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Failed Gatekeeping in Ambrosini v. Labarraque (1996)

December 28th, 2017

The Ambrosini case straddled the Supreme Court’s 1993 Daubert decision. The case began before the Supreme Court clarified the federal standard for expert witness gatekeeping, and ended in the Court of Appeals for the District of Columbia, after the high court adopted the curious notion that scientific claims should be based upon reliable evidence and valid inferences. That notion has only slowly and inconsistently trickled down to the lower courts.

Given that Ambrosini was litigated in the District of Columbia, where the docket is dominated by regulatory controversies, frequently involving dubious scientific claims, no one should be surprised that the D.C. Court of Appeals did not see that the Supreme Court had read “an exacting standard” into Federal Rule of Evidence 702. And so, we see, in Ambrosini, this Court of Appeals citing and purportedly applying its own pre-Daubert decision in 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).1 In 2000, the Federal Rule of Evidence 702 was revised in a way that extinguishes the precedential value of Ambrosini and the broad dicta of Ferebee, but some courts and commentators have failed to stay abreast of the law.

Escolastica Ambrosini was using a synthetic progestin birth control, Depo-Provera, as well as an anti-nausea medication, Bendectin, when she became pregnant. The child that resulted from this pregnancy, Teresa Ambrosini, was born with malformations of her face, eyes, and ears, cleft lip and palate, and vetebral malformations. About three percent of all live births in the United States have a major malformation. Perhaps because the Divine Being has sovereign immunity, Escolastica sued the manufacturers of Bendectin and Depo-Provera, as well as the prescribing physician.

The causal claims were controversial when made, and they still are. The progestin at issue, medroxyprogesterone acetate (MPA), was embryotoxic in the cynomolgus monkey2, but not in the baboon3. The evidence in humans was equivocal at best, and involved mostly genital malformations4; the epidemiologic evidence for the MPA causal claim to this day remains unconvincing5.

At the close of discovery in Ambrosini, Upjohn (the manufacturer of the progestin) moved for summary judgment, with a supporting affidavit of a physician and geneticist, Dr. Joe Leigh Simpson. In his affidavit, Simpson discussed three epidemiologic studies, as well as other published papers, in support of his opinion that the progestin at issue did not cause the types of birth defects manifested by Teresa Ambrosini.

Ambrosini had disclosed two expert witnesses, Dr. Allen S. Goldman and Dr. Brian Strom. Neither Goldman nor Strom bothered to identify the papers, studies, data, or methodology used in arriving at an opinion on causation. Not surprisingly, the district judge was unimpressed with their opposition, and granted summary judgment for the defendant. Ambrosini v. Labarraque, 966 F.2d 1462, 1466 (D.C. Cir. 1992).

The plaintiffs appealed on the remarkable ground that Goldman’s and Strom’s crypto-evidence satisfied Federal Rule of Evidence 703. Even more remarkably, the Circuit, in a strikingly unscholarly opinion by Judge Mikva, opined that disclosure of relied-upon studies was not required for expert witnesses under Rules 703 and 705. Judge Mikva seemed to forget that the opinions being challenged were not given in testimony, but in (late-filed) affidavits that had to satisfy the requirement of Federal Rule of Civil Procedure 26. Id. at 1468-69. At trial, an expert witness may express an opinion without identifying its bases, but of course the adverse party may compel disclosure of those bases. In discovery, the proffered expert witness must supply all opinions and evidence relied upon in reach the opinions. In any event, the Circuit remanded the case for a hearing and further proceedings, at which the two challenged expert witnesses, Goldman and Strom, would have to identify the bases of their opinions. Id. at 1471.

Not long after the case landed back in the district court, the Supreme Court decided Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). With an order to produce entered, plaintiffs’ counsel could no longer hide Goldman and Strom’s evidentiary bases, and their scientific inferences came under judicial scrutiny.

Upjohn moved again to exclude Goldman and Strom’s opinions. The district court upheld Upjohn’s challenges, and granted summary judgment in favor of Upjohn for the second time. The Ambrosinis appealed again, but the second case in the D.C. Circuit resulted in a split decision, with the majority holding that the exclusion of Goldman and Strom’s opinions under Rule 702 was erroneous. Ambrosini v. Labarraque, 101 F.3d 129 (D.C. Cir. 1996).

Although issued two decades ago, the majority’s opinion remains noteworthy as an example of judicial resistance to the existence and meaning of the Supreme Court’s Daubert opinion. The majority opinion uncritically cited the notorious Ferebee6 and other pre-Daubert decisions. The court embraced the Daubert dictum about gatekeeping being limited to methodologic consideration, and then proceeded to interpret methodology as superficially as necessary to sustain admissibility. If an expert witness claimed to have looked at epidemiologic studies, and epidemiology was an accepted methodology, then the opinion of the expert witness must satisfy the legal requirements of Daubert, or so it would seem from the opinion of the U.S. Court of Appeals for the District of Columbia.

Despite the majority’s hand waving, a careful reader will discern that there must have been substantial gaps and omissions in the explanations and evidence cited by plaintiffs’ expert witnesses. Seeing anything clearly in the Circuit’s opinion is made difficult, however, by careless and imprecise language, such as its descriptions of studies as showing, or not showing “causation,” when it could have meant only that such studies showed associations, with more or less random and systematic error.

Dr. Strom’s report addressed only general causation, and even so, he apparently did not address general causation of the specific malformations manifested by the plaintiffs’ child. Strom claimed to have relied upon the “totality of the data,” but his methodologic approach seems to have required him to dismiss studies that failed to show an association.

“Dr. Strom first set forth the reasoning he employed that led him to disagree with those studies finding no causal relationship [sic] between progestins and birth defects like Teresa’s. He explained that an epidemiologist evaluates studies based on their ‘statistical power’. Statistical power, he continued, represents the ability of a study, based on its sample size, to detect a causal relationship. Conventionally, in order to be considered meaningful, negative studies, that is, those which allege the absence of a causal relationship, must have at least an 80 to 90 percent chance of detecting a causal link if such a link exists; otherwise, the studies cannot be considered conclusive. Based on sample sizes too small to be reliable, the negative studies at issue, Dr. Strom explained, lacked sufficient statistical power to be considered conclusive.”

Id. at 1367.

Putting aside the problem of suggesting that an observational study detects a “causal relationship,” as opposed to an association in need of further causal evaluation, the Court’s précis of Strom’s testimony on power is troublesome, and typical of how other courts have misunderstood and misapplied the concept of statistical power. Statistical power is a probability of observing an association of a specified size at a specified level of statistical significance. The calculation of statistical power turns indeed on sample size, the level of significance probability preselected for “statistical significance, an assumed probability distribution of the sample, and, critically, an alternative hypothesis. Without a specified alternative hypothesis, the notion of statistical power is meaningless, regardless of what probability (80% or 90% or some other percentage) is sought for finding the alternative hypothesis. Furthermore, the notion that the defense must adduce studies with “sufficient statistical power to be considered conclusive” creates an unscientific standard that can never be met, while subverting the law’s requirement that the claimant establish causation.

The suggestion that the studies that failed to find an association cannot be considered conclusive because they “lacked sufficient statistical power” is troublesome because it distorts and misapplies the very notion of statistical power. No attempt was made to describe the confidence intervals surrounding the point estimates of the null studies; nor was there any discussion whether the studies could be aggregated to increase their power to rule out meaningful associations.

The Circuit court’s scientific jurisprudence was thus seriously flawed. Without a discussion of the end points observed, the relevant point estimates of risk ratios, and the confidence intervals, the reader cannot assess the strength of the claims made by Goldman and Strom, or by defense expert Simpson, in their reports. Without identifying the study endpoints, the reader cannot evaluate whether the plaintiffs’ expert witnesses relied upon relevant outcomes in formulating their opinions. The court viewed the subject matter from 30,000 feet, passing over at 600 mph, without engagement or care. A strong dissent, however, suggested serious mischaracterizations of the plaintiffs’ evidence by the majority.

