TORTINI

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Further Thoughts on the Carter Apportionment Case – The Pennsylvania Experience

September 20th, 2014

Carter is hard to square with commentators and precedent and the logic of the law. Juries, in their fact-finding roles, apportion in various contexts. In actions for negligence, juries consider the relative faults of the parties, and apportion responsibility in the absence of any definite quantitative basis. In considering crossclaims among defendants, juries in many states must assess each defendants relative causal contribution to the plaintiff’s overall injury and apportion liability. See, e.g., Moore v. Johns-Mansville Sales Corp., 781 F.2d 1061, 1062-65 (5th Cir. 1986) (rejecting pro-rata liability in favor of apportioned liability based upon relative causation of dose-related diseases)

Mathematical certainty is not a prerequisite to apportionment; evidence that tends to show relative proportions of damages caused by each tortfeasor, or other source, is sufficient for a jury to apportion properly. See, e.g., Scafidi v Seiler, 119 N.J. 93, 113, 574 A.2d 398 (1990) (apportionment is a traditional jury function). See also Restatement (Third) of Torts: Physical and Emotional Harm § 28, comment d (2010) (“Death as an injury may not be divisible, but damages for death are divisible.”).

As we saw in Carter, the Maryland Court of Appeals insisted upon characterizing apportionment of damages as based upon fault, when it clearly can be accomplished without reference to fault. As seen in New Jersey law and in the Restatement (Second) of Torts, apportionment on causal principles is encouraged. See Section 433A, comment a (apportionment is proper when one of the causes is the conduct of the plaintiff, regardless of whether the plaintiff’s conduct is negligent or innocent). Workman compensation cases provide many examples of fault-free, causal apportionment. See, e.g., Jenkins v. Halstead Indus., 17 Ark. App. 197, 706 S.W.2d 191 (1986) (apportionment in non-fault based workers’ compensation case). Even when apportionment is based upon fault principles, claims of synergy or mathematical inexactitude do not create a bar to reasonable divisions of damages[1].

Judges in Pennsylvania, who have heard both sides of the evidence in asbestos/smoking lung cancer cases, have upheld juries’ causal apportionments of damages. In Parker v. Bell Asbestos Mines, Ltd., plaintiff sued for her deceased husband’s death from lung cancer. Her decedent had been a heavy smoker for many years, and he had been exposed minimally to asbestos in his office job on the property of an asbestos product manufacturing plant. Plaintiffs expert witnesses (Dr. Rubin) testified that the cancer and death were the result of synergistic risk of smoking and asbestos exposure, and that they did not know how to distinguish between the risks. The defense expert witnesses (Dr. Cooper and Epstein) opined that the cancer was due solely to smoking. Judge Huyett instructed the jury that it could choose to apportion damages between asbestos and tobacco, and the jury did so. A strong panel of the Third Circuit affirmed the apportionment instruction to the jury and the jury finding. Parker v. Bell Asbestos Mines, Ltd., No. 86-1197, Slip Op. (Dec. 30, 1987) (per curiam) (Weis, Higginbotham, and Hansmann, JJ.) (affirming judgment entered on verdict that apportioned causation of lung cancer and consequent death, but remanding on a liability issue), reported only for disposition at 838 F.2d 462 (3d Cir. 1987). For about five years after Parker, the federal district courts in the Third Circuit generally followed the practice of Judge Huyett, who was affirmed by the Circuit, in giving apportionment charges[2].

The defense’s uniform success in obtaining apportionment charges in Pennsylvania law diversity cases ended with Borman v. Raymark Indus., Inc., 960 F.2d 327 (3d Cir. 1992). In Borman, neither the defendants’ (Dr. William Weiss) nor the plaintiffs’ expert witnesses (Dr. Daniel Dupont) apportioned damages in a case involving an asbestos insulator, who smoked heavily, and died of lung cancer. Borman, 960 F.2d at 331. Dr. Dupont recited the dubious 5-10-50 Mt. Sinai catechism, and gave the requisite concession that he was ignorant of any method to apportion the lung cancer outcome to asbestos and tobacco. Dr. Weiss testified that asbestos was the sole cause of Mr. Borman’s lung cancer. On this record, the trial judge, Hon. Edmund Ludwig, refused to charge the jury on apportionment. The Third Circuit affirmed on its prediction that the Pennsylvania Supreme Court would disallow apportionment because the defense expert had never been asked to apportion causation, and thus the defendants could not carry their burden of proving a reasonable basis for apportionment. Id. at 334-35.

The Borman decision raised a difficult problem, which the panel of Judges Sloviter, Scirica, and Alito, never addressed: why had the defense not carried its burden of showing a basis for apportionment when:

(1) all expert witnesses agreed that tobacco was a cause of the plaintiff’s cancer;

(2) jury heard the quantified risks of tobacco and asbestos, which showed that tobacco had been a larger risk in the plaintiff’s case; and

(3) the plaintiff’s expert witness’s admitted ignorance with respect to how the outcome might be attributed to the individual risks.

The last point would have supported a directed verdict for the defense, but given that the case was permitted to go forward, the Borman decision represents the unfair allocation of tobacco-caused (or tobacco risked) damages to defendants sued for asbestos products.[3]

Borman also poses a serious constitutional due process problem. The defendant on appeal cited to the unpublished Third Circuit opinion Court, Parker v. Bell Asbestos Mines, Ltd., No. 86-1197, slip op. at 2-7 (3d Cir. Dec. 30, 1987) (per curiam). The Circuit essentially ignored this precedent because it was unpublished and thus had no “precedential value.” 960 F.2d at 333 n.9 (3d Cir. 1992) (citing Third Circuit Internal Operating Procedure 5.6 (July 1990)). The characterization of the earlier Parker decision as having no precedential value, when it resolved the same legal issues between other parties, and provided notice to other litigants how the Third Circuit resolved the issue, was quite arbitrary.[4] The Third Circuit’s current IOP continues the distinction between precedential and non-precedential opinions. See also United States Court of Appeals for the Third Circuit Local Appellate Rule 28.3(b) (Citation Form; Certification) (Aug. 1, 2011) (“For each legal proposition supported by citations in the argument, counsel must cite to any opposing authority if such authority is binding on this court, e.g., U.S. Supreme Court decisions, published decisions of this court, or, in diversity cases, decisions of the highest state court.) (emphasis added). The upshot of the practice of marking decisions non-precedential is that judges are permitted to decide like cases differently solely because the earlier judges decided to keep their decisions “private.”

Between the Third Circuit’s Parker decision in 1987, and its Borman decision in 1992, many state court judges in Pennsylvania gave apportionment charges. Judge Della Porta’s charge in Dixon v. Celotex Corp., was typical and it resulted in the jury’s apportioning damages in a smoking lung cancer case, involving some asbestos exposure, to both tobacco and asbestos. Dixon v. Celotex Corp., Phila. Cty. Ct. C.P. No. 4576, Oct. Term 1982, Opinion Sur Post-Trial Motions at p.3 (Mar. 3, 1991) (affirming judgment entered upon jury verdict, which apportioned the causes of plaintiff’s lung cancer 65% to cigarette smoking and 35% to asbestos exposure). Judge Della Porta was especially unimpressed by the complaint that the apportionment lacked a mathematical basis with apodictic certainty:

“It is worth noting here that we engage in sophistry if it is required that some mathematical formula be presented to the jury before it can allocate percentages when there are two or more causes for one injury. Let’s not forget that this is the same jury which is asked to determine the monetary value of ‛pain and suffering’ without any guidance whatsoever on how to arrive at a fair and adequate figure.”

Id. See also Mohan v. Carey Canadian Ltd., Phila. Cty. Ct. C.P., No. 8007-3931 (Charge to Jury on April 9, 1986) (Hon. Berel Caesar) (jury instruction that pre-dated Parker: “if you find that you can reasonably split out the effects of asbestos and the injuries caused by asbestos from the injuries caused by smoking, then you should do so and assign a percentage to them.”)

In one lung cancer case, tried in 1992 in Philadelphia state court, the defense presented a defense expert witness (Dr. Theodore Rodman) that tobacco and asbestos contributed equally to plaintiff’s lung cancer. The plaintiff’s expert witness (Dr. Irwin Stoloff) hedged, but acknowledged that both asbestos and tobacco contributed, with asbestos perhaps more so. Dorothy Rothermel, Executrix of the Estate of Leland Rothermel, Deceased v. Owens-Illinois, Inc., et al., No. 8704-1464 (Philadelphia Cty. July 17, 1992) (Judge Richard B. Klein). On these facts, distinguishable from the Borman case, the trial judge gave an apportionment instruction:

The trial judge, waxing professorial, charged the jury as follows regarding the apportionment of causation:

“The next question, the first part of it is, ‛Is there a reasonable basis to apportion responsibility for Mr. Rothermel’s lung cancer between cigarette smoking and asbestos exposure’. Why did we ask that question? Because pretty much the formal statement of the law, which is put forth by a number of professors and adopted by the courts, is called the Restatement of the law. This is in torts, and says damages are to be apportioned among two or more causes when A, there are distinct harms, or B, there is a reasonable basis for determining the contribution of each cause to a single harm.

Well, there aren’t distinct harms here that we’re talking about. That would be, for example, if someone has in this kind of a context both asbestos is and emphysema from cigarette smoking. So part of your shortness of breath is caused by emphysema, and part of it is caused by asbestos if it’s symptomatic, and the doctors will tell you how much of each they think it is, but then you come to a figure. But this is one disease, lung cancer, and it’s up to you to figure out whether it’s appropriate to apportion.

* * *

The first question is do you think this is something where it’s appropriate to divide it between the two or not. If you do, then make that division[.] …[Y]ou’ve heard what the different doctors said, one says 50/50, the other says somewhat less than 50 percent due to smoking, asbestos is a little more than that, based on his reasoning.

So it’s up to you first to decide if it’s appropriate, and if it’s reasonable, there’s a reasonable way to separate the two of them out as [causative] factors and to make the allocation, and then if so, then you go to B and divide them up, just making sure that the two equal 100 percent. If you don’t think it’s appropriate to allocate between the two of them, then skip to No. 3.

* * *

. . . [W]hen you come to a damage figure, even if you have allocated between asbestos and cigarette smoking, don’t discount for that in the damage phase. We’ll do that later.”

Trial Transcript, July 2, 1990, at 117-25 (Instructions of Hon. Richard B. Klein).

The jury apportioned damages equally between asbestos and tobacco, consistent with the defense expert witness’s testimony. By post-trial motion, the defendant, Owens-Illinois, requested the trial court to mold the injury’s verdict to reflect this apportionment. The court denied this motion, 24 Phila. 332 (1992), and the Superior Court affirmed in an unpublished per curiam decision. 433 Pa. Super. 643, 638 A.2d 276 (1993). After a full briefing and oral argument in the Pennsylvania Supreme Court, that Court dismissed the appeal as having been improvidently granted. Rothermel v. Owens-Illinois Glass Co., 542 Pa. 358; 667 A.2d 2 (1995) (per curiam). In other words, the Pennsylvania justices did not want to call whether Borman had accurately predicted their decision, because they would not decide.

Pennsylvania law on apportionment, as is the case with so much of Pennsylvania products liability law, remains unclear and up in the air.


[1] See, e.g., Brisboy v. Fibreboard Corp., 429 Mich. 540, 556, 418 N.W.2d 650, 657 (1988)(upholding jury apportionment, under comparative negligence principles, of the roles of plaintiff’s cigarette smoking and the defendant’s asbestos product in causing plaintiff’s lung cancer); Hao v. Owens-Illinois, Inc., 69 Haw. 231, 738 P.2d 416 (1987) (fault-based apportionment ratio of 51% smoking to 49% asbestos affirmed); Gideon v. Johns-Manville Sales Corp., 761 F.2d 1129, 1138-40 (5th Cir. 1985) (under Texas law, determination of apportionment is for the jury; it is capable of weighing the evidence as to each potential cause); Fulgium v. Armstrong World Indus., Inc., 645 F. Supp. 761, 763 (W.D. La. 1986) (apportionment allowed under Louisiana law); Champagne v. Raybestos-Manhattan, Inc., 212 Conn. 509, 562 A.2d 1100, 1118 (1989) (commenting on the jury verdict apportioning damages: “It is the province of the jury to determine the credibility and weight to be given the evidence”)

[2] DeSilvio v. Raymark Indus., Inc., No. 86-2340, U.S.D.C., E.D. Pa., Court’s Charge and Interrogatories to the Jury, N.T. at 3.82-83 (Oct. 21, 1988) (Hon. Norma L. Shapiro) (applying New Jersey law of causal apportionment to instruct the jury that it could apportion plaintiff’s claimed fear of cancer between smoking and asbestos causes); Jordan v. Fibreboard Corp., No. 85-5655, Jury Instruction on Apportionment of lung cancer in asbestos case, June 16, 1989 (McGlynn, J.); Backman v. Celotex Corp., Civil Action No. 87-4081 (E.D. Pa. Aug. 8, 1990) (Jury Charge and Interrogatory); Henderson v. Keene Corp., Charge to the Jury and Verdict Sheet in Civ. Action No. 87-7973 (E.D. Pa. 1991) (Pollak, J.).

[3] See Richard A. Shuter, “Apportionment of Damages–Third Circuit Predicts Pennsylvania Courts Would Not Allow Jury to Apportion Liability In A Cigarette Smoking, Exposure Case–Borman v. Raymark Ind., Inc.,” 66 Temp. L. Rev. 223, 229 (1993) (“All other jurisdictions that have addressed the apportionment of damages issue in an asbestos exposure, cigarette smoking case, have permitted the jury to apportion damages.”).

[4] No citation and no precedent rules are deeply problematic, and have attracted a great deal of scholarly attention.  See Erica Weisgerber, “Unpublished Opinions: A Convenient Means to an Unconstitutional End,” 97 Georgetown L.J. 621 (2009);  Rafi Moghadam, “Judge Nullification: A Perception of Unpublished Opinions,” 62 Hastings L.J. 1397 (2011);  Norman R. Williams, “The failings of Originalism:  The Federal Courts and the Power of Precedent,” 37 U.C.. Davis L. Rev. 761 (2004);  Dione C. Greene, “The Federal Courts of Appeals, Unpublished Decisions, and the ‘No-Citation Rule,” 81 Indiana L.J. 1503 (2006);  Vincent M. Cox, “Freeing Unpublished Opinions from Exile: Going Beyond the Citation Permitted by Proposed Federal Rule of Appellate Procedure 32.1,” 44 Washburn L.J. 105 (2004);  Sarah E. Ricks, “The Perils of Unpublished Non-Precedential Federal Appellate Opinions: A Case Study of The Substantive Due Process State-Created Danger Doctrine in One Circuit,” 81 Wash. L.Rev. 217 (2006);  Michael J. Woodruff, “State Supreme Court Opinion Publication in the Context of Ideology and Electoral Incentives.” New York University Department of Politics (March 2011);   Michael B. W. Sinclair, “Anastasoff versus Hart: The Constitutionality and Wisdom of Denying Precedential Authority to Circuit Court Decisions.”  See generally The Committee for the Rule of Law (website) (collecting scholarship and news on the issue of unpublished and supposedly non-precedential opinions).

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).


				

Asbestos and Asbestos Litigation Are Forever

September 16th, 2014

When I first started practicing “asbestos law,” I routinely found copies of letters from JAG lawyers to shipyard workers, in their personnel files. The letters were notifying the workers that they had been diagnosed with asbestosis, usually by a local pulmonary physician who performed contract services for surveillance for the shipyard. The letters notified the workers that they might have rights under the Federal Employees’ Compensation Act, but emphasized that the workers had remedies against the Navy’s vendors of asbestos-containing products, and that if they sued in tort, the Navy would have a lien against any recovery. In practice, the lien was so unwieldy, that most of the Philadelphia plaintiffs’ firms would forego filing the FECA claim altogether. Thus the Navy effectively limited its liability, and kept its munitions budgets intact, while dozens of its vendors went bankrupt.

In 2011, Kara Franke and Dennis Paustenbach published a review of historical documentation of the United States Navy’s knowledge of the hazards of asbestos use in its shipyards. Kara Franke & Dennis Paustenbach, “Government and Navy knowledge regarding health hazards of Asbestos: A state of the science evaluation (1900 to 1970),” 23(S3) Inhalation Toxicology 1 (2011). Earlier, in the 1980s, Dr. Samuel Forman published a history of Navy knowledge through World War II. Samuel A. Forman, “U.S. Navy Shipyard Occupational Medicine Through World War II,” 30 J. Occup. Med. 28 (1988). Both histories serve to add valuable context to the asbestos “state of the art” story, by showing that the United States had equal or greater knowledge of the hazards of asbestos at all relevant times, and that the government was in a vastly superior position to control asbestos exposures, outfit employees and servicemen with personal protective devices, and to communicate risk information.

The subject is well covered territory, but the article approaches its subject matter from the perspective of what was known by the United States Navy, which may well have been singlehandedly responsible for exposing the greatest number of men and women to asbestos in the United States.  Back in the 1980s, Dr. Sam Forman covered a similar theme, but only through War War II.  See also Samuel A. Forman, “U.S. Navy Shipyard Occupational Medicine Through World War II,” 30 J. Occup. Med. 28 (1988); Peter A. Nowinski, “Chronology of Asbestos Regulation in United States Workplaces,” in Karen Antman & Joseph Aisner, eds., Asbestos-Related Malignancy 99 (1986) (Nowinski represented the government in direct lawsuits against the United States for its role in creating the asbestos hazards of federal and contract shipyards).

In the early days of the asbestos litigation, defendants made several attempts to implead the government, or to sue for indemnification after settling. With some few exceptions, these efforts were largely unsuccessful. Susan L. Barna, “Abandoning Ship: Government Liability for Shipyard Asbestos Exposures,” 67 New York Univ. L. Rev. 1034 (1992); Statement of Linda G. Morra, Associate Director Human Resources Division, on behalf of the United States General Accounting Office, “The Status of Asbestos Claims Against The Federal Government”; before the House Committee on the Judiciary, Subcommittee on Administrative Law and Governmental Relations (June 30, 1988).

In many states, employer knowledge was inadmissible in strict liability cases, and plaintiffs’ counsel would withdraw their negligence claims when they saw that defense counsel were prepared to implicate the government and its extensive knowledge. Unfortunately, many defense counsel failed to appreciate the potential that intermediary knowledge had for defending against punitive damage claims, which were often still in the case. And in some states, employer knowledge remained a defense in products liability trials, even when summary judgments were not given. See, e.g., In re Related Asbestos Cases, 543 F.Supp. 1142 (N.D. Calif. 1982) (permitting defendants to assert that Navy was sophisticated user as an affirmative defense at trial).

In the Philadelphia County, Pennsylvania, asbestos litigation, plaintiffs’ counsel soon learned that reverse-bifurcation fit their litigation model perfectly: quick, inexpensive trials without the bother of liability defenses. When defendants occasionally found a judge that would permit all-issue trials, and they presented “state-of-the-art” or sophisticated intermediary defenses, they often surprised themselves as well as plaintiffs’ counsel and judges with their success. See, e.g., O’Donnell v. The Celotex Corp., Phila. Cty. Ct.C.P., July 1982 Term, Case. No. 1619 (trial before Hon. Levan Gordon, and a jury; May 1989) (defense verdict in case in which plaintiffs presented negligence claims and defendants presented extensive evidence of federal government’s superior knowledge of hazard and control of workplace).

Finding admissible evidence of the government’s superior knowledge was not always an easy task. In the O’Donnell trial, defendants presented the testimony of Dr. Kindsvatter, an industrial hygienist with a doctoral degree, who had been the chief hygienist at the Philadelphia Naval Shipyard for most of the post-World War II period. Counsel also had copies of Bureau of Medicine & Surgery bulletins, with ribbons and seal authentication. These bulletins announced the Navy’s adoption of threshold limit values for asbestos, and its mandate that the values be complied with in all shipyards.

More recently, additional resources have become available, courtesy of the internet. The Navy published a safety magazine, Safety Review, starting in 1944. Glimpses of Safety Review can be found on Google Books, and “snippets” of selected volumes 17-22 can be viewed at the Hathi Trust Digital Library[1]. Hard copies of the entire Safety Review can be found in a few university libraries, with the help of World Catalog.

More recently, Archive.org has made available selected documents from a collection of documents from the United States Navy Bureau of Medicine and Surgery. This website provides a search engine and a browse by subject option. The collection on line is incomplete, but does include some issues of United States Navy Medicine, and United States Navy Medical News Letter. Here is how the webpage describes the fuller archives:

“A historical component has existed at the US Navy’s Bureau of Medicine and Surgery since May 1907 with the establishment of the Publications Office. In addition to producing The Naval Medical Bulletin, the Publications Office was responsible for producing occasional historical monographs, and maintaining a historical archive. Today the Office of Medical History’s mission has evolved to preserve and promote the history and heritage of the Navy Medical Department while serving the needs of our customers. The collection consists of publications, public records, manuscripts, personal papers, hospital plans, Navy Hygiene Museum records, biographical files, subject files, facility files, films, videos, photographs, prints, drawings, and artifacts. The OMH currently consists of over 100 collections covering over 1,000 linear feet and is staffed by a historian and an archivist.”

So apparently, more is available at the archive than is available on line. Perhaps in the fullness of time, when there is no more asbestos litigation, the archives will be fully digitized. Of course, the ship has sailed on most civilian and military asbestos exposure cases, but the web and the paper archive will contain a great number of documents that show the government’s superior knowledge with respect to the relevant hazards of asbestos, at various times.

[1] Curiously, the Hathi Trust website states that Safety Review is protected by copyright law: “Full view is not available for this item due to copyright © restrictions. Page numbers with matches are displayed without text snippets due to these restrictions. Snippets may be available for some items if you log in.” Of course, as a governmental work and publication, Safety Review is not subject to copyright protection.

The Dog That Didn’t Bark – Adverse Inferences for Expert Witnesses

September 13th, 2014

The New Jersey Supreme Court is known for bloated writing, which in the past has gotten the Court in trouble.  Witness the fiasco of the Court’s volubly outrunning its headlights to redefine strict liability to exclude the requirement of a reasonable knowability component in product liability failure-to-warn litigation. Beshada v. Johns-Manville Prods. Corp., 90 N.J. 191, 447 A.2d 539 (1982). Realizing its error, the Court attempted to correct itself a short two years later, but probably only managed to make things worse, in Feldman v. Lederle Labs., 97 N.J. 429, 479 A.2d 374 (1984). Arguably, the prestige of the New Jersey Supreme Court never recovered. See Andrew T. Berry, “Beshada v. