On the Importance of Showing Relative Risks Greater Than Two – Haack’s Arguments

Professor Susan Haack has set out, repeatedly, to criticize the judicial requirement of relative risks greater than two to support findings that exposure to a substance, process, or medication was a specific cause of a plaintiff’s injury.  If for no other reason than the frequency with which Haack has published on this same issue, her views are worth examining more closely.

Haack’s argument, typically, proceeds along the lines that requiring a relative risk greater than two (RR > 2) is improper because a RR > 2 is neither necessary nor sufficient for finding specific causation.  See, e.g., Susan Haack, “Warrant, Causation, and the Atomism of Evidence Law,” 5 Episteme 253, 261 (2008)[hereafter “Warrant“];  “Proving Causation: The Holism of Warrant and the Atomism of Daubert,” 4 J. Health & Biomedical Law 273, 304 (2008)[hereafter “Proving Causation“].

Unlike the more sophisticated reasons offered by Professor Sander Greenland, Professor Haack’s reasoning fails to understand both the law and the science.

Haack:  RR > 2 Not Sufficient

Haack argues that RR > 2 is not sufficient for two reasons:

“Epidemiological evidence of a doubling of risk is not sufficient for specific causation: first, because if the study showing a doubling of risk is poorly-designed or poorly-executed, we would have only a low epistemological likelihood of a greater than 50% statistical probability; and second, because even a well-designed and well-conducted study might also show that those subjects who develop D [some claimed causally related disease] when exposed to S [some substance] have some characteristic in common – older patients rather than younger, perhaps, or women rather than men, or the sedentary rather than the active – and our plaintiff might be an elderly, sedentary female.”

Proving Causation at 304 (emphasis added).

The first argument is largely irrelevant to the legal context in which the RR > 2 rationale arises.  Typically, plaintiffs assert general and specific causation on the basis of a complex evidentiary display.  This display includes evidence of an epidemiologic association, but the magnitude of the association is weak, with RR > 1, but < 2.  Thus the defendants challenge the attributability in the plaintiff’s individual case.  The overall evidentiary display may or may not support general causation, but even if general causation were conceded, specific causation would remain as independent factual issue.  Haack’s first “argument” is that the RR > 2 argument is insufficient because the study with RR > 2 may lack internal validity on grounds that it was poorly designed, poorly conducted, or poorly analyzed.  True, true, but immaterial.  On motions for summary judgment or directed verdict, the trial court would resolve any factual issues about disputed validity in favor of the non-moving party.  The defense may have better studies that show the RR =1, but these would not factor in the decision to grant or refuse the motion.  (If the defense can show that the plaintiffs’ studies with RR > 2 are fatally flawed, then the plaintiffs might be relegated to their studies with lower risk.)

Haack’s second reason appears to go to external validity.  She suggests that a study at issue may be in a population that shares key risk factors with the plaintiff.  Why this similarity would suggest that RR > 2 is not sufficient is quite mysterious.  External validity would support the applicability of the study, with its RR > 2, not militate against its sufficiency.  If the “characteristic in common” is the basis for an interaction with the exposure to S, then we would expect that to be shown by the data in the study; it would not, and should not, be a matter of conjecture or speculation.

Haack:  RR > 2 Not Necessary

Similarly, Haack argues that RR > 2 is not necessary for two reasons:

“And epidemiological evidence of a doubling of risk is not necessary for specific causation, either: first, because studies that fail to show a doubling of risk may be flawed – for example, by failing to take account of the period of pregnancy in which subjects are exposed to S, or by failing to take account of the fact that subjects are included who may have been exposed to S in cold medication or sleep-aids; 99 and second, because even a good epidemiological study indicating to a high degree of epistemic likelihood that there is a doubling of risk may also indicate that those subjects who develop D have some characteristic (such as being over 50 or sedentary or subject to allergies or whatever) that this plaintiff lacks.100

Proving Causation at 304 (emphasis added).