The only specific causation testimony to support plaintiff’s claims came from Goldman, in what appears to have been a “differential etiology.” Goldman purported to rule out a genetic cause, even though he had not conducted a critical family history or ordered a state-of-the-art chromosomal study. Id. at 140. Of course, nothing in a differential etiology approach would allow a physician to rule out “unknown” causes, which, for birth defects, make up the most prevalent and likely causes to explain any particular case. The majority acknowledged that these were short comings, but rhetorically characterized them as substantive, not methodologic, and therefore as issues for cross-examination, not for consideration by a judicial gatekeeping. All this is magical thinking, but it continues to infect judicial approaches to specific causation. See, e.g., Green Mountain Chrysler Plymouth Dodge Jeep v. Crombie, 508 F. Supp. 2d 295, 311 (D.Vt. 2007) (citing Ambrosini for the proposition that “the possibility of uneliminated causes goes to weight rather than admissibility, provided that the expert has considered and reasonably ruled out the most obvious”). In Ambrosini, however, Dr. Goldman had not ruled out much of anything.

Circuit Judge Karen LeCraft Henderson dissented in a short, but pointed opinion that carefully marshaled the record evidence. Drs. Goldman and Strom had relied upon a study by Greenberg and Matsunaga, whose data failed to show a statistically significant association between MPA and cleft lip and palate, when the crucial issue of timing of exposure was taken into consideration. Ambrosini, 101 F.3d at 142.

Beyond the specific claims and evidence, Judge Henderson anticipated the subsequent Supreme Court decisions in Joiner, Kumho Tire, and Weisgram, and the year 2000 revision of Rule 702, in noting that the majority’s acceptance of glib claims to have used a “traditional methodology” would render Daubert nugatory. Id. at 143-45 (characterizing Strom and Goldman’s methodologies as “wispish”). Even more importantly, Judge Henderson refused to indulge the assumption that somehow the length of Goldman’s C.V. substituted for evidence that his methods satisfied the legal (or scientific) standard of reliability. Id.

The good news is that little or nothing in Ambrosini survives the 2000 amendment to Rule 702. The bad news is that not all federal judges seem to have noticed, and that some commentators continue to cite the case, as lovely.

Probably no commentator has promiscuously embraced Ambrosini as warmly as Carl Cranor, a philosopher, and occasional expert witness for the lawsuit industry, in several publications and presentations.8 Cranor has been particularly enthusiastic about Ambrosini’s approval of expert witness’s testimony that failed to address “the relative risk between exposed and unexposed populations of cleft lip and palate, or any other of the birth defects from which [the child] suffers,” as well as differential etiologies that exclude nothing.9 Somehow Cranor, as did the majority in Ambrosini, believes that testimony that fails to identify the magnitude of the point estimate of relative risk can “assist the trier of fact to understand the evidence or to determine a fact in issue.”10 Of course, without that magnitude given, the trier of fact could not evaluate the strength of the alleged association; nor could the trier assess the probability of individual causation to the plaintiff. Cranor also has written approvingly of lumping unrelated end points, which defeats the assessment of biological plausibility and coherence by the trier of fact. When the defense expert witness in Ambrosini adverted to the point estimates for relevant end points, the majority, with Cranor’s approval, rejected the null findings as “too small to be significant.”11 If the null studies were, in fact, too small to be useful tests of the plaintiffs’ claims, intellectual and scientific honesty required an acknowledgement that the evidentiary display was not one from which a reasonable scientist would draw a causal conclusion.

1Ambrosini v. Labarraque, 101 F.3d 129, 138-39 (D.C. Cir. 1996) (citing and applying Ferebee), cert. dismissed sub nom. Upjohn Co. v. Ambrosini, 117 S.Ct. 1572 (1997) See also David E. Bernstein, “The Misbegotten Judicial Resistance to the Daubert Revolution,” 89Notre Dame L. Rev. 27, 31 (2013).

2 S. Prahalada, E. Carroad, M. Cukierski, and A.G. Hendrickx, “Embryotoxicity of a single dose of medroxyprogesterone acetate (MPA) and maternal serum MPA concentrations in cynomolgus monkey (Macaca fascicularis),” 32 Teratology 421 (1985).

3 S. Prahalada, E. Carroad, and A.G. Hendrick, “Embryotoxicity and maternal serum concentrations of medroxyprogesterone acetate (MPA) in baboons (Papio cynocephalus),” 32 Contraception 497 (1985).

4 See, e.g., Z. Katz, M. Lancet, J. Skornik, J. Chemke, B.M. Mogilner, and M. Klinberg, “Teratogenicity of progestogens given during the first trimester of pregnancy,” 65 Obstet Gynecol. 775 (1985); J.L. Yovich, S.R. Turner, and R. Draper, “Medroxyprogesterone acetate therapy in early pregnancy has no apparent fetal effects,” 38 Teratology 135 (1988).

5 G. Saccone, C. Schoen, J.M. Franasiak, R.T. Scott, and V. Berghella, “Supplementation with progestogens in the first trimester of pregnancy to prevent miscarriage in women with unexplained recurrent miscarriage: a systematic review and meta-analysis of randomized, controlled trials,” 107 Fertil. Steril. 430 (2017).

6 Ferebee v. Chevron Chemical Co., 736 F.2d 1529, 1535 (D.C. Cir.), cert. denied, 469 U.S. 1062 (1984).

7 Dr. Strom was also quoted as having provided a misleading definition of statistical significance: “whether there is a statistically significant finding at greater than 95 percent chance that it’s not due to random error.” Ambrosini at 101 F.3d at 136. Given the majority’s inadequate description of the record, the description of witness testimony may not be accurate, and error cannot properly be allocated.

8 Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 320, 327-28 (2006); see also Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 238 (2d ed. 2016).

9 Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 320 (2006).

10 Id.

11 Id. ; see also Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 238 (2d ed. 2016).

Posted in Causation, Expert Witness Discovery, Rule 702, Rule 703, Scientific Evidence, statistical evidence, Statistical Power | Comments Off on Failed Gatekeeping in Ambrosini v. Labarraque (1996)

Ferebee Revisited

December 28th, 2017

The following post was originally published on November 8, 2012, but was hacked, no doubt by the lawsuit industry, and replaced with mindless fluff as is its wont. It is now restored.

Ferebee Revisited

I used to think of the infamous Ferebee decision as the Dred Scott decision of scientific evidence; in essence, declaring that science has no validity issues that the law is bound to respect. 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). The rhetoric on expert witnesses, from the district and circuit courts in this case is sometimes jarring, but the facts of the case make the holding, rather than the expansive dicta, not so unreasonable, under all the facts and circumstances of the case.

On rereading Ferebee, I was struck by several aspects of the case that rarely are discussed when Ferebee is cited. On sober second thought, Ferebee may not be such a bad decision, especially considering that it has no continuing validity as a rule of decision for expert witness admissibility in federal court.

1. Ferebee is a government negligence case.

The plaintiff worked for the federal government when he was exposed to the herbicide paraquat. Richard Ferebee began working for the Department of Agriculture’s Beltsville Agricultural Research Center (BARC), in Beltsville, Maryland. He started spraying paraquat in the summer of 1977, and used the herbicide regularly through the time he was diagnosed with pulmonary fibrosis, in November 1979. 736 F.2d at 1531-32. Ferebee brought a failure to warn claim against the supplier of paraquat, Chevron Chemical Company. The allegations of actual or constructive knowledge of a hazard, however, could just as readily be asserted against the federal government, which owned the BARC facility, employed Ferebee, controlled and supervised his use of paraquat, and failed to comply with Chevron’s instructions. The federal government further regulated the sale and use of paraquat extensively, first by the Department of Agriculture, and later by the Environmental Protection Agency. Id. at 1532.

2. The exposure.

Ferebee filed suit in 1981, he died in 1982. His case was tried twice. In the first trial, the jury deadlocked; in the second trial, the jury returned a verdict in favor of his estate, and for his family, for $60,000. In his deposition testimony, Ferebee described how sprayed paraquat, in the summer of 1977. The chemical was diluted for use, per Chevron’s instructions. There was no evidence that Ferebee ever had direct contact with undiluted paraquat, or that the paraquat he was exposed to was not diluted according to the proportions recommended on Chevron’s label. 552 F. Supp. at 1295 & n. 3. Ferebee frequently got the chemical on his hands. 552 F. Supp. at 1294-95. Ferebee further described an occasion when he was drenched with paraquat when he walked behind a tractor that was spraying the chemical, and another incident when he used a defective sprayer that leaked paraquat “all over his pants.” 736 F.2d at 1532. On both occasions, Ferebee did not wash, and apparently went home contaminated, where he fell asleep, tired and dizzy, without showering. Id. As we will see, the exposure that Ferebee described would not have occurred had his federal employer followed the instructions on the label that it mandated. In 1978, the federal Occupational Health & Safety Administration published Guidelines on the need for protective clothing, respirators, immediate washing of contaminated skin, etc. Ferebee’s federal employer recklessly disregarded its own guidelines.

3. The warnings.

Paraquat could be sold in the United States only when labeled in accordance with EPA regulations, promulgated pursuant to the Federal Insecticide, Fungicide, and Rodenticide Act, 7 U.S.C. § 136, et seq. (FIFRA) The statute bars EPA from allowing sale of regulated herbicides, such as paraquat, unless the chemicals, as labeled, will not cause “unreasonable adverse effects on the environment.” 7 U.S.C. § 136a(c)(5)(C). Such effects are in turn defined as any unreasonable risk to man or the environment, taking into account the economic, social, and environmental costs and benefits of the use of [the] pesticide. 7 U.S.C. § 136(bb). FIFRA further requires the EPA to require labeling that is “adequate to protect health and the environment” and that is “likely to be read and understood.” 7 U.S.C. § 136(q)(1)(E). 736 F.2d at 1539-40.

Unfortunately, the courts failed to provide the complete warning label and the material data safety sheets. There are “snippets” provided, which make clear that the federal government was largely to blame for failing to comply with the directions required under FIFRA. For instance, the district court, in a footnote, acknowledged:

“For example, the label advised the user spraying paraquat to wear waterproof clothing and goggles, to avoid working in spray mist, and to wash splashes on the skin or eyes immediately with water.”

552. F. Supp. at 1304 n.40. The Court of Appeals reported that “the label, in large bold letters states:

DANGER

CAN KILL IF SWALLOWED

HARMFUL TO THE EYES AND SKIN

736 F.2d at 1536. The label also informed users to wash any exposed areas immediately, and to remove contaminated clothing. Id.

4. The Stipulation.

A key fact, rarely described or explained in discussions of the Ferebee case, is the parties’ stipulation

“that Mr. Ferebee’s only significant exposure to paraquat was on his intact skin; i.e., there was no evidence that Mr. Ferebee swallowed or inhaled paraquat, or that he spilled or sprayed it on an area of his skin upon which he had any apparent cuts or scrapes. The jury was not, of course, precluded from concluding that a person engaged in Mr. Ferebee’s line of work could have had some, or even many, minor cuts or abrasions not readily discernible to the naked eye or likely to be remembered some time later.”

552. F. Supp. at 1295 & n. 3.

Why did the plaintiffs try to present their case solely as a dermal exposure cases? As we will see, this stratagem made their medical causation case more difficult, but it avoided serious misuse and lack of proximate cause issues. Ferebee had been instructed by his co-workers and supervisors that paraquat was extremely dangerous if swallowed, and probably also if inhaled. The warning label was unequivocal in detailing the dangers and the need to avoid ingestion. (Without the full label, it is difficult to evaluate how well the label warned against inhalation, but the 1978 OSHA guidelines address the use of a proper respirator for situations in which paraquat may be inhaled.) On the other hand, the label had a weakness, which could be exploited, as long as the preemption defense could be held at bay: the label urged protective clothing, goggles, and immediate washing of contaminated skin, but it failed to describe the consequence of dermal exposure other than irritation. Ferebee could thus avoid his culpable conduct, as well as a sophisticated intermediary defense, by claiming that his exposure was only dermal.

Why did Chevron agree to the stipulation? The defendant probably felt sanguine about its preemption defense, and thus also about the adequacy of its warnings overall. The stipulation limited the plaintiff’s medical causation case to a route of exposure that put it into an arguable “first instance” case report. Chevron stood to gain a claim of “lack of notice,” and thus lack of actual or constructive knowledge of the risk of lung disease from dilute dermal exposure. The clinical presentation itself differed from many of the cases of known paraquat poisoning, see infra, and Chevron probably believed that it could deal with the medical causation claim better if exposure was limited to transdermal absorption. Curiously, Chevron did not argue that Ferebee must have had some inhalational exposure, which he almost certainly did. I suspect that Chevron’s position on inhalation was hedged because its warning label did not specify respirator usage for ordinary work exposures of applicators (as opposed to workers who handled undiluted paraquat, worked in confined spaces, etc.).

5. Medical causation

Chevron took a strident position, standing on the fact that there had been no previous documented cases of pulmonary fibrosis in workers exposed to diluted paraquat through their skin. The following facts were uncontroverted:

  • Paraquat causes pulmonary fibrosis in humans.
  • The evidence that established paraquat as a cause of pulmonary fibrosis was largely case series of acute onset of pulmonary fibrosis after ingestion.
  • Paraquat induces pulmonary fibrosis relatively rapidly.
  • Paraquat can be absorbed through the skin.
  • The parties agreed that any type of exposure – ingestion, inhalation, or dermal absorption – could cause lung damage. 552. F. Supp. at 1300 & n.28.
  • Once paraquat is ingested, inhaled, or absorbed, it can travel to the lungs.
  • Lung fibrosis caused by dermal absorption of paraquat had been described previously only with skin lesions before or after the injury. 736 F.2d at 1538.
  • The lungs are the target organ for paraquat.
  • There are numerous causes of pulmonary fibrosis (such as asbestosis, scleroderma, rheumatoid arthritis, etc.).
  • The variants of pulmonary fibrosis do not all look alike, present alike, or progress alike.
  • Mr. Ferebee had no known other disease or exposure that could account for his pulmonary fibrosis.
  • There is are cases of pulmonary fibrosis with no identifiable cause, known as idiopathic pulmonary fibrosis (IPF).
  • IPF is relatively rare; it too has a rapid onset and progression, although not as fast as the cases described after exposure to undiluted paraquat.
  • Mr. Ferebee’s medical history was largely unhelpful in explaining his clinical course.
  • Ferebee had some shortness of breath before starting to use paraquat. 552. F. Supp. at 1295.
  • Ferebee used paraquat occasionally over three years before he was diagnosed with pulmonary fibrosis.

Some observations about these facts. General causation in a sense was not contested. Paraquat causes pulmonary fibrosis. The issue was whether dilute dermal exposure over three years causes pulmonary fibrosis. Chevron stridently asserted that the “scientific method” required controlled experimental or observational (epidemiologic) studies. The problem with Chevron’s position was that general causation had already been established, and not by analytical epidemiologic studies.

6. The expert witnesses.

Ferebee was initially treated by Dr. Muhammed Yusuf, a pulmonary specialist, who diagnosed pulmonary fibrosis. Dr. Yusef referred Ferebee to the National Institutes of Health (NIH), where he came under the care of Dr. Ronald G. Crystal of the Heart, Lung, and Blood Institute. (Dr. Crystal is now at Cornell-Weill, where he is Chairman of Genetic Medicine, and he practices pulmonary medicine.)

