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The Capture of the Public Health Community by the Litigation Industry

February 10th, 2014

The American Public Health Association (APHA) is a significant organization ostensibly committed to the improvement of public health. Among its many activities, the APHA publishes a journal, the American Journal of Public Health.  Here is how the APHA describes itself and its activities to advance public health:

“The American Public Health Association champions the health of all people and all communities. We strengthen the profession of public health, share the latest research and information, promote best practices and advocate for public health issues and policies grounded in research. We are the only organization that combines a 140-plus year perspective, a broad-based member community and the ability to influence federal policy to improve the public’s health.”

How could anyone be against the APHA?

A dubious development in the APHA’s history was its evolution as a tool of the litigation industry.  In 2004, after several years of lobbying, agents of the litigation industry managed to push a policy statement past the Association’s leadership, to condemn the requirement of evidence-based reasoning in federal courts in the United States.

The litigation industry’s victory is memorialized in the “Final Minutes of Meetings of the APHA Governing Council, ” held in November 2004, when the industry’s attack on evidence-based science and data transparency, known as “Policy Number: 2004-11 Threats to Public Health Science,” was adopted as an APHA policy statement.

“2004-11” was published in the American Journal of Public Health and is still available on the APHA website, as Policy Number: 2004-11 Threats to Public Health Science.  I have excerpted contentions and recommendations from the APHA policy, in the left column of the chart, below.  My comments are on the right.

 

APHA Policy

Comment
“Acknowledging that within science, absolute proof and perfect information are rare;” Notice the false dichotomy between absolute proof and perfect information and the entire remaining spectrum of scientific information.  This dichotomization has been part of the litigation strategy of passing off hypotheses, preliminary conclusions, unreplicated findings, etc., as though they were acceptable bases for causal conclusions.
“Recognizing that special interests have exploited the nature of science, specifically scientific uncertainty, to delay protective legal and/or regulatory action;” Notice the asymmetry of the accusations; the APHA apparently has no concern for “special interests” that exploit the nature of science by passing off hypotheses as conclusions, and seek to accelerate protective legal and regulatory action by manufacturing faux scientific conclusions.
“Acknowledging that some public health decisions must be made in the absence of perfect scientific information;” “Le mieux est l’ennemi du bien.” But isn’t the good also the enemy of the shabby, dodgy, and fraudulent? Notice again the false dichotomy between “perfect” information and everything else, as though our failing to achieve the perfect opens the door to the worst. True, of course, that sometimes action is needed on incomplete records, but such action is rarely needed for compensation claims.
“Recognizing that special interests, under the guise of a call for “sound science” have sponsored and promoted changes in public policy that have weakened and continue to threaten public health protections;” If the call for sound science cannot be sustained, then this rhetorical gambit will blowback hard on those “special interests.”  Why are these putative scientists, at APHA, so afraid of sound science?
“Recognizing that special interests have challenged highly regarded public health research and researchers, and inappropriately characterized established scientific methods as ‘junk science’;” Mon Dieu!  How cheeky of those special interests.  See the discussion of Dr. Barry S. Levy, below.
“Recognizing that the Daubert decision has propagated misinterpretations and misapplications of scientific principles relied upon throughout the public health sciences, such as insisting that any epidemiologic study that is relied on to support causation demonstrate a twofold increase in risk as well as a reliance on significance testing to determine which scientific findings are to be allowed as evidence;” This contention misunderstands the basic nature of evidence law. Studies, whether they have statistically significant results, or not, are rarely admissible in evidence.  What is admissible, or not, are opinions of duly qualified expert witnesses, who explain and justify the epistemic warrant for their opinions.  With respect to general causation opinions, expert witnesses will often have to show that they have properly ruled out chance, bias, and confounding to arrive at a causal conclusions.  Significance testing can be abused, in both directions, but the APHA ignores the need for having some quantitative approach to assess random variability. As for relative risks greater than two, the APHA is correct that general causation may often be found with small relative risks, but the attribution of causation in an individual claimant often can be made only on probabilistic inferences that will require relative risks greater than two, or even larger.
“Recognizing that special interests are engaged in a campaign to extend Daubert’s reach to those states that have not embraced prescriptive definitions of scientific reliability.” So the APHA makes common cause with those “special interests,” which would abolish all limits on the admissibility of expert witness opinions, and all normative assessments of scientific research.  This position ignores the prescriptive aspect of methodology, and the nature of epistemic warrant in a methodology.

 

What follows from these contentions? 

“Therefore, APHA:”

“Opposes legislation or administrative policies that attempt to define the characteristics of valid public health science, or dictate prescriptive scientific methodologies; and” Admittedly, defining good science is very difficult, but the law often works like science as defining health as the absence of disease.  There are obviously some well-known pathologies of scientific method, and it hardly seems extravagant to urge courts to avoid flaws, fallacies, and fraud.  
“Supports the efforts of other scientific organizations to promote the government’s ability to utilize the best available science to protect the public’s health; and” Of course, sometimes the “best” available science is rather shabby. 
“Urges friend of the court briefs that address the problem inherent in the adoption of Daubert and Daubert-like court rulings, the application of Daubert in regulatory proceedings, and when judges misinterpret scientific evidence in their implementation of the Daubert ruling.” We do not see many APHA-types deploring jury verdicts that offend scientific sensibilities; and so the APHA’s urging here seems again rather one-sided and partisan.  The fact, however, that judges’ misinterpretations of scientific evidence can be criticized publicly is one of the key differences that separates judicial gatekeeping from the black box of jury determinations.

In 2005, the APHA published, in its journal, APJH, a special supplement, “Scientific Evidence and Public Policy,” with

“academic analysis of the conflicts arising in the use of science in regulatory, civil and criminal proceedings. This special issue examines how recent developments in the legal and regulatory arenas have emboldened corporations involved in civil litigation and regulatory proceedings to accuse adversaries of practicing ‘junk science’.”

Apparently, the APHA was not, and is not, concerned with the emboldening the  litigation industry and its efforts to subvert the truth-finding function of civil litigation. 

David Michaels served as the guest editor for the APJH supplement.  Michaels repeated many of the contentions of the 2004 Policy Statement, above, and he added some new ones of his own:

  • Judges are no better than juries in assessing scientific evidence.
  • Scientists evaluate all the evidence by applying a “weight-of-the-evidence” approach.
  • Uncertainty in science is normal and does not mean the underlying science flawed.

David Michaels, “Editorial: Scientific Evidence and Public Policy,” 95 (Supp. 1) Am. J. Pub. Health S5 (2005). These are all serious half truths.  Many judges are quite astute when evaluating scientific evidence, but even the lowest aptitude judges must give articulated reasons for their decisions, which opens up a public process of comment, correction, and criticism.  Juries vote in secret, without having to explain or justify their verdicts.  Scientists, metaphorically speaking, weigh evidence, as do non-scientists, but this opaque metaphor hardly explicates the process of how scientists arrive at conclusions about causal relationships.  And uncertainty is a condition of many scientific fields, but the error lies in trying to pass off tentative, uncertain, preliminary observations and findings as knowledge.

Michaels sees the development of judicial gatekeeping as favoring “the powerful,” and hurting “the weak and vulnerable.” Id. Michaels did not seem to mind if his editorial recommendations favored the litigation industry and hurt the truth.  He now heads up the Occupational Health & Safety Administration.

Here is how Michaels and the APHA described the funding for the AJPH supplement:

“Support for the supplement was provided through unrestricted funding to the Project on Scientific Knowledge and Public Policy (SKAPP) from the Common Benefit Litigation Trust, a fund established by court order in the Silicone Gel Breast Implant Products Liability Litigation. SKAPP is an initiative of scholars that examines the application of scientific evidence in the legal and regulatory arenas. SKAPP is based at the George Washington University School of Public Health and Health Services; more information is available at www.DefendingScience.org.”

See APHA website <http://www.apha.org/about/news/pressreleases/2005/05arenas.htm>, last visited on February 10, 2014.

This pseudo-disclosure is perhaps the most fraudulent aspect of the entire APHA enterprise.  The Common Benefit Trust was a fund that was held back from settlement monies paid by defendants in the silicone gel breast implant litigation.  The Trust was nothing more than the Plaintiffs’ Steering Committee’s war chest, from which it could advance litigation goals within MDL 926 (silicone breast implant cases).  Ironically, the appointment of neutral, court-appointed expert witnesses led to the triumph of “sound science,” and the collapse of the plaintiffs’ counsel house of cards.  Rather than returning their litigation expense fund to the claimants, the plaintiffs’ counsel found a more worthwhile recipient — SKAPP — to advance their litigation goals, if not for MDL 926, then for the next MDL, and the next, and the next….  See SKAPP A LOT; and Conflicted Public Interest Groups.

* * * * * * *

The same year that the APHA published the SKAPP-inspired and funded challenges to Federal Rules of Evidence 702, the APHA awarded its most prestigious award, the Sedgwick Medal, to a physician whose opinions had routinely been found to be unreliable and irrelevant in various litigation industry efforts. “Barry Levy Wins APHA’s Oldest and Most Prestigious Award, the Sedgwick Medal.” (December 11, 2005).

Perhaps the APHA had Levy in mind when it complained that “special interests have challenged highly regarded public health … researchers….”  Dr. Levy seems to have less favorable accolades from trial and appellate judges.  For instance, one federal judge found Levy engaged in a dubious enterprise to manufacture silicosis claims in Mississippi.  In re Silica Products Liability Litigation, 398 F. Supp. 2d 563, 611-16, 622 & n.100 (S.D. Texas 2005) (expressing particular disappointment with Dr. Barry Levy, who although not the worst offender of a bad lot of physicians, betrayed his “sterling credentials” in a questionable enterprise to manufacture diagnoses of silicosis for litigation).[1] Interestingly, Judge Jack’s opinion was not mentioned in the APHA press release for Dr. Levy’s award ceremony.


[1] See Schachtman, Silica Litigation: Screening, Scheming & Suing; Washington Legal Foundation Critical Legal Issues Working Paper Series No. 135 (Dec. 2005) (exploring the ethical and legal implications of the entrepreneurial litigation in which Levy and others were involved). See also Lofgren v. Motorola, Inc., 1998 WL 299925, No. CV 93-05521 (Ariz. Super. Ct., Maricopa Cty. June 1, 1998); Harman v. Lipari, N.J. L. Div. GLO-L-1375-95, Order of Nov. 3, 2000 (Tomasello, J.) (barring the use of Barry Levy in class action for medical monitoring damages); Castellow v. Chevron USA, 97 F.Supp. 2d 780, 793-95 (S.D. Tex. 2000); Knight v. Kirby Inland Marine Inc., 482 F.3d 347 (5th Cir. 2007); Watts v. Radiator Specialty Co., 990 So. 2d 143 (Miss. 2008); Aurand v. Norfolk So. Ry., 802 F.Supp.2d 950 (2011); Mallozzi v. Ecosmart Technologies, Inc., 2013 WL 2415677, No. 11-CV-2884 (SJF)(ARL) (E.D.N.Y. May 31, 2013).

