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More Case Report Mischief in the Gadolinium Litigation

November 28th, 2014

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

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

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

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

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

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

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

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

Decker at *12.

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

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

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

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

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

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

 

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Gadolinium, Nephrogenic Systemic Fibrosis, and Case Reports

November 24th, 2014

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

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

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

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

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

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

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

   *   *   *   *   *   *   *   *

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

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

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

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

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

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

Peter Tugwell, George Wells, Joan Peterson, Vivian Welch, Jacqueline Page, Carolyn Davison, Jessie McGowan, David Ramroth, and Beverley Shea, “Do Silicone Breast Implants Cause Rheumatologic Disorders? A Systematic Review for a Court-Appointed National Science Panel,” 44 Arthritis & Rheumatism 2477, 2479 (2001) (citing David Sackett, “Bias in analytic research,” 32 J. Chronic Dis. 51 (1979)).

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

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

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

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

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

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Rhetorical Strategy in Characterizing Scientific Burdens of Proof

November 15th, 2014

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

[8] Id. at 266.

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

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

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

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

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

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

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Substantial Factor Versus Sine Qua Non Causation

October 7th, 2014

In a prosecution against the eponymously named Mr. Mullet, and other Amish defendants, the Department of Justice grabbed an an Amish beard- and hair-cutting case from state authorities and cast it as a hate crime. United States v. Mullet, 868 F.Supp. 2d 618 (N.D. Ohio 2012). The criminal statute invoked by the federal prosecutors prohibits

“willfully caus[ing] bodily injury to any person . . . because of the actual or perceived . . . religion . . . of [that] person… .”

18 U.S.C. § 249(a)(2)(A). The prosecution managed to persuade the trial judge, Judge Polster, that “because of” means merely “significant motivating factor,” but the Sixth Circuit would have none of it, and reversed. United States v. Miller, 2014 U.S. App. LEXIS 16532, 2014 FED App. 0210P (6th Cir. ); see Debra Cassens Weiss, “6th Circuit reverses hate-crime convictions of Amish in beard- and hair-cutting attacks” (Aug 28, 2014).

The Court of Appeals held, in a two to one decision, that the statute required a “but for” jury instruction, reversed and remanded. Most plainly, the appellate court stated that:

“[B]ecause of” in brief means what it says: The prohibited act or motive must be an actual cause of the specified outcome.”

United States v. Miller, at *12.

The appellate court cited the common meaning of “because of” and the treatment this phrase has received in criminal[1] and civil[2] cases in the United States Supreme Court. The defendants had presented evidence of other non-religious, non-prohibited motives and thus the district court’s charge was not harmless.

The court then, rather inconsistently, pointed to the “beyond a reasonable doubt standard” and constitutional concerns over religious freedom, as requiring “but for,” despite the identical interpretive outcome in civil cases. Id. What happens when, as in Miller, there are clearly several motives involved:

“How should a jury measure whether a specific motive was significant in inspiring a defendant to act? Is a motive significant if it is one of three reasons he acted? One of ten?”

Id. at *12. The same difficulty could be raised against using the “significant” or “substantial factor” test in civil cases.

More persuasive was simply the invocation of common usage and the need to construe a statute leniently in favor of the defendant.

The dissenting judge would have brushed this all under the rug as “harmless error,” but failure to charge properly on the correct causation standard is rarely going to pass as harmless, and it did not do so here. Even the dissenter, however, acknowledged that:

“This but-for requirement is part of the common understanding of cause.”

Id. (Sargus, J., dissenting) at *46 (quoting from Burrage v. United States, 134 S. Ct. 881, 888 (2014)).

[1] Burrage v. United States, 134 S. Ct. 881, 887–89 (2014) (criminal).

[2] Univ. of Tex. Sw. Med. Ctr. v. Nassar, 133 S. Ct. 2517, 2528 (2013) (civil); Gross v. FBL Fin. Servs., Inc., 557 U.S. 167, 176–77 (2009) (civil); Safeco Ins. Co. of Am. v. Burr, 551 U.S. 47, 63–64 & n.14 (2007) (civil).

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Cancer Epidemiology 100 Years Ago

October 6th, 2014

Writing from the Department of Pathology of Columbia University, at the College of Physicians and Surgeons, Isaac Levin published a study of cancer etiology in 1910. Isaac Levin, “III. The Study of the Etiology of Cancer Based on Clinical Statistics,” 51 Ann. Surg. Jun 768 (1910). Levin looked at population and gender prevalence among cancer cases, without age correction or any statistical measure of random error. He compared population prevalence of specific or all-cause mortality without isolating exposure and outcome. Levin’s efforts were earnest, but surely they strike us as primitive. If you want to be disabused of the belief that epidemiology today is a primitive scientific enterprise, mired in methodologies and interpretative strategies of the past, Levin’s article is a welcome documentation that progress is possible and has in fact occurred.

Levin sums up what was known about occupation and cancer in 1910, which was not much:

“QUESTION 10,- OCCUPATION.–Occupation undoubtedly plays an important role in the causation of cancer. The carcinoma of the scrotum of the chimney sweeps, tumors of the bladder of the aniline workers, and X-ray cancer are well known, but it will require a great deal of research to, show how direct the influence is that these occupations exert on the causation of cancer, since only a certain number of the workers contract the disease.”

Id. at 776. No acknowledgment of dose response, or thresholds. No quantitation of risk against baselines.

Levin goes on to note that:

“[o]f extreme interest seems to be the fact, noted both in England and America, that cancer is comparatively rare among the miners. Table IV, compiled from the twelfth U. S. Census, illustrates this fact:

Table IV from Levin 1910

Table IV from Levin 1910

[Open in new window for clearer image]

Wilkesbarre and Scranton are mining towns and the death rate is lower than in Harrisburg or in the whole state of Pennsylvania. It seems also to be the opinion of the surgeons in Pennsylvania (personal communication) that cancer is rare among miners.”

Id. at 776.

There are some other quaint relics of the past here. On the questionnaire used for 4,000 cases or so, here is how Levin inquired of “Race or Nationality”

“RACE OR NATIONALITY. …………Australoid – Coolies of East India; Negroid – Negroes, Negritos of the Philippines; Mongoloid – Chinese, Japanese, American Indians, Filipinos; Melanochroic – Italians, Spaniards, Greeks, Arabs, Jews; Xanthochroic – Fair Europeans. State not only the name of the race, but also of the subdivision]”

Id. at 772. Anthropology was fairly primitive as well, in 1910.