Chevron called Dr. Carrington, who diagnosed Ferebee with IPF. Dr. Carrington challenged the plaintiffs’ expert witnesses’ opinions for lacking reliance upon controlled observational or experimental studies. 552. F. Supp. at 1301. Dr. Carrington, however, acknowledged that dermal cases are too rare for observational epidemiologic analysis, but emphasized that no animal studies of sufficient size had been done to support plaintiffs’ hypothesis. Chevron also called a Dr. Fisher, who presented a toxicokinetic (TK) analysis of Ferebee’s dermal absorption. Based upon his TK analysis, Dr. Fisher concluded that the maximal amount of paraquat absorbed by Ferebee was too small, based upon known cases and animal studies, to have caused paraquat toxicity. Id.

7. Chevron’s challenge to plaintiffs’ expert witnesses’ causation opinion.

None of the defendant’s expert witnesses examined Ferebee. The courts thought this was relevant, but they never articulated what would have been observed on physical examination that was important to resolving the differential diagnosis of paraquat toxicity versus IPF. There was no dispute that Ferebee had rapidly progressing pulmonary fibrosis. The expert witnesses on both sides evaluated Ferebee’s clinical data, presentation, clinical course, and arrived at different diagnoses. The plaintiffs’ expert witnesses’ diagnosis, however, involved a causal attribution to paraquat exposure.

The Ferebee case was litigated under Maryland law because federal statutory law requires state law to control in a wrongful death action arising out of the neglect or wrongful act of another on a federal enclave. 16 U.S.C. § 457. 736 F.2d at 1533. (Maryland law is actually favorable to a sophisticated intermediary defense, although the key decisions post-date Ferebee.) Chevron appears to have relied upon Maryland’s articulation of the Frye general acceptance doctrine, and the courts analyzed Chevron’s arguments as a Frye challenge. 552 F. Supp. at 1301; 736 F.2d at 1535. Although the use of Maryland law to determine an evidentiary issue seems suspect, Chevron pressed apparently pressed its challenge in terms of Maryland’s version of Frye, and not based upon Federal Rule of Evidence 702. The infamous language used by both the district and the circuit courts was, therefore, not an interpretation of federal law. Rule 702 was never cited or discussed in either the trial or the appellate court’s opinion.

My re-reading of Ferebee has softened my criticisms of state courts that had relied upon the case, even after the Supreme Court’s decision in Daubert. Softened but not eliminated my criticism — Ferebee is still a case largely confined to its facts, and the language quoted as a standard of admissibility is really a statement of the appellate standard of review for the jury’s determination of medical causation.

8. The judicial resolution of Chevron’s Frye challenge

The district court insightfully recognized that Chevron was demanding a level of evidence, which had never been required to establish paraquat’s generally accepted ability to cause pulmonary fibrosis. This recognition led to the district court’s colorful language:

“It is true that medical expert testimony must be grounded in proper scientific methodology, but the extremely stringent standard that defendant suggests is beyond reason. Product liability law, especially as it relates to relatively new products or those with a relatively rare yet significant danger, would be rendered next to meaningless if a plaintiff could prove he was injured by a product only after a ‘statistically significant’ number of other people were also injured. A civilized legal system does not require that much human sacrifice before it can intervene. The fact that this is the first case of this exact type-or at least the first of its exact type in which the involvement of paraquat was discovered by alert doctors — cannot be enough by itself to shield defendant from liability. Defendant’s experts were not able to fault Dr. Crystal for his basic diagnostic methodology; in fact, they used the same kinds of test results, consultations, and other tools that he did. What they disagreed with chiefly were his conclusions.”

552 F. Supp. at 1301. The important observation is that general causation had been established case series and reports of human exposure. There never was statistical evidence that had been evaluated for “significance,” to establish general causation for undiluted paraquat, and the trial court refused, under Maryland law, to require such evidence for general causation for diluted paraquat. In this context, we can see that the trial court’s suggestion that statistical significance was not required has little bearing upon, cases in which general causation could only be established using epidemiologic evidence, with its attendant statistical inferences.

Of course, the matter only became worse when Chevron persisted in its argument and presented it to a liberal panel of the D.C. Circuit. (Judge Mikva wrote the opinion for a panel that included Judge Wald, and Senior Judge Bazelon.) The panel’s decision ratcheted up the rhetoric:

“Thus, a cause-effect relationship need not be clearly established by animal or epidemiological studies before a doctor can testify that, in his opinion, such a relationship exists. As long as the basic methodology employed to reach such a conclusion is sound, such as use of tissue samples, standard tests, and patient examination, product liability does not preclude recovery until a ‘statistically significant’ number of people have been injured or until science has had the time and resources to complete sophisticated laboratory studies of the chemical. In a courtroom, the test for allowing a plaintiff to recover is not scientific certainty, but legal sufficiency; if reasonable jurors could conclude from the expert testimony that paraquat more likely than not caused Ferebee’s injury, the fact that another jury might reach the opposite conclusion or that science would require more evidence before conclusively considering the causation question resolved is irrelevant. That Ferebee’s case may have been the first of its exact type, or that his doctors may have been the first alert enough to recognize such a case, does not mean that the testimony of those doctors, who are concededly well qualified in their fields, should not have been admitted.”

736 F.2d at 1535-36 (emphasis in original).

Again, the dismissive attitude towards statistically significant evidence is limited to the context of a causal analysis that had been made, to everyone’s satisfaction, for undiluted paraquat, without the need for epidemiologic, statistical evidence. Statistical significance was never at issue. In this way, Ferebee resembles the untoward language on statistical significance from Matrixx Initiatives Inc. v. Siracusano. In both cases, statistical significance was never really at issue. In Ferebee, there was no statistical evidence needed or used to reach causal conclusions about paraquat’s ability to induce pulmonary fibrosis. In Matrixx Initiatives, allegations of statistical significance and causation were not necessary because the plaintiffs needed only to allege materiality of the facts suppressed by the company in order to plead a securities fraud case. Materiality could be established without causation, and thus neither causation nor statistical significance needed to be alleged.

As for Chevron’s Frye challenge, the district court rejected the implied call for a vote on the general acceptance of Dr. Crystal’s reasoning. Frye may require “vote counting” of some sort, but the process becomes irrelevant when virtually no one has registered to vote. Otherwise, the defense and the plaintiffs’ expert witnesses appeared to be using the same technique of arguing by analogy to accepted cases of paraquat poisoning or IPF. Dr. Crystal opined that Ferebee’s case was “similar” to three other cases he had identified. Dr. Carrington argued that Ferebee’s case was more like IPF cases, although IPF cases themselves have some clinical heterogeneity as well. Paraquat cases described onset to death as a very rapid process. Ferebee did not present with significant symptoms for three years after his first exposure, and then he survived for another two plus years. Ferebee did not report skin lesions, which had been reported in previous cases of dermal exposure leading up to pulmonary fibrosis. The case presented, on the diagnostic level, a difficult call, but it is easy to see the courts’ impatience with the defendant’s insistence upon more stringent criteria and evidence than was used to establish the causal connection with undiluted paraquat.

9. Expert witness qualifications.

Chevron never challenged Dr. Yusuf’s or Dr. Crystal’s qualifications. The oft-quoted comments about expert witness qualifications were made in the context of describing the appellate court’s standard of review, and the court’s role in not assessing credibility or weighing the evidence:

“These admonitions apply with special force in the context of the present action, in which an admittedly dangerous chemical is alleged through long-term exposure to have caused disease. Judges, both trial and appellate, have no special competence to resolve the complex and refractory causal issues raised by the attempt to link low-level exposure to toxic chemicals with human disease. On questions such as these, 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.”

736 F.2d at 1534.

This procedural posture is obviously very different from the initial determination of admissibility. As far as credentials are concerned, Drs. Yusuf and Crystal were hardly “hired guns”; both physicians were well qualified. Dr. Crystal had outstanding qualifications, and Chevron wisely never challenged them. Remarkably, this language has been mistakenly invoked as a standard for trial courts to use in determining the admissibility of expert witness opinion testimony. It is no such thing.

