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Consensus Rule – Shadows of Validity

April 26th, 2023

Back in 2011, at a Fourth Circuit Judicial Conference, Chief Justice John Roberts took a cheap shot at law professors and law reviews when he intoned:

“Pick up a copy of any law review that you see, and the first article is likely to be, you know, the influence of Immanuel Kant on evidentiary approaches in 18th Century Bulgaria, or something, which I’m sure was of great interest to the academic that wrote it, but isn’t of much help to the bar.”[1]

Anti-intellectualism is in vogue these days. No doubt, Roberts was jocularly indulging in an over-generalization, but for anyone who tries to keep up with the law reviews, he has a small point. Other judges have rendered similar judgments. Back in 1993, in a cranky opinion piece – in a law review – then Judge Richard A. Posner channeled the liar paradox by criticizing law review articles for “the many silly titles, the many opaque passages, the antic proposals, the rude polemics, [and] the myriad pretentious citations.”[2] In a speech back in 2008, Justice Stephen Breyer noted that “[t]here is evidence that law review articles have left terra firma to soar into outer space.”[3]

The temptation to rationalize, and to advocate for reflective equilibrium between the law as it exists, and the law as we think it should be, combine to lead to some silly and harmful efforts to rewrite the law as we know it.  Jeremy Bentham, Mr. Nonsense-on-Stilts, who sits stuffed in the hallway of the University of London, ushered in a now venerable tradition of rejecting tradition and common sense, in proposing all sorts of law reforms.[4]  In the early 1800s, Jeremy Bentham, without much in the way of actual courtroom experience, deviled the English bench and bar with sweeping proposals to place evidence law on what he thought was a rational foundation. As with his naïve utilitarianism, Bentham’s contributions to jurisprudence often ignored the realities of human experience and decision making. The Benthamite tradition of anti-tradition is certainly alive and well in the law reviews.

Still, I have a soft place in my heart for law reviews.  Although not peer reviewed, law reviews provide law students a tremendous opportunity to learn about writing and scholarship through publishing the work of legal scholars, judges, thoughtful lawyers, and other students. Not all law review articles are non-sense on stilts, but we certainly should have our wits about us when we read immodest proposals from the law professoriate.

*   *   *   *   *   *   *   *   *   *

Professor Edward Cheng has written broadly and insightfully about evidence law, and he certainly has the educational training to do so. Recently, Cheng has been bemused by the expert paradox, which wonders how lay persons, without expertise, can evaluate and judge issues of the admissibility, validity, and correctness of expert opinion. The paradox has long haunted evidence law, and it is at center stage in the adjudication of expert admissibility issues, as well as the trial of technical cases. Recently, Cheng has proposed a radical overhaul to the law of evidence, which would require that we stop asking courts to act as gatekeepers, and to stop asking juries to determine the validity and correctness of expert witness opinions before them. Cheng’s proposal would revert to the nose counting process of Frye and permit consideration of only whether there is an expert witness consensus to support the proffered opinion for any claim or defense.[5] Or in Plato’s allegory of the cave, we need to learn to be content with shadows on the wall rather than striving to know the real thing.

When Cheng’s proposal first surfaced, I wrote briefly about why it was a bad idea.[6] Since his initial publication, a law review symposium was assembled to address and perhaps to celebrate the proposal.[7] The papers from that symposium are now in print.[8] Unsurprisingly, the papers are both largely sympathetic (but not completely) to Cheng’s proposal, and virtually devoid of references to actual experiences of gatekeeping or trials of technical issues.

Cheng contends that the so-called Daubert framework for addressing the admissibility of expert witness opinion is wrong.  He does not argue that the existing law, in the form of Federal Rules of Evidence 702 and 703, does not call for an epistemic standard for both admitting opinion testimony, as well for the fact-finders’ assessments. There is no effort to claim that somehow four Supreme Court cases, and thousand of lower courts, have erroneously viewed the whole process. Rather, Cheng simply asserts non-expert judges cannot evaluate the reliability (validity) of expert witness opinions, and that non-expert jurors cannot “reach independent, substantive conclusions about specialized facts.”[9] The law must change to accommodate his judgment.

In his symposium contribution, Cheng expands upon his previous articulation of his proposed “consensus rule.”[10] What is conspicuously absent, however, is any example of failed gatekeeping that excluded valid expert witness opinion. One example, the appellate decision in Rosen v. Ciba-Geigy Corporation,[11] which Cheng does give, is illustrative of Cheng’s project. The expert witness, whose opinion was excluded, was on the faculty of the University of Chicago medical school; Richard Posner, the appellate judge who wrote the opinion that affirmed the expert witness’s exclusion, was on the faculty of that university’s law school. Without any discussion of the reports, depositions, hearings, or briefs, Cheng concludes that “the very idea that a law professor would tell medical school colleagues that their assessments were unreliable seems both breathtakingly arrogant and utterly ridiculous.”[12]

Except, of course, very well qualified scientists and physicians advance invalid and incorrect claims all the time. What strikes me as breathtakingly arrogant and utterly ridiculous is the judgment of a law professor who has little to no experience trying or defending Rule 702 and 703 issues labeling the “very idea” as arrogant and ridiculous. Aside from its being a petitio principia, we could probably add that the reaction is emotive, uninformed, and uninformative, and that it fails to support the author’s suggestion that “Daubert has it all wrong,” and that “[w]e need a different approach.”

Judges and jurors obviously will never fully understand the scientific issues before them.  If and when this lack of epistemic competence is problematic, we should honestly acknowledge how we are beyond the realm of the Constitution’s seventh amendment. Since Cheng is fantasizing about what the law should be, why not fantasize about not allowing lay people to decide complex scientific issues? Verdicts from jurors who do not have to give reasons for their decisions, and who are not in any sense peers of the scientists whose work they judge are normatively problematic.

Professor Cheng likens his consensus rule to how the standard of care is decided in medical malpractice litigation. The analogy is interesting, but hardly compelling in that it ignores “two schools of thought” doctrine.[13] In litigation of claims of professional malpractice, the “two schools of thought doctrine” is a complete defense.  As explained by the Pennsylvania Supreme Court,[14] physicians may defend against claims that they deviated from the standard of care, or of professional malpractice, by adverting to support for their treatment by a minority of professionals in their field:

“Where competent medical authority is divided, a physician will not be held responsible if in the exercise of his judgment he followed a course of treatment advocated by a considerable number of recognized and respected professionals in his given area of expertise.”[15]

The analogy to medical malpractice litigation seems inapt.

Professor Cheng advertises that he will be giving full-length book treatment to his proposal, and so perhaps my critique is uncharitable in looking at a preliminary, (antic?) law review article. Still, his proposal seems to ignore that “general acceptance” renders consensus, when it truly exists, as relevant to both the court’s gatekeeping decisions, and the fact finders’ determination of the facts and issues in dispute. Indeed, I have never seen a Rule 702 hearing that did not involve, to some extent, the assertion of a consensus, or the lack thereof.

To the extent that we remain committed to trials of scientific claims, we can see that judges and jurors often can detect inconsistencies, cherry picking, unproven assumptions, and other aspects of the patho-epistemology of exert witness opinions. It takes a community of scientists and engineers to build a space rocket, but any Twitter moron can determine when a rocket blows up on launch. Judges in particular have (and certainly should have) the competence to determine deviations from the scientific and statistical standards of care that pertain to litigants’ claims.

Cheng’s proposal also ignores how difficult and contentious it is to ascertain the existence, scope, and actual content of scientific consensus. In some areas of science, such as occupational and environmental epidemiology and medicine, faux consensuses are set up by would-be expert witnesses for both claimants and defendants. A search of the word “consensus” in the PubMed database yields over a quarter of a million hits. The race to the bottom is on. Replacing epistemic validity with sociological and survey navel gazing seems like a fool’s errand.

Perhaps the most disturbing aspect of Cheng’s proposal is what happens in the absence of consensus.  Pretty much anything goes, a situation that Cheng finds “interesting,” and I find horrifying:

“if there is no consensus, the legal system’s options become a bit more interesting. If there is actual dissensus, meaning that the community is fractured in substantial numbers, then the non-expert can arguably choose from among the available theories. If the expert community cannot agree, then one cannot possibly expect non-experts to do any better.”[16]

Cheng reports that textbooks and other documents “may be both more accurate and more efficient” evidence of consensus.[17] Maybe; maybe not.  Textbooks are typically often dated by the time they arrive on the shelves, and contentious scientists are not beyond manufacturing certainty or doubt in the form of falsely claimed consensus.

Of course, often, if not most of the time, there will be no identifiable, legitimate consensus for a litigant’s claim at trial. What would Professor Cheng do in this default situation? Here Cheng, fully indulging the frolic, tells us that we

“should hypothetically ask what the expert community is likely to conclude, rather than try to reach conclusions on their own.”[18]

So the default situation transforms jurors into tea-leaf readers of what an expert community, unknown to them, will do if and when there is evidence of a quantum and quality to support a consensus, or when that community gets around to articulating what the consensus is. Why not just toss claims that lack consensus support?

[1] Debra Cassens Weiss, “Law Prof Responds After Chief Justice Roberts Disses Legal Scholarship,” Am. Bar Ass’n J. (July 7, 2011).

[2] Richard A. Posner, “Legal Scholarship Today,” 45 Stanford L. Rev. 1647, 1655 (1993), quoted in Walter Olson, “Abolish the Law Reviews!” The Atlantic (July 5, 2012); see also Richard A. Posner, “Against the Law Reviews: Welcome to a world where inexperienced editors make articles about the wrong topics worse,”
Legal Affairs (Nov. 2004).

[3] Brent Newton, “Scholar’s highlight: Law review articles in the eyes of the Justices,” SCOTUS Blog (April 30, 2012); “Fixing Law Reviews,” Inside Higher Education (Nov. 19, 2012).

[4] “More Antic Proposals for Expert Witness Testimony – Including My Own Antic Proposals” (Dec. 30, 2014).

[5] Edward K. Cheng, “The Consensus Rule: A New Approach to Scientific Evidence,” 75 Vanderbilt L. Rev. 407 (2022).

[6] “Cheng’s Proposed Consensus Rule for Expert Witnesses” (Sept. 15, 2022);
“Further Thoughts on Cheng’s Consensus Rule” (Oct. 3, 2022).

[7] Norman J. Shachoy Symposium, The Consensus Rule: A New Approach to the Admissibility of Scientific Evidence (2022), 67 Villanova L. Rev. (2022).

[8] David S. Caudill, “The ‘Crisis of Expertise’ Reaches the Courtroom: An Introduction to the Symposium on, and a Response to, Edward Cheng’s Consensus Rule,” 67 Villanova L. Rev. 837 (2022); Harry Collins, “The Owls: Some Difficulties in Judging Scientific Consensus,” 67 Villanova L. Rev. 877 (2022); Robert Evans, “The Consensus Rule: Judges, Jurors, and Admissibility Hearings,” 67 Villanova L. Rev. 883 (2022); Martin Weinel, “The Adversity of Adversarialism: How the Consensus Rule Reproduces the Expert Paradox,” 67 Villanova L. Rev. 893 (2022); Wendy Wagner, “The Consensus Rule: Lessons from the Regulatory World,” 67 Villanova L. Rev. 907 (2022); Edward K. Cheng, Elodie O. Currier & Payton B. Hampton, “Embracing Deference,” 67 Villanova L. Rev. 855 (2022).

[9] Embracing Deference at 876.

[10] Edward K. Cheng, Elodie O. Currier & Payton B. Hampton, “Embracing Deference,” 67 Villanova L. Rev. 855 (2022) [Embracing Deference]

[11] Rosen v. Ciba-Geigy Corp., 78 F.3d 316 (7th Cir. 1996).

[12] Embracing Deference at 859.

[13] “Two Schools of Thought” (May 25, 2013).

[14] Jones v. Chidester, 531 Pa. 31, 40, 610 A.2d 964 (1992).

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

[16] Embracing Deference at 861.

[17] Embracing Deference at 866.

[18] Embracing Deference at 876.

Posted in Evidence, Expert Witnesses, Frye, Rule 702, Rule 703, Scientific Evidence | 1 Comment »

Oreskes Excluded as Historian Expert Witness in Mann Case

February 28th, 2023

“It has been said that though God cannot alter the past, historians can; it is perhaps because they can be useful to Him in this respect that He tolerates their existence.”    

                Samuel Butler, Erewhon Revisited, ch. 14

 

It has been a while since I have written about the scientist defamation case of brought by climate scientist and advocate, Michael E. Mann, against National Review magazine, the Competitive Enterprise Institute, and Mark Steyn.[1] Back in 2014, I commented upon the oddity of a scientist’s claim of defamation against lay people for criticizing a scientist’s work.[2] Mann took umbrage to statements, critical of his work that generated a “hockey-stick” model of global temperature rises. Defendants apparently accused Mann of “molest[ing] and tortur[ing] data in the service of politicized science[,]” “engaging in data manipulation[,]” and creating the “fraudulent climate-change ‘hockey-stick’ graph[.]”[3] Mann naturally claims that the defendants’ statements are false and defamatory; the defendants contend that their statements are true.

In the hurly burly of work and life, I lost touch with the proceedings in Mann, but recently I became aware of interesting gatekeeping rulings, issued in 2021.[4] I was particularly intrigued by the activity of Naomi Oreskes, qua historian, who sought to offer an expert witness opinion in the Mann case. On July 26, 2021, Judge Alfred S. Irving, Jr., dashed Oreskes’ hopes of testifying as an historian, and told her not to bother coming to Washington for trial.[5]

Naomi Oreskes is a “professor of the History of Science, in Harvard University. She teaches and writes about the history of science. When not riding political hobby horses, Oreskes has written about the Idiocracy’s rejection of science,[6] but she has also shown herself to be untutored in the basics of scientific and statistical method.[7]

She is an advocate who, along with her posse, frequently weighs in against oil companies in litigation.[8] Oreskes has also written extensively to demonize industry’s motives and to advance her conspiracy theories in which manufacturing industry (but not lawsuit industry) is responsible for suppressing the truth of positions that Oreskes believes fervently.[9] She has decried the political discrediting of science, while participating in a political strategy to discredit her scientific opponents.[10] The line between trust and credulity can sometimes be hard to locate.

The defendants had moved in limine to exclude Oreskes’ proferred historian testimony,[11] under the District of Columbia’s standard for admitting and excluding expert witness opinion testimony.[12] Oreskes’ opinion, at issue in the Mann case, was on

  • the general basis for finding scientific research to be reliable, and
  • that “think-tanks” (including the defendant CEI) “ignore, misrepresent, or reject” principled scientific thought on environmental issues.

On the general issue of reliability, Oreskes proferred an opinion that scientific research is made reliable by

“the collective vetting and critical interrogation of claims through scientific workshop, meetings, conferences, and above all, publication in peer-reviewed journals, formal scientific assessments and reports of government scientific agencies and laboratories.”

Even on superficial review, this description appears woefully inadequate and incomplete. For Oreskes, scientific reliability seems to be all about meetings, publications, and governmental reviews, with no room for actual data gathered in attempts to refute hypotheses, or room for interrogating the data and their quality. Nonetheless, on this general issue of reliability, the Court found her opinion to acceptable but redundant to scientific witnesses who had first-hand knowledge of Mann’s work (as opposed to an historian). On the first part of her proferred opinion, Judge Irving expressed his skepticism that Oreskes’ opinion would be helpful to the jury; Oreskes’ testimony might give the jury a framework that could be used to assess whether Mann’s work was fraudulent or not. Judge Irving held, however, that Oreskes’ testimony ran afoul of the law in failing to “to use a scientific technique which applies reliable methodologies.”[13]

On the second proferred opinion, the ad hominem attack on the bona fides of CEI and similar “think-tanks,” Judge Irving found Oreskes, in her report, failed to provide any explanation of her methodology.[14]

As was the case with several of Plaintiff’s proffered experts, Dr. Oreskes’ report was devoid of any discussion of her methodologies. Mann’s lawyers sought to remedy the omission by adverting to Oreskes’ description, in her deposition testimony, of her “content analysis” methodology, as applied to the public statements of the CEI:

“So we read the documents. And as I said before, we applied a well-established method in social science, which is broadly accepted as being, you know, a reputable method of analyzing something, content analysis, in order to show that there was this fairly substantial disparity between what the company scientists were saying in their private reports and publishing in peer-reviewed scientific literature which was essentially consistent with what other scientists were saying versus what the company was saying in public in advertisements that were aimed at the general public.

                           * * * * *

In the case of ExxonMobil, we had the opportunity to do this analysis because the company itself had made public these documents. And they claimed in public that if you read these documents, you would see that everything was fine and that ExxonMobil had done nothing wrong.

We applied a well-established method in social science, which is broadly accepted as being, you know, a reputable method of analyzing something, content analysis, in order to show that there was this fairly substantial disparity between what the company scientists were saying in their private reports and publishing in peer-reviewed scientific literature which was essentially consistent with what other scientists were saying versus what the company was saying in public in advertisements that were aimed at the general public.”[15]

Alas, it turned out that this jargon-laden description of method was irrelevant because Oreskes admitted that she had not performed a “content analysis” in the Mann case.[16] When pressed to explain the methodology actually used in the Mann case, she candidly explained:

“If you want me to tell you what my method is, it’s reading and thinking. We read. We read documents. And we think about them.”[17]

The court found this explanation more than a little problematic. “Reading and thinking about documents” are not the sort of methodologies that are beyond the ken of the jury. Oreskes’ best effort to explain what she had done left “the Court is unable to distinguish why Dr. Oreskes is more capable than the average juror, who can also read and think about documents.”[18]

The court’s inability to fathom what Oreskes might offer was not due to any judicial disability. Oreskes’ “reading and thinking” had never been peer-reviewed, had no known success rate, and could not be replicated by other experts in her field. The court saw that Oreskes’ opinion had not come from scientific method, and that her opinion would be aptly characterized “as a historical narrative or research compilation than scientific testimony.”[19] Oreskes’ opinion could not be justified as expert experiential opinion because it was not based upon her personal experience; rather, her opinion was based upon her review of documents and reports of others.

Oreskes’ “expert” witness report regaled the court with her take on CEI’s previous actions and statements. Oreskes offered the opinion that CEI has a history of opposing “progressive” policies and that it regularly advocates against “valid and widely accepted scientific research.” Judge Irving recognized that these opinions were nothing more than Oreskes’ subjective historical summary of CEI’s actions, no doubt with a heavy dose of Oreskes’ personal animus against the CEI. As Judge Learned Hand declared almost 100 years ago, “[a]rgument is argument whether in the box or at the bar, and its proper place is the last.”[20]

As for methodology, the court found none. The court agreed with the CEI that “Dr. Oreskes made no effort to compile or catalogue CEI’s publications according to an objectively defined set of metrics.” Oreskes was thus excluded from the litigation in July 2021.[21]

The plaintiff and Naomi Oreskes were not content to leave matters as they were decided in Judge Irving’s order. Mann moved for reconsideration of Oreskes’ exclusion, with a more limited proffer of testimony that would address the “importance of scientific expertise and the significance of the scientific method and peer review process in scientific debate.”[22]

In this requested do-over, Mann submitted a supplemental declaration from Oreskes, in which she elaborated upon her methodology of “contextual exposition.” Mann further argued that Oreskes should be “permitted to testify regarding scientific principles to permit the jury to understand those principles and to apply them to facts without running afoul of the general rules relating to opinion testimony.”

To this end, Oreskes would give the jury a “contextual exposition…of the character and nature of scientific research.” Mann contended that this foundational opinion testimony was “crucial to enable the jury to reach its conclusions concerning the truth or falsehood of Defendants’ objectively verifiable statements of fact about Dr. Mann and his scientific research which produced the Hockey Stick Graph.”

Essentially, Mann was seeking to have Oreskes’ testimony admitted as a “teaching expert witness,” who would not provide her own personal opinion, but who would give the jury the relevant scientific principles that they may apply to the facts of the case as they find. Judge Irving accepted this more limited proffer, and modified his earlier ruling to permit Oreskes to give the so-called “contextual information” that renders scientific research reliable, such as the peer review process.[23] As noted above, this aspect of the Oreskes’ proffered testimony appears incomplete, with emphasis on “social control,” at the expense of valid inference and data quality and integrity. 