Posted in Conflicts of Interest, Expert Witnesses, Rule 702 | Comments Off on The Capture of the Public Health Community by the Litigation Industry

The Not-So-Elite Defense Bar’s Approach to Gatekeeping

January 2nd, 2014

A couple of months ago, Professor David Bernstein posted to the Volokh Conspiracy, a short piece about some of the missteps and mistakes committed by “elite defense counsel” in litigating expert witness issues.  See David Bernstein, “The Elite Defense Bar and Expert Evidence” (Nov. 6, 2013).  Professor Bernstein makes some interesting points about questionable positions taken by “elite defense counsel” (read: “highly paid, large firm lawyers”).  For instance, according to Bernstein:

1. elite defense lawyers missed the boat early on by arguing that statistical evidence (observational epidemiology) was inadmissible or insufficient to prove general or specific causation;

2. defense counsel missed the significance of the Supreme Court’s opinion in Daubert;

3. defense counsel continued to press for Frye rule in state courts, although the Frye rule had been shown inadequate and unavailing as a rule to control medical causation opinions; and

4. defense bar has grown soft on Rule 702.

Although the charges seem at points overstated, Bernstein has presented an important indictment of the defense bar.  At the very least, the charges deserve a full exploration by a wider audience. Defense lawyers who are self-critical about their practice should certainly be concerned that someone as persistently pro-702 has taken aim at them.

On the first point, many of the early scientific causation battles were fought in tobacco litigation, in which defendants and their counsel were forced to deny and contest the obvious, the causal role for tobacco in carcinogenesis, at all costs.  The tobacco defense bar, however, should not be confused with the defense bar, generally.  Defense lawyers in Bendectin, silicone, and asbestos cases developed arguments against specious use of epidemiologic evidence, as well as sophisticated, affirmative use of epidemiologic evidence to show lack of association.  Even so, we should keep in mind that it often requires a large body of epidemiologic evidence to show “no association,” and it is not the defense’s burden to do so. 

The use of statistical or probabilistic evidence for inferring specific causation has been, and remains, problematic. See, e.g., Richard Doll, “Proof of Causality: Deduction from Epidemiological Observation,” 45 Perspectives in Biology & Medicine 499, 500 (2002) (“That asbestos is a cause of lung cancer in this practical sense is incontrovertible, but we can never say that asbestos was responsible for the production of the disease in a particular patient, as there are many other etiologically significant agents to which the individual may have been exposed, and we can speak only of the extent to which the risk of the disease was increased by the extent of his or her exposure.”) Notwithstanding the controversy, defense counsel and some astute judges have understood the indeterminate nature of statistical evidence for specific causation, and have advanced a pragmatic position of resolving specific causation controversies against plaintiffs when risk ratios failed to exceed two. See, e.g., In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 785, 836 (E.D.N.Y. 1984) (“A government administrative agency may regulate or prohibit the use of toxic substances through rulemaking, despite a very low probability of any causal relationship.  A court, in contrast, must observe the tort law requirement that a plaintiff establish a probability of more than 50% that the defendant’s action injured him. … This means that at least a two-fold increase in incidence of the disease attributable to Agent Orange exposure is required to permit recovery if epidemiological studies alone are relied upon.”), aff’d 818 F.2d 145, 150-51 (2d Cir. 1987)(approving district court’s analysis), cert. denied sub nom. Pinkney v. Dow Chemical Co., 487 U.S. 1234 (1988).

Early use of meta-analysis by plaintiffs’ expert witnesses elicited generalized attacks on meta-analysis by defense counsel.  See, e.g., In re Paoli Railroad Yard PCB Litigation, 706 F. Supp. 358, 373 (E.D. Pa. 1988) (Kelly, R., J.) (excluding plaintiffs’ expert witness Dr. William Nicholson and his testimony based upon his unpublished meta-analysis of health outcomes among PCB-exposed workers), rev’d 916 F.2d 829, 856-57 (3d Cir. 1990), cert. denied, 499 U.S. 961 (1991).  Again, it took some time for the defense to understand the potency of meta-analysis in synthesizing and presenting a summary point estimate that essentially rules out any meaningful play of chance. In the silicone gel breast implant litigation, one defense expert witness conducted and published his meta-analysis of autoimmune disease outcomes. Otto Wong, “A Critical Assessment of the Relationship between Silicone Breast Implants and Connective Tissue Diseases,” 23 Regulatory Toxicol. & Pharmacol. 74 (1996).  When the MDL 926 court got around to appointing court-appointed expert witnesses, they too picked up on the approach and made meta-analyses the hallmark of their reports. See Barbara Hulka, Betty Diamond, Nancy Kerkvliet & Peter Tugwell, “Silicone Breast Implants in Relation to Connective Tissue Diseases and Immunologic Dysfunction:  A Report by a National Science Panel to the Hon. Sam Pointer Jr., MDL 926 (Nov. 30, 1998)”; Barbara Hulka, Nancy Kerkvliet & Peter Tugwell, “Experience of a Scientific Panel Formed to Advise the Federal Judiciary on Silicone Breast Implants,” 342 New Engl. J. Med. 812 (2000).

On the second charge, many defense lawyers missed, and continue to miss, the significance of a shift to evidence-based scientific testimony, as opposed to the authority-based worldview.  When I first started trying cases, senior trial lawyers instructed me not to engage plaintiffs’ expert witnesses on substantive issues, but to limit cross-examination to “collateral attack” on bias and related issues.  The problem that I saw was that when both sides limited the attack to the other side’s expert witness’s bias, the plaintiffs won because juries were often all too willing to think the worst of defense experts, and forgive plaintiffs’ experts.  Nothing short of dramatically confronting the jury with the rubbish, inconsistencies, and incoherence spouted by the plaintiffs’ expert witnesses worked.  I quickly learned to ignore the old timers’ advice, and most of them have now dropped off.

Bernstein gives the example of the Dow Corning lawyers’ declining the Ninth Circuit’s invitation to reframe their appeal in Hopkins v. Dow Corning, 33 F.3d 1116 (9th Cir. 1994), after the Supreme Court handed down Daubert.  He may well be right about that case, but the lawyers may have been inhibited by positions that they had taken earlier in the case, before the Supreme Court breathed life into Rule 702.  Still, the Hopkins decision remains a derelict on the jurisprudential sea of expert witness law. Truth be told, there are other cases that turned out badly because of overstated or poorly framed defense arguments. 

As for their persistent affection for Frye, the defense lawyers referenced by Bernstein certainly lacked imagination, and maybe even a full measure of zeal.  The Frye case had never proven itself to be an important defense against specious expert witness opinion testimony on medical causation issues.  Daubert held out the promise that trial judges would actually have to engage with the evidence, rather than counting noses for “general acceptance,” or kicking the can, after hearing qualifications. I still recall how my colleagues and friends viewed Daubert, in 1993.  Bristol Myers Squibb and other companies were inundated by silicone breast implant cases, and plaintiffs had managed to snucker a few juries into returning large verdicts against the defendants.  Daubert was a lifeline, a way to focus trial judges’ attention on the plaintiffs’ expert witnesses and the fatally flawed, even fraudulent scientific studies that had found their way into the peer-reviewed journals, and into the courtroom.

What has happened to Daubert?  Well, of course, it is no longer Daubert, but now a much more potent statutory rule, Federal Rule of Evidence 702, as amended in 2000, and recently “restylized.”  Professor Bernstein may be on to something in calling out the hubris of big firm lawyers, who think that their prowess in  litigating scientific issues comes from charging high fees.  The sad truth is that the level of scientific and statistical acumen of lawyers generally, whether at the bench or at the bar, is low.  There is much work for law schools to do to change this situation. 

There are other forces at work in creating the phenomena described by Professor Bernstein.  Many product liability cases involve multiple defendants.  Defending such cases from the defense perspective is often like herding house cats.  Every defense counsel thinks he or she knows the best course; no one wants to do anything that raises the profile of his client or increases the cost of defense. Furthermore, products liability defense work has become increasingly “commoditized” in the last two decades.  Clients and third-party payors increasingly impose budgets that do not allow defense lawyers sufficient time to develop the necessary expertise and learning to discover, understand, and challenge plaintiffs’ scientific expert witnesses fully and effectively. There is, sadly and unfortunately, a contingent of defense lawyers who would rather see speculative claims flourish and mature into full-scale litigation, with lots of trials and appeals (and large fees), than to see specious claiming pretermitted by pre-trial judicial gatekeeping.

Another factor that may have stunted the gatekeeping process is the growth of federal (and state) multi-district litigation (MDL).  By centralizing the pre-trial handling of large, multi-plaintiff tort litigation in the hands of a single judge, the MDL process has raised the stakes for the trial judge gatekeeping.  The MDL judge is no longer deciding a single case, but the fate of thousands of claimants.  The Rule 702 process suffers in several ways.  First, many MDL judges are clearly intimidated by the life-or-death control they have over hundreds, if not thousands, of claims.  These judges may well now be inclined to deny the Rule 702 challenges, in the fond hope that juries and appellate courts will take care of the problem. Second, there is no longer the incremental decision making of case-by-case exploration of the issues.  There are economies of scale, to be sure, but the single MDL judge cannot learn from previous trial judges’ decisions and records.  The evolutionary approach of the common-law is undermined by the efficiencies of MDL procedure. Third, the MDL process blunts one of the virtues of judicial gatekeeping in requiring the transparent statement of reasons for the grant or denial of a Rule 702 motion to exclude expert evidence.  By the time the scientific, legal academic, and legal practitioner communities can weigh in on the gatekeeping process, the Rule 702 decision is a fait accompli, in the form of a single judicial decision. Compare  In re Avandia Marketing, Sales Practices and Product Liability Litigation, 2011 WL 13576, *12 (E.D. Pa. 2011) (Rufe, J.) (denying defendant’s Rule 702 motions with respect to plaintiffs’ expert witnesses’ opinions that Avandia causes heart attacks) with “FDA Drug Safety Communication: FDA requires removal of some prescribing and dispensing restrictions for rosiglitazone-containing diabetes medicines” (Nov. 25, 2013) (re-evaluating evidence that Avandia does not increase risk of heart attacks).  See also “Learning to Embrace Flawed Evidence – The Avandia MDL’s Daubert Opinion” (Jan. 10, 2011).