10. Preemption and Warnings Causation.

Ultimately, Chevron’s preemption defense was rejected by both the district and the circuit court. FIFRA preemption has had its ups and downs; no surprise there. More interesting is the emphasis that both courts gave to the important role of the employer in the case. The evidence overwhelming showed that Ferebee had never read the warning label, and thus the element of proximate causation between allegedly inadequate warning and harm was in jeopardy of going unproved. The courts, however, emphasized the role that the employer, through its supervisors and responsible co-workers, play in the complex organizational situation of a modern workplace:

“Mr. Ferebee’s situation was quite different, however. He did not purchase paraquat for his personal use; rather, it was provided to him by his employer for use on the job. The evidence showed that his principal source of information about paraquat was the oral instructions of his supervisors and co-workers, not the written label. He learned from them how to mix the product and how to spray it. It was also from this source that he learned of the danger of getting the product in his mouth: one of his co-workers warned him that if he accidently swallowed paraquat, it would ‘get in his blood’ and poison him. This is a common pattern of instruction and use of occupational materials in the workplace. Learning by doing and learning by oral instruction are tried and true methods of educating manual workers in their jobs. Therefore, although it is crucial to plaintiff’s case that someone would have read the label, it was not necessary for Mr. Ferebee to have done so. And it is obvious that one or more employees at BARC did read the label, since information did reach Mr. Ferebee about the proportions for diluting the product and about the dangers about which the label did warn. It was appropriate for the jury to infer that a warning about the danger of fatal lung disease from dermal exposure would also have been communicated to Mr. Ferebee. See Restatement (Second) of Torts § 388 comment n (seller normally entitled to assume that adequate warning will be passed on by purchaser to ultimate user); cf. Chambers v. G.D. Searle & Co., 441 F.Supp. at 381 (in product liability case involving prescription drug, relevant warning is the one given to doctor, not patient).”

552 F. Supp. at 1303-04 (internal citations omitted). So here we have Ferebee, the subject of so much derision and aspersion from defense counsel, embracing the Section 388, comment n, as well as applying learned intermediary principles to a case not involving prescription drugs. The appellate court was waxed enthusiastic about the principles of Section 388, and went so far as to cite Victor Schwartz in support:

“We live in an organizational society in which traditional common-law limitations on an actor’s duty must give way to the realities of society. *** In this case, Mr. Ferebee did not purchase the paraquat for his personal use, and there was substantial evidence that workplace communication about the dangers associated with various chemicals usually took the form of oral instructions from supervisors to workers, the latter of whom then retransmitted the information to co-workers. This, rather than individual reading of product warnings, is a typical method by which information is disseminated in the modern workplace. See Schwartz & Driver, “Warnings in the Workplace: The Need for a Synthesis of Law and Communication Theory,” 52 U. Cinn. L. Rev. 38, 66-83 (1983). The requirement that an improper warning proximately ‘cause’ the injury should be elaborated against this background. We believe Maryland would construe its tort law in this case to require only that someone in the workplace have read the label, not that Mr. Ferebee personally have read it. Because there is no dispute that one or more employees at BARC did read the label, we hold that the jury could properly have inferred that, had a warning about the danger of disease from dermal exposure been included on the label, that warning would have been communicated to Mr. Ferebee and that he would as a result have acted differently. Alternatively, the jury could have inferred that an adequate warning would have led Ferebee’s employers to undertake steps that would have protected him from paraquat poisoning-for example, provision of showers for use after spraying.”

736 F.2d at 1539 (emphasis in original; internal citation omitted). Judge Mikva’s prediction, of course, was absolutely accurate; Maryland tort law did, soon thereafter, embrace the sophisticated intermediary defense to exculpate the defendant in such remote supplier situations. See, e.g., Kennedy v. Mobay Corp., 84 Md. App. 397 (1990) (applying sophisticated user defense to bar claims against manufacturers of toluene diisocyanate), aff’d, 325 Md. 385 (1992); Higgins v. E.I. DuPont de Nemours, Inc., 671 F. Supp. 1055 (D. Md. 1987) (Maryland law; holding that manufacturer of paint was in better position than bulk supplier to communicate warnings to customers’ employees), aff’d, 863 F.2d 1162 (4th Cir. 1988). The principle invoked to excuse plaintiff from reading the warning label also works to exculpate the defendant when that warning label is otherwise adequate, or when the intermediary knows of the hazard in any event.

Posted in Causation, Rule 702, Scientific Evidence, statistical evidence | Comments Off on Ferebee Revisited

Some High-Value Targets for Sander Greenland in 2018

December 27th, 2017

A couple of years ago, Sander Greenland and I had an interesting exchange on Deborah Mayo’s website. I tweaked Sander for his practice of calling out defense expert witnesses for statistical errors, while ignoring whoopers made by plaintiffs’ expert witnesses. See “Significance Levels Made a Whipping Boy on Climate-Change Evidence: Is p < 0.05 Too Strict?” Error Statistics (Jan. 6, 2015).1 Sander acknowledged that he received a biased sample of expert reports through his service as a plaintiffs’ expert witness, but protested that defense counsel avoided him like the plague. In an effort to be helpful, I directed Sander to an example of bad statistical analysis that had been proffered by Dr Bennett Omalu, in a Dursban case, Pritchard v. Dow Agro Sciences, 705 F. Supp. 2d 471 (W.D. Pa. 2010), aff’d, 430 F. App’x 102, 104 (3d Cir. 2011).2

Sander was unimpressed with my example of Dr. Omalu; he found the example “a bit disappointing though because [Omalu] was merely a county medical examiner, and his junk analysis was duly struck. The expert I quoted in my citations was a full professor of biostatistics at a major public university, a Fellow of the American Statistical Association, a holder of large NIH grants, and his analysis (more subtle in its transgressions) was admitted” (emphasis added). Sander expressed an interest in finding “examples involving similarly well-credentialed, professionally accomplished plaintiff experts whose testimony was likewise admitted… .”

Although it was heartening to read Sander’s concurrence in the assessment of Omalu’s analysis as “junk,” Sander’s rejection of Dr. Omalu as merely a low-value target was disappointing, given that Omalu also has a master’s degree in public health, from the University of Pittsburgh, where he claims he studied with Professor Lew Kuller. Omalu has also gained some fame and notoriety for his claim to have identified the problem of chronic traumatic encephalopathy (CTE) among professional football players. After all, even Sander Greenland has not been the subject of a feature-length movie (Concussion), as has Omalu.

I lost track of our exchange in 2015, until recently I was reminded of it when reading an expert report by Professor Martin Wells. Unlike Omalu, Wells meets all the Greenland criteria for high-value targets. He is not only a full, chaired professor but also the statistics department chairman at an ivy-league school, Cornell University. Wells is a fellow of both the American Statistical Association and the Royal Statistical Society, but most important, Wells is a frequent plaintiffs’ expert witness, who is well known to Sander Greenland. Both Wells and Greenland served, side by side, as plaintiffs’ expert witnesses in the pain pump litigation.

So here is the passage in the Wells’ report that is worthy of Greenland’s attention:

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

In re Testosterone Replacement Therapy Prods. Liab. Litig., Declaration of Martin T. Wells, Ph.D., at 2-3 (N.D. Ill., Oct. 30, 2016). Unlike the Dursban litigation involving Bennett Omalu, where the “junk analysis” was excluded, in the litigation against AbbVie for its manufacture and selling of prescription testosterone supplementation, Wells’ opinions were not excluded or limited. In re Testosterone Replacement Therapy Prods. Liab. Litig., No. 14 C 1748, MDL No. 2545, 2017 WL 1833173 (N.D. Ill. May 8, 2017) (denying Rule 702 motions).

Now this statement by Wells surely offends the guidance provided by Greenland and colleagues.3 And it was exactly the sort of misrepresentation that led to a confabulation of the American Statistical Association, and that Association’s consensus statement on statistical significance.4

And here is another example, which occurs not in a distorting litigation forum, but on the pages of an occupational health journal, where the editor in chief, Anthony L. Kiorpes, ranted about the need for better statistical editing and writing in his own journal. See Anthony L Kiorpes, “Lies, damned lies, and statistics,” 33 Toxicol. & Indus. Health 885 (2017). Kiorpes decried he misuse of statistics:

“I am not implying that it is the intent of the scientists who publish in these pages to mislead readers by their use of statistics, but I submit that the misuse of statistics, whether intentional or otherwise, creates confusion and error.”

