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Weight of the Evidence in Science and in Law

July 29th, 2017

“woe to that man by whom the offense cometh”

Matthew 18:7

Weight of the evidence (WOE) has cropped up again in recent trial and appellate court proceedings involving the admissibility of scientific expert witness opinion testimony. With some consistency, the WOE approach advocated is vacuous. The proponents of WOE do not specify what type of evidence is considered, whether all evidence was considered, or how competing and conflicting evidence was weighed.

Interpreted sympathetically, WOE might be taken to mean that “scientific judgment” was exercised with respect to causal inference, without describing exactly what was done. Although sympathetic, this interpretation renders the purported methodology meaningless. WOE-ful scientists might just as well say that they used scientific method. Not surprisingly, WOE is absent from virtually all major epidemiology textbooks

Despite the vacuity of WOE, or because of it, some lawyers, who constitute the lawsuit industry, are particularly fond of WOE.¹ Expert witnesses who support the lawsuit industry have defended their “right” to inflict WOE on the litigation system, tooth and nail.²

Carl Cranor, a philosophy professor and a hired expert witness in litigation for plaintiffs’ counsel, has written about WOE and attempted to defend WOE as a scientific methodology. Cranor has caricaturized criticisms of WOE, including mine, by suggesting that the International Agency for Research on Cancer’s use of WOE rebuts my suggestion that WOE is no method at all.³ Cranor’s defense fails, however, because IARC’s method, for all its deficiencies, never invokes a method mired in WOE.

Perhaps the Lawsuit Industry likes WOE as much as it likes the equally vague term, “link.” WOE frees them from the requirement of any meaningful methodology, which means that any conclusion is possible. Under WOE, any conclusion can survive gatekeeping as an opinion. WOE frees the putative expert witness from the need to consider the quality of research. WOE-ful authors such as Carl Cranor invoke WOE or seek to inflict WOE without mentioning the crucial “nuts and bolts” of scientific inference, such as concepts of

Internal and external validity
Assessment of random error
Assessment of known and residual confounding
Known and potential threats to validity in
Appropriate methods of systematic review
Appropriate synthesis across studies, such as systematic review and meta-analysis

These important concepts are lost in the miasma of WOE.

In the published scientific literature, it is a commonplace that WOE is either poorly or not defined and specified. The phrase is vague and ambiguous; its use, inconsistent.⁴ Even authors sympathetic to the WOE mission have reluctantly concluded that the term is most often used in a way that “does not lend itself to transparency or repeatability except in simple cases.”⁵

Another reason that WOE resonates so strongly with the Lawsuit Industry is that having expert witnesses proclaim WOE as their methodology permits trial counsel to claim that the proffered opinions are immune to gatekeeping because, after all, weight-of-the-evidence questions are for the jury. Lawyers learn early on about WOE factual issues in appellate review of a wide variety of evidentiary and sufficiency issues in criminal and civil cases.⁶ Unless against the great WOE, WOE questions are for the jury.

Even venerable judges fall for this semantic confusion. In 1995, the Second Circuit, before the major revision of Rule 702, in 2000, noted that in discharging their gatekeeping role, trial judges do not assume:

“‘the role of St. Peter at the gates of heaven, performing a searching inquiry into the depth of an expert witness’s soul’ that would ‘inexorably lead to evaluating witness credibility and weight of the evidence, the ageless role of the jury’.”

McCullock v. H.B. Fuller Co., 61 F.3d 1038, 1045 (2d Cir.1995) (internal citations omitted).

Of course, the expert witness’s soul is not at issue, but his methodology is. More important, however, note how the appellate court adverted to “weight of the evidence” as something that the jury must evaluate, along with witness credibility. The expert witness WOE litigation strategy deliberately trades upon the confusion between WOE in the allocation between judge and jury, and valid scientific methodology in causal inference. McCullock is proof that judges can be, and are, bamboozled by the litigation strategy.

Twenty years after McCullock, federal appellate judges are still falling for the deliberate confusion between legal and scientific WOE. The Ninth Circuit recently held that the reliability test of Federal Rule of Evidence 702 is:

“‘is not the correctness of the expert’s conclusions but the soundness of his methodology’, and when an expert meets the threshold established by Rule 702, the expert may testify and the fact finder decides how much weight to give that testimony. Challenges that go to the weight of the evidence are within the province of a fact finder, not a trial court judge. A district court should not make credibility determinations that are reserved for the jury.”

City of Pomona v. SQM North America Corp., 750 F.3d 1036, 1044 (9th Cir. 2014) (internal citation omitted), cert. denied, 135 S. Ct. 870 (2014). Characterizing a methodological dispute as one that “merely” concerns the “weight of the evidence” is a strategy to remove the dispute from judicial gatekeeping altogether.

Recently, the Third Circuit displayed this confusion of WOE with methodological impropriety by mischaracterizing failure to correct for multiple testing as merely an improper calculation that ordinarily goes to the weight of the evidence, not its admissibility. Karlo v. Pittsburgh Glass Works, LLC, 849 F.3d 61, 83 (3d Cir. 2017).

The Third Circuit, in Karlo, cited to a Supreme Court case that predated Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579 (1993), and which did involve any Rule 702 challenge to the use of a flawed statistical analysis. In Bazemore v. Friday, 478 U.S. 385, 400 (1986), plaintiffs sued as a class for employment discrimination, and sought to show the discrimination through the use of a regression analysis. The defense challenged the plaintiffs’ regression on grounds that key variables were omitted. The Court rejected a sufficiency challenge to a finding of discrimination in plaintiffs’ class action, and noted:

“Normally, failure to include variables will affect the analysis’ probativeness, not its admissibility.”

The lesson of the last two decades of judicial gatekeeping is that methodological infirmity will affect both probitiveness and admissibility⁷. Courts cannot escape their important gatekeeping duties by shifting their responsibility to juries under the guise of WOE.

1 See, e.g., “WOE-fully Inadequate Methodology – An Ipse Dixit By Another Name” (May 1, 2012); “As They WOE, So No Recovery Have the Reeps,” (May 22, 2013).

2 See Schachtman, “Desultory Thoughts on Milward v. Acuity Specialty Products,” (Oct. 2015).

3 Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 146 (2d ed. 2016) (citing and selectively quoting from Schachtman, “WOE-fully Inadequate Methodology – An Ipse Dixit By Another Name” (May 1, 2012)).

4 See Charles Menzie, Miranda Hope Henning, Jerome Cura, Kenneth Finkelstein, Jack Gentile, James Maughan, David Mitchell, Stephen Petron, Bonnie Potocki, Susan Svirsky & Patti Tyler, “A weight-of-evidence approach for evaluating ecological risks; report of the Massachusetts Weight-of-Evidence Work Group,” 2 Human Ecological Risk Assessment 277, 279 (1996) (“although the term ‘weight of evidence’ is used frequently in ecological risk assessment, there is no consensus on its definition or how it should be applied”); Sheldon Krimsky, “The weight of scientific evidence in policy and law,” 95 Am. J. Pub. Health S129 (2005) (“However, the term [WOE] is applied quite liberally in the regulatory literature, the methodology behind it is rarely explicated.”); V. H. Dale, G.R. Biddinger, M.C. Newman, J.T. Oris, G.W. Suter II, T. Thompson, et al., “Enhancing the ecological risk assessment process,” 4 Integrated Envt’l Assess. Management 306 (2008) (“An approach to interpreting lines of evidence and weight of evidence is critically needed for complex assessments, and it would be useful to develop case studies and/or standards of practice for interpreting lines of evidence.”); Douglas L. Weed, “Weight of Evidence: A Review of Concept and Methods,” 25 Risk Analysis 1545 (2005) (noting the “lack of definition of the term weight of evidence, multiple uses of the term and a lack of consensus about its meaning, and the many different kinds of weights, both qualitative and quantitative which can be used in risk assessment”); R.G. Stahl Jr., “Issues addressed and unaddressed in EPA’s ecological risk guidelines,” 17 Risk Policy Report 35 (1998) (noting that U.S. Environmental Protection Agency’s guidelines for ecological weight-of-evidence approaches to risk assessment fail to provide guidance); Glenn W. Suter, Susan M. Cormier, “Why and how to combine evidence in environmental assessments: Weighing evidence and building cases,” 409 Sci. Total Env’t 1406, 1406 (2011) (noting arbitrariness and subjectivity of WOE “methodology”).

5 See Igor Linkov, Drew Loney, Susan Cormier, F. Kyle Satterstrom, and Todd Bridges, “Weight-of-evidence evaluation in environmental assessment: review of qualitative and quantitative approaches,” 407 Sci. Total Env’t 5199, 5203 (2009).

6 See, e.g., People v. Collier, 146 A.D.3d 1146, 1147-48, 2017 NY Slip Op 00342 (N.Y. App. Div. 3d Dep’t, Jan. 19, 2017) (rejecting appeal based upon defendant’s claim that conviction was against “weight of the evidence”); Venson v. Altamirano, 749 F.3d 641, 656 (7th Cir. 2014) (noting “new trial is appropriate if the jury’s verdict is against the manifest weight of the evidence”).

7 David L. Faigman, Christopher Slobogin & John Monahan, “Gatekeeping Science: Using the Structure of Scientific Research to Distinguish Between Admissibility and Weight in Expert Testimony,” 110 Northwestern L. Rev. 859, 865 (2016) (“An expert economist in an employment discrimination case who admittedly fails to control for a key variable such as seniority or wage structure in a regression analysis has committed a general error that should lead to exclusion by a judge… .”).

Posted in Causation, Rule 702, Scientific Evidence | Comments Off on Weight of the Evidence in Science and in Law

Slemp Trial Part 5 – Daniel W. Cramer

July 24th, 2017

The case of talc and ovarian cancer is a difficult and close case on general causation. Although I do not believe that the plaintiffs have made their case, their causal claims do not have the usual earmarks of “junk science,” so readily visible in many other litigations, such as the Zoloft birth defects cases.

Dr. Daniel Cramer is a physician and an epidemiology. He holds the title of professor of epidemiology at the Harvard University Chan School Of Public Health, as well as a professor of obstetrics, gynecology, and reproductive biology, at the Harvard Medical School. The plaintiffs called Cramer to testify on causation issues.

Cramer could have been purely duplicative as a witness, but he was used primarily on specific causation with a big boost on general causation because of his many publications on talc and ovarian cancer (a subject generally missing from Graham Colditz’s C.V.). The planned testimony for Cramer was to try to present the causal attribution of Slemp’s tumor to talc, with the understanding that since specific implied general causation, the plaintiff would obtain corroborating testimony on general causation as well.

With respect to Slemp’s known risk factors, such as her massive obesity and heavy smoking history, Cramer attempted to quantify her ex ante risks based upon her medical chart and from using risk ratios from available epidemiologic studies. Predictably, Cramer tried to diminish these ex ante risks by a highly selective reading of Slemp’s charts, but he ably deflected cross-examination criticisms by characterizing questions as quibbles and volunteering that he was not trying to ascribe plaintiff’s ovarian cancer exclusively to talc. Similarly, Cramer attempted to present the highest ex ante risk ratio for Slemp’s talc exposure, through his characterizations of her case as involving bilateral tumors and other features. Cramer tried to diminish the risk factor of obesity by claiming that fat women use talc more and that there was “synergy” between obesity and talc use. Cramer never described the evidentiary basis for this claimed synergy, or whether it was multiplicative or something less dramatic.

Interestingly, risk ratios from groups (epidemiologic studies) were used to describe her individual risks. The defense did not actively challenge this procedure. The premise of Cramer’s approach was that if an individual patient had a previous exposure or lifestyle variable that has been causally associated with ovarian cancer, then those exposures and lifestyle variables all participating in actually causing the patient’s cancer. As noted in the summary of Graham Colditz’s testimony, this assumption by Cramer is disputed. Cramer never attempted to justify the assumption by reference to any body of scientific evidence, or text. For Mrs. Slemp, Cramer opined that talc (as well as obesity and smoking) caused her serous borderline ovarian tumors. This conclusion was driven by his assumption that if Slemp had an exposure to a known cause of ovarian cancer, then it must have played a “substantial” role in causing the cancer.

Cross-Examination

The defense vigorously challenged Cramer for having failed to discuss causation in his publications. Most of these publications were epidemiologic studies, which did not necessarily provide an opportunity for full-ranging discussions of causal conclusions. Cramer effectively parried by noting that causation is not established by a single study, and single-study reports were not an appropriate vehicle for a full review and analysis of causation. As for his reviews and opinion pieces, Cramer defended his failure to state a clear causal conclusion on grounds that he had urged warning labels for personal talc products, and that a causal conclusion was not needed to justify such a warning because even a potential risk of ovarian cancer outweighed the negligible benefit of using talc in personal hygiene.

The defense plowed on with its claim that many studies lacked statistical significance, but Cramer generally lost defense counsel in technical details. For Cramer’s estimation of Slemp’s ex ante risk ratio from talc exposure, the defense challenged Cramer’s use of a one-tailed test of significance¹. Cramer offered a half-hearted defense of a one-sided test in this context, and used the questions as an opportunity to repeat how low the p-value was with respect to the general association between talc and ovarian cancer. Cramer muddied the water by claiming that this calculation was superseded by further refinement of his estimate, which took into account the bilaterality of Slemp’s tumors, which obviated his one-sided confidence interval calculation. Although the details were not entirely forthcoming, the jury would not likely have seen this exchange as anything other than a quibble. The defense’s claim that Cramer had violated the “rules of epidemiology” never got off the ground, and given that the defense never presented an epidemiologist, the claim of counsel never was grounded in actual evidence.

Counterfactual Causation

The most important cross-examination of Dr. Cramer came from both J & J’s and Imerys’ counsel on the issue of counterfactual causation. Defense counsel asked Cramer, in several different ways, whether Ms. Slemp would have avoided having ovarian cancer if she had not used talc. Cramer stridently and belligerently refused to answer the question. The trial judge showed no interest in obtaining an answer to these questions. In the last effort to obtain a response from Cramer on “but for” causation, Cramer simply refused:

“I am not going to opine on the topic because it is not the task I was charged with.”

In other words, plaintiffs’ counsel and Cramer had discussed his inability to answer the counterfactual question, and decided it was simply better not respond to the question altogether. Since Mr. Smith, plaintiffs’ counsel, did not “task” him with counterfactual causation, Cramer was not going to answer it. Cramer’s intransigence was remarkable because the counterfactual question is an important component to causal inference in epidemiologic science. See, e.g., Michael Höfler, “Causal inference based on counterfactuals,” 5 BMC Med. Research Methodology 28 (2005).

