclusion of “class effect” among the other selective serotonin reuptake inhibitors (SSRIs), such as Zoloft (sertraline), Celexa (citalopram), and Prozac (fluoxetine). Indeed, the FDA requested the manufacturer of paroxetine to undertake additional research to look at teratogenicity of paroxetine, as well as the possibility of class effects. That research never showed an SSRI teratogenicity class effect.

A “suggestion” from the FDA of an adverse effect is sufficient to launch a thousand litigation complaints, which were duly filed against GlaxoSmithKline. The plaintiffs’ counsel recruited Dr. Bérard to serve as an expert witness in support of a wide array of birth defects in Paxil cases. In her hands, the agency’s “suggestion” of causation became a conclusion. The defense challenged Bérard’s opinions, but the federal court motion to exclude her causal opinions were taken under advisement, without decision. Hayes v. SmithKline Beecham Corp., 2009 WL 4912178 (N.D. Okla. Dec. 14, 2009). One case in state court went to trial, with a verdict for plaintiffs.

Despite Dr. Bérard;s zealous advocacy for a causal association between Paxil and birth defects, she declined to assert any association between maternal use of the other, non-paroxetine SSRIs and birth defects. Here is an excerpt from her Rule 26 report in a paroxetine case:

“Taken together, the available scientific evidence makes it clear that Paxil use during the first trimester of pregnancy is an independent risk factor that at least doubles the risk of cardiovascular malformations in newborns at all commonly used doses. This risk has been consistent and was further reinforced by repeated observational study findings as well as meta-analyses results. No such associations were found with other types of SSRI exposures during gestation.”2

In her sworn testimony, Dr. Bérard made clear that she really meant what she had written in her report, about exculpating the non-paroxetine SSRIs of any association with birth defects:

“Q. Is it fair to say that you will not be offering an opinion that SSRIs as a class, or individual SSRIs other than Paxil increased the risk of cardiovascular malformations in newborns?

A. This is not what I was asked to do.

Q. But in fact you actually write in your report that you don’t believe there’s sufficient data to reach any conclusion about other SSRIs, true?

A. Correct.”3

In 2010, Dr. Bérard, along with two professional colleagues, published what they called a systematic review of antidepressant use in pregnancy and birth outcomes.4 In this review, Bérard specifically advised that paroxetine should be avoided by women of childbearing age, but she and her colleagaues affirmatively encouraged use of other SSRIs, such as fluoxetine, sertraline, and citalopram:

“Clinical Approach: A Brief Overview

“For women planning a pregnancy or when a treatment initiation during pregnancy is deemed necessary, the decision should rely not only on drug safety data but also on other factors such as the patient’s condition, previous response to other antidepressants, comorbidities, expected adverse effects and potential interactions with other current pharmacological treatments. Since there is a more extensive clinical experience with SSRIs such as fluoxetine, sertraline, and citalopram, these agents should be used as first-line therapies. Whenever possible, one should refrain from prescribing paroxetine to women of childbearing potential or planning a pregnancy. However, antenatal screening such as fetal echocardiography should be considered in a woman exposed prior to finding out about her pregnancy.”5

When Bérard wrote and published her systematic review, she was still actively involved as an expert witness for plaintiffs in lawsuits against the manufacturers of paroxetine. In her 2010 review, Dr. Bérard gave no acknowledgment of monies earned in her capacity as an expert witness, and her disclosure of potential conflicts of interest was limited to noting that she was “a consultant for a plaintiff in the litigation involving Paxil.”6 In fact, Bérard had submitted multiple reports, testified at deposition, and had been listed as a testifying expert witness in many cases involving Paxil or paroxetine.

Not long after the 2010 review article, Glaxo settled most of the pending paroxetine birth defect cases, and the plaintiffs’ bar pivoted to recast their expert witnesses’ opinions as causal teratogenic conclusions about the entire class of SSRIs. In 2012, the federal courts established a “multi-district litigation,” MDL 2342, for birth defect cases involving Zoloft (sertraline), in the Philadelphia courtroom of Judge Cynthia Rufe, in the Eastern District of Pennsylvania.

Notwithstanding her 2010 clinical advice that pregnant women with depression should use fluoxetine, sertraline, or citalopram, Dr. Bérard became actively involved in the new litigation against the other, non-Paxil SSRI manufacturers. By 2013, Dr. Bérard was on record as a party expert witness for plaintiffs, opining that setraline causes virtually every major congenital malformation.7

In the same year, 2013, Dr. Bérard published another review article on teratogens, but now she gave a more equivocal view of the other SSRIs, claiming that they were “known carcinogens,” but acknowledging in a footnote that teratogenicity of the SSRIs was “controversial.”8 Incredibly, this review article states that “Anick Bérard and Sonia Chaabane have no potential conflicts of interest to disclose.”9

Ultimately, Dr. Bérard could not straddle her own contradictory statements and remain upright, which encouraged the MDL court to examine her opinions closely for methodological shortcomings and failures. Although Bérard had evolved to claim a teratogenic “class effect” for all the SSRIs, the scientific support for her claim was somewhere between weak to absent.10 Perhaps even more distressing, many of the pending claims involving the other SSRIs arose from pregnancies and births that predated Bérard’s epiphany about class effect. Finding ample evidence of specious claiming, the federal court charged with oversight of the sertraline birth defect claims excluded Dr. Bérard’s causal opinions for failing to meet the requirements of Federal Rule of Evidence 702.11

Plaintiffs sought to substitute Nicholas Jewell for Dr. Bérard, but Dr. Jewell fared no better, and was excluded for other methodological shenanigans.12 Ultimately, a unanimous panel of the United States Court of Appeals, for the Third Circuit, upheld the expert witness exclusions.13

1 See “FDA Advising of Risk of Birth Defects with Paxil; Agency Requiring Updated Product Labeling,” P05-97 (Dec. 8, 2005) (emphasis added).