Not surprisingly, plaintiffs’ counsel have gotten better at dressing up weak and fatally flawed evidence as “inference to the best explanation,” or “weight of the evidence” evaluations that have the appearance without the reality of scientific conclusions. And as evidenced by the Third Edition of the Reference Manual on Scientific Evidence, and many recent 702 decisions in the Circuits (and Matrixx Initiatives in the Supreme Court), the federal judiciary has lost its will and its way in applying Rule 702. An activist core of federal trial and appellate courts have shown increasing hostility and outright disregard for the gatekeeping process, and a willingness to disregard the language of the statute, Supreme Court precedent, and sound scientific and statistical methodology.  Rule 702 in its present form is a strong rule, but unfortunately it is neutralized in the hands of weak judges who cannot or will not explore the intricate methodological issues raised by Rule 702 and 703 motions.

The phenomenon identified by Professor Bernstein may be real, but like many natural (and unnatural) phenomena, the causes are not always easily discerned. The phenomenon and its causes are worth a deeper exploration.

Posted in Expert Witnesses, Rule 702 | Comments Off on The Not-So-Elite Defense Bar’s Approach to Gatekeeping

Gastwirth on the Wells Case

December 27th, 2013

One of the high points of 2013 for me was the Practicing Law Institute seminar on expert witness gatekeeping.  I am indebted to my co-chair David Cohen, and the talented participants, Dr. David Garabrant, Joe Cecil, Mary Wells, and Mike Williams.  I learned a great deal from all of them, even when we disagreed.

At the seminar, which addressed the slippage in the federal judiciary’s fidelity to Rule 702 text and principles, Joe Cecil kindly reminded me of Professor Gastwirth’s contribution on the Wells v. Ortho Pharmaceutical Corp., 615 F. Supp. 262, 298 (N.D. Ga. 1985), aff’d and rev’d in part on other grounds, 788 F.2d 741 (11th Cir.), cert. denied, 479 U.S.950 (1986).  Joseph L. Gastwirth, “The need for careful evaluation of epidemiological evidence in product liablility cases: a reexamination of Wells v. Ortho and Key Pharmaceuticals,” 2 Law, Probability and Risk 151 (2003).

The Supreme Court recently reinvigorated the Wells case, and like Frankenstein’s monster, it walks again.  Matrixx Initiatives, Inc. v. Siracusano, 131 S. Ct. 1309 (2011).  See also “Matrixx Unloaded.”  As a result of the Matrixx decision, I revisited the untoward Wells decision several times this year. See “Wells v. Ortho Pharmaceutical Corp. Reconsidered – Part 1”; and here, here, here, here, and here.  Joe’s reminder, however, provoked me to look one more time at Wells, through the lens of Gastwirth’s review.

Gastwirth is a well-known statistician, not a lawyer.  His article undertakes some interesting sensitivity analyses of the potential role of one known confounder in the epidemiologic studies of spermicides and birth defects, cited by witnesses in Wells. Not surprisingly, Gastwirth confuses important legal concepts, when he contends that science and law have different goals because science has the luxury of waiting for additional studies to resolve indeterminate datasets.  Gastwirth at 154. Gastwirth suggests that in law, causality determinations turn on fairness, but in science, they turn on the truth.  Gastwirth offers no support for his assertion, and there is much law to the contrary.  Federal Rule of Evidence 102, for instance, explains the “Purpose” of the Federal Rules and how they should be construed:

“These rules should be construed so as to administer every proceeding fairly, eliminate unjustifiable expense and delay, and promote the development of evidence law, to the end of ascertaining the truth and securing a just determination.”

Truth does count, at least in some courts, and it is hard to imagine a case in which the goals of truth and justice are bifurcated. Gastwirth sees law courts as unable to avoid judgment when the evidentiary display is weakly developed or not replicated, but he is wrong.  Courts can, do, and should avoid permitting judgments based upon indeterminate datasets.

Gastwirth also contends that the duty to warn in tort is based upon a possibility of causation, and he opines that this is perfectly satisfactory.  Gastwirth at 155.  Gastwirth cites the Restatement (Third) a/Torts for his view, but the Restatement does not couch the duty to warn as predicated upon merely possible risk:

“A defendant will not be liable under an implied warranty of merchantability for failure to warn about risks that were not reasonably foreseeable at the time of sale or could not have been discovered by way of reasonable testing prior to marketing the product. A manufacturer will be held to the standard of knowledge of an expert in the appropriate field, and will remain subject to a continuing duty to warn of risks discovered following the sale of the product at issue.”

Id. (emphasis added).  Gastwirth fails to explain why the epistemic standard of the Restatement should be diluted to include merely possible risks; nor does he explain why the law should impose a duty because a minority of so-called experts claim knowledge of the existence of a risk, whether potential or known.

Risks are based upon known causal relationships, viewed ex ante rather than post hoc.  Gastwirth attempts to defend the Wells decision on the basis that the trial judge, Judge Shoob, could have correctly found a possible risk, but this was not then or now the standard for imposing a duty to warn.  Even if possibilities were the basis for a duty to warn, the courts in Wells had to find sufficient evidence of cause in fact between the spermicidal jelly and the birth defect present in the infant plaintiff.  No merely possible risk could have satisfied this burden, and Gastwirth avoids this important issue in his review.  Ultimately, Gastwirth fails to come to grips with how the Wells courts artificially distinguished two causation standards – warning-harm and product-harm.  Gastwirth at 184.

When courts are required to work with an epistemic standard for evaluating opinions about causal claims, they will often confront sincere beliefs supported by “putative” justifications, but which turn out to be untrue.  The obvious implication is that the causal opinions were not “true” when offered, and the asserted, putative justification was no justification at all.  Twenty years post-Daubert should have made our courts more sensitive to the pathology of claiming, or pathoepistemology, as I call it.

Although Gastwirth is intent to show that the district and circuit court decisions in Wells were reasonable given the record evidence at the time of their decisions, Gastwirth’s defense is tepid at best. Gastwirth concedes that the plaintiffs’ evidence in the Wells case was not very convincing, and he is quick to point out that he does not conclude that spermicides cause limb reduction defects (although he does believe that the data were sufficient for his idiosyncratic diluted duty-to-warn legal standard:

 “The epidemiological evidence in the Wells case surely was not very convincing and it is understandable that scientists and legal scholars might desire stronger scientific evidence before holding a defendant liable. What seems unfortunate is the lack of discussion of the part of the record most supportive of the legal decisions from the published criticisms.201 While it is reasonable to ask how much evidence should be required before a warning is required, is it fair to rely on studies that were published after the time of exposure to assess the producer’s duty at the time?”

Gastwirth at 184-85.  The equivocation in this passage between assessing causation for a duty to warn and for product harm is typical of Gastwirth’s confusion throughout this article.  As noted, Gastwirth appears to believe it is sufficient to show the plausibility of the causal relationship such that the trial court’s findings of a duty to warn, and a breach of that duty, were reasonably supported:

“It should be stressed that our examination of the studies does not conclude that exposure to spermicides causes limb reduction defects. 202 Indeed, the studies published in the 1980s are sensitive to the potential effect of unmeasured known potential risk factors that were not controlled for in the analysis. Many studies observed that it is difficult to rule out small but meaningful risks given their sample size or that more studies including potential confounding variables be carried out before a scientific conclusion can be reached.203”

Gastwirth at 185 & n.202.  So small increased risks were difficult to rule in or rule out, but then how can a judgment for plaintiffs be sustained unless, as I have shown elsewhere, Judge Shoob improperly placed the burden of proof upon the defendant?  The studies published in the 1980s may have been sensitive to the potential effect of unmeasured and uncontrolled known potential risks, but Judge Shoob clearly was not sensitive to the problem at all.

Other problems abound. The studies involved in the Wells case not only failed to account for the few known confounders at the time, but they could not and did not sort out the residual confounding.  Gastwirth concedes the point in a footnote, in which he cites a paper by Professor Gary Shaw on the role of multivitamin use in preventing birth defects. See Gastwirth at 185 & n. 202 (citing Shaw et al., “Maternal Periconceptional Use of Multivitamins and Reduced Risk for Conotruncal Heart Defects and Limb Deficiencies Among Offspring,” 59 Am. J. Med. Genetics 536 (1995) (showing that children of mothers who had taken vitamins and folic acid had a 30-35% lower risk of limb defects).  Gastwirth sees the discovery of causes not previously controlled for in the spermicide/birth defect studies of the 1980s as example of the differences between scientific and legal judgments.  Another way to look at such discoveries is to impose some standard of intellectual modesty upon courts in basing their findings upon speculative causal claims.

Gastwirth’s casual dismissiveness of the need for replication in a legal standard of causation is difficult to square with his acknowledgment that early studies often prove misleading about the existence of a true risk.  Gastwirth, for instance, acknowledges that later publications quite commonly do not support initial hypotheses.  Gastwirth at 179, 184 (citing Michael B. Bracken, “Spermicidal Contraceptives and Poor Reproductive Outcomes: The Epidemiologic Evidence Against an Association,” 151 Am. J. Obstet. & Gyncecol. 552, 555 (1985)).  Gastwirth channels the anti-manufacturer Zeitgeist for his claim that “firms” may not report studies that show risk, but he ignores the pervasive, prevalent practice of academic and advocacy scientists’ not publishing negative studies in the first place, and even later in the natural history of scientific controversies.

Ultimately, however, Gastwirth’s own judgment is a self-fulfilling prophecy of how the law and science should part company over false-positive assertions of causality.  Fortunately, the law has evolved in a different direction, towards convergence of scientific and legal modes of assessing causal claims.  Now judges must evolve as well.

Posted in Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Gastwirth on the Wells Case

Pennsylvania Superior Court Takes The Bite Out of Fixodent Claims

December 12th, 2013

In the spring of 2012, Judge Sandra Mazer Moss granted summary judgment to Proctor & Gamble, after excluding, on Frye grounds, plaintiff’s expert witnesses who opined that plaintiff suffered zinc neurotoxicity from his use of Fixodent.  Jacoby v. Rite Aid Corp., 2012 Phila. Ct. Com. Pl. LEXIS 208 (2012).  See “Philadelphia Plaintiff’s Claims Against Fixodent Prove Toothless” (May 2, 2012).  Judge Moss’s exclusion of plaintiff’s expert witnesses involved a careful analysis of the evasive, hand-waving tactics of the witnesses.  Among the plaintiff’s team of expert witnesses was Dr. Martyn Smith, the chief hand waver and obscurantist in Milward v. Acuity Specialty Products Group, Inc., 664 F.Supp. 2d 137 (D. Mass. 2009), rev’d, 639 F.3d 11 (1st Cir. 2011), cert. denied, U.S. Steel Corp. v. Milward, ___ U.S. ___, 2012 WL 33303 (2012).