In law, as in science, the counterfactual questions put to Cramer, are essential. Conduct or a product cannot be a legal cause of harm unless that cause alone, or acting in concert with other causes, was enough to result in the injury. Although legal treatises speak of “substantial factor,” the American Law Institute (ALI) defined that phrase (outside the context of overdetermined effects) negatively to make clear that “the actor’s negligent conduct is not a substantial factor in bringing about harm to another if the harm would have been sustained even if the actor had not been negligent.” Restatement (Second) of Torts § 432 (1965).

Given the mischief generated by some courts and commentators² with respect to “substantial factor,” the ALI abandoned the phrase altogether in its most recent Restatement of the law of torts. In the current Restatement, the ALI has emphasized that the imposition of liability require that the harm claimed is one that would not have occurred in the absence of (“but for”) the defendant’s negligent conduct. Restatement (Third) of Torts: Physical and Emotional Harm § 26 cmt. J (2010); see also June v. Union Carbide Corp., 577 F.3d 1234, 1244 (10th Cir. 2009) (no material difference between Second and Third Restatements; holding that ‘‘a defendant cannot be liable to the plaintiff unless its conduct is either (a) a but-for cause of the plaintiff’s injury or (b) a necessary component of a causal set that (probably) would have caused the injury in the absence of other causes.’’).

Dr. Cramer’s refusal to answer the key counterfactual question about talc and Ms. Slemp’s ovarian cancer points to a lawlessness, both scientific and legal, in the proceedings in St. Louis, Missouri.

1 See “FAQ: What are the differences between one-tailed and two-tailed tests?” Institute for Digital Research and Education.

2 See David A. Fischer, “Insufficient Causes,” 94 Kent. L. J. 277, 277 (2005-06) (criticizing judicial obtuseness in misinterpreting the earlier Restatement’s use of “substantial factor”).

Posted in Causation, Risk and Risk Factor | Comments Off on Slemp Trial Part 5 – Daniel W. Cramer

David Rosner’s Document Repository

July 23rd, 2017

David Rosner and Gerald Markowitz are leftist labor and social historians in Columbia University and City University of New York, respectively. Both are frequently disclosed by plaintiffs’ counsel as expert witnesses on historical issues, and both often testify at asbestos and other personal injury trials¹. Markowitz has been excluded in at least one reliability challenge².

The two historians, who appear so often together on plaintiffs’ designations that they are sometime referred to as a unified persona, Rosnowitz, have create a website, “Project Toxicdocs,” supposedly in an alpha version³.

The Toxic Docs website does not identify Rosner and Markowitz by name as authors or sponsors, but the website’s content and goals bear their indelible stamp, as well as the concordance of their institutional affiliations of Columbia and CUNY. The website promises “[b]lazingly fast” searches and access to previously confidential, classified industry documents on “industrial poisons”:

“This dataset and website contain millions of pages of previously secret documents about toxic substances. They include secret internal memoranda, emails, slides, board minutes, unpublished scientific studies, and expert witness reports — among other kinds of documents — that emerged in recent toxic tort litigation.

Over the next couple years, we’ll be constantly adding material from lawsuits involving lead, asbestos, silica, and PCBs, among other dangerous substances. Innovations in parallel and cloud computing have made conversion of these documents into machine-readable, searchable text a far faster process than would have been the case just a decade ago.”

Similar efforts have been put into place for documents collected in tobacco and other litigations⁴. David Egilman, another regular testifier for the Lawsuit Industry once maintained a website with a large library of documents he relied upon for his ethics and state-of-the-art opinion testimony in various litigations.

A trial run through the “dataset” for the search term “silicosis” turned up 44 documents, most of which had nothing to do with silica or silicosis, and many of which were duplicates. Remarkably, there were no documents from government or labor unions.

We are sure that these historian expert witnesses will improve their efforts to be comprehensive and balanced, with practice.

1 See, e.g., Garcia v. Lone Star Indus., Case No. D-149, 527, 1997 WL 34904089 (Dist. Ct. Tex., Jefferson Cty., 1997) (identifying Rosner and Markowitz as testifying expert witnesses for plaintiff); City of Milwaukee v NL Industries, Inc., Circuit Ct., Milwaukee Cty., Wisc., 2007 WL 4676349 (Jan. 16, 2007) (referencing litigation report of Rosner and Markowitz); Gibson v. American Cyanamid Co., 719 F. Supp. 2d 1031, 1048 (E.D. Wis. 2010) (noting Rosner and Markowitz’s declaration for plaintiffs); Rhode Island v. Lead Industries Ass’n, C.A. No. PC 99-5226, Rhode Island Superior Court, Providence (Feb. 26, 2007) (discussing Rosner and Markowitz’s testimony on post-verdict motions); Altria Group, Inc. v. Good, No. 07-562, U.S. Sup. Ct., Amicus Brief of Allan M. Brandt, Robert N. Proctor, David M. Burns, Jonathan M. Samet, and David Rosner (June 18, 2008) (all amici except Rosner disclosed their litigation activities); Burton v. American Cyanamid Co., 775 F. Supp. 2d 1093 (E.D. Wis. 2011) (noting Rosner and Markowitz’s testimony in lead pigment case); California v. Atlantic Richfield Co., Santa Clara Super. Ct., Calif., No. 1-00-CV-788657, 2013 WL 4425657 (July 15, 2013) (noting Rosner’s testimony); Ostenrieder v. Rohm & Haas Co., Phila. Ct. C.P. Case No. 150602485, Motion in Limine to Exclude Testimony of Gerald Markowitz and David Rosner (filed by Rohm & Haas Co., subsidiary of Dow Chemical Co., June 18, 2015); Dumas v. ABB Group, Inc., civ. action no. 13-229-SLR-SRF (D. Del. Sept. 30, 2015) (referencing Rosner’s report for plaintiffs); Assenzio v. A.O. Smith Water Prods. Co., docket nos. 190008/12, 190026/12, 190200/12, 190183/12, 190184/12, NY Sup. Ct., NY Cty. (Feb. 5, 2015) (noting that Rosner testified for plaintiffs); Noll v American Biltrite, Inc., 188 Wash. App. 572, 355 P.3d 279 (Wash. Ct. App. June 29, 2015), aff’d, 355 P.3d 279 (Wash. 2015) (deposition of Gerald Markowitz given on behalf of plaintiff); Schwartz v. Honeywell Internat’l, Inc., 66 N.E.3d 118 (Ohio Ct. App. 2016) (same), app. granted, 148 Ohio St. 3d 1442, 72 N.E.3d 656 (2017); Clair v. Monsanto Co., 412 S.W.3d 295 (Mo. App. 2013) (noting Rosner as plaintiff’s expert witness); New v. Borg-Warner Corp., No. 13-cv-00675, 2015 WL 5166946 (W.D. Mo., Sept. 3, 2015) (identifying Rosner and Markowitz as plaintiff’s expert witnesses); Begin v. Air & Liquid Corp., Case No. 3:15-cv-830-SMY-DGW (S.D. Ill. May 10, 2016) (striking designation of plaintiff’s expert witness David Rosner as untimely in asbestos case); Rost v. Ford Motor Co., 151 A.3d 1032 (Pa. 2016) (noting Rosner and Markowitz as amici authors; no disclosure of litigation income); Dominick v. A.O. Smith Water Products, CA2014-000232, NY Sup. Ct., Oneida Cty., Notes of Testimony of David Rosner, Mar. 18, 2017 (Press Release from Plaintiffs’ law firm).

2 Quester v. B.F. Goodrich Co., Cuyahoga Cty., Ohio, C.P. Case No. 30-509539 (Jan. 12, 2008) (excluding Markowitz’s testimony as impermissible attempt to introduce expert witness opinion on defendants’ intent and motive).

3 Presumably an alpha version is one that has not made it to beta.

4 See “Truth Tobacco Industry Documents,” and “Tobacco Archives.”

Posted in Historian Testimony, State of the Art | Comments Off on David Rosner’s Document Repository

Slemp Trial Part 4 – Graham Colditz

July 22nd, 2017

The Witness

Somehow, in opposition to two epidemiologists presented by the plaintiff in Slemp, the defense managed to call none. The first of the plaintiffs’ two epidemiology expert witnesses was Graham A. Colditz, a physician with doctoral level training in epidemiology. For many years, Colditz was a professor at the Harvard School of Public Health. Colditz left Harvard to become the Niess-Gain Professor at Washington University St. Louis School of Medicine, where he is also the Associate Director for Prevention and Control at the Alvin J. Siteman Cancer Center.

Colditz is a senior epidemiologist, with many book and article publications to his credit. Although he has not published a causal analysis of ovarian cancer and talc, Colditz was an investigator on the well-known Nurses’ Health Study. One of Colditz’s publications on the Nurses’ cohort featured an analysis of talc use and ovarian cancer outcomes.

Although he is not a frequent testifying expert witness, Colditz is no stranger to the courtroom. He was a regular protagonist in the estrogen-progestin hormone replacement therapy (HRT) litigation, which principally involves claims of female breast cancer. Colditz has a charming Australian accent, with a voice tremor that makes him sound older than 63, and perhaps even more distinguished. He charges $1,500 per hour for his testimonial efforts, but is quick to point out that he has given thousands to charity. At his hourly rate, we can be sure he needs tax deductions of some kind.

In discussing his own qualifications, Colditz was low-key and modest except for what seemed like a strange claim that his HRT litigation work for plaintiffs led the FDA to require a boxed warning of breast cancer risk on the package insert for HRT medications. This claim is certainly false, and an extreme instance of post hoc ergo propter hoc. Colditz gilded the lilly by claiming that he does not get involved unless he believes that general causation exists between the exposure or medication and the disease claimed. Since he has only been a plaintiffs’ expert witness, this self-serving claim is quite circular.

The Examinations

The direct and cross-examinations of Dr. Colditz were long and tedious. Most lawyers are reluctant to have an epidemiologists testify at all, and try to limit the length of their examinations, when they must present epidemiologic testimony. Indeed, the defense in Slemp may have opted to present a clinician based upon the prejudice against epidemiologists testifying about quantitative data and analysis. In any event, Colditz’s direct examination went not hours, but days, as did the defense’s cross-examination.

The tedium of the direct examination was exacerbated by the shameless use of leading, loaded, and argumentative questions by plaintiff’s counsel, Allen Smith. A linguistic analysis might well show that Smith spoke 25 to 30 words for every one word spoken by Colditz on direct examination. Even aside from the niceties of courtroom procedure, the direct examination was lacking in aesthetic qualities. Still, it is hard to argue with a $110 million verdict, which cries out for explanation.

There were virtually no objections to Smith’s testifying in lieu of Colditz, with Colditz reduced to just “yes.” Sometimes, Colditz waxed loquacious, and answered, “yes, sir.” From judicial responses to other objections, however, it was clear that the trial court would have provided little control of the leading and argumentative questions.

Smith’s examination also took Colditz beyond the scope of his epidemiologic expertise in to ethics, social policy, and legal requirements of warnings, again without judicial management or control. We learned, over objection, from Colditz of all witnesses that the determination of causation has nothing to do with whether a warning should be given.

The Subject Matter

Colditz was clearly familiar with the subject matter, and allowed Smith to testify for him on a fairly simplistic level. The testimony was a natural outgrowth of his professional interests, and Colditz must have appeared to have been a credible expert witness, especially in a St. Louis courtroom, given that he was in a leadership role at the leading cancer center in that city.

With Smith’s lead, Colditz broached technical issues of bias evaluation, meta-analysis and pooling, which would never be addressed later by a defense expert witness at an equal level of expertise, sophistication, and credibility. Colditz offered criticisms of the Gonzalez (Sister Study) and the latency built into the observation period of that cohort, and he introduced the concept of Berkson bias in some of the case-control studies. Neither of these particular criticisms was rebutted in the defense case, again raising the question whether the defense expert witness, Dr. Huh, a clinician specializing in gynecologic oncology, was an appropriate foil for the line up of plaintiffs’ expert witness. Dr. Colditz was able to talk authoritatively (and in some cases misleadingly) about issues, which Dr. Huh could not contradict effectively, even if he were to have tried.

Colditz characterized his involvement in the talc cases as starting with his conducting a systematic review, undertaken for litigation, but still systematic. As a professor of epidemiology, Colditz should know what a systematic review is, although he never fully described the process on either direct or cross-examinations. No protocol for the systematic review was adduced into evidence. Sadly, the defense expert witness, Dr. Huh, never stated that he had done a systematic review; nor did he offer any criticisms of Dr. Colditz’s systematic review. Indeed, Huh admitted that he had not read Colditz’s testimony. In general, observing Colditz’s testimony after having watched Dr. Huh testify shouted MISMATCH.

The Issues

Statistical Significance

The beginning point of a case such as Slemp, involving a claim that talc causes ovarian cancer, and that it caused her ovarian cancer, is whether there is supporting epidemiology for the claim. As Sir Austin Bradford Hill put it over 50 years ago:

“Disregarding then any such problem in semantics we have this situation. Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance. What aspects of that association should we especially consider before deciding that the most likely interpretation of it is causation?”

Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295, 295 (1965). Colditz, and plaintiff’s counsel, did not run away from the challenge; they embraced statistical significance and presented an argument for why the association was “clear-cut” (not created by bias or confounding).

In one of his lengthy, leading questions, plaintiffs’ counsel attempted to suggest that statistical significance, or a confidence interval that excluded a risk ratio of 1.0, excluded bias as well as chance. Colditz to his credit broke from the straight jacket of “yes, sirs,” and disagreed as to bias. Smith, perhaps chastised then took a chance and asked an open-ended question about what a confidence interval was. With the bit in his mouth, Colditz managed to describe the observed confidence interval incorrectly as providing the range within which the point estimate would fall 95% of the time if the same study were repeated many times! There is a distribution of 95% confidence intervals, which cover the true parameter 95% of the time, assuming a correct statistical model, random sampling, and no bias or confounding. For the observed confidence interval, the true value is either included or not. Perhaps Colditz was thinking of a prediction interval, but Smith had asked for a definition of a confidence interval, and the jury got non-sense.

Dose Response

Colditz parsed the remaining Bradford Hill factors, and opined that exposure-gradient or dose response was good to have but not necessary to support a causal conclusion. Colditz opined, with respect to whether the statistical assessment of a putative dose-response should include non-exposed women, that the non-exposed women should be excluded. This was one of the few technical issues that Dr. Huh engaged with, in the defense case, but Dr. Colditz was not confronted with any textbooks or writings that cast doubt on his preference for excluding non-users.