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The Last Squirmish Between Irving Selikoff and Sir Richard Doll

September 30th, 2014

In one of his last publications before he died, Dr. Selikoff reflected on the ethical dimensions of epidemiology. He recounted the development of our understanding of the lung cancer hazards of asbestos and smoking, and noted that there had been “random instances” of lung cancer cases reported among asbestos workers in the 1930s and 1949s, but “[w]ith the continued growth of the asbestos industry, it was deemed wise to epidemiologically examine the proposed association. This was done in an elegant, innovative, well-considered study by Richard Doll [7], a study which anyone of us would have been proud to report in 1955.” Irving J. Selikoff, “Statistical Compassion,” 55 J. Clin. Epidemol. 141S, 142S (1991).

Despite his praise for Doll’s work, Selikoff goes on to downplay Doll’s achievement by explaining how Doll supposedly missed a synergistic multiplicative interaction between asbestos exposure and smoking, which Selikoff claimed to have found a decade later:

“Not only was the association [with smoking] not yet established, indicating the need for its investigation in cohort studies, but smoking histories were not available (and indeed, many of the workers involved may not have smoked cigarettes, having begun their asbestos exposure at a time when cigarette smoking was considerably less common, even among blue collar workers). We would want such information now, but these studies were accomplished at an earlier, less informed, time.”

Id. at 143S

This short passage is revealing. In 1955, epidemiology was still a relatively young science, and it was Doll who energetically was developing and implementing its methods. Doll’s use of his cohort study was not undertaken just because it was deemed “wise,” but because the method had evolved to the point that Doll could cast offer the asbestos company in question a reasonably rigorous method of answering their “wise” concern.

Contrary to Selikoff’s suggestions, the smoking association was better established in 1955, when Doll published, than was the asbestosis association. By the time Doll published his famous paper on the association between asbestosis and lung cancer, he had published three studies on the association between smoking and lung cancer. Interestingly, Doll later acknowledged that his failure to obtain smoking histories was purely an oversight. By the time Selikoff undertook his studies of asbestos insulators in the late 1950s, a wise investigator would have known that he needed to be very careful smoking histories to study the role of asbestos in an exposed cohort.

Perhaps more revealing yet, however, was Selikoff’s counterfactual assertion that Doll’s 1955 study was conducted too early to assess the role of tobacco in lung cancers observed in the early 1950s. By the early 1950s, cigarette smoking was well established in both in the U.K., and in the U.S., and had been so for several decades. Here are the data for the United States:

 

Correlation between smoking and lung cancer in US males, showing a 20-year time lag between increased smoking rates and increased incidence of lung cancer.

Correlation between smoking and lung cancer in US males, showing a 20-year time lag between increased smoking rates and increased incidence of lung cancer.

National Cancer Institute Figure 2003

And here are the data from the United Kingdom:

 

Figure 1

Figure 1

Figure 1, from Robert Platt, et al., Smoking and Health: A Report of The Royal College of Physicians of London on Smoking in relation to Cancer of the Lung and Other Diseases 3 (1962).

 

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Common Law Causal Apportionment – Each Dog Had His Day

September 27th, 2014

Some legal scholars have suggested that apportionment of damages by causation is a 20th century reform to the common law[1]. This strikes view strikes me as ignoring the late 20th century American courts’ penchant for favoring joint and several liability, without apportionment, and its hostility or refusal to permit causal apportionments. See, e.g., Carter v. The Wallace & Gale Asbestos Settlement Trust, 439 Md. 333, 96 A.3d 147 (2014). See also “Maryland Refuses Apportionment in Asbestos Lung Cancer Cases – Carter” (Sept. 19, 2014); “Further Thoughts on the Carter Apportionment Case – The Pennsylvania Experience” (Sept. 20, 2014).

The common law, as it developed in the United States from the early 19th century, was hospitable to apportionments that avoided “entire” or “joint and several” liability. Apportionments of single harms were often permitted and encouraged by the use of reasonable estimates of relative causal contributions. The common law generally provided that entire liability, and its procedural consequences similar to joint and several liability, did not apply to concurrent or successive tortfeasors whose acts (or products) cause distinct injuries or cause an injury that can be reasonably apportioned.

Asbestos (and other similar) cases raise interesting questions about the divisibility and apportionment of physical injuries and resulting impairment or death. Asbestosis represented the cumulative fibrotic result from multiple exposures to asbestos, over the course of an entire occupational exposure. For workers who were exposed to asbestos that came from different manufacturers’ products, the workers’ asbestosis represents the cumulative, single result of all the exposures that resulted in pulmonary deposition of fibers. A very slight, passing exposure may not have contributed at all to pulmonary deposition and retention. Heavier, more sustained exposures might contribute to the overall fiber burden, but certainly not equally. Exposures, deposition, and retention would be expected to vary in proportion to the use and dustiness (asbestos) of each product, weighted by the duration of exposure from each product. If all products were used equally, and were equally dusty, then perhaps they all could be taken to contribute equally. This last hypothetical, however, ignores the reality of market dominance of a few manufacturers, such as Johns-Manville up through the end of asbestos use in insulation.

The situation with mesothelioma is more complicated because not all commercial asbestos fiber types have the same potency with respect to causing mesothelioma. Crocidolite fiber has a potency an order of magnitude greater than amosite fiber. Chrysotile, even with some tremolite contamination, is orders of magnitude below crocidolite in its ability to cause mesothelioma, if it does so at all. These complexities of varying potency can be modeled by dustiness, duration of exposure, intensity of exposure, and potency factors. A further consideration is that mesothelioma arises from one or a few cells deranged by an asbestos fiber in close proximity. Increasing exposure would appear to increase the risk of malignant change, but the change is likely a local phenomenon, not the result of total fiber burden. (Increasing total fiber burden, however, represents an increasing risk of mesothelioma induction.) The assessment of causal responsibility is essential an attribution based upon ex ante risk, not actual causation. Given this reality, there is no reason that the causation cannot and should not be apportioned by the magnitude of the risk, modeled as suggested above.

The scholar’s suggestion that apportionment is a new-fangled development in tort law, and a reform of the common law, does not appear to hold up on close scrutiny. The common law dealt with combined causes in a variety of situations, and liberally permitted apportionment even for single harms, when there was a rational basis.  As Restatement (Second) of Torts makes clear, even so-called distinct harms may require some “rough” estimation in attributing damages to the tortfeasors responsible for the different harms. Restatement (Second) of Torts § 433A (1965). Comment b to this section rather circularly defines “distinct harms” as those “results which, by their nature, are more capable of apportionment.” The comment states a hypothetical case and suggested resolution, which are, however, more helpful:

“If two defendants independently shoot the plaintiff at the same time, and one wounds him in the arm and the other in the leg, the ultimate result may be a badly damaged plaintiff in the hospital, but it is still possible, as a logical, reasonable, and practical matter, to regard the two wounds as separate injuries, and as distinct wrongs. The mere coincidence in time does not make the two wounds a single harm, or the conduct of the two defendants one tort. There may be difficulty in the apportionment of some elements of damages, such as the pain and suffering resulting from the two wounds, or the medical expenses, but this does not mean that one defendant must be liable for the distinct harm inflicted by the other. It is possible to make a rough estimate which will fairly apportion such subsidiary elements of damages.”

