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Professor Faigman on the Dual Goals of the Daubert Revolution

March 9th, 2013

Academic commentators on Daubert and its progeny tend to fall into two camps:  acolytes and heretics.  The acolytes have generally supported the changes brought about by Daubert and the ultimate statutory embrace of active expert witness gatekeeping.  The heretics have maintained a rearguard action against Daubert, and Rule 702; they have tried to undermine gatekeeping at every turn.

Among the chief acolytes is David Faigman, whose books and articles have contributed substantially to the discussions and debates about the law of scientific evidence and expert witnesses.  Professor Faigman’s recent article is an important contribution to the law review literature on Daubert.  David L. Faigman, “The Daubert Revolution and the Birth of Modernity:  Managing Scientific Evidence in the Age of Science,” 102 U.C. Davis Law Rev. 101 (2013) [“Revolution”].  It is well worth reading.

Professor Faigman declares himself “a fan” of Daubert, and embraces the revolution in expert witness law heralded by the Supreme Court’s 1993 decision.  Id. at 103.  He emphasizes that the decision, quickly approaching its 20th anniversary, was truly revolutionary in how the federal courts engaged with expert witness opinion testimony, and that the consequences of the revolution are still taking shape.  Id.

Faigman acknowledges that Daubert and its progeny, and the statutory embrace of gatekeeping in Rule 702, at the end of the last millennium, were important developments in ensuring the epistemic warrant of federal courts’ judgments.  Some authors, hostile to the gatekeeping enterprise, have suggested that this aspect of Daubert resulted from persistent pressures from the defense bar and industry to limit plaintiffs’ access to the courts.  Faigman does not address such suggestions, and I believe that they are cynical and incorrect.  The federal courts, by the mid-1980’s, were deeply embarrassed by the scientific community’s opprobrium, meted out over notorious decisions, such as Wells v. Ortho Pharmaceutical Corp., 615 F. Supp. 262 (N.D. Ga. 1985), aff’d and rev’d in part on other grounds, 788 F.2d 741 (11th Cir.), cert. denied, 479 U.S.950 (1986).  See also In re Air Crash Disaster at New Orleans, 795 F.2d 1230, 1234 (5th Cir. 1986) (“Our message to our able trial colleagues: it is time to take hold of expert testimony in federal trials.”).  Daubert and its progeny were, in my view, the judicial response to the scientific community’s criticisms.

Faigman’s thesis in this paper, however, lies elsewhere.  He argues that the Supreme Court’s excursions into expert evidence law, in Daubert and in the later cases, were intended primarily to give trial courts greater control over their dockets by being able to excluding dubious testimony and to grant summary dispositions.  Revolution at 104  Scientific verisimilitude was secondary to docket control.  Id. at 105.

Faigman’s thesis is plausible and should be taken seriously.  The first three cases in the “Revolution,” Daubert, Joiner, and Kumho Tire, were all tort cases with “mass tort” overtones.  Daubert was one of many Bendectin cases.  Joiner was a case involving occupational PCB exposures.  If the tenuous scientific opinions were deemed “admissible,” there were sure to be many more such cases.  And Kumho Tire was a case involving dubious allegations of a defect in a tire, the sort of allegations that plague American industry because they are so easy to manufacture, and so costly to defend.

Faigman builds an impressive case for the proposition that the justices really were trying to give trial courts managerial power to control their own dockets by filtering out essential, but deficient, expert witness testimony. Id. at 118.  After all, if the Supreme Court were really interested in improving judicial use of scientific evidence, why would it have created an abuse of discretion standard for reviewing Rule 702 determinations? The abuse standard signals that decisions either way are tolerable if they are accompanied by the right verbiage and procedural steps.

Faigman also points out that the abuse-of-discretion standard deprives the appellate courts of any meaningful review of the validity of scientific opinion testimony. The claims and conclusions advanced by expert witnesses in individual cases will often be of interest and importance to scientists, policy makers, plaintiffs, defendants, beyond the confines of the individual case.  The appellate courts are in a better position to ascertain validity questions, and maintain consistency in them, as a matter of law.  Freed of the pressures of trial courts, and with input from amici curiae, the appellate court can evaluate validity issues more deliberately with a view to harmonizing competing factors across many cases.  The scientific issues are, in any event, often non-case specific, or they have the tendency to recur in many cases of the same type.  Id. at 131.

Faigman’s thesis sheds light upon who the heretics are, and why they have worked so hard to undermine expert witness gatekeeping.  At stake is not only greater scientific validity, but also summary disposition of litigation rent-seeking. Rule 702 gatekeeping challenges judges and commentators to identify their priorities:  commitment to scientific principles or to litigation as an alternative to regulation and legislation on behalf of a special constituency.

There are some ironies inherent in Faigman’s thesis.  The trial bench has been reluctant to exercise its gatekeeping function as a method of docket control.  Instead, it has moved towards greater use of pre-trial consolidations in multi-district litigations to achieve economies of scale.  The MDL trend, however, has its problems.  Placing responsibility for expert witness gatekeeping in the MDL court may be counter to its “pre-trial” rationale of the MDL statute.  Furthermore, exercising gatekeeping across hundreds or thousands of cases heightens and highlights the anxieties, fears, distaste, and institutional incompetence for deciding scientific issues. The move toward MDL handling has had the apparent result of diluting the gatekeeping mandate and reducing the use of summary dispositions.

The procedural and the validity goals of Daubert are quite independent.  Validity may have been, as Faigman argues, a secondary goal for the Justices, but it was a worthy goal in and of itself.  I believe Professor Faigman would agree.  In describing the Supreme Court’s path on validity, Faigman notes that there were two competing models of expert witness admissibility determinations that vied for acceptance:  Frye, and then Daubert.  Id. at 105. He likens Frye to nose counting among the “relevant” scientific community for support of the witness’s methodology.  All a trial judge need do is identify the relevant community and then to count the noses.  Daubert represented a possible alternative:

“to charge judges with the responsibility to consider the methods and principles underlying proffered expert opinion and have them make the validity determination.”

Id. at 105.  Making trial judges responsible for warranting the validity of scientific evidence, and ultimately all expert witness opinion testimony, was one of the important changes that resulted in the Revolution and its embrace of “good grounds” or epistemic validity:

“[p]roposed testimony must be supported by appropriate validation.”

Daubert v. Merrell Dow Pharm., 509 U.S. 579, 590 (1993)

Professor Faigman correctly observes that, although lawyers and lower court judges have obsessed over the so-called Daubert factors, the actual holding of Daubert was “the requirement that an expert’s testimony pertain to ‘scientific knowledge’ establishes a standard of evidentiary reliability.” Revolution at 111 (quoting Daubert, 509 U.S. at 590).  Despite the improvident dictum about focus on methodology and not on conclusions, the Supreme Court, in Daubert, had made clear that there are necessary implications of Rule 702’s requirement that expert witness testimony relate to specialized “knowledge”:

“This entails a preliminary assessment of whether the reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts in issue.”

Daubert, 509 U.S. at 592-93.

Professor Faigman writes to point out the erroneous interpretations and distortions of Daubert, its progeny, and Rule 702:

“The holding of Daubert is the requirement that judges find as a preliminary fact that the methods and principles underlying proffered expert testimony are sufficiently valid to support that testimony. The four ‘Daubert factors’ were offered as guidelines to help courts assess expert testimony.”

Revolution at 114.

Faigman’s writing is a useful reminder to those judges and commentators who would simplify and abridge the entire gatekeeping project into one or another dictum found in Daubert (or Joiner or Kumho Tire), and who ignore the actual holding of the cases, or the mandate of the subsequent statute. For those writers who try to evade the difficult scientific determinations and discriminations inherent in evaluating causal claims and other scientific opinions, Faigman reminds us that Justice Breyer, in his concurrence in Joiner, was not shy about pointing out that gatekeeping:

“will sometimes ask judges to make subtle and sophisticated determinations about scientific methodology and its relation to the conclusions an expert witness seeks to offer.”

General Electric Company v. Joiner, 522 U.S. 136, 118 S. Ct. 512, 520 (1997) (Breyer, J., concurring).  I take Faigman’s essay as an eloquent importuning of the judiciary to heed Justice Breyer, to stop whining, and to start learning.

It is a measure of Professor Faigman’s concern for the accuracy and validity of scientific testimony that he cannot bring himself to address a third way:  ignore validity, reliability, sufficiency, and simply allow expert witnesses to battle out.

This third way was what really prevailed before Daubert in much of civil litigation over health effects.  The Frye rule was rarely if ever applied to such cases, and most states excepted the opinion testimony of physicians, in any event.  Before Frye, we had whatever was dished up by ready, willing, able (and sufficiently glib) testifiers.  To be sure, expert witnesses had to be qualified, but the threshold was astonishingly low.  In Pennsylvania, for instance, the standard is that the putative “expert” must have “a reasonable pretense of expertise.” See, e.g., Ruzzi v. Butler Petroleum Co., 527 Pa. 1, 9-10 (1991); Kuisis v. Baldwin-Lima-Hamilton Corp.,457 Pa. 321, 319 A.2d 914 (1974)(“the witness must have a reasonable pretension to specialized knowledge on the subject under investigation”).  The federal courts were not far behind. Ferebee v. Chevron Chem. Co., 552 F. Supp. 1297 (D.D.C. 1982), aff’d, 736 F.2d 1529 (D.C. Cir.), cert. denied, 469 U.S. 1062 (1984).

Indeed, there is a pervasive, reactionary movement afoot, among judges and academic commentators to return to the wild, woolly days, celebrated in Ferebee’s famous dictum:

“On questions … which stand at the frontier of current medical and epidemiological inquiry, if experts are willing to testify that such a link exists, it is for the jury to decide whether to credit such testimony.”

Ferebee, 736 F.2d at 1534.  This third way then is simply to delegate to the expert witnesses themselves to assess the “weight of the evidence,” and offer up their opinions, without any scrutiny from the courts as to the validity or sufficiency of the bases for those opinions. This retrograde step is not just the stuff of naive law student musings. See, e.g., Note, “Admitting Doubt: A New Standard for Scientific Evidence,” 123 Harv. L. Rev. 2021 (2010). Reactionaries in the Academy and in the judiciary are intent to reduce gatekeeping to a weak test of relevancy, without any determination of content validity.

Posted in Expert Witnesses, Rule 702, Scientific Evidence, Trial Procedure | Comments Off on Professor Faigman on the Dual Goals of the Daubert Revolution

Milward Symposium Organized By Plaintiffs’ Counsel and Witnesses

February 16th, 2013

The criticisms of corporate free speech are motivated, at bottom, over hostility to the views that would likely flow from corporate speech. In this age, it is a marvel that there is such hostility to free expression of ideas.  We should be much more focused on validity and factual accuracy of arguments than on sponsorship.  Sometimes, even the most biased sources manage to stumble upon the truth.

Still, sponsorship remains a major debating point for those who cannot or will not take the time to evaluate the merits of an issue.  The Center for Progressive Reform (CPR) is, like many American corporations, a nonprofit organization, but it aspires to be a “research and educational organization.” The CPR’s principal aims deal with protecting health and safety against occupational and environmental harms.  These are laudable goals even if the CPR is predictably a voice of entrenched interest groups, such as the litigation industry, also known as the plaintiffs’ tort bar.

One of the CPR’s key activities is “[d]efending clean science from political or corporate interference.” The CPR raises interesting questions about what is “clean,” and what is “dirty” science, and whether it is willing to defend science from all political and corporate interference, or only that interference with which it disagrees.