On Monday, December 9, 2013, after a careful review, the Pennsylvania Superior Court affirmed summary judgment for Proctor & Gamble in the Jacoby case. Jacoby v. Rite Aid Corp., Pa. Super. Ct. No. 1508 EDA 2012 (Dec. 9, 2013) [Slip op.]  The Superior Court panel, consisting of Judges Stevens, Lazarus, and Colville, largely adopted Judge Moss’s analysis and affirmed in a signed, but unpublished, opinion by Judge Lazarus. 

Like Judge Moss before them, the Panel saw through the attempt to pass off “Weight of the Evidence” (WOE) and “Totality of the Evidence” (TOE) as scientific methodologies.  The witnesses, Martyn Smith and others, failed to specify what evidence they weighed, how they weighed the evidence, and what the weights supposedly were.  Another expert witness vaguely pointed to the “Naranjo scale” in support of interpreting case reports to show causal association, but this scale was similarly incompetent other than as a crude “plausibility” scale for assessing case reports.

The Superior Court’s decision in Jacoby is noteworthy on several important issues. There was no material issue as to whether zinc at some dose and duration of exposure can cause neuropathies.  The Court saw, however, that the important issue was whether zinc in the form, dose, and duration ingested by plaintiff can cause the outcome he experienced, and whether his exposure to zinc in Fix-o-dent actually caused his alleged injury.  The Superior Court re-affirmed Pennsylvania’s case law that makes extrapolation from different doses, different durations, and different biological circumstances, a “novel” claim that is subject to the gatekeeping by the so-called Frye standard. Slip op. at 11.

The Superior Court’s opinion astutely observed that the issue was not whether WOE and TOE are accepted scientific methodologies, but whether expert witness Martyn Smith can “evade a reasoned Frye inquiry merely by making reference to accepted methods in the abstract.”  Id. at 12 (citing Betz, at 58).  When pressed, Martyn Smith’s invocation of WOE amounted to little more than a distortion and abridgment of the Bradford Hill factors.  The Superior Court recognized, however, that the Bradford Hill guidelines provide an evaluative process to consider whether an association, after first being shown to be clear cut and not attributable to chance, is causal or spurious.  Id. at 13.  As Bradford Hill postulated the question that arises before his famous nine factors come into the analysis:

“Disregarding then any such problem in semantics we have this situation. Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance. What aspects of that association should we especially consider before deciding that the most likely interpretation of it is causation?”

Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295, 295 (1965) (emphasis added).

In this case, Smith never got off the dime with his evasive tactics.  He did not identify a quantified association that could be assessed for the play of random variation, or bias and confounding.  Smith tried to suggest that a mere possibility of an association was sufficient to invoke the Bradford Hill guidelines, but the Superior Court rejected this attempt to invent a new-age scientific method. Slip op. at 13.

The Superior Court acknowledged that the scientific literature describes WOE as varying from nothing more than “seat-of-the-pants qualitative assessment” to “aggregating diverse modalities.”  Id. at 14.  In Smith’s hands, WOE was little more than a personal, subjective opinion, an ipse dixit dressed as a scientific opinion.  Smith never defined his WOE approach, and the other witnesses never defined their TOE approach.  The plaintiffs’ witnesses in Jacoby failed to offer an accepted methodology when they failed to identify the forms of evidence they considered, and how they went about weighing the evidence upon which they had relied.  Id. at 15.

In a brief discussion, the Panel also embraced another basic evidentiary principle to dismiss a common tactic in specious claiming. The plaintiffs’ challenged defendants’ pharmokinetic study and tried to suggest that their deconstruction counted as affirmative evidence to support their own theory of biological fate and distribution. Id. at 16.  The Superior Court saw through the ruse; the plaintiffs had not created affirmative evidence for their theory by arguing that the defendants’ study was flawed. 

The Superior Court squarely confronted the limitations and inadequacy of relying upon descriptive, anecdotal case reports. Case reports provide a narrative and temporal history of events with respect to exposure and outcome, but they cannot fully account for confounding by known and unknown factors.  Case reports represent post hoc assessments that were not planned, and therefore lack data that would permit distinguishing coincidence from causality.  Id. at 17 (citing Dr. Lorene Nelson’s report).  See In re Denture Cream Prods. Liab. Litig., 795 F. Supp. 2d 1345 (S.D. Fla.2011).

Proctor & Gamble had the good fortunate to have obtained a good ruling in the MDL litigation in the Southern District of Florida, which no doubt helped focus the gatekeeping process in Pennsylvania state court. Unfortunately, the Superior Court Panel chose not to publish its decision.  This decision is regrettable for its inconsistency with the transparency and due process expected of all courts.  See Erica Weisgerber, “Unpublished Opinions: A Convenient Means to an Unconstitutional End,” 97 Georgetown L.J. 621 (2009).

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Avoiding Nonsense About Science — Ask For The Evidence

November 25th, 2013

Sense about Science is a British charitable organization that is devoted to helping people understand scientific and medical claims. Sense about Science acknowledges that:

“Sharing scientific reasoning involves giving people the tools to question pseudoscience and misleading claims, to help cut through the noise around scientific or medical issues.”

To further its laudable goals, Sense about Science has launched an “Ask for Evidence Campaign”:

“We hear daily claims about what is good for our health, bad for the environment, how to improve education, cut crime, treat disease or improve agriculture. Some are based on reliable evidence and scientific rigour. Many are not.  How can we make companies, politicians, commentators and official bodies accountable for the claims they make? If they want us to vote for them, believe them or buy their products, then we should Ask for Evidence.”

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Mr. Nicholas Kristof grew up on a cherry farm, and went on to a successful academic and writing career. For over a decade,  Kristof has written “columns” for The New York Times, a public platform that has helped him win two Pulitzer Prizes.  Sometimes, Kristof’s early experience in cherry picking has helped him with discussions of scientific issues, which seem more like “Nonsense about Science.”  Consider yesterday’s New York Times, in which, Kristof combines cherry picking with scare mongering.  See “Danger Lurks in That Mickey Mouse Couch”:

“RESEARCHERS this summer purchased 42 children’s chairs, sofas and other furniture from major retailers and tested them for toxic flame retardants that have been linked to cancer, birth defects, diminished I.Q.’s and other problems.”

Besides the vague and conclusory language of “links,” Kristof does not cite a scintilla of evidence; instead he cites opinion from an environmentalist organization, Center for Environmental Health (CEH).  What is the CEH?  From its website, the CEH appears to be a group led by actors, community activists, politicians, self-styled “philanthropists,” advocates for “environmental justice.”  No serious scientists appear on the CEH’s board of directors, or on its staff, which is populated mostly by lawyers and activists.

Does the CEH, without the benefit of real scientific talent, marshal serious scientific evidence?  You should judge for yourself by reading the webpage that Kristof cites.  See CEH, “Playing on Poisons: Children’s Furniture Found with Harmful Flame Retardant Chemicals” (November 20, 2013).  If diligent readers of Kristof’s column were to read his “source,” they would find only hand waving and opinionated pronouncements without any reference to supporting scientific studies. Perhaps there is something to the accusations made by Kristof and his band of “environmental justice” advocates, but nothing in the column or its sources would shed any light on the matter. 

Mr. Kristof prefers to deal in vague, if not meaningless terms, such as “links” between chemical exposures and myriad dire outcomes.  He patronizes readers by giving them no understanding of the quantity or quality of the evidence that supports his innuendo.  Kristof repeats his bad, unscientific brand of journalism on his blog. See Nicholas Kristof, “Are You Sitting Down? On a Couch?” (Nov. 23, 2013).

Citing regulatory approval of the fire retardants at issue, the American Chemistry Council has taken Mr. Kristof to task.  See “New York Times columnist and new docudrama mislead public on importance of flame retardants, strong fire safety standards” (Nov. 23, 2013).  The Council’s webpage points to other sites that provide some additional evidence of regulatory approvals and efficacy testing of fireproofing chemicals, but it does not list the chemicals involved, and it does not address the biological causal claims made by Kristof and the CEH.  Nor does the American Chemistry Council mention that the litigation industry (a/k/a plaintiffs’ bar) has waged war against the use of companies for using natural, flammable fabrics and materials.

The Sense about Science organization focuses upon scientific nonsense mostly in the United Kingdom.  Kristof’s brand of hit-and-run journalism illustrates that we very much need a similar organization in the United States.  The discussion and debate over health issues should not take place by the trading of assertions and adjectives, without reference to the actual evidence at hand.  Interestingly, in the same issue of the New York Times, which carried Kristof’s column, two reporters, Walt Bodganich and Glenn Silber, covered a flawed forensics investigation in Florida.  Bodganich & Silber, “Two Gunshots on a Summer Night,” New York Times, A1 (Nov. 24, 2013).  In almost four full pages of coverage, these Times reporters analyze the circumstantial and forensic evidence in great detail to expose a flawed police investigation.  Although the death involved, and the police incompetence suggested by these journalists, is a tragedy, the inability of a newspaper to cover a story that alleges many thousands of deaths, with any attention to the actual evidence, is a much greater tragedy.

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The aversion to reading and understanding the actual scientific evidence finds ample expression in the legal arena. In the recent case of Jackson v. Pollion, the Seventh Circuit chided the lawyers, and trial judges, for their failure to examine and understand the scientific evidence at issue in the merits of the case. Jackson v. Pollion, No. No. 12-2682 (7th Cir. Oct. 28, 2013) (Posner, J.).  Judge Posner argued the noteworthiness of the lapse by the advocates and the judges:

“This lapse is worth noting because it is indicative of a widespread, and increasingly troublesome, discomfort among lawyers and judges confronted by a scientific or other technological issue.”

Slip op. at 2.

And in more Kierkegaardian terms, Judge Posner admonishes the legal profession:

“The legal profession must get over its fear and loathing of science.”

Slip op. at 8.

Indeed!  Judge Posner’s admonition is undermined by the current Federal Rule of Evidence, which diminish the value of underlying data and evidence in expert witness opinion.  Rule 702 makes opinion admissible, and Rule 703 acknowledges that much of the bases for expert witness opinion will itself be inadmissible.  The structure of the Federal Rules of Evidence, however, undermines the importance of underlying evidence by not requiring that expert witnesses disclose the facts and data upon which they rely.