The above hypothetical is very much analogous to cases that occur in asbestos personal injury and property damage litigation. The Restatement also provides for apportionment of damages in cases in which the plaintiff suffers a single but divisible harm. Restatement § 433A(1)(b). Apportionment is permitted for such a harm when “there is a reasonable basis for determining the contribution of each cause.” Id. at comment d, the Restatement gives several examples of joint torts that can be apportioned by cause. Of particular interest is the suggestion that:

“Apportionment is commonly made in cases of private nuisance, where the pollution of a stream, or flooding, or smoke or dust or noise, from different sources, has interfered with the plaintiff’s use or enjoyment of his land. Thus where two or more factories independently pollute a stream, the plaintiff’s use of the water may be treated as divisible in terms of degree, and may be apportioned among the owners of the factories, on the basis of the respective quantities of pollution discharged into the stream.”

Id. See also 1 S. Speiser, C. Krause & A. Gans, The American Law of Torts at § 3.12 & note 88 (1983 & Supp. 1984) (collecting cases on joint flooding and polluting). Like a stream wasted by pollution, a person’s lungs impaired by fibrosis should be divisible “in terms of degrees” of contribution to the outcome.

Some of the earliest cases giving rise to an apportionment of property damages have involved the worrying and killing of sheep by dogs belonging to two or more persons. Many of these early cases involved the propriety of joinder of the dog owners and the resultant joint liability. Under the common-law approach to joinder, courts found it “repugnant to the plainest principles of justice to say that the dogs of different persons, by joining in doing mischief could make the owners jointly liable.” Russell v. Tomlinson & Hawkins, 2 Conn. 206 (1817). Consequently, if two dogs, each belonging to different persons, run together and kill the plaintiff’s sheep, each owner is liable only for the sheep his dog killed. Id. (“no man can be liable for the mischief done by the dog of another, unless he had some agency in causing the dog to do it.”) Van Steenburgh v. Tobias, 17 Wend. 562 (N.Y. 1837) (affirming nonsuit based upon misjoinder because joinder was error unless defendants jointly liable). The court in Van Steenburgh noted that the imposition of joint liability on the owner of one dog, which happened to unite with other dogs in destroying a herd, would be unjust. Id. at 564. The difficulty in estimating the separate injury done by each dog does not permit imposing liability for the entire damage. Id. at 563.

In Adams v. Hall, 2 Vt. 9 (1829), the court rejected the plaintiff’s argument that the damage done to his property, a herd of sheep, was entire. Id. at 10, 11. Because the damage done by each defendant’s dog was separate, the defendants were misjoinded under the then current procedural rules. Id. at 11.

In Buddington v. Shearer, 37 Mass. (20 Pick.) 477 (1838), the court acknowledged that the plaintiff would have some difficulty in proving which dog caused what distinct harm, but that under the circumstances, the trier of fact could reasonably apportion damages equally on the assumption that the dogs were capable of equal mischief. Id. at 479-80.

In the absence of a statute, the rule requiring apportionment in dog and sheep cases remains valid. See Miller v. Prough, 203 Mo. App. 413, 425, 221 S.W. 159 (1920) (each owner of a dog may not be liable for the entire damage; evidence of relative size and ferocity sufficient to permit the jury to apportion damages); Stine v. McShane, 55 N.D. 745, 746 214 N.W. 906 (1927) (in absence of a joint tort or a statute modifying the common law, plaintiff can recover only those damages occasioned by that defendant’s conduct); Nohre v. Wright, 98 Minn. 477, 478-79, 108 N.W. 865 (1906) (each dog owner is liable separately for the damages done by his animal); Anderson v. Halverson, 126 Iowa 125, 127, 101 N.W. 781 (1904) (reversing judgment for defendant dog owner because although plaintiff could not show which defendant’s dog killed which sheep, the jury should have been allowed to consider defendant’s liability with proper instructions on apportionment), Denny v. Correll, 9 Ind. 72, 73 (1857) (per curiam) (reversing joint judgment against defendant dog owners); Dyer v. Hutchins, 87 Tenn. 198, 199, 10 S.W. 194 (1889)(each defendant dog owner is responsible only for the depradations of his own animal).

The validity of the apportionments made for separate harms in dog and sheep cases continued into the second half of the 20th century, as evidenced by the following illustration in the Second Restatement:

“Five dogs owned by A and B enter C’s farm and kill ten of C’s sheep. There is evidence that three of the dogs are owned by A and two by B, and that all of the dogs are of the same general size and ferocity.”

Second Restatement § 433A, illustration 3. Based upon these facts, the Second Restatement would hold A liable for the value of six of the sheep, and B liable for four. Id.

The destruction of a field or its crops presents a case of harm, which courts have often treated as single but divisible. In Powers v. Kindt, 13 Kan. 74 (1874), the plaintiff sued for the damage inflicted to his crops by cattle belonging to two unrelated parties. Noting that the plaintiff had suffered a single injury to his property, the court held that the damages for the single injury should be apportioned by the relative number of each defendant’s cattle. Id. at 83. In Wood v. Snider, 187 N.Y. 28, 79 N.E. 858 (1907), the plaintiff sued an owner of cattle, which had trespassed along with the cattle belonging to other persons, on the plaintiff’s land. Id. at 36, 79 N.E. 858. The court noted that the cattle were all on the plaintiff’s land and that they all caused equal damage to the plaintiff, and, therefore, each cattle owner was liable for his proportionate share of the entire damages. Id. Accord Pacific Live Stock Co. v. Murray, 45 Or. 103, 76 P. 1079 (1904) (the proper measure of plaintiff’s damages was the value of pasturage consumed by defendant’s sheep, not the mischief done by animals belonging to other persons); Hill v. Chappel Brothers of Montana, 93 Mont. 92, 103, 18 P. 2d 1106 (1933) (jury allowed to make the best possible estimate of the portion of damages attributable to the defendant’s horses).

Other courts, in considering animal trespass cases, have not emphasized whether they viewed the plaintiff’s injury as single or several. Rather, these courts, simply have stressed the reasonable divisibility of damages and the appropriateness of apportioning damages accordingly. Westgate v. Carr, 43 Ill. 450, 454-44 (1867) (each defendant cattle owner is liable only for the damage done by his cattle); State v. Wood, 59 N.J.L. 112, 113-14, 35 A. 654 (1896) (each dog’s trampling of the plaintiff’s cabbage patch is a separate harm; each owner is liable only for the harm his dog caused); King v. Ruth, 136 Miss. 377, 381,101 So. 500 (1924) (each dog owner is liable only for the damages done by his animals’ separate and distinct trespass). See also Cogswell v. Murphy, 46 Iowa 44 (1877) (reversing judgment against defendant cattle owners because of misjoinder of parties).