The American litigation industry is represented by a highly politicized “corporation,” the American Association for Justice (AAJ), previously known by the more revealing name, Association of Trial Lawyers of America (ATLA®).   The AAJ describes itself as a corporation, or a “collective,” that supports plaintiff trial lawyers as their “collective voice … on Capitol Hill and in courthouses across the nation … .” The Robert A. Habush Foundation is endowed by the AAJ, and serves as an educational mission.  Through the Habush Foundation, the AAJ funds educational programs, “think tanks,” and writing projects designed to influence judges, law professors, lawyers, and the public, on issues of importance to the AAJ:  “the civil justice system and individual rights” for bigger, better, and more profitable litigation outcomes.

Of the two organizations, the CPR, and the AAJ/ATLA, the CPR has the more disinterested stance, in theory. The AAJ may be a “not-for-profit,” but it represents the interests of one of the most powerful, and wealthiest, interest groups in American society — the plaintiffs’ bar.

Last May, the CPR sponsored a symposium in Washington D.C. on one of the most controversial, and reactionary decisions involving federal gatekeeping of expert witness testimony, Milward v. Acuity Specialty Products Group, Inc., 664 F.Supp. 2d 137 (D. Mass. 2009), rev’d, 639 F.3d 11 (1st Cir. 2011), cert. denied, U.S. Steel Corp. v. Milward, ___ U.S. ___, 2012 WL 33303 (2012).  The CPR’s interest in the Milward decision is clear.  One of CPR’s member “scholars,” Carl Cranor, was a partisan expert witness in Milward.  The trial court had excluded Cranor’s testimony; a panel of the First Circuit of the Court of Appeals reversed and ordered that Cranor and the plaintiffs’ other expert witnesses be heard at trial.  See Milward — Unhinging the Courthouse Door to Dubious Scientific Evidence (Sept. 2, 2011); WOE-fully Inadequate Methodology – An Ipse Dixit By Another Name (May 2, 2012).  The Milward decision embraced a vacuous methodology sometimes called “weight of the evidence” (WOE) or “inference to the best explanation,” which had been previously rejected by other Circuits, as well as by the United States Supreme Court, in General Electric Co. v. Joiner, 522 U.S. 136 (1997).

The agenda for the symposium, “Toxic Tort Litigation after Milward v. Acuity Specialty Products,” reflects the CPR’s role, in conjunction with the Wake Forest Journal of Law and Public Policy, in sponsoring the event.  The connection between the CPR and Wake Forest Law School may not be obvious.  CPR board member, Sid Shapiro, is a law professor at Wake Forest.  Shapiro and CPR member Thomas McGarity presented at the symposium. So did Professor Steve Gold, who has been an enthusiastic cheerleader for the Milward decision.  Law professors Michael Green and Joseph Sanders also presented.  There was only one practicing lawyer involved in the symposium, Texas plaintiffs’ lawyer, Steve Jensen, of Allen Stewart, P.C.  Mr. Jensen is a past chair of the AAJ’s Section on Toxic, Environmental, and Pharmaceutical Torts.

No defense counsel participated.

The proceedings of the Milward symposium will be published in an upcoming issue (volume 3, no. 1) of the Wake Forest Journal of Law and Public Policy.  This issue is scheduled to include papers from the presenters, along with one additional author, Carl Cranor.

The website of the Wake Forest Journal of Law & Policy describes the symposium:

In Milward v. Acuity Products, 639 F.3d 11 (1st Cir. 2011), the First Circuit became the first court – either federal or state – to allow a “weight of the evidence” methodology for assessing causation in a toxic tort case. The plaintiff had alleged that exposure to defendant’s benzene-containing products caused his rare leukemia (Acute Promyelocytic Leukemia (“APL”)).  His expert witness, a leading toxicologist and expert on benzene, surveyed five lines of scientific evidence from the peer-reviewed literature, and concluded the available evidence, taken as a whole, supported the inference that benzene exposure can cause APL.  The lower court, following a common post-Daubert approach, excluded the testimony “because no one line of evidence supported a reliable inference of causation, [and] an inference of causation based on the totality of the evidence was unreliable.”  The First Circuit rejected this “atomistic” approach, noting that the district court did not have the authority to exclude evidence because reasonable experts may disagree about what it means.

This symposium will explore the implications of Milward for toxic tort litigation in the federal and state courts, including whether it correctly applies Daubert v. Merrell Dow Pharmaceuticals, Inc., 509, U.S. 579 (1993).  * * * Speakers are invited to comment on any aspect on Milward that they find interesting and important, including the following issues:

  1. What role does the weight of the evidence methodology play in scientific risk assessment, and what are the implications of this role for tort litigation?
  2. Should well-founded testimony based on a weight of the evidence methodology be admissible in toxic tort litigation?  Does the Restatement of Torts (Third) § 28 cmt. c concerning the role of scientific judgment in adjudicating general causation support the admissibility of such testimony?
  3. Does the reliance of regulatory agencies, such as EPA, on a weight of the evidence methodology for purposes of regulating toxic chemicals support the result in Milward?  Or are there differences in the legal and policy judgments being made by regulators and judges that distinguish regulatory agencies from courts?
  4. What are the legal and policy implications of Milward for the future of toxic tort litigation?

The Journal also notes the sponsorship of the CPR, and, in a cryptic paragraph, reports that

“CPR thanks the Robert L. Habush Foundation for its support of the symposium.”

Most casual readers will not likely recognize the Habush foundation for what it is: an arm of AAJ/ATLA.  I suppose it was too painful for Wake Forest or the CPR to acknowledge openly that the litigation industry itself supported this symposium.  Some may find irony in the CPR’s past criticism of Citizens United v. Federal Election Commission, 558 U.S. 310 (2010), when its current status as a conduit for litigation industry money to support scholarship in that industry’s interests.  See Daniel Farber, “Of the Corporations, By the Corporations, For the Corporations? The Meaning of the Citizens United Decision” (Jan. 21, 2010).

Professor Steve Gold’s paper, “When Certainty Dissolves into Probability: A Legal Vision of Toxic Causation for the Post-Genomic Era,” has been posted at the Social Science Research Network.  Steve Jensen’s contribution to the symposium has been published as well, in the AAJ’s trade journal.  Steve Baughman Jensen, “Reframing the Daubert Issue in Toxic Tort Cases,” Trial (Feb. 2013).

Posted in Conflicts of Interest, Expert Witnesses, Rule 702 | Comments Off on Milward Symposium Organized By Plaintiffs’ Counsel and Witnesses

Reanalysis of Epidemiologic Studies – Not Intrinsically WOEful

December 27th, 2012

A recent student law review article discusses reanalyses of epidemiologic studies, an important, and overlooked topic in the jurisprudence of scientific evidence.  Alexander J. Bandza, “Epidemiological-Study Reanalyses and Daubert: A Modest Proposal to Level the Playing Field in Toxic Tort Litigation,” 39 Ecology L. Q. 247 (2012).

In the Daubert case itself, the Ninth Circuit, speaking through Judge Kozinksi, avoided the methodological issues raised by Shanna Swan’s reanalysis of Bendectin epidemiologic studies, by assuming arguendo its validity, and holding that the small relative risk yielded by the reanalysis would not support a jury verdict of specific causation. Daubert v. Merrell Dow Pharm., Inc., 43 F.3d 1311, 1317–18 (9th Cir. 1995).

There is much that can, and should, be said about reanalyses in litigation and in the scientific process, but Bandza never really gets down to the business at hand. His 36 page article curiously does not begin to address reanalysis until the bottom of the 20th page. The first half of the article, and then some, reviews some time-worn insights and factoids about scientific evidence. Finally, at page 266, the author introduces and defines reanalysis:

“Reanalysis occurs ‘when a person other than the original investigator obtains an epidemiologic data set and conducts analyses to evaluate the quality, reliability or validity of the dataset, methods, results or conclusions reported by the original investigator’.”

Bandza at 266 (quoting Raymond Neutra et al., “Toward Guidelines for the Ethical Reanalysis and Reinterpretation of Another’s Research,” 17 Epidemiology 335, 335 (2006).

Bandza correctly identifies some of the bases for judicial hostility to re-analyses. For instance, some courts are troubled or confused when expert witnesses disagree with, or reevaluate, the conclusions of a published article. The witnesses’ conclusions may not be published or peer reviewed, and thus the proffered testimony fails one of the Daubert factors.  Bandza correctly notes that peer review is greatly overrated by judges. Bandza at 270. I would add that peer review is an inappropriate proxy for validity, a “test,” which reflects a distrust of the unpublished.  Unfortunately, this judicial factor ignores the poor quality of much of what is published, and the extreme variability in the peer review process. Judges overrate peer review because they are desperate for a proxy for validity of the studies relied upon, which will allow them to pass their gatekeeping responsibility on to the jury. Furthermore, the authors’ own conclusions are hearsay, and their qualifications are often not fully before the court.  What is important is the opinion of the expert witness who can be cross-examined and challenged.  See “FOLLOW THE DATA, NOT THE DISCUSSION.” What counts is the validity of the expert witness’s reasoning and inferences.

Bandza’s article, which by title advertises itself to be about re-analyses, gives only a few examples of re-analyses without much detail.  He notes concerns that reanalyses may impugn the reputation of published scientists, and burden them with defending their data.  Who would have it any other way? After this short discussion, the article careens into a discussion of “weight of the evidence” (WOE) methodology. Bandza tells us that the rejection of re-analyses in judicial proceedings “implicitly rules out using the weight-of-the-evidence methodology often appropriate for, or even necessary to, scientific analysis of potentially toxic substances.” Bandza at 270.  This argument, however, is one sustained non-sequitur.  WOE is defined in several ways, but none of the definitions require or suggest the incorporation of re-analyses. Re-analyses raise reliability and validity issues regardless whether an expert witness incorporates them into a WOE assessment. Yet Bandza tells us that the rejection of re-analyses “Implicitly Ignores the Weight-of-the-Evidence Methodology Appropriate for the Scientific Analysis of Potentially Toxic Substances.” Bandza at 274. This conclusion simply does not follow from the nature of WOE methodology or reanalyses.

Bandza’s ipse dixit raises the independent issue whether WOE methodology is appropriate for scientific analysis. WOE is described as embraced or used by regulatory agencies, but that description hardly recommends the methodology as the basis for a scientific, as opposed to a regulatory, conclusion.  Furthermore, Bandza ignores the ambiguity and variability of WOE by referring to it as a methodology, when in reality, WOE is used to describe a wide variety of methods of reasoning to a conclusion. Bandza cites Douglas Weed’s article on WOE, but fails to come to grips with the serious objections raised by Weed in his article to the use of WOE methodologies.  Douglas Weed, “Weight of Evidence: A Review of Concept and Methods,” 25 Risk Analysis 1545, 1546–52 (2005) (describing the vagueness and imprecision of WOE methodologies). See also “WOE-fully Inadequate Methodology – An Ipse Dixit By Another Name.”

Bandza concludes his article with a hymn to the First Circuit’s decision in Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11 (1st Cir. 2011). Plaintiffs’ expert witness, Dr. Martyn Smith claimed to have performed a WOE analysis, which in turn was based upon a re-analysis of several epidemiologic studies. True, true, and immaterial.  The re-analyses were not inherently a part of a WOE approach. Presumably, Smith re-analyzed some of the epidemiologic studies because he felt that the data as presented did not support his desired conclusion.  Given the motivations at work, the district court in Milward was correct to look skeptically and critically at the re-analyses.

Bandza notes that there are procedural and evidentiary safeguards in federal court against unreliable or invalid re-analyses of epidemiologic studies.  Bandza at 277. Yes, there are safeguards but they help only when they are actually used. The First Circuit in Milward reversed the district court for looking too closely at the re-analyses, spouting the chestnut that the objections went to the weight not the admissibility of the evidence.  Bandza embraces the rhetoric of the Circuit, but he offers no description or analysis of the liberties that Martyn Smith took with the data, or the reasonableness of Smith’s reliance upon the re-analyzed data.