Judge Irving’s reconsideration gave Oreskes a very limited remit to testify at trial. His Honor emphasized, however, that most of what she had originally proposed for her testimony was “unreliable and irrelevant.” Oreskes will not be allowed to give her opinion over the history of “the debate over anthropogenic climate change,” or hold forth with opinions about the history and character of CEI’s “agenda.” Judge Irving reiterated his finding that Oreskes’ opinions on these matters “are not demonstrably the product of any scientific principle or method, and are largely irrelevant.”[24]

Furthermore, Oreskes will not be allowed to discuss Mann’s work, or whether or not his methodology is valid, or whether there is evidence or not of data manipulation or fraudulent behavior. As Judge Irving summarized the matter:

“Dr. Oreskes’ opinion in that regard would be entirely speculative given that she has not demonstrated any particular expertise or experience regarding Dr. Mann’s research. Neither her original expert report nor her supplemental declaration indicates any intimate knowledge of Dr. Mann’s work. Further, Dr. Oreskes’ expert report identifies her as an expert in the history of science and in geology, not as an expert in climate reconstruction. Dr. Oreskes has not demonstrated any specialized knowledge or experience concerning the substantive or factual aspects of the MBH research.”

Judge Irving also excised Oreskes’ claim, made in her belated supplemental declaration, that there is a consensus about the cause of climate change, or that there is a political and ideological basis for CEI’s opposition to the consensus. After all, Mann’s work could have been fraudulent, even if other, sound scientific work came to the same conclusion, and even if that conclusion were widely shared.[25]

The choice of Naomi Oreskes to serve as an expert witness was dubious on several fronts.  First, as a partisan in the climate science debates, Oreskes hardly brought objectivity to the courtroom to support plaintiff Michael Mann. While attacking CEI for political and ideological bias, Oreskes’ helped showcase her own biases, which have long been on display.[26] Mann would be more effectively served by presenting an expert on scientific method who was not such an extreme advocate. Second, as shown by her misidentification of the burden of proof with the coefficient of confidence, Oreskes previously had shown a lack of understanding of scientific and statistical method.[27] Mann might have considered that his case would be better supported by someone who had not made such glaring mistakes, in front of a national audience.

As for whether the historian aspect of Oreskes’ testimony could ever have succeeded, I am more doubtful. Historians who “read and think” often have little to offer beyond what lawyers can accomplish using documents presented to the trier of fact for interpretation.[28]

Presenting historian “expert” witnesses is a commonplace in occupational exposure litigations, involving silicosis or claimed asbestos-related diseases.[29] The use of such expert witnesses leads to serious abuses, by which argument and advocacy are surreptitiously presented as history.[30] Judge Irving’s exclusion of Naomi Oreskes is a valuable precedent for bench and bar.

Trial is set for June 12, 2023.

[1] Michael E. Mann v. National Review, CA 008263 B (filed in 2012, in the Washington, DC Superior Court, Civil Division).

[2] See “Climategate on Appeal” (Aug. 17, 2014).

[3] Competitive Enter. Inst. v. Mann, 150 A.3d 1213, 1262-64 (D.C. 2016), as amended (Dec. 13, 2018), cert denied 140 S. Ct. 344 (2019).

[4] There is a useful compendium of rulings available through the CEI website.

[5] See District of Columbia Superior Court Order on Expert Witnesses (July 26, 2021) [Order]. T.C. Kelly, “Expert Testimony Excluded in Michael Mann Defamation Lawsuit,” Expert Pages (Aug. 11, 2021).

[6] Naomi Oreskes, Why Trust Science? (2019).

[7] See “Playing Dumb on Statistical Significance” (Jan. 4, 2015); “ The Rhetoric of Playing Dumb on Statistical Significance – Further Comments on Oreskes” (Jan. 20, 2015); “Significance Levels Made Whipping Boy on Climate Change Evidence; Is 0.05 too Strict?” Error Statistics (Jan. 4, 2015).

[8] See, e.g., Brief of Amici Curiae Robert Brulle, Center for Climate Integrity, Justin Farrell, Benjamin Franta, Stephan Lewandowsky, Naomi Oreskes, and Geoffrey Supran in Support of Appellees and Affirmance, County of San Mateo v. Chevron Corp., Nos. 18-15499, 18-15502, 18-15503, 18-16376 at 2 (9th Cir. 2019); Brief of Amici Curiae Robert Brulle, Center for Climate Integrity, Justin Farrell, Benjamin Franta, Stephan Lewandowsky, Naomi Oreskes, Geoffrey Supran and the Union of Concerned Scientists, City of Oakland v. B.P. PLC, No. No. 18-16663 (9th Cir. Mar. 20, 2019); Brief of Amici Curiae Robert Brulle, Center for Climate Integrity, Justin Farrell, Benjamin Franta, Stephan Lewandowsky, Naomi Oreskes, Geoffrey Supran and the Union of Concerned Scientists, Mayor and City Council of Baltimore  v BP PLC, No. 19-1644 (4th Cir. Sept. 3, 2019).

[9] Naomi Oreskes & Erik M. Conway, Merchants of Doubt: How a Handful of Scientists Obscured the Truth on Issues from Tobacco Smoke to Global Warming (2010); Naomi Oreskes & Erik M. Conway, “Defeating the merchants of doubt,” 465 Nature 686 (2010). See also Geoffrey Supran & Naomi Oreskes, “Assessing ExxonMobil’s climate change communications (1977–2014),” 12 Envt’l Research Letters (Aug. 2017). Remarkably, Oreskes declared no conflicts of interest in this publication.

[10] Zoë Corbyn, “Naomi Oreskes: ‘Discrediting science is a political strategy’,” The Guardian (Nov. 2019).

[11] See Defendants Competitive Enterprise Institute and Rand Simberg’s Motion in Limine to Exclude the Expert Testimony of Dr. Naomi Oreskes (“MIL Oreskes”), filed on March 3, 2021.

[12] The standard is substantially the same as that articulated in Federal Rule of Evidence 702; see Motorola Inc. v. Murray, 147 A.3d 751 (D.C. Ct. App. 2016) (applying standard to case involving claims of brain cancer from the use of mobile telephones).

[13] Order at 23-24.

[14] Judge Irving noted that failure to explain methodology was a fatal flaw, citing Sacchetti v. Gallaudet Univ., 344 F. Supp. 3d 233, 250-51 (D.D.C. 2018).

[15] Plaintiff’s Opposition, Oreskes Deposition v.2 at 55:12-56:5.

[16] Id. at 33:5-15.

[17] Id. at 34:13-15.

[18] Order at 24-25 (citing Parsi v. Daioleslam, 852 F. Supp. 2d 82, 89 (D.D.C. 2012) (rejecting an expert opinion based solely on the experts “reading and viewing” and finding that reading, alone, does not constitute an acceptable methodology).

[19] Id. The court acknowledged that expert witness opinion could be “experiential,” but such a case, the witness must explain “how that experience leads to the conclusions reached, why that experience is a sufficient basis for the opinion and how that experience is reliably applied to the facts.” Id. (citing Arias v. DynCorp., 928 F. Supp. 2d 10, 15-16 (D.D.C 2013).

[20] Nichols v. Universal Pictures Corp., 45 F.2d 119, 123 (2d Cir. 1930).

[21] Order at 25.

[22] Court Order on Expert Witnesses, in Michael E. Mann v. National Review, CA 008263 B, Washington, D.C, Superior Court, Civil Division (Jan. 22, 2022)

[Order II at 20].

[23] Order II at 22.

[24] Order II at 22-23.

[25] Order II at 23-24.

[26] See, e.g., Naomi Oreskes  & Erik M. Conway, The Big Myth: How American Business Taught Us to Loathe Government and Love the Free Market (2023).

[27] Oreskes, in the past, has shown a stunning disregard for the meaning of scientific and statistical concepts.[27]

[28] See, e.g., Quester v. B.F. Goodrich Co., Cuyahoga Cty., Ohio, C.P. Case No. 03-509539 (Jan. 12, 2008) (excluding historian Gerald Markowitz’s testimony as impermissible attempt to introduce expert witness opinion on defendants’ intent and motive) (Sweeney, J.).

[29] Nathan A. Schachtman, “On Deadly Dust and Histrionic Historians: Preliminary Thoughts on History and Historians as Expert Witnesses,” 2 Mealey’s Silica Litigation Report Silica 1, 2 (November 2003); Nathan Schachtman & John Ulizio, “Courting Clio:  Historians and Their Testimony in Products Liability Action,” in: Brian Dolan & Paul Blanc, eds., At Work in the World: Proceedings of the Fourth International Conference on the History of Occupational and Environmental Health, Perspectives in Medical Humanities, University of California Medical Humanities Consortium, University of California Press (2012); Scott Kozak, “Use and Abuse of ‘Historical Experts’ in Toxic Tort Cases,” in Toxic & Hazardous Substances Litigation (March 2015).

[30] See How Testifying Historians Are Like Lawn-Mowing Dogs” (May 15, 2010); “Courting Clio: Historians and Their Testimony in Products Liability Litigation” (May 24, 2010);  A Walk on the Wild Side (July 16, 2010); Counter Narratives for Hire (Dec. 13, 2010); “Narratives & Historians for Hire” (Dec. 15, 2010); “Courting Clio: Historians Under Oath – Part 1” (Dec. 17, 2011); “Courting Clio: Historians Under Oath – Part 2” (Dec. 17, 2011); “What Happens When Historians Have Bad Memories” (Mar. 15, 2014); “Too Many Narratives – Historians in the Dock” (July 14, 2014); Historians Noir (Nov. 18, 2014); “Lawyers as Historians” (Feb. 2, 2016); “Succès de scandale – With Thanks to Rosner & Markowitz” (Mar. 26, 2017); “More Rosner-Markowitz Faux History of Workplace Safety” (July 9, 2020).

Posted in Historian Testimony, Scientific Misconduct | 5 Comments »

Selikoff Timeline & Asbestos Litigation History (Revised)

February 26th, 2023

The critics and cheerleaders of Dr. Irving John Selikoff agree that he was a charming, charismatic, and courageous man, a compassionate physician, and a zealous advocate for worker safety and health. The consensus falls apart over the merits of Selikoff’s actual research, his credentials, and his advocacy tactics.[1]

Selikoff’s collaborators, protégés, and fellow travelers tend to brand any challenge or criticism as “scurrilous.”[2] They attack the messenger for attacking the messenger, who attacked the messenger, u.s.w.. Certainly in his lifetime, Selikoff attracted harsh and vituperative attacks, some of which were mean-spirited and even anti-semitic. Although I am not a Jew, I am, following Jonathan Miller, “Jew-ish, just not the whole hog.” As such, I can appreciate the ire of some of Selikoff’s defenders over the nature of these attacks.

Selikoff’s legitimate achievements should not be diminished, and his defenders are correct to bemoan the ad hominem attacks on Selikoff, based upon ethnicity and personal characteristics. Some attacks, however, were merited. The time has come to stop evaluating the message by its messenger, and to pay attention to the evidence. Selikoff’s defenders and hagiographers are wrong, therefore, to claim that Selikoff’s training, scientific acumen, advocacy, and false positive claims are somehow off limits. Selikoff advanced his scientific and political agenda by promoting his reputation and work, and he thus put his credentials, work, and methods into issue. Selikoff’s contributions to public health in publicizing the dangers of high exposure, long-term asbestos exposure do not privilege every position he took. Selikoff is a difficult case because he was wrong on many issues, and his reputation, authority and prestige ultimately became much greater than the evidence would ultimately support.

Although Selikoff died in 1992, his legacy lives on in the perpetual litigation machine that is run by the litigation industry and Selikoff’s juniors and imitators, who serve as testifying expert witnesses. One of Selikoff’s great achievements, the federalization of worker safety and health in the Williams-Steiger Occupational Safety and Health Act of 1970,[3] languishes because of inadequate resources for enforcement and frivolous efforts to address non-existent problems, such as the lowering of the crystalline silica permissible exposure limit. Activists have taken to redress the problem by advocating for nugatory “warnings” from remote suppliers, in the face of employer failures to monitor and supervise workers and the workplace, and to provide administrative, engineering, and personal protective controls.

Selikoff diverted regulatory attention from asbestos fiber type, with the result that the OSHA PELs were lowered for both chrysotile and amphibole asbestos, thus leaving the ultra-hazardous crocidolite asbestos in use. Selikoff perpetuated a good deal of mischief and misinformation to keep his myth that all fiber types are the same (and that “asbestos is asbestos is asbestos”). In doing so, he actually hurt many people.

An anonymous snark on Wikipedia noted some of my blog posts about Selikoff, and offered the lame criticism that my writings were not peer reviewed.[4] The snark (Tweedale?) was of course correct on this limited point, but generally in this field, peer review is worth a warm bucket of spit. And there is the matter that the anonymous critic was offering a criticism that was also not peer reviewed.

Selikoffophiles continue to tell tall tales about Selikoff’s work and in particular about how he became involved in asbestos medicine.[5]  So here is a timeline of Selikoff’s life and asbestos work, an update of an earlier version. If anyone notes an error or inconsistency in this time line, please let me know, provide better sources, and ask for a correction. If I am wrong, I will readily note the correction and eat my words, but I am sure they will be quite digestible.[6]

1915-01-15.  Irving John Selikoff was born as Irving Selecoff in the brain basket of America, Brooklyn, New York, to Abraham and Matilda (Tillie) Selecoff.[7]  His father, Abraham, was born on April 6, 1885, in the Kyiv oblast of what is now Ukraine.[8]

1920.  According to the 1920 census, the Selekoff family lived at 816 179th Street, in the Bronx. Irving’s father, Abraham, was self-employed as a hat manufacturer, doing business later as United Headwear Corporation.[9]  The family had two children, Irving, and his older sister, Gladys.

1930. The asbestos workers’ journal published a story about the (non-malignant) risks of asbestos exposure.[10]

1935-06.  Selikoff was graduated from Columbia University, with a B.S. degree.

1935-12-24.  Selikoff arrived in Boston from Yarmouth, Nova Scotia, on the S.S. Yarmouth, on December 24, 1935, apparently en route from Scotland.

1936.  Dr. Alice Hamilton, physician and noted labor activist, wrote in a labor union journal to urge more attention to industrial dusts, the knowledge of dangers of which was[11] “still very limited except with regard to silica and asbestos.”

1936-08.  Selikoff sat for the university entrance boards in Scotland.

1936-09-27.  Selikoff married Lydia Kapilian, in the Bronx.[12]

1936-10-12. Irving Selecoff arrives in Liverpool, from New York, aboard the S.S. Samaria.

1936-10.  Selikoff entered Anderson’s College of Medicine, in Glasgow, Scotland.[13]

1936-12-28. Irving John Selikoff is listed in the UK, Medical and Dental Students Registers, 1882-1937, registration date December 28, 1936, in Scotland.

1936.  Alice Hamilton published an article on the risks and benefits of industrial asbestos use, in a key labor unionist journal. Alice Hamilton, “Industrial Poisons,” 43 The American Federationist 707-13 (1936).

1937-04-26.  Selikoff arrived in New York, from Greenock, Scotland, on the S.S. Carinthia.

1937-10-10. Irving Selecoff arrived in Glasgow, Scotland, from New York City, on board the SS. Cameronia.

1938-07-14.  Irving J. Selecoff arrived in Quebec, Canada, from Greenock, Scotland, on the S.S. Duchess Atholl.

1939-06-24.  Irving Selecoff arrived in New York, from Liverpool, London, on the S.S. Mauretania. Because of the developing hostilities in Europe, Selikoff apparently did not return to Glasgow, in the fall of 1939.

1939-11.  Unable to return to Scotland, Selikoff applied to Melbourne University for coursework to finish his non-degree course of qualification for medication practice in the United Kingdom.[14]

1940-03-04.  Selecoff (as his name was then often spelled) arrived in Vancouver from Sydney, on the S.S. Aorangi.

1940-04.  Irving Selikoff was living with his parents, and his married sister and her family, in Rye, New York, according to the 1940 census, taken on April 10, 1940.

1940-05-27.  Selikoff enrolled in the University of Melbourne as a non-degree student, for coursework to finish his qualification for medical license in Scotland.[15]

1941-03-24.  John Selecoff arrived in Los Angeles, California, from Sydney, Australia, on the S.S. Mariposa. According to Bartrip, Selikoff had completed his last course at the University of Melbourne, for his “tailor-made” program, on

1941-02-27. Selikoff never gained entrance to a degree program at Melbourne.[16]

1941-04-21. Irving John Selikoff registered for the draft, in Port Chester, New York.

1941.  Selikoff joined the Mount Sinai Hospital as an assistant in Anatomy and Pathology, “immediately following his university training.”[17]

1943-11-01.  Selikoff received an M.D., degree from Middlesex University,[18] after two semesters in residence. This school was regarded as “substandard” and not approved by the American Medical Association. The school lost its accreditation in 1946, and closed.[19] After receiving this degree, Selikoff continued his efforts to return to Scotland, to complete his “triple qualification” for medical licensure in Scotland, which would allow him to sit for the licensing examination in one of the United States.

1943 – 1944.  Selikoff served as an intern, at the Beth Israel Hospital, in Newark, New Jersey.[20]

1944 – 1946. Selikoff served as a resident, at the Sea View Hospital, in New York City.[21]

1945-04-23.  Selikoff was listed in the British Medical Registry, based upon his qualification by the Scottish Conjoint Board for his work at Anderson’s and his non-degree work at the University of Melbourne.[22]

1943-06-02. Irving J Selecoff arrived in Montreal, Quebec, Canada, from Liverpool, aboard the S.S. Axel Johnson.

1945-06-02.  Selikoff arrived in Montreal, Quebec, from Liverpool, England, on the S.S. Axel Johnson.

1945-12-21. Selikoff’s mother, Tillie, died.

1946-02.  Selikoff married Celia Schiffrin in Manhattan.[23]  It was the second marriage for both bride and groom.

1947.  After having left Mt. Sinai Hospital, in 1943, for an internship and a residency, Selikoff resumed his association with Mt. Sinai Hospital.[24]

1947-06-30. Selikoff’s father, Abraham Selecoff, married Anna Susser, in Manhattan.[25]

1949.  Selikoff opened a medical office at 707 Broadway, Paterson, New Jersey,[26] not far from a factory run by the Union Asbestos and Rubber Company (UNARCO). In the same year, the Selikoffs were living at 965 Fifth Avenue, near 78th Street, in Manhattan.[27]

1950.  Selikoff’s medical practice in Paterson, New Jersey, afforded him the opportunity to observe “the incidence of lung disease among workers at the Union Asbestos and Rubber Company (UNARCO),”[28] which operated one of its factories in Paterson.

1950-04-05. Irving J. Selikoff and his wife Celia resided at 93 Broadway, Paterson, New Jersey, USA, according to the 1950 census. By the early 1950s, Selikoff and his wife had moved to 505 Upper Boulevard, Ridgewood, New Jersey.

1951.  New Jersey lawyer Carl Gelman retained Dr. Irving Selikoff to examine 17 workers from the Paterson plant of Union Asbestos and Rubber Company (UNARCO). Gelman filed workers’ compensation claims on behalf of the UNARCO workers.[29]

1952.  Supported by Selikoff’s report, UNARCO worker Anton Szczesniak settled his worker’s compensation case, involving “intestinal cancer,” for $2,000 in 1952.[30] Selikoff published data on the carcinogenicity of amosite in 1972,[31]  a delay of twenty years.[32]

1952.  Selikoff and colleagues published the results of a clinical trial of isoniazid for tuberculosis patients.[33]

1952.  Selikoff was featured in Life magazine coverage of isoniazid, a chemotherapy for tuberculosis.[34]

1952.  Selikoff was an assistant attending physician for thoracic diseases in the department of thoracic diseases at Mt. Sinai Hospital. In this year, Selikoff delivered the monthly Physiological Chemistry Seminar lecture at Mt. Sinai Hospital on: “Antitubercular Hydrazines,” along with Drs. H. H. Fox and Richard J. Schnitzer, of Hoffman-La Roche.