Apportionments of damages for indivisible harms are routinely made in cases involving the flooding of land from multiple sources. In Griffith v. Kerrigan, 109 Cal. App. 2d 637, 241 P.2d 296 (1952), a typical joint-flooding case, the plaintiff sued for damage to his peach orchard, caused by excessive underground water seepage from one defendant’s irrigation of an adjacent rice paddy, and from another defendant’s nearby canal. Id. at 638, 241 P.2d 296. The trial court entered judgment for the plaintiff against the remaining defendant for only the harm caused by that defendant. Id. Both parties appealed. On appeal, the plaintiff claimed that each defendant was the proximate cause of the entire harm, and therefore, she was entitled to a judgment for the entire amount of damages proved at trial. Relying on Restatement of Torts Section 881, the predecessor to Section 433A of the Second Restatement, the Griffith court rejected the plaintiff’s contention that damage and liability were entire. Id. at 639, 241 P.2d 296. The appellate court was satisfied that the estimates of the relative percentages of water from all possible sources were a sufficient evidentiary basis for making a reasonable apportionment of the damages. Id.

The defendants[2] in Griffith also appealed on grounds that the expert witness testimony given at trial established that no exact apportionment was possible. Because of this lack of precision, the defendants contended that the plaintiff had failed to carry his burden of proving each defendant’s causal role. Id. at 640, 241 P.2d 296. The appellate count expressly rejected the defendants’ contention and held that the expert witness’s estimate was a sufficient basis for the apportionment. Id.

The holdings in Griffith are based upon well-established precedents and principle of justice. Joint and several liability in such a case would allow “a plaintiff to overwhelm a defendant with claims for damages out of all proportion to his wrongdoing …” William Tackaberry Co. v. Sioux City Service Co.,154 Iowa 358, 377-78, 132 N.W. 945 (1911) (extensively reviewing authorities and rejecting joint and several liability for property damage caused by flooding from multiple causes; Boulger v. Northern Pacific Railroad Co., 41 N.D. 316, 324, 171 N.W. 632, (1918) (imposing entire liability on a party responsible for only a portion of the harm caused by a flood would be contrary to law and justice).

In Sellick v. Hall, 47 Conn. 260 (1879), the court held that regarding parties that independently damaged plaintiff’s property by flooding as joint tortfeasors was error. Id. at 273. Each party can be liable only for that portion of the harm, which he caused. Id. at 274. Although apportionment might be difficult in some cases, the court noted that juries are often entrusted with difficult factual judgments. Id. The plaintiff should not, therefore, be denied any recovery; nor should one defendant be “loaded with damages to not legally liable, simply because the exact ascertainment of the proper amount is a matter of practical difficulty.” Id.

The common law saw that any hardship to the plaintiff in not being able to assert joint and several liability was fairly mitigated by plaintiff’s being relieved of the requirement to prove the precise damage inflicted by each defendant. William Tackaberry Co. v. Sioux City Service, Co. 154 Iowa at 377, 132 N.W. 945; Griffith v. Kerrigan, 109 Cal. App. 2d. at 640, 241 P.2d 296. A reasonable basis for apportioning the single harm among multiple causes is sufficient to support an apportionment of damages. Sloggy v. Dilworth, 38 Minn. 179, 185, 36 N.W. 451 (1888) (rejecting entire liability; apportionment for damage to plaintiff’s crops caused by flooding from multiple causes may be based on the relative contribution of each party): Blaisdell v.Stephens, 14 Nev. 17, 19 (1879)(reversing joint judgment in a flooding case); Verheyen v. Dewey, 27 Idaho 1, 11-12, 146 P. 1116 (1915)(reversing joint judgment; each party should be responsible only for that portion of the flood that damaged plaintiff’s property): Ryan Gulch Reservoir Co. v. Swartz, 77 Colo. 60, 234 P. 1059, 1061 (1925) (rejecting joint liability for independent flooders of plaintiff’s land); Miller v. Highland Ditch Co., 87 Cal. 430, 431, 23 P. 550 (1891)(reversing joint judgment against defendants, whose irrigation ditches independently overflowed and deluged plaintiff’s land).

When two or more independent tortfeasors separately pollute the air or water and the consequences combine to form a single injury, each tortfeasor will be liable only for the consequences of his independent tortious act and will not be liable for the entire injury. Oakwood Homeowners Assoc. v. Maration Oil Co., 104 Mich. App. 689, 305 N.W.2d 567 (Mich. App. 1981). In Oakwood, the appellate court sustained the trial court’s jury instruction that the jury should separate the injuries caused to the plaintiff by the defendant from the injuries caused by other tortfeasors if they could do so.

“If two or more persons acting independently tortiously cause distinct harms or a single harm for which there is a reasonable basis for division according to the contribution of each, each is subject to liability only for the portion of the total harm that he himself caused.”

Oakwood Homeowners, 305 N.W.2d at 569.

In Maas v. Perkins, 42 W.2d 38, 253 P.2d 427 (Wash. 1953), the Supreme Court of Washington held that, while two alleged tortfeasors, accused of having contributed to the damage caused by oil sludge draining onto plaintiffs’ property, could be joined in one action, their liability was several and not joint. Plaintiffs would not be relieved of their burden that a particular defendant caused damage of a specified amount. Although the court admitted of the difficulty of such proof, the court required some basis for the allocation of the total damage. 42 W.2d 38, 253 P.2d at 430. The Maas decision followed the rule previously set out in Snavely v. City of Goldendale, 10 Wash. 2d 453, 117 P.2d 221 (1941, where a downstream farmer alleged that a municipality and a slaughterhouse discharged refuse into the Little Klickitat River. The court affirmed the rule that tortfeasors independently contributing to the pollution of a stream cannot be held jointly liable for the common injury. The basis of the court’s decision was fairness.

“[I]t might work great injustice to hold one responsible for the entire injurious effect of the pollution of a stream brought about by himself and others in varying degrees.”

Snavely, 117 P.2d at 224.

Courts have consistently viewed the rule of apportionment and several liability as a rule of fairness. Courts have been unwilling to impose liability on one tortfeasor for the acts of another over which the first had no control and where the only logical connection was some similarity of consequences.