Plausibility

Plaintiff’s counsel spent a great deal of time, mostly reading lengthy passages of articles on this or that plausible mechanism for talc’s causing human ovarian cancer, only to have Colditz, with little or no demonstrated expertise in biological mechanism, say “yes.” Some articles discussed that talc use was a modifiable risk and that avoiding perineal talc use “may” reduce ovarian cancer risk. Smith would read (accurately) and then ask Colditz whether he agreed that avoiding talc use would reduce ovarian cancer in women. Colditz himself catches and corrects Smith, some times, but not others.

Smith read from an article that invokes a claim that asbestos (with definition as to what mineral) causes ovarian cancer. Colditz agreed. Smith testified that talc has asbestos in it, and Colditz agreed. Smith read from an article that stated vaguely that talc is chemically similar to asbestos and thus this creates plausibility for a causal connection between talc and cancer. Colditz agreed, without any suggestion that he understands whether or not talc is morphologically similar to asbestos. It seems unlikely that Colditz had any real expertise to offer here, but Smith could not resist touching all bases with Colditz; and the defense did not object or follow up on these excesses.

Smith and Colditz, well mostly Smith, testified that tubal ligation reduces the otherwise observed increased risk of ovarian cancer from talc use. Smith here entrusts Colditz with providing the common-sense explanation. There is no meaningful cross-examination on this “jury friendly” point.

Consistency

Colditz testifed that the studies, both case-control and cohort studies, were consistent in showing an increased risk of ovarian cancer in association with talc use. Indeed, the studies are mostly consistent; the issue is whether they are consistently biased or consistently showing the true population risk. The defense chose to confront Colditz with the lack of statistical significance in some studies (with elevated risk ratios) as though these studies were inconsistent with the studies that found similar risk ratios, with p-values less than 5%. This confrontation did not go well for the defense, either on cross-examination of Colditz, or on direct examination of Dr. Huh. Colditz backed up his opinion on consistency with the available meta-analyses, which find very low p-values for the summary estimate of risk ratio for talc use and ovarian cancer.

Unlike the Zoloft case¹, in which consistency was generated across different end points by cherry picking, the consistency in the talc case was evidenced by a consistent elevation of risk ratios for the same end point, across studies. When subgroups of ovarian cell or tumor types were examined, statistical significance was sometimes lost, but the direction of the risk ratio above one was maintained. Meta-analyses generated summary point estimates with very low p-values.

The Gold Standard

Colditz further gilded the consistency lilly by claiming that the Terry study², a pooled analysis of available case-control studies, was the “gold standard” in this area of observational epidemiology. Smith and Colditz presented at some length as to how the Cochrane Collaboration has labeled combined “individual patient data” (IPD) analyses as the gold standard. Colditz skimmed over the Cochrane’s endorsement of IPD analyses as having been made in the context of systematic reviews, involving primarily randomized clinical trials, for which IPD analyses allow time-to-event measurements, which can substantially modify observed risk ratios, and even reverse their direction. The case-control studies in the Terry pooled analysis did not have anything like the kind of prospectively collected individual patient data, which would warrant holding the Terry paper up as a “gold standard,” and Terry and her co-authors never made such a claim for their analysis. Colditz’s claim about the Terry study cried out for strong rebuttal, which never came.

The defense should have known that this hyperbolic testimony would be forthcoming, but they seemed not to have a rebuttal planned, other than dismissing case-controls studies generally as smaller than cohort studies. Rather than “getting into the weeds” about the merits of pooled analyses of observational studies, as opposed to clinical trials, the defense continued with its bizarre stance that the cohort studies were better because larger, while ignoring that they are smaller with respect to number of ovarian cancer cases and have less precision than the case-control studies. See “New Jersey Kemps Ovarian Cancer – Talc Cases” (Sept. 16, 2016). The defense also largely ignored Colditz’s testimony that exposure data collected in the available cohort studies was of limited value because lacking in details about frequency and intensity of use, and in some cases, collected on only one occasion.

Specific Causation

Colditz disclaimed the ability or intention to offer a specific causation opinion about Ms. Slemp’s ovarian cancer. Nonetheless, Colditz volunteered that “cancer is multifactorial,” which says very little because it says so much. In plaintiffs’ counsel’s hands, this characterization became a smokescreen to indict every possible present risk factor as playing a part in the actual causation of a particular case, such as Ms. Slemp’s case. No matter that the plaintiff was massively obese, and a smoker; every risk factor present must be, by fiat, in the “causal pie.”

But this would seem not to be Colditz’s own opinion. Graham Colditz has elsewhere asserted that an increased risk of disease cannot be translated into the “but-for” standard of causation³:

“Knowledge that a factor is associated with increased risk of disease does not translate into the premise that a case of disease will be prevented if a specific individual eliminates exposure to that risk factor. Disease pathogenesis at the individual level is extremely complex.”

Just because a risk factor (assuming it is real and causal) is present does not put in the causal set.

Cross-Examination

The direct examination of Graham Colditz included scurrilous attacks on J & J’s lobbying, paying FDA user fees, and other corporate conduct, based upon documents of which Colditz had not personal knowledge. Colditz was reduced to nothing more than a backboard, off which plaintiff’s counsel could make his shots. On cross, the defense carefully dissected this direct examination and obtained disavowals from Colditz that he had suggested any untoward conduct by J & J. The jury could have been spared their valuable time by a trial judge who did not allow the scurrilous, collateral attacks in the first place.

The defense also tried to diminish Dr. Colditz’s testimony as an opinion coming from a non-physician. The problem, however, was that Colditz is a physician, who understands the biological issues, even if he is not a pathologist, toxicologist, or oncologist. Colditz did not offer opinions about Slemp’s medical treatment, and there was nothing in this line of cross-examination that lessened the impact of Colditz’s general causation testimony.

Generally, the cross-examination did not hurt Dr. Colditz’s strongly stated opinion that talc causes ovarian cancer. The defense (and plaintiff’s counsel before them) spent an inordinate amount of time on why Dr. Colditz has not updated his website to state publicly that talc causes ovarian cancer. Colditz blamed the “IT” guys, a rather disingenuous excuse. His explanation on direct, and on cross, as to why he could not post his opinion on his public-service website was so convoluted, however, that there was no clear admission or inference of dereliction. Colditz was permitted to bill his opinion, never posted to his institution’s website, as a “consensus opinion,” endorsed by several researchers, based upon hearsay emails and oral conversations.

1 See In re Zoloft Prod. Liab. Litig., No. 16-2247 , __ F.3d __, 2017 WL 2385279, 2017 U.S. App. LEXIS 9832 (3d Cir. June 2, 2017) (affirming exclusion of dodgy opinion, which involved changing subgroup end points across studies of maternal sertraline use and infant cardiac birth defects ).

2 Kathryn L. Terry, et al., “Genital powder use and risk of ovarian cancer: a pooled analysis of 8,525 cases and 9,859 controls,” 6 Cancer Prev. & Research 811 (2013).

3 Graham A. Colditz, “From epidemiology to cancer prevention: implications for the 21st Century,” 18 Cancer Causes Control 117, 118 (2007).

Posted in Causation, Meta-analysis, Scientific Evidence | Comments Off on Slemp Trial Part 4 – Graham Colditz

Welding Litigation – Another Positive Example of Litigation-Generated Science

July 11th, 2017

In a recent post¹, I noted Samuel Tarry’s valuable article² for its helpful, contrarian discussion of the importance of some scientific articles with litigation provenances. Public health debates can spill over to the courtroom, and developments in the courtroom can, on occasion, inform and even resolve those public health debates that gave rise to the litigation. Tarry provided an account of three such articles, and I provided a brief account of another article, a published meta-analysis, from the welding fume litigation.

The welding litigation actually accounted for several studies, but in this post, I detail the background of another published study, this one an epidemiologic study by a noted Harvard epidemiologist. Not every expert witness’s report has the making of a published paper. In theory, if the expert witness has conducted a systematic review, and reached a conclusion that is not populated among already published papers, we might well expect that the witness had achieved the “least publishable unit.” The reality is that most causal claims are not based upon what could even remotely be called a systematic review. Given the lack of credibility to the causal claim, rebuttal reports are likely to have little interest to serious scientists.

Martin Wells

In the welding fume cases, one of plaintiffs’ hired expert witnesses, Martin Wells, a statistician, proffered an analysis of Parkinson’s disease (PD) mortality among welders and welding tradesmen. Using the National Center for Health Statistics (NCHS) database, Wells aggregated data from 1993 to 1999, for PD among welders and compared this to PD mortality among non-welders. Wells claimed to find an increased risk of PD mortality among younger (under age 65 at death) welders and welding tradesmen in this dataset.

The defense sought discovery of Wells’s methods and materials, and obtained the underlying data from the NCHS. Wells had no protocol, no pre-stated commitment to which years in the dataset he would use, and no pre-stated statistical analysis plan. At a Rule 702 hearing, Wells was unable to state how many welders were included in his analysis, why he selected some years but not others, or why he had selected age 65 as the cut off. His analyses appeared to be pure data dredging.

As the defense discovered, the NCHS dataset contained mortality data for many more years than the limited range employed by Wells in his analysis. Working with an expert witness at the Harvard School of Public Health, the defense discovered that Wells had gerrymandered the years included (and excluded) in his analysis in a way that just happened to generate a marginally, nominally statistically significant association.

NCHS Welder Age Distribution

The defense was thus able to show that the data overall, and in each year, were very sparse. For most years, the value was either 0 or 1, for PD deaths under age 65. Because of the huge denominators, however, the calculated mortality odds ratios were nominally statistically significant. The value of four PD deaths in 1998 is clearly an outlier. If the value were three rather than four, the statistical significance of the calculated OR would have been lost. Alternatively, a simple sensitivity test suggests that if instead of overall n = 7, n were 6, statistical significance would have been lost. The chart below, prepared at the time with help from Dr. David Schwartz, of Innovative Science solutions, shows the actual number of “underlying cause” PD deaths that were in the dataset for each year in the NCHS dataset, and how sparse and “granular” these data were:

A couple of years later, the Wells’ litigation analysis showed up as a manuscript, with only minor changes in its analyses, and with authors listed as Martin T. Wells and Katherine W. Eisenberg, in the editorial offices of Neurology. Katherine W. Eisenberg, AB and Martin T. Wells, Ph.D., “A Mortality Odds Ratio Study of Welders and Parkinson Disease.” Wells disclosed that he had testified for plaintiffs in the welding fume litigation, but Eisenberg declared no conflicts. Having only an undergraduate degree, and attending medical school at the time of submission, Ms. Eisenberg would not seem to have had the opportunity to accumulate any conflicts of interest. Undisclosed to the editors of Neurology, however, was that Ms. Eisenberg was the daughter of Theodore (Ted) Eisenberg, a lawyer who taught at Cornell University and who represented plaintiffs in the same welding MDL as the one in which Wells testified. Inquiring minds might have wondered whether Ms. Eisenberg’s tuition, room, and board were subsidized by Ted’s earnings in the welding fume and other litigations. Ted Eisenberg and Martin Wells had collaborated on many other projects, but in the welding fume litigation, Ted worked as an attorney for MDL welding plaintiffs, and Martin Wells was compensated handsomely as an expert witness. The acknowledgment at the end of the manuscript thanked Theodore Eisenberg for his thoughtful comments and discussion, without noting that he had been a paid member of the plaintiff’s litigation team. Nor did Wells and Eisenberg tells the Neurology editors that the article had grown out of Wells’ 2005 litigation report in the welding MDL.

The disclosure lapses and oversights by Wells and the younger Eisenberg proved harmless error because Neurology rejected the Wells and Eisenberg paper for publication, and it was never submitted elsewhere. The paper used the same restricted set of years of NCHS data, 1993-1999. The defense had already shown, through its own expert witness’s rebuttal report, that the manuscript’s analysis achieved statistical significance only because it omitted years from the analysis. For instance, if the authors had analyzed 1992 through 1999, their Parkinson’s disease mortality point estimate for younger welding tradesmen would no longer have been statistically significant.

Robert Park

One reason that Wells and Eisenberg may have abandoned their gerrymandered statistical analysis of the NCHS dataset was that an ostensibly independent group³ of investigators published a paper that presented a competing analysis. Robert M. Park, Paul A. Schulte, Joseph D. Bowman, James T. Walker, Stephen C. Bondy, Michael G. Yost, Jennifer A. Touchstone, and Mustafa Dosemeci, “Potential Occupational Risks for Neurodegenerative Diseases,” 48 Am. J. Ind. Med. 63 (2005) [cited as Park (2005)]. The authors accessed the same NCHS dataset, and looked at hundreds of different occupations, including welding tradesmen, and four neurodegenerative diseases.

Park, et al., claimed that they looked at occupations that had previously shown elevated proportional mortality ratios (PMR) in a previous publication of the NIOSH. A few other occupations were included; in all their were hundreds of independent analyses, without any adjustment for multiple testing. Welding occupations⁴ were included “[b]ecause of reports of Parkinsonism in welders [Racette et al.,, 2001; Levy and Nassetta, 2003], possibly attributable to manganese exposure (from welding rods and steel alloys)… .”⁵ Racette was a consultant for the Lawsuit Industry, which had been funded his research on parkinsonism among welders. Levy was a testifying expert witness for Lawsuit, Inc. A betting person would conclude that Park had consulted with Wells and Eisenberg, and their colleagues.

These authors looked at four neurological degenerative diseases (NDDs), Alzheimer’s disease, Parkinson’s disease, motor neuron disease, and pre-senile dementia. The authors looked at NCHS death certificate occupational information from 1992 to 1998, which was remarkable because Wells had insisted that 1992 somehow was not available for inclusion in his analyses. During 1992 to 1998, in 22 states, there were 2,614,346 deaths with 33,678 from Parkinson’s diseases. (p. 65b). Then for each of the four disease outcomes, the authors conducted an analysis for deaths below age 65. For the welding tradesmen, none of the four NDDs showed any associations. Park went on to conduct subgroup analyses for each of the four NDDs for death below age 65. In these subgroup analyses for welding tradesmen, the authors purported to find only an association only with Parkinson’s disease:

“Of the four NDDs under study, only PD was associated with occupations where arc-welding of steel is performed, and only for the 20 PD deaths below age 65 (MOR=1.77, 95% CI=1.08-2.75) (Table V).”

Park (2005), at 70.

The exact nature of the subgroup was obscure, to say the least. Remarkably, Park and his colleagues had not calculated an odds ratio for welding tradesmen under age 65 at death compared with non-welding tradesmen under age 65 at death. The table’s legend attempts to explain the authors’ calculation:

“Adjusted for age, race, gender, region and SES. Model contains multiplicative terms for exposure and for exposure if age at death <65; thus MOR is estimate for deaths occurring age 65+, and MOR, age <65 is estimate of enhanced risk: age <65 versus age 65+”

In other words, Park looked to see whether welding tradesmen who died at a younger age (below age 65) were more likely to have a PD cause of death than welding tradesmen who died an older age (over age 65). The meaning of this internal comparison is totally unclear, but it cannot represent a comparison of welder’s with non-welders. Indeed, every time, Park and his colleagues calculated and reported this strange odds ratio for any occupational group in the published paper, the odds ratio was elevated. If the odds ratio means anything, it is that younger Parkinson’s patients, regardless of occupation, are more likely to die of their neurological disease than older patients. Older men, regardless of occupation, are more likely to die of cancer, cardiovascular disease, and other chronic diseases. Furthermore, this age association within (not between) an occupational groups may be nothing other than a reflection of the greater severity of early-onset Parkinson’s disease in anyone, regardless of their occupation.

Like the manuscript by Eisenberg and Wells, the Park paper was an exercise in data dredging. The Park study reported increased odds ratios for Parkinson’s disease among the following groups on the primary analysis:

biological, medical scientists [MOR 2.04 (95% CI, 1.37-2.92)]

clergy [MOR 1.79 (95% CI, 1.58-2.02)]

religious workers [MOR 1.70 (95% CI, 1.27-2.21)]

college teachers [MOR 1.61 (95% CI, 1.39-1.85)]

social workers [MOR 1.44 (95% CI, 1.14-1.80)]

As noted above, the Park paper reported all of the internal mortality odds ratios for below versus above age 65, within occupational groups were nominally statistically significantly elevated. Nonetheless, the Park authors were on a mission, and determined to make something out of nothing, at least when it came to welding and Parkinson’s disease among younger patients. The authors’ conclusion reflected stunningly poor scholarship:

“Studies in the US, Europe, and Korea implicate manganese fumes from arc-welding of steel in the development of a Parkinson’s-like disorder, probably a manifestation of manganism [Sjogren et al., 1990; Kim et al., 1999; Luccini, et al., 1999; Moon et al., 1999]. The observation here that PD mortality is elevated among workers with likely manganese exposures from welding, below age 65 (based on 20 deaths), supports the welding-Parkinsonism connection.”

Park (2005) at 73.

Stunningly bad because the cited papers by Sjogren, Luccini, Kim, and Moon did not examine Parkinson’s disease as an outcome; indeed, they did not even examine a parkinsonian movement disorder. More egregious, however, was the authors’ assertion that their analysis, which compared the odds of Parkinson’s disease mortality between welders under age 65 to that mortality for welders over age 65, supported an association between welding and “Parkinsonism.”

Every time the authors conducted this analysis internal to an occupational group, they found an elevation among under age 65 deaths compared with over age 65 deaths within the occupational group. They did not report comparisons of any age-defined subgroup of a single occupational group with similarly aged mortality in the remaining dataset.

Elan Louis

The plaintiffs’ lawyers used the Park paper as “evidence” of an association that they claimed was causal. They were aided by a cadre of expert witnesses who could cite to a paper’s conclusions, but could not understand its methods. Occasionally, one of the plaintiffs’ expert witnesses would confess ignorance about exactly what Robert Park had done in this paper. Elan Louis, one of the better qualified expert witnesses on the side of claimants, for instance, testified in the plaintiffs’ attempt to certify a national medical monitoring class action for welding tradesmen. His testimony about what to make of the Park paper was more honest than most of the plaintiffs’ expert witnesses:

Q. My question to you is, is it true that that 1.77 point estimate of risk, is not a comparison of this welder and allied tradesmen under this age 65 mortality, compared with non-welders and allied tradesmen who die under age 65?

A. I think it’s not clear that the footnote — I think that the footnote is not clearly written. When you read the footnote, you didn’t read the punctuation that there are semicolons and colons and commas in the same sentence. And it’s not a well constructed sentence. And I’ve gone through this sentence many times. And I’ve gone through this sentence with Ted Eisenberg many times. This is a topic of our discussion. One of the topics of our discussions. And it’s not clear from this sentence that that’s the appropriate interpretation. * * * However, the footnote, because it’s so poorly written, it obscures what he actually did. And then I think it opens up alternative interpretations.

Q. And if we can pursue that for a moment. If you look at other tables for other occupational titles, or exposure related variables, is it true that every time that Mr. Park reports on that MOR age under 65, that the estimate is elevated and statistically significantly so?

A. Yes. And he uses the same footnote every time. He’s obviously cut and paste that footnote every single time, down to the punctuation is exactly the same. And I would agree that if you look for example at table 4, the mortality odds ratios are elevated in that manner for Parkinson’s Disease, with reference to farming, with reference to pesticides, and with reference to farmers excluding horticultural deaths.

Deposition testimony of Elan Louis, at p. 401-04, in Steele v. A. O. Smith Corp., no. 1:03 CV-17000, MDL 1535 (Jan. 18, 2007). Other less qualified, or less honest expert witnesses on the plaintiffs’ side were content to cite Park (2005) as support for their causal opinions.

Meir Stampfer

The empathetic MDL trial judge denied the plaintiffs’ request for class certification in Steele, but individual personal injury cases continued to be litigated. Steele v. A.O. Smith Corp., 245 F.R.D. 279 (N.D. Ohio 2007) (denying class certification); In re Welding Fume Prods. Liab. Litig., No. 1:03-CV-17000, MDL 1535, 2008 WL 3166309 (N.D. Ohio Aug. 4, 2008) (striking pendent state-law class actions claims)

Although Elan Louis was honest enough to acknowledge his own confusion about the Park paper, other expert witnesses continued to rely upon it, and plaintiffs’ counsel continued to cite the paper in their briefs and to use the apparently elevated point estimate for welders in their cross-examinations of defense expert witnesses. With the NCHS data in hand (on a DVD), defense counsel returned to Meir Stampfer, who had helped them unravel the Martin Wells’ litigation analysis. The question for Professor Stampfer was whether Park’s reported point estimate for PD mortality odds ratio was truly a comparison of welders versus non-welders, or whether it was some uninformative internal comparison of younger welders versus older welders.

The one certainty available to the defense is that it had the same dataset that had been used by Martin Wells in the earlier litigation analysis, and now by Robert Park and his colleagues in their published analysis. Using the NCHS dataset, and Park’s definition of a welder or a welding tradesman, Professor Stampfer calculated PD mortality odds ratios for each definition, as well as for each definition for deaths under age 65. None of these analyses yielded statistically significant associations. Park’s curious results could not be replicated from the NCHS dataset.

For welders, the overall PD mortality odds ratio (MOR) was 0.85 (95% CI, 0.77–0.94), for years 1985 through 1999, in the NCHS dataset. If the definition of welders was expanded to including welding tradesmen, as used by Robert Park, the MOR was 0.83 (95% CI, 0.78–0.88) for all years available in the NCHS dataset.

When Stampfer conducted an age-restricted analysis, which properly compared welders or welding tradesmen with non-welding tradesmen, with death under age 65, he similarly obtained no associations for PD MOR. For the years 1985-1991, death under 65 from PD, Stampfer found MORs 0.99 (95% CI, 0.44–2.22) for just welders, and 0.83 (95% CI, 0.48–1.44) all welding tradesmen.

And for 1992-1999, the years used by Park (2005), and similar to the date range used by Martin Wells, for PD deaths at under age 65, for welders only, Stampfer found a MOR of 1.44 (95% CI, 0.79–2.62), and for all welding tradesmen, 1.20 (95% CI, 0.79–1.84)

None of Park’s slicing, dicing, and subgrouping of welding and PD results could be replicated. Although Dr. Stampfer submitted a report in Steele, there remained the problem that Park (2005) was a peer-reviewed paper, and that plaintiffs’ counsel, expert witnesses, and other published papers were citing it for its claimed results and errant discussion. The defense asked Dr. Stampfer whether the “least publishable unit” had been achieved, and Stampfer reluctantly agreed. He wrote up his analysis, and published it in 2009, with an appropriate disclosure⁶. Meir J. Stampfer, “Welding Occupations and Mortality from Parkinson’s Disease and Other Neurodegenerative Diseases Among United States Men, 1985–1999,” 6 J. Occup. & Envt’l Hygiene 267 (2009).

Professor Stampfer’s paper may not be the most important contribution to the epidemiology of Parkinson’s disease, but it corrected the distortions and misrepresentations of data in Robert Park’s paper. His paper has since been cited by well-known researchers in support of their conclusion that there is no association between welding and Parkinson’s disease⁷. Park’s paper has been criticized on PubPeer, with no rebuttal⁸.

Almost comically, Park has cited Stampfer’s study tendentiously for a claim that there is a healthy worker bias present in the available epidemiology of welding and PD, without noting, or responding to, the devastating criticism of his own Park (2005) work:

“For a mortality study of neurodegenerative disease deaths in the United States during 1985 – 1999, Stampfer [61] used the Cause of Death database of the US National Center for Health Statistics and observed adjusted mortality odds ratios for PD of 0.85 (95% CI, 0.77 – 0.94) and 0.83 (95% CI, 0.78 – 0.88) in welders, using two definitions of welding occupations [61]. This supports the presence of a significant HWE [healthy worker effect] among welders. An even stronger effect was observed in welders for motor neuron disease (amyotrophic lateral sclerosis, OR 0.71, 95% CI, 0.56 – 0.89), a chronic condition that clearly would affect welders’ ability to work.”

Robert M. Park, “Neurobehavioral Deficits and Parkinsonism in Occupations with Manganese Exposure: A Review of Methodological Issues in the Epidemiological Literature,” 4 Safety & Health at Work 123, 126 (2013). Amyotrophic lateral sclerosis has a sudden onset, usually in middle age, without any real prodomal signs or symptoms, which would keep a young man from entering welding as a trade. Just shows you can get any opinion published in a peer-reviewed journal, somewhere. Stampfer’s paper, along with Mortimer’s meta-analysis helped put the kabosh on welding fume litigation.

Addendum

A few weeks ago, the Sixth Circuit affirmed the dismissal of a class action that was attempted based upon claims of environmental manganese exposure. Abrams v. Nucor Steel Marion, Inc., Case No. 3:13 CV 137, 2015 WL 6872511 (N. D. Ohio Nov. 9, 2015) (finding testimony of neurologist Jonathan Rutchik to be nugatory, and excluding his proffered opinions), aff’d, 2017 U.S. App. LEXIS 9323 (6th Cir. May 25, 2017). Class plaintiffs employed one of the regulators, Jonathan Rutchik, from the welding fume parkinsonism litigation).

1 See “Samuel Tarry’s Protreptic for Litigation-Sponsored Publications” (July 9, 2017).

2 Samuel L. Tarry, Jr., “Can Litigation-Generated Science Promote Public Health?” 33 Am. J. Trial Advocacy 315 (2009)

3 Ostensibly, but not really. Robert M. Park was an employee of NIOSH, but he had spent most of his career working as an employee for the United Autoworkers labor union. The paper acknowledged help from Ed Baker, David Savitz, and Kyle Steenland. Baker is a colleague and associate of B.S. Levy, who was an expert witness for plaintiffs in the welding fume litigation, as well as many others. The article was published in the “red” journal, the American Journal of Industrial Medicine.

4 The welding tradesmen included in the analyses were welders and cutters, boilermakers, structural metal workers, millwrights, plumbers, pipefitters, and steamfitters. Robert M. Park, Paul A. Schulte, Joseph D. Bowman, James T. Walker, Stephen C. Bondy, Michael G. Yost, Jennifer A. Touchstone, and Mustafa Dosemeci, “Potential Occupational Risks for Neurodegenerative Diseases,” 48 Am. J. Ind. Med. 63, 65a, ¶2 (2005).

5 Id.

6 “The project was supported in part through a consulting agreement with a group of manufacturers of welding consumables who had no role in the analysis, or in preparing this report, did not see any draft of this manuscript prior to submission for publication, and had no control over any aspect of the work or its publication.” Stampfer, at 272.

7 Karin Wirdefeldt, Hans-Olov Adami, Philip Cole, Dimitrios Trichopoulos, and Jack Mandel, “Epidemiology and etiology of Parkinson’s disease: a review of the evidence,” 26 Eur. J. Epidemiol. S1 (2011).

8 The criticisms can be found at <https://pubpeer.com/publications/798F9D98B5D2E5A832136C0A4AD261>, last visited on July 10, 2017.

Posted in Scientific Evidence, Scientific Publishing, statistical evidence, Underlying Data | Comments Off on Welding Litigation – Another Positive Example of Litigation-Generated Science

Slemp Trial Part 3 – The Defense Expert Witness – Huh

July 9th, 2017

On June 19, 2017, the U.S. Supreme Court curtailed the predatory jurisdictional practices of the lawsuit industry in seeking out favorable trial courts with no meaningful connection to their claims. See Bristol-Myers Squib Co. v. Superior Court, No. 16-466, 582 U.S. ___ (June 19, 2017). The same day, the defendants in a pending talc cancer case in St. Louis filed a motion for a mistrial. Swann v. Johnson & Johnson, Case No. 1422-CC09326-01, Division 10, Circuit Court of St. Louis City, Missouri. Missouri law may protect St. Louis judges from having to get involved in gatekeeping scientific expert witness testimony, but when the Supreme Court speaks to the requirements of the federal constitution’s due process clause, even St. Louis judges must listen. Bristol-Myers held that the constitution limits the practice of suing defendants in jurisdictions unrelated to the asserted claims, and the St. Louis trial judge, Judge Rex Burlison, granted the requested mistrial in Swann. As a result, there will not be another test of plaintiffs’ claims that talc causes ovarian cancer, and the previous Slemp case will remain an important event to interpret.

The Sole Defense Expert Witness

Previous posts¹ addressed some of the big picture issues as well as the opening statements in Slemp. This posts turns to the defense expert witness, Dr. Walter Huh, in an attempt to understand how and why the jury returned its egregious verdict. Juries can, of course, act out of sympathy, passion, or prejudice, but their verdicts are usually black boxes when it comes to discerning their motivations and analyses. A more interesting and fruitful exercise is to ask whether a reasonable jury could have reached the conclusion in the case. The value of this exercise is limited, however. A reasonable jury should have reasonable expertise in the subject matter, and in our civil litigation system, this premise is usually not satisfied.

Dr. Walter Huh, a gynecologic oncologist, was the only expert witness who testified for the defense. As the only defense witness, and as a clinician, Huh had a terrible burden. He had to meet and rebut testimony outside his fields of expertise, including pathology, toxicology, and most important, epidemiology. Huh was by all measures well-spoken, articulate, and well-qualified as a clinical gynecologic oncologist. Defense counsel and Huh, however, tried to make the case that Huh was qualified to speak to all issues in the case. The initial examination on qualifications was long and tedious, and seemed to overcompensate for the obvious gaps in Dr. Huh’s qualifications. In my view, the defense never presented much in the way of credible explanations about where Huh had obtained the training, experience, and expertise to weigh in on areas outside clinical medicine. Ultimately, the cross-examination is the crucial test of whether this strategy of one witness for all subjects can hold. The cross-examination of Dr. Huh, however, exposed the gaps in qualifications, and more important, Dr. Huh made substantive errors that were unnecessary and unhelpful to the defense of the case.