The evidence law of some states is to the contrary.  Consider Hansen v. Wyeth Inc., 77 Pa. D. & C.4th 501, 2005 WL 3068256 (Phila. Cty. Ct. Com.Pl. 2005) (Bernstein, J.).  The Hansen case focused on the testimony that was given by Dr. Harris Busch in a fenfluramine products liability case in Philadelphia.  Some may recall Busch as a veteran plaintiffs’ expert witness from the silicone gel breast implant litigation.  See Hon. Jack B. Weinstein, “Preliminary Reflections on Administration of Complex Litigation” 2009 Cardozo L. Rev. de novo 1, 14 (2009) (describing plaintiffs’ expert witnesses in silicone litigation as “charlatans” and the litigation as largely based upon fraud). 

In Hansen, Busch testified that Wyeth had been negligent, but on post-trial motions, Judge Bernstein found that:

“The doctor’s opinion, however, was presented in conclusory form and was ‘generically’ predicated on voluminous materials.”

Hansen, 77 Pa. D. & C.4th at 501.

Applying Pennsylvania’s version of Rule 705, which incorporated the state’s traditional common-law approach, Judge Bernstein held that Dr. Busch’s failure to give a detailed accounting of the evidentiary basis for his opinion rendered his opinion inadmissible.  Pennsylvania Rule 705 provides:

“Disclosure of facts or data underlying expert opinion.

The expert may testify in terms of opinion or inference and give reasons therefore; however the expert must testify as to the facts or data on which the opinion or inference is based.”

Hansen, 77 Pa. D. & C.4th at 504 (citing and quoting Rule 705).  The Pennsylvania version of Rule 705 differs significantly from the Federal Rule of Evidence 705 by requiring actual disclosure of the evidence upon which an expert witness opines.  In Pennsylvania state court, it is not sufficient for juries or judges to evaluate expert witness testimony upon looks, demeanor, apparent bias, and the like:

“While most rules of evidence concern the admission of facts, Rule 705 concerns itself not with admission but disclosure. Absent a clear disclosure of the factual basis of opinion testimony, an expert’s opinion does not so much assist the jury with their determination of the facts as replace the jury’s essential factfinding  role. Without a clear disclosure, the jury has no basis for determining whether the facts as understood or assumed by the expert are compatible with the facts as the jury finds them to be. Thus, Rule 705 was adopted to preserve the exclusive  factfinding function of the jury.”

Id. at 507 (internal citations omitted).  Pennsylvania Rule of Evidence 705 requires specificity by the testifying expert witness in identifying the actual basis for his or her opinion:

“The Rule 705 requirement of presenting the ‘facts and data’ which form the basis of the opinion may not be satisfied by a mere formalistic recitation of the material reviewed or considered. That pro forma routine absolutely obscures what Rule 705 intends to clarify and is tantamount to the clearly impermissible tactic of offering an opinion based on ‘all the evidence’.”

Id. at 511 -12 (internal citations omitted).

The omission of the Pennsylvania rule from federal practice and many other states’ practices illustrates our legal system’s failure to insist upon showing the factfinder the actual evidence.  We have a long way to go, in journalism, politics, and law, to become an evidence-based society.

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Bendectin, Diclegis & The Philosophy of Science

October 26th, 2013

In April of this year, the United States Food and Drug Administration (FDA) approved Diclegis, a combination of doxylamine succinate and pyridoxine hydrochloride for sale in the United States, for pregnant women experiencing nausea and vomiting. See FDA News Release, “FDA approves Diclegis for pregnant women experiencing nausea and vomiting,” (April 8, 2013). The return of this drug to the United States market was held up as a triumph of science over the will of the lawsuit industry. See Gideon Koren, “The Return to the USA of the Doxylamine-Pyridoxine Delayed Release Combination (Diclegis®) for Morning Sickness — A New Morning for American Women,” 20 J. Popul. Ther. Clin. Pharmacol. e161 (2013).

The sponsor of the drug, Duchesnay USA, wisely did not use the medication’s former name, Bendectin, which was the victim of a litigation industry jihad in the late 1970s through the mid-1990s. The plaintiffs’ lawyers’ war against Bendectin and its United States manufacturer is chronicled in two book-length accounts, and hundreds of articles. See Joseph Sanders, Bendectin on Trial: A Study of Mass Tort Litigation (Ann Arbor 1998); Michael D. Green, Bendectin and Birth Defects: The Challenges of Mass Toxic Substances Litigation (Philadelphia 1996).

As recently approved by the FDA, Declegis is categorized as “Pregnancy Category A,” which means that it is medication indicated for use in pregnant women. Most drugs are not tested in pregnant women in randomized clinical trials for obvious ethical and practical reasons. Perhaps one of the good things that came out of the Bendectin litigation wars was that Bendectin became one of the most intensely studied medications available for pregnant women. Another good thing was the achievement of evidence-based standards for expert witness opinion testimony in federal court. See David Bernstein, “Bendectin is Back” (April 9, 2013).

According to FDA regulations, Category A is defined:

“(1) Pregnancy category A. If adequate and well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of a risk in later trimesters), the labeling must state: ‘Pregnancy Category A. Studies in pregnant women have not shown that (name of drug) increases the risk of fetal abnormalities if administered during the first (second, third, or all) trimester(s) of pregnancy. If this drug is used during pregnancy, the possibility of fetal harm appears remote. Because studies cannot rule out the possibility of harm, however, (name of drug) should be used during pregnancy only if clearly needed.’ The labeling must also contain a description of the human studies. If animal reproduction studies are also available and they fail to demonstrate a risk to the fetus, the labeling must also state: ‘Reproduction studies have been performed in (kinds of animal(s)) at doses up to (x) times the human dose and have revealed no evidence of impaired fertility or harm to the fetus due to (name of drug).’ The labeling must also contain a description of available data on the effect of the drug on the later growth, development, and functional maturation of the child.

21 CFR § 201.57 (c)(9)(i)(A)(1) (April 2012).

A Litmus Test for Philosophy of Science?

The inability to discriminate between valid and invalid science should be a disqualifying characteristic in a putative philosopher of science, or a putative expert, for that matter. Professor Susan Haack, whose writings provide both insight and confusion on the role of science in the law, revealed her robust biases and prejudices in commenting upon the Bendectin litigation. These revelations should raise red flags about her objectivity in commenting on the legal process. See Susan Haack, “Irreconcilable Differences? The Troubled Marriage of Science and Law,” 72 Law & Contemporary Problems 1 (2009).

Haack’s paper on the marital discord was based upon her presentation at the Fourth Coronado Conference, organized by SKAPP (The Project on Scientific Knowledge and Public Policy), an ideological group dedicated to opening the courthouse doors to every quackacademic theory, and shadily funded by the litigation industry of plaintiffs’ lawyers from their left-over spoils from the silicone breast implant litigation. See SKAPP A LOT (April 30, 2010); “Haacking at the Truth – Part Two” (Oct. 31, 2010).

Haack provided examples of “marginal” science and witnesses who disturb her for biases and prejudices she perceives in these witnesses. Haack focuses upon Dr. Robert Brent, a toxicologist, who appears to her as Merrell Dow’s expert witness “always ready to testify that Bendectin does not cause birth defects.” Id. At 17. Haack presented no evidence or basis to suggest that Brent was wrong, and indeed, Brent published widely on his views of the subject. Multiple publications do not necessarily mean that Brent was right, but at least he was willing to subject himself to professional peer review, and post-publication, professional challenges. Still, Haack is distressed that Dr Robert Brent opines with “unwarranted certainty” that Bendectin does not cause birth defects, but she offers no suggestion or support that his certainty was or is misplaced.

In stark contrast, Haack expressed no discomfort with Bendectin plaintiffs’ expert witness, Dr Done, or with the facile ease with which he opined with scientific certainty that Bendectin causes birth defects. Here there really is a great deal of empirical evidence, and along with the FDA’s recent approval of Diclegis for use in pregnant women, the evidence has vindicated Dr. Brent’s views on the safety and efficacy of Bendectin/Diclegis. Dr. Done’s subjective appreciation of “flaws” in some clinical studies does not turn criticism into affirmative evidence in favor of the opinion that he so zealously, and overzealously, advocated in many Bendectin cases, for his own substantial pecuniary benefit. What is remarkable about Haack’s article is that she singles out Dr. Brent in the context of a discussion of “marginal” and “willing” testifying scientists, but she omits any mention of the plaintiffs’ cadre of ready, willing, and somewhat disreputable testifiers. Perhaps even more remarkable is that Haack overlooks that Dr. Done was essentially fired from his university for his entrepreneurial testimonial activities of dubious scientific worth, and that he probably lied about his credentials. See Michael Green, Bendectin and Birth Defects: The Challenges of Mass Toxic Substances Litigation 280 – 82 (Philadelphia 1996) (citing decisional law in which Done’s lack of veracity was judicially noted).

Of course, what is most remarkable about Haack’s infatuation with Dr. Alan Done and his mosaic theory is that the theory was the concoction of plaintiffs’ lawyer, Barry Nace, and that the theory leads to such a palpably incorrect result. Barry Nace was one of the lead plaintiffs’ counsel in the Bendectin litigation. Nace was also formerly President of the litigation industry’s principal lobbying organization, the American Trial Lawyers Association (now the AAJ). After the second Ninth Circuit Daubert decision, Nace declined to pursue one of his Bendectin cases, and his client sued him. Nace’s attorney moved for summary judgment in August 1998, on grounds that included the assertion that “courts soundly and uniformly reject the notion that Bendectin causes birth defects.” See David Bernstein, “A Day Late and a Dollar Short on Bendectin” (June 28, 2005).

This is the same Barry Nace lauded by Michael Green for having devised the notorious matrix theory of scientific evidence (a.k.a. the tsumish theory). Michael D. Green, “Pessimism About Milward,” 3 Wake Forest J. Law & Policy41, 62-63 (2013). Professor Haack sees Nace’s matix theory as the practical application of some of her theories. Susan Haack, “Irreconcilable Differences? The Troubled Marriage of Science and Law,” 72 Law & Contemporary Problems 1, 17 (2009); Susan Haack, “Proving Causation: The Holism of Warrant and the Atomism of Daubertm” 4 J. Health & Biomedical Law 273, 274-78 (2008). Haack’s embrace of the dubious Bendectin causal claims as supported by her matrix theory of causal inference raises the issue why we should credit a theory in the face of such a compelling counter example? As Professor Ronald Allen put the matter, before Bendectin was reintroduced into the United States market this year:

“Given the weight of evidence in favor of Bendectin’s safety, it seems peculiar to argue for mosaic evidence from a case in which it would have plainly been misleading.”