There is no necessary connection between WOE methodologies and re-analyses of epidemiologic studies.  Re-analyses can be done properly to support or deconstruct the conclusions of published papers.  As Bandza points out, some re-analyses may go on to be peer reviewed and published themselves.  Validity is the key, and WOE methodologies have little to do with the process of evaluating the original or the re-analyzed study.

 

 

Posted in Causation, Data Sharing, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Reanalysis of Epidemiologic Studies – Not Intrinsically WOEful

Litmus Tests

December 27th, 2012

Rule 702 is, or is not, a litmus test for expert witness opinion admissibility.  Relative risk is, or is not, a litmus test for specific causation.  Statistical significance is, or is not, a litmus test for reasonable reliance upon the results of a study.  It is relatively easy to find judicial opinions on either side of the litmus divide.  Compare National Judicial College, Resource Guide for Managing Complex Litigation at 57 (2010) (Daubert is not a litmus test) with Cryer v. Werner Enterprises, Inc., Civ. Action No. 05-S-696-NE, Mem. Op. & Order at 16 n. 63 (N.D. Ala. Dec. 28, 2007) (describing the Eleventh Circuit’s restatement of Rule 702’s “litmus test” for the methodological reliability of proffered expert witness opinion testimony).

The “litmus test“ is one sorry, overworked metaphor.  Perhaps its appeal has to do with a vague collective memory that litmus paper is one of those “things of science,” which we used in high school chemistry, and never had occasion to use again. Perhaps, litmus tests have the appeal of “proofiness.”

The reality is different. The litmus test is a semi-quantitative test for acidity or alkalinity.  Neutral litmus is purple.  Under acidic conditions, litmus turns red; under basic conditions, it turns blue.  For some time, scientists have used pH meters when they want a precise quantification of acidity or alkalinity.  Litmus paper is a fairly crude test, which easily discriminates  moderate acidity from alkalinity (say pH 4 from pH 11), but is relatively useless for detecting an acidity at pH or 6.95, or alkalinity at 7.05.

So what exactly are legal authors trying to say when they say that some feature of a test is, or is not, a “litmus test”? The litmus test is accurate, but not precise at the important boundary at neutrality.  The litmus test color can be interpreted for degree of acidity or alkalinity, but it is not the preferred method to obtain a precise measurement. Saying that a judicial candidate’s views on abortion are a litmus test for the Senate’s evaluation of the candidate makes sense, given the relative binary nature of the outcome of a litmus test, and the polarization of political views on abortion. Apparently, neutral views or views close to neutrality on abortion are not a desideratum for judicial candidates.  A cruder, binary test is exactly what is desired by politicians.

The litmus test that is used for judicial candidates does not seem to work so well when used to describe scientific or statistical inference.  The litmus test is well understood, but fairly obsolete in modern laboratory practice.  When courts say things, such as statistical significance is not a litmus test for acceptability of a study’s results, clearly they are correct because measure of random error is only one aspect of judging a body of evidence for, or against, an association.  Yet courts seem to imply something else, at least at times:

statistical significance is not an important showing in making a case that an exposure is reliably associated with a particular outcome.

Here courts are trading in half truths.  Statistical significance is quantitative, and the choice of a level of significance is not based upon immutable law. So like the slight difference between a pH of 6.95 and 7.05, statistical significance tests have a boundary issue.  Nonetheless, a consideration of random error cannot be dismissed or overlooked on the theory that significance level is not a “litmus test.”  This metaphor obscures and attempts to excuse sloppy thinking.  It is time to move beyond this metaphor.

Posted in Rule 702, Scientific Evidence, statistical evidence | Comments Off on Litmus Tests

Lumpenepidemiology

December 24th, 2012

Judge Helen Berrigan, who presides over the Paxil birth defects MDL in New Orleans, has issued a nicely reasoned Rule 702 opinion, upholding defense objections to plaintiffs expert witnesses, Paul Goldstein, Ph.D., and Shira Kramer, Ph.D. Frischhertz v SmithKline Beecham EDLa 2012 702 MSJ Op.

The plaintiff, Andrea Frischhertz, took GSK’s Paxil, a selective serotonin reuptake inhibitor (SSRI), for depression while pregnant with her daughter, E.F. The parties agreed that E.F. was born with a deformity of her right hand.  Plaintiffs originally claimed that E.F. had a heart defect, but their expert witnesses appeared to give up this claim at deposition, as lacking evidential support.

Adhering to Daubert’s Epistemiologic Lesson

Like many other lower federal courts, Judge Berrigan focused her analysis on the language of Daubert v. Merrell Dow Pharmaceuticals Inc., 509 U.S. 579 (1993), a case that has been superseded by subsequent cases and a revision to the operative statute, Rule 702.  Fortunately, the trial court did not lose sight of the key epistemological teaching of Daubert, which is based upon Rule 702:

“Regarding reliability, the [Daubert] Court said: ‘the subject of an expert’s testimony must be “scientific . . . knowledge.” The adjective “scientific” implies a grounding in the methods and procedures of science. Similarly, the word “knowledge” connotes more than subjective belief or unsupported speculation’.”

Slip Op. at 3 (quoting Daubert, 509 U.S. at 589-590).

There was not much to the plaintiffs’ expert witnesses’ opinion beyond speculation, but many other courts have been beguiled by speculation dressed up as “scientific … knowledge.”  Dr. Goldstein relied upon whole embryo culture testing of SSRIs, but in the face overwhelming evidence, Dr. Goldstein was forced to concede that this test may generate hypotheses about, but cannot predict, human risk of birth defects.  No doubt this concession made the trial court’s decision easier, but the result would have been required regardless of Dr. Goldstein’s exhibition of truthfulness at deposition.

Statistical Association – A Good Place to Begin

More interestingly, the trial court rejected the plaintiffs’ expert witnesses’ efforts to leapfrog finding a statistically significant association to parsing the so-called Bradford Hill factors:

“The Bradford-Hill criteria can only be applied after a statistically significant association has been identified. Federal Judicial Center, Reference Manual on Scientific Evidence, 599, n.141 (3d. ed. 2011) (“In a number of cases, experts attempted to use these guidelines to support the existence of causation in the absence of any epidemiologic studies finding an association . . . . There may be some logic to that effort, but it does not reflect accepted epidemiologic methodology.”). See, e.g., Dunn v. Sandoz Pharms., 275 F. Supp. 2d 672, 678 (M.D.N.C. 2003). Here, Dr. Goldstein attempted to use the Bradford-Hill criteria to prove causation without first identifying a valid statistically significant association. He first developed a hypothesis and then attempted to use the Bradford-Hill criteria to prove it. Rec. Doc. 187, Exh. 2, depo. Goldstein, p. 103. Because there is no data showing an association between Paxil and limb defects, no association existed for Dr. Goldstein to apply the Bradford-Hill criteria. Hence, Dr. Goldstein’s general causation opinion is not reliable.”

Slip op. at 6.

The trial court’s rejection of Dr. Goldstein’s attempted end run is particularly noteworthy given the Reference Manual’s weak-kneed attempt to suggest that this reasoning has “some logic” to it.  The Manual never articulates what “logic” commends Dr. Goldstein’s approach; nor does it identify any causal relationship ever established with such paltry evidence in the real world of science. The Manual does cite several legal cases that excused or overlooked the need to find a statistically significant association, and even elevated such reasoning into legally acceptable, admissibility method.  See Reference Manual on Scientific Evidence at 599 n. 141 (describing cases in which purported expert witnesses attempted to use Bradford Hill factors in the absence of a statistically significant association; citing Rains v. PPG Indus., Inc., 361 F. Supp. 2d 829, 836–37 (S.D. Ill. 2004); ); Soldo v. Sandoz Pharms. Corp., 244 F. Supp. 2d 434, 460–61 (W.D. Pa. 2003).  The Reference Manual also cited cases, without obvious disapproval, which completely dispatched with any necessity of considering any of the Bradford Hill factors, or the precondition of a statistically significant association.  See Reference Manual at 599 n. 144 (citing Cook v. Rockwell Int’l Corp., 580 F. Supp. 2d 1071, 1098 (D. Colo. 2006) (“Defendants cite no authority, scientific or legal, that compliance with all, or even one, of these factors is required. . . . The scientific consensus is, in fact, to the contrary. It identifies Defendants’ list of factors as some of the nine factors or lenses that guide epidemiologists in making judgments about causation. . . . These factors are not tests for determining the reliability of any study or the causal inferences drawn from it.“).

Shira Kramer Takes Her Lumpings

The plaintiffs’ other key expert witness, Dr. Shira Kramer, was a more sophisticated and experienced obfuscator.  Kramer attempted to provide plaintiffs with a necessary association by “lumping” all birth defects together in her analysis of epidemiologic data of birth defects among children of women who had ingested Paxil (or other SSRIs).  Given the clear evidence that different birth defects arise at different times, based upon interference with different embryological processes, the trial court discerned this “lumping” of end points to be methodologically inappropriate.  Slip op. at 8 (citing Chamber v. Exxon Corp., 81 F. Supp. 2d 661 (M.D. La. 2000), aff’d, 247 F.3d 240 (5th Cir. 2001) (unpublished).

Without her “lumping”, Dr. Kramer was left with only a weak, inconsistent claim of biological plausibility and temporality. Finding that Dr. Kramer’s opinion had outrun her headlights, Judge Berrigan, excluded Dr. Kramer as an expert witness, and granted GSK summary judgment.

Merry Christmas!

 

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence, statistical evidence | Comments Off on Lumpenepidemiology

Egilman Petitions the Supreme Court for Review of His Own Exclusion in Newkirk v. Conagra Foods

December 13th, 2012

Last year, the Ninth Circuit of the United States Court of Appeals affirmed a district judge’s decision to exclude Dr David S. Egilman from testifying in a consumer-exposure diacetyl case.  Newkirk v. Conagra Foods Inc., 438 Fed.Appx. 607  (9th Cir. 2011).  The plaintiff moved on, but his expert witness could not let his exclusion go.

To get the full “flavor” of this diacetyl case, read the district court’s opinion, which excluded Egilman and other witnesses, and entered summary judgment for the defense. Newkirk v. Conagra Foods, Inc., 727 F. Supp. 2d 1006  (E.D. Wash. July 2, 2010).  Here is the language that had Dr. Egilman popping mad:

“In other parts of his reports and testimony, Dr. Egilman relies on existing data, mostly in the form of published studies, but draws conclusions far beyond what the study authors concluded, or Dr. Egilman manipulates the data from those studies to reach misleading conclusions of his own. See Daubert I, 509 U.S. at 592–93, 113 S.Ct. 2786.”

727 F. Supp. 2d at 1018.

This language, cut Dr. Egilman to the kernel, and provoked him to lodge a personal appeal to the Ninth Circuit, based in part upon the economic harm done to his litigation consulting and testimonial practice. (See attached Egilman Motion Appeal Diacetyl Exclusion 2011 and Egilman Declaration Newkirk Diacetyl Appeal 2011.)  Not only did the exclusion hurt Dr. Egilman’s livelihood, but also his eleemosynary endeavors:

“The Daubert ruling eliminates my ability to testify in this case and in others. I will lose the opportunity to bill for services in this case and in others (although I generally donate most fees related to courtroom testimony to charitable organizations, the lack of opportunity to do so is an injury to me). Based on my experience, it is virtually certain that some lawyers will choose not to attempt to retain me as a result of this ruling. Some lawyers will be dissuaded from retaining my services because the ruling is replete with unsubstantiated pejorative attacks on my qualifications as a scientist and expert. The judge’s rejection of my opinion is primarily an ad hominem attack and not based on an actual analysis of what I said – in an effort to deflect the ad hominem nature of the attack the judge creates ‘straw man’ arguments and then knocks the straw men down, without ever addressing the substance of my positions.”

Egilman Declaration in Newkirk at Paragraph 11.

The Ninth Circuit affirmed Dr. Egilman’s exclusion, Newkirk v. Conagra Foods, Inc., 438 Fed. Appx. 607 (9th Cir. 2011).  See “Ninth Circuit Affirms Rule 702 Exclusion of Dr David Egilman in Diacetyl Case.

This year, the Ninth Circuit dismissed his personal appeal for lack of standing.  Egilman v. Conagra Foods, Inc., 2012 WL 3836100 (9th Cir. 2012). Previously, I suggested that the Ninth Circuit had issued a judgment from which there will be no appeal.  I may have been mistaken.  Last week, counsel for Dr. Egilman filed a petition for certiorari in the United States Supreme Court.  Smarting from the district court’s attack on his character and professionalism, Dr. Egilman is seeking the personal right to appeal an adverse Rule 702 ruling.  The Circuit split, which Dr. Egilman hopes will get him a hearing in the Supreme Court, involves the issue whether he, as a non-party witness, must intervene in the proceedings in order to preserve his right to appeal:

“Whether a nonparty to a district court proceeding has a right to appeal a decision that adversely affects his interest, as the Second, Sixth, and D.C. Circuits hold, or whether, as six other circuit courts hold, the nonparty must intervene or otherwise participate in the district court proceedings to have a right to appeal.”

Egilman Pet’n Cert Newkirk v Conagra SCOTUS at 5 (Dec. 2012).  Of course there is also a split among courts about Dr. Egilman reliability.

And who represents Dr. Egilman?  Counsel of record is Alexander A. Reinert, who teaches at Cardozo Law School, here in New York.  Dr. Egilman and Reinert have published several articles together, within the scope of Dr. Egilman’s litigation-oriented practice.[i]  In the past, I have commented upon Reinert’s work.  See, e.g., Schachtman, “Confidence in Intervals and Diffidence in the Courts” (May 8, 2012 ) (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)). It should be interesting to see what mischief Egilman & Reinert can make in the Supreme Court.

[i] David S. Egilman & Alexander A. Reinert, “Corruption of Previously Published Asbestos Research,” 55 Arch. Envt’l Health 75 (2000); David S. Egilman & Alexander A. Reinert,“Asbestos Exposure and Lung Cancer: Asbestosis Is Not Necessary,” 30 Am. J. Indus. Med. 398 (1996); David S. Egilman & Alexander A. Reinert, “The Asbestos TLV: Early Evidence of Inadequacy,” Am. J. Indus. Med. 369 (1996);  David S. Egilman & Alexander A. Reinert,“The Origin and Development of the Asbestos Threshold Limit Value: Scientific Indifference and Corporate Influence,”  25 Internat’l J. Health Serv. 667 (1995).

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Bad Gatekeeping or Missed Opportunity – Allen v. Martin Surfacing

November 30th, 2012

Sometimes when federal courts permit dubious causation opinion testimony over Rule 702 objections, the culprit is bad lawyering by the opponent of the proffered testimony.  Allen v. Martin Surfacing, 263 F.R.D. 47 (D. Mass. 2009), may be an important example.

THE CLAIMS

Daniel Allen was the former football coach of the College of The Holy Cross, in Worcester, Massachusetts.  In spring of 2001, defendant Martin Surfacing refinished the gymnasium floor at the college.  Coach Allen was exposed to solvent fumes, including toluene fumes, during defendant’s work, as well as for a couple of months afterwards.   While exposed, Allen experienced “dizziness, headaches, and disorientation.” 263 F.R.D. at 51.  After the gym floor resurfacing was completed, Allen experienced other symptoms, such as fatigue, muscle weakness, and fasciculations in his lower limbs.  In January 2002, at the age of 45, Allen was diagnosed with amyotrophic lateral sclerosis (ALS).  Id. Allen’s condition progressed, and he died three years later, in May 2004.  Id. at 52.

Allen’s family sued for wrongful death.  The parties’ apparently agreed on the following:

  • ALS occurs as a sporadic ALS, as well as “familial ALS,”
  • the cause of sporadic ALS is unknown,
  • Allen developed and died of sporadic ALS,
  • no air sampling established overexposure to any chemical,
  • there were no reliable exposure models to quantify Allen’s exposures,
  • there are no known causes of sporadic ALS, and
  • toluene did not cause Allen’s ALS

Remarkably, defendant lost the Rule 702 challenge to plaintiffs’ expert witnesses’ opinion testimony.  It is easy to suspect that the district judge was sleep at the gate, and that his gatekeeping was deficient.  A close read of the opinion supports the view that this was not Rule 702’s finest moment, but much more was going on to get to admissibility.

First, the plaintiffs’ counsel cleverly avoided running into a wall by avoiding a claim that toluene caused Allen’s ALS. Instead, plaintiffs’ claimed that toluene accelerated the onset of the disease.  This claim was equally dubious, but it allowed the expert witnesses to avoid a mountain of medical opinion, authoritative and well-supportive, that there is no known cause of sporadic ALS.

Second, the plaintiffs’ counsel took the initiative by filing an affirmative motion to admit the testimony of their expert witnesses.  Rather than ceding the initiative to the defendant, the plaintiffs seized the initiative and had the first and last word on admissibility.  As a result, plaintiffs were able to present and frame their witnesses’ opinions sympathetically rather than defensively.

Third, the plaintiffs had the good fortune of the defendant’s counsel’s apparent failure to find the key fallacies, invalidities, and flaws in plaintiffs’ questionable expert witness opinions.

The Allen case teaches that sometimes good lawyering can win a losing case.

The plaintiffs’ counsel retained and presented an array of expert witnesses who might be the usual suspects in a district court’s exclusion of expert witness testimony:

None of these four expert witnesses was a specialist in ALS or ALS causation; none was a neurologist; none had ever addressed ALS causation in a peer-reviewed article.  All four witnesses were frequent testifiers in tort litigation, and some have are repeat offenders when it comes to offering questionable or excludable opinion testimony.  Somehow, the defense dashed this opportunity by retaining only one expert, Dean M. Hashimoto, M.D., J.D., M.P.H., who was also not a specialist in ALS, who was not a neurologist, and who had never published anything on ALS.  And to make matters worse, the defense proceeded to challenge the plaintiffs’ expert witnesses for lack of qualifications!

The defense’s challenges to qualifications takes up a good deal of Judge Saylor’s published opinion, which illustrates the maxim that judges have short attention spans, and you should not waste the opportunity of a motion on an issue that is so easily decided against you.  The scientific issues are difficult and the temptation to avoid them is great.  By leading with an issue that will almost certainly lose, the defense wasted a valuable advocacy opportunity to show the court the fallacious reasoning in the plaintiffs’ case.  By submitting reports from only one expert witness, who had all the deficiencies claimed in the plaintiffs’ set of witnesses, the defense exhibited a duplicity that must have seriously undermined its credibility for the entire set of Rule 702 motion issues.

THE WITNESSES

Dr. Christine Oliver has been testifying in asbestos and other occupational lung disease cases for decades.  She is a pulmonary physician on staff at Massachusetts General Hospital, in Boston, and an associate professor of clinical medicine at the Harvard Medical School.  She is board certified in internal medicine and in occupational medicine (American Board of Preventive Medicine), and her clinical interests are asthma occupational lung disease, and health hazards of construction work.  If the defense had presented real expert witnesses in ALS causation, Dr. Oliver’s expertise would have seemed quite irrelevant.  Dr. Oliver has, as well as I can determine, never researched or published on ALS causation.  She has, however, published on “multiple chemical sensitivity,” which should give a disinterested court some pause.  See L. Christine Oliver and Alison Johnson, “Multiple Chemical Sensitivity: Reflections” (Nov. 4, 2011).

Richard Clapp, professor emeritus at the Boston University School of Public Health, is a known purveyor of dubious courtroom testimony. See, e.g., Sutera v. The Perrier Group of America Inc., 986 F.Supp. 655 (D. Mass. 1997).  He is a frequent testifier and a charter member of the surreptitiously funded SKAPP organization.  Clapp is a non-physician epidemiologist, who has never published on ALS.

Marcia Ratner Ph.D. may be best known for her possession of mace and an unlicensed gun, but she does occasionally show up in civil litigation as an expert witness.  See “Quincy District Court News,” Patriot Ledger June 09, 2010 (reporting that Ratner pleaded guilty to criminal possession of mace and a firearm).

Ratner is a postdoctoral researcher at Boston University, where she works as a neurotoxicologist.  She does not appear to have ever published a peer-reviewed paper on ALS or ALS causation.  Plaintiffs’ counsel claimed that she was researching a new drug with therapeutic potential for ALS treatment, although they were quite sketchy about details.  Ratner does not appear to hold any NIH grants for ALS drug research.

[Please see update on the discussion of Dr. Ratner at http://schachtmanlaw.com/gatekeeping-in-allen-v-martin-surfacing-postscript/]

William Ewing, an industrial hygienist, frequently testifies in asbestos litigation.  He offered no opinion on causation.

Against this field of witnesses, the defense punted on presenting its own witness with relevant expertise. Dr. Dean M. Hashimoto, the defense’s sole witness on causation, is a physician, lawyer, and has a master’s degree in occupational health.  Hashimoto has no specialized training in ALS or clinical neurology, although he serves on the Massachusetts Workers’ Compensation Board. A pubmed search  shows that Hashimoto has never published on the neurology or causation of ALS.

CAUSATION

The plaintiffs had a huge problem to avoid:  ALS has no known cause.  Counsel table could be filled up with textbooks and review articles, but perhaps the following, lengthy quote from the National Institute for Neurological Disorders and Stroke website suffices to make the point:

“What causes ALS?

The cause of ALS is not known, and scientists do not yet know why ALS strikes some people and not others. An important step toward answering that question came in 1993 when scientists supported by the National Institute of Neurological Disorders and Stroke (NINDS) discovered that mutations in the gene that produces the SOD1 enzyme were associated with some cases of familial ALS. This enzyme is a powerful antioxidant that protects the body from damage caused by free radicals. Free radicals are highly reactive molecules produced by cells during normal metabolism. If not neutralized, free radicals can accumulate and cause random damage to the DNA and proteins within cells. Although it is not yet clear how the SOD1 gene mutation leads to motor neuron degeneration, researchers have theorized that an accumulation of free radicals may result from the faulty functioning of this gene. In support of this, animal studies have shown that motor neuron degeneration and deficits in motor function accompany the presence of the SOD1 mutation.

Studies also have focused on the role of glutamate in motor neuron degeneration. Glutamate is one of the chemical messengers or neurotransmitters in the brain. Scientists have found that, compared to healthy people, ALS patients have higher levels of glutamate in the serum and spinal fluid. Laboratory studies have demonstrated that neurons begin to die off when they are exposed over long periods to excessive amounts of glutamate. Now, scientists are trying to understand what mechanisms lead to a buildup of unneeded glutamate in the spinal fluid and how this imbalance could contribute to the development of ALS.

Autoimmune responses—which occur when the body’s immune system attacks normal cells—have been suggested as one possible cause for motor neuron degeneration in ALS. Some scientists theorize that antibodies may directly or indirectly impair the function of motor neurons, interfering with the transmission of signals between the brain and muscles.

In searching for the cause of ALS, researchers have also studied environmental factors such as exposure to toxic or infectious agents. Other research has examined the possible role of dietary deficiency or trauma. However, as of yet, there is insufficient evidence to implicate these factors as causes of ALS.

Future research may show that many factors, including a genetic predisposition, are involved in the development of ALS.”

NINDS – “Amyotrophic Lateral Sclerosis (ALS) Fact Sheet.”