The defense pitched the notion that Dr. Huh somehow trumped all the expert witnesses called by plaintiff because Huh was the “only physician heard by the jury” in court. Somehow, I wonder whether the jury was so naïve. It seems like a poor strategic choice to hope that the biases of the jury in favor of the omniscience of physicians (over scientists) will carry the day.

There were, to be sure, some difficult clinical issues, on which Dr. Huh could address within his competence. Cancer causation itself is a multi-disciplinary science, but in the case of a disease, such as ovarian cancer, with a substantial base-rate in the general population and without any biomarker of a causal pathway between exposure and outcome, epidemiology will be a necessary tool. Huh was thus forced to “play” on the plaintiffs’ expert witnesses’ home court, much to his detriment.

General Causation

Don’t confuse causation with links, association, and risk factors

The defense strong point is that virtually no one, other than the plaintiffs’ expert witnesses themselves, and only in the context of litigation, has causally attributed ovarian cancer to talc exposure. There are, however, some ways that this point can be dulled in the rough and tumble of trial. Lawyers, like journalists, and even some imprecise scientists, use a variety of terms such as “risk,” “risk factor,” “increased risk,” and “link,” for something less than causation. Sometimes these terms are used deliberately to try to pass off something less than causation as causation; sometimes the speaker is confused; and sometimes the speaker is simply being imprecise. It seems incumbent upon the defense to explain the differences between and among these terms, and to stick with a consistent, appropriate terminology.

One instance in which Dr. Huh took his eye off the “causation ball,” arose when plaintiffs’ counsel showed him a study conclusion that talc use among African American women was statistically significantly associated with ovarian cancer. Huh answered, non-responsively, “I disagree with the concept that talc causes ovarian cancer.” The study, however, did not advance a causal conclusion and there was no reason to suggest to the jury that he disagreed with anything in the paper; rather it was the opportunity to repeat that association is not causation, and the article did not contradict anything he had said.

Similarly, Dr. Huh was confronted with several precautionary recommendations that women “may” benefit from avoiding talc. Remarkably, Huh simply disagreed, rather than making the obvious point that the recommendation was not stated as something that would in fact benefit women.

When witnesses answer long, involved questions, with a simple “yes,” then they may have made every implied proposition in the questions into facts in the case. In an exchange between plaintiff’s counsel and Huh, counsel asked whether a textbook listed talc as a risk factor.² Huh struggled to disagree, which disagreement tended to impair his credibility, for disagreeing with a textbook he acknowledged using and relying upon. Disagreement, however, was not necessary; the text merely stated that “talc … may increase risk.” If “increased risk” had been defined and explained as something substantially below causation, then Huh could have answered simply “yes, but that quotation does not support a causal claim.”

At another point, plaintiffs’ counsel, realizing that none of the individual studies reached a causal conclusion, asked whether it would be improper for a single study to give such a conclusion. It was a good question, with a solid premise, but Dr. Huh missed the opportunity for explaining that the authors of all the various individual studies had not conducted systematic reviews that advanced the causal conclusion that plaintiffs would need. Certainly, the authors of individual studies were not prohibited from taking the next step to advance a causal conclusion in a separate paper with the appropriate analysis.

Bradford Hill’s Factors

Dr. Huh’s testimony provided the jury with some understanding of Sir Austin Bradford Hill’s nine factors, but Dr. Huh would have helped himself by acknowledging several important points. First, as Hill explained, the nine factors are invoked only after there is a clear-cut (valid) association beyond that which we care to attribute to chance. Second, establishing all nine factors is not necessary. Third, some of the nine factors are more important than others.

Study validity

In the epidemiology of talc and ovarian cancer, statistical power and significance are not the crucial issues; study validity is. It should have been the plaintiff’s burden to rule out bias, and confounding, as well as chance. Hours had passed in the defense examination of Dr. Huh before study validity was raised, and it was never comprehensively explained. Dr. Huh explained recall bias as a particular problem of case-control studies, which made up the bulk of evidence upon which plaintiffs’ expert witnesses relied. A more sophisticated witness on epidemiology might well have explained that the selection of controls can be a serious problem without obvious solutions in case-control studies.

On cross-examination, plaintiffs’ counsel, citing Kenneth Rothman, asked whether misclassification bias always yields a lower risk ratio. Dr. Huh resisted with “not necessarily,” but failed to dig in whether the conditions for rejecting plaintiffs’ generalization (such as polychotomous exposure classification) obtained in the relevant cohort studies. More importantly, Huh missed the opportunity to point out that the most recent, most sophisticated cohort study reported a risk ratio below 1.0, which on the plaintiffs’ theory about misclassification would have been even lower than 1.0 than reported in the published paper. Again, a qualified epidemiologist would not have failed to make these points.

Dr. Huh never read the testimony of one of the plaintiffs’ expert witnesses on epidemiology, Graham Colditz, and offered no specific rebuttal of Colditz’s opinions. With respect to the other of plaintiffs’ epidemiology expert witness, Dr. Cramer, Huh criticized him for engaging in post-hoc secondary analyses and asserted that Cramer’s meta-analysis could not be validated. Huh never attempted to validate the meta-analysis himself; nor did Huh offer his own meta-analysis or explain why a meta-analysis of seriously biased studies was unhelpful. These omissions substantially blunted Huh’s criticisms.

On the issue of study validity, Dr. Huh seem to intimate that cohort studies were necessarily better than case-control studies because of recall bias, but also because there are more women involved in the cohort studies than in the case-control studies. The latter point, although arithmetically correct, is epidemiologically bogus. There are often fewer ovarian cancer cases in the cohort study, especially if the cohort is not followed for a very long time. The true test comes in the statistical precision of the point estimate, relative risk or odds ratio, in the different type of study. The case-control studies often generate much more precise point estimates as seen from their narrower confidence intervals. Of course, the real issue is not precision here, but accuracy. Still, Dr. Huh appeared to have endorsed the defense counsel misleading argument about study size, a consideration that will not help the defense when the contentions of the parties are heard in scientific fora.

Statistical Significance

Huh appeared at times to stake out a position that if a study does not have statistical significance, then we must accept the null hypothesis. I believe that most careful scientists would reject this position. Null studies simply fail to reject the null hypothesis.

Although there seems to be no end to fallacious reasoning by plaintiffs, there is a particular defense fallacy seen in some cases that turn on epidemiology. What if we had 10 studies that each found an elevated risk ratio of 1.5, with two-tailed 95 percent confidence intervals of 0.92 – 2.18, or so. Can the defense claim victory because no study is statistically significant? Huh seemed to suggest so, but this is clearly wrong. Of course, we might ask why no one conducted the 11^th study, with sufficient power to detect a risk ratio of 1.5, at the desired level of significance. But parties go to trial with the evidence they have, not what they might want to have. On the above 10-study hypothetical, a meta-analysis might well be done (assuming the studies could be appropriately included), and the summary risk ratio for all studies would be 1.5, and highly statistically significant.

On the question of talc and ovarian cancer, there were several meta-analyses at issue, and so the role of statistical significance of individual studies was less relevant. The real issue was study validity. This issue was muddled by assertions that risk ratios such as 2.05 (95%, 0.94 – 4.47) were “chance findings.” Chance may not have been ruled out, but the defense can hardly assert that chance and chance alone produced the findings; otherwise, it will be sunk by the available meta-analyses.

Strength of Association

The risk ratios involved in most of the talc ovarian cancer studies are small, and that is obviously an important factor to consider in evaluating the studies for causal conclusions. Still, it is also obvious that sometimes real causal associations can be small in magnitude. Dr Huh could and should have conceded in direct that small associations can be causal, but explained that validity concerns about the studies that show small associations become critical. Examples would have helped, such as the body of observational epidemiology that suggested that estrogen replacement therapy in post-menopausal women provided cardiovascular benefit, only to be reversed by higher quality clinical trials. Similarly, observational studies suggested that lung cancer rates were reduced by Vitamin A intake, but again clinical trial data showed the opposite.

Consistency of Studies

Are studies that have statistically non-significant risk ratios above 1.0 inconsistent with studies that find statistically significant elevated risk ratios? At several points, Huh appears to say that such a group of studies is inconsistent, but that is not necessarily so. Huh’s assertion provoked a good bit of harmful cross-examination, in which he seemed to resist the notion that meta-analysis could help answer whether a group of studies is statistically consistent. Huh could have conceded the point readily but emphasized that a group of biased studies would give only a consistently biased estimate of association.

Authority

One of the cheapest tricks in the trial lawyers’ briefcase is the “learned treatise” exception to the rule against hearsay.”³ The lawyer sets up witnesses in deposition by obtaining their agreement that a particular author or text is “authoritative.” Then at trial, the lawyer confronts the witnesses with a snippet of text, which appears to disagree with the expert witnesses’ testimony. Under the rule, in federal and in some state courts, the jury may accept the snippet or sound bite as true, and also accept that the witnesses do not know what they are talking about when they disagree with the “authoritative” text.

The rule is problematic and should have been retired long ago. Since 1663, the Royal Society has sported the motto: “Nullius in verba.” Disputes in science are resolved with data, from high-quality, reproducible experimental or observational studies, not with appeals to the prestige of the speaker. And yet, we lawyers will try, and sometimes succeed, with this greasy kidstuff approach cross-examination. Indeed, when there is an opportunity to use it, we may even have an obligation to use so-called learned treatises to advance our clients’ cause.

In the Slemp trial, the plaintiff’s counsel apparently had gotten a concession from Dr. Huh that plaintiff’s expert witness on epidemiology, Dr. Daniel Cramer, was “credible and authoritative.” Plaintiff’s counsel then used Huh’s disagreement with Cramer’s testimony as well as his published papers to undermine Huh’s credibility.

This attack on Huh was a self-inflicted wound. The proper response to a request for a concession that someone or some publication is “authoritative,” is that this word really has no meaning in science. “Nullius in verba,” and all that. Sure, someone can be a respected research based upon past success, but past performance is no guarantee of future success. Look at Linus Pauling and Vitamin C. The truth of a conclusion rests on the data and the soundness of the inferences therefrom.

Collateral Attacks

The plaintiff’s lawyer in Slemp was particularly adept at another propaganda routine – attacking the witness on the stand for having cited another witness, whose credibility in turn was attacked by someone else, even if that someone else was a crackpot. Senator McCarthy (Joseph not Eugene) would have been proud of plaintiff’s lawyer’s use of the scurrilous attack on Paolo Boffetta for his views on EMF and cancer, as set out in Microwave News, a fringe publication that advances EMF-cancer claims. Now, the claim that non-ionizing radiation causes cancer has not met with much if any acceptance, and Boffetta’s criticisms of the claims are hardly unique or unsupported. Yet plaintiff’s counsel used this throw-away publication’s characterization of Boffetta as “the devil’s advocate,” to impugn Boffetta’s publications and opinions on EMF, as well as Huh’s opinions that relied upon some aspect of Boffetta’s work on talc. Not that “authority” counts, but Boffetta is the Associate Director for Population Sciences of the Tisch Cancer Institute and Chief of the Division of Cancer Prevention and Control of the Department of Oncological Sciences, at the Mt. Sinai School of Medicine in New York. He has published many epidemiologic studies, as well as a textbook on the epidemiology of cancer.⁴

The author from the Microwave News was never identified, but almost certainly lacks the training, experience, and expertise of Paolo Boffetta. The point, however, is that this cross-examination was extremely collateral, had nothing to do with Huh, or the issues in the Slemp case, and warranted an objection and admonition to plaintiff’s counsel for the scurrilous attack. An alert trial judge, who cared about substantial justice, might have shut down this frivolous, highly collateral attack, sua sponte. When Huh was confronted with the “devil’s advocate” characterization, he responded “OK,” seemingly affirming the premise of the question.

Specific Causation

Dr. Huh and the talc defendants took the position that epidemiology never informs assessment of individual causation. This opinion is hard to sustain. Elevated risk ratios reflect more individual cases than expected in a sample. Epidemiologic models are used to make individual predictions of risk for purposes of clinical monitoring and treatment. Population-based statistics are used to define range of normal function and to assess individuals as impaired or disabled, or not.

At one point in the cross-examination, plaintiffs’ counsel suggested the irrelevance of the size of relative risk by asking whether Dr. Huh would agree that a 20% increased risk was not small if you are someone who has gotten the disease. Huh answered “Well, if it is a real association.” This answer fails on several levels. First, it conflates “increased risk” and “real association” with causation. The point was for Huh to explain that an increased risk, if statistically significant, may be an association, but it is not necessary causal.

Second, and equally important, Huh missed the opportunity to explain that even if the 20% increased risk was real and causal, it would still mean that an individual patient’s ovarian cancer was most likely not caused by the exposure. See David H. Schwartz, “The Importance of Attributable Risk in Toxic Tort Litigation,” (July 5, 2017).

Conclusion

The defense strategy of eliciting all their scientific and medical testimony from a single witness was dangerous at best. As good a clinician as Dr. Huh appears to be, the defense strategy did not bode well for a good outcome when many of the scientific issues were outside of Dr. Huh’s expertise.

1 “The Slemp Case, Part I – Jury Verdict for Plaintiff – 10 Initial Observations” (May 13, 2017); The Slemp Case, Part 2 – Openings (June 10, 2017).

2 Jonathan S. Berek & Neville F. Hacker, Gynecologic Oncology at 231 (6th ed. 2014).

3 See “Trust-Me Rules of Evidence” (Oct. 18 2012).

4 See, e.g., Paolo Boffetta, Stefania Boccia, Carol La Vecchia, A Quick Guide to Cancer Epidemiology (2014).

Posted in Causation, Meta-analysis, statistical evidence | Comments Off on Slemp Trial Part 3 – The Defense Expert Witness – Huh

Samuel Tarry’s Protreptic for Litigation-Sponsored Publications

July 9th, 2017

Litigation-related research has been the punching bag of self-appointed public health advocates for some time. Remarkably, and perhaps not surprising to readers of this blog, many of the most strident critics have deep ties to the lawsuit industry, and have served the plaintiffs’ bar loyally and zealously for many years.¹^,²^,³^,⁴ And many of these critics have ignored or feigned ignorance of the litigation provenance of much research that they hold dear, such as Irving Selikoff’s asbestos research undertaken for the asbestos workers’ union and its legal advocates. These critics’ campaign is an exquisite study in hypocrisy.