Ronald J. Allen and Esfand Nafisi, “Daubert and its Discontents,” 76 Brooklyn L. Rev. 132, 148 (2010). Peculiar indeed. Professor Allen’s point is important for its wide-ranging implications. Methodologies that yield false-positive results are unreliable. Perhaps a methodology can be saved if we could quantify that a given methodology rarely yields such false results, but the matrix theory of Barry Nace and his expert witnesses seems so vague and insubstantial that no one, in all likelihood, could frame a test for the generalized approach. Expert witnesses perhaps should be judged by their track record over time, as well. See David Kaye, “The Experts in Daubert.”[1]

 

[1] Dr. Alan Done (pediatrician, pharmacology, toxicology); Dr. Jay Glasser (biostatistician, epidemiologist); Dr. Adrian Gross (veterinarian); Dr. Stuart Newman (developmental biologist); Dr. Wayne Snodgrass (Assoc. Professor of Pediatrics, Pharmacology, and Toxicology); Dr. Shanna Swan (epidemiologist); Dr. Johannes Thiersch (pathologist and pharmacologist); Dr. John Palmer (Professor of pharmacology).

 

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Power in the Reference Manual for Scientific Evidence

June 15th, 2013

The Third Edition of the Reference Manual on Scientific Evidence (2011) [RMSE3ed] treats statistical power in three of its chapters, those on statistics, epidemiology, and medical testimony.  Unfortunately, the treatment is not always consistent.

The chapter on statistics has been consistently among the best and most frequently ignored content of the three editions of the Reference Manual.  The most recent edition offers a good introduction to basic concepts of sampling, random variability, significance testing, and confidence intervals.  David H. Kaye & David A. Freedman, “Reference Guide on Statistics,” in RMSE3ed 209 (2011).  Kaye and Freedman provide an acceptable non-technical definition of statistical power:

“More precisely, power is the probability of rejecting the null hypothesis when the alternative hypothesis … is right. Typically, this probability will depend on the values of unknown parameters, as well as the preset significance level α. The power can be computed for any value of α and any choice of parameters satisfying the alternative hypothesis. … Frequentist hypothesis testing keeps the risk of a false positive to a specified level (such as α = 5%) and then tries to maximize power. Statisticians usually denote power by the Greek letter beta (β). However, some authors use β to denote the probability of accepting the null hypothesis when the alternative hypothesis is true; this usage is fairly standard in epidemiology. Accepting the null hypothesis when the alternative holds true is a false negative (also called a Type II error, a missed signal, or a false acceptance of the null hypothesis).”

Id. at 254 n.106

The definition is not, however, without problems.  First, it introduces a nomenclature issue likely to be confusing for judges and lawyers. Kaye and Freeman use β to denote statistical power, but they acknowledge that epidemiologists use β to denote the probability of a Type II error.  And indeed, both the chapters on epidemiology and medical testimony use β to reference Type II error rate, and thus denote power as the complement of β, or (1- β).  See Michael D. Green, D. Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” in RMSE3ed 549, 582, 626 ; John B. Wong, Lawrence O. Gostin, and Oscar A. Cabrera, Abogado, “Reference Guide on Medical Testimony,” in RMSE3ed 687, 724.  This confusion in nomenclature is regrettable, given the difficulty many lawyers and judges seem have in following discussions of statistical concepts.

Second, the reason for introducing the confusion about β is doubtful.  Kaye and Freeman suggest that statisticians usually denote power by β, but they offer no citations.  A quick review (not necessarily complete or even a random sample) suggests that many modern statistics texts denote power as (1- β).  See, e.g., Richard D. De Veaux, Paul F. Velleman, and David E. Bock, Intro Stats 545-48 (3d ed. 2012); Rand R. Wilcox, Fundamentals of Modern Statistical Methods 65 (2d ed. 2010).  At the end of the day, there really is no reason for the conflicting nomenclature and the likely confusion it engenders.  Indeed, the duplicative handling of statistical power, and other concepts, suggests that it is time to eliminate the repetitive discussions, in favor of one, clear, thorough discussion in the statistics chapter.

Third, Kaye and Freeman problematically refer to β as the probability of accepting the null hypothesis when elsewhere they more carefully instruct that a non-significant finding results in not rejecting the null hypothesis as opposed to accepting the null.  Id. at 253.  See also Daniel Rubinfeld, “Reference Guide on Multiple Regression,“ in RMSE3d 303, 321 (describing a p-value > 5% as leading to failing to reject the null hypothesis).

Fourth, Kaye and Freedman’s discussion of power, unlike most of their chapter, offers advice that is controversial and unclear:

“On the other hand, when studies have a good chance of detecting a meaningful association, failure to obtain significance can be persuasive evidence that there is nothing much to be found.”

RMSE3d at 254. Note that the authors leave open what a legal or clinically meaningful association is, and thus offer no real guidance to judges on how to evaluate power after data are collected and analyzed.  As Professor Sander Greenland has argued, in legal contexts, this reliance upon observed power (as opposed to power as a guide in determining appropriate sample size in the planning stages of a study) is arbitrary and “unsalvageable as an analytic tool.”  See Sander Greenland, “Nonsignificance Plus High Power Does Not Imply Support Over the Alternative,” 22 Ann. Epidemiol. 364, 364 (2012).

The chapter on epidemiology offers similar controversial advice on the use of power:

“When a study fails to find a statistically significant association, an important question is whether the result tends to exonerate the agent’s toxicity or is essentially inconclusive with regard to toxicity.93 The concept of power can be helpful in evaluating whether a study’s outcome is exonerative or inconclusive.94  The power of a study is the probability of finding a statistically significant association of a given magnitude (if it exists) in light of the sample sizes used in the study. The power of a study depends on several factors: the sample size; the level of alpha (or statistical significance) specified; the background incidence of disease; and the specified relative risk that the researcher would like to detect.95  Power curves can be constructed that show the likelihood of finding any given relative risk in light of these factors. Often, power curves are used in the design of a study to determine what size the study populations should be.96”

Michael D. Green, D. Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” RMSE3ed 549, 582.  Although the authors correctly emphasize the need to specify an alternative hypothesis, their discussion and advice are empty of how that alternative should be selected in legal contexts.  The suggestion that power curves can be constructed is, of course, true, but irrelevant unless courts know where on the power curve they should be looking.  The authors are correct that power is used to determine adequate sample size under specified conditions, but again, the use of power curves in this setting is today rather uncommon.  Investigators select a level of power corresponding to an acceptable Type II error rate, and an alternative hypothesis that would be clinically meaningful for their research, in order to determine their sample size. Translating clinical into legal meaningfulness is not always straightforward.

In a footnote, the authors of the epidemiology chapter note that Professor Rothman has been “one of the leaders in advocating the use of confidence intervals and rejecting strict significance testing.” RMSE3d at 579 n.88.  What the chapter fails, however, to mention is that Rothman has also been outspoken in rejecting post-hoc power calculations that the epidemiology chapter seems to invite:

“Standard statistical advice states that when the data indicate a lack of significance, it is important to consider the power of the study to detect as significant a specific alternative hypothesis. The power of a test, however, is only an indirect indicator of precision, and it requires an assumption about the magnitude of the effect. In planning a study, it is reasonable to make conjectures about the magnitude of an effect to compute study-size requirements or power. In analyzing data, however, it is always preferable to use the information in the data about the effect to estimate it directly, rather than to speculate about it with study-size or power calculations (Smith and Bates, 1992; Goodman and Berlin, 1994; Hoening and Heisey, 2001). Confidence limits and (even more so) P-value functions convey much more of the essential information by indicating the range of values that are reasonably compatible with the observations (albeit at a somewhat arbitrary alpha level), assuming the statistical model is correct. They can also show that the data do not contain the information necessary for reassurance about an absence of effect.”

Kenneth Rothman, Sander Greenland, and Timothy Lash, Modern Epidemiology 160 (3d ed. 2008).  See also Kenneth J. Rothman, “Significance Questing,” 105 Ann. Intern. Med. 445, 446 (1986) (“[Simon] rightly dismisses calculations of power as a weak substitute for confidence intervals, because power calculations address only the qualitative issue of statistical significance and do not take account of the results already in hand.”)

The selective, incomplete scholarship of the epidemiology chapter on the issue of statistical power is not only unfortunate, but it distorts the authors’ evaluation of the sparse case law on the issue of power.  For instance, they note:

“Even when a study or body of studies tends to exonerate an agent, that does not establish that the agent is absolutely safe. See Cooley v. Lincoln Elec. Co., 693 F. Supp. 2d 767 (N.D. Ohio 2010).  Epidemiology is not able to provide such evidence.”

RMSE3d at 582 n.93; id. at 582 n.94 (“Thus, in Smith v. Wyeth-Ayerst Labs. Co., 278 F.Supp. 2d 684, 693 (W.D.N.C. 2003), and Cooley v. Lincoln Electric Co., 693 F. Supp. 2d 767, 773 (N.D. Ohio 2010), the courts recognized that the power of a study was critical to assessing whether the failure of the study to find a statistically significant association was exonerative of the agent or inconclusive.”)

Here Green, Freedman, and Gordis shift the burden to the defendant and make the burden one of absolute certainty in the product’s safety.  This is not a legal standard. The cases they cite amplify the error. In Cooley, for instance, the defense expert would have opined that welding fume exposure did not cause parkinsonism or Parkinson’s disease.  Although the expert had not conducted a meta-analysis, he had reviewed the confidence intervals around the point estimates of the available studies.  Many of the point estimates were at or below 1.0, and in some cases, the upper bound of the confidence interval excluded 1.0.  The trial court expressed its concern that the expert witness had inferred “evidence of absence” from “absence of evidence.”  Cooley v. Lincoln Elec. Co., 693 F. Supp. 2d 767, 773 (N.D. Ohio 2010).  This concern, however, was misguided given that many studies had tested the claimed association, and that virtually every case-control and cohort study had found risk ratios at or below 1.0, or very close to 1.0.  What the court in Cooley, and the authors of the epidemiology chapter in the RSME3d have lost sight of, is that when the hypothesis is repeatedly tested, with failure to reject the null hypothesis, and with point estimates at or very close to 1.0, and with narrow confidence intervals, then the claimed association is probably incorrect.  See, e.g., Anthony J. Swerdlow, Maria Feychting, Adele C. Green, Leeka Kheifets, David A. Savitz, International Commission for Non-Ionizing Radiation Protection Standing Committee on Epidemiology, “Mobile Phones, Brain Tumors, and the Interphone Study: Where Are We Now?” 119 Envt’l Health Persp. 1534, 1534 (2011) (“Although there remains some uncertainty, the trend in the accumulating evidence is increasingly against the hypothesis that mobile phone use can cause brain tumors in adults.”).