As a result, the plaintiffs adopted a strategy of confession and avoidance; they renounced any claim that they were asserting a causal claim.  Instead, they insisted that they were “merely” claiming that toluene exposure had accelerated the onset of sporadic ALS in Coach Allen.  This mere claim, however, was actually a causal claim in disguise, and the district judge was taken in by the ruse.  If plaintiffs were claiming that toluene can accelerate the onset of ALS by a meaningful period of time (years), then they were making a causal claim, legally and scientifically.  A shift in the age of onset of a sporadic disease is a causal claim, and it requires supporting evidence, not hand waving.

PLAUSIBLE MECHANISM

One scientist could postulate a reasonable mechanism even for a sporadic disease.  Professional journals and textbooks are filled with such speculation.  These postulations are part of science in that they inform research hypotheses and funding, but they are not conclusions of causality.  The quote above from the NINDS discusses the lack of an anti-oxidizing enzyme and glutamate toxicity as potential mechanisms in familial ALS, but even there, the authors are appropriately modest in avoiding a claim to know the pathogenesis of familial ALS.

The plaintiffs’ approach was to take the suggestion of a mechanism, misrepresent it as a known mechanism, and then claim that toluene activated glutamate toxicity and exercised an oxidizing effect on neurons. The plaintiffs’ team had no basis for claiming that short-term exposure to solvents, or toluene specifically, translated into a toxicity to the relevant human motor neurons that are involved in ALS.  It is a long stretch from suggesting a mechanism to documenting the mechanism to be actually at work in producing, or accelerating, a disease in humans.

A typical statement, from the Yale School of Medicine, Division of Neurology, in 2012:

“Why the motor neurons begin to die is still unknown. Recent evidence, however, have implicated glutamate excitotoxicity, free radical toxicity, and mitochondrial dysfunction as possible mechanisms, and this is an area of active research.”

“Amyotrophic Lateral Sclerosis (ALS)” (emphasis added).   See also Adams and Victor’s Principles of Neurology 1157-58 (7th ed. 2001) (noting that the pathogenesis of ALS and similar motor neuron diseases is not known).

The district judge seemed mesmerized by Ratner’s having providing a biologically plausible theory for tying ALS progression to toluene exposure.  263 F.R.D. at 60.  Judge Saylor stated that the defense did not address any flaw in Ratner’s methodology other than to point out that her theory was not supported by epidemiology.  The court seemed to equate providing a plausible theory with establishing a scientific conclusion.  More to the point, the court was truly asleep at its gatekeeping task because Ratner’s theory actually presupposed that she knew that Coach Allen was going to develop ALS in any event, only not as early as 2001.  The court faulted the defense for not showing that Ratner’s (and the other plaintiffs’ witnesses’) theory was unreliable, but the burden was on the plaintiffs to show reliability.  Id.  The court not only faulted the defense for carrying a burden it did not have, but it overlooked the very telling criticisms of Ratner’s theories of acceleration and mechanism.

EXCUSES – EPIDEMIOLOGY

Plaintiffs’ expert witnesses had a welter of excuses as to why there was no epidemiologic data to support their theories.  The absence of statistical significance, according to plaintiffs’ expert witnesses does not mean that a study should be disregarded.  Id. at 58.  Their claim is superficially true, but a study not disregarded does not necessarily support a causal inference, either alone or conjunction with other such studies. Similarly, plaintiffs’ claim that flawed studies should not be disregarded is also a half truth.  A flawed study may lead to a much better one, which can support valid inferences.  Flawed studies are thus part of the scientific process because they may lead to a self-correcting triangulation of the truth, but there is little to recommend relying upon flawed studies to support scientific conclusions of causality.  Nevertheless, the district court appeared to swallow these half truths, whole.

Ratner also advanced a claim that the acceleration theory had not been subjected to epidemiologic analysis because of “funding limitations, as most funding goes toward finding treatment or cures for the disease, not towards finding what accelerates the course of the disease.”  Id. at 59 n. 14.  The district court repeats this excuse without critical thought.  If a commonly used solvent such as toluene accelerated the onset of a terrible disease such as ALS by decades, such a putative effect would be amenable to epidemiologic analysis and would be a source of incredible concern and funding efforts by the NIH, NINDS, NIEHS, and other granting agencies and organizations.  Despite excusifying verbiage, Ratner maintained that there were no epidemiologic data that refuted her novel acceleration.  Id. at 59.  Of course, if her excuses were taken seriously, then this absence of refutation was fairly irrelevant, but in any event, this supposed absence could not support the reliability of Ratner’s inferences or conclusions.

The defense focused on the lack of short-term exposures in epidemiologic studies, and also the lack of statistical significance in some studies.  What appears to have been missing from both sides was a comprehensive analysis of the available epidemiologic data.  If long-term exposure were associated with earlier age of onset of ALS, or even a greater risk of ALS, then it would have given some support to Ratner’s novel theory.  The defense appeared to punt on the epidemiology by claiming its irrelevance.  It might have been helpful to point out internal as well as external validity issues to the court.

As for both sides citing different studies, and no side presenting a comprehensive view of the epidemiologic evidence, the court could have given some consideration to the ethical considerations of the incomplete presentation:

“Basis of Expert Medical Testimony

The testimony of an expert medical witness should be founded on a thorough and critical review of the pertinent medical and scientific facts, available data, and relevant literature.”

Ethical Guidelines for Occupational and Environmental Medicine Physicians Serving as Expert Witnesses (Oct. 25, 2007).

DIFFERENTIAL DIAGNOSIS

The plaintiffs’ claim that they were not asserting causation was disingenuous.  As noted above, acceleration of onset is a form of causation.  Of course, exposure to a neurotoxic material, with some symptoms, might have made Allen more aware of other symptoms, and so the time to diagnosis was abbreviated.  The plaintiffs, however, were claiming more than earlier ascertainment; they claimed the toluene exposure caused an underlying disease process to accelerate.

Oliver actually went further and performed an invalid differential etiologic analysis. Oliver reviewed medical records and claimed to have applied “differential diagnosis to the review.”  Id. at 63. This claim was quite bogus because there was no dispute that Allen had and died of ALS, but the district court was beguiled.  Having ruled out family history, Oliver claimed to then rule out other “putative causes” of ALS:  “pesticides and agricultural chemicals containing solvents, 60-hertz magnetic fields, and welding fumes.”  Id. at 63.  In one fell swoop, Oliver created several known causes to be ruled out, and then ruled them out in Allen’s case.  This is remarkable given that NINDS and most of medical sciences does not recognize any known or putative causes of sporadic ALS, and that Oliver failed to rule out the one potential cause that some scientists take seriously:  cigarette smoking.  See, e.g., Hao Wang, Éilis J. O’Reilly, Marc G. Weisskopf, Giancarlo Logroscino, Marji L. McCullough, Michael Thun, Arthur Schatzkin, Laurence N. Kolonel, Alberto Ascherio, “Smoking and risk of amyotrophic lateral sclerosis: a pooled analysis of 5 prospective cohorts” 68 Arch. Neurol. 207 (2011); A. Alonso, G. Logroscino, M.A. Hernán, “Smoking and the risk of amyotrophic lateral sclerosis: a systematic review and meta-analysis,” 81 J. Neurol. Neurosurg. & Psychiatry 1249 (2010); F. Fang & W. Ye, “Smoking may be considered an established risk factor for sporadic ALS,” 74 Neurology 1927 (2010).

Of course, Oliver, and the entire plaintiffs’ expert witness team failed to rule out the most obvious, most prevalent explanation for Allen’s ALS:  unknown.

GENETIC SUSCEPTIBILITY

Ratner testified “to a reasonable degree of scientific certainty that Allen was genetically predisposed to develop ALS and would have developed and died from ALS later in his life.”  263 F.R.D. at 61.  This assertion was truly an incredible, unsupported, unverifiable, and unfalsifiable statement.  If a drug company ever made a similarly unsupported claim in an electronically transmitted document, the Department of Justice would prosecute it for wire fraud.  United States v. Harkonen, 2010 WL 2985257 (N.D. Calif. 2010).

The parties had essentially stipulated that Allen did not suffer from familial ALS, and neither Ratner nor anyone else identified any gene that was responsible for his “susceptibility.”  The district court, of course, did not report how Ratner could possibly have known that Allen was going to develop ALS, only at some unspecified date later than the date when Allen first became aware of signs and symptoms of motor neuron disease.  The district court announced that plaintiffs’ expert witnesses were not propounding “junk science,” but perhaps the heavy perfume helped masquerade the garbage.

POST HOC ERGO PROPTER HOC

The court conclusorily noted, without explanation, that the temporal relationship between exposure and disease manifestation would allow a conclusion of causality:

“Finally, after interpreting the data within a chronological context, the clinician may conclude that the patient’s disease is a neurotoxic illness.”

Id. at 61.  The court appears to accept the temporal pattern as sufficient in itself, or with other information, to support the conclusion.  This reasoning is fallacious.

AGE OF ONSET

Allen developed ALS when he was 45 years old.  Ratner reasoned that the average age of onset was 60, and Allen developed his disease “much earlier than would be expected”; therefore toluene accelerated the onset of Allen’s disease.  Id. at 61. The problem is that there is no “therefore” that can reasonably be claimed in the court’s sentence.

Most publications put the mean and median of age of ALS onset around 55 years, but even if the court were to accept Ratner’s reference to 60 as correct, surely the court recognized that half the cases therefore occurred below the age of 60.  The question of course is the variability in age of onset, and the court’s opinion is silent about the scatter or distribution of age-of-onset data.  Ratner’s reasoning was prima facie invalid unless there was additional information to show a very narrow distribution of age of onset around the mean.  It is difficult to discern whether the defense made this point, but Ratner could not have supported this counterfactual claim.

Here is what the ALS association has to say about the issue:

“Most people who develop ALS are between the ages of 40 and 70, with an average age of 55 at the time of diagnosis. However, cases of the disease do occur in persons in their twenties and thirties.”

“Who Gets ALS.”

Ratner essentially conceded that her argument was vacuous and invalid.  When confronted at her deposition about whether age of onset greater than the mean would have changed her opinion, she emphatically denied its relevance:

“My opinion would be the same even if that guy died at 60 instead of 75 and had history of this exposure … but you wouldn’t have bothered to depose me in that case… . Somebody else has moved down from where they are to here. But it may not result in a lawsuit, and I wouldn’t be here, because— I wouldn’t be here.”

Ratner Deposition at 172-3.

RULE 702 ANALYSIS

The district court recognized the novelty of Ratner’s analysis, but opined that Ratner, Oliver, and Clapp had provided sufficient cumulative evidence to support their theories.  263 F.R.D. at 61.  The trial court apparently conducted a Rule 702 hearing, over three days. Both sides filed what appears to have been extensive briefing and affidavits.  There are some huge gaps in the reasoning of the plaintiffs’ expert witnesses, and in the district court’s opinion.  Perhaps those gaps could be filled in with volumes of testimony.  My unscientific opinion is to doubt it. Although the plaintiffs should have had the burden of showing admissibility, the defendant had the practical burden of illustrating the analytical gaps, ipse dixit, fallacies, and invalid inferences that were before the court.  The defense may have indeed pointed out such problems, which were fulsomely present, but the district court’s opinion does not report the obvious defense arguments.  Without more background information, it is difficult to evaluate comprehensively the court’s or the defense’s handling of the scientific issues that were clearly before the court on the Rule 702 motions.  What is clear from what the district court reports is, however, sufficient to document an unsatisfactory judicial review of the evidence discussed.

