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First Amendment Rights of the Litigation Industry

December 21st, 2014

When a Wall Street Journal opinion piece stated that “the plaintiffs bar is all but running the Senate[1],” Frederick Martin (“Fred”) Baron, former president of the litigation industry’s Association of Trial Lawyers of America (ATLA), reportedly quipped that “I really, strongly disagree with that. Particularly the ‘all but’.” Baron, affectionately known as “Robber Baron” for his aggressive advocacy for uninjured asbestos claimants and questionable deposition coaching tactics, was the ultimate Democratic party insider. He was the finance chair of John Edwards’ ill-fated presidential campaign, and the sugar daddy for Rielle Hunter, the mother of Edwards’ out-of-wedlock child. You cannot get more “inside” than that.

Robber Baron died in 2008, but his legacy is a reminder of the hypocrisy of those who decry the Citizens United[2] opinion, which held that corporations and unions have first amendment rights to speak in ways that might influence the outcomes of elections. While many fuss over “corporate” speech, the litigation industry has operated largely without constraint. Last year, for example, plaintiffs’ counsel, Edward F. Blizzard, and representatives of the litigation industry’s ATLA, now operating under the self-serving name, American Association for Justice (AAJ), met with Food and Drug Administration officials to influence agency policy on generic medication warnings. This week, the Times featured front-page coverage of how the litigation industry has co-opted the policies and agendas of the States’ attorneys general, and directed their targeting of corporations. See Eric Lipton, “Lawyers Create Big Paydays by Coaxing Attorneys General to Sue,” New York Times (Dec. 18, 2014).

The litigation industry makes its presence felt in many ways, sometimes as an omnipresent threat that influences business and professional judgments. President Obama criticized Sony’s decision to pull down The Interview, as an undue concession to terrorists. See “Sony’s Decision to Pull Movie Is a ‘Mistake,’ Obama Says.” Obama went so far as to express his wish that “they’d spoken to me first.” But would Obama, or anyone, have been able to control the litigation industry’s second-guessing of Sony’s or any individual theater owner’s decision to show the movie?

Lipton’s article is a vivid reminder that the plaintiffs’ trial bar remains the largest rent-seeking lobby in the United States.

[1] John Fund, “Have You Registered to Sue?” Wall Street Journal (Nov. 6, 2002).

[2] Citizens United v. Federal Election Comm’n, 558 U.S. 310 (2010).

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Showing Causation in the Absence of Controlled Studies

December 17th, 2014

The Federal Judicial Center’s Reference Manual on Scientific Evidence has avoided any clear, consistent guidance on the issue of case reports. The Second Edition waffled:

“Case reports lack controls and thus do not provide as much information as controlled epidemiological studies do. However, case reports are often all that is available on a particular subject because they usually do not require substantial, if any, funding to accomplish, and human exposure may be rare and difficult to study. Causal attribution based on case studies must be regarded with caution. However, such studies may be carefully considered in light of other information available, including toxicological data.”

F.J.C. Reference Manual on Scientific Evidence at 474-75 (2d ed. 2000). Note the complete lack of discussion of base-line risk, prevalence of exposure, and external validity of the “toxicological data.”

The second edition’s more analytically acute and rigorous chapter on statistics generally acknowledged the unreliability of anecdotal evidence of causation. See David Kaye & David Freedman, “Reference Guide on Statistics,” in F.J.C. Reference Manual on Scientific Evidence 91 – 92 (2d ed. 2000).

The Third Edition of the Reference Manual is even less coherent. Professor Berger’s introductory chapter[1] begrudgingly acknowledges, without approval, that:

“[s]ome courts have explicitly stated that certain types of evidence proffered to prove causation have no probative value and therefore cannot be reliable.59”

The chapter on statistical evidence, which had been relatively clear in the second edition, now states that controlled studies may be better but case reports can be helpful:

“When causation is the issue, anecdotal evidence can be brought to bear. So can observational studies or controlled experiments. Anecdotal reports may be of value, but they are ordinarily more helpful in generating lines of inquiry than in proving causation.14”

Reference Manual at 217 (3d ed. 2011). The “generally” is given no context or contour for readers. These authors fail to provide any guidance on what will come from anecdotal evidence, or when and why anecdotal reports may do more than merely generating “lines of inquiry.”

In Matrixx Initiatives Inc. v. Siracusano, 131 S. Ct. 1309 (2011), the Supreme Court went out of its way, way out of its way, to suggest that statistical significance was not always necessary to support conclusions of causation in medicine. Id. at 1319. The Court cited three Circuit court decisions to support its suggestion, but two of three involved specific causation inferences from so-called differential etiologies. General causation was assumed in those two cases, and not at issue[2]. The third case, the notorious Wells v. Ortho Pharmaceutical Corp., 788 F. 2d 741, 744–745 (11th Cir. 1986), was also cited in support of the suggestion that statistical significance was not necessary, but in Wells, the plaintiffs’ expert witnesses actually relied upon studies that claimed at least nominal statistical significance. Wells was and remains representative of what is possible and results when trial judges ignore the constraints of study validity. The Supreme Court, in any event, abjured any intent to specify “whether the expert testimony was properly admitted in those cases [Wells and others],” and the Court made no “attempt to define here what constitutes reliable evidence of causation.” 131 S. Ct. at 1319.

The causal claim in Siracusano involved anosmia, loss of the sense of smell, from the use of Zicam, zinc gluconate. The case arose from a motion to dismiss the complaint; no evidence was ever presented or admitted. No baseline risk of anosmia was pleaded; nor did plaintiffs allege that any controlled study demonstrated an increased risk of anosmia from nasal instillation of zinc gluconate. There were, however, clinical trials conducted in the 1930s, with zinc sulfate for poliomyelitis prophylaxis, which showed a substantial incidence of anosmia in the treated children[3]. Matrixx tried to argue that this evidence was unreliable, in part because it involved a different compound, but this argument (1) in turn demonstrated a factual issue that required discovery and perhaps a trial, and (2) traded on a clear error in asserting that the zinc in zinc sulfate and zinc gluconate were different, when in fact they are both ionic compounds that result in zinc ion exposure, as the active constituent.

The position stridently staked out in Matrixx Initiatives is not uncommon among defense counsel in tort cases. Certainly, similar, unqualified statements, rejecting the use of case reports for supporting causal conclusions, can be found in the medical literature[4].

When the disease outcome has an expected value, a baseline rate, in the exposed population, then case reports simply confirm what we already know: cases of the disease happen in people regardless of their exposure status. For this reason, medical societies, such as the Teratology Society, have issued guidances that generally downplay or dismiss the role that case reports may have in the assessment and determination of causality for birth defects:

“5. A single case report by itself is not evidence of a causal relationship between an exposure and an outcome.  Combinations of both exposures and adverse developmental outcomes frequently occur by chance. Common exposures and developmental abnormalities often occur together when there is no causal link at all. Multiple case reports may be appropriate as evidence of causation if the exposures and outcomes are both well-defined and low in incidence in the general population. The use of multiple case reports as evidence of causation is analogous to the use of historical population controls: the co-occurrence of thalidomide ingestion in pregnancy and phocomelia in the offspring was evidence of causation because both thalidomide use and phocomelia were highly unusual in the population prior to the period of interest. Given how common exposures may be, and how common adverse pregnancy outcome is, reliance on multiple case reports as the sole evidence for causation is unsatisfactory.”

The Public Affairs Committee of the Teratology Society, “Teratology Society Public Affairs Committee Position Paper Causation in Teratology-Related Litigation,” 73 Birth Defects Research (Part A) 421, 423 (2005).

When the base rate for the outcome is near zero, and other circumstantial evidence is present, some commentators insist that causality may be inferred from well-documented case reports:

“However, we propose that some adverse drug reactions are so convincing, even without traditional chronological causal criteria such as challenge tests, that a well documented anecdotal report can provide convincing evidence of a causal association and further verification is not needed.”

Jeffrey K. Aronson & Manfred Hauben, “Drug safety: Anecdotes that provide definitive evidence,” 333 Brit. Med. J. 1267, 1267 (2006) (Dr. Hauben was medical director of risk management strategy for Pfizer, in New York, at the time of publication). But which ones are convincing, and why?

        *        *        *        *        *        *        *        *        *

Dr. David Schwartz, in a recent blog post, picked up on some of my discussion of the gadolinium case reports (see here and there), and posited the ultimate question: when are case reports sufficient to show causation? David Schwartz, “8 Examples of Causal Inference Without Data from Controlled Studies” (Dec. 14, 2014).

Dr. Schwartz discusses several causal claims, all of which gave rise to litigation at some point, in which case reports or case series played an important, if not dispositive, role:

  1.      Gadolinium-based contrast agents and NSF
  2.      Amphibole asbestos and malignant mesothelioma
  3.      Ionizing radiation and multiple cancers
  4.      Thalidomide and teratogenicity
  5.      Rezulin and acute liver failure
  6.      DES and clear cell vaginal adenocarcinoma
  7.      Vinyl chloride and angiosarcoma
  8.      Manganese exposure and manganism

Dr. Schwartz’s discussion is well worth reading in its entirety, but I wanted to emphasize some of Dr. Schwartz’s caveats. Most of the exposures are rare, as are the outcomes. In some cases, the outcomes occur almost exclusively with the identified exposures. All eight examples pose some danger of misinterpretation. Gadolinium-based contrast agents appear to create a risk of NSF only in the presence of chronic renal failure. Amphibole asbestos, and most importantly, crocidolite causes malignant mesothelioma after a very lengthy latency period. Ionizing radiation causes some cancers that are all-too common, but the presence of multiple cancers in the same person, after a suitable latency period, is distinctly uncommon, as is the level of radiation needed to overwhelm bodily defenses and induce cancers. Thalidomide was associated by case reports fairly quickly with phocomelia, which has an extremely low baseline risk. Other birth defects were not convincingly demonstrated by the case series. Rezulin, an oral antidiabetic medication, was undoubtedly causally responsible for rare cases of acute liver failure. Chronic liver disease, however, which is common among type 2 diabetic patients, required epidemiologic evidence, which never materialized[5].