For some time, I have argued that the standards for conflict-of-interest disclosures should be applied symmetrically and comprehensively to include positional conflicts, public health and environmental advocacy, as well as litigation consulting or testifying for any party. Conflicts should be disclosed, but they should not become a facile excuse or false justification for dismissing research, regardless of the party that sponsored it.⁵ Scientific studies should be interpreted scientifically – that is carefully, thoroughly, and rigorously – regardless whether they are conducted and published by industry-sponsored, union-sponsored, or Lord help us, even lawyer-sponsored scientists.

Several years ago, a defense lawyer, Samuel Tarry, published a case series of industry-sponsored research or analysis, which grew out of litigation, but made substantial contributions to the scientific understanding of claimed health risks. See Samuel L. Tarry, Jr., “Can Litigation-Generated Science Promote Public Health?” 33 Am. J. Trial Advocacy 315 (2009). Tarry’s paper is a helpful corrective to the biased (and often conflicted) criticisms of industry-sponsored research and analysis by the lawsuit industry and its scientific allies and consultants. It an ocean of uninformative papers about “Daubert,” Tarry’s paper stands out and should be required reading for all lawyers who practice in the area of “health effects litigation.”

Tarry presented a brief summary of the litigation context for three publications that deserve to remembered and used as exemplars of important, sound, scientific publications that helped changed the course of litigations, as well as the scientific community’s appreciation of prior misleading contentions and publications. His three case studies grew out of the silicone-gel breast implant litigation, the latex allergy litigation, and the never-ending asbestos litigation.

1. Silicone

There are some glib characterizations of the silicone gel breast implant litigation as having had no evidentiary basis. A more careful assessment would allow that there was some evidence, much of it fraudulent and irrelevant. See, e.g., Hon. Jack B. Weinstein, “Preliminary Reflections on Administration of Complex Litigation” 2009 Cardozo L. Rev. de novo 1, 14 (2009) (describing plaintiffs’ expert witnesses in the silicone gel breast implant litigation as “charlatans” and the litigation as largely based upon fraud). The lawsuit industry worked primarily through so-called support groups, which in turn funded friendly, advocate physicians, who in turn testified for plaintiffs and their lawyers in personal injury cases.

When the defendants, such as Dow Corning, reacted by sponsoring serious epidemiologic analyses of the issue whether exposure to silicone gel was associated with specific autoimmune or connective tissue diseases, the plaintiffs’ bar mounted a conflict-of-interest witch hunt over industry funding.⁶ Ultimately, the source of funding became obviously irrelevant; the concordance between industry-funded and all high quality research on the litigation claims was undeniable. Obvious that is to court-appointed expert witnesses⁷, and to a blue-ribbon panel of experts in the Institute of Medicine⁸.

2. Latex Hypersensitivity

Tarry’s second example comes from the latex hypersensitivity litigation. Whatever evidentiary basis may have existed for isolated cases of latex allergy, the plaintiffs’ bar had taken and expanded into a full-scale mass tort. A defense expert witness, Dr. David Garabrant, a physician and an epidemiologist, published a meta-analysis and systematic review of the extant scientific evidence. David H. Garabrant & Sarah Schweitzer, “Epidemiology of latex sensitization and allergies in health care workers,” 110 J. Allergy & Clin. Immunol. S82 (2002). Garabrant’s formal, systematic review documented his litigation opinions that the risk of latex hypersensitivity was much lower than claimed and not the widespread hazard asserted by plaintiffs and their retained expert witnesses. Although Garabrant’s review did not totally end the litigation and public health debate about latex, it went a long way toward ending both.

3. Fraudulent Asbestos-Induced Radiography

I still recall, sitting at my desk, my secretary coming into my office to tell me excitedly that a recent crop of silicosis claimants had had previous asbestosis claims. When I asked how she knew, she showed me the computer print out for closed files for another client. Some of the names were so distinctive that the probability that there were two men with the same name was minuscule. When we obtained the closed files from storage, sure enough, the social security numbers matched, as did all other pertinent data, except that what had been called asbestosis previously was now called silicosis.

My secretary’s astute observation was mirrored in the judicial proceedings of Judge Janis Graham Jack, who presided over MDL 1553. Judge Jack, however, discovered something even more egregious: in some cases, a single physician interpreted a single chest radiograph as showing either asbestosis or silicosis, but not both. The two, alternative diagnoses were recorded in two, separate reports, for two different litigation cases against different defendants. This fraudulent practice, as well as others, are documented in Judge Jack’s extraordinary, thorough opinion. See In re Silica Prods. Liab. Litig., 398 F. Supp. 2d 563 (S.D. Tex. 2005)⁹.

The revelations of fraud in Judge Jack’s opinion were not entirely surprising. As everyone involved in asbestos litigation has always known, there is a disturbing degree of subjectivity in the interpretation of chest radiographs for pneumoconiosis. The federal government has long been aware of this problem, and through the Centers for Disease Control and the National Institute of Occupational Safety and Health, has tried to subdue extreme subjectivity by creating a pneumoconiosis classification schemed for chest radiographs known as the “B-reader” system. Unfortunately, B-reader certification meant only that physicians could achieve inter-observer and intra-observer reproducibility of interpretations on the examination, but they were free to peddle extreme interpretations for litigation. Indeed, the B-reader certification system exacerbated the problem by creating a credential that was marketed to advance the credibility of some of the most biased, over-reading physicians in asbestos, silica, and coal pneumoconiosis litigation.

Tarry’s third example is a study conducted under the leadership of the late Joseph Gitlin, at Johns Hopkins Medical School. With funding from defendants and insurers, Dr. Joseph Gitlin conducted a concordance study of films that had been read by predatory radiologists and physicians as showing pneumoconiosis. The readers in his study found a very low level of positive films (less than 5%), despite their having been interpreted as showing pneumoconiosis by the litigation physicians. See Joseph N. Gitlin, Leroy L. Cook, Otha W. Linton, and Elizabeth Garrett-Mayer, “Comparison of ‘B’ Readers’ Interpretations of Chest Radiographs for Asbestos Related Changes,” 11 Acad. Radiol. 843 (2004); Marjorie Centofanti, “With thousands of asbestos workers demanding compensation for lung disease, a radiology researcher here finds that most cases lack merit,” Hopkins Medicine (2006). As with the Sokol hoax, the practitioners of post-modern medicine cried “foul,” and decried industry sponsorship, but the disparity between courtroom and hospital medicine was sufficient proof for most disinterested observers that there was a need to fix the litigation process.

Meretricious Mensuration¹⁰ – Manganese Litigation Example

Tarry’s examples are important reminders that corporate sponsorship, whether from the plaintiffs’ lawsuit industry or from manufacturing industry, does not necessarily render research tainted or unreliable. Although lawyers often confront exaggerated or false claims, and witness important, helpful correctives in the form of litigation-sponsored studies, the demands of legal practice and “the next case” typically prevent lawyers from documenting the scientific depredations and their rebuttals. Sadly, unlike litigations such as those involving Bendectin and silicone, the chronicles of fraud and exaggeration are mostly closed books in closed files in closed offices. These examples need the light of day and a fresh breeze to disseminate them widely in both the scientific and legal communities, so that all may have a healthy appreciation for the value of appropriately conducted studies generated in litigation contexts.

As I have intimated elsewhere, the welding fume litigation is a great example of specious claiming, which ultimately was unhorsed by publications inspired or funded by the defense. In the typical welding fume case, plaintiff claimed that exposure to manganese in welding fume caused Parkinson’s disease or manganism. Although manganism sounds as though it must be a disease that can be caused only by manganese, in the hands of plaintiffs’ expert witnesses, manganism became whatever ailment plaintiffs claimed to have suffered. Circularity and perfect definitional precision were achieved by semantic fiat.

The Sanchez-Ramos Meta-Analysis

Manganese Madness was largely the creation of the Litigation Industry, under the dubious leadership of Dickie Scruggs & Company. Although the plaintiffs enjoyed a strong tail wind in the courtroom of an empathetic judge, they had difficulties in persuading juries and ultimately decamped from MDL 1535, in favor of more lucrative targets. In their last hurrah, however, plaintiffs retained a neurologist, Juan Sanchez-Ramos, who proffered a biased, invalid synthesis, which he billed as a meta-analysis¹¹.

Sanchez-Ramos’s meta-analysis, such as it was, provoked professional disapproval and criticism from the defense expert witness, Dr. James Mortimer. Because the work product of Sanchez-Ramos was first disclosed in deposition, and not in his Rule 26 report, Dr. Mortimer undertook belatedly a proper meta-analysis.¹² Even though Dr. Mortimer’s meta-analysis was done in response to the Sanchez-Ramos’s improper, tardy disclosure, the MDL judge ruled that Mortimer’s meta-analysis was too late. The effect, however, of Mortimer’s meta-analysis was clear in showing that welding had no positive association with Parkinson’s disease outcomes. The MDL 1535 resolved quickly thereafter, and with only slight encouragement, Dr. Mortimer published a further refined meta-analysis with two other leading neuro-epidemiologists. See James Mortimer, Amy Borenstein, and Lorene Nelson, “Associations of welding and manganese exposure with Parkinson disease: Review and meta-analysis,” 79 Neurology 1174 (2012). See also “Manganese Meta-Analysis Further Undermines Reference Manual’s Toxicology Chapter” (Oct. 15, 2012).

1 See, e.g., David Michaels & Celeste Monforton, “Manufacturing Uncertainty Contested Science and the Protection ofthe Public’s Health and Environment,” 95 Am. J. Pub. Health S39, S40 (2005); David Michaels & Celeste Monforton, “How Litigation Shapes the Scientific Literature: Asbestos and Disease Among Automobile Mechanics,” 15 J. L. & Policy 1137, 1165 (2007). Michaels had served as a plaintiffs’ paid expert witness in chemical exposure litigation, and Monforton had been employed by labor unions before these papers were published, without disclosure of conflicts.

2 Leslie Boden & David Ozonoff, “Litigation-Generated Science: Why Should We Care?” 116 Envt’l Health Persp. 121, 121 (2008) (arguing that systematic distortion of the scientific record will result from litigation-sponsored papers even with disclosure of conflicts of interest). Ozonoff had served as a hired plaintiffs’ expert witnesses on multiple occasion before the publication of this article, which was unadorned by disclosure.

3 Lennart Hardell, Martin J. Walker, Bo Walhjalt, Lee S. Friedman, and Elihu D. Richter, “Secret Ties to Industry and Conflicting Interest in Cancer Research,” 50 Am. J. Indus. Med. 227, 233 (2007) (criticizing “powerful industrial interests” for “undermining independent research on hazard and risk,” in a “red” journal that is controlled by allies of the lawsuit industry). Hardell was an expert witness for plaintiffs in mobile phone litigation in which plaintiffs claimed that non-ionizing radiation caused brain cancer. In federal litigation, Hardell was excluded as an expert witness when his proffered opinions were found to be scientifically unreliable. Newman v. Motorola, Inc., 218 F. Supp. 2d. 769, 777 (D. Md. 2002), aff’d, 78 Fed. Appx. 292 (4th Cir. 2003).

4 See David Egilman & Susanna Bohme, “IJOEH and the Critique of Bias,” 14 Internat’l J. Occup. & Envt’l Health 147, 148 (2008) (urging a Marxist critique that industry-sponsored research is necessarily motivated by profit considerations, and biased in favor of industry funders). Although Egilman usually gives a disclosure of his litigation activities, he typically characterizes those activities as having been for both plaintiffs and defendants, even though his testimonial work for defendants is minuscule.

5 Kenneth J. Rothman, “Conflict of Interest: The New McCarthyism in Science,” 269 J. Am. Med. Ass’n 2782 (1993).

6 See Charles H. Hennekens, I-Min Lee, Nancy R. Cook, Patricia R. Hebert, Elizabeth W. Karlson, Fran LaMotte; JoAnn E. Manson, and Julie E. Buring, “Self-reported Breast Implants and Connective- Tissue Diseases in Female Health Professionals: A Retrospective Cohort Study, 275 J. Am. Med. Ass’n 616-19 (1998) (analyzing established cohort for claimed associations, with funding from the National Institutes of Health and Dow Corning Corporation).

7 See Barbara Hulka, Betty Diamond, Nancy Kerkvliet & Peter Tugwell, “Silicone Breast Implants in Relation to Connective Tissue Diseases and Immunologic Dysfunction: A Report by a National Science Panel to the Hon. Sam Pointer Jr., MDL 926 (Nov. 30, 1998).” The court-appointed expert witnesses dedicated a great deal of their professional time to their task of evaluating the plaintiffs’ claims and the evidence. At the end of the process, they all published their litigation work in leading journals. See Barbara Hulka, Nancy Kerkvliet & Peter Tugwell, “Experience of a Scientific Panel Formed to Advise the Federal Judiciary on Silicone Breast Implants,” 342 New Engl. J. Med. 812 (2000); Esther C. Janowsky, Lawrence L. Kupper., and Barbara S. Hulka, “Meta-Analyses of the Relation between Silicone Breast Implants and the Risk of Connective-Tissue Diseases,” 342 New Engl. J. Med. 781 (2000); Peter Tugwell, George Wells, Joan Peterson, Vivian Welch, Jacqueline Page, Carolyn Davison, Jessie McGowan, David Ramroth, and Beverley Shea, “Do Silicone Breast Implants Cause Rheumatologic Disorders? A Systematic Review for a Court-Appointed National Science Panel,” 44 Arthritis & Rheumatism 2477 (2001).

8 Stuart Bondurant, Virginia Ernster, and Roger Herdman, eds., Safety of Silicone Breast Implants (Institute of Medicine) (Wash. D.C. 1999).

9 See also Lester Brickman, “On the Applicability of the Silica MDL Proceeding to Asbestos Litigation, 12 Conn. Insur. L. J. 289 (2006); Lester Brickman, “Disparities Between Asbestosis and Silicosis Claims Generated By Litigation Screenings and Clinical Studies,” 29 Cardozo L. Rev. 513 (2007).

10 This apt phraseology is due to the late Keith Morgan, whose wit, wisdom, and scientific acumen are greatly missed. See W. Keith C. Morgan, “Meretricious Mensuration,” 6 J. Eval. Clin. Practice 1 (2000).

11 See Deposition of Dr. Juan Sanchez-Ramos, in Street v. Lincoln Elec. Co., Case No. 1:06-cv-17026, 2011 WL 6008514 (N.D. Ohio May 17, 2011).

12 See Deposition of Dr. James Mortimer, in Street v. Lincoln Elec. Co., Case No. 1:06-cv-17026, 2011 WL 6008054 (N.D. Ohio June 29, 2011).