1954.  UNARCO closed its Paterson, New Jersey plant, and moved it to Tyler, Texas.[35]

1955.  Selikoff received the Albert Lasker Clinical Medical Research Award for his work on the clinical trial of isoniazid to treat tuberculosis, along with Walsh McDermott and Carl Muschenheim, of the Hoffmann-La Roche Research Laboratories, and Edward H. Robitzek, of the Squibb Institute for Medical Research.[36]

1955.  Selikoff’s involvement in the isoniazid clinical trials continued to attract media attention. His first television appearance was panned, but he would later develop considerable public speaking skills.[37]

1955.  Sir Richard Doll published his epidemiologic study of lung cancer among British asbestos workers.[38]  This study was known to Selikoff, who relied upon it in his litigation reports to support the compensation claims of asbestos workers in the 1950s.[39]

1955. In 1955, American labor unions were well aware of the claim that asbestos causes lung cancer. Herbert K. Abrams, union physician and the Medical Director of Local 25 Chicago, Building Service Employees International Union, concluded that asbestos causes cancer in a prominent union journal.[40]

1956.  Selikoff became an associate attending physician for thoracic disease at Mt. Sinai Hospital.

1957.  For many years, Frederick Legrand had been a pipecoverer and asbestos worker for asbestos contracting firms. In February 1956, Legrand filed a successful claim for worker’s compensation for disability due to asbestosis.[41] Attorney William L. Brach filed perhaps the first civil action (as opposed to worker’s compensation claim), on behalf of LeGrand, against Johns-Manville, for asbestos-related disease, on July 17, 1957. Frederick LeGrande v. Johns-Manville Prods. Corp., No. 741-57 (D.N.J.).[42] Trial commenced on March 4, 1959, before the Hon. Honorable Reynier J. Wortendyke, Jr. In the middle of trial, Johns-Manville (JM)  settled the case for $35,000.[43] According to various accounts, JM badly mishandled the defense by falsely asserting that it had no knowledge of potential asbestosis hazards to end-users such as LeGrand. The defense had the dual liability of both being untrue and depriving JM of affirmative defenses of contributory negligence and assumption of risk. JM was apparently able to obtain a stipulation that LeGrand’s condition was not the result of asbestos in JM’s product, which JM used to hide the JM settlement from subsequent claimants. Frederick Legrand died in the fall of 1959.[44]

1957-07. The asbestos insulators’ union’s periodical, distributed to its members, notes that “[t]he problem of hazardous materials was again discussed with the importance of using preventative measures to eliminate inhalation. It is suggested that, when working under dusty conditions, respirators should be used at all times and gloves whenever conditions warrant.”[45]

1957-10. President Sickles, at the International Convention of the Asbestos Heat, Frost and Insulators Union, reported to his union’s delegates that he, “[b]eing well aware of the health hazards in the Asbestos industry, requested authority for the General Executive Board to make a study of the health hazards … that will enable the Board to adopt any policies that will tend to protect the health of our International membership.”[46]

1960.  Dr. J. Christopher Wagner published a case series of mesothelioma among persons exposed to crocidolite, in the region of South Africa where crocidolite is mined and milled. After this publication, the causal role of crocidolite became quickly accepted in the scientific and medical community.[47]

1960-1961.  Selikoff published two papers on the patho-physiology of asbestosis, based on data from 17 UNARCO workers,[48] obtained from his medico-legal evaluations of the men.[49]

 

Irving and Celia Selikoff from their 1961 Brazilian visa documents

1961-05. Asbestos insulators’ union discussed collaboration with scientists to discuss lung cancer and other diseases among its membership.[50]  Union members, intensely interested in legal redress for compensation, became aware of Selikoff’s research hypothesis in advance of Selikoff’s survey of the members’ smoking habits, which the workers had a motive to under report.

1961-11. The Asbestos insulators’ union’s magazine featured a full page warning of the grim reaper urging insulators to “Wear Your Respirator.”[51] The warning was developed under the guidance of C. V. Krieger of Local No. 28, Safety Superintendent at the Long Beach Naval Shipyard.

1962-07-12.  Selikoff visited Asbestos Corporation of America, an intermediary broker of asbestos fibers. In a memorandum Selikoff prepared from his discussions with Wade I. Duym, the general manager of the company, and others, he detailed the widespread use of amphibole asbestos fibers in a variety of products. He noted that amosite was used primarily in the insulation trade, and that it was the asbestos “of choice” for sprayed-on products, high temperature insulating cements and pipecovering (magnesia and calcium silicates). Selikoff described crocidolite, from Africa and Bolivia, as a strong, chemically resistant, relatively inexpensive fiber that was used in asbestos cement products, and in Kent cigarette filters.

1962-09. Selikoff presented to a meeting of the Asbestos Workers, to request their help in conducting his study of insulator mortality and morbidity. Irving Selikoff, “Speech at Asbestos Workers’ Union Annual Meeting,” The Asbestos Worker 8 (Sept. 1962).

1962.  Asbestos insulators’ union acknowledged that its leadership has been collaborating with Dr. Irving Selikoff.[52] In September 1962, Selikoff and colleagues began physical examinations of members of the New York and New Jersey locals.[53] `

1962.  In a publication for Naval personnel, with virtually no circulation in the general industrial community, the United States government acknowledged that shipyard and on-board exposures greatly exceeded the ACGIH’s then current TLV for asbestos.[54]

1963.  Selikoff established the Environmental Sciences Laboratory, later known as the Division of Environmental and Occupational Medicine, in would become the Mt. Sinai School of Medicine’s Department of Community Medicine.

1963-02. The asbestos insulation workers’ union announces that it has begun a large-scale program of examinations for asbestos-related disease in the members of the New York and New Jersey locals.[55]

1964.  Selikoff published his first article on cancer in a cohort of union asbestos insulators from New York and New Jersey.[56] Selikoff and his co-authors failed to disclose funding from the union, or the union members’ awareness of the research hypotheses under investigation.

1964.  In October 1964, Selikoff organized and co-chaired (with Dr. Jacob Churg) a conference, “The Biological Effects of Asbestos, for the New York Academy of Sciences, in New York City. The conference featured presentations and papers from many international investigators. Several presenters, including Selikoff, documented the prevalent use of amphibole asbestos (both crocidolite and amosite) in the United States.[57]

1965.  Papers presented at the 1964 New York Academy of Sciences conference were published in late 1965, in a non-peer reviewed publication, volume 132, of the Annals of the New York Academy of Sciences.

1965.  Selikoff testified on behalf of an insulator who claimed that asbestos exposure caused his colorectal cancer.[58] Forty years later, the Institute of Medicine (now the National Academy of Medicine) comprehensively reviewed the extant evidence and announced that the evidence was “suggestive but not sufficient to infer a causal relationship between asbestos exposure and pharyngeal, stomach, and colorectal cancers.”[59] None of Selikoff’s publications, including those on asbestos and colorectal cancer, disclosed his litigation testimonies for claimants.

1966 – 1972.  Selikoff continued to testify frequently in civil action and in worker compensation proceedings for claimants who alleged asbestos-related injuries.[60]  In 1972, Andrew Haas, President of the asbestos workers’ union thanked Selikoff for his “frequent” expert witness testimony on behalf of union members.[61]

1967-09. In an address to the International Association of Heat and Frost Insulators and Asbestos Workers, Selikoff acknowledged the widespread use of amosite, particularly in shipyards, the absence of lung cancer among non-smoking insulation workers, and the failure of more than 9 out of 10 insulators to wear respirators on dusty jobs. See Irving J. Selikoff, Address to the delegates of the twenty-first convention of the International Association of Heat and Frost Insulators and Asbestos Workers at 8, 9-10, 24 (Chicago, Illinois, Sept. 1967) (“I have yet to see a lung cancer in an asbestos worker who didn’t smoke cigarettes. … “[C]ancer of the lung could be wiped out in your trade if you people wouldn’t smoke cigarettes, period.”).

1968-09.  Selikoff “warns” the United States of asbestos hazards that existed and continue to exist in the government’s shipyards.[62] The warning was largely about seeking media attention by Selikoff; the government, and especially the Navy, had long known of asbestos hazards.[63]

1968-05.  Selikoff testified that all fibers are equally potent, to Congress in support of a bill that would become the OSH Act.

1968. The Mount Sinai School of Medicine opened in 1968, as part of The City University of New York. The first class in the newly formed medical school had 36 students in the entering class. The school was chartered in 1963. It is now known as the Icahn School of Medicine at Mount Sinai.

1969.  Selikoff served as president of the New York Academy of Sciences.

1969-05. Selikoff acknowledged that only four percent of insulators wore a mask despite extensive warnings.[64]

1972.  In a published study of variability in the interpretation of chest radiographs, Selikoff was shown consistently to over-read chest radiographs for potential asbestos-related abnormalities, when compared with other pulmonary experts on pneumoconiosis.[65]

1973.  Selikoff testified for the government in United States v. Reserve Mining Co., No. 5-72 Civil 19 (D. Minn. Sept. 21, 1973).[66]  On September 20, Selikoff testified about the town where Reserve Mining’s taconite mine was located: “I think we ought to have a sign at the entrance to sections of the town ‘Please Close Your Windows Before Driving Through’. I certainly would want to close mine.” When his testimony continued the following day, Selikoff acknowledged that he had been “facetious” in his previous day’s testimony.[67]

1974. After having given “facetious” testimony, Selikoff reduced his testifying activities. Marxist historians Jock McCulloch and Geoffrey Tweedale have falsely suggested that Selikoff “avoided the drama of the courtroom and the role of the expert witness” because of the drain on his time, his desire to avoid antagonizing industry, and his need to prevent discovery of trade union medical files.[68]

1974-05-20.  Selikoff’s father, Abraham Selecoff, died in Florida.[69]

1974.  Selikoff published a review on asbestos and gastrointestinal cancer, without disclosing his funding from the asbestos insulation union or his receipt of fees for litigation work in which he maintained a causal relationship in advance of any data.[70]

1978-07.  The National Cancer Institute (NCI) invited Dr. Hans Weill to co-chair a conference on lung cancer surveillance. Ten days later, the NCI retracted the invitation. When Weill inquired about the reasons for the shoddy treatment, an NCI official (Margaret Sloan) told him that “representatives of organized labor” objected to his participation. Sloan’s superior at NCI stated that Selikoff had raised the question whether the conference’s recommendations would lose credibility if Weill were a co-chair. When asked about his role in this sordid affair, Selikoff equivocated, saying he had “simply” said that “[s]ince Weill was a consultant to the Asbestos Information Center, I didn’t know if this would enhance or detract from hearing all points of view.”[71]

1979-11-05.  Barry Castleman, career testifier for the asbestos lawsuit industry, prepared a memorandum to Selikoff to urge him to resist allowing discovery of asbestos worker union members’ knowledge of the hazards of asbestos.[72]

1980-07-29.  A Newsday journalist reports that Selikoff is loath to talk about himself, and that he threatens to cut short the interview when asked about his background.[73]

1981.  Sir Richard Doll and Professor Richard Peto published a rebuttal to wildly exaggerated asbestos risk assessments based upon Selikoff’s insulator studies.[74]

1984.  Selikoff prepared a report on his group’s epidemiologic study of Electric Boat employees, who were engaged in the construction of submarines.[75]  The data did not fit the Mt. Sinai Catechism of large increased risks.[76]  Selikoff never published these data in a medical journal or a textbook.[77]

1985-03-10. Selikoff retires from Mount Sinai Medical School.[78]

1986-03.  Selikoff’s wife, Celia, died.[79]

1987 – 1989.  Selikoff’s insulator cohort study data took on an outsize importance in litigation because of plaintiffs’ heavy reliance upon his studies in court cases. When litigants asked for these data, Selikoff consistently refused to share, which necessitated federal court intervention.[80]

1988.  Selikoff and William Nicholson prepared a manuscript report of a study of the mortality experience at a New Jersey asbestos product manufacturing plant of Johns Manville.[81] Their report documented the substantial use of crocidolite in various products, and the resulting horrific mesothelioma mortality at this plant. Selikoff never published this crocidolite-exposed cohort, although he tirelessly republished his insulator cohort data repeatedly with the misrepresentation that the insulators were not exposed to crocidolite.

1990-06-07. Selikoff conspired with Ron Motley and others to pervert the course of justice by inviting judges with active asbestos dockets to a one-sided conference on asbestos science, and to pay for their travel and lodging. In his invitation to this ex parte soirée, Selikoff failed to mention that the funding came from plaintiffs’ counsel.[82]  Shortly after the Third Circuit spoke on the Mt. Sinai dress rehearsal for the plaintiffs’ asbestos property damage trial case, Judge Jack Weinstein issued a curious mea culpa. Because of a trial in progress, Judge Weinstein did not attend the “Third Wave” conference, but he and a state judge (Justice Helen Freedman) attended an ex parte private luncheon meeting with Dr. Selikoff. Here is how Judge Weinstein described the event:

“But what I did may have been even worse [than Judge Kelly’s conduct that led to his disqualification]. A state judge and I were attempting to settle large numbers of asbestos cases. We had a private meeting with Dr. Irwin [sic] J. Selikoff at his hospital office to discuss the nature of his research. He had never testified and would never testify. Nevertheless, I now think that it was a mistake not to have informed all counsel in advance and, perhaps, to have had a court reporter present and to have put that meeting on the record.”[83]

What is curious is that Judge Weinstein, usually a careful judge and scholar, was so incorrect about Dr. Selikoff’s having never testified. His error could have been avoided by a simple search in the Westlaw or LexisNexis databases. Judge Weinstein’s account points directly to Dr. Selikoff as the source for this falsehood.[84]

1990-10-02.  Selikoff wrote to Judge Jack Weinstein and Justice Helen Freedman, presumably after the “regrettable” ex parte luncheon meeting, to hold forth with his views on the health effects of occupational and para-occupational exposure to asbestos.

1992-05-20.  Selikoff died several months before the U.S. Court of Appeals for the Third Circuit condemned the Selikoff-Motley conspiracy.[85]

2013.  Follow up of the national insulator cohort fails to support multiplicative interaction between smoking and asbestos for lung cancer outcomes in the absence of asbestosis.[86]

[1] Rachel Maines, Asbestos and Fire: Technological Tradeoffs and the Body at Risk 155 (2005) (“charming, courageous, and compassion medical professional with more charisma than credentials”).

[2] Jock McCulloch & Geoffrey Tweedale, “Shooting the messenger: the vilification of Irving J. Selikoff,” 37 Internat’l J. Health Services 619 (2007); “Scientific Prestige, Reputation, Authority & The Creation of Scientific Dogmas” (Oct. 4, 2014); David Egilman, Geoffrey Tweedale, Jock McCulloch, William Kovarik, Barry Castleman, William Longo, Stephen Levin, and Susanna Rankin Bohme, “P.W.J. Bartrip’s Attack on Irving J. Selikoff,” 46 Am. J. Indus. Med. 151, 152 (2004) [Egilman (2004)].

[3] 84 Stat. 1590, et seq., 29 U.S.C. § 651, et seq.

[4] “The Legacy of Irving Selikoff & Wicked Wikipedia” (Mar. 1, 2015). See also “Hagiography of Selikoff” (Sept. 26, 2015); “Historians Should Verify Not Vilify or Abilify – The Difficult Case of Irving Selikoff” (Jan. 4, 2014).

[5] See, e.g., Philip Landrigan, “Stephen Levin, MD, honored with the Collegium Ramazzini’s Irving J. Selikoff Memorial Award in 2009.”

[6] See Wikipedia, “Irving Selikoff” (last visited Dec. 4, 2018).

[7] Kings County Birth Certificate no. 4595 (Jan. 15, 1915). His family later adopted the surname Selikoff. Irving Selikoff’s social security records list his father as Abraham Selikoff and his mother as Tillie Katz.

[8] Abraham Selecoff World War II draft registration, serial no. U1750.

[9] Abraham Selecoff World War II draft registration, serial no. U1750.

[10] See “The Asbestos Menace,” The Asbestos Worker 9-11 (Sept. 1930).

[11] Alice Hamilton, “Industrial Poisons,” American Federationist (1936). This journal was “The Official Magazine of the American Federation of Labor.”

[12] Bronx marriage certificate no. 8246 (1936); Bronx marriage license no. 8652 (1936). Irving’s parents were listed as Abraham Selikoff and Tillie Katz. His residence was at 109 W. 112th Street. Lydia was listed as the daughter of Mendel Kapilian and Bessie Weller. Irving and Lydia were divorced sometime between 1939 and 1941. The marriage certificates stated Lydia to have been 21 years old. Her Social Security records (SSN 112-052-2143), however, gave her birth date as April 22, 1917, (making her 19), and subsequent marriage names of Quint and Teichner.

[13] This and other details of Selikoff’s medical education come from Peter Bartrip’s exposé. Although Bartrip’s research was attacked for its allegedly gratuitous attacks on Selikoff’s research prowess, Bartrip’s account of Selikoff’s medical education in Scotland, Australia, and the United States has gone largely unrebutted, and must for the present be accepted. Peter W.J. Bartrip, “Irving John Selikoff and the Strange Case of the Missing Medical Degrees,” 58 J. History Med. 8 (2003) [Bartrip 2003]; Peter Bartrip, “Around the World in Nine Years: A Medical Education Revisited,” 59 J. History of Med. 135 (2004). One group of plaintiffs’ expert witnesses took Bartrip to task for not disclosing that he had served as a defense expert witness, but none of the complainants disclosed their substantial testimonial adventures for the litigation industry! While making some interesting points, these critics of Bartrip did not really contest his historical work on Selikoff: “Bartrip’s critiques of Anderson’s College (AC) and Middlesex University School of Medicine (MSUM) may be accurate, but are beside the point.” David Egilman, Geoffrey Tweedale, Jock McCulloch, William Kovarik, Barry Castleman, William Longo, Stephen Levin, and Susanna Rankin Bohme, “P.W.J. Bartrip’s Attack on Irving J. Selikoff,” 46 Am. J. Indus. Med. 151, 152 (2004).

[14] Bartrip 2003, at 15 & n.44-51.

[15] Bartrip 2003, at 17 & n.54-55.

[16] Bartrip 2003 at 18.

[17] William J. Nicholson & Alvin S. Teirstein, “Remembering Irving J. Selikoff,”  61 Mt. Sinai J. Med. 500 (1994) [Nicholson & Teirstein]. This account seems doubtful; Selikoff would not have an M.D. degree until 1943, and then from a school that was about to lose its accreditation.

[18] See Stephen Rushmore, “Middlesex University School of Medicine,” 230 New Engl. J. Med. 217 (1944).

[19] Anthony Seaton, “The Strange Case of Irving Selikoff,” 60 Occup. Med. 53 (2010); Peter W.J. Bartrip, “Irving John Selikoff and the Strange Case of the Missing Medical Degrees,” 58 J. History Med. 3, 27 & n.88-92 (2003) [cited as Bartrip].

[20] Bartrip 2003 at 22.

[21] Bartrip 2003 at 22.

[22] Bartrip 2003 at 21.

[23] New York County marriage license no. 3879 (Feb. 2, 1946). Celia had been married to Nathan Michaels in 1937. Manhattan Marriage License no. 21454 (1937).

[24] Nicholson & Teirstein.

[25] Manhattan Marriage License  21527 (1947).

[26] City Directory of Paterson, New Jersey at p. 218 (1949).

[27] Manhattan Telephone Directory (1949).

[28] George W. Conk, “Deadly Dust: Occupational Health and Safety as a Driving Force in Workers’ Compensation Law and the Development of Tort Doctrine,” 69 Rutgers L. Rev. 1140, 1154 & n. 136 (2017).

[29] Jon L. Gelman, “History of Asbestos and the Law” (Jan. 2, 2001). Carl Gelman was a life-long Paterson resident. His legal practice specialized in workers’ compensation, and he chaired state bar association’s workers’ compensation section for several years. His practice represented claimants from 1936, until his retirement in 1986. In the mid-1970s, with Karl Asch, Gelman’s firm sued asbestos suppliers to Raybestos Manhattan on behalf of multiple employees.Gelman died on February 24, 2009. “Obituary for Carl Gelman,” The Record/Herald News (Mar. 16, 2009); “163 Who Had Jobs at Raybestos Sue,” N.Y. Times (May 7, 1975). The suit for $326 million settled for $15.5 million.

[30] Barry I. Castleman, Asbestos: Medical and Legal Aspects at 142 (1984); Matt Mauney, “Unarco,” Mesothelioma Center (Nov. 2018). Of course, there were no data to support this claim in 1952. Selikoff was publically and positionally committed to his causal hypothesis as a conclusion well in advance of conducting any studies or having any supporting data.

[31] Irving J. Selikoff, E. Cuyler Hammond, and Jacob Churg, “The carcinogenicity of amosite asbestos,” 25 Arch. Envt’l Health 183 (1972). This 1972 publication was the first epidemiologic study on the carcinogenicity of amosite.

[32] David E. Lilienfeld, “The Silence: The Asbestos Industry and Early Occupational Cancer Research – A Case Study,” 81 Am. J. Pub. Health 791 (1991).

[33] Irving J. Selikoff, Edward H. Robitzek, and George G. Ornstein, “Treatment of pulmonary tuberculosis with hydrazine derivatives of isonicotinic acid,” 150 J. Am. Med. Ass’n 973 (1952).

[34] “TB Milestone,” Life (Mar. 3, 1952).

[35] Irving J. Selikoff, “Asbestos in Paterson, New Jersey and Tyler, Texas – A Tale of Two Cities,” Transcript of Lecture (Houston, Texas, Oct. 11, 1979).

[36] See “Isoniazid for treating tuberculosis.”

[37] See “Medical Horizons,” Broadcasting * Telecasting at 14 (Nov. 21, 1955) (describing Selikoff as a plodding presenter). See also “Irving Selikoff – Media Plodder to Media Zealot” (Sept. 9, 2014).

[38] Richard Doll, “Mortality from Lung Cancer in Asbestos Workers,”  12 Br. J. Indus. Med. 81 (1955).