The Cooley court’s comments have some validity when applied to a single study, but not to the impressive body of exculpatory epidemiologic evidence that pertains to welding fume and Parkinson’s disease.  Shortly after the Cooley case was decided, a published meta-analysis of welding fume or manganese exposure demonstrated a reduced level of risk for Parkinson’s disease among persons occupationally exposed to welding fumes or manganese.  James Mortimer, Amy Borenstein, and Lorene Nelson, “Associations of welding and manganese exposure with Parkinson disease: Review and meta-analysis,” 79 Neurology 1174 (2012).

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Sympathy for the Diablo — Peppermint Barry vs Spicy Seafood Pasta

June 12th, 2013

Barry S. Levy is a physician, author, performer, and political activist.   Dr. Levy is a past president of the American Public Health Association, which conferred upon him its oldest and most prestigious award, the Sedgwick Memorial Medal, in 2005, for his outstanding achievements in public health.

Levy has been received other, less favorable notice from trial and appellate judges.  For instance, one federal judge found Levy engaged in a dubious enterprise to manufacture silicosis claims in Mississippi.  In re Silica Products Liability Litigation, 398 F. Supp. 2d 563, 611-16, 622 & n.100 (S.D. Texas 2005) (expressing particular disappointment with Dr. Barry Levy, who although not the worst offender of a bad lot of physicians, betrayed his “sterling credentials” in a questionable enterprise to manufacture diagnoses of silicosis for litigation). See also Schachtman, Silica Litigation: Screening, Scheming & Suing; Washington Legal Foundation Critical Legal Issues Working Paper Series No. 135 (Dec. 2005) (exploring the ethical and legal implications of the entrepreneurial litigation in which Levy and others were involved).

Unfortunately, In re Silica was not an isolated case.  See, e.g., Lofgren v. Motorola, Inc., 1998 WL 299925, No. CV 93-05521 (Ariz. Super. Ct., Maricopa Cty. June 1, 1998); Harman v. Lipari, N.J. L. Div. GLO-L-1375-95, Order of Nov. 3, 2000 (Tomasello, J.) (barring the use of Barry Levy in class action for medical monitoring damages); Castellow v. Chevron USA, 97 F.Supp. 2d 780, 793-95 (S.D. Tex. 2000); Knight v. Kirby Inland Marine Inc., 482 F.3d 347 (5th Cir. 2007); Watts v. Radiator Specialty Co., 990 So. 2d 143 (Miss. 2008); Aurand v. Norfolk So. Ry., 802 F.Supp.2d 950 (2011).

Now, once again, right here in River City, Dr. Levy has stepped out of bounds, and has been stripped of his mantle of testifying expert witness.  Mallozzi v. Ecosmart Technologies, Inc., 2013 WL 2415677, No. 11-CV-2884 (SJF)(ARL) (E.D.N.Y. May 31, 2013).

Over the course of a few minutes, plaintiff Velio Mallozi applied a “couple of ounces” of EcoSmart Organic Home Pest Control product to the foundation of his home, and a few squirts inside.  The product used, EcoSmart, contains plant oils, including one percent peppermint oil.  Id. at *1.  Mallozi did not experience any acute ill effects from his organic pest control efforts, and later went to dinner at an [unidentified] Italian restaurant, where he enjoyed a meal of “spaghetti with seafood.”  Id. at *10.  Perhaps seafood diablo, but Judge Feuerstein doesn’t say.

After the seafood spaghetti meal, Mallozi experienced a serious bout of laryngopharyngeal reflux (LPR).  With sympathy for the diablo, Mallozi sued only EcoSmart, on the claim that his inhaling some spray, with its 1% peppermint oil, caused his LPR.

The Mallozis sought out B.S. Levy to support the claimed relationship.  Levy did not disappoint.  He rendered a report that asserted that the few minutes of inhaling minor amounts of peppermint oil causes relaxation of the lower esophogeal sphincter, and consequently LPR.  Id. at *5.  Levy relied upon four articles to support this claim, but Judge Feuerstein refused to accept the claim of support, at face value.  Her Honor reviewed each study, only to find that the exposures that were associated with relaxation of G.I. smooth muscle, for a short period of about 20 minutes, were trials of ingested peppermint oil, at significantly greater doses, over lengthy periods of observation.  Id. at *6.  The studies individually and collectively did not support Levy’s opinion.

One of the papers on Levy’s reliance list was a case report of a patient that suffered burns in her mouth from ingestion of pure peppermint oil. The court found that this case report, involving large doses of pure peppermint oil, with an outcome different from claimed by Mallozi, was irrelevant.  Id. Even if it were construed to offer some support, the anecdotal nature of the case report, lacking controls, renders the report an unreliable basis for a causal conclusion.  Id.

The trial court found that B.S. Levy’s analysis ignored the crucial roles of dose, duration, route of exposure, and the nature of plaintiff’s condition, LPR.   Id. at *8.  The court held that Levy’s opinion did not satisfy the requirements of Rule 702.  The plaintiffs failed to show that Levy’s opinion was supported sufficiently by facts or data, and they failed to show that his opinion was the product of applying reliable methods and principles.  Id.

Judge Feuerstein, having found that Levy’s opinion on general causation between EcoSmart and LPR was bereft of validity, could have stopped without addressing specific causation.  Such an approach would have had the virtue of judicial economy, but would have left out some delicious facts.  Levy purportedly used some sort of differential etiology to infer the cause of plaintiff’s LPR, but he omitted meaningful consideration of plaintiff’s having had a history of severe severe gastroesophageal reflux disease (GERD), which predated his bout of LPR.  Indeed, plaintiff’s GERD had been so severe that he had been previously hospitalized for GERD after ingesting coffee and donuts.   Judge Feuerstein found Levy’s iterative disjunctive syllogism invalid for having failed to address the prior history of GERD, and the intervening role of the pasta and seafood dinner, in bringing on the LPR.  Id. at *10-11.

The Material Safety Data Sheet Ploy

Judge Feuerstein also demonstrated a careful understanding of the meaning and role of the Material Data Safety Sheet (MSDS).  EcoSmart’s MSDS contained a warning that some sensitive persons may experience dizziness or irritation of their nasal passages, and that ingestion may cause GI irritation.  Id. at *13.  Dr. Levy had embraced this MSDS language as an “admission,” but he did not analyze the sources of information or their validity.  The MSDS warning, as required by law, addresses the potential hazard of the ingredient, peppermint oil, irrespective of dose, concentration, or route of administration.  Id., citing Moore v. Ashland Chem. Inc., 151 F.3d 269, 278 (5th Cir.1998); Turner v. Iowa Fire Equip. Co., 229 F.3d 1202, 1209 (8th Cir.2000); Ingram v. Solkatronic Chem., Inc., No. 04–CV–0287, 2005 WL 3544244, at *6 (N.D.Okla. Dec. 28, 2005)).

The Treating Physician Echo

Apparently one of Mr. Mallozzi’s treating physicians joined the fray with echoes of Levy’s opinion.  Judge Feuerstein recognized that treating physicians are subject to the requirements of Rule 702, and that a me-too opinion deserved the me-too result.  Id. at *13, citing Davids v. Novartis Pharm. Corp., 857 F.Supp. 2d 267, 280 (E.D.N.Y. 2012).

Pasta and Peppermints

Bad sense, innocence, cripplin’ my mind.
Old medical records I just can’t find.
Too much Cajun spice, and I forgot about GERD.
Incense and peppermints, haven’t you heard?
But who cares, it’s just litigation.
Lots to win, but nothing to lose.

Incense and peppermints, meaningless claims.
Turn on, drop in, toxins are all the same

Throw your pride to the side; it’s what you must do.

Daubert is politics; 702.
A yardstick for lunatics, your point of view.
The court cares what games you choose.
You have lots to win, but nothing to lose

(adapted from, and with apologies to, Strawberry Alarm Clock)

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The Mt. Sinai Catechism

June 7th, 2013

There are mythologies in science as there in religion.  Back in the day, Dr. Irving Selikoff invented a catchy catechism about synergistic interaction between asbestos and smoking in producing lung cancer.  Selikoff’s study of insulators advanced lung cancer point estimates for asbestos alone, for smoking alone, and for asbestos and smoking together:  5-10-50, which became incorporated in innumerable textbooks, articles, expert witness reports, and court opinions.

E. Cuyler Hammond, Irving J. Selikoff,  and Herbert Seidman, “Asbestos Exposure, Cigarette Smoking and Death Rates,” 330 Ann. N.Y. Acad. Sci. 473, 487 (1979).  Selikoff tells us that each insulator, starting in 1961, answered “a detailed questionnaire,” and later, repeat questionnaires on their smoking histories.  Id. at 475.

“Of the 8220 men who answered the questionnaire, 891 (11%) said that they had never smoked regularly; 488 (6%) had a history of pipe or cigar smoking but never smoked cigarettes regularly and; 6841 (83%) were either current or ex-cigarette smokers. Some of the cigarette smokers also smoked pipes or cigars or had done so in the past.”

Id. at 481.

The 5 supposedly represented the relative risk of asbestos exposure alone in insulators who did not smoke; the 10 supposedly represented the relative risk of smoking alone in the non-insulator general population of smokers; and the 50 represented the relative risk of insulators who had smoked.  Selikoff claimed that his data supported a multiplicative model of synergistic interaction between smoking and asbestos exposure.

Like other mythologies, there was a good bit of exaggeration and fabrication in Selikoff’s story. First, the non-smoking relative risk was based upon the observed risk ratio among insulators who “never smoked regularly.”  Smoking data were collected by survey, and the actual questionnaires and definition have never been published or provided by Selikoff and his colleagues.  Even taken at face value, “never smoked regularly” is not the same as non-smoker.  Adding that the insulators union was widely engaged in personal injury litigation, and that the membership had a strong motive to downplay their smoking histories, this exposure information becomes suspect.

The non-asbestos smoking lung cancer point estimate (10) was equally dubious.  The ten-fold risk statistic represented an average smoking lung cancer risk in the first Cancer Prevention Survey (CPS-1).  The insulators who smoked were rarely average smokers, and the CPS-1 point estimate was superseded within a couple of years by the new, revised CPS-II overall smoking lung cancer point estimate that was greater than twenty.  The CPS-II results were published in the 1980s and early 1990s, but Selikoff and his protégés contained to testify to the 5-10-50. See, e.g., Shopland, “Smoking-Attributable Cancer Mortality in 1991: Is Lung Cancer Now the Leading Cause of Death Among Smokers in the United States?” 83 J. Nat’l Cancer Inst. 1142 (1991).

These problems and others led astute authors to note their dissent from the simplistic multiplicative model.  F. Douglas K. Liddell, “The Interaction of Asbestos and Smoking in Lung Cancer,” 45 Ann. Occup. Hyg. 341 (2001) (“Both cigarette smoke and inhaled asbestos fibres can cause lung cancer, but the assessment of how these agents act in combination is a matter of great difficulty.”)

Despite the serious problems with the multiplicative model, Selikoff’s wanton republication of the 5-10-50 data, and the popularity of these data with testifying expert witnesses and regulating agencies, cemented their use in litigation. Consider, for instance, how the orthodoxy infiltrated the ostensibly neutral Reference Manual on Scientific Evidence, which proclaimed the multiplicative synergy of smoking and asbestos in its second edition:

“Occupational asbestos exposure in nonsmokers increases the risk of lung cancer by a factor of about five, from about 11 per 100,000, for nonsmoking industrial workers not exposed to asbestos to about 58 per 100,000 for nonsmoking asbestos workers; a significant smoking history increases the rate of lung cancer by a factor of at least ten. See U.S. Surgeon Gen., U.S. Dep’t of Health & Human Servs., The Health Consequences of Smoking: Cancer and Chronic Lung Disease in the Workplace 216 (1985); see also Rodolfo Saracci, “The Interactions of Tobacco Smoking and Other Agents in Cancer Etiology,” 9 Epidemiologic Revs. 175, 176–80 (1987). Because the effects of smoking and asbestos are multiplicative for lung cancer, the population of smoking asbestos workers has a lung cancer incidence of 5 times 10, or 50 times the background rates, rather than the 15-fold increase predicted by adding the separate risks. See U.S. Surgeon Gen., U.S. Dep’t of Health & Human Servs., supra, at 216–17.”

Mary Sue Henifin, Howard M. Kipen, and Susan R. Poulter, “Reference Guide on Medical Testimony,” in Federal Judicial Center, Reference Manual on Scientific Evidence 439, 476 & n. 136 (2d ed. 2000).  Dr. Kipen was a protégé of Dr. Selikoff.  The reference to the multiplicative mantra was eliminated from the Third Edition of the Reference Manual.

Back in April of this year, some other Selikoff protégés were busy trying to rehabilitate the 5-10-50 mantra, with a new study. Science Daily earnestly reported news of the new study as though it were ground breaking.  See “Asbestos Exposure, Asbestosis, and Smoking Combined Greatly Increase Lung Cancer Risk” (Apr. 12, 2013)  (reporting on the in-press version of Steve Markowitz, Stephen Levin, Albert Miller, and Alfredo Morabia, “Asbestos, Asbestosis, Smoking and Lung Cancer: New Findings from the North American Insulator Cohort,” Am. J. Respir. & Critical Care Med. (2013)).  Interestingly, only Stephen Levin, who died over a year ago, is listed as affiliated with the Mt. Sinai School of Medicine.  Although some of the other authors had previous affiliations with Mt. Sinai, they are now listed at the Center for the Biology of Natural Systems, Queens College – CUNY.

Science Daily quotes lead author Markowitz as saying that “[t]he interactions between asbestos exposure, asbestosis and smoking, and their influence on lung cancer risk are incompletely understood.”  It seems unlikely that this new article will shed much light on the problem.   The authors claim to apply and extend Selikoff’s approach from previous publications.  This new publication thus incorporates the serious problems that had afflicted Selikoff’s papers, especially his use of CPS-I to provide a point estimate for smoking alone (the alleged 10 in the 5-10-50 theory).  Here is the abstract of the paper:

“Rationale

Asbestos, smoking, and asbestosis increase lung cancer risk in incompletely elucidated ways. Smoking cessation among asbestos-exposed cohorts has been little studied.

Objectives

To measure the contributions of asbestos exposure, asbestosis, smoking and their interactions to lung cancer risk in an asbestos-exposed cohort, and to describe their reduction in lung cancer risk when they stop smoking.

Methods

We examined lung cancer mortality obtained through the National Death Index for 1981-2008 for 2,377 male North American insulators for whom chest x-ray, spirometric, occupational and smoking data were collected in 1981- 1983 and for 54,243 non-asbestos exposed blue collar male workers from Cancer Prevention Study II for whom occupational and smoking data were collected in 1982.

Measurements and Main Results

Lung cancer caused 339 (19%) insulator deaths. Lung cancer mortality was increased by asbestos exposure among non-smokers [rate ratio = 3.6 (95% CI: 1.7-7.6)], by asbestosis among non-smokers [rate ratio = 7.40 (95% CI, 4.0-13.7], and by smoking without asbestos exposure [rate ratio = 10.3 (95% CI, 8.8-12.2)]. The joint effect of smoking and asbestos alone was additive [rate ratio = 14.4 (95% CI, 10.7-19.4)] and with asbestosis, supra-additive [rate ratio = 36.8 (95% CI, 30.1-46.0)]. Insulator lung cancer mortality halved within 10 years of smoking cessation and converged with that of never-smokers 30 years following smoking cessation.

Conclusions

Asbestos increases lung cancer mortality among non-smokers. Asbestosis further increases the lung cancer risk and, considered jointly with smoking, has a supra-additive effect. Insulators benefit greatly by quitting smoking.”

The big news that Steven Markowitz did not trumpet in the press releases was that in the absence of asbestosis, there was no multiplicative interaction.  The asbestos-alone (point estimate) is still suspect.  The paper characterizes this point estimate as applying to non-smokers without asbestosis, but given this group’s history of equivocating between “never smoked regularly” and “non-smoker,” and the difficulty in obtaining accurate smoking histories from men enmeshed in litigation over respiratory claims, the asbestos-alone point estimate remains doubtful.  Curiously, the smoking histories were collected in 1981-83, but there is no mention of any attempt to verify the histories against smoking histories provided by the study participants in earlier versions of Selikoff’s studies on the insulators.

Similarly, the smoking-alone point estimate is incredible.  The authors purport to draw the smoking-alone risk ratio from CPS-II; yet the risk ratio presented (10.3) is less than half that reported in multiple publications of the CPS-II study.  Markowitz and colleagues cite to two papers for the 10.3 point estimate; neither appears to support this number.  Steven Stellman & Lawrence, “Smoking habits and tar levels in a new American Cancer Society prospective study of 1.2 million men and women,” 76 J. Nat’l Cancer Inst. 1057 (1986); Michael Thun, Eugenia Calle, Carmen Rodriguez, and Phyllis Wingo, “Epidemiological research at the American Cancer Society. 9 Cancer Epidemiol. Biomarkers & Prevention 861 (2000).  I would welcome contradiction from anyone who can find the point estimate in the cited papers.

Consider one of the most recent publications, which drew upon CPS-II data, in the New England Journal of Medicine.  For men who were current smokers, compared with men who never smoked, the relative risk of lung cancer mortality was 24.97. Michael Thun, Brian Carter, Diane Feskanich, Neal D. Freedman, Ross Prentice, Alan D. Lopez, Patricia Hartge, and Susan M. Gapstur, “50-Year Trends in Smoking-Related Mortality in the United States,” 368 New Engl. J. Med. 351 (2013).

The Markowitz, Levin, Miller paper is still “in press.”  There is still time for the editors to take a closer look.  There is also time for the editors to insist upon a disclosure of the authors’ conflicts of interest. See, e.g., Wannall v. Honeywell Internat’l, Inc., Civ. Action No. 10-351 (BAH), 2013 U.S. Dist. LEXIS 68523 (D.D.C. May 14, 2013) (discussing Markowitz’s participation as an expert witness).

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The Doubling Dose

June 5th, 2013

Sander Greenland and others have raised various theoretical objections to the argument that relative risks should exceed two before attribution can be made in specific cases.  In large part, Greenland’s objections turn on conjecture that risks are not stochastically distributed in the population samples studied in epidemiologic studies.  These objections are potentially true, but the burden remains on the proponent.  When there is serious evidence of latency or bimodal distribution, then epidemiologic studies or clinical trials can be adapted to examine the risk in the relevant subgroup.  When this is done, the relative risk argument once again is unavoidable.  For many exposures and conditions of interest, epidemiologic studies have evolved to accommodate the relevant model of risk distribution.

Despite Greenland’s speculative objections, the concept of a doubling dose has been widely advocated by scientists. The following are a few of such endorsements:

Philip Enterline, “Attributability in the Face of Uncertainty,” 78 (Supp.) Chest 377, 377, 378 (1980);

Otto Wong, “Using Epidemiology to Determine Causation in Disease,” 3 Natural Resources & Env’t 20, 23 (1988); Ben Armstrong, Claude Tremblay, and Gilles Theriault, “Compensating Bladder Cancer Victims Employed in Aluminum Reduction Plants,” 30 J. Occup. Med. 771 (1988);

Joshua Muscat & Michael Huncharek, “Causation and disease: Biomedical science in toxic tort litigation,” 31 J. Occup. Med. 997 (1989);

Troyen A. Brennan, “Can Epidemiologists Give Us Some Specific Advice?” 1 Courts, Health Science & the Law 397, 398 (1991)(“This indeterminancy complicates any case in which epidemiological evidence forms the basis for causation, especially when attributable fractions are lower than 50%.  In such cases, it is more probable than not that the individual has her illness as a result of unknown causes, rather than as a result of exposure to hazardous substance.”);

Mark R. Cullen & Linda Rosenstock, “Principles and Practice of Occupational and Environmental Medicine,” chap. 1, in Linda Rosenstock & Marc Cullen, eds., Textbook of Clinical Occupational and Environmental Medicine 1, 13-14 (Phila. 1994);

David F. Goldsmith & Susan G. Rose, “Establishing Causation with Epidemiology,” in Tee L. Guidotti & Susan G. Rose, eds., Science on the Witness Stand:  Evaluating Scientific Evidence in Law, Adjudication, and Policy 57, 60 (OEM Press 2001)(“A relative risk greater than 2.0 produces an attributable risk (sometimes called attributable risk percent10) or an attributable fraction that exceeds 50%.  An attributable risk greater than 50% also means that ‘it is more likely than not’, or, in other words, there is a greater than 50% probability that the exposure to the risk factor is associated with disease.”)

Below, I have updated once again the case law on the issue of using relative and attributable risks to satisfy plaintiff’s burden of showing, more likely than not, that an exposure or condition caused a plaintiff’s disease or injury.

See , for the updated the case law on the issue of using relative and attributable risks to satisfy plaintiff’s burden of showing, more likely than not, that an exposure or condition caused a plaintiff’s disease or injury.

 

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