2 Bérard Report in Hayes v. SmithKline Beecham Corp, 2009 WL 3072955, at *4 (N.D. Okla. Feb. 4, 2009) (emphasis added).

3 Deposition Testimony of Anick Bérard, in Hayes v. SmithKline Beecham Corp., at 120:16-25 (N.D. Okla. April 2009).

4 Marieve Simoncelli, Brigitte-Zoe Martin & Anick Bérard, “Antidepressant Use During Pregnancy: A Critical Systematic Review of the Literature,” 5 Current Drug Safety 153 (2010).

5 Id. at 168b.

6 Id. at 169 (emphasis added).

7 See Anick Bérard, “Expert Report” (June 19, 2013).

8 Sonia Chaabanen & Anick Bérard, “Epidemiology of Major Congenital Malformations with Specific Focus on Teratogens,” 8 Current Drug Safety 128, 136 (2013).

9 Id. at 137b.

10 See, e.g., Nicholas Myles, Hannah Newall, Harvey Ward, and Matthew Large, “Systematic meta-analysis of individual selective serotonin reuptake inhibitor medications and congenital malformations,” 47 Australian & New Zealand J. Psychiatry 1002 (2013).

11 See In re Zoloft (Sertraline Hydrochloride) Prods. Liab. Litig., MDL No. 2342; 26 F.Supp. 3d 449 (E.D.Pa. 2014) (Rufe, J.). Plaintiffs, through their Plaintiffs’ Steering Committee, moved for reconsideration, but Judge Rufe reaffirmed her exclusion of Dr. Bérard. In re Zoloft (Sertraline Hydrochloride) Prods. Liab. Litig., MDL No. 2342; 12-md-2342, 2015 WL 314149 (E.D. Pa. Jan. 23, 2015) (Rufe, J.) (denying PSC’s motion for reconsideration). See “Zoloft MDL Relieves Matrixx Depression” (Jan. 30, 2015).

12 See In re Zoloft Prods. Liab. Litig., No. 12–md–2342, 2015 WL 7776911 (E.D. Pa. Dec. 2, 2015) (excluding Jewell’s opinions as scientifically unwarranted and methodologically flawed); In re Zoloft Prod. Liab. Litig., MDL NO. 2342, 12-MD-2342, 2016 WL 1320799 (E.D. Pa. April 5, 2016) (granting summary judgment after excluding Dr. Jewell). See also “The Education of Judge Rufe – The Zoloft MDL” (April 9, 2016).

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The Joiner Finale

March 23rd, 2019

“This is the end
Beautiful friend

This is the end
My only friend, the end”

Jim Morrison, “The End” (c. 1966)

The General Electric Co. v. Joiner, 522 U.S. 136 (1997), case was based upon polychlorinated biphenyl exposures (PCB), only in part. The PCB part did not hold up well legally in the Supreme Court; nor was the PCB lung cancer claim vindicated by later scientific evidence. See “How Have Important Rule 702 Holdings Held Up With Time?” (Mar. 20, 2015).

The Supreme Court in Joiner reversed and remanded the case to the 11th Circuit, which then remanded the case back to the district court to address claims that Mr. Joiner had been exposed to furans and dioxins, and that these other chemicals had caused, or contributed to, his lung cancer, as well. Joiner v. General Electric Co., 134 F.3d 1457 (11th Cir. 1998) (per curiam). Thus the dioxins were left in the case even after the Supreme Court ruled.

After the Supreme Court’s decision, Anthony Roisman argued that the Court had addressed an artificial question when asked about PCBs alone because the case was really about an alleged mixture of exposures, and he held out hope that the Joiners would do better on remand. Anthony Z. Roisman, “The Implications of G.E. v. Joiner for Admissibility of Expert Testimony,” 1 Res Communes 65 (1999).

Many Daubert observers (including me) are unaware of the legal fate of the Joiners’ claims on remand. In the only reference I could find, the commentator simply noted that the case resolved before trial.[1] I am indebted to Michael Risinger, and Joseph Cecil, for pointing me to documents from PACER, which shed some light upon the Joiner “endgame.”

In February 1998, Judge Orinda Evans, who had been the original trial judge, and who had sustained defendants’ Rule 702 challenges and granted their motions for summary judgments, received and reopened the case upon remand from the 11th Circuit. In March, Judge Evans directed the parties to submit a new pre-trial order by April 17, 1998. At a status conference in April 1998, Judge Evans permitted the plaintiffs additional discovery, to be completed by June 17, 1998. Five days before the expiration of their additional discovery period, the plaintiffs moved for additional time; defendants opposed the request. In July, Judge Evans granted the requested extension, and gave defendants until November 1, 1998, to file for summary judgment.

Meanwhile, in June 1998, new counsel entered their appearances for plaintiffs – William Sims Stone, Kevin R. Dean, Thomas Craig Earnest, and Stanley L. Merritt. The docket does not reflect much of anything about the new discovery other than a request for a protective order for an unpublished study. But by October 6, 1998, the new counsel, Earnest, Dean, and Stone (but not Merritt) withdrew as attorneys for the Joiners, and by the end of October 1998, Judge Evans entered an order to dismiss the case, without prejudice.

A few months later, in February 1999, the parties filed a stipulation, approved by the Clerk, dismissing the action with prejudice, and with each party to bear its own coasts. Given the flight of plaintiffs’ counsel, the dismissals without and then with prejudice, a settlement seems never to have been involved in the resolution of the Joiner case. In the end, the Joiners’ case fizzled perhaps to avoid being Frye’d.

And what has happened since to the science of dioxins and lung cancer?

Not much.