[39] Selikoff letter to Thomas Mancuso (Mar. 30, 1989).

[40] Herbert K. Abrams, “Cancer in Industry,” American Federationist (1955). Dr. Abrams’ article was republished in many union newsletters. See Herbert K. Abrams, “Cancer in Industry,” 69 The Painter & Decorator 15, 16 (Mar. 1955); see also Lester Breslow, LeMar Hoaglin, Gladys Rasmussen & Herbert K. Abrams, “Occupations and Cigarette Smoking as Factors in Lung Cancer,” 44 Am. J. Pub. Health. 171, 171 (1954).

[41] A. C. & S., Inc. v. Asner, 104 Md. App. 608, 633, 657 A.2d 379 (Md. Ct. Spec. App. 1995).

[42] Paul Brodeur, Outrageous Misconduct: The Asbestos Industry on Trial 236-39 (1985). According to Brodeur’s account, Johns-Manville’s defense was clever by halves. By claiming that the company had no knowledge that asbestos could be harmful to applicators such as LeGrand, the company deprived itself of assumption-of-risk and contributory negligence defenses.  The company also set itself up to be brutally contradicted by internal documents and communications that showed an awareness of hazards to pipecoverers. By the time J-M understood that the question of responsibility required acknowledging potential hazards that were in the control of the contractors themselves (such as the use of proper respirators and the like), the company filed for bankruptcy.

[43] Greg Gordon, “Health studies drew little action,” Star Tribune (Nov. 9, 2003); Wondie Russell, “Memorandum re Frederick LeGrande v. J-M Products Corp,”(Nov. 3, 1982).

[44] The Freehold Transcript and The Monmouth Inquirer (Freehold, New Jersey) at 17 (Thurs., Oct. 22, 1959).

[45] Asbestos Worker (July 1957).

[46] The Asbestos Worker at 1 (Oct, 1957) (reporting on the Asbestos Workers’ 19th General Convention).

[47] See J. Christopher Wagner, C.A. Sleggs, and Paul Marchand, “Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province,” 17 Br. J. Indus. Med. 260 (1960); J. Christopher Wagner, “The discovery of the association between blue asbestos and mesotheliomas and the aftermath,” 48 Br. J. Indus. Med. 399 (1991).

[48] Arthur M. Langer, “Asbestos Studies in the Environmental Sciences Laboratory Mount Sinai School of Medicine 1965 – 1985: Investigations Reflecting State-of-the-Art; Contributions to the Understanding of Asbestos Medicine” (Unpublished MS, Nov. 7, 2008).

[49] Alvin S. Tierstein, A. Gottlieb, Mortimer E. Bader, Richard A. Bader & Irving Selikoff, “Pulmonary mechanics in asbestosis of the lungs,” 8 Clin. Res. 256 (1960); Mortimer E. Bader, Richard A. Bader & Irving Selikoff, “Pulmonary function in asbestosis of the lung; an alveolar-capillary block syndrome, 30 Am. J. Med. 235 (1961).

[50] Asbestos Worker (May 1961) (“The subject matter of Health Hazards was discussed and President Sickles reported on the possibility of an early meeting with people connected with the Medical Association for the purpose of running various tests on certain materials used by our membership in order to determine the extent of their contribution to lung cancer, silicosis, asbestosis, tuberculosis, etc.”).

[51] 15 The Asbestos Worker at 29 (Nov. 1961).

[52] Asbestos Worker (May 1962) (“President Sickles advised the Board as to a meeting which had been held with Vice President Rider and a Dr. Irving Selikoff, of the Paterson Clinic in connection with our issue on Health Hazards and the Committee on Health Hazards with the approval of the Board instructed President Sickles to continue his efforts in this direction.”)

[53] Asbestos Worker at 25 (Feb. 1963).

[54] Capt. H.M. Robbins & William T. Marr, “Asbestosis,” 19 Safety Review 10 (1962) (noting that asbestos dust counts of 200 million particles per cubic foot were not uncommon during insulation ripouts onboard naval vessels).

[55] “Progress Report on Health Hazards,” 16 The Asbestos Worker 25 (Feb. 1963) (the examination were arranged by President Carl Sickles, Vice-President Hugh Mulligan and Vice-President George Rider of the Health Hazards Committee).

[56] Irving J. Selikoff, Jacob Churg, and E. Cuyler Hammond, “Asbestos Exposure and Neoplasia,” 188 J. Am. Med. Ass’n 22 (1964).

[57] Irving J. Selikoff, Jacob Churg, E. Cuyler Hammond, “The Occurrence of Asbestosis among Insulation Workers in the United States,” 132 Ann. N.Y. Acad. Sci. 139, 142 (1965) (“In later specimens so obtained, crocidolite has also been found. Moreover, materials used for ship insulation, while containing the same amounts of asbestos as above, began in 1934 to have significant amounts of amosite in addition to chrysotile, because of the lighter weight of the material.”); Harrington, “Chemical Studies of Asbestos,” 132 Ann. N.Y. Acad. Sci. 31, 41 (1965) (reporting the finding of chrysotile and crocidolite asbestos in equal proportions in specimens of 85% magnesia pipe-covering sections); N.W. Hendry, “The Geology, Occurrences, and Major Uses of Asbestos 132 Annals N.Y. Acad. Sci. 12, 19 (1965) (reporting that, in 1963, the U.S. used  22,000 tons of amosite in manufactured products, and 17,000 tons of crocidolite in acid-resistent filters, packings, insulations, and certain types of lagging. United States Department of Commerce statistics show that for the years 1957 to 1962, more crocidolite was used in the United States than was amosite. In 1962, the use of blue was twice as great as that for brown. 132 Ann. N.Y. Acad. Sci. at 753, Table 17 (1965); see also id. at 762, Table 23 (1965) (South African blue fiber imports exceeded brown fiber imports, starting about 1954). See also “Selikoff and the Mystery of the Disappearing Amphiboles” (Dec. 10, 2010); James R. Millette, Steven Compton, and Christopher DePasquale, “Microscopical Analyses of Asbestos-Cement Pipe and Board,” 66 The Microscope 3 (2018) (reporting analyses of cement formulations with substantial crocidolite).

[58]  “Health Hazard Progress Notes,”16 The Asbestos Worker 13 (May 1966) (“A recent decision has widened the range of compensable diseases for insulation workers even further. A member of Local No. 12. Unfortunately died of a cancer of the colon. Dr. Selikoff reported to the compensation court that his research showed that these cancers of the intestine were at least three times as common among the insulation workers as in men of the same age in the general population. Based upon Dr. Selikoff’s testimony, the Referee gave the family a compensation award, holding that the exposure to many dusts during employment was responsible for the cancer. The insurance company appealed this decision. A special panel of the Workman’s Compensation Board reviewed the matter and agreed with the Referee’s judgement and affirmed the compensation award. This was the first case in which a cancer of the colon was established as compensable and it is likely that this case will become an historical precedent.”)

[59] Jonathan Samet, et al., eds., Institute of Medicine Review of Asbestos: Selected Cancers (2006); see also Richard Doll & Julian Peto, Asbestos: Effects on health of exposure to asbestos 8 (1985) (“In particular, there are no grounds for believing that gastrointestinal cancers in general are peculiarly likely to be caused by asbestos exposure.”).

[60] “Selikoff and the Mystery of the Disappearing Testimony” (Dec. 3, 2010); see, e.g., Barros v. United States, 147 F.Supp. 340, 343-44 (E.D.N.Y. 1957) (noting that Dr. Selikoff testified for seaman suing for maintenance and cure as a result of a slip and fall; finding for respondent against libelant); DeRienzo v. Passaic Fire Dept., reported in The News (Paterson, New Jersey) at 27 (Feb. 14, 1957) (Selikoff was a witness for the claimant); Bradshaw v. Twin City Insulation Co. Ltd., Indus. Ct. Indiana, Claim No. O.D.1454 (Oct. 14, 1966); Bradshaw v. Johns-Manville Sales Corp., Civ. Action No. 29433, E. D. Mich. S. Div. (July 6, 1967); Bambrick v. Asten Hill Mfg. Co., Pa. Cmwlth. Ct. 664 (1972); Tomplait v. Combustion Engineering Inc.., E. D. Tex. Civ. Action No. 5402 (March 4, 1968); Babcock & Wilcox, Inc. v. Steiner, 258 Md. 468, 471, 265 A.2d 871 (1970) (affirming workman compensation award for asbestosis); Rogers v. Johns-Manville Products Corp., Cir. Ct. Mo., 16th Jud. Cir., Div. 9, Civ. Action No. 720,071 (Feb. 19, 1971); Utter v. Asten-Hill Mfg. Co., 453 Pa. 401 (1973); Karjala v Johns-Manville Products Corp., D. Minn., Civ. Action Nos. 5–71 Civ. 18, and Civ. 40 (Feb. 8, 1973); Culp Industrial Insulation v. Commonwealth of Pennsylvania Workmen’s Compensation Appeal Board, 57 Pa. Commonwealth Ct. 599, 601-602 (1981).

[61] Andrew Haas, Comments from the General President, 18 Asbestos Worker (Nov. 1972); see also Peter W.J. Bartrip, “Irving John Selikoff and the Strange Case of the Missing Medical Degrees,” 58 J. History Med. 3, 27 & n.88-92 (2003) (citing Haas).

[62] Thomas O’Toole, “U.S. Warned of Asbestos Peril,” Wash. Post. A4 (Dec. 4, 1968).

[63] “The United States Government’s Role in the Asbestos Mess” (Jan. 31, 2012). See also Kara Franke & Dennis Paustenbach, “Government and Navy knowledge regarding health hazards of Asbestos: A state of the science evaluation (1900 to 1970),” 23(S3) Inhalation Toxicology 1 (2011); Capt. H.M. Robbins & W.T. Marr, “Asbestosis,” Safety Review (Oct. 1962); See also Walter Olson, “Asbestos awareness pre-Selikoff,” (Oct. 19, 2007).

[64] “Green Sheet,” The Asbestos Worker (May 1969).

[65] See Charles E. Rossiter, “Initial repeatability trials of the UICC/Cincinnati classification of the radiographic appearances of pneumoconioses,” 29 Brit. J. Indus. Med. 407 (1972) (among physician readers of chest radiographs, Selikoff was at the extreme of least likely to call a film normal (less than half the average of all readers), and the most likely to interpret films to show excess profusion of small irregular linear densities). See “Selikoff and the Mystery of the Disappearing Asbestosis” (Dec. 6, 2010). The unions, of course, interested in maximizing compensation for their members loved Selikoff’s over-reading of chest films. Selikoff’s colleagues (Ruth Lilis) routinely teased Selikoff about not being able to read chest radiographs. Selikoff was rumored to have taken and failed the NIOSH B-Reader examination, a rumor which needs to be resolved by a FOIA request.

[66] United States v. Reserve Mining Co. See United States v. Reserve Mining Co., 56 F.R.D. 408 (D.Minn.1972); Armco Steel Corp. v. United States, 490 F.2d 688 (8th Cir. 1974); United States v. Reserve Mining Co., 380 F.Supp. 11 (D.Minn.1974); Reserve Mining Co. v. United States, 498 F.2d 1073 (8th Cir. 1974); Minnesota v. Reserve Mining Co., 418 U.S. 911 (1974); Minnesota v. Reserve Mining Co., 419 U.S. 802 (1974); United States v. Reserve Mining Co., 394 F.Supp. 233 (D.Minn.1974); Reserve Mining Co. v. Environmental Protection Agency, 514 F.2d 492 (8th Cir. 1975); Minnesota v. Reserve Mining Co., 420 U.S. 1000, 95 S.Ct. 1441, 43 L.Ed.2d 758 (1975); Reserve Mining Co. v. Lord, 529 F.2d 181 (8th Cir. 1976); United States v. Reserve Mining Co., 408 F.Supp. 1212 (D.Minn.1976); United States v. Reserve Mining Co., 412 F.Supp. 705 (D.Minn.1976); United States v. Reserve Mining Co., 417 F.Supp. 789 (D.Minn.1976); United States v. Reserve Mining Co., 417 F.Supp. 791 (D.Minn.1976); 543 F.2d 1210 (1976).

[67] Robert V. Bartlett, The Reserve Mining Controversy: Science, Technology, and Environmental Quality 140-41 (1980) (describing Selikoff’s testimony).

[68] Jock McCulloch & Geoffrey Tweedale, Defending the Indefensible: The Global Asbestos Industry and its Fight for Survival: The Global Asbestos Industry and its Fight for Survival 95 & n.36 (2008). These authors ignored other reasons Selikoff later stood down from the witness chair: his self-serving insistence upon the importance of his own research detracted from the work of previous authors (e.g., Sir Richard Doll, J. Christopher Wagner, et al.) in litigation of personal injury claims of asbestos health effects. Plaintiffs’ counsel needed to push back the dates of first knowledge of asbestos health effects well before Selikoff’s first insulator study in 1964. The litigation industry needed Selikoff to continue to generate publicity, and to stop testifying. Selikoff surely must have had some concerns about how further testifying would eventually lead to questions about his credentials. Furthermore, Selikoff had an entire generation of younger, less politically visible colleagues at Mt. Sinai to fill the ranks of expert witnesses for the litigation industry (Miller, Levin, Nicholson, Lillis, Daum, Anderson, Frank, et al.).

[69] Obituary for Abraham Selecoff, The Miami Herald (May 22, 1974).

[70] Irving J. Selikoff, “Epidemiology of gastrointestinal cancer,” 9 Envt’l Health Persp. 299 (1974) (arguing for causal conclusion between asbestos and all gastrointestinal cancers).

[71] Nicholas Wade, “The Science and Politics of a Disinvitation,” 201 Science 892 (1978) (commenting that the NCI was negligent in failing to evaluate the ad hominem opinions given to it by Selikoff).

[72] See “The Selikoff – Castleman Conspiracy” (Mar. 13, 2011); “What Happens When Historians Have Bad Memories” (Mar. 15, 2014); “Castleman-Selikoff – Can Their Civil Conspiracy Survive Death?” (Dec. 3, 2018). In 2014, Castleman testified that he has no recollection of the memorandum, but he did not deny that had written it.

[73] B.D. Colen, “Knowing When the Chemistry is Right,” Newsday (Suffolk Edition) (Melville, New York) at 85 (Tue., July 29, 1980).

[74] See Richard Doll & Richard Peto, “The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today,” 66 J. Nat’l Cancer Inst. 1191 (1981).

[75] Irving Selikoff & William Nicholson, “Mortality Experience of 1,918 Employees of the Electric Boat Company, Groton, Connecticut January 1, 1967 – June 30, 1978” (Jan. 27, 1984).

[76] “The Mt. Sinai Catechism” (June 5, 2013).

[77] “Irving Selikoff and the Right to Peaceful Dissembling” (June 5, 2013).

[78] Leo H. Caney, “Noted Cancer Researcher Altering Role,” N.Y. Times (Mar. 10, 1985).

[79] Celia Selikoff Social Security Records, SSN 064-12-6401. Celia was born on Sept. 12, 1908.

[80] A New York state trial court initially sided with Selikoff over this subpoena battle. In re R.J. Reynolds Tobacco Co., 136 Misc.2d 282, 518 N.Y.S.2d 729 (N.Y. Sup. Ct., N.Y. Cty. 1987). The federal court subsequently required Selikoff to honor another litigant’s subpoena. In re American Tobacco Co., 866 F.2d 552 (2d Cir. 1989).

[81] William J. Nicholson & Irving J. Selikoff, “Mortality experience of asbestos factory workers; effect of differing intensities of asbestos exposure”: unpublished manuscript produced in litigation (1988) (“[O]ther asbestos varieties (amosite, crocidolite, anthophyllite) were also used for some products. In general, chrysotile was used for textiles, roofing materials, asbestos cements, brake and friction products, fillers for plastics, etc.; chrysotile with or without amosite for insulation materials; chrysotile and crocidolite for a variety of asbestos cement products.”).

[82] In re School Asbestos Litigation, 977 F.2d 764 (3d Cir. 1992). See Cathleen M. Devlin, “Disqualification of Federal Judges – Third Circuit Orders District Judge James McGirr Kelly to Disqualify Himself So As To Preserve ‘The Appearance of Justice’ Under 28 U.S.C. § 455 – In re School Asbestos Litigation (1992),” 38 Villanova L. Rev. 1219 (1993); Bruce A. Green, “May Judges Attend Privately Funded Educational Programs? Should Judicial Education Be Privatized?: Questions of Judicial Ethics and Policy,” 29 Fordham Urb. L.J. 941, 996-98 (2002).

[83] Jack B. Weinstein, “Learning, Speaking, and Acting: What Are the Limits for Judges?” 77 Judicature 322, 326 (May-June 1994) (emphasis added). Judge Weinstein’s false statement that Selikoff “had never testified” not only reflects an incredible and uncharacteristic naiveté by a distinguished evidence law scholar, but the false statement was in a journal, Judicature, which was widely circulated to state and federal judges. The source of the lie appears to have been Selikoff himself in the ethically dodgy ex parte meeting with judges actively presiding over asbestos personal injury cases.

[84] Jack B. Weinstein, “Learning, Speaking, and Acting: What Are the Limits for Judges?” 77 Judicature 322, 326 (May-June 1994). The point apparently weighed on Judge Weinstein’s conscience. He repeated his mea culpa almost verbatim, along with the false statement about Selikoff’s never having testified, in a law review article in 1994, and then incorporated the misrepresentation into a full-length book. See Jack B. Weinstein, “Limits on Judges’ Learning, Speaking and Acting – Part I- Tentative First Thoughts: How May Judges Learn?” 36 Ariz. L. Rev. 539, 560 (1994) (“He [Selikoff] had never testified and would   never testify.”); Jack B. Weinstein, Individual Justice in Mass Tort Litigation: The Effect of Class Actions, Consolidations, and other Multi-Party Devices 117 (1995) (“A court should not coerce independent eminent scientists, such as the late Dr. Irving Selikoff, to testify if, like he, they prefer to publish their results only in scientific journals.”).

[85] Social Security records for Irving John Selikoff, social sec. no. 085-16-1882. See Bruce Lambert, “Irving J. Selikoff Is Dead at 77; TB Researcher Fought Asbestos,” N.Y. Times (May 22, 1992).

[86] Steve Markowitz, Stephen Levin, Albert Miller, and Alfredo Morabia, “Asbestos, Asbestosis, Smoking and Lung Cancer: New Findings from the North American Insulator Cohort,” Am. J. Respir. & Critical Care Med. (2013)).

Posted in Asbestos, Expert Witnesses, State of the Art | 5 Comments »

Reference Manual – Desiderata for 4th Edition – Part VI – Rule 703

February 17th, 2023

One of the most remarkable, and objectionable, aspects of the third edition was its failure to engage with Federal Rule of Evidence of 703, and the need for courts to assess the validity of individual studies relied upon. The statistics chapter has a brief, but important discussion of Rule 703, as does the chapter on survey evidence. The epidemiology chapter mentions Rule 703 only in a footnote.[1]

Rule 703 appears to be the red-headed stepchild of the Federal Rules, and it is often ignored and omitted from so-called Daubert briefs.[2] Perhaps part of the problem is that Rule 703 (“Bases of an Expert”) is one of the mostly poorly drafted rules in the Federal Rules of Evidence:

“An expert may base an opinion on facts or data in the case that the expert has been made aware of or personally observed. If experts in the particular field would reasonably rely on those kinds of facts or data in forming an opinion on the subject, they need not be admissible for the opinion to be admitted. But if the facts or data would otherwise be inadmissible, the proponent of the opinion may disclose them to the jury only if their probative value in helping the jury evaluate the opinion substantially outweighs their prejudicial effect.”

Despite its tortuous wording, the rule is clear enough in authorizing expert witnesses to rely upon studies that are themselves inadmissible, and allowing such witnesses to disclose the studies that they have relied upon, when there has been the requisite showing of probative value that outweighs any prejudice.

The statistics chapter in the third edition, nonetheless, confusingly suggested that

“a particular study may use a method that is entirely appropriate but that is so poorly executed that it should be inadmissible under Federal Rules of Evidence 403 and 702. Or, the method may be inappropriate for the problem at hand and thus lack the ‘fit’ spoken of in Daubert. Or the study might rest on data of the type not reasonably relied on by statisticians or substantive experts and hence run afoul of Federal Rule of Evidence 703.”[3]

Particular studies, even when beautifully executed, are not admissible. And particular studies are not subject to evaluation under Rule 702, apart from the gatekeeping of expert witness opinion testimony that is based upon the particular studies. To be sure, the reference to Rule 703 is important and welcomed counter to the suggestion, elsewhere in the third edition, that courts should not look at individual studies. The independent review of individual studies is occasionally lost in the shuffle of litigation, and the statistics chapter is correct to note an evidentiary concern whether each individual study may or may not be reasonably relied upon by an expert witness. In any event, reasonably relied upon studies do not ipso facto become admissible.