Id. at 885. Kiorpes then proceeded to hold himself up as Exhibit A to his screed:

“Remember that p values are estimates of the probability that the null hypothesis (no difference) is true.”

Id. Uggh; we seem to be back sliding after the American Statistical Association’s consensus statement.

“Almost all scientists have stated (or have been tempted to state) something like ‘the mean of Group A was greater than that of Group B, but the difference was not statistically significant’. With very few exceptions (which I will mention below), this statement is nonsense.”

* * * * *

“What the statistics are indicating when the p-value is greater than 0.05 is that there is ‘no difference’ between group A and group B.”

Id. at 886.

Let’s hope that this gets Sander Greenland away from his biased sampling of expert witnesses, off the backs of defense expert witnesses, and on to some of the real culprits out there, in the new year.

1 See also “Sander Greenland on ‘The Need for Critical Appraisal of Expert Witnesses in Epidemiology and Statistics’” (Feb. 8, 2015).

2 See also “Pritchard v. Dow Agro – Gatekeeping Exemplified” (Aug. 25, 2014); “Omalu and Science — A Bad Weld” (Oct. 22, 2016); Brian v. Association of Independent Oil Distributors, No. 2011-3413, Westmoreland Cty. Ct. Common Pleas, Order of July 18, 2016 (excluding Dr. Omalu’s testimony on welding and solvents and Parkinson’s disease).

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

4 Ronald L. Wasserstein & Nicole A. Lazar, “American Statistical Association Statement on statistical significance and p values,” 70 Am. Statistician 129 (2016)

Posted in Cognitive Biases, Conflicts of Interest, Expert Witnesses, Rule 702, statistical evidence | Comments Off on Some High-Value Targets for Sander Greenland in 2018

Gatekeeping of Expert Witnesses Needs a Bair Hug

December 20th, 2017

For every Rule 702 (“Daubert”) success story, there are multiple gatekeeping failures. See David E. Bernstein, “The Misbegotten Judicial Resistance to the Daubert Revolution,” 89 Notre Dame L. Rev. 27 (2013).1 Exemplars of inadequate expert witness gatekeeping in state or federal court abound, and overwhelm the bar. The only solace one might find is that the abuse-of-discretion appellate standard of review keeps the bad decisions from precedentially outlawing the good ones.

Judge Joan Ericksen recently provided another Berenstain Bears’ example of how not to keep the expert witness gate, in litigation claims that the Bair Hugger forced air warming devices (“Bair Huggers”) cause infections. In re Bair Hugger Forced Air Warming, MDL No. 15-2666, 2017 WL 6397721 (D. Minn. Dec. 13, 2017). Although Her Honor properly cited and quoted Rule 702 (2000), a new standard is announced in a bold heading:

“Under Federal Rule of Evidence 702, the Court need only exclude expert testimony that is so fundamentally unsupported that it can offer no assistance to the jury.”

Id. at *1. This new standard thus permits largely unsupported opinion that can offer bad assistance to the jury. As Judge Ericksen demonstrates, this new standard, which has no warrant in the statutory text of Rule 702 or its advisory committee notes, allows expert witnesses to rely upon studies that have serious internal and external validity flaws.

Jonathan Samet, a specialist in pulmonary medicine, not infectious disease or statistics, is one of the plaintiffs’ principal expert witnesses. Samet relies in large measure upon an observational study2, which purports to find an increased odds ratio for use of the Bair Hugger among infection cases in one particular hospital. The defense epidemiologist, Jonathan B. Borak, criticized the McGovern observational study on several grounds, including that the study was highly confounded by the presence of other known infection risks. Id. at *6. Judge Ericksen characterized Borak’s opinion as an assertion that the McGovern study was an “insufficient basis” for the plaintiffs’ claims. A fair reading of even Judge Ericksen’s précis of Borak’s proffered testimony requires the conclusion that Borak’s opinion was that the McGovern study was invalid because of data collection errors and confounding. Id.

Judge Ericksen’s judicial assessment, taken from the disagreement between Samet and Borak, is that there are issues with the McGovern study, which go to “weight of the evidence.” This finding obscures, however, that there were strong challenges to the internal and external validity of the study. Drawing causal inferences from an invalid observational study is a methodological issue, not a weight-of-the-evidence problem for the jury to resolve. This MDL opinion never addresses the Rule 703 issue, whether an epidemiologic expert would reasonably rely upon such a confounded study.

The defense proffered the opinion of Theodore R. Holford, who criticized Dr. Samet for drawing causal inferences from the McGovern observational study. Holford, a professor of biostatistics at Yale University’s School of Public Health, analyzed the raw data behind the McGovern study. Id. at *8. The plaintiffs challenged Holford’s opinions on the ground that he relied on data in “non-final” form, from a temporally expanded dataset. Even more intriguingly, given that the plaintiffs did not present a statistician expert witness, plaintiffs argued that Holford’s opinions should be excluded because

(1) he insufficiently justified his use of a statistical test, and

(2) he “emphasizes statistical significance more than he would in his professional work.”

Id.

The MDL court dismissed the plaintiffs’ challenge on the mistaken conclusion that the alleged “contradictions between Holford’s practice and his testimony impugn his credibility at most.” If there were truly such a deviation from the statistical standard of care, the issue is methodological, not a credibility issue of whether Holford was telling the truth. And as for the alleged over-emphasis on statistical significance, the MDL court again falls back to the glib conclusions that the allegation goes to the weight, not the admissibility of expert witness opinion testimony, and that plaintiffs can elicit testimony from Dr Samet as to how and why Professor Holford over-emphasized statistical significance. Id. Inquiring minds, at the bar, and in the academy, are left with no information about what the real issues are in the case.

Generally, both sides’ challenges to expert witnesses were denied.3 The real losers, however, were the scientific and medical communities, bench, bar, and general public. The MDL court glibly and incorrectly treated methodological issues as “credibility” issues, confused sufficiency with validity, and banished methodological failures to consideration by the trier of fact for “weight.” Confounding was mistreated as simply a debating point between the parties’ expert witnesses. The reader of Judge Ericksen’s opinion never learns what statistical test was used by Professor Holford, what justification was needed but allegedly absent for the test, why the justification was contested, and what other test was alleged by plaintiffs to have been a “better” statistical test. As for the emphasis given statistical significance, the reader is left in the dark about exactly what that emphasis was, and how it led to Holford’s conclusions and opinions, and what the proper emphasis should have been.

Eventually appellate review of the Bair Hugger MDL decision must turn on whether the district court abused its discretion. Although appellate courts give trial judges discretion to resolve Rule 702 issues, the appellate courts cannot reach reasoned decisions when the inferior courts fail to give even a cursory description of what the issues were, and how and why they were resolved as they were.

2 P. D. McGovern, M. Albrecht, K. G. Belani, C. Nachtsheim, P. F. Partington, I. Carluke, and M. R. Reed, “Forced-Air Warming and Ultra-Clean Ventilation Do Not Mix: An Investigation of Theatre Ventilation, Patient Warming and Joint Replacement Infection in Orthopaedics,” 93 J. Bone Joint 1537 (2011). The article as published contains no disclosures of potential or actual conflicts of interest. A persistent rumor has it that the investigators were funded by a commercial rival to the manufacturer of the Bair Hugger at issue in Judge Ericksen’s MDL. See generally, Melissa D. Kellam, Loraine S. Dieckmann, and Paul N. Austin, “Forced-Air Warming Devices and the Risk of Surgical Site Infections,” 98 Ass’n periOperative Registered Nurses (AORN) J. 354 (2013).

3 A challenge to plaintiffs’ expert witness Yadin David was sustained to the extent he sought to offer opinions about the defendant’s state of mind. Id. at *5.