In 2006, the National Research Council published a monograph on dioxin, which took the controversial approach of focusing on all cancer mortality rather than specific cancers that had been suggested as likely outcomes of interest. See David L. Eaton (Chairperson), Health Risks from Dioxin and Related Compounds – Evaluation of the EPA Reassessment (2006). The validity of this approach, and the committee’s conclusions, were challenged vigorously in subsequent publications. Paolo Boffetta, Kenneth A. Mundt, Hans-Olov Adami, Philip Cole, and Jack S. Mandel, “TCDD and cancer: A critical review of epidemiologic studies,” 41 Critical Rev. Toxicol. 622 (2011) (“In conclusion, recent epidemiological evidence falls far short of conclusively demonstrating a causal link between TCDD exposure and cancer risk in humans.”

In 2013, the Industrial Injuries Advisory Council (IIAC), an independent scientific advisory body in the United Kingdom, published a review of lung cancer and dioxin. The Council found the epidemiologic studies mixed, and declined to endorse the compensability of lung cancer for dioxin-exposed industrial workers. Industrial Injuries Advisory Council – Information Note on Lung cancer and Dioxin (December 2013). See also Mann v. CSX Transp., Inc., 2009 WL 3766056, 2009 U.S. Dist. LEXIS 106433 (N.D. Ohio 2009) (Polster, J.) (dioxin exposure case) (“Plaintiffs’ medical expert, Dr. James Kornberg, has opined that numerous organizations have classified dioxins as a known human carcinogen. However, it is not appropriate for one set of experts to bring the conclusions of another set of experts into the courtroom and then testify merely that they ‘agree’ with that conclusion.”), citing Thorndike v. DaimlerChrysler Corp., 266 F. Supp. 2d 172 (D. Me. 2003) (court excluded expert who was “parroting” other experts’ conclusions).

Last year, an industrial cohort, followed for two decades found no increased risk of lung cancer among workers exposed to dioxin. David I. McBride, James J. Collins, Thomas John Bender, Kenneth M Bodner, and Lesa L. Aylward, “Cohort study of workers at a New Zealand agrochemical plant to assess the effect of dioxin exposure on mortality,” 8 Brit. Med. J. Open e019243 (2018) (reporting SMR for lung cancer 0.95, 95%CI: 0.56 to 1.53)

[1] Morris S. Zedeck, Expert Witness in the Legal System: A Scientist’s Search for Justice 49 (2010) (noting that, after remand from the Supreme Court, Joiner v. General Electric resolved before trial)

 

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Daubert Retrospective – Statistical Significance

January 5th, 2019

The holiday break was an opportunity and an excuse to revisit the briefs filed in the Supreme Court by parties and amici, in the Daubert case. The 22 amicus briefs in particular provided a wonderful basis upon which to reflect how far we have come, and also how far we have to go, to achieve real evidence-based fact finding in technical and scientific litigation. Twenty-five years ago, Rules 702 and 703 vied for control over errant and improvident expert witness testimony. With Daubert decided, Rule 702 emerged as the winner. Sadly, most courts seem to ignore or forget about Rule 703, perhaps because of its awkward wording. Rule 702, however, received the judicial imprimatur to support the policing and gatekeeping of dysepistemic claims in the federal courts.

As noted last week,1 the petitioners (plaintiffs) in Daubert advanced several lines of fallacious and specious argument, some of which was lost in the shuffle and page limitations of the Supreme Court briefings. The plaintiffs’ transposition fallacy received barely a mention, although it did bring forth at least a footnote in an important and overlooked amicus brief filed by American Medical Association (AMA), the American College of Physicians, and over a dozen other medical specialty organizations,2 all of which both emphasized the importance of statistical significance in interpreting epidemiologic studies, and the fallacy of interpreting 95% confidence intervals as providing a measure of certainty about the estimated association as a parameter. The language of these associations’ amicus brief is noteworthy and still relevant to today’s controversies.

The AMA’s amicus brief, like the brief filed by the National Academies of Science and the American Association for the Advancement of Science, strongly endorsed a gatekeeping role for trial courts to exclude testimony not based upon rigorous scientific analysis:

“The touchstone of Rule 702 is scientific knowledge. Under this Rule, expert scientific testimony must adhere to the recognized standards of good scientific methodology including rigorous analysis, accurate and statistically significant measurement, and reproducibility.”3

Having incorporated the term “scientific knowledge,” Rule 702 could not permit anything less in expert witness testimony, lest it pollute federal courtrooms across the land.

Elsewhere, the AMA elaborated upon its reference to “statistically significant measurement”:

“Medical researchers acquire scientific knowledge through laboratory investigation, studies of animal models, human trials, and epidemiological studies. Such empirical investigations frequently demonstrate some correlation between the intervention studied and the hypothesized result. However, the demonstration of a correlation does not prove the hypothesized result and does not constitute scientific knowledge. In order to determine whether the observed correlation is indicative of a causal relationship, scientists necessarily rely on the concept of “statistical significance.” The requirement of statistical reliability, which tends to prove that the relationship is not merely the product of chance, is a fundamental and indispensable component of valid scientific methodology.”4

And then again, the AMA spelled out its position, in case the Court missed its other references to the importance of statistical significance:

“Medical studies, whether clinical trials or epidemiologic studies, frequently demonstrate some correlation between the action studied … . To determine whether the observed correlation is not due to chance, medical scientists rely on the concept of ‘statistical significance’. A ‘statistically significant’ correlation is generally considered to be one in which statistical analysis suggests that the observed relationship is not the result of chance. A statistically significant correlation does not ‘prove’ causation, but in the absence of such a correlation, scientific causation clearly is not proven.9”5

In its footnote 9, in the above quoted section of the brief, the AMA called out the plaintiffs’ transposition fallacy, without specifically citing to plaintiffs’ briefs:

“It is misleading to compare the 95% confidence level used in empirical research to the 51% level inherent in the preponderance of the evidence standard.”6

Actually the plaintiffs’ ruse was much worse than misleading. The plaintiffs did not compare the two probabilities; they equated them. Some might call this ruse, an outright fraud on the court. In any event, the AMA amicus brief remains an available, citable source for opposing this fraud and the casual dismissal of the importance of statistical significance.