Posted in Asbestos, Causation, Conflicts of Interest, Meta-analysis, Rule 702, Scientific Evidence, Scientific Misconduct | Comments Off on Samuel Tarry’s Protreptic for Litigation-Sponsored Publications

Every Time a Bell Rings

July 1st, 2017

“Every time a bell rings, an angel gets his wings.”
Zuzu Bailey

And every time a court issues a non-citable opinion, a judge breaks fundamental law. Whether it wants to or not, a common law court, in deciding a case, creates precedent, and an expectation and a right that other, similarly situated litigants will be treated similarly. Deciding a case and prohibiting its citation deprives future litigants of due process and equal protection of the law. If that makes for more citable opinions, more work for judges and litigants, so be it; that is what our constitution requires.

Back in 2015, Judge Bernstein issued a ruling in a birth defects case in which the mother had claimed to have taken sertraline during pregnancy and this medication use caused her child to be born with congenital malformations. Applying what Pennsylvania courts insist is a Frye standard, Judge Bernstein excluded the proffered expert witness testimony that attempted to draw a causal connection between the plaintiff’s birth defect and the mother’s medication use. Porter v. SmithKline Beecham Corp., No. 03275, 2015 WL 5970639 (Phila. Cty. Pennsylvania, Ct. C.P. October 5, 2015) (Mark I. Bernstein, J.) Judge Bernstein has since left the bench, but he was and is a respected commentator on Pennsylvania evidence¹, even if he was generally known for his pro-plaintiff views on many legal issues. Bernstein’s opinion in Porter was a capable demonstration of how Pennsylvania’s Frye rule can be interpreted to reach essentially the same outcome that is required by Federal Rule of Evidence 702. See “Demonstration of Frye Gatekeeping in Pennsylvania Birth Defects Case” (Oct. 6, 2015); In re Zoloft Prod. Liab. Litig., No. 16-2247 , __ F.3d __, 2017 WL 2385279 , 2017 U.S. App. LEXIS 9832 (3d Cir. June 2, 2017) (affirming exclusion of dodgy statistical analyses and opinions, and the trial court’s entry of summary judgment on claims that sertraline causes birth defects).

In May of this year, the Pennsylvania Superior Court affirmed Judge Bernstein’s judgment, and essentially approved and adopted his reasoning. Porter v. SmithKline Beecham Corp., No. 3516 EDA 2015,2017 WL 1902905 (Pa. Super. May 8, 2017). What the Superior Court purport to giveth, the Superior Court taketh away. The Porter decision is franked as a “Non-Precedential Decision – See Superior Court I.O.P. 65.37.”

What is this Internal Operating Procedure that makes the Superior Court think that it can act and decide cases without creating precedent? Here is the relevant text from the Pennsylvania Code:

An unpublished memorandum decision shall not be relied upon or cited by a Court or a party in any other action or proceeding, except that such a memorandum decision may be relied upon or cited

when it is relevant under the doctrine of law of the case, res judicata, or collateral estoppel, and

when the memorandum is relevant to a criminal action or proceeding because it recites issues raised and reasons for a decision affecting the same defendant in a prior action or proceeding.

210 Pa. Code § 65.37. Unpublished Memoranda Decisions. So, in other words, it is secret law.

No citation and no precedent rules are deeply problematic, and have attracted a great deal of scholarly attention². And still, courts engage in this problematic practice. Prohibiting citation of Superior Court decisions in Pennsylvania is especially problematic in a state in which the highest court hears relatively few cases, and where the Justices involve themselves in internecine disputes. As other commentators have noted, prohibiting citation to prior decisions admitting or excluding expert witness testimony stunts the development of an area of evidence law, in which judges and litigants are often confused and in need of guidance. William E. Padgett, “‘Non-Precedential’ Unpublished Decisions in Daubert and Frye Cases, Often Silenced,” Nat’l L. Rev. (2017). The abuses of judge-made secret law from uncitable decisions has been abolished in the federal appeals courts for over a decade³. It is time for the state courts to follow suit.

1 See, e.g., Mark I. Bernstein, Pennsylvania Rules of Evidence (2017).

2 See Erica Weisgerber, “Unpublished Opinions: A Convenient Means to an Unconstitutional End,” 97 Georgetown L.J. 621 (2009); Rafi Moghadam, “Judge Nullification: A Perception of Unpublished Opinions,” 62 Hastings L.J. 1397 (2011); Norman R. Williams, “The failings of Originalism: The Federal Courts and the Power of Precedent,” 37 U.C.. Davis L. Rev.761 (2004); Dione C. Greene, “The Federal Courts of Appeals, Unpublished Decisions, and the ‘No-Citation Rule,” 81 Indiana L.J. 1503 (2006); Vincent M. Cox, “Freeing Unpublished Opinions from Exile: Going Beyond the Citation Permitted by Proposed Federal Rule of Appellate Procedure 32.1,” 44 Washburn L.J. 105 (2004); Sarah E. Ricks, “The Perils of Unpublished Non-Precedential Federal Appellate Opinions: A Case Study of The Substantive Due Process State-Created Danger Doctrine in One Circuit,” 81 Wash. L.Rev. 217 (2006); Michael J. Woodruff, “State Supreme Court Opinion Publication in the Context of Ideology and Electoral Incentives.” New York University Department of Politics (March 2011); Michael B. W. Sinclair, “Anastasoff versus Hart: The Constitutionality and Wisdom of Denying Precedential Authority to Circuit Court Decisions”; Thomas Healy, “Stare Decisis as a Constitutional Requirement,” 104 W. Va. L. Rev. 43 (2001); David R. Cleveland & William D. Bader, “Precedent and Justice,” 49 Duq. L. Rev. 35 (2011); Johanna S. Schiavoni, “Who’s Afraid of Precedent,” 49 UCLA L. Rev. 1859 (2002); Salem M. Katsh and Alex V. Chachkes, “Constitutionality of ‘No-Citation’ Rules,” 3 J. App. Prac. & Process 287 (2001); David R. Cleveland, “Appellate Court Rules Governing Publication, Citation, and Precedent of Opinions: An Update,” 16 J. App. Prac. & Process 257 (2015). See generally The Committee for the Rule of Law (website) (collecting scholarship and news on the issue of unpublished and supposedly non-precedential opinions). The problem even has its own Wikipedia page. See “Non-publication of legal opinions in the United States.”

3 See Fed. R. App. Proc. 32.1 (prohibiting federal courts from barring or limiting citation to unpublished federal court opinions, effective after Jan. 1, 2007).

Posted in Causation, Expert Witnesses, Frye, Rule 702 | Comments Off on Every Time a Bell Rings

Belgian Waffles and Post Hoc Ergo Propter Hoc

June 22nd, 2017

In language that could well be a Sokol hoax on the vacuousness of post-modernist non-thinking, the Court of Justice of the European Union issued a press release to announce its judgment in N.W. v. Sanofi Pasteur MSD, Case C-621/15 (Luxembourg, 21 June 2017). With European hypersensitivity to public disclosure, and in recognition of the right to be forgotten, the plaintiffs are known only as the “W” family. Mr. J. W. received Sanofi’s hepatitis B vaccine between late 1998 and the middle of 1999. In the summer of 1999, Mr. W. began to experience symptoms, which led to a diagnosis of multiple sclerosis over a year later, in November 2000. J.W. and his family sued Sanofi Pasteur in 2006. J.W. died in 2012.

The Ws filed their case in Paris, where the courts found for Sanofi Pasteur. The Cour d’Appel de Paris, impressed by the lack of scientific consensus to support W’s causal claim, held that the plaintiffs had failed to demonstrate causality. The Cour d’Appel de Paris court dismissed the W’s case. The dismissal was remarkable in the context of credulous French courts that had routinely recognized such claims. See C. Rougé-Maillart, N. Guillaume, N. Jousset, and M, Penneau, “Recognition by French courts of compensation for post-vaccination multiple sclerosis: the consequences with regard to expert practice,”47 Med. Sci. Law 185 (2007) (summarizing the course of M.S. and hepatitis B vaccination litigation in France). The Ws appealed further to the French Cour de Cassation (Court of Cassation), which punted to the EU Court of Justice, to ask whether the EU directive on liability for defective products required a different result than handed down by the Cour d’Appel.

The “Court of Justice” stated that the claimants had the burden of proof, but dubiously framed the causation issue as a choice between “certain and irrefutable evidence” and evidence of a “sufficiently high degree of probability.” What gives rise to sufficiently high degree of probability? In bold type, the EU press release announces that:

“Where there is a lack of scientific consensus, the proof of the defect of the vaccine and of a causal link between the defect and the damage suffered may be made out by serious, specific and consistent evidence.”

But what is “serious, specific, and consistent evidence”? Scouring both the press release and the full decision of the Court provides one answer:

Anecdotes. Unspecified number of case reports of multiple sclerosis occurring in patients after vaccination, without regard to an anticipated or expected incidence of the disease in the vaccinated population suffices. The Court of Justice sums up the Ws’ case as a showing that:

“The temporal proximity between the administering of a vaccine and the occurrence of a disease, the lack of personal and familial history of the person vaccinated and the existence of a significant number of reported cases of the disease occurring following such vaccines being administered may, where applicable, constitute sufficient evidence to make out such proof.”

The significant number of cases is never quantified or even described. The “sufficiently high probability” is never quantified or described. Presumably, the judges in Brussels can count, and the probability is some number greater than zero, but less than 1. The Court of Justice follows many other lay courts in falsely dichotomizing scientific disputes as involving either “certain, irrefutable” evidence or something less, and good enough for government (judicial) work. Even its representation of the Ws’ evidence as “serious, specific and consistent” and its suggestion of a “sufficiently high” probability are false, at least without spelling out the evidentiary base of the anecdotal evidence that is elevated to legally sufficient in the eyes of the Court of Justice. The Court fails to acknowledge, as a Court of Justice should, that large, high quality epidemiologic studies fail to find associations between hepatitis B vaccination and multiple sclerosis. See, e.g., Annette Langer-Gould, Lei Qian, Sara Y. Tartof, PhD; Sonu M. Brara, Steve J. Jacobsen, Brandon E. Beaber, Lina S. Sy, Chun Chao, Rulin Hechter, Hung Fu Tseng, “Vaccines and the Risk of Multiple Sclerosis and Other Central Nervous System Demyelinating Diseases,” 71 J. Am. Med. Ass’n Neurol. 1506 (2014); Miguel A. Hernán & Susan S. Jick, “Hepatitis B vaccination and multiple sclerosis: the jury is still out,” 15 Pharmacoepidemiology & Drug Safety 653 (2006).

The European right to be forgotten has apparently been extended to scientific evidence. There may be reasons more legitimate than racist xenophobia to exit the European Union.

Posted in Causation, Scientific Evidence | Comments Off on Belgian Waffles and Post Hoc Ergo Propter Hoc

The Slemp Case, Part 2 – Openings

June 10th, 2017

“The Slemp Case, Part I – Jury Verdict for Plaintiff – 10 Initial Observations” (May 13, 2017)

The legal community is still trying to grasp the enormity of the $110M verdict against Johnson & Johnson, in the Slemp case. J & J says it will appeal, but resolution of legal issues will not necessarily clarify what happened factually in the Slemp case. Some legal commentators have attempted superficial analyses that try to correlate case outcomes with how cases are selected for trial in Missouri. In the five talc trials to date, plaintiffs have prevailed (with fulsome verdicts) in both cases in which plaintiffs’ counsel selected the case for trial. See Amy Rubenstein and Malerie Ma Roddy, “Talc Talk: 1 Of These Verdicts Is Not Like The Others,” Law360 (June 1, 2017). In the three other cases, selected by defense counsel, the defense has lost two of the three cases, again with outlandish verdicts. No statistical analysis of these correlations will suggest that the selection process is correlated with verdict outcome. If there is no general causation, then selection of plaintiff for trial should not correlate with outcome. More important, the Missouri verdicts cannot be reconciled with the ruling by Judge Johnson in the New Jersey talc cases. Carl v. Johnson & Johnson, No. ATL-L-6546-14, 2016 WL 4580145 (N.J. Super. Ct. Law Div., Atl. Cty., Sept. 2, 2016); see also “New Jersey Kemps Ovarian Cancer – Talc Cases” (Sept. 16, 2016).

A manufacturer is legally held to the standard of having expert knowledge of the hazards of a product, and warning about those hazards that are not common knowledge. The conflicts noted above, and the exculpatory views of various professional groups and federal and international agencies should mean, in a sane system of products liability law, that a manufacturer would have no liability in the ovarian cancer – talc cases. A recent review concluded:

“While mechanistic, pathology, and animal studies do not support evidence for the carcinogenicity of talc on the ovarian epithelium 329, epidemiological studies have indicated an association with talc use and increased OC [ovarian cancer] risk.”

Brett M. Reid, Jennifer B. Permuth, Thomas A. Sellers, “Epidemiology of ovarian cancer: a review,” Cancer Biol. Med. 14 (2017). The authors went on, however, to note that the association was not consistently found among studies, and that the IARC had rejected the causal contention as having been shown. How on this evidence, can a manufacturer be held liable for not warning of a causal connection? And how could a manufacturer be found to have acted maliciously or outrageously, with substantial scientific support?

What is needed is careful, detailed evaluation of the actual evidence at trial. The International Agency for Research on Cancer (IARC), the FDA, the NTP, and virtually every other agency and professional group that has addressed the question whether talc causes ovarian cancer, have declared that there is no causal connection established. Have the plantiffs in these cases hit a treasure trove of data not seen by the scientific and regulatory community? Or have plaintiffs exploited the weaknesses of the jury system, and advanced arguments and evidence that would never move a panel of disinterested scientists?

Meaningful analyses of the talc trials are not likely to happen from hipshot commentary. Fortunately, Courtroom View Network videotaped the Slemp trial from openings to return of verdict, which has created a rich resource for lawyers, legal analysts, political scientists, scientists, and regulators to judge the efficacy and content of courtroom presentations of complex scientific evidence.

Less is More, Except When Less is Just Less

There are two common, glib pronouncements you can often hear uttered in defense counsel confabulations. The first is “Less is More.” The second is “Let’s not get into weeds.” These generalizations cannot be tested with jury research in which both sides’ presentations are often no longer than 60 minutes, or so. Actual research of trial research rarely can move beyond anecdotal observations.