Manganism, by definition, is the cause of manganism, but extremely high levels of manganese exposure, and specific speciation of the manganese, are essential to the causal connection. Manganism raises another issue often seen in so-called signature diseases: diagnostic accuracy. Unless the diagnostic criteria have perfect (100%) specificity, with no false-positive diagnoses, then once again, we expect false-positive cases to appear when the criteria are applied to large numbers of people. In the welding fume litigation, where plaintiffs’ counsel and physicians engaged in widespread, if not wanton, medico-legal screenings, it was not surprising that they might find occasional cases that appeared to satisfy their criteria. Of course, the more the criteria are diluted to accommodate litigation goals, the more likely there will be false positive cases.[6]

Dr. Schwartz identifies some common themes and important factors in identifying the bases for inferring causality from uncontrolled evidence:

“(a) low or no background rate of the disease condition;

(b) low background rate of the exposure;

(c) a clear understanding of the mechanism of action.”

These factors and perhaps others should not be confused with strict criteria here. The exemplar cases suggest a family resemblance of overlapping factors that help support the inference, even against the most robust skepticism.

In litigation, defense counsel typically argue that analytical epidemiology is always necessary, and plaintiffs’ counsel claim epidemiology is never needed. The truth is more nuanced and conditional, but the great majority of litigated cases do require epidemiology for health effects because the claimed harms are outcomes that have an expected incidence or prevalence in the exposed population irrespective of exposure.

[1] Reference Manual on Scientific Evidence at 23 (3d ed. 2011) (citing “Cloud v. Pfizer Inc., 198 F. Supp. 2d 1118, 1133 (D. Ariz. 2001) (stating that case reports were merely compilations of occurrences and have been rejected as reliable scientific evidence supporting an expert opinion that Daubert requires); Haggerty v. Upjohn Co., 950 F. Supp. 1160, 1164 (S.D. Fla. 1996), aff’d, 158 F.3d 588 (11th Cir. 1998) (“scientifically valid cause and effect determinations depend on controlled clinical trials and epidemiological studies”); Wade-Greaux v. Whitehall Labs., Inc., 874 F. Supp. 1441, 1454 (D.V.I. 1994), aff’d, 46 F.3d 1120 (3d Cir. 1994) (stating there is a need for consistent epidemiological studies showing statistically significant increased risks).”)

[2] Best v. Lowe’s Home Centers, Inc., 563 F. 3d 171, 178 (6th Cir 2009); Westberry v. Gislaved Gummi AB, 178 F. 3d 257, 263–264 (4th Cir. 1999).

[3] There may have been a better argument for Matrixx in distinguishing the method and place of delivery of the zinc sulfate in the polio trials of the 1930s, but when Matrixx’s counsel was challenged at oral argument, he asserted simply, and wrongly, that the two compounds were different.

[4] Johnston & Hauser, “The value of a case report,” 62 Ann. Neurology A11 (2007) (“No matter how compelling a vignette may seem, one must always be concerned about the reliability of inference from an “n of one.” No statistics are possible in case reports. Inference is entirely dependent, then, on subjective judgment. For a case meant to suggest that agent A leads to event B, the association of these two occurrences in the case must be compared to the likelihood that the two conditions could co-occur by chance alone …. Such a subjective judgment is further complicated by the fact that case reports are selected from a vast universe of cases.”); David A. Grimes & Kenneth F. Schulz, “Descriptive studies: what they can and cannot do,” 359 Lancet 145, 145, 148 (2002) (“A frequent error in reports of descriptive studies is overstepping the data: studies without a comparison group allow no inferences to be drawn about associations, causal or otherwise.”) (“Common pitfalls of descriptive reports include an absence of a clear, specific, and reproducible case definition, and interpretations that overstep the data. Studies without a comparison group do not allow conclusions about cause and disease.”); Troyen A. Brennan, “Untangling Causation Issues in Law and Medicine: Hazardous Substance Litigation,” 107 Ann. Intern. Med. 741, 746 (1987) (recommending that testifying physicans “[a]void anecdotal evidence; clearly state the opposing side is relying on anecdotal evidence and why that is not good science.”).

[5] See In re Rezulin, 2004 WL 2884327, at *3 (S.D.N.Y. 2004).

[6] This gaming of diagnostic criteria has been a major invitation to diagnostic invalidity in litigation over asbestosis and silicosis in the United States.

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Power at the FDA

December 11th, 2014

For six years, the Food and Drug Administration (FDA) has been pondering a proposed rule to abandon the current system of pregnancy warning categories for prescription drugs. Last week, the agency finally published its final rule for pregnancy and lactation labeling[1]. The rule, effective in June 2015, will require removal of the current category labeling, A, B, C, D, or X, in favor of risk statements and narrative summaries of the human, animal, and pharmacologic data for adverse maternal and embryo/fetal outcomes.

The labeling system, which will be phased out, discouraged or prohibited inclusion of actual epidemiologic data results for teratogenicity. With sponsors required to present actual data, the agency voiced a concern whether prescribing physicians, who are the intended readers of the labeling, interpret a statistically non-significant result as showing a lack of association:

“We note that it is difficult to be certain that a lack of findings equates to a lack of risk because the failure of a study to detect an association between a drug exposure and an adverse outcome may be related to many factors, including a true lack of an association between exposure and outcome, a study of the wrong population, failure to collect or analyze the right data endpoints, and/or inadequate power. The intent of this final rule is to require accurate descriptions of available data and facilitate the determination of whether the data demonstrate potential associations between drug exposure and an increased risk for developmental toxicities.[2]”

When human epidemiologic data are available, the agency had proposed the following for inclusion in drug labeling[3]:

“Narrative description of risk(s) based on human data. FDA proposed that when there are human data, the risk conclusion must be followed by a brief description of the risks of developmental abnormalities as well as other relevant risks associated with the drug. To the extent possible, this description must include the specific developmental abnormality (e.g., neural tube defects); the incidence, seriousness, reversibility, and correctability of the abnormality; and the effect on the risk of dose, duration of exposure, and gestational timing of exposure. When appropriate, the description must include the risk above the background risk attributed to drug exposure and confidence limits and power calculations to establish the statistical power of the study to identify or rule out a specified level of risk (proposed [21 C.F.R.] § 201.57(c)(9)(i)(C)(4)).”

The agency rebuffed comments that physicians would be unable to interpret confidence intervals, and confused by actual data and the need to interpret study results. The agency’s responses to comments to the proposed rule note that the final rule requires a description of the data, and its limitations, in approved labeling[4]:

‘‘Confidence intervals and power calculations are important for the review and interpretation of the data. As noted in the draft guidance on pregnancy and lactation labeling, which is being published concurrently with the final rule, the confidence intervals and power calculation, when available, should be part of that description of limitations.’’

The agency’s insistence upon power calculations is surprising. The proposed rule talked about requiring ‘‘confidence limits and power calculations to establish the statistical power of the study to identify or rule out a specified level of risk (proposed § 201.57(c)(9)(i)(C)(4)).” The agency’s failure to retain the qualification of power, at some specified level of risk, makes the requirement meaningless. A study with ample power to find a doubling of risk may have low power to find a 20% increase in risk. Power is dependent upon the specified alternative to the null hypothesis, as well as the level of alpha, or statistical significance.

The final rule omits all references to power and power calculations, with or without the qualifier of at some specified level of risk, from the revised sections of part 201; indeed the statistical concepts of power and confidence interval do not show up at all, other than a vague requirement that the limitation of data from epidemiologic studies be described[5]:

‘‘(3) Description of human data. For human data, the labeling must describe adverse developmental outcomes, adverse reactions, and other adverse effects. To the extent applicable, the labeling must describe the types of studies or reports, number of subjects and the duration of each study, exposure information, and limitations of the data. Both positive and negative study findings must be included.”

Presumably, the proposed rule’s requirement of providing power calculations and confidence intervals is part of the future requirement to describe data limitations. The agency, however, omitted this level of detail from the revised regulation.

The same day that the FDA issued the final rule, it also issued a draft guidance on pregnancy and lactation labeling, for public comment[6].