The third edition’s chapter on Survey Research contains the most explicit direction on Rule 703, in terms of courts’ responsibilities.  In that chapter, the authors instruct that Rule 703:

“redirect[ed] attention to the ‘validity of the techniques employed’. The inquiry under Rule 703 focuses on whether facts or data are ‘of a type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject’.”[4]

Although Rule 703 is clear enough on admissibility, the epidemiology chapter described epidemiologic studies broadly as admissible if sufficiently rigorous:

“An epidemiologic study that is sufficiently rigorous to justify a conclusion that it is scientifically valid should be admissible, as it tends to make an issue in dispute more or less likely.”[5]

The authors of the epidemiology chapter acknowledge, in a footnote, “that [h]earsay concerns may limit the independent admissibility of the study, but the study could be relied on by an expert in forming an opinion and may be admissible pursuant to Fed. R. Evid. 703 as part of the underlying facts or data relied on by the expert.”[6]

This footnote is curious, and incorrect. There is no question that hearsay “concerns” “may limit” admissibility of a study; hearsay is inadmissible unless there is a statutory exception.[7] Rule 703 is not one of the exceptions to the rule against hearsay in Article VIII of the Federal Rules of Evidence. An expert witness’s reliance upon a study does not make the study admissible. The authors cite two cases,[8] but neither case held that reasonable reliance by expert witnesses transmuted epidemiologic studies into admissible evidence. The text of Rule 703 itself, and the overwhelming weight of case law interpreting and applying the rule,[9]  makes clear that the rule does not render scientific studies admissible. The two cases cited by the epidemiology chapter, Kehm and Ellis, both involved “factual findings” in public investigative or evaluative reports, which were independently admissible under Federal Rule of Evidence 803(8)(C).[10] As such, the cases failed to support the chapter’s suggestion that Rule 703 is a rule of admissibility for epidemiologic studies. The third edition thus, in one sentence, confused Rule 703 with an exception to the rule against hearsay, which would prevent the statistically based epidemiologic studies from being received in evidence. The point was reasonably clear, however, that studies “may be offered” to explain an expert witness’s opinion. Under Rule 705, that offer may also be refused.

The Reference Manual was certainly not alone in advancing the notion that studies are themselves admissible. Other well-respected evidence scholars have misstated the law on this issue.[11] The fourth edition would do well to note that scientific studies, and especially epidemiologic studies, involve multiple levels of hearsay. A typical epidemiologic study may contain hearsay leaps from patient to clinician, to laboratory technicians, to specialists interpreting test results, back to the clinician for a diagnosis, to a nosologist for disease coding, to a national or hospital database, to a researcher querying the database, to a statistician analyzing the data, to a manuscript that details data, analyses, and results, to editors and peer reviewers, back to study authors, and on to publication. Those leaps do not mean that the final results are thus untrustworthy or not reasonably relied upon, but they do raise well-nigh insuperable barriers to admissibility. The inadmissibility of scientific studies is generally not problematic because Rule 703 permits testifying expert witnesses to formulate opinions based upon facts and data, which are not themselves admissible in evidence. The distinction between relied upon, and admissible, studies is codified in the Federal Rules of Evidence, and in virtually every state’s evidence law.

The fourth edition might well also note that under Rule 104(a), the Rules of Evidence themselves do not govern a trial court’s preliminary determination, under Rules 702 or 703, of the admissibility of an expert witness’s opinion, or the appropriateness of reliance upon a particular study. Although Rule 705 may allow disclosure of facts and data described in studies, it is not an invitation to permit testifying expert witnesses to become a conduit for off-hand comments and opinions in the introduction or discussion sections of relied upon articles.[12] The wholesale admission of such hearsay opinions undermines the court’s control over opinion evidence. Rule 703 authorizes reasonable reliance upon “facts and data,” not every opinion that creeps into the published literature.

Reference Manual’s Disregard of Study Validity in Favor of the “Whole Tsumish”

The third edition evidence considerable ambivalence in whether trial judges should engage in resolving disputes about the validity of individual studies relied upon by expert witnesses. Since 2000, Rule 702 clearly required such engagement, which made the Manual’s hesitancy, on the whole, unjustifiable.  The ambivalence with respect to study validity, however, was on full display in the late Professor Margaret Berger’s chapter, “The Admissibility of Expert Testimony.”[13] Berger’s chapter criticized “atomization,” or looking at individual studies in isolation, a process she described pejoratively as “slicing-and-dicing.”[14]

Drawing on the publications of Daubert-critic Susan Haack, Berger appeared to reject the notion that courts should examine the reliability of each study independently.[15] Berger described the “proper” scientific method, as evidenced by works of the International Agency for Research on Cancer (IARC), the Institute of Medicine, the National Institute of Health, the National Research Council, and the National Institute for Environmental Health Sciences, “is to consider all the relevant available scientific evidence, taken as a whole, to determine which conclusion or hypothesis regarding a causal claim is best supported by the body of evidence.”[16]

Berger’s description of the review process, however, was profoundly misleading in its incompleteness. Of course, scientists undertaking a systematic review identify all the relevant studies, but some of the “relevant” studies may well be insufficiently reliable (because of internal or external validity issues) to answer the research question at hand. All the cited agencies, and other research organizations and researchers, exclude studies that are fundamentally flawed, whether as a result of bias, confounding, erroneous data analyses, or related problems. Berger cited no support for her remarkable suggestion that scientists do not make “reliability” judgments about available studies when assessing the “totality of the evidence.”[17]

Professor Berger, who had a distinguished career as a law professor and evidence scholar, died in November 2010, before the third edition was published. She was no friend of Daubert,[18] but her antipathy remarkably outlived her. Berger’s critical discussion of “atomization” cited the notorious decision in Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11, 26 (1st Cir. 2011), which was decided four months after her passing.[19]

Professor Berger’s contention about the need to avoid assessments of individual studies in favor of the whole “tsumish” must also be rejected because Federal Rule of Evidence 703 requires that each study considered by an expert witness “qualify” for reasonable reliance by virtue of the study’s containing facts or data that are “of a type reasonably relied upon by experts in the particular field forming opinions or inferences upon the subject.” One of the deeply troubling aspects of the Milward decision is that it reversed the trial court’s sensible decision to exclude a toxicologist, Dr. Martyn Smith, who outran his headlights on issues having to do with a field in which he was clearly inexperienced – epidemiology.

Another curious omission in the third edition’s discussions of Milward is the dark ethical cloud of misconduct that hovers over the First Circuit’s reversal of the trial court’s exclusions of Martyn Smith and Carl Cranor. On appeal, the Council for Education and Research on Toxics (CERT) filed an amicus brief in support of reversing the exclusion of Smith and Cranor. The CERT amicus brief, however, never disclosed that CERT was founded by Smith and Cranor, and that CERT funded Smith’s research.[20]

Rule 702 requires courts to pay attention to, among other things, the sufficiency of the facts and data relied upon by expert witnesses. Rule 703’s requirement that individual studies must be reasonably relied upon is an important additional protreptic against the advice given by Professor Berger, in the third edition.

[1] The index notes the following page references for Rule 703: 214, 361, 363-364, and 610 n.184.

[2] See David E. Bernstein & Eric G. Lasker,“Defending Daubert: It’s Time to Amend Federal Rule of Evidence 702,” 57 William & Mary L. Rev. 1, 32 (2015) (“Rule 703 is frequently ignored in Daubert analyses”);  Schachtman, “Rule 703 – The Problem Child of Article VII,” 17 Proof 3 (Spring 2009); Schachtman “The Effective Presentation of Defense Expert Witnesses and Cross-examination of Plaintiffs’ Expert Witnesses”; at the ALI-ABA Course on Opinion and Expert Witness Testimony in State and Federal Courts (February 14-15, 2008). See also Julie E. Seaman, “Triangulating Testimonial Hearsay: The Constitutional Boundaries of Expert Opinion Testimony,” 96 Georgetown L.J. 827 (2008); “RULE OF EVIDENCE 703 — Problem Child of Article VII” (Sept. 19, 2011); “Giving Rule 703 the Cold Shoulder” (May 12, 2012); “New Reference Manual on Scientific Evidence Short Shrifts Rule 703,” (Oct. 16, 2011).

[3] RMSE3d at 214.

[4] RMSE3d at 364 (internal citations omitted).

[5] RMSE 3d at 610 (internal citations omitted).

[6] RSME3d at 601 n.184.

[7] Rule 802 (“Hearsay Rule”) “Hearsay is not admissible except as provided by these rules or by other rules prescribed by the Supreme Court pursuant to statutory authority or by Act of Congress.”

[8] Kehm v. Procter & Gamble Co., 580 F. Supp. 890, 902 (N.D. Iowa 1982) (“These [epidemiologic] studies were highly probative on the issue of causation—they all concluded that an association between tampon use and menstrually related TSS [toxic shock syndrome] cases exists.”), aff’d, 724 F.2d 613 (8th Cir. 1984); Ellis v. International Playtex, Inc., 745 F.2d 292, 303 (4th Cir. 1984). The chapter also cited another the en banc decision in Christophersen for the proposition that “[a]s a general rule, questions relating to the bases and sources of an expert’s opinion affect the weight to be assigned that opinion rather than its admissibility. . . . ” In the Christophersen case, the Fifth Circuit was clearly addressing the admissibility of the challenged expert witness’s opinions, not the admissibility of relied-upon studies. Christophersen v. Allied-Signal Corp., 939 F.2d 1106, 1111, 1113-14 (5th Cir. 1991) (en banc) (per curiam) (trial court may exclude opinion of expert witness whose opinion is based upon incomplete or inaccurate exposure data), cert. denied, 112 S. Ct. 1280 (1992).

[9] Interestingly, the authors of this chapter abandoned their suggestion, advanced in the second edition, that studies relied upon “might qualify for the learned treatise exception to the hearsay rule, Fed. R. Evid. 803(18), or possibly the catchall exceptions, Fed. R. Evid. 803(24) & 804(5).” which was part of their argument in the Second Edition. RMSE 2d at 335 (2000). See also RMSE 3d at 214 (discussing statistical studies as generally “admissible,” but acknowledging that admissibility may be no more than permission to explain the basis for an expert’s opinion, which is hardly admissibility at all).

[10] See Ellis, 745 F.2d at 299-303; Kehm, 724 F.2d at 617-18. These holdings predated the Supreme Court’s 1993 decision in Daubert, and the issue whether they are subject to Rule 702 has not been addressed.  Federal agency factual findings have been known to be invalid, on occasion.

[11] David L. Faigman, et al., Modern Scientific Evidence: The Law and Science of Expert Testimony v.1, § 23:1,at 206 (2009) (“Well conducted studies are uniformly admitted.”).

[12] Montori, et al., “Users’ guide to detecting misleading claims in clinical research reports,” 329 Br. Med. J. 1093, 1093 (2004) (advising readers on how to avoid being misled by published literature, and counseling readers to “Read only the Methods and Results sections; bypass the Discussion section.”)  (emphasis added).

[13] RSME 3d 11 (2011).

[14] Id. at 19.

[15] Id. at 20 & n. 51 (citing Susan Haack, “An Epistemologist in the Bramble-Bush: At the Supreme Court with Mr. Joiner,” 26 J. Health Pol. Pol’y & L. 217–37 (1999).

[16] Id. at 19-20 & n.52.

[17] See Berger, “The Admissibility of Expert Testimony,” RSME 3d 11 (2011).  Professor Berger never mentions Rule 703 at all!  Gone and forgotten.

[18] Professor Berger filed an amicus brief on behalf of plaintiffs, in Rider v. Sandoz Pharms. Corp., 295 F.3d 1194 (11th Cir. 2002).

[19] Id. at 20 n.51. (The editors note that the published chapter was Berger’s last revision, with “a few edits to respond to suggestions by reviewers.”) The addition of the controversial Milward decision cannot seriously be considered an “edit.”

[20] “From Here to CERT-ainty” (June 28, 2018); “ THE COUNCIL FOR EDUCATION AND RESEARCH ON TOXICS” (July 9, 2013).

Posted in Causation, Evidence, Reference Manual on Scientific Evidence, Rule 702, Rule 703 | 17 Comments »

Reference Manual – Desiderata for 4th Edition – Part V – Specific Tortogens

February 14th, 2023

Examples are certainly helpful to explain and to show judges how real scientists reach causal conclusions. The Reference Manual should certainly give such examples of how scientists determine whether a claim has been adequately tested, and whether the claim has eliminated the myriad kinds of error that threaten such claims and require us to withhold our assent. The third edition of the Manual, however, advances some dodgy examples, without any data or citations. I have already pointed out that the third edition’s reference to clear cell adenocarcinoma of the vagina in young women as a “signal” disease caused only by DES is incorrect.[1] There are, alas, other troubling examples in the third edition, which are due for pruning.

Claimed Interaction Between Asbestos and Tobacco Risks for Lung Cancer

The third edition’s chapter on epidemiology discusses the complexities raised by potential interaction between multiple exposures. The discussion is appropriately suggesting that a relative risk cannot be used to determine the probability of individual causation “if the agent interacts with another cause in a way that results in an increase in disease beyond merely the sum of the increased incidence due to each agent separately.” The suggestion is warranted, although the chapter then is mum on whether there are other approaches that can be invoked to derive probabilities of causation when multiple exposures interact in a known way. Then the authors provided an example:

“For example, the relative risk of lung cancer due to smoking is around 10, while the relative risk for asbestos exposure is approximately 5. The relative risk for someone exposed to both is not the arithmetic sum of the two relative risks, that is, 15, but closer to the product (50- to 60-fold), reflecting an interaction between the two.200 Neither of the individual agent’s relative risks can be employed to estimate the probability of causation in someone exposed to both asbestos and cigarette smoke.”[2]

Putting aside for the moment the general issue of interaction, the chapter’s use of the Mt. Sinai catechism, of 5-10-50, for asbestos and tobacco smoking and lung cancer, is a poor choice. The evidence for multiplicative interaction was advanced by the late Irving Selikoff, and frankly the evidence was never very good. The supposed “non-smokers” were really “never smoked regularly,” and the smoking histories were taken by postcard surveys. The cohort of asbestos insulators was well aware of the study hypothesis, in that many of its members had compensations claims, and they had an interest in downplaying their smoking.  Indeed, the asbestos workers’ union helped fund Selikoff’s work, and Selikoff had served as a testifying expert witness for claimants.

Given that “never smoked regularly” is not the same as never having smoked, and given that the ten-fold risk from smoking-alone was already an underestimate of lung cancer risk from smoking alone, the multiplicative model never was on a firm basis.  The smoking-alone risk ratio was doubled in the American Cancer Society’s Cancer Prevention Survey Numbers One and Two, but the Mt. Sinai physicians, who frequently testified in lawsuits for claimants steadfastly held to their outdated statistical control group.[3] It is thus disturbing that the third edition’s authors trotted out a summary of asbestos / smoking lung cancer risks based upon Selikoff’s dodgy studies of asbestos insulation workers. The 5-10-50 dogma was already incorrect when the first edition went to press.

Not only were Selikoff’s study probably incorrect when originally published, updates to the insulation worker cohort published after his death, specifically undermine the multiplicative claim. In a 2013 publication by Selikoff’s successors, asbestos and smoking failed to show multiplicative interaction.  Indeed, occupational asbestos exposure that had not manifested in clinically apparent asbestosis did not show any interaction with smoking.  Only in a subgroup of insulators with clinically detectable asbestosis did the asbestosis and smoking show “supra-additive” (but not multiplicative) interaction.[4]

Manganese and Parkinson’s Disease

Table 1, of the toxicology chapter in the third edition, presented a “Sample of Selected Toxicological End Points and Examples of Agents of Concern in Humans.” The authors cautioned that the table was “not an exhaustive or inclusive list of organs, end points, or agents. Absence from this list does not indicate a relative lack of evidence for a causal relation as to any agent of concern.”[5] Among the examples presented in this Table 1 was neurotoxicity in the form of “Parkinson’s disease and manganese”[6]

The presence of this example of this example in Table 1 is curious on a number of fronts. First, one of the members of the Development Committee for the third edition was Judge Kathleen O’Malley, who presided over a multi-district litigation involving claims for parkinsonism and Parkinson’s disease against manufacturers of welding rods. It seemed unlikely that Judge O’Malley would have overlooked this section. See, e.g., In re Welding Fume Prods. Liab. Litig., 245 F.R.D. 279 (N.D. Ohio 2007) (exposure to manganese fumes allegedly increased the risk of later developing brain damage). More important, however, the authors’ inclusion of Parkinson’s disease as an outcome from manganese exposure is remarkable because that putative relationship has been extensively studied and rejected by leading researchers in the field of movement disorders.[7] In 2010, neuro-epidemiologists published a comprehensive meta-analysis that confirmed the absence of a relationship between manganese exposure and Parkinson’s disease.[8] The inclusion in Table 1 of a highly controversial relationship, manganese-Parkinson’s disease, suggests either undisclosed partisanship or ignorance of the relevant scientific evidence.

Mesothelioma

The toxicology chapter of the third edition also weighed in on mesothelioma as a supposed signature disease of asbestos exposure. The chapter’s authors described mesothelioma as “almost always caused by asbestos,”[9] which was no doubt true when mesothelioma was first identified as caused by fibrous amphibole minerals.[10] The last two decades, however, has seen a shift in the incidence of mesothelioma among industrially exposed workers, which reveals more cases without asbestos exposure and with other potential causes. Leading scientists in the field have acknowledged non-asbestos causes,[11] and recently researchers have identified genetic mutations that completely account for the causation of individual cases of mesothelioma.[12] It is time for the fourth edition to acknowledge other causes of mesothelioma, and to offer judges and lawyers guidance on genetic causes of sporadic diseases.

[1] See “Reference Manual – Desiderata for the Fourth Edition – Signature Disease” (Jan. 30, 2023).

[2] RMSE3d at 615 & n. 200. The chapter fails to cite support for the 5-10-50 dogma, but it is readily recognizable as the Mt. Sinai Catechism that was endlessly repeated by Irving Selikoff and his protégés.

[3] Michael J. Thun, Cathy A. Day-Lally, Eugenia E. Calle, W. Dana Flanders, and Clark W Heath, “Excess mortality among cigarette smokers: Changes in a 20-year interval,” 85 Am. J. Public Health 1223 (1995).

[4] Steve Markowitz, Stephen Levin, Albert Miller, and Alfredo Morabia, “Asbestos, Asbestosis, Smoking and Lung Cancer: New Findings from the North American Insulator Cohort,” 188 Am. J. Respir. & Critical Care Med. 90 (2013); see “The Mt. Sinai Catechism” (June 7, 2013).

[5] RMSE3d at 653-54.

[6] Reference Manual at 653.

[7] See e.g., Karin Wirdefeldt, Hans-Olaf Adami, Philip Cole, Dimitrios Trichopoulos, and Jack Mandel, “Epidemiology and etiology of Parkinson’s disease: a review of the evidence. 26 European J. Epidemiol. S1, S20-21 (2011); Tomas R. Guilarte, “Manganese and Parkinson’s Disease: A Critical Review and New Findings,” 118 Environ Health Perspect. 1071, 1078 (2010) (“The available evidence from human and nonhuman primate studies using behavioral, neuroimaging, neurochemical, and neuropathological end points provides strong support to the hypothesis that, although excess levels of [manganese] accumulation in the brain results in an atypical form of parkinsonism, this clinical outcome is not associated with the degeneration of nigrostriatal dopaminergic neurons as is the case in PD [Parkinson’s disease].”)

[8] James Mortimer, Amy Borenstein, and Lorene Nelson, “Associations of welding and manganese exposure with Parkinson disease: Review and meta-analysis,” 79 Neurology 1174 (2012).

[9] Bernard D. Goldstein & Mary Sue Henifin, “Reference Guide on Toxicology,” RMSE3d 633, 635 (2011).

[10] See J. Christopher Wagner, C.A. Sleggs, and Paul Marchand, “Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province,” 17 Br. J. Indus. Med. 260 (1960); J. Christopher Wagner, “The discovery of the association between blue asbestos and mesotheliomas and the aftermath,” 48 Br. J. Indus. Med. 399 (1991); see also Harriet Hardy, M.D., Challenging Man-Made Disease:  The Memoirs of Harriet L. Hardy, M.D. 95 (1983); “Harriet Hardy’s Views on Asbestos Issues” (Mar. 13, 2013).

[11] Richard L. Attanoos, Andrew Churg, Allen R. Gibbs, and Victor L. Roggli, “Malignant Mesothelioma and Its Non-Asbestos Causes,” 142 Arch. Pathol. & Lab. Med. 753 (2018).