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Bad Gatekeeping or Missed Opportunity – Allen v. Martin Surfacing

Wells v. Ortho Pharmaceutical Corp. Reconsidered – Part 6

November 21st, 2012

In 1984, before Judge Shoob gave his verdict in the Wells case, another firm filed a birth defects case against Ortho for failure to warn in connection with its non-ionic surfactant spermicides, in the same federal district court, the Northern District of Georgia. The mother in Smith used Ortho’s product about the same time as the mother in Wells (in 1980).  The case was assigned to Judge Shoob, who recused himself.  Smith v. Ortho Pharmaceutical Corp., 770 F. Supp. 1561, 1562 n.1 (N.D. Ga. 1991) (no reasons for the recusal provided).  The Smith case was reassigned to Judge Horace Ward, who entertained Ortho’s motion for summary judgment in July 1988.  Two and one-half years later, Judge Ward granted summary judgment to Ortho on grounds that the plaintiffs’ expert witnesses’ testimony was not based upon the type of data reasonably relied upon by experts in the field, and was thus inadmissible under Federal Rule of Evidence 703. 770 F. Supp. at 1681.

A prevalent interpretation of the split between Wells and Smith is that the scientific evidence developed with new studies, and that the scientific community’s views matured in the five years between the two district court opinions. The discussion in Modern Scientific Evidence is typical:

“As epidemiological evidence develops over time, courts may change their view as to whether testimony based on other evidence is admissible. In this regard it is worth comparing Wells v. Ortho Pharmaceutical Corp., 788 F.2d 741 (11th Cir. 1986), with Smith v. Ortho Pharmaceutical Corp., 770 F. Supp. 1561 (N.D. Ga. 1991). Both involve allegations that the use of spermicide caused a birth defect. At the time of the Wells case there was limited epidemiological evidence and this type of claim was relatively novel.  In a bench trial the court found for the plaintiff.  *** The Smith court, writing five years later, noted that, ‘The issue of causation with respect to spermicide and birth defects has been extensively researched since the Wells decision.’ Smith v. Ortho Pharmaceutical Corp., 770 F. Supp. 1561, 1563 (N.D. Ga. 1991).”

1 David L. Faigman, Michael J. Saks, Joseph Sanders, and Edward K. Cheng, Modern Scientific Evidence:  The Law and Science of Expert Testimony, “Chapter 23 – Epidemiology,” § 23:4, at 213 n.12 (West 2011) (internal citations omitted).

Although Judge Ward was being charitable to his judicial colleague, this attempt to reconcile Wells and Smith does a disservice to Judge Ward’s hard work in Smith, and Judge Shoob’s errors in Wells.

Even a casual reading of Smith and Wells reveals that the injuries were completely differently.  Plaintiff Crystal Smith was born with a chromosomal defect known as Trisomy-18; Plaintiff Katie Wells was born with limb reduction deficits.   Some studies relevant to one injury had no information about the other.  Other studies, which addressed both injuries, yielded different results for the different injuries.  Although some additional studies were available to Judge Ward in 1988, this difference is hardly the compelling difference between the two cases.

Perhaps the most important difference between the cases is that in Smith, the biologically plausibility that spermicides could cause a Trisomy-18 was completely absent.  The chromosomal defect arises from a meiotic disjunction, an error in meiosis that is part of the process in which germ cells are formed.  Simply put, spermicides arrive on the scene too late to cause a Trisomy-18.  Notwithstanding the profound differences between the injuries involved in Wells and Smith, the Smith plaintiffs sought the application of collateral estoppel.  Judge Ward refused this motion, on the basis of the factual differences in the cases, as well as the availability of new evidence.  770 F.Supp. at 1562.

The difference in injuries, however, was not the only important difference between these two cases.  Wells was actually tried, apparently without any challenge under Frye, or Rules 702 or 703, to the admissibility of expert witness testimony.  There is little to no discussion of scientific validity of studies, or analysis of the requisites for evaluating associations for causality.  It is difficult to escape the conclusion that Judge Shoob decided the Wells case on the basis of superficial appearances, and that he frequently ignored validity concerns in drawing invidious distinctions between plaintiffs’ and defendant’s expert witnesses and their “credibility.”  Smith, on the other hand, was never tried.  Judge Ward entertained and granted dispositive motions for summary judgment, on grounds that the plaintiffs’ expert witnesses’ testimony was inadmissible. Legally, the cases are light years apart.

In Smith, Judge Ward evaluated the same FDA reports and decisions seen by Judge Shoob.  Judge Ward did not, however, dismiss these agency materials simply because one or two of dozens of independent scientists involved had some fleeting connection with industry. 770 F.Supp. at 1563-64.

Judge Ward engaged with the structure and bases of the expert witnesses’ opinions, under Rules 702 and 703.  The Smith case thus turned on whether expert witness opinions were admissible, an issue not considered or discussed in Wells.  As was often the case before the Supreme Court decided Daubert in 1993, Judge Ward paid little attention to Rule 702’s requirement of helpfulness or knowledge.  The court’s 702 analysis was limited to qualifications.  Id. at 1566-67.  The qualifications of the plaintiffs’ witnesses were rather marginal.  They relied upon genetic and epidemiologic studies, but they had little training or experience in these disciplines. Finding the plaintiffs’ expert witnesses to meet the low threshold for qualification to offer an opinion in court, Judge Ward focused on Rule 703’s requirement that expert witnesses reasonably rely upon facts and data that are not otherwise admissible.

The trial court in Smith struggled with how it should analyze the underpinnings of plaintiffs’ witnesses’ proffered testimony.  The court acknowledged that conflicts between expert witnesses typically raise questions of weight, not admissibility.  Id. at 1569.  Ortho had, however, challenged plaintiffs’ witnesses for having given opinions that lacked a “sound underlying methodology.” Id.  The trial court found at least one Fifth Circuit case that suggested that Rule 703 requires trial courts to evaluate the reliability of expert witnesses’ sources.  Id. (citing Soden v. Freightliner Corp., 714 F.2d 498, 505 (5th Cir. 1983). Elsewhere, the trial court also found precedent from Judge Weinstein’s opinion in Agent Orange, as well as Court of Appeals decisions involving Bendectin, all of which turned to Rule 703 as the legal basis for reviewing, and in some cases limiting or excluding expert witness opinion testimony.  Id.

The defendant’s argument under Rule 703 was strained; Ortho argued that the plaintiffs’

“experts’ selection and use of the epidemiological data is faulty and thus provides an insufficient basis upon which experts in the field of diagnosing the source of birth defects normally form their opinions. The defendant also contends that the plaintiffs’ experts’ data on genetics is not of the kind reasonably relied upon by experts in field of determining causation of birth defects.”

Id. at 1572.  Nothing in Rule 703 addresses the completeness or thoroughness of expert witnesses in their consideration of facts and data; nor does Rule 703 address the sufficiency of data or the validity vel non of inferences drawn from facts and data considered.  Nonetheless, the trial court in Smith took Rule 703 as its legal basis for exploring the epistemic warrant for plaintiffs’ witnesses’ causation opinions.

Although plaintiffs’ expert witnesses stated that they had relied upon epidemiologic studies and method, the trial court in Smith went beyond their asseverations.  The Smith trial court explored the credibility of these witnesses at a whole other level.  The court reviewed and discussed the basic structure of epidemiologic studies, and noted that the objective of such studies is to provide a statistical analysis:

“The objective of both case-control and cohort studies is to determine whether the difference observed in the two groups, if any, is ‘statistically significant’, (that is whether the difference found in the particular study did not occur by chance alone).40 However, statistical methods alone, or the finding of a statistically significant association in one study, do not establish a causal relationship.41 As one authority states:

‘Statistical methods alone cannot establish proof of a causal relationship in an association’.42

As a result, once a statistical association is found in an epidemiological study, that data must then be evaluated in a systematic manner to determine causation. If such an association is present, then the researcher looks for ‘bias’ in the study.  Bias refers to the existence of factors in the design of a study or in the manner in which the study was carried out which might distort the result.43

If a statistically significant association is found and there is no apparent ‘bias’, an inference is created that there may be a cause-and-effect relationship between the agent and the medical effect. To confirm or rebut that inference, an epidemiologist must apply five criteria in making judgments as to whether the associations found reflect a cause-and-effect relationship.44 The five criteria are:

1. The consistency of the association;

2. The strength of the association;

3. The specificity of the association;

4. The temporal relationship of the association; and,

5. The coherence of the association.

Assuming there is some statistical association, it is these five criteria that provide the generally accepted method of establishing causation between drugs or chemicals and birth defects.45 ”

The Smith court acknowledged that there were differences of opinion in weighting these five factors, but that some of them were very important to drawing a reliable inference of causality.  Id. at 1775.

A major paradigm shift thus separates Wells and Smith.  The trial court in Wells contented itself with superficial and subjective indicia of witnesses’ personal credibility; the trial in Smith delved into the methodology of drawing an appropriate scientific conclusion about causation.  Telling was the Smith court’s citation to Moultrie v. Martin, 690 F.2d 1078, 1082 (4th Cir. 1982) (“In borrowing from another discipline. a litigant cannot be selective in which principles are applied.”).  770 F.Supp. at 1575 & n.45.  Gone is the Wells retreat from engagement with science, and the dodge that the court must make a legal, not a scientific decision.

Applying the relevant principles, the Smith court found that the plaintiffs’ expert witnesses had deviated from the scientific standards of reasoning and analysis:

“It is apparent to the court that the testimony of Doctors Bussey and Holbrook is insufficiently grounded in any reliable evidence. * * * The conclusions Doctors Bussey and Holbrook reach are also insufficient as a basis for a finding of causality because they fail to consider critical information, such as the most relevant epidemiologic studies and the other possible causes of disease.81

The court finds that the opinions of plaintiffs’ experts are not based upon the type of data reasonably relied upon by experts in determining the cause of birth defects. Experts in determining birth defects rely upon a consensus in genetic or epidemiological investigations or specific generally accepted studies in these fields. While a consensus in genetics or epidemiology is not a prerequisite to a finding of causation in any and all birth defect cases, Rule 703 requires some reliable evidence for the basis of an expert’s opinion.

Experts in determining birth defects also utilize methodologies and protocols not followed by plaintiffs’ experts. Without a well-founded methodology, opinions which run contrary to the consensus of the scientific community and are not supported by any reliable data are necessarily speculative and lacking in the type of foundation necessary to be admissible.

For the foregoing reasons, the court finds that plaintiffs have failed to produce admissible evidence sufficient to show that defendant’s product caused Crystal’s birth defects.”

Id. at 1581.  Rule 703 was forced into a service to filter out methodologically specious opinions.

Not all was smooth sailing for Judge Ward.  Like Judge Shoob, Judge Ward seemed to think that a physical examination of the plaintiff provided helpful, relevant evidence, but he never articulated what the basis for this opinion was. (His Honor did note that the parties agreed that the physical examination offered no probative evidence about causation.  Id. at 1572 n.32.) No harm came of this opinion.  Judge Ward wrestled with the lack of peer review in some unpublished studies, and the existence of a study only in abstract form.  See, e.g., id. at 1579 (“a scientific study not subject to peer review has little probative value”); id. at 1578 (insightfully noting that an abstract had insufficient data to permit a reader to evaluate its conclusions).  The Smith court recognized the importance of statistical analysis, but it confused Bayesian posterior probabilities with significance probabilities:

“Because epidemiology involves evidence on causation derived from group based information, rather than specific conclusions regarding causation in an individual case, epidemiology will not conclusively prove or disprove that an agent or chemical causes a particular birth defect. Instead, its probative value lies in the statistical likelihood of a specific agent causing a specific defect. If the statistical likelihood is negligible, it establishes a reasonable degree of medical certainty that there is no cause-and-effect relationship absent some other evidence.”

The confusion here is hardly unique, but ultimately it did not prevent Judge Ward from reaching a sound result in Smith.

What intervened between Wells and Smith was not any major change in the scientific evidence on spermicides and birth defects; the sea change came in the form of judicial attitudes toward the judge’s role in evaluating expert witness opinion testimony.  In 1986, for instance, after the Court of Appeals affirmed the judgment in Wells, Judge Higginbotham, speaking for a panel of the Fifth Circuit, declared:

“Our message to our able trial colleagues: it is time to take hold of expert testimony in federal trials.”