One other amicus brief touched on the plaintiffs’ statistical shanigans. The Product Liability Advisory Council, National Association of Manufacturers, Business Roundtable, and Chemical Manufacturers Association jointly filed an amicus brief to challenge some of the excesses of the plaintiffs’ submissions.7  Plaintiffs’ expert witness, Shanna Swan, had calculated type II error rates and post-hoc power for some selected epidemiologic studies relied upon by the defense. Swan’s complaint had been that some studies had only 20% probability (power) to detect a statistically significant doubling of limb reduction risk, with significance at p < 5%.8

The PLAC Brief pointed out that power calculations must assume an alternative hypothesis, and that the doubling of risk hypothesis had no basis in the evidentiary record. Although the PLAC complaint was correct, it missed the plaintiffs’ point that the defense had set exceeding a risk ratio of 2.0, as an important benchmark for specific causation attributability. Swan’s calculation of post-hoc power would have yielded an even lower probability for detecting risk ratios of 1.2 or so. More to the point, PLAC noted that other studies had much greater power, and that collectively, all the available studies would have had much greater power to have at least one study achieve statistical significance without dodgy re-analyses.

1 “The Advocates’ Errors in Daubert” (Dec. 28, 2018).

2 American Academy of Allergy and Immunology, American Academy of Dermatology, American Academy of Family Physicians, American Academy of Neurology, American Academy of Orthopaedic Surgeons, American Academy of Pain Medicine, American Association of Neurological Surgeons, American College of Obstetricians and Gynecologists, American College of Pain Medicine, American College of Physicians, American College of Radiology, American Society of Anesthesiologists, American Society of Plastic and Reconstructive Surgeons, American Urological Association, and College of American Pathologists.

3 Brief of the American Medical Association, et al., as Amici Curiae, in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006285, at *27 (U.S., Jan. 19, 1993)[AMA Brief].

4 AMA Brief at *4-*5 (emphasis added).

5 AMA Brief at *14-*15 (emphasis added).

6 AMA Brief at *15 & n.9.

7 Brief of the Product Liability Advisory Council, Inc., National Association of Manufacturers, Business Roundtable, and Chemical Manufacturers Association as Amici Curiae in Support of Respondent, as Amici Curiae, in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006288 (U.S., Jan. 19, 1993) [PLAC Brief].

8 PLAC Brief at *21.

Posted in Evidence, Expert Witnesses, Rule 702, Rule 703, statistical evidence, Statistical Power | Comments Off on Daubert Retrospective – Statistical Significance

The Advocates’ Errors in Daubert

December 28th, 2018

Over 25 years ago, the United States Supreme Court answered a narrow legal question about whether the so-called Frye rule was incorporated into Rule 702 of the Federal Rules of Evidence. Plaintiffs in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), appealed a Ninth Circuit ruling that the Frye rule survived, and was incorporated into, the enactment of a statutory evidentiary rule, Rule 702. As most legal observers can now discern, plaintiffs won the battle and lost the war. The Court held that the plain language of Rule 702 does not memorialize Frye; rather the rule requires an epistemic warrant for the opinion testimony of expert witnesses.

Many of the sub-issues of the Daubert case are now so much water over the dam. The case involved claims of birth defects from maternal use of an anti-nausea medication, Bendectin. Litigation over Bendectin is long over, and the medication is now approved for use in pregnant women, on the basis of a full new drug application, supported by clinical trial evidence.

In revisiting Daubert, therefore, we might imagine that legal scholars and scientists would be interested in the anatomy of the errors that led Bendectin plaintiffs stridently to maintain their causal claims. The oral argument before the Supreme Court is telling with respect to some of the sources of error. Two law professors, Michael H. Gottesman, for plaintiffs, and Charles Fried, for the defense, squared off one Tuesday morning in March 1993. A review of Gottesman’s argument reveals several fallacious lines of argument, which are still relevant today:

A. Regulation is Based Upon Scientific Determinations of Causation

In his oral argument, Gottesman asserted that regulators (as opposed to the scientific community) are in charge of determining causation,1 and environmental regulations are based upon scientific causation determinations.2 By the time that the Supreme Court heard argument in the Daubert case, this conflation of scientific and regulatory standards for causal conclusions was fairly well debunked.3 Gottesman’s attempt to mislead the Court failed, but the effort continues in courtrooms around the United States.

B. Similar Chemical Structures Have the Same Toxicities

Gottesman asserted that human teratogenicity can be determined from similarity in chemical structures with other established teratogens.4 Close may count in horseshoes, but in chemical structural activities, small differences in chemical structures can result in huge differences in toxicologic or pharmacologic properties. A silly little methyl group on a complicated hydrocarbon ring structure can make a world of difference, as in the difference between estrogen and testosterone.

C. All Animals React the Same to Any Given Substance

Gottesman, in his oral argument, maintained that human teratogenicity can be determined from teratogenicity in non-human, non-primate, murine species.5 The Court wasted little time on this claim, the credibility of which has continued to decline in the last 25 years.