[12] Angela Bononia, Qian Wangb, Alicia A. Zolondick, Fang Baib, Mika Steele-Tanjia, Joelle S. Suareza , Sandra Pastorinoa, Abigail Sipesa, Valentina Signoratoa, Angelica Ferroa, Flavia Novellia , Jin-Hee Kima, Michael Minaaia,d, Yasutaka Takinishia, Laura Pellegrinia, Andrea Napolitanoa, Ronghui Xua , Christine Farrara , Chandra Goparajua, Cristian Bassig, Massimo Negrinig, Ian Paganoa , Greg Sakamotoa, Giovanni Gaudinoa, Harvey I. Pass, José N. Onuchic , Haining Yang, and Michele Carbone, “BAP1 is a novel regulator of HIF-1α,” 120 Proc. Nat’l Acad. Sci. e2217840120 (2023).

Posted in Causation, Reference Manual on Scientific Evidence | 1 Comment »

Reference Manual – Desiderata for 4th Edition – Part IV – Confidence Intervals

February 10th, 2023

Putting aside the idiosyncratic chapter by the late Professor Berger, most of the third edition of the Reference Manual presented guidance on many important issues.  To be sure, there are gaps, inconsistencies, and mistakes, but the statistics chapter should be a must-read for federal (and state) judges. On several issues, especially statistical in nature, the fourth edition could benefit from an editor to ensure that the individual chapters, written by different authors, actually agree on key concepts.  One such example is the third edition’s treatment of confidence intervals.[1]

The “DNA Identification” chapter noted that the meaning of a confidence interval is subtle,[2] but I doubt that the authors, David Kaye and George Sensabaugh, actually found it subtle or difficult. In the third edition’s chapter on statistics, David Kaye and co-author, the late David A. Freedman, gave a reasonable definition of confidence intervals in their glossary:

“confidence interval. An estimate, expressed as a range, for a parameter. For estimates such as averages or rates computed from large samples, a 95% confidence interval is the range from about two standard errors below to two standard errors above the estimate. Intervals obtained this way cover the true value about 95% of the time, and 95% is the confidence level or the confidence coefficient.”[3]

Intervals, not the interval, which is correct. This chapter made clear that it was the procedure of obtaining multiple samples with intervals that yielded the 95% coverage. In the substance of their chapter, Kaye and Freedman are explicit about how intervals are constructed, and that:

“the confidence level does not give the probability that the unknown parameter lies within the confidence interval.”[4]

Importantly, the authors of the statistics chapter named names; that is, they cited some cases that butchered the concept of the confidence interval.[5] The fourth edition will have a more difficult job because, despite the care taken in the statistics chapter, many more decisions have misstated or misrepresented the meaning of a confidence interval.[6] Citing more cases perhaps will disabuse federal judges of their reliance upon case law for the meaning of statistical concepts.

The third edition’s chapter on multiple regression defined confidence interval in its glossary:

“confidence interval. An interval that contains a true regression parameter with a given degree of confidence.”[7]

The chapter avoided saying anything obviously wrong only by giving a very circular definition. When the chapter substantively described a confidence interval, it ended up giving an erroneous one:

“In general, for any parameter estimate b, the expert can construct an interval around b such that there is a 95% probability that the interval covers the true parameter. This 95% confidence interval is given by: b ± 1.96 (SE of b).”[8]

The formula provided is correct, but the interpretation of a 95% probability that the interval covers the true parameter is unequivocably wrong.[9]

The third edition’s chapter by Shari Seidman Diamond on survey research, on the other hand, gave an anodyne example and a definition:

“A survey expert could properly compute a confidence interval around the 20% estimate obtained from this sample. If the survey were repeated a large number of times, and a 95% confidence interval was computed each time, 95% of the confidence intervals would include the actual percentage of dentists in the entire population who would believe that Goldgate was manufactured by the makers of Colgate.

                 *  *  *  *

Traditionally, scientists adopt the 95% level of confidence, which means that if 100 samples of the same size were drawn, the confidence interval expected for at least 95 of the samples would be expected to include the true population value.”[10]

Similarly, the third edition’s chapter on epidemiology correctly defined the confidence interval operationally as a process of iterative intervals that collectively cover the true value in 95% of all the intervals:

“A confidence interval provides both the relative risk (or other risk measure) found in the study and a range (interval) within which the risk likely would fall if the study were repeated numerous times.”[11]

Not content to leave it well said, the chapter’s authors returned to the confidence interval and provided another, more problematic definition, a couple of pages later in the text:

“A confidence interval is a range of possible values calculated from the results of a study. If a 95% confidence interval is specified, the range encompasses the results we would expect 95% of the time if samples for new studies were repeatedly drawn from the same population.”[12]

The first sentence refers to “a study”; that is, one study, one range of values. The second sentence then tells us that “the range” (singular, presumably referring back to the single “a study”), will capture 95% of the results from many resamplings from the same population. Now the definition is not framed with respect to the true population parameter, but the results from many other samples. The authors seem to have given the first sample’s confidence interval the property of including 95% of all future studies, and that is incorrect. From reviewing the case law, courts remarkably have gravitated to the second, incorrect definition.

The glossary to the third edition’s epidemiology chapter clearly, however, runs into the ditch:

“confidence interval. A range of values calculated from the results of a study within which the true value is likely to fall; the width of the interval reflects random error. Thus, if a confidence level of .95 is selected for a study, 95% of similar studies would result in the true relative risk falling within the confidence interval.”[13]

Note that the sentence before the semicolon talked of “a study” with “a range of values,” and that there is a likelihood of that range including the “true value.” This definition thus used the singular to describe the study and to describe the range of values.  The definition seemed to be saying, clearly but wrongly, that a single interval from a single study has a likelihood of containing the true value. The second full sentence ascribed a probability, 95%, to the true relative risk’s falling within “the interval.” To point out the obvious, “the interval,” is singular, and refers back to “a study,” also singular. At best, this definition was confusing; at worst, it was wrong.

The Reference Manual has a problem beyond its own inconsistencies, and the refractory resistance of the judiciary to statistical literacy. There are any number of law professors and even scientists who have held out incorrect definitions and interpretations of confidence intervals.  It would be helpful for the fourth edition to caution its readers, both bench and bar, to the prevalent misunderstandings.

Here, for instance, is an example of a well-credentialed statistician, who gave a murky definition in a declaration filed in federal court:

“If a 95% confidence interval is specified, the range encompasses the results we would expect 95% of the time if samples for new studies were repeatedly drawn from the same population.”[14]

The expert witness correctly identifies the repeated sampling, but specifies a 95% probability to “the range,” which leaves unclear whether it is the range of all intervals or “a 95% confidence interval,” which is in the antecedent of the statement.

Much worse was a definition proffered in a recent law review article by well-known, respected authors:

“A 95% confidence interval, in contrast, is a one-sided or two-sided interval from a data sample with 95% probability of bounding a fixed, unknown parameter, for which no nondegenerate probability distribution is conceived, under specified assumptions about the data distribution.”[15]

The phrase “for which no nondegenerate probability distribution is conceived,” is unclear as to whether the quoted phrase refers to the confidence interval or to the unknown parameter. It seems that the phrase modifies the noun closest to it in the sentence, the “fixed, unknown parameter,” which suggests that these authors were simply trying to emphasize that they were giving a frequentist interpretation and not conceiving of the parameter as a random variable as Bayesians would. The phrase “no nondegenerate” appears to be a triple negative, since a degenerate distribution is one that does not have a variation. The phrase makes the definition obscure, and raises questions what is being excluded by the phrase.

The more concerning aspect of the quoted footnote is its obfuscation of the important distinction between the procedure of repeatedly calculating confidence intervals (which procedure has a 95% success rate in the long run) and the probability that any given instance of the procedure, in a single confidence interval, contains the parameter. The latter probability is either zero or one.

The definition’s reference to “a” confidence interval, based upon “a” data sample, actually leaves the reader with no way of understanding the definition to be referring to the repeated process of sampling, and the set of resulting intervals. The upper and lower interval bounds are themselves random variables that need to be taken into account, but by referencing a single interval from a single data sample, the authors misrepresent the confidence interval and invite a Bayesian interpretation.[16]

Sadly, there is a long tradition of scientists and academics in giving errant definitions and interpretations of the confidence interval.[17] Their error is not harmless because they invite the attribution of a high level of probability to the claim that the “true” population measure is within the reported confidence interval. The error encourages readers to believe that the confidence interval is not conditioned upon the single sample result, and it misleads readers into believing that not only random error, but systematic and data errors are accounted for in the posterior probability.[18] 

[1] “Confidence in Intervals and Diffidence in the Courts” (Mar. 4, 2012).

[2] David H. Kaye & George Sensabaugh, “Reference Guide on DNA Identification Evidence” 129, 165 n.76.

[3] David H. Kaye & David A. Freedman, “Reference Guide on Statistics” 211, 284-5 (Glossary).

[4] Id. at 247.

[5] Id. at 247 n.91 & 92 (citing DeLuca v. Merrell Dow Pharms., Inc., 791 F. Supp. 1042, 1046 (D.N.J. 1992), aff’d, 6 F.3d 778 (3d Cir. 1993); SmithKline Beecham Corp. v. Apotex Corp., 247 F. Supp. 2d 1011, 1037 (N.D. Ill. 2003), aff’d on other grounds, 403 F.3d 1331 (Fed. Cir. 2005); In re Silicone Gel Breast Implants Prods. Liab. Litig, 318 F. Supp. 2d 879, 897 (C.D. Cal. 2004) (“a margin of error between 0.5 and 8.0 at the 95% confidence level . . . means that 95 times out of 100 a study of that type would yield a relative risk value somewhere between 0.5 and 8.0.”).

[6] See, e.g., Turpin v. Merrell Dow Pharm., Inc., 959 F.2d 1349, 1353–54 & n.1 (6th Cir. 1992) (erroneously describing a 95% CI of 0.8 to 3.10, to mean that “random repetition of the study should produce, 95 percent of the time, a relative risk somewhere between 0.8 and 3.10”); American Library Ass’n v. United States, 201 F.Supp. 2d 401, 439 & n.11 (E.D.Pa. 2002), rev’d on other grounds, 539 U.S. 194 (2003); Ortho–McNeil Pharm., Inc. v. Kali Labs., Inc., 482 F.Supp. 2d 478, 495 (D.N.J.2007) (“Therefore, a 95 percent confidence interval means that if the inventors’ mice experiment was repeated 100 times, roughly 95 percent of results would fall within the 95 percent confidence interval ranges.”) (apparently relying party’s expert witness’s report), aff’d in part, vacated in part, sub nom. Ortho McNeil Pharm., Inc. v. Teva Pharms Indus., Ltd., 344 Fed.Appx. 595 (Fed. Cir. 2009); Eli Lilly & Co. v. Teva Pharms, USA, 2008 WL 2410420, *24 (S.D. Ind. 2008) (stating incorrectly that “95% percent of the time, the true mean value will be contained within the lower and upper limits of the confidence interval range”); Benavidez v. City of Irving, 638 F.Supp. 2d 709, 720 (N.D. Tex. 2009) (interpreting a 90% CI to mean that “there is a 90% chance that the range surrounding the point estimate contains the truly accurate value.”); Pritchard v. Dow Agro Sci., 705 F. Supp. 2d 471, 481, 488 (W.D. Pa. 2010) (excluding Dr. Bennet Omalu who assigned a 90% probability that an 80% confidence interval excluded relative risk of 1.0), aff’d, 430 F. App’x 102 (3d Cir.), cert. denied, 132 S. Ct. 508 (2011); Estate of George v. Vermont League of Cities and Towns, 993 A.2d 367, 378 n.12 (Vt. 2010) (erroneously describing a confidence interval to be a “range of values within which the results of a study sample would be likely to fall if the study were repeated numerous times”); Garcia v. Tyson Foods, 890 F. Supp. 2d 1273, 1285 (D. Kan. 2012) (quoting expert witness Robert G. Radwin, who testified that a 95% confidence interval in a study means “if I did this study over and over again, 95 out of a hundred times I would expect to get an average between that interval.”); In re Chantix (Varenicline) Prods. Liab. Litig., 889 F. Supp. 2d 1272, 1290n.17 (N.D. Ala. 2012); In re Zoloft Products, 26 F. Supp. 3d 449, 454 (E.D. Pa. 2014) (“A 95% confidence interval means that there is a 95% chance that the ‘‘true’’ ratio value falls within the confidence interval range.”), aff’d, 858 F.3d 787 (3d Cir. 2017); Duran v. U.S. Bank Nat’l Ass’n, 59 Cal. 4th 1, 36, 172 Cal. Rptr. 3d 371, 325 P.3d 916 (2014) (“Statisticians typically calculate margin of error using a 95 percent confidence interval, which is the interval of values above and below the estimate within which one can be 95 percent certain of capturing the ‘true’ result.”); In re Accutane Litig., 451 N.J. Super. 153, 165 A.3d 832, 842 (2017) (correctly quoting an incorrect definition from the third edition at p.580), rev’d on other grounds, 235 N.J. 229, 194 A.3d 503 (2018); In re Testosterone Replacement Therapy Prods. Liab., No. 14 C 1748, MDL No. 2545, 2017 WL 1833173, *4 (N.D. Ill. May 8, 2017) (“A confidence interval consists of a range of values. For a 95% confidence interval, one would expect future studies sampling the same population to produce values within the range 95% of the time.”); Maldonado v. Epsilon Plastics, Inc., 22 Cal. App. 5th 1308, 1330, 232 Cal. Rptr. 3d 461 (2018) (“The 95 percent ‘confidence interval’, as used by statisticians, is the ‘interval of values above and below the estimate within which one can be 95 percent certain of capturing the “true” result’.”); Escheverria v. Johnson & Johnson, 37 Cal. App. 5th 292, 304, 249 Cal. Rptr. 3d 642 (2019) (quoting uncritically and with approval one of plaintiff’s expert witnesses, Jack Siemiatycki, who gave the jury an example of a study with a relative risk of 1.2, with a “95 percent probability that the true estimate is between 1.1 and 1.3.” According to the court, Siemiatycki went on to explain that this was “a pretty tight interval, and we call that a confidence interval. We call it a 95 percent confidence interval when we calculate it in such a way that it covers 95 percent of the underlying relative risks that are compatible with this estimate from this study.”); In re Viagra (Sildenafil Citrate) & Cialis (Tadalafil) Prods. Liab. Litig., 424 F.Supp.3d 781, 787 (N.D. Cal. 2020) (“For example, a given study could calculate a relative risk of 1.4 (a 40 percent increased risk of adverse events), but show a 95 percent “confidence interval” of .8 to 1.9. That confidence interval means there is 95 percent chance that the true value—the actual relative risk—is between .8 and 1.9.”); Rhyne v. United States Steel Corp., 74 F. Supp. 3d 733, 744 (W.D.N.C. 2020) (relying upon, and quoting, one of the more problematic definitions given in the third edition at p.580: “If a 95% confidence interval is specified, the range encompasses the results we would expect 95% of the time if samples for new studies were repeatedly drawn from the population.”); Wilant v. BNSF Ry., C.A. No. N17C-10-365 CEB, (Del. Super. Ct. May 13, 2020) (citing third edition at p.573, “a confidence interval provides ‘a range (interval) within which the risk likely would fall if the study were repeated numerous times’.”; “[s]o a 95% confidence interval indicates that the range of results achieved in the study would be achieved 95% of the time when the study is replicated from the same population.”); Germaine v. Sec’y Health & Human Servs., No. 18-800V, (U.S. Fed. Ct. Claims July 29, 2021) (giving an incorrect definition directly from the third edition, at p.621; “[a] “confidence interval” is “[a] range of values … within which the true value is likely to fall[.]”).

[7] Daniel Rubinfeld, “Reference Guide on Multiple Regression” 303, 352.

[8] Id. at 342.

[9] See Sander Greenland, Stephen J. Senn, Kenneth J. Rothman, John B. Carlin, Charles Poole, Steven N. Goodman, and Douglas G. Altman, “Statistical tests, P values, confidence intervals, and power: a guide to misinterpretations,” 31 Eur. J. Epidemiol. 337, 343 (2016).

[10] Shari Seidman Diamond, “Reference Guide on Survey Research” 359, 381.

[11] Michael D. Green, D. Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” 549, 573.

[12] Id. at 580.

[13] Id. at 621.

[14] In re Testosterone Replacement Therapy Prods. Liab. Litig., Declaration of Martin T. Wells, Ph.D., at 2-3 (N.D. Ill., Oct. 30, 2016). 

[15] Joseph Sanders, David Faigman, Peter Imrey, and A. Philip Dawid, “Differential Etiology: Inferring Specific Causation in the Law from Group Data in Science,” 63 Arizona L. Rev. 851, 898 n.173 (2021).

[16] The authors are well-credentialed lawyers and scientists. Peter Imrey, was trained in, and has taught, mathematical statistics, biostatistics, and epidemiology. He is a professor of medicine in the Cleveland Clinic Lerner College of Medicine. A. Philip Dawid is a distinguished statistician, an Emeritus Professor of Statistics, Cambridge University, Darwin College, and a Fellow of the Royal Society. David Faigman is the Chancellor & Dean, and the John F. Digardi Distinguished Professor of Law at the University of California Hastings College of the Law. Joseph Sanders is the A.A. White Professor, at the University of Houston Law Center. I have previously pointed this problem in these authors’ article. “Differential Etiologies – Part One – Ruling In” (June 19, 2022).

[17] See, e.g., Richard W. Clapp & David Ozonoff, “Environment and Health: Vital Intersection or Contested Territory?” 30 Am. J. L. & Med. 189, 210 (2004) (“Thus, a RR [relative risk] of 1.8 with a confidence interval of 1.3 to 2.9 could very likely represent a true RR of greater than 2.0, and as high as 2.9 in 95 out of 100 repeated trials.”); Erica Beecher-Monas, Evaluating Scientific Evidence: An Interdisciplinary Framework for Intellectual Due Process 60-61 n. 17 (2007) (quoting Clapp and Ozonoff with obvious approval); Déirdre Dwyer, The Judicial Assessment of Expert Evidence 154-55 (Cambridge Univ. Press 2008) (“By convention, scientists require a 95 per cent probability that a finding is not due to chance alone. The risk ratio (e.g. ‘2.2’) represents a mean figure. The actual risk has a 95 per cent probability of lying somewhere between upper and lower limits (e.g. 2.2 ±0.3, which equals a risk somewhere between 1.9 and 2.5) (the ‘confidence interval’).”); Frank C. Woodside, III & Allison G. Davis, “The Bradford Hill Criteria: The Forgotten Predicate,” 35 Thomas Jefferson L. Rev. 103, 110 (2013) (“A confidence interval provides both the relative risk found in the study and a range (interval) within which the risk would likely fall if the study were repeated numerous times.”); Christopher B. Mueller, “Daubert Asks the Right Questions:  Now Appellate Courts Should Help Find the Right Answers,” 33 Seton Hall L. Rev. 987, 997 (2003) (describing the 95% confidence interval as “the range of outcomes that would be expected to occur by chance no more than five percent of the time”); Arthur H. Bryant & Alexander A. Reinert, “The Legal System’s Use of Epidemiology,” 87 Judicature 12, 19 (2003) (“The confidence interval is intended to provide a range of values within which, at a specified level of certainty, the magnitude of association lies.”) (incorrectly citing the first edition of Rothman & Greenland, Modern Epidemiology 190 (Philadelphia 1998);  John M. Conley & David W. Peterson, “The Science of Gatekeeping: The Federal Judicial Center’s New Reference Manual on Scientific Evidence,” 74 N.C.L.Rev. 1183, 1212 n.172 (1996) (“a 95% confidence interval … means that we can be 95% certain that the true population average lies within that range”).

[18] See Brock v. Merrill Dow Pharm., Inc., 874 F.2d 307, 311–12 (5th Cir. 1989) (incorrectly stating that the court need not resolve questions of bias and confounding because “the studies presented to us incorporate the possibility of these factors by the use of a confidence interval”). Bayesian credible intervals can similarly be misleading when the interval simply reflects sample results and sample variance, but not the myriad other ways the estimate may be wrong.

Posted in Evidence, Expert Witnesses, Reference Manual on Scientific Evidence, statistical evidence | No Comments »

Reference Manual – Desiderata for 4th Edition – Part III – Differential Etiology

February 1st, 2023

Admittedly, I am playing the role of the curmudgeon here by pointing out errors or confusions in the third edition of the Reference Manual.  To be sure, there are many helpful and insightful discussions throughout the Manual, but they do not need to be revised.  Presumably, the National Academies and the Federal Judicial Center are undertaking the project of producing a fourth edition because they understand that revisions, updates, and corrections are needed. Otherwise, why bother?

To be sure, there are aspects of the third edition’s epidemiology chapter that get some important points right. 