Posted in Causation, Conflicts of Interest, Data Sharing, Rule 702, Rule 703, Scientific Evidence, Underlying Data | Comments Off on Gatekeeping of Expert Witnesses Needs a Bair Hug

Stuck in Silicone

December 12th, 2017

There was a time when silicone chemistry, biocompatibility, toxicity, and litigation weighed upon my mind. What started with a flurry of scientific interest, led to a media free for all, then FDA Commissioner David Kessler’s moratorium on silicone breast implants, and then to a feeding frenzy for the lawsuit industry. Ultimately, the federal court system found its way to engage four non-party expert witnesses, who cut through the thousands of irrelevant documents that plaintiffs’ counsel used to obfuscate the lack of causation evidence. The court-appointed experts in MDL 926 were unanimous in their rejection of the plaintiffs’ claims.1 Not long after, the Institute of Medicine (now the National Academy of Medicine) issued its voluminous review of the scientific evidence, again with the conclusion that the evidence, when viewed scientifically and critically, showed a lack of association between silicone and autoimmune disease.2

Along the way to this definitive end of the lawsuit industry’s assault on the medical device industry, the parties assembled in the courtroom of the Hon. Jack B. Weinstein, for Rule 702 hearings on the opinions proffered by the plaintiffs’ expert witnesses. Judge Weinstein, along with the late Judge Harold Baer, of the Southern District of New York, and Justice Lobis, of the New York Supreme Court, held hearings that lasted two weeks, and entertained virtually unlimited argument. In characteristic style, Judge Weinstein did not grant the defendants’ Rule 702 motions; rather he cut right to the heart of the matter, and granted summary judgment in favor of the defense on plaintiffs’ claims of systemic diseases.3

Over a dozen years later, in reflecting upon a long judicial career that involved many so-called mass torts, Judge Weinstein described the plaintiffs’ expert witnesses more plainly as “charlatans” and the silicone litigation as largely based upon fraud.4

****************************

Last week, I received an email from Arthur E. Brawer, who represented himself to be an Associate Clinical Professor of Medicine.5 Dr. Brawer kindly forwarded some of his publications on the subject of silicone toxicity.6 Along with the holiday gift, Dr Brawer also gave me a piece of his mind:

“I recommend you rethink your prior opinions on the intersection of science and the law as it relates to this issue, as you clearly have no idea what you are talking about regarding the matter of silicone gel-filled breast implants. Perhaps refresher courses in biochemistry and biophysics at a major university might wake you up.”

Wow, that woke me up! Who was this Dr Brawer? His name seemed vaguely familiar. I thought he might have been a lawsuit industry expert witness I encountered in the silicone litigation, but none of his articles had a disclosure of having been a retained expert witness. Perhaps that was a mere oversight on his part. Still, I went to my archives, where I found the same Dr Brawer engaged in testifying for plaintiffs all around the country. In one early testimonial adventure, Brawer described how he came up with his list of signs and symptoms to use to define “silicone toxicity”:

Q. Doctor, if a patient presented to you with green hair and claimed that her green hair was attributable to her silicone breast implants, unless you could find another explanation for that green hair, you’d put that on your list of signs and symptoms; right?

A. The answer is yes.

Notes of Testimony of Arthur E. Brawer, at 465:7-12, in Merlin v. 3M Co., No. CV-N-95-696-HDM (D. Nev.Dec. 11, 1995) (Transcript of Rule 702 hearing)

A year later, Brawer’s opinions were unceremoniously excluded in a case set for trial in Dallas, Texas.7 Surely this outcome, along with Judge Weinstein’s rulings, the findings of the court-appointed witnesses in MDL 926, and the conclusions of the Institute of Medicine would have discouraged this Brawer fellow from testifying ever again?

Apparently not. Brawer, like the Black Knight in Monty Python and the Holy Grail, still lives and breathes, but only to be cut again and again. A quick Westlaw search turned up another, recent Brawer testimonial misadventure in Laux v. Mentor Worldwide, LLC, case no. 2:16-cv-01026, 2017 WL 5235619 (C.D. Calif., Nov. 8, 2017).8 Plaintiff Anita Laux claimed that she developed debilitating “biotoxin” disease from her saline-filled silicone breast implants. In support, she proffered the opinions of three would-be expert witnesses, a plastic surgeon (Dr Susan Kolb), a chemist (Pierre Blais), and a rheumatologist (Arthur Brawer).

Plaintiffs’ theory of biotoxin disease causation started with Blais’ claim to have found mold debris in the plaintiff’s explanted implants. The court found Blais unqualified, however, to offer an opinion on microbiology or product defects, and his opinions in the case, unreliable. Id. at *4-6. Dr Kolb, the author of The Naked Truth about Breast Implants, attempted to build upon Blais’ opinions, a rather weak foundation, to construct a “differential diagnosis.” In reasoning that Ms. Laux’s medical complaints arose from a mold infection, Kolb asserted that she had ruled out all other sources of exposure to mold. Unfortunately, Kolb either forgot or chose to hide correspondence with Ms. Laux, in which the plaintiff directly provided Kolb with information about prior environmental mold exposure on multiple occasions. Id. at *3. The trial court severely deprecated Kolb’s rather selective and false use of facts used to make the attribution of Ms. Laux’s claimed medical problems.

Dr Brawer, the author of Holistic Harmony: A Guide To Choosing A Competent Alternative Medicine Provider (1999), and my recent email correspondent, also succumbed to Judge Wright’s gatekeeping in Laux. The court found that Brawer had given a toxicology opinion with no supporting data. His report was thus both procedurally deficient under Federal Rule of Civil Procedure 26, and substantively deficient under Federal Rule of Evidence 702. Finding Brawer’s report “so lacking of scientific principles and methods,” and thus unhelpful and unreliable, the trial court excluded his report and precluded his testimony at trial. Id. at *7.

Thankfully, the ghost of litigations past, communicating now by email, can be safely disregarded. And I do not have to dig my silicone polymer chemistry and biochemistry textbooks out of storage.

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

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

3 See In re Breast Implant Cases, 942 F. Supp. 958 (E. & S.D.N.Y. 1996) (granting summary judgment because of insufficiency of plaintiffs’ evidence, but specifically declining to rule on defendants’ Rule 702 and Rule 703 motions).

5 At the Drexel University School of Medicine, in Philadelphia, as well as the Director of Rheumatology at Monmouth Medical Center, in Long Branch, New Jersey.

6 Included among the holiday gift package was Arthur E. Brawer, “Is Silicone Breast Implant Toxicity an Extreme Form of a More Generalized Toxicity Adversely Affecting the Population as a Whole?,”1 Internat’l Ann. Med. (2017); Arthur E. Brawer, “Mechanisms of Breast Implant Toxicity: Will the Real Ringmaster Please Stand Up,”1 Internat’l Ann. Med. (2017); Arthur E. Brawer, “Destiny rides again: the reappearance of silicone gel-filled breast implant toxicity,” 26 Lupus 1060 (2017); Arthur E. Brawer, “Silicon and matrix macromolecules: new research opportunities for old diseases from analysis of potential mechanisms of breast implant toxicity,” 51 Medical Hypotheses 27 (1998).

7 Bailey v. Dow Corning Corp., c.a. 94-1199-A (Dallas Cty. Texas Dist. Ct., Sept. 15, 1996).

8 I later found that another blog had reviewed the Laux decision. Stephen McConnell, “C.D. Cal. Excludes Three Plaintiff Experts in Breast Implant Case,” Drug & Device Law (Nov. 16, 2017).

Posted in Causation, Conflicts of Interest, Expert Witness Hall of Shame, Rule 702, Scientific Evidence, Scientific Misconduct | Comments Off on Stuck in Silicone

Manufacturing Consent

December 2nd, 2017

David Michaels along with other “political” scientists, and the lawsuit industry, have worked assiduously over the last several decades to delegitimize discussion, debate, and controversy over scientific claims.1 Their key goals have been to attempt to disqualify manufacturing industry and any scientist with the slightest manufacturing industry contact. Their attempts to disqualify other interlocutors is, however, highly asymmetrical. If those with connections to manufacturing industry criticize studies or causal conclusions, then we hear that the criticism is corrupt. If those with connections to manufacturing industry embrace studies that show favored associations, or causal conclusions, then we hear that the embrace of advocacy positions was an “admission,” reluctantly given but “forced” by overwhelming evidence. In other words, the attempts to disqualify interlocutors are made only when the speakers articulate criticism of the claims of advocacy science.