The guidance recommends what the regulation, in its final form, does not require specifically. First, the guidance recommends omission of individual case reports from the human data section, because:

‘‘Individual case reports are rarely sufficient to characterize risk and therefore ordinarily should not be included in this section.[7]”

And for actual controlled epidemiologic studies, the guidance suggests that:

‘‘If available, data from the comparator or control group, and data confidence intervals and power calculations should also be included.[8]”

Statistically, this guidance is no guidance at all. Power calculations can never be presented without a specified alternative hypothesis to the null hypothesis of no increased risk of birth defects. Furthermore, virtually no study provides power calculations of data already acquired and analyzed for point estimates and confidence intervals. The guidance is unclear as to whether sponsors should attempt to calculate power from the data in a study, and try to anticipate what level of specified risk is of interest to the agency and to prescribing physicians. More disturbing yet is the agency’s failure to explain why it is recommending both confidence intervals and power calculations, in the face of many leading groups’ recommendations to abandon power calculations when confidence intervals are available for the analyzed data.[9]

[1] Dep’t of Health & Human Services, Food & Drug Admin., 21 CFR Part 201, Content and Format of Labeling for Human Prescription Drug and Biological Products; Requirements for Pregnancy and Lactation Labeling; Pregnancy, Lactation, and Reproductive Potential: Labeling for Human Prescription Drug and Biological Products—Content and Format; Draft Guidance for Industry; Availability; Final Rule and Notice, 79 Fed. Reg. 72064 (Dec. 4, 2014) [Docket No. FDA–2006–N–0515 (formerly Docket No. 2006N–0467)]

[2] Id. at 72082a.

[3] Id. at 72082c-083a.

[4] Id. at 72083c.

[5] Id. at 72102a (§ 201.57(c)(9)(i)(D)(3)).

[6] U.S. Department of Health and Human Services, Food and Drug Administration, Pregnancy, Lactation, and Reproductive Potential: Labeling for Human Prescription Drug and Biological Products — Content and Format DRAFT GUIDANCE (Dec. 2014).

[7] Id. at 12.

[8] Id.

[9] See, e.g., Vandenbroucke, et al., “Strengthening the reporting of observational studies in epidemiology (STROBE):  Explanation and elaboration,” 18 Epidemiology 805, 815 (2007) (Section 10, sample size) (“Do not bother readers with post hoc justifications for study size or retrospective power calculations. From the point of view of the reader, confidence intervals indicate the statistical precision that was ultimately obtained. It should be realized that confidence intervals reflect statistical uncertainty only, and not all uncertainty that may be present in a study (see item 20).”); Douglas Altman, et al., “The Revised CONSORT Statement for Reporting Randomized Trials:  Explanation and Elaboration,” 134 Ann. Intern. Med. 663, 670 (2001) (“There is little merit in calculating the statistical power once the results of the trial are known, the power is then appropriately indicated by confidence intervals.”).

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More Case Report Mischief in the Gadolinium Litigation

November 28th, 2014

The Decker case is one curious decision, by the MDL trial court, and the Sixth Circuit. Decker v. GE Healthcare Inc., ___ F.3d ___, 2014 FED App. 0258P, 2014 U.S. App. LEXIS 20049 (6th Cir. Oct. 20, 2014). First, the Circuit went out of its way to emphasize that the trial court had discretion, not only in evaluating the evidence on a Rule 702 challenge, but also in devising the criteria of validity[1]. Second, the courts ignored the role and the weight being assigned to Federal Rule of Evidence 703, in winnowing the materials upon which the defense expert witnesses could rely. Third, the Circuit approved what appeared to be extremely asymmetric gatekeeping of plaintiffs’ and defendant’s expert witnesses. The asymmetrical standards probably were the basis for emphasizing the breadth of the trial court’s discretion to devise the criteria for assessing scientific validity[2].

In barring GEHC’s expert witnesses from testifying about gadolinium-naive nephrogenic systemic fibrosis (NSF) cases, Judge Dan Polster, the MDL judge, appeared to invoke a double standard. Plaintiffs could adduce any case report or adverse event report (AER) on the theory that the reports were relevant to “notice” of a “safety signal” between gadolinium-based contrast agents in MRI and NSF. Defendants’ expert witnesses, however, were held to the most exacting standards of clinical identity with the plaintiff’s particular presentation of NSP, biopsy-proven presence of Gd in affected tissue, and documentation of lack of GBCA-exposure, before case reports would be permitted as reliance materials to support the existence of gadolinium-naïve NSF.

A fourth issue with the Decker opinion is the latitude it permitted the district court to allow testimony from plaintiffs’ pharmacovigilance expert witness, Cheryl Blume, Ph.D., over objections, to testify about the “signal” created by the NSF AERs available to GEHC. Decker at *11. At the same trial, the MDL judge prohibited GEHC’s expert witness, Dr. Anthony Gaspari, to testify that the AERs described by Blume did not support a clinical diagnosis of NSF.

On a motion for reconsideration, Judge Polster reaffirmed his ruling on grounds that

(1) the AERs were too incomplete to rule in or rule out a diagnosis of NSF, although they were sufficient to create a “signal”;

(2) whether the AERs were actual cases of NSF was not relevant to their being safety signals;

(3) Dr. Gaspari was not an expert in pharmacovigilance, which studied “signals” as opposed to causation; and

(4) Dr. Gaspari’s conclusion that the AERs were not NSF was made without reviewing all the information available to GEHC at the time of the AERs.

Decker at *12.

The fallacy of this stingy approach to Dr. Gaspari’s testimony lies in the courts’ stubborn refusal to recognize that if an AER was not, as a matter of medical science, a case of NSF, then it could not be a “signal” of a possible causal relationship between GBCA and NSF. Pharmacovigilance does not end with ascertaining signals; yet the courts privileged Blume’s opinions on signals even though she could not proceed to the next step and evaluate diagnostic accuracy and causality. This twisted logic makes a mockery of pharmacovigilance. It also led to the exclusion of Dr. Gaspari’s testimony on a key aspect of plaintiffs’ liability evidence.

The erroneous approach pioneered by Judge Polster was compounded by the district court’s refusal to give a jury instruction that AERs were only relevant to notice, and not to causation. Judge Polster offered his reasoning that “the instruction singles out one type of evidence, and adds, rather than minimizes, confusion.” Judge Polster cited the lack of any expert witness testimony that suggested that AERs showed causation and “besides, it doesn’t matter because those patients are not, are not the plaintiffs.” Decker at *17.

The lack of dispute about the meaning of AERs would have seemed all the more reason to control jury speculation about their import, and to give a binding instruction on AERs and their limited significance. As for the AER patients’ not being the plaintiffs, well, the case report patients were not the plaintiffs, either. This last reason is not even wrong[3]. The Circuit, in affirming, turned a blind eye to the district court’s exercise of discretion in a way that systematically increased the importance of Blume’s testimony on signals, while systematically hobbling the defendant’s expert witnesses.

[1] “THE STANDARD OF APPELLATE REVIEW FOR RULE 702 DECISIONS” (Nov. 12, 2014).

[2] “Gadolinium, Nephrogenic Systemic Fibrosis, and Case Reports” (Nov. 24, 2014).

[3] “Das ist nicht nur nicht richtig, es ist nicht einmal falsch!” The quote is attributed to Wolfgang Pauli in R. E. Peierls, “Wolfgang Ernst Pauli, 1900-1958,” 5 Biographical Memoirs Fellows Royal Soc’y 175, 186 (1960).

 

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The Shyster Files – Racketeering in Silicosis Litigation

November 26th, 2014

David Rosner and Gerald Markowitz trace the silicosis compensation issues back to debates at the 1935 National Silicosis Conference, where representatives of labor and management squared off on the appropriate criteria for compensation.

David Rosner & Gerald Markowitz, Deadly Dust: Silicosis and the On-Going Struggle to Protect Workers’ Health at 110-15 (Ann Arbor 2006). Labor’s representative argued that silicosis should be defined by inhaling silica dust, which would have made every case of respiratory disease compensable. A lawyer who represented industry, Alfred C. Hirth, argued that compensation should be tied to disability.

Although Hirth acknowledged that silicosis was an employer problem[1], Rosner and Markowitz give a typically uncharitable assessment of Hirth’s ideas, even though the labor view that any silica inhalation constituted silicosis was demonstrably wrong at the time, and more so today. The authors quote Hirth as decrying the “[i]gnorance and sensational journalism” that has given rise to the then “the popular belief … that to inhale silica is to have silicosis.” Plus ça change, plus c’est la même chose!

Rosner and Markowitz then hone in on one sentence in Hirth’s presentation, where he criticizes the:

“shyster lawyer and quack doctor, who have been with the United States always, but whom we hope we may someday exterminate.”

Deadly Dust at 113. Here they launch the charge that Hirth was an anti-semite because he was against shysters and quacks, and even hoped, not unreasonably, that someday we might be rid of them.  The historians urge that we:

“Note the anti-Semitism implied by the use of shyster and the call for extermination, which echoed the views of the Nazi and the anti-Semites during the 1930s.”

Id. at 113n.19. Really?

Now when I first read this passage in Deadly Dust, I was puzzled. My grandmother, a sweet, charming Jewish lady, who could curse in several languages, including Yiddish, would regularly rant about the shysters about in the world. As far as I can recall, her usage was non-denominational, non-racial, non-ethnic. It was an equal opportunity epithet. So I decided to dig a little deeper into the alleged “implication” seen by Markowitz and Rosner. Everything I could find pointed to both Jewish hypersensitivity and linguistic ignorance in the authors of the Deadly Dust.

Fanciful Etymology

Here is what the venerable Oxford English Dictionary has to say about shyster:

“shyster slang. [Of obscure origin. It might be f. shy a. (sense 7, disreputable) + -ster; but this sense of the adj. is app. not current in the U.S.]

1. A lawyer who practises in an unprofessional or tricky manner; especially, one who haunts the prisons and lower courts to prey on petty criminals; hence, any one who conducts his business in a tricky manner.”