Again, Haack’s reasoning is nothing other than an invitation to speculate.  Sure, studies with RR < 2 may be flawed, but the existence of flaws in the studies is hardly a warrant for the true RR > 2.  The evidence is the thing; and she is quick to point out elsewhere:  absence of evidence is not evidence of absence.  And so a flawed study is not particularly probative of anything; it cannot be made into affirmative evidence of the opposite result by the existence of a flaw.  Haack seems to be suggesting that the studies at issue, with RR < 2, may be biased low by misclassification or other systemic bias.  Again, true, true, and immaterial.  An epidemiologic study may suffer bias (or not), but if it does, the usual path is conduct the study again without the previous bias.  Sometimes the data may be re-analyzed, and the march of progress is in the direction of having underlying data accessible to permit some degree of re-analysis.  In any event, cases with RR < 2, or RR = 2, are not transformed into cases of RR > 2, solely by hand waving or speculation over the existence of potential bias.  The existence and direction of the bias remains something that must be shown by competent evidence.

As for the second argument, again, Haack invokes external invalidity as a possible reason that a RR > 2 does not necessarily require a finding for plaintiff.  The plaintiff may be sufficiently different from study participants such that the RR > 2 is not relevant.  This argument hardly undermines a requirement for a RR > 2, based upon a relevant study.

These arguments are repeated virtually verbatim in Proving Causation, where Haack asserts for the same reasons that a RR > 2 is neither necessary nor sufficient for showing specific causation.  Proving Causation at 261.

In an unpublished paper, which Haack has presented several times over the last few years, she has criticized the RR >2 argument as an example of flawed “probabilism” in the law.  Susan Haack, “Risky Business:  Statistical Proof of Individual Causation,” in Jordi Ferrer Beltrán, ed., Casuación y atribución de responsibilidad (Madrid: Marcial Pons, forthcoming)[hereafter Risky Business]; Presentation at the Hastings Law School (Jan. 20, 2012);  Presentation at University of Girona (May 24, 2011)

While there is some merit to Haack’s criticisms of probabilism, they miss the important point, which is that sometimes probabilistic inference is all there is.  Haack cites the New Jersey Supreme Court’s decision in Landrigan as supporting her notion that “other evidence,” presumably particularistic, plaintiff-specific evidence, plus a RR < 2 will suffice:

“The following year (1992), in Landrigan, the Supreme Court of New Jersey briskly observed that ‘a relative risk of 2.0 is not so much a password to a finding of causation as one piece of evidence among others’.”

Risky Business at 22 (citing and quoting Landrigan v. Celotex Corp., 127 N.J. 404, 419, 605 A.2d 1079 (1992)).

Haack, however, advances a common, but mistaken reading of Landrigan, where the Court blurred the distinction between sufficiency and admissibility of expert witness opinion on specific causation.  Landrigan, and another case, Caterinicchio v. Pittsburgh Corning Corp., 127 N.J. 428, 605 A.2d 1092 (1992), were both tried to juries, about the same time, in different counties in New Jersey.  (My former partner Terri Keeley tried Landrigan; I tried Caterinicchio.)  There was no motion to exclude expert witness testimony in either case; nor was there a motion for summary judgment ever lodged pre-trial.  Both cases involved motions for directed verdict, in which the defense invited the trial courts to accept the plaintiffs’ expert witnesses’ opinions, arguendo, and to focus on the inference of specific causation, which was drawn upon the assertion that both Mr. Landrigan and Mr. Caterinicchio had an increased risk of colorectal cancer as a result of their occupational asbestos exposure.  Admissibility was never in issue.

There were no valid biomarkers, no “fingerprints” of causation; no evidence of either plaintiff’s individual, special vulnerability.  The plaintiffs had put in their cases and rested; the trial courts were required to assume that the facts were as presented by the plaintiffs.  All the plaintiffs had offered, however, of any possible relevance, was a relative risk statistic. The trial courts in both cases granted the directed verdicts, and separate panels of the New Jersey Appellate Division affirmed.  Riding roughshod over the evidence, the New Jersey Supreme Court granted certification in both cases, and reversed and remanded for new trials.

Haack does an admirable job of echoing the speculation advanced by plaintiffs on appeal, in both Landrigan and Caterinicchio.  She speculates that the plaintiffs may have had greater than average exposure, or that they were somehow more vulnerable than the average exposed person in the relevant studies.

To paraphrase a Rumsfeldian bon mot:  The litigants must go to trial with the evidence that they have.

Both cases were remanded for new trials.  What is often not reported or discussed in connection with these two cases is that plaintiffs’ counsel dismissed Landrigan before proceeding with a new trial.  Caterinicchio was indeed retried — to a defense verdict.

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