In Slemp, the defense case went took up two days. The plaintiffs’ case took 12 days. The plaintiff presented multiple medical expert witnesses, including two epidemiologists who have been involved in studying talc and ovarian cancer, and publishing on the issue, for decades. The defense presented just one expert witness, Dr. Warner Huh, a gynecologic oncologist. Dr. Huh claimed to have epidemiologic expertise by virtue of his work on studies on cervical cancer screening. Dr. Huh, as we will see, never explained how, when, and where he received training in epidemiologic study design and biostatistics. This defense strategy on expert witnesses requires careful analysis. Furthermore, the plaintiffs’ counsel presented a minimally qualified regulatory expert witness to serve primarily as a document reader. The defense effectively cross-examined this witness by showing his ignorance and selectivity in document reading and presentation. J & J, however, never called a fact witness, or corporate witness, to give viva voce testimony, that rebutted the innuendo, defamations, and characterizations of the company by plaintiffs’ counsel.

The Opening “Statements”

Perhaps it is best to begin at the beginning. Voir dire is not available at Courtroom View Network, but the opening statements are on line. There is a widespread myth that Hans Zeisel’s research established that most cases are won in the openings. Zeisel debunked that reading of his work, without disagreeing that the first impressions of opening statement can be powerful. See Hans Zeisel, “A Jury Hoax: The Superpower of the Opening Statement,” 14 Litigation 17 (Summer 1988). Inquiring minds might want to know how the openings statements went for the parties involved in Slemp.

Counsel for the plaintiff and for the two defendants (J & J, Imerys) all gave strong arguments that went well beyond stating what the evidence will show. All counsel worked hard to establish ethos and pathos, but plaintiff’s counsel excelled at creating the appearance of scientific logos, even when there was none. Defense counsel, on the other hand, tried to avoid talking about epidemiology for the most part. When the defense did discuss epidemiology, they made some disturbing, unnecessary mistakes.

Plaintiffs’ Opening

The plaintiff’s opening was noteworthy for its fear mongering. There are some authors who seem to want to take credit for a so-called reptile strategy, but fear mongering has been part of the dark side of rhetoric since at least the dawn of recorded history.¹ Edmund Burke captured the sum and substance of the reptile strategy, which was so much on display in 18^th century politics:

“No passion so effectually robs the mind of all its powers of acting and reasoning as fear.”

Edmund Burke, A Philosophical Inquiry into The Origin of Our Ideas of The Sublime And Beautiful – With Several Other Additions at Sect. II. Terror (1757). Plaintiff’s counsel argued that all women, everywhere [including the women jurors and the male jurors’ female kin] are threatened by the evil corporate behemoth that sells baby powder. Women, everywhere, are developing ovarian cancer by the millions because they have used talcum powder. Only this jury can stop the carnage because regulators have ignored the situation. Regulators and the scientific establishment are venal, and J & J has bought them off. Steve Bannon would be proud.

The plaintiff’s counsel argued that J & J’s talcum powder contains not one, not two, but three carcinogens: talc, asbestos, and heavy metals. Talc, of course, is the focus of the claim and the trial, but what about the other two? Plaintiffs’ counsel did not advert to any evidence or opinion that heavy metals cause ovarian cancer; nor did he even slow down to say what heavy metals he was claiming were present. The evidence that asbestos causes ovarian cancer is perhaps marginally credible, but the causal conclusion is still doubtful. The studies that suggest an association are generally poorly done and heavily confounded. The real issue, however, with the asbestos claim, other than its effectiveness in instilling fear and knee-jerk reactions among lay jurors, is that it obscures an important issue whether the tremolite that sometimes accompanies talc in serpentine rock deposits is actually tremolite asbestos. Tremolite, as a mineral, has numerous crystallogaphic “habits,” including acicular fibers, angular particles, plates, etc.² Some time ago, the federal government adopted a convention of counting anything as a “fiber,” if it were greater than 5 μm in length, and it had an aspect ratio of at least three to one. Another agency, the U.S. EPA adopted a minimal 5:1 aspect ratio, but both federal regulatory definitions disregard both mineralogical and biological considerations for what is a “fiber” with biological effects. Pace Melanie³, a thing is not a phallic system if it is just longer than it is wide, and a tremolite cleavage fragment is not a fiber, even if it is three times longer than wide.

There were other notable rhetorical moves in Plaintiff’s opening statement. In most other litigations, Plaintiffs run away from the need to rule out random error in studies that their expert witnesses proffer as support for causal claims. See, e.g., In re Zoloft (Sertraline Hydrochloride) Products Liability Litigation, U.S. Court of Appeals, 3rd Circuit, No. 16-2247 (June 2, 2017). In doing so, Plaintiffs often distort the consensus views about statistical significance, from the American Statistical Association⁴ and other groups. In the Slemp case, however, Plaintiff’s counsel swung to an opposite extreme by over-endorsing statistical significance as the apparent end-all and be-all for assessing causality. Study validity, whether internal or external, received no serious mention; bias in the studies relied upon was not discussed in any meaningful way.

To highlight the disingenuousness of the Plaintiffs’ opening with respect to failing to consider study validity and bias, and its over-endorsement of statistical significance, the Plaintiff later in the trial flashed sound bites from a report, commissioned by J & J, on the claimed causal connection. The report was by done other than Professor Kenneth Rothman, along with others. Professor Rothman has been in the forefront of criticizing the use of statistical significance testing as a bright-line criterion for causation. Rothman, along with Jonathan Samet (hardly a defense friendly epidemiologist) and Harris Pastides, reported, in 2000, that there was a “statistically significant” association, but demurred on causation because of the problem of study bias and validity:

“A weighted average of the results from epidemiologic studies to date measuring the relation between talc and ovarian cancer risk gives an overall relative risk of 1.31, with a 95% confidence interval of 1.21-1.41. Bias and causation are competing explanations for the weak positive association observed. This weak association could be an underestimate of a stronger association if there are errors in measuring talc exposure that apply uniformly to all study subjects (non-differential misclassification). On the other hand, non-differential misclassification does not bias an association that is null to begin with, so postulating non-differential misclassification cannot shed light on whether the association results from a causal relation or not. Most of the published studies are interview-based case-control studies, subject to recall bias, which can readily give rise to associations of this magnitude. The evidence from these studies regarding recall bias is mixed. Uncontrolled confounding can also easily explain associations this weak; although no single confounding factor would seem to account for the overall effect, the combined effect of several such unidentified confounders could do so. In considering these competing explanations of bias and causation, the evidence in favor of a causal explanation is only the overall weak association of a relative risk of 1.31. The lack of a plausible biologic mechanism, on the other hand, weighs against a causal interpretation. Also weighing against a causal explanation is the dose-response pattern among talc users, which is an inverse trend for both duration of use and frequency of use. A causal relation would predict a positive trend, not an inverse trend. Based on these considerations, we suggest that the evidence to date does not indicate that talc can be ‘reasonably anticipated to be a human carcinogen’.”

Kenneth J. Rothman Harris Pastides Jonathan Samet, “Interpretation of Epidemiologic Studies on Talc and Ovarian Cancer,” (Nov. 28, 2000).

From a rhetorical perspective, one of the more interesting moves in Plaintiff’s opening was a pivot from causation to association. Without ever really discussing the standards or factors for inferring causation, Plaintiff’s counsel invoked regulatory standards and avoided addressing himself to the Missouri standard of causation. The standards for whether to warn and for determining cause in fact were conflated and confused, in what seemed liked a deliberate effort.

Defense Openings

J & J’s Opening

The defense strategies were apparent enough. The defense emphasized that Ms. Slemp had a serous borderline tumor (SBT). The emphasis appeared to be a plea of confession and avoidance. In other words, maybe there is something going on with talc and ovarian cancer, but this is an SBT, and it is different, so you do not need to worry too much about the more general claim that talc causes ovarian cancer. SBTs are a subset of epithelial ovarian tumors, often characterized as semi-malignant, with a more favorable outcome than other ovarian epithelial tumors. The defense also strived to shift the spotlight to Ms. Slemp and her strikingly poor health, preëxisting her cancer diagnosis, as well as her massive obesity and her heavy smoking, both risk factors for ovarian cancer.

On the positive side, J & J’s counsel anticipated and warned the jury that plaintiffs’ expert witnesses would be seriously challenged on their post-hoc analyses and their failing to share their causal conclusions with the scientific community. J & J’s counsel did engage on the general causation claim, but mostly to argue that most governmental agencies and professional organizations have refused to accept the causal claim. To the limited extent that J & J got into the “weeds,” it identified the Bradford Hill factors as the generally accepted decision procedure for reaching causal conclusions. So far, so good (except for the insistence upon referring to Sir Austin as Sir Bradford, as though Bradford was the man’s first name). What defense counsel did not say, astonishingly, is that Sir Austin’s nine factors require a necessary predicate that is satisfied when:

“Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance.”

Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295, 295 (1965). See “Woodside & Davis on the Bradford Hill Considerations” (Aug. 23, 2013). To be sure, there are any number of studies on talc and ovarian cancer that satisfy Hill’s requirement of an association not attributable to the play of chance, but what is lacking is the clear-cut association; that is, the associations that are “statistically significant” have not ruled out bias and confounding. The defense opening did introduce the concept of recall bias, which plays an important part in undermining the validity of the available case-control studies. What the defense did not say, however, is that misclassification biases in cohort studies do not always bias towards the null, and even if they did, then the latest cohort study (with a hazard ratio below 1.0) would have had a risk ratio even lower than 1.0 than what was reported.

The defense did emphasize the absence of the Bradford Hill factors for plausibility and dose response. A more sophisticated analysis would have acknowledged what Sir Austin had over 60 years ago: plausibility or explanation is not necessary to infer causation. Not all the Bradford Hill factors are equal, and the defense diluted the analysis by falsely elevating one factor, plausibility, to the status of a necessary criterion.

The defense opening also had some dubious moves. It deprecated case-control studies as inferior to cohort studies, both as a general proposition and specifically with respect to talc. Case-control studies are generally harder to do, as the Plaintiffs’ bar learned when it based an entire mass tort litigation on a single case-control study, the so-called Yale Hemorrhagic Stroke Project.⁵ The Plaintiffs won the Daubert war⁶ in that litigation, but lost their jury trials because juries ultimately saw the methodological flaws that the MDL court disregarded. The general proposition that cohort studies are always superior to case-control studies, however, is doubtful. The defense did not need to stake out this claim, especially since it was not going to call an epidemiologist to testify.

Some of the claims that the defense committed to in its opening were as stunning as they were dubious. J & J’s counsel promised that he would show that talc has been proven safe. That claim is, however, beyond what the available science can show, especially with a plethora of statistically significant associations in case-control studies. J & J need only show that the plaintiffs’ claim has not been established, but it created an unnecessary burden of proving safety. The rhetorical value of the claim is obvious, but promising to show something that cannot be delivered seems like a recipe for disaster. $110 million is a disaster.

Then there was a defense claim that epidemiology cannot show that talc causes ovarian cancer. The claim was unclear as to whether epidemiology cannot establish general or specific causation, and vague as to whether the inability resulted from the weak, equivocal evidence in the instance of talc and ovarian cancer, or some deeper inability that stems from the nature of the evidence itself. Of course, given that there is an expected base rate of ovarian cancer in the general population, epidemiology will be required, even if it may not be sufficient. But if epidemiology alone is not sufficient, then what else is required? The defense never clarified its claim.

As for specific causation, the notion that epidemiology never informs individual patient predictions or causal assessments seems far fetched. If are dealing with a case of mesothelioma and occupational crocidolite exposure, with relative risks in the thousands, the attribution based upon the existence of a very high relative risk seems eminently reasonable. The same with maternal thalidomide use and an infant’s phocomelia, even though there is a baseline risk of phocomelia. Even in the case of a heavy smoker and lung cancer, with relative risks in the range of 20 to 40, inferring specific causation seems like a sound inference, especially in the absence of evidence that the risk is segregated in some subgroup of the population that suffers the outcome.

Imerys’s Opening

Counsel for Imerys also gave an opening statement, which started on common defense themes of the need to reserve judgment until all evidence is heard, and the need to consider context for statements. Imerys echoed the dubious claims that epidemiology can never inform inferences about individual patients, that epidemiology has determined that talc is safe, that cohort studies are always better than case-control studies, and that cohort studies are better because they have many thousand of women in them as opposed to “just a handful” in case-control studies.

Imerys, however, soon wandered into territory that affirmatively undermined J & J’s defense. First, it applauded itself for having warned of “possible causation,” which tended to concede the point to plaintiffs that there is a duty to warn of possibly caused outcomes. Second, Imerys appropriately urged its bulk supplier defense, which placed the spotlight on J & J’s alleged culpability.

The Imerys lawyer may have offended the Missouri jury by referring to talc as a mineral formed millions of years ago. A large percentage of Americans believe that the Earth was created less than 6,000 years ago. And yet, we still believe that allowing ordinary citizens to decide scientific issues is a good thing!

In its opening, Imerys also misstated the law to its own detriment. In discussing its obligations to warn, Imerys asserted that as a mining company it had to follow the rules established by OSHA. Actually, not. Mining companies are under the jurisdiction of the Mining Safety and Health Administration (MSHA), and OSHA Hazards Communication regulations did not apply to mining companies for the years involved in the Slemp case. See Memorandum from Patricia K. Clark, Director of OSHA Compliance Programs, to Regional Administrators re Hazard Communication and Mining Operations (Mar. 3, 1992).

1 See also Anthony Pratkanis & Elliot Aronson, Age of Propaganda: The Everyday Use and Abuse of Persuasion at 210 (2000) (“[A]ll other things being equal, the more frightened a person is by a communication, the more likely her or she is to take positive preventive action.”); H.L. Mencken, In Defence of Women § 13 “Women and the Emotions” (1923) (“The whole aim of practical politics is to keep the populace alarmed (and hence clamorous to be led to safety) by menacing it with an endless series of hobgoblins, most of them imaginary.”); Conor Boyack, Feardom: How Politicians Exploit Your Emotions and What You Can Do to Stop Them (2014).

2 John W. Anthony, Richard A. Bideaux, Kenneth W. Bladh, and Monte C. Nichols, The Handbook of Mineralogy, vol. II (1995).

3 Melanie Safka, “Psychotherapy” (“A thing is a phallic symbol if it’s longer than it’s wide”).

4 Ronald L. Wasserstein & Nicole A. Lazar, “The ASA’s Statement on p-Values: Context, Process, and Purpose,” The American Statistician, available online (Mar. 7, 2016), in-press at DOI:10.1080/00031305.2016.1154108, <http://dx.doi.org/10.1080/>.

5 Walter N. Kernan, Catherine M. Viscoli, et al., “Phenylpropanolamine and the Risk of Hemorrhagic Stroke,” 343 New Engl. J. Med. 1826 (2000).

6 See In re Phenylpropanolamine Prod. Liab. Litig., 289 F. 2d 1230 (2003).

Posted in Asbestos, Causation, Scientific Evidence | Comments Off on The Slemp Case, Part 2 – Openings

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