David Zaruk has argued that the techniques used to squelch criticism of advocacy science bear an uncanny resemblance to the techniques used by fascists generally. See David Zaruk, “Ten Practices Linking Environmentalism with Fascism,” Riskmonger (Dec. 2, 2017). Although Zaruk’s argument may appear hyperbolic, there is no denying that advocacy scientists (not merely in the field of environmentalism) have used the rhetorical devices that are used by intellectual bullies everywhere. In the case of advocacy scientists, one of their key maneuvers has been to privilege advocacy scientists who speak for their favored positions, for the lawsuit industry, and for self-styled public interest groups by ignoring their potential conflicts of interest, while diminishing the substantive content of all “opposition” voices by pejoratively characterizing their opponents’ motivation as “manufacturing doubt.” Of course, the deepest irony is that before there was manufacturing doubt, there was manufacturing consent.2 The unkindest thing that can, and must be said, of the current enthusiasm for attacking dissident scientists is not that the attacks are fascist, but that they are unscientific.

The likes of David Michaels have sought to manufacture consent on various health effects issues, by selectively and asymmetrically accusing scientists of conflicts of interest, or trying to pervert the course of science. These attacks on “dissidents” assume the truth of the contested causal conclusions, and then proceed to call out the dissidents for casting doubt on the “truth” in favor of falsehood. What this mobbing of dissidents ignores is the basic normative structure of science, which requires doubt.

One of the first sociologists of science, Robert Merton, described four institutional imperatives of science: universality, communitarianism, disinterestedness, and “organized skepticism.”3 Scientists are committed to methodologies and an institutional ethos that require searching scrutiny of claims to scientific knowledge. The scientific advocates who would silence criticism with accusations of “manufacturing doubt” ignore the epistemic importance of dissent and disagreement in science. The prevalent attempts to squelch dissent as “manufacturing doubt” is thus unscientific and dangerous.4

1 See, e.g., David Michaels, Doubt is Their Product: How Industry’s War on Science Threatens Your Health (2008); David Michaels, “Manufactured Uncertainty: Protecting Public Health in the Age of Contested Science and Product Defense,” 1076 Ann. N.Y. Acad. Sci. 149 (2006); David Michaels, “Mercenary Epidemiology – Data Reanalysis and Reinterpretation for Sponsors with Financial Interest in the Outcome,” 16 Ann. Epidemiol. 583 (2006); David Michaels & Celeste Monforton, “Manufacturing Uncertainty: Contested Science and the Protection of the Public’s Health and Environment,” 95 Amer. J. Public Health S39 (2005); David Michaels, “Doubt is their Product,” 292 Sci. Amer. 74 (June 2005).

2 See generally Edward S. Herman & Noam Chomsky, Manufacturing Consent (1988).

3 Robert K. Merton, “The Normative Structure of Science,” in Robert K. Merton, The Sociology of Science: Theoretical and Empirical Investigations, chap. 13, at 267, 270 (1973).

4 See Inmaculada de Melo-Mmartín and Kristen Intemann, “Who’s afraid of dissent? Addressing concerns about undermining scientific consensus in public policy developments,” 22 Persp. on Science 593 (2014).

Posted in Causation, Public Nuisances, Scientific Evidence | Comments Off on Manufacturing Consent

Copywrongs in the Academic-Publishing Industrial Complex

December 1st, 2017

Works of the United States government, including works prepared by its officers and employees, do not qualify for copyright protection. 17 U.S.C. § 105. Such works are in the “public domain,” and may be freely distributed. Works in the public domain thus include academic papers written by governmental scientists and published in proprietary academic journals. The journals cannot acquire a copyright in what was in the public domain ab initio.

And yet, proprietary journals routinely charge customers for works in the public domain. There appears to be no meaningful regulation of the academic publishing world, where publishers sometimes commandeer $60 or more per article, and charge yet again for access to supplementary data and materials. Charging fees such as these for what belongs to the public is worse than ludicrous; it’s piracy! See Ryan Merkley, “You Pay to Read Research You Fund. That’s Ludicrous,” Wired (April 18, 2016).

In an era when publishers complain and sue over unauthorized distribution of articles, it is remarkable that publishers are so cavalier about their own copywrongs. Paywall Watch is a website that has set its mission to call out proprietary academic publishers for improperly charging money to distribute articles that are in the public domain. See Dalmeet Singh Chawla, “Website Flags Wrongly Paywalled Papers,” The Scientist (May 31, 2017). From a casual review of the Paywall Watch website, there appear to be many offending instances of publisher piracy.

In addition to overt copywrongs, there is the more prevalent issue raised by publishers profiteering from selling papers based upon federally funded research. Federal regulations and Executive Orders direct federal agencies to ensure that taxpayers do not pay twice for federally funded research, even research conducted by non-governmental employees. See “Expanding Public Access to the Results of Federally Funded Research,” (Feb. 22, 2013); Office of Science and Technology Policy, “Memorandum on Public Access” (2013). Despite President Obama’s support, powerful congressional patrons of the Academic-Publishing complex, from both sides of the aisle, have shilled for protectionist legislation. See “Beware the Academic-Publishing Complex!” (Jan. 11, 2012) (discussing Congresswoman Carolyn Maloney’s efforts to press special interest legislation for Elsevier). Compliance with the federal open-access mandate is poor.

* * * * * * *

A group of authors, led by scientists from Divisions of the National Institute for Occupational Safety and Health, in Cincinnati, Ohio, recently published an epidemiologic study of cancer outcomes in workers exposed to polychlorinated biphenyls (PCBs). Avima M. Ruder, Misty J. Hein, Nancy B. Hopf, and Martha A. Waters, “Cancer incidence among capacitor manufacturing workers exposed to polychlorinated biphenyls,” 60 Am. J. Indus. Med. 198 (2017) [cited below as Ruder]. The NIOSH authors published their study in the “Red Journal,” the American Journal of Industrial Medicine, edited by Steven B. Markowitz and Rodney Ehrlich, who are well-known in lawsuit industry circles.

Ruder’s article contained a clear disclaimer:

“This article is a U.S. Government work and is in the public domain in the USA.”

Ruder’s publisher, John Wiley & Sons, blithely ignored the disclaimer and hid the article behind a paywall (at the relatively low, one-time price of $38.00, U.S.). And that is too bad because Ruder’s work has generally shown that there is not much to the claim that PCBs cause lung cancer, a claim that caused quite a stir in the United States Supreme Court, twenty years ago. See General Electric Co. v. Joiner, 522 U.S. 136 (1997). Ruder and colleagues found a slightly raised incidence of lung cancer, risk ratio 1.16, but they readily acknowledged that without smoking history data, this small risk could not be interpreted causally. Ruder at 205 (2017); see also Avima M. Ruder, Misty J. Hein, Nancy B. Hopf, and Martha A. Waters, “Mortality among 24,865 workers exposed to polychlorinated biphenyls (PCBs) in three electrical capacitor manufacturing plants: A ten-year update,”217 Internat’l J. Hyg. & Envt’l Health 176 (2014). In a previous analysis of lung cancer mortality in the full cohort, the elevation had disappeared when short-term workers (fewer than 90 days on the job) were removed from the analysis. The long-term workers, with obviously much greater potential for cumulative and peak exposures, showed a lung cancer standardized mortality ratio of 0.99, ever so slightly less lung cancer than expected among non-exposed workers. Ruder at 205. See “How Have Important Rule 702 Holdings Held Up With Time?” (Mar. 20, 2015); “The Joiner Finale.”

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