In Farley v. Crystal Coal & Coke Co., 85 W.Va. 595, 102 S.E. 265 (1920), the Supreme Court of Appeals of West Virginia held that six separate mine operators, alleged to have polluted with slag, cinder and sewage the stream on which plaintiff’s farm was situated, could not be jointly liable for damage caused by the pollution:

“In the actual infliction of the injury there was nothing more than a combination, effected by natural causes of the consequences or results or the wrongful acts, in which the parties did not act. This of course does not absolve them from liability, but it does away with the ground or basis of joint liability and liability for entire damages. Each is liable only for the consequences of his own wrong and must be sued alone for the damages.”

Farley, 102 S.E. at 268.

Similarly, the court in Watson v. Pyramid Oil Co., 198 Ky. 135, 248 S.W. 227 (1923), was moved by considerations of fairness to adopt the rule of apportionment and several liability. Watson held that several refining companies could not be liable for the damage caused by each other’s operations. Otherwise, it reasoned “a defendant who had contributed to the injury in the slightest degree would be liable for all the damage caused by the wrongful acts of all the others.” 198 Ky. 135, 248 S.W. at 228.

In a case concerning noise pollution, the Georgia Court of Appeals held that a city operating an airport and the airlines using it were not jointly liable for damage caused to the plaintiff by a low flying aircraft. City of Atlanta v. Cherry, 84 Ga. App. 728, 67 S.E.2d 317 (Ga. App. 1951).

The Florida Supreme Court has held that joint liability would not be imposed on up-river phosphate producers despite the intermingling of the consequences of their tortious acts for the downstream riparian owners. Synnes v. Prarie Pebble Phosphate Co., 66 Fla. 27, 63 So. 1 (Fla. 1913); Standard Phosphate Co. v. Lunn, 66 Fla. 220, 63 So. 429 (Fla. 1913).

Apportionment, with burden on the plaintiff, was applied in personal injuries as well, at common law. In City of Mansfield v. Brister, 76 Ohio 270, 81 N.E. 631 (1907), the plaintiff, a riparian proprietor, sued the city for damage to his health caused by the pollution of Ritter’s Run. Ritter’s Run was found to have been fouled by five sewers, only one of which had been constructed by the city. The trial court instructed that jury that it was unnecessary to find that the city had caused the entire injury in order to find it liable for the damage. The Ohio Supreme Court deemed this error, and reversed. In a thoughtful opinion, the court discussed the contemporary authority. The court found the difficulty of apportionment presented no compelling reason to relieve the plaintiff from the obligation of proving that the damages sought from a defendant sprung from the act of that defendant:

“Each is liable only to the extent of the wrong committed by him. The fact that it is difficult to separate the injury done by each one from the others furnishes no reason for holding that one tortfeasor should be liable for act of others with whom he is not acting in concert.”

City of Mansfield, 76 Ohio 270, 81 N.E. at 633.

The suggestion of legal scholars that causal apportionment was a 20th century reform seems misguided. The mantra of “joint and several” has often clouded consideration of the fairness and practicality of causal apportionment in many kinds of personal injury cases.

[1] Michael D. Green, “Second Thoughts about Apportionment in Asbestos Litigation,” 37 Southwestern Univ. L. Rev. 531 (2008) (“The idea that liability is not all or nothing—a basic tenet of the common law—but could be apportioned in a fine-grained manner—that is using a scale of 100, whether you call it comparative negligence, fault, responsibility, or causation—is a reform of the twentieth century and one of the most influential in tort law of that century.”).

[2] Interesting how the procedure at that time put the defendants into the position that plaintiffs today take with respect to apportionment.

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Big Blue & The Sophisticated User and Intermediary Defenses

September 26th, 2014

Two particularly perfidious myths perpetrated by the asbestos litigation industry is that crocidolite was not used in the United States, and that chrysotile is as potent in causing mesothelioma as is crocidolite. Both myths are untrue, but they have become current articles of faith among the “The Lobby.” See “Selikoff and the Mystery of the Disappearing Amphiboles” (Dec. 10, 2010).

Because of the flagrant falsehoods imbedded in the Lobby’s mythology, I am always fascinated to see incontrovertible evidence of the use of crocidolite. Crocidolite is a blue fiber, and Johns-Manville (JM) was the “Big Blue” of the North American asbestos industry. JM used crocidolite in several products, but perhaps best known is its incorporation of blue fiber into asbestos cement products, known as Transite. One of JM’s manufacturing facilities, where crocidolite was used, was in Stockton, California, a.k.a. Fat City.

The JM Stockton plant was the situs of a recent sophisticated intermediary case, which is set for argument soon before the California Supreme Court. Webb v. Special Electric Company, Inc., 214 Cal. App. 4th 595, 153 Cal. Rptr. 3d 882, 888 (2013). See Monica Williams Monroe “Is There a Duty to Warn Even the Most Sophisticated User?”(July 23, 2014); “California Supreme Court Set To Untangle Webb” (July 7, 2013). The JM Stockton facility was, at one time, the largest consumer of asbestos in California, for use in making Transite (asbestos-cement) pipe products. See Asbestos:  The Magic Mineral (JM Brochure). In 1982, JM sold the Stockton facility to the J-M Manufacturing Co., and the J-M A/C Pipe Corp., which were unaffiliated with JM. “Johns-Manville Sells Pipe Unit” N.Y. Times (Dec. 21, 1982)[1].

Back in April 2001, the Kazan firm obtained a substantial jury verdict against J-M A/C Pipe Company, on behalf an employer who had worked there since 1959. Hardcastle v. J-M A/C Pipe Corp., Alameda County Superior Court No. 830058-2 (Jury verdict, April 21, 2001). The employer claimed untruthfully that it had never been sued, and had to confront allegations that it had cheated on air quality testing. The jury found J-M A/C Pipe Co. liable for negligence, with actual malice.

Given the actual knowledge and sophistication of the employer, one would expect that there was no need for an outside vendor of asbestos to warn the employer of its hazards, especially not after the early 1960s. Such a defense appears to have been interposed in one unreported California case. Ransom v. Calaveras Asbestos Ltd., No. B207018 (Cal. App. 2d Dist., Div. 5) (Mar. 4, 2009) (unpublished). Plaintiff claimed that his lung cancer was related to occupational exposure at the Stockton plant. Dr. Samuel Hammar, a pathologist, testified conclusorily that “each and every occupational exposure to asbestos” was a substantial factor. Dr. B.S. Levy offered testimony on epidemiology of asbestos fiber types. Somehow the court got the idea that “there were no distinctions in the effect of the types of asbestos to which plaintiff was exposed.” Id. Mistakes were made, and not much seems to have come of the sophisticated intermediary defense.