 In re Air Crash Disaster at New Orleans, 795 F.2d 1230, 1234 (5th Cir. 1986).  By the time the motion for summary judgment in Smith was decided, that time had come.

Posted in Causation, Data Sharing, Frye, Rule 702, Rule 703, Scientific Evidence, statistical evidence | Comments Off on Wells v. Ortho Pharmaceutical Corp. Reconsidered – Part 6

Evidence-Based Specific Causation

November 7th, 2012

In the last post, I discussed an important article by Professors Davidson and Guzelian, on the legal implications of evidence-based medicine (EBM).  Terence M. Davidson & Christopher P. Guzelian, “Evidence-based Medicine (EBM): The (Only) Means for Distinguishing Knowledge of Medical Causation from Expert Opinion in the Courtroom,” 47 Tort Trial & Ins. Practice L. J. 741 (2012) [cited as Davidson].

Their criticism of the deficiencies in current gatekeeping practice cries out for reform of much current judicial practice.  Education of the judiciary in EBM would be helpful to both plaintiffs and defendants in civil cases, as well as prosecutors and defendants in criminal cases.  I will leave for another day a discussion of whether the boundary between knowledge and “mere opinion” is so easily discernible.

Although the authors’ call for EBM in judicial decisions is timely and needed, I noted my dissent to their assessment of one defense expert witness’s specific causation opinion in the hormone therapy litigation. Davidson and Guzelian criticize one district judge for having admitted the challenged testimony of a defense expert witness, Dr. Blaustein, who opined that (1) estrogen + progesterone combination post-menopausal hormone replacement therapy (CHRT) has not been shown to cause breast cancer, and (2) there is no generally accepted method for determining a cause of a woman’s breast cancer.  Cross v. Wyeth Pharms., Inc., CASE NO.: 8:06-cv-429-T-23AEP, 2011 U.S. Dist. LEXIS 89078; 2011 WL 3498305 (M.D. Fla. 2011) (Merryday, J.).

Here is how Davidson & Guzelian put the matter:

“Blaustein also opined that there is no generally accepted method for diagnosing specific medical causation—that is, whether a medical intervention or treatment, even if it is known to generally cause a result ‘X’ (e.g., breast cancer), caused a particular patient’s result ‘X’. Blaustein’s statement, accepted by the judge as befitting of presentation to the jury, is ‘simply false’.”

The claim that Blaustein’s statement is “simply false” is pretty strong for both general and specific causation, and partially explains my initial dissent.  The prestige of the Women’s Health Initiative (WHI), a large, randomized, clinical meta-trial of  CHRT, with its finding of an increased risk for breast cancer among women, certainly has made Dr. Blaustein’s opinion on general causation a distinctly minority view.  There are, however, some careful authors who have challenged the findings of the WHI on grounds of internal and external validity.  See, e.g., Samuel Shapiro, Richard Farmer, Helen Seaman, J. C. Stevenson, “Does hormone replacement therapy cause breast cancer? An application of causal principles to three studies: part 2. The Women’s Health Initiative: estrogen plus progestogen,” 37 J. Family Planning & Reproductive Health Care 165, 165 (2011) (“HRT with estrogen plus progestogen may or may not increase the risk of breast cancer, but the WHI did not establish that it does.”).  In any event, given the state of the science, most defendants would hedge their position on general causation even if they stopped short of saying it was not established.  Still, the validity concerns may cause us to have some doubts that the conclusions drawn from the WHI and other studies are truly “knowledge.”

Professor Guzelian has persuaded me that their indictment of Blaustein’s opinion on specific causation is correct, at least technically.  There are, to be sure, a few genetic causes of breast cancer, such as the BrCa 1, and 2, genes, which can cause breast cancer, and which, if present in a particular woman, would constitute an adequate description of the cause of that woman’s cancer.  Blaustein claimed that there is no generally accepted method for attributing an individual woman’s breast cancer to known causes, and Davidson and Guzelian are correct that Blaustein’s claim is, therefore, “simply false.”

Given how cursory and conclusory the trial court’s opinion is, Davidson and Guzelian’s derision is, however, relatively uncharitable.  We can probably credit the plaintiff’s counsel with sufficient entrepreneurial savvy to have not pressed the claims of a woman who had a known genetic cause of breast cancer.  And we can similarly credit the defense counsel with sufficient intelligence not to have overlooked the presence of such a gene if it were present.

With genetic causes taken out of the equation, Blaustein’s opinion seems fairly unremarkable.  Even if the criticism of the trial court’s refusal to preclude Dr. Blaustein’s testimony on general causation were correct under Federal Rule of Evidence 702, Davidson and Guzelian have failed to make their case against the trial court, and Dr. Blaustein, on specific causation.

Here is what Davidson and Guzelian have to say about Blaustein’s specific causation opinion:

“EBM has documented and catalogued the best practices regarding how to diagnose whether generally applicable evidence-based conclusions hold for specific patients.51 Moreover, even if in a specific case it were plausible to assert that it is impossible to reach a specific causation conclusion for a particular patient’s condition using the scientific method, that is very different than saying that there is no scientific method for analyzing specific causation. According to EBM’s strictures, Blaustein’s proposed blanket denial of the possibility of specific causation should have been precluded from his testimony.52”

Davidson at 757. The footnotes in this passage are to the section of an article on evidence-based toxicology, which deals with attribution of an adverse drug reaction.  Philip Guzelian et al., “Evidence-Based Toxicology: A Comprehensive Framework for Causation,” 24 Human & Experimental Toxicol. 161, 190-91 (Table 9) (2005) (presenting “an overview of evidence-based specific causation diagnostic criteria”). Putting aside the very substantial differences between cancer causation and the general run of adverse drug reactions, we can see that the proposed criteria for specific causation in the referenced article contain this extremely important criterion:

“No good alternative candidate (unexplained exacerbation or recurrence of underlying illness).”

Id.  Specific causation in a breast cancer case falls outside this criterion because most cases of breast cancer (with the exception of the genetic cases mentioned above) have no identifiable risk factor.  Dr. Blaustein’s opinion on specific causation — that there is no generally accepted method for attributing breast cancer to exogenous cause(s) — seems then exactly on point, even on the EBM criteria for specific causation urged by the authors.

In Cross, the trial court does not provide any insight into the basis for the plaintiffs’ challenge to Blaustein’s specific causation opinion, and I am aware of none.  The trial court does not give us any particulars of the plaintiff’s use of CHRT or development of breast cancer, and there is no suggestion that she had an extraordinarily high risk (say > 10-fold increase, which I have never seen reported, in any event).

The plaintiffs did not attempt to infer causation from risk.  Perhaps they thought better of it, or perhaps one of their testifying epidemiologists, Dr. Graham Colditz, refused to support such an inference:

“Knowledge that a factor is associated with increased risk of disease does not translate into the premise that a case of disease will be prevented if a specific individual eliminates exposure to that risk factor. Disease pathogenesis at the individual level is extremely complex. As Rose stated, a preventive measure that brings large benefits to the community offers little to each participating individual [3]. Accordingly, epidemiology must be harnessed to identify the population level strategies that will reduce the burden of illness.”

Graham A. Colditz, “From epidemiology to cancer prevention: implications for the 21st Century,” 18 Cancer Causes Control 117, 118 (2007).  Professor Colditz’ view is hardly unique; there are many similar refusals to base an inference of specific causation upon an increased risk, whether or not that increased risk is quantified as a relative risk greater than two.  The late David Freedman, who was the co-author of the chapters on statistics in all three editions of the Reference Manual on Scientific Evidence, was also a naysayer when it came to transmuting risk into cause:

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

David Freedman & Philip Stark, “The Swine Flu Vaccine and Guillaine-Barré Syndrome:  A Case Study in Relative Risk and Specific Causation,” 64 Law & Contemporary Problems 49, 61 (2001).

The plaintiffs’ challenge to Blaustein’s claim that there was no “generally accepted” method for specific causal attribution took the form of advancing their own “method”:  differential diagnosis. At face value, the plaintiffs’ use of differential diagnosis to advance a claim of specific causation is “simply false.”  There was no dispute about diagnosis, and no differential diagnosis at issue.  Unfortunately, courts have permitted lawyers to corrupt the meaning of differential diagnosis and contend that it covers something akin to differential etiology.

Davidson and Guzelian, in their reference back to an earlier article on evidence-based toxicology, embrace differential etiology as a method of specific case attribution.  I agree that there is really no dispute about the logically validity of such reasoning, generally.  The logic of differential etiology is simple.  If you can specify all the known causes of a disease, and eliminate all but one cause, then you have ruled in the specific cause.  Logically, this is an iterative disjunctive syllogism, also known as the process of elimination.  The syllogism requires an exhaustive statement of disjuncts, with the negation of all but one:

A v B v C v D

~A and ~B and ~ C.

Therefore, D.

In “The Adventure of the Beryl Coronet,” Sir Arthur Conan Doyle had his famous detective, Sherlock Holmes, articulate this method in ordinary English, with a bit more flair:

“It is an old maxim of mine that when you have excluded the impossible, whatever remains, however improbable, must be the truth.”

Arthur Conan Doyle, The Penguin Complete Sherlock Holmes 315 (Penguin 1981). The process of elimination was a mainstay of Holmes’ forensic thought:

“Eliminate all other factors, and the one which remains must be the truth.”

“The Sign of the Four,” chap. 1 (“The Science of Deduction”), in Arthur Conan Doyle, The Penguin Complete Sherlock Holmes at 92 (Penguin 1981).

The problem of course is, for a disease such as breast cancer, is that one of the disjuncts has been, and will remain, for some time: the proposition that this case is “idiopathic” or “sporadic.” The plaintiffs in Cross did not advance any plausible method for eliminating this disjunct.  As a result, they can never arrive at a conclusion that CHRT was a cause of Ms. Cross’s breast cancer.  The closest they can get to their desired conclusion with this “method,” once they have eliminated genetic causes, is a conclusion that:

The case is idiopathic OR the case resulted from CHRT.

This conclusion is not really a conclusion at all, but an indeterminate statement, which would be quite unhelpful to the trier in deciding the case. Furthermore, as the case is described by the trial court’s opinion, the plaintiffs did not even attempt a quantification of the probability of each of these two disjuncts.  Thus, the plaintiffs failed to offer any substantial evidence that a jury could believe to find in their favor on specific causation.  The trial court was correct to reject the challenge to Dr. Blaustein’s specific causation opinion, but the court should have granted the defendants’ challenge to the plaintiffs’ expert witnesses, who had no method at all on the crucial element of specific causation.

Interestingly, one of the plaintiffs’ better arguments against Dr. Blaustein was that he was, as a clinician, unqualified to opine on causation.  Cross, *9.  The trial court did not elaborate on the argument other than to point out that plaintiffs had emphasized that Dr. Blaustein relied upon his “unquantifiable and untested clinical experience.” Cross, *10. The courts have been remarkably resistant to the argument that physicians are generally unqualified to interpret scientific evidence of causation.  Sadly, there is a good deal of empirical evidence to show that physicians are not particularly well trained in statistics or in interpreting clinical research.  See, e.g., Donna Windish, Stephen Huot, and Michael Green, “Medicine Residents’ Understanding of the Biostatics and Results in the Medical Literature,” 298 J. Am. Med. Ass’n 1010, 1010 (2007) (“Most residents in this study lacked the knowledge in biostatistics to interpret many of the results in published clinical research.”).