Nothing there to support the authors’ character assassination, but perhaps the English are just too polite? Here is the earthier, more down-to-Earth, American Heritage Dictionary (4th ed. 2000):

“shyster.  NOUN: Slang An unethical, unscrupulous practitioner, especially of law.

ETYMOLOGY: Probably alteration of German Scheisser, son of a bitch, bastard, from scheissen, to defecate … .”

Now we are getting to fundamentals. The Merriam Webster dictionary is in line with the defecator, which accords with my sense of lawyers who file fraudulent lawsuits:

“a person who is professionally unscrupulous especially in the practice of law or politics :  pettifogger.  Origin of SHYSTER: probably from German Scheisser, literally, defecator.  First Known Use: 1844”

The less venerable, crowd-sourced Wikipedia notes that

“Various false etymologies have suggested an anti-Semitic origin, but there is no proof for that.[3]”

Wikipedia entry for “shyster” (citing Michael Quinion “Shyster” World Wide Words (19 May 2007).

“Shysters” in Court

My view of the usage and etymology of shyster would appear to have the highest judicial authority. When some puglistic contracts turned puglistic, Lennox Lewis sued Don King in cases that spanned the Atlantic Ocean. At some point, King, with his gloves off and his mouth open, called Judd Berstein, Lewis’s attorney, a “shyster lawyer.” Berstein claimed that these were fighting words, or at least suing words, but the House of Lords disagreed. Lennox Lewis v Don King, [2004] EWCA Civ1329 (House of Lords, Supreme Court of Judicature).

Burstein’s claim, in his action for libel, turned on the assertion that calling a Jewish lawyer a “shyster lawyer” was anti-semitic (and defamatory). The appellate court (Lord Chief Justice Mummery and the eponymously named Lord Justice Laws) noted, with apparent approval, that the court below had diligently searched but failed to find any support for Burstein’s claim:

“It seems clear from a web search of 900 dictionaries (including specifically American ones) that there is no support for the word ‘shyster’ having any anti-semitic connotations.”

Id. at para. 18.

Shysters to the Right of Me; Shysters to the Left

In playing the “shyster” card, Rosner and Markowitz protest too much. They are so intent upon painting industry as unreasonable, that they overlook that the litigious behavior of the shyster lawyers in the 1930s embarrassed labor. There were, to be sure, real cases of silicosis, with real impairment, and real disability, even if the diagnostic criteria and classification of silicosis were in flux. Liability was contested in many of the “real cases,” which made administrative compensation boards such as workman’s compensation courts more attractive to many in labor unions than were litigation solutions. Here is what one labor union publication of the time had to say about the explosion of silicosis litigation in the 1930s:

“It is estimated that today in the United States there are approximately $500,000,000 in damage suits pending against employers. Many of these are legitimate, many admittedly racketeering. But just as medical research has demonstrated that one disease can be cured by the injection of another into the system, so in the end this regretable [sic] racketeering in damage suits — this ambulance chasing and canvassing of hospital beds by shyster lawyers and quack doctors — may prove to be the beneficent agent that shall cure big business of the greed and insensitiveness that places profits above human lives.”

“Silicosis Prevention” 72 Internat’l Molders’ J. 1 (July 1936) (emphasis added) (republished from the American Federationist (June 1936)).

So everyone agreed that there were shysters out in the land, and in court. The difference between labor and management is that labor wanted to use the shysters and fraudulent lawsuits in the hope that they would pressure industry into providing safer workplaces. And industry somehow objected to being besmirched by the shysters.

 

[1] See Alfred C. Hirth, Silicosis as an Employer Problem (1935).

 

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History – Lies My Teacher Told Me

November 26th, 2014

James W. Loewen, a professor of history, has been one of the most untiring critics of how history is taught and practiced in the United States. A large part of his criticism derives from the overt politicization of the teaching of history, especially the heavy hand of school boards and textbook committees in their selection of “appropriate textbooks” for high school students. See James W. Loewen, Lies My Teacher Told Me: Everything Your American History Textbook Got Wrong (2007). The disgraceful “conservative” sanitizing of United States highschoolers’ history textbooks is almost equal to the heavy-handed Marxist bent of some University professors. The politicization of history may be unavoidable, but we should be alert to the intellectual depredations from the right and the left.

*     *     *     *     *     *

I recently saw the self-styled social history of silicosis, Deadly Dust, by David Rosner and Gerald Markowitz, cited in a trial court brief. The cite was to the original edition, but it led me to read the “new and expanded” edition[1], published in 2006. Expanded, but not exactly super-sized, and with the same empty calories as before. The authors’ Preface to the second edition relays an air of excitement about recent (at the time of publication) media suggestions that silicosis may be the “new asbestosis.[2]” Of course, the authors were excited because the uptick in silicosis litigation around 2003, based almost exclusively upon fraudulent filings, brought them engagements as compensated expert witnesses for plaintiffs’ counsel.

The Preface also confesses that before their initial edition, the authors were ignorant about silicosis. And because they are so well read they assumed that their not having heard of silicosis meant that silicosis must have disappeared from the literature. Id. at xiii. This fallacious confusion between absence of evidence and evidence of absence pervades the entire book. Their first edition was written with this confirmation bias dominating their narrative:

“The book we wrote tells the story of a condition that dominated public health, medical, labor, and popular discourse on disease in the 1930s but that virtually vanished from popular and professional consciousness after World War II. How, we asked, could a chronic disease that took decades to develop and that was assumed to affect hundreds of thousands of American workers disappear from the literature and public notice in less than a decade? This question is the basis for Deadly Dust, and we believe that we answered it, providing a cultural, medical, and political model of how we, as a society, decide to recognize or forget about illness.”

Deadly Dust at xiv (emphasis added). The second edition is more of the same biased narrative.

Also clear from their Preface is the authors’ messianic complex. I now know why they have repeatedly attacked me for having criticized them: It is important for them to be seen as having been resistant victims of industry, indeed, especially if they are triumphant victims:

“We are particularly proud that lawyers for various industries have sought to get judges to exclude our book from court cases.”

Id. at xvi. Of course, from the lawyers’ perspective, a book such as Deadly Dust has many layers of evidentiary problems, running from authentication of documents, to multiple layers of hearsay, legal and logical relevancy, and rampant, subjective opinion spread throughout the narrative.

The “virtually vanished” phrase caused me to revisit[3] my previous quantitative assessment of discussions of silicosis in the popular and medical literature. The National Library of Medicine PubMed database is expanding back into the past, adding old journals and their articles to the database. Here is the most recent tally, by decade of articles with keyword “silicosis”:

Date Range                    Number of Articles from Keyword Search

1940 – 1949                      119

1950 – 1959                    1,436

1960 – 1969                    1,868

1970 – 1979                    1,176

1980 – 1989                       940

1990 – 1999                       883

2000 – 2009                      860

2010 — present                  498

The Rosner/Markowitz claim about silicosis “virtually vanishing” from professional discourse after World War II, is an assertion that is completely belied by the evidence. Google’s Ngram function further confirms the incorrectness of the fundamental premise of Deadly Dust:

Silicosis Ngram 1920 - 2010

Silicosis Ngram 1920 – 2010

The Google chart shows that although there was a peak around 1940, the level of referencing silicosis remained at or above the level for the mid-1930s until 1960, and never retreated to levels as low as for 1930-32.

This false premise, that silicosis vanished, or virtually vanished, from the medical literature, is the starting point for Rosner and Markowitz’ faux conspiracy charge against industry for suppressing discussion, when the reality was exactly the opposite. What follows from the false premise is a false set of conclusions.

[1] David Rosner & Gerald Markowitz, Deadly Dust: Silicosis and the On-Going Struggle to Protect Workers’ Health (Ann Arbor 2006).

[2] citing Jonathan Glater, “Suits on Silica Being Compared to Asbestos Cases,” New York Times (Sept. 6, 2003), C-1 (quoting one defense lawyer as saying that “I actually thought that we had made the world safe for sand.”).

[3] See Schachtman, “Conspiracy Theories: Historians, In and Out of Court” (April 17, 2013).

 

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Gadolinium, Nephrogenic Systemic Fibrosis, and Case Reports

November 24th, 2014

Gadolinium (Gd) is a rare earth element. In its ionic form (+3), gadolinium is known to be highly toxic to humans. Gadolinium is strongly paramagnetic, which makes it a valuable contrast agent in for magnetic resonance imaging (MRI). The gadolinium is administered intravenously in a chelated form before MRI. In its chelated form, the ion is escorted out of the body through the kidneys before exposure to free Gd ion occurs. Or that was the theory.

Nephrogenic systemic fibrosis (NSF) is a rare, painful, incurable progressive connective tissue disease. NSF manifests with skin thickening and fibrosis, tethering, which means it cannot be pulled away from body. Some patients may develop extracutaneous fibrosis of muscle, lymph nodes, pleura, and other internal organs. Elana J. Bernstein, Christian Schmidt-Lauber, and Jonathan Kay, “Nephrogenic systemic fibrosis: A systemic fibrosing disease resulting from gadolinium exposure,” 26 Best Practice & Research Clin. Rheum. 489, 489 (2012).

