TORTINI

For your delectation and delight, desultory dicta on the law of delicts.

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]  SeeFollow 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.

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.).

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 MisdeedsColumbia 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 SeeToxicHistorians 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).

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).