The sophisticated user defense seems to have gone better in a jury trial that ended with a defense verdict last month. Plaintiffs sued Special Electric for having brokered South African crocidolite fiber to the Stockton facility, and for having caused plaintiff’s mesothelioma. See “Special Electric Secures Defense Verdict In San Francisco Asbestos Trial” (Sept. 24, 2014). Plaintiffs called a physician, Barry Horn, M.D., and an industrial hygienist, William Ewing, CIH, as expert witnesses, to support their consumer expectations test for design defect. The defense called no witness, but defended on theory that the plaintiff, Mr. Dennis Hill, had been trained in, and aware of, the hazards of asbestos by the mid-1970s. Martha Joan Hill v. A.C.& S. Inc., et al., San Francisco County Superior Court (trial Sept. 2 through 10, with verdict returned Sept. 10, 2014) (Hon. Richard B. Ulmer, Dept. 624, and a jury).

It is a safe bet that Mr. Hill, and his union, had known about asbestos hazards for much longer than acknowledged. Mr. Hill’s demise is sad outcome to the crocidolite tragedy, for which his employer was and should have responsible. Almost as sad is forcing a remote supplier of crocidolite to defend itself for having brokered asbestos to the one of the world’s most knowledgeable users of the natural material.

[1] The Stockton plant was organized by the Machinists District Lodge 115, Local Lodge 1549, from 1958, on. Johns-Manville Sales Corp. v. National Labor Relations Board, 906 F.2d 1428 (10th Cir. 1990). The sale of the facility took place on the heels of a violent strike, in which the union showed it, too, could act maliciously and violently.

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Maryland Refuses Apportionment in Asbestos Lung Cancer Cases – Carter

September 19th, 2014

In Carter v. The Wallace & Gale Asbestos Settlement Trust, 439 Md. 333, 96 A.3d 147 (2014), the Maryland Court of Appeals missed an opportunity to place causal apportionment of damages in asbestos cases on a sound legal and factual basis. Instead, the Court misinterpreted the law to be about fault instead of causation, and it failed to come to terms with the facts that supported apportionment.

Carter was a consolidation of four lung cancer cases for trial before a single jury. All plaintiffs had substantial smoking histories, with varying degrees of asbestos exposure. None of the plaintiffs had been an insulator or worked in an asbestos factory. In one of the cases, involving Roger C. Hewitt, Sr., defendant Wallace & Gale Asbestos Settlement Trust[1] proffered a report of its expert witness, Dr. Gerald R. Kerby, who opined that the Mr. Hewitt’s lung cancer and death was apportionable, 3:1, between two causes, smoking and asbestos. 96 A.3d at 151-52.

The plaintiffs’ expert witness, Dr. Steven Zimmet provides the catechistic testimony, based upon the Mt. Sinai scriptures. Zimmet testified that “he could not differentiate between the two causes because the two exposures [asbestos and tobacco] are ‛not just additive, they are synergistic which means they multiple exposures’.” Id. at 151. Of course, Zimmet’s profession of ignorance was hardly probative of whether an apportionment could be made. The distinction, however, between knowledge that something cannot be done, and ignorance as to how it might be done, was lost upon the trial judge, who was wildly dismissive of the proffered opinion from Dr. Kerby:

“No, I understand there is a statistical basis for likelihood of risk. But in a given—with a given plaintiff, I don’t know how you can apportion it. But, you know, I guess, the witness can say what he says if he is qualified to say it. But I’m not going to give an instruction on this because it is not — I don’t perceive it at this point to be the law in these types of cases.

* * *

You can apportion risk. I don’t know how, in an individual plaintiff[‘s] case, you can apportion damages. I don’t know. It is a mystery to me. We’ll find out. The doctor will show up and we will hear about it.”

Id. at 151.

The trial judge excluded Dr. Kerby’s apportionment opinion, based upon a filed offer of proof, and refused to charge the jury on apportionment of damages. As for the jury instruction on apportionment, the trial judge ventured that the defendant was asking to the jury to make “a very unscientific wild guess.” Id. at 151. Of course, allowing the jury to decide any causation claim upon evidence of increased risk sanctions wild guesses and unscientific speculation. Risk is not causation. See, e.g., Guinn v. AstraZeneca Pharms., 602 F.3d 1245, 1255 (11th Cir. 2010) (“An expert, however, cannot merely conclude that all risk factors for a disease are substantial contributing factors in its development. ‘The fact that exposure to [a substance] may be a risk factor for [a disease] does not make it an actual cause simply because [the disease] developed.’”) (internal citation omitted). See also 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.”). Given that courts have put juries into the business of making wild guesses, the trial court failed to explain why it could not make a guess based upon the same sort of increased risk evidence that would support a finding of causation against the asbestos defendant alone.

The jury returned verdicts for all four plaintiffs, and the defendant appealed. The Maryland Special Court of Appeals reversed and remanded the Hewitt case for a new trial.[2] Wallace & Gale Trust v. Carter, 65 A.3d 749, 752 (Md. App. 2013). The Maryland Court of Appeals, however, took the plaintiff’s appeal, and reinstated the verdict in favor of the Hewitt family[3].

The Court of Appeals did not fuss over the general statement of Maryland law of apportionment of damages, which has adopted the American Law Institute’s Restatement (Second) of Torts § 433A (1965), which provides:

“(1) Damages for harm are to be apportioned among two or more causes where

          (a) there are distinct harms, or

(b) there is a reasonable basis for determining the contribution of each  cause to a single harm.

(2) Damages for any other harm cannot be apportioned among two or more causes.”

Id. at 157-58, quoting the Restatement. The Court did not explain why it was relying upon a portion of the Restatement, which has been superseded by the Restatement Third of Torts: Apportionment of Liability § 26 (2000).

In any event, the Court of Appeals did recognize that the crucial issue was whether there was a reasonable basis for determining the contribution of each cause to a single harm. On this issue, the Carter court took its lead from antiquated dicta from a treatise, 30 years out of date. W. Page Keeton, et al., Prosser and Keeton on Torts § 52, at 345 (5th ed. 1984). See Georgetown Law Library, “Torts Law Treatises” (“This classic hornbook on torts is no longer up-to-date… .”). The Court quoted:

“The distinction is one between injuries which are reasonably capable of being separated and injuries which are not. If two defendants, struggling for a single gun, succeed in shooting the plaintiff, there is no reasonable basis for dividing the injury between them, and each will be liable for all of it. If they shoot the plaintiff independently, with separate guns, and the plaintiff dies from the effect of both wounds, there can still be no division, for death cannot be divided or apportioned except by an arbitrary rule devised for that purpose. If they merely inflict separate wounds, and the plaintiff survives, a basis for division exists, because it is possible to regard the two wounds as separate injuries; and the same of course is true for wounds negligently inflicted…. Upon the same basis, if two defendants each pollute a stream with oil, in some instances it may be possible to say that each has interfered to a separate extent with the plaintiff’s rights in the water, and to make some division of the damages. It is not possible if the oil is ignited, and burns the plaintiff’s barn.”