D. The Transposition Fallacy

Perhaps of greatest interest to me was Gottesman’s claim that the probability of the claimed causal association can be determined from the p-value or from the coefficient of confidence taken from the observational epidemiologic studies of birth defects among children of women who ingested Bendectin in pregancy; a.k.a. the transposition fallacy.6

All these errors are still in play in American courtrooms, despite efforts of scientists and scientific organizations to disabuse judges and lawyers. The transposition fallacy, which has been addressed in these pages and elsewhere at great length seems especially resilient to educational efforts. Still, the fallacy was as well recognized at the time of the Daubert argument as it is today, and it is noteworthy that the law professor who argued the plaintiffs’ case, in the highest court of the land, advanced this fallacious argument, and that the scientific and statistical community did little to nothing to correct the error.7

Although Professor Gottesman’s meaning in the oral argument is not entirely clear, on multiple occasions, he appeared to have conflated the coefficient of confidence, from confidence intervals, with the posterior probability that attaches to the alternative hypothesis of some association:

“What the lower courts have said was yes, but prove to us to a degree of statistical certainty which would give us 95 percent confidence that the human epidemiological data is reflective, that these higher numbers for the mothers who used Bendectin were not the product of random chance but in fact are demonstrating the linkage between this drug and the symptoms observed.”8

* * * * *

“… what was demonstrated by Shanna Swan was that if you used a degree of confidence lower than 95 percent but still sufficient to prove the point as likelier than not, the epidemiological evidence is positive… .”9

* * * * *

“The question is, how confident can we be that that is in fact probative of causation, not at a 95 percent level, but what Drs. Swan and Glassman said was applying the Rothman technique, a published technique and doing the arithmetic, that you find that this does link causation likelier than not.”10

Professor Fried’s oral argument for the defense largely refused or failed to engage with plaintiffs’ argument on statistical inference. With respect to the “Rothman” approach, Fried pointed out that plaintiffs’ statistical expert witness, Shanna swan, never actually employed “the Rothman principle.”11

With respect to plaintiffs’ claim that individual studies had low power to detect risk ratios of two, Professor Fried missed the opportunity to point out that such post-hoc power calculations, whatever validity they might possess, embrace the concept of statistical significance at the customary 5% level. Fried did note that a meta-analysis, based upon all the epidemiologic studies, rendered plaintiffs’ power complaint irrelevant.12

Some readers may believe that judging advocates speaking extemporaneously about statistical concepts might be overly harsh. How well then did the lawyers explain and represent statistical concepts in their written briefs in the Daubert case?

Petitioners’ Briefs

Petitioners’ Opening Brief

The petitioners’ briefs reveal that Gottesman’s statements at oral argument represent a consistent misunderstanding of statistical concepts. The plaintiffs consistently conflated significance probability or the coefficient of confidence with the civil burden of proof probability:

“The crux of the disagreement between Merrell’s experts and those whose testimony is put forward by plaintiffs is that the latter are prepared to find causation more probable than not when the epidemiological evidence is strongly positive (albeit not at a 95% confidence level) and when it is buttressed with animal and chemical evidence predictive of causation, while the former are unwilling to find causation in the absence of an epidemiological study that satisfies the 95% confidence level.”13

After giving a reasonable fascimile of a definition of statistical significance, the plaintiffs’ brief proceeds to confuse the complement of alpha, or the coefficient of confidence (typically 95%), with probability that the observed risk ratio in a sample is the actual population parameter of risk:

“But in toxic tort lawsuits, the issue is not whether it is certain that a chemical caused a result, but rather whether it is likelier than not that it did. It is not self-evident that the latter conclusion would require eliminating the null hypothesis (i.e. non-causation) to a confidence level of 95%.30” 14

The plaintiffs’ brief cited heavily to Rothman’s textbook, Modern Epidemiology, with the specious claim that the textbook supported the plaintiffs’ use of the coefficient of confidence to derive a posterior probability (> 50%) of the correctness of an elevated risk ratio for birth defects in children born to mothers who had taken Bendectin in their first trimesters of pregnancy:

“An alternative mechanism has been developed by epidemiologists in recent years to give a somewhat more informative picture of what the statistics mean. At any given confidence level (e.g. 95%) a confidence interval can be constructed. The confidence interval identifies the range of relative risks that collectively comprise the 95% universe. Additional confidence levels are then constructed exhibiting the range at other confidence levels, e.g., at 90%, 80%, etc. From this set of nested confidence intervals the epidemiologist can make assessments of how likely it is that the statistics are showing a true association. Rothman, Tab 9, pp. 122-25. By calculating nested confidence intervals for the data in the Bendectin studies, Dr. Swan was able to determine that it is far more likely than not that a true association exists between Bendectin and human limb reduction birth defects. Swan, Tab 12, at 3618-28.”15

The heavy reliance upon Rothman’s textbook at first blush appears confusing. Modern Epidemiology makes one limited mention of nested confidence intervals, and certainly never suggests that such intervals can provide a posterior probability of the correctness of the hypothesis. Rothman’s complaints about reliance upon “statistical significance,” however, are well-known, and Rothman himself submitted an amicus brief16 in Daubert, a brief that has its own problems.17

In direct response to the Rothman Brief,18 Professor Alvin Feinstein filed an amicus brief in Daubert, wherein he acknowledged that meta-analyses and re-analyses can be valid, but these techniques are subject to many sources of invalidity, and their employment by careful practitioners in some instances should not be a blank check to professional witnesses who are supported by plaintiffs’ counsel. Similarly, Feinstein acknowledged that standards of statistical significance:

“should be appropriately flexible, but they must exist if science is to preserve its tradition of intellectual discipline and high quality research.”19

Petitioners’ Reply Brief

The plaintiffs’ statistical misunderstandings are further exemplified in their Reply Brief, where they reassert the transposition fallacy and alternatively state that associations with p-values greater than 5%, or 95% confidence intervals that include the risk ratio of 1.0, do not show the absence of an association.20 The latter point was, of course irrelevant in the Daubert case, in which plaintiffs had the burden of persuasion. As in their oral argument through Professor Gottesman, the plaintiffs’ appellate briefs misunderstand the crucial point that confidence intervals are conditioned upon the data observed from a particular sample, and do not provide posterior probabilities for the correctness of a claimed hypothesis.