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Evidence-Based Specific Causation

Broadbent on the Relative Risk > 2 Argument

October 31st, 2012

Alex Broadbent, of the University of Johannesburg, Department of Philosophy, has published a paper that contributes to the debate over whether a relative risk (RR) greater than (>) two is irrelevant, helpful, necessary, or sufficient in inferring that an exposure more likely than not caused an individual claimant’s disease. Alex Broadbent, “Epidemiological Evidence in Proof of Specific Causation,” 17 Legal Theory 237 (2011) [cited as Broadbent].  I am indebted to his having called his paper to my attention. Professor Broadbent’s essay is clearly written, which is helpful in assessing the current use of the RR > 2 argument in judicial decisions.

General vs. Specific Causation

Broadbent carefully distinguishes between general and specific causation.  By focusing exclusively upon specific causation (and assuming that general causation is accepted), he avoids the frequent confusion over when RR > 2 might play a role in legal decisions. Broadbent also “sanitizes” his portrayal of RR by asking us to assume that “the RR is not due to anything other than the exposure.” Id. at 241. This is a BIG assumption and a tall order for observational epidemiologic evidence.  The study or studies that establishes the RR we are reasoning from must be free of bias and confounding. Id.  Broadbent does not mention, however, the statistical stability of the RR, which virtually always will be based upon a sample, and thus subject to the play of random error.  He sidesteps the need for statistical significance in comparing two proportions, but the most charitable interpretation of his paper requires us to assume further that the hypothetical RR from which we are reasoning is sufficiently statistically stable that random error, along with bias and confounding, can be also ruled out as likely explanations for the RR > 1.

Broadbent sets out to show that RR > 2 may, in certain circumstances, suffices to show specific causation, but he argues that RR > 2 is never logically necessary, and must never be required to support a claim of specific causation.  Broadbent at 237.  On the same page in which he states that epidemiologic evidence of increased risk is a “last resort,” Broadbent contradicts himself by stating RR > 2 evidence “must never be required,” and then, in an apparent about face, he argues:

“that far from being epistemically irrelevant, to achieve correct and just outcomes it is in fact mandatory to take (high-quality) epidemiological evidence into account in deciding specific causation. Failing to consider such evidence when it is available leads to error and injustice. The conclusion is that in certain circumstances epidemiological evidence of RR > 2 is not necessary to prove specific causation but that it is sufficient.”

Id. at 237 (emphasis added). I am not sure how epidemiologic evidence can be mandatory but never logically necessary, and something that we should never require.

Presumably, Broadbent is using “to prove” in its legal and colloquial sense, and not as a mathematician.  Let us also give Broadbent his assumptions of “high quality” epidemiologic studies, with established general causation, and ask why, and explore when and whether, RR > 2 is not necessary to show specific causation.

The Probability of Causation vs. The Fact of Causation

Broadbent notes that he is arguing against what he perceives to be Professor Haack’s rejection of probabilistic inference, which would suggest that epidemiologic evidence is “never sufficient to establish specific causation.” Id. at 239 & n.3 (citing Susan Haack, “Risky Business: Statistical Proof of Individual Causation,” in Causación y Atribucion de Responsabilidad (J. Beltran ed., forthcoming)). He correctly points out that sometimes the probabilistic inference is the only probative inference available to support specific causation.  His point, however, does not resolve the dispute; it suffices only to show that whether we allow the probabilistic inference may be outcome determinative in many lawsuits.  Broadbent characterizes Haack’s position as one of two “serious mistakes in judicial and academic literature on this topic.”  Broadbent at 239.  The other alleged mistake is the claim that RR > 2 is needed to show specific causation:

“What follows, I conclude, is that epidemiological evidence is relevant to the proof of specific causation. Epidemiological evidence says that a particular exposure causes a particular harm within a certain population. Importantly, it quantifies: it says how often the exposure causes the harm. However, its methods are limited: they measure only the net effect of the exposure, leaving open the possibility that the exposure is causing more harm than the epidemiological evidence suggests—but ruling out the possibility that it causes less. Accordingly I suggest that epidemiological evidence can be used to estimate a lower bound on the probability of causation but that no epidemiological measure can be required. Thus a relative risk (RR, defined in Section II) of greater than 2 can be used to prove causation when there is no other evidence; but RR < 2 does not disprove causation. Given high-quality epidemiological evidence, RR > 2 is sufficient for proof of specific causation when no other evidence is available but not necessary when other evidence is available.”

Some of this seems reasonable enough.  Contrary to the claims of authors such as Haack and Wright, Broadbent maintains that some RR evidence is relevant and indeed probative of specific causation.  In a tobacco lung cancer, with a plaintiff who has smoked three packs a day, for 50 years (and RR > 50), we can confidently attribute the lung cancer to smoking, and rest assured that background cosmic radiation did not likely play a substantial role. The RR quantifies the strength of the association, and it does lead us to a measure of “attributable risk” (AR), also known as the attributable fraction (AF):

AR = 1 – 1/RR.

So far, so good.

Among the perplexing statements above, however, Broadbent suggests that:

1. The methods of epidemiologic evidence measure only the net effect of the exposure.  Epidemiologic evidence (presumably the RR or other risk ratio) provides a lower bound on the probability of causation.  I take up this suggestion in discussing Broadbent’s distinction between the “excess fraction,” and the “etiologic fraction,” below.

2. A RR > 2 “can be used to prove causation when there is no other evidence; but RR < 2 does not disprove causation.” (My emphasis.) When an author is usually clear about his qualifications, and his language generally, it is distressing for him to start comparing apples to oranges.  Note that RR > 2 suffices “when there is no other evidence,” but the parallel statement about RR < 2 is not similarly qualified, and the statement about RR < 2 is framed in terms of disproof of causation. Even if the RR < 2 did not “disprove” specific causation, when there was no other evidence, it would not prove causation.  And if there is no other evidence, judgment for the defense must result. Broadbent fails to provide us a persuasive scenario in which a RR ≤ 2, with no other evidence, would support an inference of specific causation.

Etiological Fraction vs. Excess Fraction — Occam’s Disposable Razor

Broadbent warns that the expression “attributable risk” (AR or “attributable fraction,” AF) is potentially misleading.  The numerical calculation identifies the excess number of cases, above “expected” per base rate, and proceeds from there.  The AR thus identifies the “excess fraction,” and not the “etiological fraction,” which is the fraction of all cases in which exposure makes a contribution. Broadbent tells us that:

“Granted a sound causal inference, we can infer that all the excess cases are caused by the exposure. But we cannot infer that the remaining cases are not caused by the exposure. The etiologic fraction—the cases in which the exposure makes a causal contribution—could be larger. Roughly speaking, this is because, in the absence of substantive biological assumptions, it is possible that the exposure could contribute to cases that would have occurred12 even without the exposure.13 For example, it might be that smoking is a cause of lung cancer even among some of those who would have developed it anyway. The fact that a person would have developed lung cancer anyway does not offer automatic protection against the carcinogenic effects of cigarette smoke (a point we return to in Section IV).”

Id. at 241. In large measure here, Broadbent has adopted (and acknowledged) his borrowings from Professor Sander Greenland.  Id. at 242 n.11. The argument  still fails.  What Broadbent has interposed is a “theoretical possibility” that the exposure in question may contribute to those cases that would have occurred anyway.  Note that raising theoretical possibilities here now alters the hypothetical; Broadbent is no longer working from a hypothetical that we have a RR and no other evidence.  Even more important, we are left guessing what it means to say that an exposure causes some cases that would have occurred anyway.  If we accept the postulated new evidence at face value, we can say confidently that the exposure is not the “but for” cause of the case at issue.  Without sufficient evidence of “but for” causation, plaintiff will lose. Furthermore, we are being told to add a new fact to the hypothetical, namely that the non-excess cases are causally over-determined.  If this is the only additional new fact being added, a court might invoke the rule in Summers v. Tice, but even so, the defense will be entitled to a directed verdict if the RR < 2. (If the RR = 2, I suppose, the new fact, and the change in the controlling rule, might alter the result.)

Exposures that Cause Some and Prevent Some Cases of Disease

Broadbent raises yet another hypothetical possibility, which adds to, and materially alters,  his original hypothetical.  If the exposure in question, causes some cases, and prevents others, then the RR ≤ 2 will not permit us to infer that a given case is less likely than not the result of the exposure.  (Broadbent might have given an example of what he had in mind, from well-established biological causal relationships; I am skeptical that he would have found one that would have satisfactorily made his argument.) The bimodal distribution of causal effects is certainly not typical of biological processes, but even if we indulge the “possibility,” we are now firmly in the realm of speculation.  This is a perfectly acceptable realm for philosophers, but in court, we want evidence.  Assuming that the claimant could present such evidence, finders of fact would still founder because the new evidence would leave them guessing whether the claimant was a person who would have gotten the disease anyway, or got it because of the exposure, or even got it in spite of the exposure.

Many commentators who urge a “probability of [specific] causation” approach equate the probability of causation (PC) with the AR.  Broadbent argues that because of the possibility that some biological model results in the etiologic fraction exceeded the excess fraction, the usual equation of PC = AR, must be represented as an equality:

PC ≥ AR

While the point is logically unexceptional, Broadbent must concede that some other evidence, which supports and justifies the postulated biological model, is required to change the equality to an inequality.  If no other evidence besides the RR is available, we are left with the equality.  Broadbent tells us that the biological model “often” requires that the etiological fraction exceeds the excess fraction, but he never tells us how often, or how we would ascertain the margin of error.  Id. at 256.

Broadbent does not review any of the decided judicial cases to point out which ones involved biological models that invalidated the equality.  Doing so would be an important exercise because it might well show that even where PC ≥ AR, with a non-quantified upper bound, the plaintiff might still fail in presenting a prima facie case of specific causation.  Suppose the population RR for the exposure in question were 1.1, and we “know” (and are not merely speculating) that the etiological fraction > excess fraction.   Unless we know how much greater is the etiological fraction, such that we can recalculate the PC, then we are left agnostic about specific causation.

Broadbent treats us to several biological scenarios in which PC possibly is greater than AR.  All of these scenarios violate his starting premiss that we have a RR with no other evidence. For instance, Broadbent hypothesizes that exposure might accelerate onset of a disease.  Id. at 256. This biological model of acceleration can be established with the same epidemiologic evidence that established the RR for the population.  Epidemiologists will frequently look at time windows from onset of exposure to explore whether there is an acceleration of onset of cases in a younger age range that offsets a deficit later in the lives of the exposed population.  If there were firm evidence of such a phenomenon, then we would look to the RR within the relevant time window.  If the relevant RR ≤ 2, the biological model will have added nothing to the plaintiff’s case.

Broadbent cites Greenland for the proposition that PC > AR:

“We know of no cancer or other important chronic disease for which current biomedical knowledge allows one to exclude mechanisms that violate the assumptions needed to claim that PC = [AF].”

Id. at 259, quoting form Sander Greenland & James Robins, “Epidemiology, Justice, and the Probability of Causation,” 40 Jurimetrics J. 321, 325 (2000).  Here, not only has Broadbent postulated a mechanism that makes PC > AR, but he has shifted the burden of proof to the defense to exclude it!

The notion that the etiological fraction may exceed the excess fraction is an important caveat.  Courts and lawyers should take note.  It will not do, however, wave hands and exclaim that the RR > 2 is not a “litmus test,” and proceed to let any RR > 1, or even RR ≤ 1 support a verdict.  The biological models that may push the etiological fraction higher than the excess fraction can be tested, and quantified, with the same epidemiologic approaches that provided a risk ratio, in the first place.  Broadbent gives us an example of this sort of hand waving:

“Thus, for example, evidence that an exposure would be likely to aggravate an existing predisposition to the disease in question might suffice, along with RR between 1 and 2, to make it more likely than not that the claimant’s disease was caused by the exposure.”

Id. at 275. This is a remarkable, and unsupported claim.  The magnitude of the aggravation might still leave the RR ≤ 2.  What is needed is evidence that would allow quantification of the risk ratio in the scenario presented. Speculation will not do the trick; nor will speculation get the case to a jury, or support a verdict.

 

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