As a diagnostic entity, NSF is a relatively recent discovery. The first case was noted in 1997, in California. Within a few years, the differential diagnostic criteria to distinguish NSF from other fibrotic diseases were developed. Centers for Disease Control, “Fibrosing skin condition among patients with renal disease–United States and Europe, 1997–2002,” 51 MMWR Morbidity and Mortality Weekly Report 25 (2002). Physicians identified the condition among patients with renal insufficiency who had received MRI with a gadolinium-based contrast agent (GBCA). Given the rarity of both the exposure (GBCA and renal insufficiency) and the outcome (NSF), the relationship between NSF and the use of gadolinium-containing contrast agents for magnetic resonance imaging (MRI) was discovered largely from case reports. A case registry is maintained at Yale University, and has identified 380 cases to date. Shawn E. Cowper, “Nephrogenic Systemic Fibrosis” at the website for The International Center for Nephrogenic Systemic Fibrosis Research (ICNSFR) [last updated June 15, 2013).

The little epidemiology that exists on the subject generally has found that all “cases” had exposure to Gd[1]. Or almost all. There have been occasional cases found without reported exposure to GBCA. Indeed, one case of NSF without prior GBCA was reported last month in the dermatological literature. C. Ross, N. De Rosa, G. Marshman, D. Astill, “Nephrogenic systemic fibrosis in a gadolinium-naïve patient: Successful treatment with oral sirolimus,” Australas. J. Dermatol. (2014); doi: 10.1111/ajd.12176. [Epub ahead of print].

In litigation, the usual scenario is that plaintiffs and their counsel and expert witnesses want to offer case reports or case series as probative of a causal association between an exposure and a particular disease outcome. In the silicone gel breast implant litigation, women, who self-characterized themselves “victims,” shouted outside courtrooms, “We are the evidence.”

When the outcome in question has a baseline rate, and the exposure is widespread, this strategy is usually illegitimate and most courts have limited or prohibited the obvious attempt to prejudice the jury by the use of evidence that has little or no probative value.

The causal connection between NSF and GBCA, described above, was postulated on the basis of case reports, but this is not really a rejection of the general rule about case reports. NSF is an extremely rare outcome, and GBCA administered to patients with serious kidney insufficiency is a fairly rare exposure. In addition, gadolinium ion has a known human toxicity, and the connection between renal insufficiency and Gd toxicity is rather straightforward. The insufficiency of the kidney function results in longer “in residence” times for the GBCA, with the consequence that the gadolinium disassociates from its chelating agent, and the free Gd ion does its damage. Furthermore, biopsies of affected tissues show an uptake of gadolinium in NSF patients.

   *   *   *   *   *   *   *   *

GE Healthcare manufactures Omniscan, a GBCA, for use as an MRI-contrast medium. Given the recently discovered dangers of GBCAs in vulnerable patients, Omniscan has been a magnet for lawsuits, with the peak intensity of the litigation field in the MDL courtroom of federal district courtroom of Judge Dan Polster. Judge Polster tried the first Omniscan case, which resulted in a verdict for the plaintiff. GE appealed, complaining about several of Judge Polster’s rulings, including the uneven handling of case reports. Last month, the Sixth Circuit affirmed. Decker v. GE Healthcare Inc., ___ F.3d ___, 2014 FED App. 0258P, 2014 U.S. App. LEXIS 20049 (6th Cir. Oct. 20, 2014).

General causation between GBCAs and NSF was apparently not disputed in Decker. Although plaintiffs in the GBCA litigation established the causality of GABC in producing NSF, by case reports, Judge Polster refused to permit GEHC’s expert witnesses to testify about their reliance upon case reports of gadolinium-naïve cases of NSF; that is, the court disallowed testimony about reported cases that occurred in the absence of GBCA exposure[2]. Id. at *9. Judge Polster found that the reported gadolinium-naïve case reports were “methodologically flawed” because they did not adequately show that the NSF patients in question lacked Gd exposure, with tissue biopsy or other means. Id. at * 10. The district court speculated that there may have Gd exposure from a non-MRI procedure, but never explained what non-MRI procedure would involve internal administration of GBCA. Nor did the district court address the temporal relationship between this undocumented, conjectured non-MRI gadolinium-based imaging procedure and the onset of the reported patient’s NSF.

Before trial defendant GEHC moved for reconsideration of the district court’s previous decision on defensive use of gadolinium-naïve case reports, based upon on a then recent publication of a “purported” case of gadolinium-naïve NSF. Id. at *8. A quick read of the late-breaking case study shows that it was more than a “purported” case. A.A. Lemy, et al., “Revisiting nephrogenic systemic fibrosis in 6 kidney transplant recipients: a single-center experience,” 63 J. Am. Acad. Dermatol. 389 (2010). The cited paper by Lemy had diagnosed NSF in a patient without GBCA exposure, and mass spectrometry testing of affected tissue revealed no Gd. The district court, however, dismissed the Lemy case as irrelevant unless GEHC’s expert witnesses could demonstrate that Lemy’s patient number 5 and the plaintiff were so clinical similar that “it was probable that Mr. Decker’s NSF was not caused by his 2005 Omniscan [exposure].”

The Sixth Circuit affirmed this “tails they win; heads you lose” approach to gatekeeping as all within the scope of the district court’s exercise of discretion. Lemy’s case number 5 and Mr. Decker both had NSF, and yet the courts do not describe clinical varieties among NSF, which vary based upon their relatedness to gadolinium exposure. It would seem that the courts were imposing an extremely heavy burden on the defense to show that the gadolinium-naïve cases were absolutely free of Gd exposure, and that they resembled the particular plaintiff’s NSF diagnosis in every respect. Without any evidence of diagnostic disease criteria sensitivity and specificity, and positive predictive value for the criteria, the district and the appellate courts seem to have accepted glib demands for absolute identity between the plaintiff’s NSF manifestation and any candidate Gd-free NSF case. Given that there is clinical heterogeneity among Gd-NSF cases, and that causality was basically inferred from cases and case series, the courts’ reasoning seems strained.

The appellate court also seemed blithely unaware of the fallacious circularity of permitting a diagnostic entity to be defined based upon exposure, thereby preventing any fair test of the hypothesis that all NSF cases are caused by gadolinium. This fallacy was advanced in the silicone gel breast implant litigation, where the litigation industry shrank from claims that silicone caused classic connective tissue diseases, in the face of exculpatory epidemiologic studies. The claimants retreated to a claim that silicone caused a “new” disease that was defined by mostly vague, self-reported symptoms [so very different from NSF in this respect], in conjunction with silicone exposure. The court-appointed expert witnesses, however, would have none of these shenanigans:

“The National Science Panel concluded that they do not yet support the inclusion of SSRD [systemic silicone-related disease] in the list of accepted diseases, for 4 reasons. First, the requirement of the inclusion of the putative cause (silicone exposure) as one of the criteria does not allow the criteria set to be tested objectively without knowledge of the presence of implants, thus incurring incorporation bias (27).”

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, 2479 (2001) (citing David Sackett, “Bias in analytic research,” 32 J. Chronic Dis. 51 (1979)).

Of course, NSF does not share the dubious provenance of SSRD, or SAD [silicone-associated disorder] as it was sometimes known. Still, the analytic studies that have shown that NSF cases all, or mostly, had GBCA exposure, explicitly refrained from defining the NSF case as including gadolinium exposure.

Decker is thus a curious case. The trial and appellate court talked about preventing the defense expert witnesses from relying upon case reports that were “methodologically flawed,” but the courts never mentioned Federal Rule of Evidence 703, which should have been the basis for such selective pruning of the expert witnesses’ reliance materials. And then there is the matter that even if GEHC were correct about Gd-free NSF cases, the attributable risk for NSF to prior Gd exposure is almost certainly very high, and the debate over whether NSF is a “signature” disease was not likely going to affect the case outcome.

Decker can perhaps best be understood as a dispute about specific causation, with established general causation, in which the relative risk of NSF from GBCA exposure is extraordinarily high among patients with renal insufficiency. If there are other causes of NSF, they are considerably more rare than GBCA/renal insufficiency exposed cases. In the face of this very high attributable risk, GE’s expert witnesses’ discussions of an idiopathic or other cause was too speculative to pass muster under Rule 702.

[1] Elana J. Bernstein, Tamara Isakova, Mary E. Sullivan, Lori B. Chibnik, Myles Wolf & Jonathan Kay, “Nephrogenic systemic fibrosis is associated with hypophosphataemia: a case–control study,” 53 Rheumatology 1613 (2014); T.R. Elmholdt, M. Pedersen, B. Jørgensen, K. Søndergaard, J.D. Jensen, M. Ramsing, and A.B. Olesen, “Nephrogenic systemic fibrosis is found only among gadolinium-exposed patients with renal insufficiency: a case-control study from Denmark,” 165 Br. J. Dermatol. 828 (2011); P. Marckmann, “An epidemic outbreak of nephrogenic systemic fibrosis in a Danish hospital,” 66 Eur. J. Radiol. 187 (2008) (reporting all patients had gadodiamide-enhanced magnetic resonance imaging and severe renal insufficiency before onset of NSF); P. Marckmann, L. Skov, K. Rossen, J.G. Heaf, and H.S. Thomsen, “Case-control study of gadodiamide-related nephrogenic systemic fibrosis,” 22 Nephrol. Dialysis &Transplant. 3174 (2007) (all 19 cases in case-control study had prior exposure to gadolinium (Gd)-containing magnetic resonance imaging contrast agents); Centers for Disease Control, “Nephrogenic Fibrosing Dermopathy Associated with Exposure to Gadolinium-Containing Contrast Agents — St. Louis, Missouri, 2002–2006,” 56 MMWR Morbidity and Mortality Weekly Report (Feb. 23, 2007).