Defense Brief

The defense brief spent little time on the statistical issue or plaintiffs’ misstatements, but dispatched the issue in a trenchant footnote:

“Petitioners stress the controversy some epidemiologists have raised about the standard use by epidemiologists of a 95% confidence level as a condition of statistical significance. Pet. Br. 8-10. See also Rothman Amicus Br. It is hard to see what point petitioners’ discussion establishes that could help their case. Petitioners’ experts have never developed and defended a detailed analysis of the epidemiological data using some alternative well-articulated methodology. Nor, indeed, do they show (or could they) that with some other plausible measure of confidence (say, 90%) the many published studies would collectively support an inference that Bendectin caused petitioners’ limb reduction defects. At the very most, all that petitioners’ theoretical speculations do is question whether these studies – as the medical profession and regulatory authorities in many countries have concluded – affirmatively prove that Bendectin is not a teratogen.”21

The defense never responded to the specious argument, stated or implied within the plaintiffs’ briefs, and in Gottesman’s oral argument, that a coefficient of confidence of 51% would have generated confidence intervals that routinely excluded the null hypothesis of risk ratio of 1.0. The defense did, however, respond to plaintiffs’ power argument by adverting to a meta-analysis that failed to find a statistically significant association.22

The defense also advanced two important arguments to which the plaintiffs’ briefs never meaningfully responded. First, the defense detailed the “cherry picking” or selective reliance engaged in by plaintiffs’ expert witnesses.23 Second, the defense noted that plaintiffs’ had a specific causation problem in that their expert witnesses had been attempting to infer specific causation based upon relative risks well below 2.0.24

To some extent, the plaintiffs’ statistical misstatements were taken up by an amicus brief submitted by the United States government, speaking through the office of the Solicitor General.25 Drawing upon the Supreme Court’s decisions in race discrimination cases,26 the government asserted that epidemiologists “must determine” whether a finding of an elevated risk ratio “could have arisen due to chance alone.”27

Unfortunately, the government’s brief butchered the meaning of confidence intervals. Rather than describe the confidence interval as showing what point estimates of risk ratios are reasonable compatible with the sample result, the government stated that confidence intervals show “how close the real population percentage is likely to be to the figure observed in the sample”:

“since there is a 95 percent chance that the ‘true’ value lies within two standard deviations of the sample figure, that particular ‘confidence interval’ (i.e., two standard deviations) is therefore said to have a ‘confidence level’ of about 95 percent.” 28

The Solicitor General’s office seemed to have had some awareness that it was giving offense with the above definition because it quickly added:

“While it is customary (and, in many cases, easier) to speak of ‘a 95 percent chance’ that the actual population percentage is within two standard deviations of the figure obtained from the sample, ‘the chances are in the sampling procedure, not in the parameter’.”29

Easier perhaps but clearly erroneous to speak that way, and customary only among the unwashed. The government half apologized for misleading the Court when it followed up with a better definition from David Freedman’s textbook, but sadly the government lawyers were not content to let the matter sit there. The Solicitor General office’s brief obscured the textbook definition with a further inaccurate and false précis:

“if the sampling from the general population were repeated numerous times, the ‘real’ population figure would be within the confidence interval 95 percent of the time. The ‘real’ figure would be outside that interval the remaining five percent of the time.”30

The lawyers in the Solicitor General’s office thus made the rookie mistake of forgetting that in the long run, after numerous repeated samples, there would be numerous confidence intervals, not one. The 95% probability of containing the true population value belongs to the set of the numerous confidence intervals, not “the confidence interval” obtained in the first go around.

The Daubert case has been the subject of nearly endless scholarly comment, but few authors have chosen to revisit the parties’ briefs. Two authors have published a paper that reviewed the scientists’ amici briefs in Daubert.31 The Rothman brief was outlined in detail; the Feinstein rebuttal was not substantively discussed. The plaintiffs’ invocation of the transposition fallacy in Daubert has apparently gone unnoticed.

1 Oral Argument in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 754951, *5 (Tuesday, March 30, 1993) [Oral Arg.]

2 Oral Arg. at *6.

3 In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 781 (E.D.N.Y.1984) (“The distinction between avoidance of risk through regulation and compensation for injuries after the fact is a fundamental one.”), aff’d in relevant part, 818 F.2d 145 (2d Cir. 1987), cert. denied sub nom. Pinkney v. Dow Chemical Co., 484 U.S. 1004 (1988).

4 Org. Arg. at *19.

5 Oral Arg. at *18-19.

6 Oral Arg. at *19.

7 See, e.g., “Sander Greenland on ‘The Need for Critical Appraisal of Expert Witnesses in Epidemiology and Statistics’” (Feb. 8, 2015) (noting biostatistician Sander Greenland’s publications, which selectively criticize only defense expert witnesses and lawyers for statistical misstatements); see also “Some High-Value Targets for Sander Greenland in 2018” (Dec. 27, 2017).

8 Oral Arg. at *19.

9 Oral Arg. at *20

10 Oral Arg. at *44. At the oral argument, this last statement was perhaps Gottesman’s clearest misstatement of statistical principles, in that he directly suggested that the coefficient of confidence translates into a posterior probability of the claimed association at the observed size.

11 Oral Arg. at *37.

12 Oral Arg. at *32.

13 Petitioner’s Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1992 WL 12006442, *8 (U.S. Dec. 2, 1992) [Petitioiner’s Brief].

14 Petitioner’s Brief at *9.

15 Petitioner’s Brief at *n. 36.

16 Brief Amici Curiae of Professors Kenneth Rothman, Noel Weiss, James Robins, Raymond Neutra and Steven Stellman, in Support of Petitioners, 1992 WL 12006438, Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. S. Ct. No. 92-102 (Dec. 2, 1992).