(1) The chapter at least acknowledges that small relative risks (1 < RR <3) may be insufficient to support causal inferences.[1]

(2) The chapter correctly notes that the method known as “differential etiology” addresses only specific causation, and that the method presupposes that general causation has been established.[2]

(3) The third edition correctly observes that clinicians generally are not concerned with etiology as much as with diagnosis of disease.[3] The authors of the epidemiology chapter correctly observe that “[f]or many health conditions, the cause of the disease or illness has no relevance to its treatment, and physicians, therefore, do not employ this term or pursue that question.”[4] This observation alone should help trial courts question whether many clinicians have even the pretense of expertise to offer expert causation opinions.[5]

(4) With respect to so-called differential etiology, the third edition correctly states that this mode of reasoning is a logically valid argument if premises are true; that is, general causation must be established for each “differential etiology.” The epidemiology chapter observes that “like any scientific methodology, [differential etiology] can be performed in an unreliable manner.”[6]

(5) The third edition reports that the differential etiology argument as applied in litigation is often invalid because not all the differentials other than the litigation claim have been ruled out.[7]

(6) The third edition properly notes that for diseases for which the causes are largely unknown, such as most birth defects, a differential etiology is of little benefit.[8] Unfortunately, the third edition offered no meaningful guidance for how courts should consider differential etiologies offered when idiopathic cases make up something less “than largely,” (0% < Idiopathic < 10%, 20%, 30%, 40, 50%, etc.).The chapter acknowledges that:

“Although differential etiologies are a sound methodology in principle, this approach is only valid if … a substantial proportion of competing causes are known. Thus, for diseases for which the causes are largely unknown, such as most birth defects, a differential etiology is of little benefit.”[9]

Accordingly, many cases reject proffered expert witness testimony on differential etiology, when the witnesses failed to rule out idiopathic causes in the case at issue. What is a substantial proportion?  Unfortunately, the third edition did not attempt to quantify or define “substantial.” The inability to rule out unknown etiologies remains the fatal flaw in much expert witness opinion testimony on specific causation.

Errant Opinions on Differential Etiology

The third edition’s treatment of differential etiology does leave room for improvement. One glaring error is the epidemiology chapter’s assertion that “differential etiology is a legal invention not used by physicians.”[10] Indeed, the third edition provides a definition for “differential etiology” that reinforces the error:

“differential etiology. Term used by the court or witnesses to establish or refute external causation for a plaintiff’s condition. For physicians, etiology refers to cause.”[11]

The third edition’s assertion about legal provenance and exclusivity can be quickly dispelled by a search on “differential etiology” in the National Library of Medicine’s PubMed database, which shows up dozens of results, going back to the early 1960s. Some citations are supplied in the notes.[12] A Google Ngram for “differential etiology” in American English shows prevalent usage well before any of the third edition’s cited cases:

The third edition’s erroneous assertion about the provenance of “differential etiology” has been echoed by other law professors. David Faigman, for instance, has claimed that in advancing differential etiologies, expert witnesses were inventing wholesale an approach that had no foundation or acceptance in their scientific disciplines:

“Differential etiology is ostensibly a scientific methodology, but one not developed by, or even recognized by, physicians or scientists. As described, it is entirely logical, but has no scientific methods or principles underlying it. It is a legal invention and, as such, has analytical heft, but it is entirely bereft of empirical grounding. Courts and commentators have so far merely described the logic of differential etiology; they have yet to define what that methodology is.”[13]

Faigman’s claim that courts and commentators have not defined the methodology underlying differential etiology is wrong. Just as hypothesis testing is predicated upon a probabilistic version of modus tollens, differential etiology is based upon “iterative disjunctive syllogism,” or modus tollendo ponens. Basic propositional logic recognizes that such syllogisms are valid arguments,[14] in which one of its premises is a disjunction (P v Q), and the other premise is the negation of one of the disjuncts:

P v Q

~P­­­_____

∴ Q

If we expand the disjunctive premise to more than one disjunction, we can repeat the inference (iteratively), eliminating one disjunct at a time, until we arrive at a conclusion that is a simple, affirmative proposition, without any disjunctions in it.

P v Q v R

~P­­­_____

∴ Q v R

     ~Q­­­_____

∴ R

Hence, the term “iterative disjunctive syllogism.” Sherlock Holmes’ fans, of course, will recognize that iterative disjunctive syllogism is nothing other than the process of elimination, as explained by the hero of Sir Arthur Conan Doyle’s short stories.[15]

The fourth edition should correct the error of the third edition, and it should dispel the strange notion that differential etiology is not used by scientists or clinicians themselves.

Supreme Nonsense on Differential Etiology

In 2011, the Supreme Court addressed differential etiology in a case, Matrixx Initiatives, in stunningly irrelevant and errant dicta. The third edition did not discuss this troublesome case, in which the defense improvidently moved to dismiss a class action complaint for securities violations allegedly arising from the failure to disclose multiple adverse event reports of anosmia from the use of the defendant’s product, Zicam. The basic reason for the motion on the pleadings was that the plaintiffs’ failed to allege a statistically significant and causally related increased risk of anosmia.  The Supreme Court made short work of the defense argument because material events, such as an FDA recall, did not require the existence of a causal relationship between Zicam use and anosmia. The defense complaints about statistical significance, causation, and their absence, were thus completely beside the point of the case.  Nonetheless, it became the Court’s turn for improvidence in addressing statistical and causation issues not properly before it. With respect to causation, the Court offered this by way of obiter dictum:

“We note that courts frequently permit expert testimony on causation based on evidence other than statistical significance. See, e.g., Best v. Lowe’s Home Centers, Inc., 563 F. 3d 171, 178 (6th Cir 2009); Westberry v. Gislaved Gummi AB, 178 F. 3d 257, 263–264 (4th Cir. 1999) (citing cases); Wells v. Ortho Pharmaceutical Corp., 788 F. 2d 741, 744–745 (11th Cir. 1986). We need not consider whether the expert testimony was properly admitted in those cases, and we do not attempt to define here what constitutes reliable evidence of causation.”[16]

This part of the Court’s opinion was stunningly wrong about the Court of Appeals’ decisions on statistical significance[17] and on causation. The Best and the Westberry decisions were both cases that turned on specific, not general, causation.  Statistical significance this was not part of the reasoning or rationale of the cited cases on specific caustion. Both cases assumed that general causation was established, and inquired into whether expert witnesses could reasonably and validly attribute the health outcome in the case to the exposures that were established causes of such outcomes.  The Court’s selection of these cases, quite irrelevant to its discussion, appears to have come from the Solicitor General’s amicus brief in Matrixx, but mindlessly adopted by the Court.

Although cited for an irrelevant proposition, the Supreme Court’s selection of the Best’s case was puzzling because the Sixth Circuit’s discussion of the issue is particularly muddled. Here is the relevant language from Best:

“[A] doctor’s differential diagnosis is reliable and admissible where the doctor

(1) objectively ascertains, to the extent possible, the nature of the patient’s injury…,

(2) ‘rules in’ one or more causes of the injury using a valid methodology,

and

(3) engages in ‘standard diagnostic techniques by which doctors normally rule out alternative causes” to reach a conclusion as to which cause is most likely’.”[18]

Of course, as the authors of the third edition’s epidemiology chapter correctly note, physicians rarely use this iterative process to arrive at causes of diseases in an individual; they use it to identify the disease or disease process that is responsible for the patient’s signs and symptoms.[19] The Best court’s description does not make sense in that it characterizes the process as ruling in “one or more” causes, and then ruling out alternative causes.  If an expert had ruled in only one cause, then there would be no need or opportunity to rule out an alternative cause.  If the one ruled-in cause was ruled out for other reasons, then the expert witness would be left with a case of idiopathic disease.

In any event, differential etiology was irrelevant to the general causation issue raised by the defense in Matrixx Initiatives. After the Supreme Court correctly recognized that causation was largely irrelevant to the securities fraud claim, it had no reason to opine on general causation.  Certainly, the Supreme Court had no reason to cite two cases on differential etiology in a case that did not even require allegations of general causation. The fourth edition of the Reference Manual should put Matrixx Initatives in its proper (and very limited) place.

[1] RMSE3d at 612 & n.193 (noting that “one commentator contends that, because epidemiology is sufficiently imprecise to accurately measure small increases in risk, in general, studies that find a relative risk less than 2.0 should not be sufficient for causation. The concern is not with specific causation but with general causation and the likelihood that an association less than 2.0 is noise rather than reflecting a true causal relationship. See Michael D. Green, “The Future of Proportional Liability,” in Exploring Tort Law (Stuart Madden ed., 2005); see also Samuel M. Lesko & Allen A. Mitchell, “The Use of Randomized Controlled Trials for Pharmacoepidemiology Studies,” in Pharmacoepidemiology 599, 601 (Brian Strom ed., 4th ed. 2005) (“it is advisable to use extreme caution in making causal inferences from small relative risks derived from observational studies”); Gary Taubes, “Epidemiology Faces Its Limits,” 269 Science 164 (1995) (explaining views of several epidemiologists about a threshold relative risk of 3.0 to seriously consider a causal relationship); N.E. Breslow & N.E. Day, “Statistical Methods in Cancer Research,” in The Analysis of Case-Control Studies 36 (IARC Pub. No. 32, 1980) (“[r]elative risks of less than 2.0 may readily reflect some unperceived bias or confounding factor”); David A. Freedman & Philip B. Stark, “The Swine Flu Vaccine and Guillain-Barré Syndrome: A Case Study in Relative Risk and Specific Causation,” 64 Law & Contemp. Probs. 49, 61 (2001) (“If the relative risk is near 2.0, problems of bias and confounding in the underlying epidemiologic studies may be serious, perhaps intractable.”). For many other supporting comments and observations, see “Small Relative Risks and Causation” (June 28, 2022).

[2] RMSE3d. at 618 (“Although differential etiologies are a sound methodology in principle, this approach is only valid if general causation exists … .”). In the case of a novel putative cause, the case may give rise to a hypothesis that the putative cause can cause the outcome, in general, and did so in the specific case.  That hypothesis must, of course, then be tested and supported by appropriate analytical methods before it can be accepted for general causation and as a putative specific cause in a particular individual.

[3] RMSE3d at 617.

[4] RMSE3d at 617 & n. 211 (citing Zandi v. Wyeth, Inc., No. 27-CV-06-6744, 2007 WL 3224242 (D. Minn. Oct. 15, 2007) (observing that physicians do assess the cause of patients’ breast cancers)).

[5] See, e.g., Tamraz v. BOC Group Inc., No. 1:04-CV-18948, 2008 WL 2796726 (N.D.Ohio July 18, 2008)(denying Rule 702 challenge to treating physician’s causation opinion), rev’d sub nom. Tamraz v. Lincoln Elec. Co., 620 F.3d 665 (6th Cir. 2010)(carefully reviewing record of trial testimony of plaintiffs’ treating physician; reversing judgment for plaintiff based in substantial part upon treating physician’s speculative causal assessment created by plaintiffs’ counsel), cert. denied, ___ U.S. ___ , 131 S. Ct. 2454 (2011).

[6] RMSE3d at 617-18 & n. 215.

[7] See, e.g, Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013) (excluding plaintiffs’ expert witnesses on specific causation), aff’d sub nom., Milward v. Rust-Oleum Corp., 820 F.3d 469 (1st Cir. 2016). Interestingly, the earlier appellate journey taken by the Milward litigants resulted in a reversal of a Rule 702 exclusion of plaintiff’s general causation expert witnesses. That reversal meant that there was no longer a final judgment.  The exclusion of specific causation witnesses was affirmed by the First Circuit, and the general causation opinion was no longer necessary to the final judgment. See “Differential Diagnosis in Milward v. Acuity Specialty Products Group” (Sept. 26, 2013); “Differential Etiology and Other Courtroom Magic” (June 23, 2014).

[8] RMSE3d at 617-18 & n. 214.

[9] See RMSE at 618 (internal citations omitted).

[10] RMSE3d at 691 (emphasis added).

[11] RMSE3d at 743.

[12] See, e.g., Kløve & D. Doehring, “MMPI in epileptic groups with differential etiology,” 18 J. Clin. Psychol. 149 (1962); Kløve & C. Matthews, “Psychometric and adaptive abilities in epilepsy with differential etiology,” 7 Epilepsia 330 (1966); Teuber & K. Usadel, “Immunosuppression in juvenile diabetes mellitus? Critical viewpoint on the treatment with cyclosporin A with consideration of the differential etiology,” 103  Fortschr. Med. 707 (1985); G.May & W. May, “Detection of serum IgA antibodies to varicella zoster virus (VZV)–differential etiology of peripheral facial paralysis. A case report,” 74 Laryngorhinootologie 553 (1995); Alan Roberts, “Psychiatric Comorbidity in White and African-American Illicity Substance Abusers” Evidence for Differential Etiology,” 20 Clinical Psych. Rev. 667 (2000); Mark E. Mullinsa, Michael H. Leva, Dawid Schellingerhout, Gilberto Gonzalez, and Pamela W. Schaefera, “Intracranial Hemorrhage Complicating Acute Stroke: How Common Is Hemorrhagic Stroke on Initial Head CT Scan and How Often Is Initial Clinical Diagnosis of Acute Stroke Eventually Confirmed?” 26 Am. J. Neuroradiology 2207 (2005); Qiang Fua, et al., “Differential Etiology of Posttraumatic Stress Disorder with Conduct Disorder and Major Depression in Male Veterans,” 62 Biological Psychiatry 1088 (2007); Jesse L. Hawke, et al., “Etiology of reading difficulties as a function of gender and severity,” 20 Reading and Writing 13 (2007); Mastrangelo, “A rare occupation causing mesothelioma: mechanisms and differential etiology,” 105 Med. Lav. 337 (2014).

[13] David L. Faigman & Claire Lesikar, “Organized Common Sense: Some Lessons from Judge Jack Weinstein’s Uncommonly Sensible Approach to Expert Evidence,” 64 DePaul L. Rev. 421, 439, 444 (2015). See also “David Faigman’s Critique of G2i Inferences at Weinstein Symposium” (Sept. 25, 2015).

[14] See Irving Copi & Carl Cohen Introduction to Logic at 362 (2005).

[15] See, e.g., Doyle, The Blanched Soldier (“…when you have eliminated all which is impossible, then whatever remains, however improbable, must be the truth.”); Doyle, The Beryl Coronet (“It is an old maxim of mine that when you have excluded the impossible, whatever remains, however improbable, must be the truth.”); Doyle, The Hound of the Baskervilles (1902) (“We balance probabilities and choose the most likely. It is the scientific use of the imagination.”); Doyle, The Sign of the Four, ch 6 (1890)(“‘You will not apply my precept’, he said, shaking his head. ‘How often have I said to you that when you have eliminated the impossible, whatever remains, however improbable, must be the truth? We know that he did not come through the door, the window, or the chimney. We also know that he could not have been concealed in the room, as there is no concealment possible. When, then, did he come?”)

[16] Matrixx Initiatives, Inc. v. Siracusano, 131 S. Ct. 1309, 1319 (2011). 

[17] The citation to Wells was clearly wrong in that the plaintiffs in that case had, in fact, relied upon studies that were nominally statistically significant, and so the Wells court could not have held that statistical significance was unnecessary.

[18] Best v. Lowe’s Home Centers, Inc., 563 F.3d 171, 179, 183-84 (6th Cir. 2009).

[19] See generally Harold C. Sox, Michael C. Higgins, and Douglas K. Owens, Medical Decision Making (2d ed. 2014). 

Posted in Causation, Reference Manual on Scientific Evidence, Rule 702 | 2 Comments »

Reference Manual – Desiderata for 4th Edition – Part II – Epidemiology & Specific Causation

January 31st, 2023

There are many nits that a reader could pick with the third edition of the Reference Manual, but one non-trivial issue is raised by the epidemiology chapter’s pronouncement that:

“Epidemiology is concerned with the incidence of disease in populations, and epidemiologic studies do not address the question of the cause of an individual’s disease178.”[1]

According to the Manual’s authors, the so-called specific-causation question is “beyond the domain of the science of epidemiology.” Epidemiologists do not investigate whether “an agent caused a specific plaintiff’s disease.”[2] The chapter insists that “[t]his question is not a question that is addressed by epidemiology. Rather, it is a legal question with which numerous courts have grappled.”[3]

Later on in the chapter, the authors repeat their opinion when they insist that the use of a threshold relative risk is “not epidemiology or an inquiry that an epidemiologist would undertake.”[4]

Strictly speaking the authors are correct that an epidemiologic study itself typically does not address the question individual causation. The authors of an epidemiologic study have no one person in mind, as does the factfinder in a civil action. The notion that epidemiology as a scientific discipline does not address the question of individual causation, however, seems just wrong. Tellingly, the authors’ footnote pointed to case law and a law review article, and not a single scientific source. The chapter does reference another legal source, the Third Restatement, which repeats the gist of the epidemiology chapter’s categorical statement:

“Scientists who conduct group studies do not examine specific causation in their research. No scientific methodology exists for assessing specific causation for an individual based on group studies. Nevertheless, courts have reasoned from the preponderance-of-the-evidence standard to determine the sufficiency of scientific evidence on specific causation when group-based studies are involved.”[5]

The chapter’s broad, sweeping characterization fails to consider:

  • genome-wide association studies that may identify genes or mutations that are highly penetrant and which identify a causal association in the carriers of the genes; and
  • epidemiologic studies that identify associations, shown to be causal, with risk ratios sufficiently great (say over 20) such that virtually all cases of the studied outcome would be avoided by removing the exposure that gave rise to such a large risk ratio; and
  • epidemiologic studies that allow causal associations to be inferred in limited sub-populations, with sufficiently high relative risks that the studies support specific causation opinions.

Perhaps even more important than the above counter-examples, the chapter authors ignore the myriad instances in which epidemiologic studies and clinical trials, and analyses of both, directly inform clinical judgments about individual patients or subjects. Clinicians use studies of groups, such as clinical trials, to identify therapeutic benefits from medications and other interventions.  These data directly inform their prescription decisions for individual patients, or their decisions to recommend surgical or other medical interventions to individuals.[6] The classic text on medical decision making describes how group-level data provide the basis for individual clinical decisions on therapy:

“1.5 How do I choose among several risky treatment alternatives?

Choosing among risky treatment alternatives is difficult because the outcome of most treatments is uncertain: some people respond to treatment but others do not. If the outcome of a treatment is governed by chance, a clinician cannot know in advance which outcome of the treatment will result. Under these circumstances, the best way to achieve a good outcome is to choose the treatment alternative whose average outcome is best. This concept is called expected value decision making.”[7]

Medical practitioners and scientists frequently use epidemiologic data, based upon “group-based data” to make individual diagnostic judgments. The inferences from group data to individual range abound in the diagnostic process itself, where the specificity and sensitivity of disease signs and symptoms are measured by group data. Physicians must rely upon group data to make prognoses for individual patients, and they rely upon group data to predict future disease risks for individual patients. Future disease risks, as in the Framingham risk score for hard coronary heart disease, or the Gale model for breast cancer risk, are, of course, based upon “group-based data.”[8] A search on the phrase “prediction models” yielded 662,297 results in the National Library of Medicine PubMed database.

The epidemiology chapter has taken its position on the irrelevance of epidemiology to specific causation through all three editions of the Reference Manual.  Perhaps its authors will rethink their dogma in the fourth.

[1] RMSE3d at 608. The internal footnote, 178, pointed to: “178. See DeLuca v. Merrell Dow Pharms., Inc., 911 F.2d 941, 945 & n.6 (3d Cir. 1990) (“Epidemiological studies do not provide direct evidence that a particular plaintiff was injured by exposure to a substance.”) (emphasis added in this post). The emphasis in the quote is mine because the DeLuca court suggested by implication that epidemiologic studies provided the basis for inferences about specific causation. The footnote also cited another case that simply cited an earlier edition of the Manual, which hardly advances the inquiry into whether the Manual was correct in the first place. See In re Viagra Prods. Liab. Litig., 572 F. Supp. 2d 1071, 1078 (D. Minn. 2008) (“Epidemiology focuses on the question of general causation (i.e., is the agent capable of causing disease?) rather than that of specific causation (i.e., did it cause a disease in a particular individual?)” (quoting the second edition of this reference guide)). Finally, the Manual cited a state court case, In re Asbestos Litig,, 900 A.2d 120, 133 (Del. Super. Ct. 2006), and a law review article, Michael Dore, “A Commentary on the Use of Epidemiological Evidence in Demonstrating Cause-in-Fact,” 7 Harv. Envtl. L. Rev. 429, 436 (1983).” Admittedly, the chapter’s position can be found in writings of other legal commentators, although repetition hardly makes it any less wrong. See, e.g., Andrew See, “Use of Human Epidemiology Studies in Proving Causation,” 67 Def. Couns. J. 478, 478 (2000) (“Epidemiology studies are relevant only to the issue of general causation and cannot establish whether an exposure or factor caused disease or injury in a specific individual.”); Melissa Moore Thomson, Causal Inference in Epidemiology: Implications for Toxic Tort Litigation, 71 N.C. L. Rev. 247, 255 (1992) (“statistic-based epidemiological study results should not be applied directly to establish the likelihood of causation in an individual plaintiff”); 

[2] RMSE3d at 609 & n.179. Inconsistently, the epidemiology chapter reports, without criticism, that some courts have allowed expert witnesses to opine about specific causation, without detailing how epidemiologic science was helpful to the specific causation issues. See RMSE3d at 609 n. 181 (citing Ambrosini v. Labarraque, 101 F.3d 129, 137–41 (D.C. Cir. 1996); Zuchowicz v. United States, 870 F. Supp. 15 (D. Conn. 1994); Landrigan v. Celotex Corp., 605 A.2d 1079, 1088–89 (N.J. 1992)).