96 A.3d at 158, quoting Prosser and Keeton on Torts § 52, at 345-47 (5th ed. 1984) (internal citations omitted). As can be seen from the language quoted by Court, the venerable, but out-dated text never even considered an apportionment of an injury where the only information about causation was the existence of ex ante risks. Conspicuously absent from the hornbook are any examples of cases in which causation itself is predicated upon quantitative risk estimates, which in turn could readily supply the basis for apportionment.

As for the science, the Court of Appeals cited a textbook written by plaintiffs’ lawyers:

“asbestos and tobacco smoke are complex carcinogens that can affect multiple steps in the multistage process of cancer evolution, and that the combined effects will depend on the relative magnitude of each carcinogen at each stage. As reported in different studies, the interactive effect ranges from less than additive to supramultiplicative [sic] but the model for insulation workers approximates a multiplicative effect. If the multistage model of carcinogenesis holds, and asbestos and smoking act at different stages, then a multiplicative relationship follows.”

96 A.3d at 160-61, quoting from George A. Peters & Barbara J. Peters, Asbestos Pathogenesis and Litigation, 13 The Sourcebook on Asbestos Diseases: Medical, Legal, and Technical Aspects 149 (1996). Peters and Peters is a consulting and law firm in Santa Monica. Barbara J. Peters is a lawyer and a member of the Consumer Attorneys Association of Los Angeles, the Consumer Attorneys Association of California, and the Association of Trial Lawyers of America.

If the Court of Appeals had even bothered to read the plaintiffs’ lawyer tract, it would have seen that even the Peters had qualified their opinion, in their 1996 book, by suggesting that the “model for insulation workers approximates a multiplicative effect.” Id. (emphasis added). Mr. Hewitt had been a crane operator, which hardly involves the same level of exposure as an asbestos insulator, and the evidence for multiplicative synergy is sorely lacking outside a few, heavily exposed cohorts such as insulation workers. In any event, the Court of Appeals failed to explain or justify why a multiplicative model, even if it were appropriate, is decisive of the issue whether or not there was a reasonable basis for apportionment.

While we might excuse the Court of Appeals’ missteps in interpreting scientific evidence, even if filtered through funnels created by the plaintiffs’ expert witness Zimmet and the law firm of Peters & Peters, harder to forgive is the Court’s bobbling the interpretation of apportionment in New Jersey courts. The Special Court of Appeals had relied upon the New Jersey Dafler case, which affirmed a jury’s apportionment of damages in an asbestos and smoking lung cancer case. Dafler v. Raymark Industries, Inc., 259 N.J.Super. 17, 611 A.2d 136 (App. Div.1992), aff’d 132 N.J. 96, 622 A.2d 1305 (1993) (per curiam). In Dafler, the plaintiff’s expert witness made the usual protestations that the outcome, lung cancer, was indivisible, and the defense expert witness opined that smoking was the sole cause. The New Jersey appellate courts held that it would be manifestly unjust to attribute 100% of the lung cancer to smoking when no expert witness testified to such an allocation.

The Court of Appeals correctly pointed out that New Jersey cases are not binding upon it and that it would choose not to do so, which was its wont. The Court then proceeded to ignore that the Dafler holding was explicitly adopted by the New Jersey Supreme Court, and that the holding was based upon a causal, not a fault-based, apportionment. Indeed, the Court of Appeals went as far as to declare that the Dafler case was based upon fault principles because the Appellate Division there had stated that “apportionment is also consistent with the principles of the Comparative Negligence Act.” 96 A.3d at 155, quoting from Dafler, 259 N.J.Super. at 35, 611 A.2d at 145 (emphasis added). What the Maryland Court of Appeals failed to realize, however, was that the Dafler case was tried in New Jersey’s regime of hyper-strict asbestos liability, in which evidence of fault is excluded. Of necessity, the evidence and the verdict in Dafler were based exclusively upon causal determinants, not fault principles. Indeed, the Appellate Division’s “also” emphasized here in the quote from Dafler makes clear that the Appellate Division was merely noting that New Jersey juries are asked to make similar assessments of comparative contributions in fault, and that making such an assessment is not beyond the jury’s function or competence.

Two judges, in Carter, dissented in a polite, factual opinion that tore away at the majority opinion. The dissent noted that in Maryland, as in most states, workman’s compensation judges apportion causal shares to single injuries all the time. 96 A.3d at 173. And the dissent dug deeper into New Jersey law, as well as other foreign states, to expose the majority’s poor scholarship:

“Death may be indivisible as to result, but it is not per se incapable of apportionment. Many courts around the country have permitted apportionment in death cases. See e.g., Brisboy v. Fibreboard Corp., 429 Mich. 540, 418 N.W.2d 650, 655 (1988) (permitting apportionment of damages in a wrongful death action based on smoking history and asbestos exposure); Champagne v. Raybestos–Manhattan, Inc., 212 Conn. 509, 562 A.2d 1100, 1118 (1989) (same); see also Poliseno v. General Motors Corp., 328 N.J.Super. 41, 744 A.2d 679, 687 (2000) (concluding that while death is indivisible as to result, it is capable of apportionment in terms of causation). … In my view, a categorical rule that death is an indivisible injury incapable of apportionment speeds past an accepted principle of law: death can be capable of apportionment as to damages, but not as to fault. See Restatement (Third) of Torts: Physical and Emotional Harm § 28, cmt. d (2010) (“Death as an injury may not be divisible, but damages for death are divisible.”); see also Gerald W. Boston, Toxic Apportionment: A Causation and Risk Contribution Model, 25 Envtl. L. 549, 568–69 (1995) (stating that although “comment i [to the Restatement (Second) of Torts § 443A] states that death is the quintessential indivisible harm … deaths attributable to toxic causes, as when a plaintiff dies from lung cancer brought about by the combined effects of smoking and asbestos exposure, each of the contributing causes can be compared and the harm apportioned on that basis.”).

Id. at 173.

The dissent saw clearly that the characterization of apportionment in New Jersey law, relied upon by the intermediate appellate court, was not a mere matter of opinion. The majority of the Court of Appeals was wrong, as a matter of fact, in claiming that apportionment of damages in New Jersey was based upon fault. Id. at 174, citing Poliseno v. General Motors Corp., 328 N.J.Super. 41 55-56, 744 A.2d 679, 687-88 (2000), for clear distinguishing between apportionment based upon causation as opposed to fault.

The dissent also called out the majority for the disturbing partisanship in adopting plaintiffs’ lawyers’ and plaintiffs’expert witness’s opinions on apportionment, without any consideration of the excluded expert witness’s contrary opinions. See Gerald W. Boston, Toxic Apportionment: A Causation and Risk Contribution Model, 25 Envt’l L. 549, 555 (1995) (cited by dissenters for his conclusion that “[i]f the plaintiff’s asbestos exposure and his smoking are both shown to be causal factors in the plaintiff’s lung cancer, then the loss is necessarily capable of apportionment on the basis of the relative risks demonstrated for each kind of toxic exposure.”).