[2] T.A. Collidge, P.C. Thomson, P.B. Mark, et al., “Gadolinium-Enhanced MR Imaging and Nephrogenic Systemic Fibrosis: Retrospective Study of a Renal Replacement Therapy Cohort,” 245 Radiology 168-175 (2007); I.M. Wahba, E.L. Simpson, and K. White, “Gadolinium Is Not The Only Trigger For Nephrogenic Systemic Fibrosis: Insights From Two Cases And Review Of The Recent Literature,” 7 Am. J. Transplant. 1 (2007); A. Deng, D.B. Martin, et al., “Nephrogenic Systemic Fibrosis with a Spectrum of Clinical and Histopathological Presentation: A Disorder of Aberrant Dermal Remodeling,” 37 J. Cutan. Pathol. 204 (2009).

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Historians Noir

November 18th, 2014

David Rosner and Gerald Markowitz are two “labor” historians who make it their business to testify as historian expert witnesses in occupational and environmental disease cases. They apparently do not like lawyers who argue that they should have less business in the courts[1]. Rosner and Markowitz have obsessed about my article critical of their scholarship, and about historian witnesses, but rather than respond as scholars, they have responded largely ad hominem by suggesting that my criticisms were motivated by their testifying for the litigation industry. They have accused me of “attacking the messenger,” and they have responded by attacking the messenger. And their “attacks,” feeble though they may be, have come repetitively[2], suggesting some obsession and compulsion.

Last month[3], Professor Rosner gave a public lecture on his testimonial adventures as an historian expert witness, “Judging Science: The Historian, the Courts, & Discerning Responsibility for Environmental Pollution.” The lecture, given at Columbia University’s Heyman Center, lasted a little over an hour, exemplifies Rosner’s approach to “historifying,” as well as why courts should be wary of permitting such testimony. Here is how the Heyman Center’s website describes the talk:

“Over the past twenty years a vast public negotiation has taken place over the causes of, and responsibility for, disease. For the most part this discussion has flown under the radar of doctors, historians and public health professionals. This talk will look at a number of environmental pollution and public health cases over the course of the past two decades in which Professor Rosner has participated.”

Rosner begins by recounting his initial involvement in litigation, in Texas cases involving claims for silicosis. Rosner asserts that his involvement was necessitated by the defendants’ position that no one had ever heard of silicosis, and that silicosis had vanished from the medical literature after 1940. Rosner’s characterization of the claims and defenses of the Odessa sandblasting cases is, however, badly flawed, and his suggestion that silicosis had disappeared from the medical literature at the end of the 1930s is simply false.

According to Rosner (about 22:40 into the video), Histrionic Historians was an “attack” made in response to his, and his friend Gerald Markowitz’s, testimony in the Odessa, Texas case. Wrong. By the time Histrionic Historians was published, Rosner and Markowitz were listed as retained expert witnesses in hundreds if not thousands of cases, in the silicosis MDL, see In re Silica Prods. Liab. Litig., 398 F. Supp. 2d 563 (S.D. Tex. 2005), and they were showing up in several other isolated cases around the country. One of the Odessa silicosis cases had gone up to the Texas Supreme Court, which reversed the judgment for plaintiff on the ground that the jury must consider the knowledge and role of the intermediary employer in the context of an occupational disease claim against a remote supplier. Humble Sand & Gravel, Inc. v. Gomez, 146 S.W.3d 170 (Tex. 2004). The cases in front of Judge Jack were, of course, mostly fraudulent, and the liability in the remaining cases was almost tenuous to non-existent. In his Heyman Center lecture last month, Rosner suggests that my article was an attempt to “take back” from him and Markowitz, the narrative that had been historically controlled by industry (around 34:50 of the video). The fact is, however, that industry never controlled the silicosis narrative, which was played out in the 1930s by organized labor, government, academics, and industry. Histrionic Historians was only a preliminary essay designed to show that the Rosner narrative was false.

Towards the end of his lecture, Rosner attempts to describe the consequences of the workman’s compensation system. He argues that byssinosis, anthracosilicosis, and asbestosis were once considered “silicosis,” on the theory that silica was doing the damage, a stunning claim considering that byssinosis is caused by cotton dust, and does not involve any mineral dust of any kind. According to Rosner, the other pneumoconioses were “politically divided off of the silicosis issue” so that workers could regain the ability to sue, since workers could not sue for silicosis (due to statutory employer immunity). Video at 59:15-40. With no regard for the medical or scientific history of the knowledge of the various pneumoconioses, Rosner states that asbestosis and byssinosis were:

“in some sense created as clinical entities because of the political implications of being identified as silicosis after 1940. Silicosis was no longer compensable and so you had to find new definitions. It is a very interesting history of these disease that were once considered forms of silicosis.”

Video at 1:00:30-51. Very interesting, and entirely bogus. Asbestosis and silicosis were considered distinct diseases well before 1940, and medical science distinguished the two pneumoconioses as having different causes, different diagnostic criteria, and different sequelae. And neither asbestos nor cotton dust contains silica. A great example of the misinformation that historians unfamiliar with the relevant medical history can spout.

Historians’ Acting Badly

In response to a question from the audience, Professor Rosner recounts the events of an historical society meeting at which he and his colleagues learned that the President had been consulting for tobacco defendants in litigation. Apparently, this revelation almost led to fistfights in the halls. So much for diversity and tolerance! Video around 1:10:00. Rosner tells us that he is one of only about three historians who have decided to work for plaintiffs and labor unions. Video at 1:09:45.

Standards for Historian Testimony

Rosner criticizes the historians who testify for tobacco defendants on the grounds that they were not shown everything known (secretly) by the tobacco companies. These historian thus testified on only the public record, and their testimony was thus misleading. According to Rosner, you (the aspiring historian expert witness) “must see everything”; “you are entitled to see all the documents.” Otherwise, you are at risk of being given documents selectively by instructing counsel. Video at 1:11:10-29. There could be a semblance of a criterion in Rosner’s remarks for evaluating historian expert witness testimony. Rosner, understandably however, states that he does not know whether he wants the American Historian Association to become involved in policing historian witness testimony.

Historian Testimony – Beyond the Ken?

Rosner fielded a question from the audience about how courts viewed historian testimony. Of course, Rosner is not a lawyer, and his answer did not attempt to summarize the judicial antipathy towards historian testimony when not necessary. Instead, Rosner focused on his own niche of testifying in lead, asbestos, and silica cases, where courts have been more indulgent of permitting historian expert witness testimony. “They [the courts] are getting used to it,” Rosner reports. “Juries love” historian testimony because historians speak English, and “they understand it,” unlike the scientific testimony in the case. According to Rosner, historians are not pretending to have a special expertise that the jury cannot understand, and the materials relied upon do not require interpretation by an expert the way scientific studies do. Video at 1:12:24-14:04. Q.E.D.!

[1] Nathan Schachtman & John Ulizio, “Courting Clio:  Historians and Their Testimony in Products Liability Action,” in: Brian Dolan & Paul Blanc, eds., At Work in the World: Proceedings of the Fourth International Conference on the History of Occupational and Environmental Health, Perspectives in Medical Humanities, University of California Medical Humanities Consortium, University of California Press (2012); Schachtman, “On Deadly Dust & Histrionic Historians 041904,” Mealey’s Silica Litigation Report Vol. 2, No. 3 (Nov. 2003). See also “How Testifying Historians Are Like Lawn-Mowing Dogs” (May 15, 2010); A Walk on the Wild Side (July 16, 2010); Counter Narratives for Hire (Dec. 13, 2010).

[2] Four articles dwell on the issue. See D. Rosner & G. Markowitz, “The Trials and Tribulations of Two Historians:  Adjudicating Responsibility for Pollution and Personal Harm, 53 Medical History 271, 280-81 (2009); D. Rosner & G. Markowitz, “L’histoire au prétoire.  Deux historiens dans les procès des maladies professionnelles et environnementales,” 56 Revue D’Histoire Moderne & Contemporaine 227, 238-39 (2009); David Rosner, “Trials and Tribulations:  What Happens When Historians Enter the Courtroom,” 72 Law & Contemporary Problems 137, 152 (2009); David Rosner & Gerald Markowitz, “The Historians of Industry” Academe (Nov. 2010). To these publications, these “forensic historians” have added yet another recitation in an epilogue to a revised edition of one of their books. Gerald Markowitz and David Rosner, Deceit and Denial: The Deadly Politics of Industrial Pollution at 313-14 (U. Calif. rev. ed. 2013).

[3] October 22, 2014.

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Rhetorical Strategy in Characterizing Scientific Burdens of Proof

November 15th, 2014

The recent opinion piece by Kevin Elliott and David Resnik exemplifies a rhetorical strategy that idealizes and elevates a burden of proof in science, and then declares it is different from legal and regulatory burdens of proof. Kevin C. Elliott and David B. Resnik, “Science, Policy, and the Transparency of Values,” 122 Envt’l Health Persp. 647 (2014) [Elliott & Resnik]. What is astonishing about this strategy is the lack of support for the claim that “science” imposes such a high burden of proof that we can safely ignore it when making “practical” legal or regulatory decisions. Here is how the authors state their claim:

“Very high standards of evidence are typically expected in order to infer causal relationships or to approve the marketing of new drugs. In other social contexts, such as tort law and chemical regulation, weaker standards of evidence are sometimes acceptable to protect the public (Cranor 2008).”