[3] RMSE3d at 609.

[4] RMSE3d at 611 n.186.

[5] See Restatement (Third) of Torts: Liability for Physical and Emotional Harm § 28 cmt.

c(3) (2010) (cited at RMSE3d at 610 n.182).

[6] See, e.g., Robert H. Fletcher, Suzanne W. Fletcher, and Grant S. Fletcher, Clinical Epidemiology: The Essentials (5th ed. 2015) (treating prognosis, diagnosis, treatment, and prevention as topics of consideration, all involving individual patient decisions, in clinical epidemiology); Grobbee & Arno W. Hoes, Clinical Epidemiology: Principles, Methods, and Applications for Clinical Research (2d ed. 2015).

[7] Harold C. Sox, Michael C. Higgins & Douglas K. Owens, Medical Decision Making 6 (2d ed. 2013).

[8] See, e.g., Ewout W. Steyerberg. Clinical Prediction Models: A Practical Approach to Development, Validation, and Updating (2d ed. 2019).

Posted in Uncategorized | 3 Comments »

Reference Manual – Desiderata for 4th Edition – Part I – Signature Diseases

January 30th, 2023

The fourth edition of the Reference Manual on Scientific Evidence is by all accounts under way. Each of the first three editions represented an improvement over previous editions, but the last edition continued to have substantive problems. The bar, the judiciary, and the scientific community hopefully await an improved fourth edition. Although I have posted previously about issues in the third edition, I am updating and adding to what I have written.[1]  There were only a few reviews and acknowledgments of the third edition.[2] The editorial staff provided little to no opportunity for comments in advance of the third edition, and to date, there has been no call for public comment about the pending fourth edition. I hope there will be more opportunity for the legal and scientific community to comment in the production of the fourth edition.

There are several issues raised by the third edition’s treatment of specific causation, which I hope will be improved in the fourth edition. One such issue is the epidemiology chapter’s brief discussion of so-called signature diseases. The chapter takes the curious position that epidemiology has nothing to say about individual or specific causation, a position I will discuss in later posts. The chapter, however, carves out a limited exception to its (questionable) edict that epidemiology does not concern itself with specific causation.  The chapter tells us, uncontroversially, that some diseases do not occur without exposure to a specific chemical or substance. In my view, the authors of this chapter then go astray in telling us that “[a]bestosis is a signature disease for asbestos, and vaginal adenocarcinoma (in young adult women) is a signature disease for in utero DES exposure.”

Now, by definition, only asbestos can cause asbestosis, but asbestosis presents clinically in a way that is indistinguishable in many cases from idiopathic pulmonary fibrosis and other interstitial fibrotic diseases of the lungs. Over the years, the diagnostic criteria for asbestosis have changed, but these criteria have always had a specificity and sensitivity less than 100%. Saying that a case of asbestosis must have been caused by asbestos begs the clinical question whether the case really is asbestosis.

The chapter’s characterization of vaginal adenocarcinoma as a signature disease of in utero DES exposure is also not correct.  Although this cancer in young women is extremely rare, there is a baseline risk that allows the calculation of relative risks for young women exposed in utero. In older women, the relative risks are lower because the baseline risks are higher, and because the effect of DES is diminished for older onset cases.[3] The disease was known before the use of DES in pregnant women began after World War II.[4]

For support of their discussion of “signal diseases,” the authors of the epidemiology chapter chose, remarkably, to cite an article that was over 25 years old (now over 35 years old) at the time the third edition was published.[5] The referenced passage asks us to:

“Consider tort claims for what have come to be called signature disease. These are diseases characteristically caused by only a few substances – such as the vaginal adenocarcinoma usually associated with exposure to DES in utero – and mesothelioma, a cancer of the pleura caused almost exclusively by exposure to asbestos fibers in the air.”[6]

Well, “usually associated” does equal signature disease.[7] The relative risks for smoking and some kinds of lung cancer are higher than for DES in utero and clear cell vaginal adenocarcinoma, but no one calls lung cancer a signature disease of smoking. (Admittedly, smoking is the major cause and perhaps the most preventable cause of lung cancer in Western countries.)

The third edition’s reference to a source that describes mesothelioma as “caused almost exclusively by exposure to asbestos fibers” is also out of date.[8] Recognizing that casual comments and citations can influence credulous judges, the authors of the fourth edition should strive for greater accuracy in their discussions of such scientific issues. It may be time to find new examples of signature disease.

[1] “Reference Manual on Scientific Evidence v4.0” (Feb. 28, 2021); “Reference Manual on Scientific Evidence – 3rd Edition is Past Its Expiry” (Oct. 17, 2021). 

[2] See, e.g., Adam Dutkiewicz, “Book Review: Reference Manual on Scientific Evidence, Third Edition,” 28 Thomas M. Cooley L. Rev. 343 (2011); John A. Budny, “Book Review: Reference Manual on Scientific Evidence, Third Edition,” 31 Internat’l J. Toxicol. 95 (2012); James F. Rogers, Jim Shelson, and Jessalyn H. Zeigler, “Changes in the Reference Manual on Scientific Evidence (Third Edition),” Internat’l Ass’n Def. Csl. Drug, Device & Biotech. Comm. Newsltr. (June 2012). See Schachtman “New Reference Manual’s Uneven Treatment of Conflicts of Interest” (Oct. 12, 2011).

[3] Janneke Verloop, Flora E. van Leeuwen, Theo J. M. Helmerhorst, Hester H. van Boven, and Matti A. Rookus, “Cancer risk in DES daughters,” 21 Cancer Causes & Control 999 (2010).

[4] See “Risk Factors for Vaginal Cancer,” American Cancer Soc’y website (last visited Jan. 29, 2023).

[5] Kenneth S. Abraham & Richard A. Merrill, Scientific Uncertainty in the Courts, 2 Issues Sci. & Tech. 93, 101 (Winter 1986).

[6] Id.

[7] See, e.g., Kadir Güzin, Semra Kayataş Eserm, Ayşe Yiğit, and Ebru Zemheri, “Primary clear cell carcinoma of the vagina that is not related to in utero diethylstilbestrol use,” 3 Gynecol. Surg. 281 (2006).

[8] Michele Carbone, Harvey I. Pass, Guntulu Ak, H. Richard Alexander Jr., Paul Baas, Francine Baumann, Andrew M. Blakely, Raphael Bueno, Aleksandra Bzura, Giuseppe Cardillo, Jane E. Churpek, Irma Dianzani, Assunta De Rienzo, Mitsuru Emi, Salih Emri, Emanuela Felley-Bosco, Dean A. Fennell, Raja M. Flores, Federica Grosso, Nicholas K. Hayward, Mary Hesdorffer, Chuong D. Hoang, Peter A. Johansson, Hedy L. Kindler, Muaiad Kittaneh, Thomas Krausz, Aaron Mansfield, Muzaffer Metintas, Michael Minaai, Luciano Mutti, Maartje Nielsen, Kenneth O’Byrne, Isabelle Opitz, Sandra Pastorino, Francesca Pentimalli, Marc de Perrot, Antonia Pritchard, Robert Taylor Ripley, Bruce Robinson, and Valerie Rusch, “Medical and Surgical Care of Patients With Mesothelioma and Their Relatives Carrying Germline BAP1 Mutations,” 17 J. Thoracic Oncol. 873 (2022). See also Mitchell Cheung, Yuwaraj Kadariya, Eleonora Sementino, Michael J. Hall, Ilaria Cozzi, Valeria Ascoli, Jill A. Ohar, and Joseph R. Testa, “Novel LRRK2 mutations and other rare, non-BAP1-related candidate tumor predisposition gene variants in high-risk cancer families with mesothelioma and other tumors,” 30 Human Molecular Genetics 1750 (2021); Thomas Wiesner, Isabella Fried, Peter Ulz, Elvira Stacher, Helmut Popper, Rajmohan Murali, Heinz Kutzner, Sigurd Lax, Freya Smolle-Jüttner, Jochen B. Geigl, and Michael R. Speicher, “Toward an Improved Definition of the Tumor Spectrum Associated With BAP1 Germline Mutations,” 30 J. Clin. Oncol. e337 (2012); Alexandra M. Haugh, BA1; Ching-Ni Njauw, MS2,3; Jeffrey A. Bubley, et al., “Genotypic and Phenotypic Features of BAP1 Cancer Syndrome: A Report of 8 New Families and Review of Cases in the Literature,” 153 J.Am. Med. Ass’n Dermatol. 999 (2017).

Posted in Asbestos, Causation, Reference Manual on Scientific Evidence | 6 Comments »

Mass Tortogenesis

January 22nd, 2023

Mass torts are created much as cancer occurs in humans. The multistage model of tortogenesis consists of initiating and promoting events. The model describes, and in some cases, can even predict mass torts. The model also offers insights into prevention.

INITIATION

Initiating events can take a variety of forms. A change in a substance’s categorization in the International Agency for Research on Cancer’s treatment of cancer “hazards” will often initiate a mass tort by stirring interest in the lawsuit industry. A recent example of an IARC pronouncement’s initiating mass tort litigation is its reclassification of glyphosate as a “probable” human carcinogen.  Although the IARC monograph was probably flawed at its inception, and despite IARC’s specifying that its use of “probable” has no quantitative meaning, the IARC glyphosate monograph was a potent initiator of mass tort litigation against the manufacturer of glyphosate.

Regulatory rulemaking will often initiate a mass tort. Asbestos litigation existed as workman’s compensation cases from the 1930s, and as occasional, isolated cases against manufacturers, from the late 1950s.[1] By 1970, federal regulation of asbestos, in both occupational and environmental settings, however, helped create a legal perpetual motion machine that is still running, half a century later.

Publication of studies, especially with overstated results, will frequently initiate a mass tort. In 2007, the New England Journal of Medicine published a poorly done meta-analysis by Dr. Steven Nissen, on the supposed risk of heart attack from the use of rosiglitazone (Avandia).[2] Within days, lawsuits were filed against the manufacturer, GlaxoSmithKline, which ultimately paid over six billion dollars in settlements and costs.[3] Only after the harm of this mass tort was largely complete, the results of a mega-trial, RECORD,[4] became available, and the FDA changed its regulatory stance on rosiglitazone.[5]

More recently, on October 17, 2022, the Journal of the National Cancer Institute, published an observational epidemiologic study, “Use of Straighteners and Other Hair Products and Incident Uterine Cancer.”[6] Within a week or two, lawsuits began to proliferate. The authors were equivocal about their results, refraining from using explicit causal language, but suggesting that specific (phthalate) chemicals were “driving” the association:

“Abstract

Background

Hair products may contain hazardous chemicals with endocrine-disrupting and carcinogenic properties. Previous studies have found hair product use to be associated with a higher risk of hormone-sensitive cancers including breast and ovarian cancer; however, to our knowledge, no previous study has investigated the relationship with uterine cancer.

Methods

We examined associations between hair product use and incident uterine cancer among 33947 Sister Study participants aged 35-74 years who had a uterus at enrollment (2003-2009). In baseline questionnaires, participants in this large, racially and ethnically diverse prospective cohort self-reported their use of hair products in the prior 12 months, including hair dyes; straighteners, relaxers, or pressing products; and permanents or body waves. We estimated adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) to quantify associations between hair product use and uterine cancer using Cox proportional hazard models. All statistical tests were 2-sided.

Results

Over an average of 10.9 years of follow-up, 378 uterine cancer cases were identified. Ever vs never use of straightening products in the previous 12 months was associated with higher incident uterine cancer rates (HR= 1.80, 95% CI = 1.12 to 2.88). The association was stronger when comparing frequent use (> 4 times in the past 12 months) vs never use (HR=2.55, 95% CI = 1.46 to 4.45; P trend=.002). Use of other hair products, including dyes and permanents or body waves, was not associated with incident uterine cancer.

Conclusion

These findings are the first epidemiologic evidence of association between use of straightening products and uterine cancer. More research is warranted to replicate our findings in other settings and to identify specific chemicals driving this observed association.”

The JNCI article might be considered hypothesis generating, but we can observe the article, in real time, initiating a mass tort. A petition for “multi-district litigation” status was filed not long after publication, and the lawsuit industry is jockeying for the inside post in controlling the litigation. Although the authors acknowledged that their findings were “novel,” and required more research, the lawsuit industry did not.

PROMOTION OF INITIATED MASS TORTS

As noted, within days of publication of the JNCI article on hair straighteners and uterine cancer, lawyers filed cases against manufacturers and sellers of hair straighteners. Mass tort litigation is a big business, truly industrial in scale, with its own eco-system of litigation finance, and claim finding and selling. Laws against champerty and maintenance have gone the way of the dodo. Part of the ethos of this eco-system is the constant deprecation of manufacturing industry’s “conflicts of industry,” while downplaying the conflicts of the lawsuit industry.

Here is an example of an email that a lawsuit industry lawyer might have received last month. The emphases below are mine:

“From:  ZZZ

To:  YYYYYYYYY

Date:  12/XX/2022
Subject:  Hair relaxer linked to cancer

Hi,

Here is the latest information on the Hair Relaxer/Straightener tort.

A recent National Institute of Health sister study showed proof that hair straightener products are linked to uterine cancer.

Several lawsuits have been filed against cosmetic hair relaxer companies since the release of the October 2022 NIH study.

The potential plaintiff pool for this case is large since over 50,000 women are diagnosed yearly.

A motion has been filed with the Judicial Panel on Multi District Litigation to have future cases moved to a class action MDL.

There are four cosmetic hair relaxers that are linked to this case so far.  Dark & Lovely, Olive Oil Relaxer, Motions, and Organic Root Stimulator.

Uterine fibroids and endometriosis have been associated with phthalate metabolites used in hair relaxers.

Are you looking to help victims in this case

ZZZ can help your firm sign up these thousands of these claimants monthly with your hair relaxer questionnaire, criteria, retainer agreement, and Hippa without the burden of doing this in house at an affordable cost per signed retainer for intake fees.

  • ZZZ intake fees are as low as $65 dollars per signed based upon a factors which are criteria, lead conversion %, and length of questionnaire.  Conversion rates are averaging 45%.
  • I can help point you in the right direction for reputable marketing agencies if you need lead sources or looking to purchase retainers.  

Please contact me to learn more about how we can help you get involved in this case.

Thank you,

ZZZ”

As you can see from ZZZ’s email, the JNCI article was the tipping point for the start of a new mass tort. ZZZ, however, was a promoter, not an initiator. Consider the language of ZZZ’s promotional efforts:

“Proof”!

As in quod erat demonstrandum.

Where is the Department of Justice when you have the makings of a potential wire fraud case?[7]

And “link.” Like sloppy journalists, the lawsuit industry likes to link a lot.

chorizo sausage links (courtesy of Wikipedia)[8]

And so it goes.

Absent from the promotional email are of course, mentions of the “novelty” of the JNCI paper’s finding, its use of dichotomized variables, its multiple comparisons, or its missing variables. Nor will you see any concern with how the JNCI authors inconsistently ascertained putative risk factors. Oral contraception was ascertained for over 10 years before base line, but hair straightener use was ascertained only for one year prior to baseline.

SYSTEMIC FAILURES TO PREVENT MASS TORTOGENESIS

Human carcinogenesis involves initiation and promotion, as well as failure of normal defense mechanisms against malignant transformation. Similarly, mass tortogenesis involves failure of defense mechanisms. Since 1993, the federal courts have committed to expert witness gatekeeping, by which they exclude expert witnesses who have outrun their epistemic headlights. Gatekeeping in federal court does not always go well, as for example in the Avandia mass tort, discussed above. In state courts, gatekeeping is a very uneven process.

Most states have rules or law that looks similar to federal law, but state judges, not uncommonly, look for ways to avoid their institutional responsibilities. In a recent decision involving claims that baby foods allegedly containing trace metals cause autism, a California trial judge shouted “not my job”[9]:

 “Under California law, the interpretation of epidemiological data — especially data reported in peer-reviewed, published articles — is generally a matter of professional judgment outside the trial court’s purview, including the interpretation of the strengths and weaknesses of a study’s design. If the validity of studies, their strengths and weaknesses, are subject to ‘considerable scientific interpretation and debate’, a court abuses its discretion by ‘stepping in and resolving the debate over the validity of the studies’. Nor can a court disregard ‘piecemeal … individual studies’ because it finds their methodology, ‘fully explained to the scientific community in peer-reviewed journals, to be misleading’ – ‘it is essential that… the body of studies be considered as a whole’. Flaws in study methodology should instead be ‘explored in detail through cross-examination and with the defense expert witnesses’ and affect ‘the weight[,] not the admissibility’ of an expert’s opinions.”

When courts disclaim responsibility for ensuring validity of evidence used to obtain judgments in civil actions, mass tortogenesis is complete, and the victim, the defendants, often must undergo radical treatment.

[1] The first civil action appears to have been filed by attorney William L. Brach on behalf of Frederick LeGrande, against Johns-Manville, for asbestos-related disease, on July 17, 1957, in LeGrande v. Johns-Manville Prods. Corp., No. 741-57 (D.N.J.).

[2] Steven E. Nissen, M.D., and Kathy Wolski, M.P.H., “Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes,” 356 New Engl. J. Med. 2457, 2457 (2007).

[3] In re Avandia Marketing, Sales Practices and Product Liability Litigation, 2011 WL 13576, *12 (E.D. Pa. 2011) (Rufe, J.).  See “Learning to Embrace Flawed Evidence – The Avandia MDL’s Daubert Opinion” (Jan. 10, 2011). Failed expert witness opinion gatekeeping promoted the mass tort into frank mass tort.

[4] Philip D. Home, Stuart J Pocock, et al., “Rosiglitazone Evaluated for Cardiovascular Outcomes in Oral Agent Combination Therapy for Type 2 Diabetes (RECORD),” 373 Lancet 2125 (2009) (reporting hazard ratios for cardiovascular deaths 0.84 (95% C.I., 0·59–1·18), and for myocardial infarction, 1·14 (95% C.I., 0·80–1·63). See “Revisiting the Avandia Scare: Results from the RECORD Trial” DiaTribe Learn (updated Aug. 14, 2021).

[5] FDA Press Release, “FDA requires removal of certain restrictions on the diabetes drug Avandia” (Nov. 25, 2013). And in December 2015, the FDA abandoned its requirement of a Risk Evaluation and Mitigation Strategy for Avandia. FDA, “Rosiglitazone-containing Diabetes Medicines: Drug Safety Communication – FDA Eliminates the Risk Evaluation and Mitigation Strategy (REMS)” (Dec. 16, 2015).

[6] Che-Jung Chang, Katie M O’Brien, Alexander P Keil, Symielle A Gaston, Chandra L Jackson, Dale P Sandler, and Alexandra J White, “Use of Straighteners and Other Hair Products and Incident Uterine Cancer,”114 J.Nat’l Cancer Instit. 1636 (2022).

[7] See, e.g., United States v. Harkonen, 2010 WL 2985257, at *5 (N.D. Calif. 2010) (denying defendant’s post–trial motions to dismiss the indictment, for acquittal, or for a new trial), aff’d, 510 Fed. Appx. 633, 2013 WL 782354, 2013 U.S. App. LEXIS 4472 (9th Cir. March 4, 2013), cert. denied 134 S.Ct. 824 (2013).

[8] See https://en.wikipedia.org/wiki/List_of_sausages.

[9] NC v Hain Celestial Group, Inc., 21STCV22822, Slip op. sur motion to exclude expert witnesses, Cal. Super. Ct. (Los Angeles May 24, 2022) (internal citations omitted).

Posted in Public Nuisances, Rule 702, Scientific Evidence, Scientific Publishing | 2 Comments »

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The opinions, statements, and asseverations expressed on Tortini are my own, or those of invited guests, and these writings do not necessarily represent the views of clients, friends, or family, even when supported by good and sufficient reason.