18 Brief Amicus Curiae of Professor Alvan R. Feinstein in Support of Respondent, in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court no. 92-102, 1993 WL 13006284, at *2 (U.S., Jan. 19, 1993) [Feinstein Brief].

19 Feinstein Brief at *19.

20 Petitioner’s Reply Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006390, at *4 (U.S., Feb. 22, 1993).

21 Respondent’s Brief in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006277, at n. 32 (U.S., Jan. 19, 1993) [Respondent Brief].

22 Respondent Brief at *4.

23 Respondent Brief at *42 n.32 and 47.

24 Respondent Brief at *40-41 (citing DeLuca v. Merrell Dow Pharms., Inc., 911 F.2d 941, 958 (3d Cir. 1990)).

25 Brief for the United States as Amicus Curiae Supporting Respondent in Daubert v. Merrell Dow Pharmaceuticals, Inc., U.S. Supreme Court No. 92-102, 1993 WL 13006291 (U.S., Jan. 19, 1993) [U.S. Brief].

26 See, e.g., Hazelwood School District v. United States, 433 U.S. 299, 308-312

(1977); Castaneda v. Partida, 430 U.S. 482, 495-499 & nn.16-18 (1977) (“As a general rule for such large samples, if the difference between the expected value and the observed number is greater than two or three standard deviations, then the hypothesis that the jury drawing was random would be suspect to a social scientist.”).

27 U.S. Brief at *3-4. Over two decades later, when politically convenient, the United States government submitted an amicus brief in a case involving alleged securities fraud for failing to disclose adverse events of an over-the-counter medication. In Matrixx Initiatives Inc. v. Siracusano, 131 S. Ct. 1309 (2011), the securities fraud plaintiffs contended that they need not plead “statistically significant” evidence for adverse drug effects. The Solicitor General’s office, along with counsel for the Food and Drug Division of the Department of Health & Human Services, in their zeal to assist plaintiffs disclaimed the necessity, or even the importance, of statistical significance:

“[w]hile statistical significance provides some indication about the validity of a correlation between a product and a harm, a determination that certain data are not statistically significant … does not refute an inference of causation.”

Brief for the United States as Amicus Curiae Supporting Respondents, in Matrixx Initiatives, Inc. v. Siracusano, 2010 WL 4624148, at *14 (Nov. 12, 2010).

28 U.S. Brief at *5.

29 U.S. Brief at *5-6 (citing David Freedman, Freedman, R. Pisani, R. Purves & A. Adhikari, Statistics 351, 397 (2d ed. 1991)).

30 U.S. Brief at *6 (citing Freedman’s text at 351) (emphasis added).

31 See Joan E. Bertin & Mary S. Henifin, Science, Law, and the Search for Truth in the Courtroom: Lessons from Dauburt v. Menell Dow,” 22 J. Law, Medicine & Ethics 6 (1994); Joan E. Bertin & Mary Sue Henifin, “Scientists Talk to Judges: Reflections on Daubert v. Merrell Dow,” 4(3) New Solutions 3 (1994). The authors’ choice of the New Solutions journal is interesting and curious. New Solutions: A journal of Environmental and Occupational Health Policy was published by the Oil, Chemical and Atomic Workers International Union, under the control of Anthony Mazzocchi (June 13, 1926 – Oct. 5, 2002), who was the union’s secretary-treasurer. Anthony Mazzocchi, “Finding Common Ground: Our Commitment to Confront the Issues,” 1 New Solutions 3 (1990); see also Steven Greenhouse, “Anthony Mazzocchi, 76, Dies; Union Officer and Party Father,” N.Y. Times (Oct. 9, 2002). Even a cursory review of this journal’s contents reveals how concerned, even obsessed, the union was interested and invested in the litigation industry and that industry’s expert witnesses. 

 

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence, statistical evidence | Comments Off on The Advocates’ Errors in Daubert

Selikoff Timeline & Asbestos Litigation History

December 20th, 2018

This post has been updated here.

Posted in Asbestos, Expert Witnesses, Historian Testimony | Comments Off on Selikoff Timeline & Asbestos Litigation History

“Each and Every Exposure” Is a Substantial Factor

December 3rd, 2018

“Every time a bell rings an angel gets his wings”
… It’s a Wonderful Life (1946)

Every time a plaintiff shows the smallest imaginable exposure, there is a full recovery.
… The American tort system.

 

In 1984, Philadelphia County had a non-jury system for asbestos personal injury cases, with a right to “appeal” for a de novo trial with a jury. The non-jury trials were a wonderful training ground for a generation of trial lawyers, and for a generation or two of testifying expert witnesses. When I started to try asbestos cases as a young lawyer, the plaintiffs’ counsel had already taught their expert witnesses to include the “each and every exposure” talismanic language in their direct examination testimonies on the causation of the plaintiffs’ condition. The litigation industry had figured out that this expression would help avoid a compulsory non-suit on proximate causation.