Id.[1] Remarkably, the authors cite no statute, no case law, and no legal treatise for the proposition that the tort law standard for causation is somehow lower than for a scientific claim of causality. Similarly, the authors cite no support for their claim that regulatory pronouncements are judged under a lower burden. One only need consider the burden a sponsor faces in establishing medication efficacy and safety in a New Drug Application before the Food and Drug Administration.  Of course, when agencies engage in assessing causal claims regarding safety, they often act under regulations and guidances that lessen the burden of proof from what we would be required in a tort action.[2]

And most important, Elliott and Resnik fail to cite to any work of scientists for the claim that scientists require a greater burden of proof before accepting a causal claim. When these authors’ claims of differential burdens of proof were challenged by a scientist, Dr. David Schwartz, in a letter to the editors, the authors insisted that they were correct, again citing to Carl Cranor, a non-lawyer, non-scientist:

“we caution against equating the standards of evidence expected in tort law with those expected in more traditional scientific contexts. The tort system requires only a preponderance of evidence (> 50% likelihood) to win a case; this is much weaker evidence than scientists typically demand when presenting or publishing results, and confusion about these differing standards has led to significant legal controversies (Cranor 2006).”

Reply to Dr. Schwartz. The only thing the authors added to the discussion was to cite to the same work by Carl Cranor[3], but change the date of the book.

Whence comes the assertion that science has a heavier burden of proof? Elliott and Resnik cite Cranor for their remarkable proposition, and so where did Cranor find support for the proposition at issue here? In his 1993 book, Cranor suggests that we “can think of type I and II error rates as “standards of proof,” which begs the question whether they are appropriately used to assess significance or posterior probabilities[4]. Cranor goes so far in his 1993 as to describe the usual level of alpha as the “95%” rule, and that regulatory agencies require something akin to proof “beyond a reasonable doubt,” when they require two “statistically significant” studies[5]. Thus Cranor’s opinion has its origins in his commission of the transposition fallacy[6].

Cranor has persisted in his fallacious analysis in his later books. In his 2006 book, he erroneously equates the 95% coefficient of statistical confidence with 95% certainty of knowledge[7]. Later in the text, he asserts that agency regulations are written when supported by “beyond a reasonable doubt.[8]”

To be fair, it is possible to find regulators stating something close to what Cranor asserts, but only when they themselves are committing the transposition fallacy:

“Statistical significance is a mathematical determination of the confidence in the outcome of a test. The usual criterion for establishing statistical significance is the p-value (probability value). A statistically significant difference in results is generally indicated by p < 0.05, meaning there is less than a 5% probability that the toxic effects observed were due to chance and were not caused by the chemical. Another way of looking at it is that there is a 95% probability that the effect is real, i.e., the effect seen was the result of the chemical exposure.”

U.S. Dep’t of Labor, Guidance for Hazard Determination for Compliance with the OSHA Hazard Communication Standard (29 CFR § 1910.1200) Section V (July 6, 2007).

And it is similarly possible to find policy wonks expressing similar views. In 1993, the Carnegie Commission published a report in which it tried to explain away junk science as simply the discrepancy in burdens of proof between law and science, but its reasoning clearly points to the Commission’s commission of the transposition fallacy:

“The reality is that courts often decide cases not on the scientific merits, but on concepts such as burden of proof that operate differently in the legal and scientific realms. Scientists may misperceive these decisions as based on a misunderstanding of the science, when in actuality the decision may simply result from applying a different norm, one that, for the judiciary, is appropriate.  Much, for instance, has been written about ‘junk science’ in the courtroom. But judicial decisions that appear to be based on ‘bad’ science may actually reflect the reality that the law requires a burden of proof, or confidence level, other than the 95 percent confidence level that is often used by scientists to reject the possibility that chance alone accounted for observed differences.”

The Carnegie Commission on Science, Technology, and Government, Report on Science and Technology in Judicial Decision Making 28 (1993)[9].

Resnik and Cranor’s rhetoric is a commonplace in the courtroom. Here is how the rhetorical strategy plays out in courtroom. Plaintiffs’ counsel elicits concessions from defense expert witnesses that they are using the “norms” and standards of science in presenting their opinions. Counsel then argue to the finder of fact that the defense experts are wonderful, but irrelevant because the fact finder must decide the case on a lower standard. This stratagem can be found supported by the writings of plaintiffs’ counsel and their expert witnesses[10]. The stratagem also shows up in the writings of law professors who are critical of the law’s embrace of scientific scruples in the courtroom[11].

The cacophony of error, from advocates and commentators, have led the courts into frequent error on the subject. Thus, Judge Pauline Newman, who sits on the United States Court of Appeals for the Federal Circuit, and who was a member of the Committee on the Development of the Third Edition of the Reference Manual on Scientific Evidence, wrote in one of her appellate opinions[12]:

“Scientists as well as judges must understand: ‘the reality that the law requires a burden of proof, or confidence level, other than the 95 percent confidence level that is often used by scientists to reject the possibility that chance alone accounted for observed differences’.”

Reaching back even further into the judiciary’s wrestling with the issue of the difference between legal and scientific standards of proof, we have one of the clearest and clearly incorrect statements of the matter[13]:

“Petitioners demand sole reliance on scientific facts, on evidence that reputable scientific techniques certify as certain. Typically, a scientist will not so certify evidence unless the probability of error, by standard statistical measurement, is less than 5%. That is, scientific fact is at least 95% certain.  Such certainty has never characterized the judicial or the administrative process. It may be that the ‘beyond a reasonable doubt’ standard of criminal law demands 95% certainty.  Cf. McGill v. United States, 121 U.S.App. D.C. 179, 185 n.6, 348 F.2d 791, 797 n.6 (1965). But the standard of ordinary civil litigation, a preponderance of the evidence, demands only 51% certainty. A jury may weigh conflicting evidence and certify as adjudicative (although not scientific) fact that which it believes is more likely than not. ***”

The 95% certainty appears to derive from 95% confidence intervals, although “confidence” is a technical term in statistics, and it most certainly does not mean the probability of the alternative hypothesis under consideration.  Similarly, the probability that is less than 5% is not the probability that the null hypothesis is correct. The United States Court of Appeals for the District of Columbia thus fell for the rhetorical gambit in accepting the strawman that scientific certainty is 95%, whereas civil and administrative law certainty is a smidgeon above 50%.

We should not be too surprised that courts have erroneously described burdens of proof in the realm of science. Even within legal contexts, judges have a very difficult time articulating exactly how different verbal formulations of the burden of proof translate into probability statements. In one of his published decisions, Judge Jack Weinstein reported an informal survey of judges of the Eastern District of New York, on what they believed were the correct quantizations of legal burdens of proof. The results confirm that judges, who must deal with burdens of proof as lawyers and then as “umpires” on the bench, have no idea of how to translate verbal formulations into mathematical quantities: Fatico

U.S. v. Fatico, 458 F.Supp. 388 (E.D.N.Y. 1978). Thus one judge believed that “clear, unequivocal and convincing” required a higher level of proof (90%) than “beyond a reasonable doubt,” and no judge placed “beyond a reasonable doubt” above 95%. A majority of the judges polled placed the criminal standard below 90%.

In running down Elliott, Resnik, and Cranor’s assertions about burdens of proof, all I could find was the commonplace error involved in moving from 95% confidence to 95% certainty. Otherwise, I found scientists declaring that the burden of proof should rest with the scientist who is making the novel causal claim. Carl Sagan famously declaimed, “extraordinary claims require extraordinary evidence[14],” but he appears never to have succumbed to the temptation to provide a quantification of the posterior probability that would cinch the claim.

If anyone has any evidence leading to support for Resnik’s claim, other than the transposition fallacy or the confusion between certainty and coefficient of statistical confidence, please share.

 

[1] The authors citation is to Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice (NY 2008). Professor Cranor teaches philosophy at one of the University of California campuses. He is neither a lawyer nor a scientist, but he does participate with some frequency as a consultant, and as an expert witness, in lawsuits, on behalf of claimants.

[2] See, e.g., In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 781 (E.D.N.Y. 1984) (Weinstein, J.) (“The distinction between avoidance of risk through regulation and compensation for injuries after the fact is a fundamental one.”), aff’d 818 F.2d 145 (2d Cir. 1987) (approving district court’s analysis), cert. denied sub nom. Pinkney v. Dow Chemical Co., 487 U.S. 1234 (1988).

[3] Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice (NY 2006).

[4] Carl F. Cranor, Regulating Toxic Substances: A Philosophy of Science and the Law at 33-34 (Oxford 1993) (One can think of α, β (the chances of type I and type II errors, respectively and 1- β as measures of the “risk of error” or “standards of proof.”) See also id. at 44, 47, 55, 72-76.

[5] Id. (squaring 0.05 to arrive at “the chances of two such rare events occurring” as 0.0025).