The Carter case comes about a year after the Court of Appeals reversed a careful opinion of the Special Court of Appeals, and held that plaintiffs’ expert witnesses may testify that each exposure, however small, represents a substantial contributing factor to a plaintiff’s asbestos-related disease. Dixon v. Ford Motor Co., 433 Md. 137 (2013). Science seems not to play well in asbestos cases before the high court of Maryland.

[1] Apparently, the Trust was inappropriately named a Settlement Trust, probably by plaintiffs’ counsel creditors who had apparently hoped it would simply be a cash delivery device.

[2] Colleen K. O’Brien, “Trial Court Erred by Excluding Defense Expert Testimony on Cigarette Smoking As Contributing to Plaintiff’s Lung Cancer” (May 2013); Arlow M. Linton, “Maryland: Failure to Allow Apportionment of Causes of Lung Cancer is Reversible Error” (Oct. 28, 2013).

[3] Colleen K. O’Brien, “Trial Court Properly Excluded Defense Expert Testimony on Cigarette Smoking as Contributing to Plaintiff’s Lung Cancer in Asbestos Case” (Aug. 19, 2014).


				


				
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Railroading Scientific Evidence of Causation in Court

				August 31st, 2014 

				

					
Harold Tanfield spent 40 years or so working for Consolidated Rail Corporation (and its predecessors), from 1952 to 1992.  Mr. Tanfield’s widow sued Conrail, under the Federal Employers’ Liability Act (“FELA”), 45 U.S.C.A. §§ 51-60, for negligently overexposing her late husband to diesel fumes, which allegedly caused him to develop lung cancer. Tanfield v. Leigh RR, No. A-4170-12T2, New Jersey Superior Court, App. Div. (Aug. 11, 2014) Slip op. at 3. [cited below as Tanfield].


The trial court granted Conrail summary judgment on grounds that plaintiff failed to show that Conrail had breached a duty of care.  The appellate court reversed and remanded for trial. The Appellate Division’s decision is “per curiam,” and franked “not for publication without the approval of the Appellate Division.” Only two of the usual three appellate judges participated.  The panel decided the case one week after it was submitted.


The plaintiff relied upon two witness, a co-worker of her husband, and an expert witness, Steven R. Tahan, M.D.  Dr. Tahan is a pathologist, an Associate Professor, Department of Pathology, Harvard Medical School, and the Director of Dermatopathology, Beth Israel Deaconess Medical Center.  Dr. Tahan’s website lists melanoma as his principal research interest. A PubMed search reveals no publications on diesel fume, occupational disease, or lung cancer.  Dr. Tahan’s principal research interest, skin pathology, was decidedly not at issue in the Tanfield case.


The panel of the Appellate Division quoted from the relevant paragraphs of Tahan’s report:


“Mr. Tanfield was a railroad worker for 35 years, where he was exposed to a large number of carcinogenic chemicals and fumes, including asbestos, antimony, arsenic, benzene, beryllium, cadmium, carbon disulfide, cyanide, DDT, diesel fumes, diesel fuel, dioxins, ethylbenzene, lead, methylene chloride, mercury, naphthalene, petroleum hydrocarbon, polychlorinated biphenyls, polynuclear aromatic hydrocarbons, toluene, vinyl acetate, and other volatile organics.


I have reviewed the cytology and biopsy slides from the right lung and confirm that he had a poorly differentiated malignant non-small cell carcinoma with both adenocarcinomatous and squamous features.  I have reached the following conclusions to a reasonable degree of medical certainty based on review of the above materials, my education, training, and experience, and review of published studies.


Mr. Tanfield’s more than 35 year substantial occupational exposure to an extensive array of carcinogens and diesel fumes without provision of protective equipment such as masks, respirators, and other filters created a long-term hazard that substantially multiplied his risk for developing lung cancer over the baseline he had as a former smoker.  It is more likely than not that his occupational exposure to diesel fumes and other carcinogenic toxins present in his workplace was a significant causative factor for his development of lung cancer and death from his cancer.”


Tanfield at 6-7.


Mr. Tanfield’s co-worker testified to what appeared to him to be excessive diesel fumes in the workplace, but there is no mention of any quantitative or qualitative evidence to any other lung carcinogen.  The Appellate Division states that the above three paragraphs represent the substance of Dr. Tahan’s report, and so it appears that there is no quantification of Tanfield’s smoking abuse, or the length of time between his discontinuing his smoking and the diagnosis of his lung cancer.  There is no discussion of any support for the alleged interaction between risks, or for any quantification of the extent of his increased risk from his lifestyle choices as opposed to his workplace exposure(s). There is no discussion of what Dr. Tahan visualized in his review of cytology and pathology slides, which permitted him to draw inferences about the actual causes of Mr. Tanfield’s lung cancer.


The trial judge proceeded on the assumption that there was an adequate proffer of expert opinion on causation, but that Dr. Tahan’s opinions on the failure to provide masks or respirators was a “net opinion,” a bit out of Tahan’s area of expertise.  Tanfield at 8. The Appellate Division apparently thought having a skin pathologist opine about the duty of care for a railroad was good enough for government work.  The appellate court gave the widow the benefit of the lower evidentiary threshold for negligence under FELA, which supposedly excuses the lack of an industrial hygiene opinion.  Tanfield at 10.  According to the two-judge panel, “[t]he doctor’s [Tahan’s] opinions are backed by professional literature and by his own considerable years of research and experience.” Tanfield at 11.  The Panel’s statement is all the more remarkable given that Tahan had never published on lung cancer, exposure assessments, or industrial hygiene measures; the vaunted experience of this witness was irrelevant to the issues in the case. Perhaps even more disturbing are the gaps in the proofs concerning the lack of causal connection between many of the alleged exposures and lung cancer generally, any discussion that the level of exposure to diesel fumes, from 1952 to 1992, was such that the railroads knew or should have known that that level of diesel fume caused lung cancer in workers.  And then there is the lurking probability that Mr. Tanfield’s smoking was the sole cause of his lung cancer.


Over 50 years ago, the New York Court of Appeals rejected a claim for leukemia, based upon allegations of benzene exposure, without any quantification of risk from the alleged exposure.  Miller v. National Cabinet Co., 8 N.Y.2d 277, 283-84, 168 N.E.2d 811, 813-15, 204 N.Y.S.2d 129, 132-34, modified on other grounds, 8 N.Y.2d 1025, 70 N.E.2d 214, 206 N.Y.S.2d 795 (1960). It is time to raise the standard for New Jersey courts’ consideration of epidemiologic evidence.

				


				
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