Back in those wild, woolly frontier days, I encountered the slick Dr. Joseph Sokolowski (“Sok”), a pulmonary physician in private practice in New Jersey. Sok, like many other pulmonary physicians in the Delaware Valley area, had seen civilian workers referred by Philadelphia Naval Shipyard to be evaluated for asbestosis. When the plaintiff-friendly physicians diagnosed asbestosis, a few preferred firms would then pursue their claims under the Federal Employees Compensation Act (FECA). The United States government would notify the workers of their occupational disease, and urge them to pursue the government’s outside vendors of asbestos-containing materials, with a reminder that the government had a lien against any civil action recovery. The federal government thus made common cause with the niche law practices of workers’ compensation lawyers,1 and helped launch the tsunami of asbestos litigation.2

Sok was perfect for his role in the federal kick-back scheme. He could deliver the most implausible testimony, and weather brutal cross-examination without flinching. He had the face of a choir boy, and his service as an outside examiner for the Navy Yard employees gave his diagnoses the apparent imprimatur of the federal government. Although Sok had no real understanding of epidemiology, he could readily master the Selikoff litany of 5-10-50, for relative risks for lung cancer, from asbestos alone (supposedly), from smoking alone, and from asbestos and smoking combined, respectively. And he similarly mastered his lines that “each and every exposure” is substantial, when pressed on whether and how exposure to a minor vendor’s product was a substantial factor. Back in those days, before Johns-Manville (JM) Corporation went bankrupt, honest witnesses at the Navy Yard acknowledged that JM supplied the vast majority of asbestos products, but that testimony changed literally over the course of a trial day, when the plaintiffs’ bar learned of the JM bankruptcy.

It was into this topsy-turvy litigation world, I was thrown. I had the sense that there was no basis for the “each and every exposure” opinion, but my elders at the defense bar seemed to avoid the opinion studiously on cross-examination. I recall co-defendants’ counsels’ looks of horror and disapproval when I broached the topic in my first cross-examination. Sok had known to incorporate the “each and every exposure” opinion into his direct testimony, but he had no intelligible response to my question about what possible basis there was for the opinion. “Well, we have to blame each and every exposure because we have no way distinguish among exposures.” I could not let it lie there, and so I asked: “So your opinion about each and every exposure is based upon your ignorance?” My question was quickly met with an objection, and just as quickly with a rather loud and disapproving, “Sustained!” When Sok finished his testimony, I moved to strike his substantial factor opinion as having no foundation, but my motion was met with by judicial annoyance and apathy.

And so I learned that science and logic had nothing to do with asbestos litigation. Some determined defense counsel persevered, however, and in the face of over one hundred bankruptcies,3 a few courts started to take the evidence and arguments against the “every exposure” testimony, seriously. Last week, the New York Court of Appeals, New York’s highest court, agreed to state out loud that the plaintiffs’ “every exposure” theory had no clothes, no foundation, and no science. Juni v. A.O. Smith Water Products Co., No. 123, N.Y. Court of Appeals (Nov. 27, 2018).4

In a short, concise opinion, with a single dissent, the Court held that plaintiffs’ evidence (any exposure, no matter how trivial) in a mesothelioma death case was “insufficient as a matter of law to establish that respondent Ford Motor Co.’s conduct was a proximate cause of the decedent’s injuries.” The ruling affirmed the First Department’s affirmance of a trial court’s judgment notwithstanding the $11 million jury verdict against Ford.5 Arguing for the proposition that every exposure is substantial, over three dozen scientists, physicians, and historians, most of whom regularly support and testify for the litigation industry, filed a brief in support of the plaintiffs.6 The Atlantic Legal Foundation filed an amicus brief on behalf of several scientists,7 and I had the privilege of filing an amicus brief on behalf of the Coalition for Litigation Justice and nine other organizations in support of Ford’s positions.8

It has been 34 years since I first encountered the “every exposure is substantial” dogma in a Philaddelphia courtroom. Some times in litigation, it takes a long time to see the truth come out.

1 E.g., Shein and Brookman; Greitzer & Locks; both of Philadelphia.

2 Encouraging litigation against its suppliers, the federal government pulled off a coup of misdirection. First, it deflected public censure from the Navy and other governmental branches for its own carelessness in the use, installation, and removal of asbestos-containing insulations. Second, the government winnowed the ranks of older, better compensated workers. Third, and most diabolically, the government, which was self-insured for FECA claims, recovered most of their outlay when its former employees recovered judgments or settlements against the government’s outside asbestos product vendors. “The United States Government’s Role in the Asbestos Mess” (Jan. 31, 2012). See also Walter Olson, “Asbestos awareness pre-Selikoff,” Point of Law (Oct. 19, 2007); “The U.S. Navy and the asbestos calamity” Point of Law (Oct. 9, 2007).

4 The plaintiffs were represented by Alani Golanski of Weitz & Luxenberg LLP.

6 Abby Lippman, Annie Thebaud Mony, Arthur L. Frank, Barry Castleman, Bruce P. Lanphear,

Celeste Monforton, Colin L. Soskolne, Daniel Thau Teitelbaum, Dario Consonni, Dario Mirabelli, David Egilman, David F. Goldsmith, David Ozonoff, David Rosner, Fiorella Belpoggi, James Huff, John Heinzow, John M. Dement, John Coulter Maddox, Karl T. Kelsey, Kathleen Ruff, Kenneth D. Rosenman, L. Christine Oliver, Laura Welch, Leslie Thomas Stayner, Morris Greenberg, Nachman Brautbar, Philip J. Landrigan, Xaver Baur, Hans-Joachim Woitowitz, Bice Fubini, Richard Kradin, T.K. Joshi, Theresa S. Emory, Thomas H. Gassert,

Tony Fletcher, and Yv Bonnier Viger.

7 John Henderson Duffus, Ronald E. Gots, Arthur M. Langer, Robert Nolan, Gordon L. Nord, Alan John Rogers, and Emanuel Rubin.

8 Amici Curiae Brief of Coalition for Litigation Justice, Inc., Business Council of New York State, Lawsuit Reform Alliance of New York, New York Insurance Association, Inc., Northeast Retail Lumber Association, National Association of Manufacturers, Chamber of Commerce of the U.S.A., American Tort Reform Association, American Insurance Association, and NFIB Small Business Legal Center Supporting Defendant-Respondent Ford Motor Company.

Posted in Asbestos, Causation, Expert Witnesses | Comments Off on “Each and Every Exposure” Is a Substantial Factor

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