[6] Michael D. Green, “Science Is to Law as the Burden of Proof is to Significance Testing: Book Review of Cranor, Regulating Toxic Substances: A Philosophy of Science and the Law,” 37 Jurimetrics J. 205 (1997) (taking Cranor to task for confusing significance and posterior (burden of proof) probabilities). At least one other reviewer was not as discerning as Professor Green and fell for Cranor’s fallacious analysis. Steven R. Weller, “Book Review: Regulating Toxic Substances: A Philosophy of Science and Law,” 6 Harv. J. L. & Tech. 435, 436, 437-38 (1993) (“only when the statistical evidence gathered from studies shows that it is more than ninety-five percent likely that a test substance causes cancer will the substance be characterized scientifically as carcinogenic … to determine legal causality, the plaintiff need only establish that the probability with which it is true that the substance in question causes cancer is at least fifty percent, rather than the ninety-five percent to prove scientific causality”).

[7] Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice 100 (2006) (incorrectly asserting, without further support, that “[t]he practice of setting α =.05 I call the “95% rule,” for researchers want to be 95% certain that when knowledge is gained [a study shows new results] and the null hypothesis is rejected, it is correctly rejected.”).

[8] Id. at 266.

[9] There were some scientists on the Commission’s Task Force, but most of the members were lawyers.

[10] Jan Beyea & Daniel Berger, “Scientific misconceptions among Daubert gatekeepers: the need for reform of expert review procedures,” 64 Law & Contemporary Problems 327, 328 (2001) (“In fact, Daubert, as interpreted by ‛logician’ judges, can amount to a super-Frye test requiring universal acceptance of the reasoning in an expert’s testimony. It also can, in effect, raise the burden of proof in science-dominated cases from the acceptable “more likely than not” standard to the nearly impossible burden of ‛beyond a reasonable doubt’.”).

[11] Lucinda M. Finley, “Guarding the Gate to the Courthouse:  How Trial Judges Are Using Their Evidentiary Screening Role to Remake Tort Causation Rules,” 336 DePaul L. Rev. 335, 348 n. 49 (1999) (“Courts also require that the risk ratio in a study be ‘statistically significant,’ which is a statistical measurement of the likelihood that any detected association has occurred by chance, or is due to the exposure. Tests of statistical significance are intended to guard against what are called ‘Type I’ errors, or falsely ascribing a relationship when there in fact is not one (a false positive).” Finley erroneously ignores the conditioning of the significance probability on the null hypothesis, and she suggests that statistical significance is sufficient for ascribing causality); Erica Beecher-Monas, Evaluating Scientific Evidence: An Interdisciplinary Framework for Intellectual Due Process 42 n. 30, 61 (2007) (“Another way of explaining this is that it describes the probability that the procedure produced the observed effect by chance.”) (“Statistical significance is a statement about the frequency with which a particular finding is likely to arise by chance.″).

[12] Hodges v. Secretary Dep’t Health & Human Services, 9 F.3d 958, 967 (Fed. Cir. 1993) (Newman, J., dissenting) (citing and quoting from the Report of the Carnegie Commission on Science, Technology, and Government, Science and Technology in Judicial Decision Making 28 (1993).

[13] Ethyl Corp. v. EPA, 541 F.2d 1, 28 n.58 (D.C. Cir.), cert. denied, 426 U.S. 941 (1976).

[14] Carl Sagan, Broca’s Brain: Reflections on the Romance of Science 93 (1979).

Posted in Causation, Rule 702, Scientific Evidence | Comments Off on Rhetorical Strategy in Characterizing Scientific Burdens of Proof

 THE STANDARD OF APPELLATE REVIEW FOR RULE 702 DECISIONS

November 12th, 2014

Back in the day, some Circuits of the United States Court of Appeal embraced an asymmetric standard of review of district court decisions concerning the admissibility of expert witness opinion evidence. If the trial court’s decision was to exclude an expert witness, and that exclusion resulted in summary judgment, then the appellate court would take a “hard look” at the trial court’s decision. If the trial court admitted the expert witness’s opinions, and the case proceeded to trial, with opponent of the challenged expert witness losing the verdict, then the appellate court would take a not-so “hard look” the trial court’s decision to admit the opinion. In re Paoli RR Yard PCB Litig., 35 F.3d 717, 750 (3d Cir.1994) (Becker, J.), cert. denied, 115 S.Ct.1253 (1995).

In Kumho Tire, the 11th Circuit followed this asymmetric approach, only to have the Supreme Court reverse and render. Unlike the appellate procedure followed in Daubert, the high Court took the extra step of applying the symmetrical standard of review, presumably for the didactic purpose of showing the 11th Circuit how to engage in appellate review. Carmichael v. Kumho Tire Co., 131 F.3d 1433 (11th Cir. 1997), rev’d sub nom. Kumho Tire Co. v. Carmichael, 526 U.S. 137, 158-59 (1999).

If anything is clear from the Kumho Tire decision, courts do not have discretion to apply an asymmetric standard to their evaluation of a challenge, under Federal Rule of Evidence 702, to a proffered expert witness opinion. Justice Stephen Breyer, in his opinion for the Court, in Kumho Tire, went on to articulate the requirement that trial courts must inquire whether an expert witness ‘‘employs in the courtroom the same level of intellectual rigor that characterizes the practice of an expert in the relevant field.’’ Kumho Tire Co. v. Carmichael, 526 U.S. 137, 152 (1999). Again, trial courts do not have the discretion to abandon this inquiry.

The “same intellectual rigor” test may have some ambiguities that make application difficult. For instance, identifying the “relevant” field or discipline may be contested. Physicians traditionally have not been trained in statistical analyses, yet they produce, and rely extensively upon, clinical research, the proper conduct and interpretation of which requires expertise in study design and data analysis. Is the relevant field biostatistics or internal medicine? Given that the validity and reliability of the relied upon studies come from biostatistics, courts need to acknowledge that the rigor test requires identification of the “appropriate” field — the field that produces the criteria or standards of validity and interpretation.

Justice Breyer did grant that trial courts must have some latitude in determining how to conduct their gatekeeping inquiries. Some cases may call for full-blown hearings and post-hearing proposed findings of fact and conclusions of law; some cases may be easily decided upon the moving papers. Justice Breyer’s grant of “latitude,” however, wanders off target:

“The trial court must have the same kind of latitude in deciding how to test an expert’s reliability, and to decide whether or when special briefing or other proceedings are needed to investigate reliability, as it enjoys when it decides whether that expert’s relevant testimony is reliable. Our opinion in Joiner makes clear that a court of appeals is to apply an abuse-of-discretion standard when it ‛review[s] a trial court’s decision to admit or exclude expert testimony’. 522 U. S. at 138-139. That standard applies as much to the trial court’s decisions about how to determine reliability as to its ultimate conclusion. Otherwise, the trial judge would lack the discretionary authority needed both to avoid unnecessary ‛reliability’ proceedings in ordinary cases where the reliability of an expert’s methods is properly taken for granted, and to require appropriate proceedings in the less usual or more complex cases where cause for questioning the expert’s reliability arises. Indeed, the Rules seek to avoid ‛unjustifiable expense and delay’ as part of their search for ‛truth’ and the ‛jus[t] determin[ation]’ of proceedings. Fed. Rule Evid. 102. Thus, whether Daubert ’s specific factors are, or are not, reasonable measures of reliability in a particular case is a matter that the law grants the trial judge broad latitude to determine. See Joiner, supra, at 143. And the Eleventh Circuit erred insofar as it held to the contrary.”

Kumho, 526 U.S. at 152-53.

Now the segue from discretion to fashion the procedural mechanism for gatekeeping review to discretion to fashion the substantive criteria or standards for determining “intellectual rigor in the relevant field” represents a rather abrupt shift. The leap from discretion to fashion procedure to discretion to fashion substantive criteria of validity has no basis in prior law, in linguistics, or in science. For instance, Justice Breyer would be hard pressed to uphold a trial court’s refusal to consider bias and confounding in assessing whether epidemiologic studies established causality in a given case, notwithstanding the careless language quoted above.

The troubling nature of Justice Breyer’s language did not go unnoticed at the time of the Kumho Tire case. Indeed, three of the Justices in Kumho Tire concurred to clarify:

“I join the opinion of the Court, which makes clear that the discretion it endorses—trial-court discretion in choosing the manner of testing expert 1reliability—is not discretion to abandon the gatekeeping function. I think it worth adding that it is not discretion to perform the function inadequately.”

Kumho Tire Co. v. Carmichael, 526 U.S. 137, 158-59 (1999) (Scalia, J., concurring, with O’Connor, J., and Thomas, J.)

Of course, this language from Kumho Tire really cannot be treated as binding after the statute interpreted, Rule 702, was modified in 2000. The judges of the inferior federal courts have struggled with Rule 702, sometimes more to evade its reach than to perform gatekeeping in an intelligent way. Quotations of passages from cases decided before the statute was amended and revised should be treated with skepticism.

Recently, the Sixth Circuit quoted Justice Breyer’s language about latitude from Kumho Tire, in the Circuit’s decision involving GE Healthcare’s radiographic contrast medium, Omniscan. Decker v. GE Healthcare Inc., 2014 U.S. App. LEXIS 20049, at *29 (6th Cir. Oct. 20, 2014). Although the Decker case is problematic in many ways, the defendant did not challenge general causation between gadolinium and nephrogenic systemic fibrosis, a painful, progressive connective tissue disease, which afflicted the plaintiff. It is unclear exactly what sort of latitude in applying the statute, the Sixth Circuit was hoping to excuse.

Posted in Rule 702, Scientific Evidence | Comments Off on  THE STANDARD OF APPELLATE REVIEW FOR RULE 702 DECISIONS

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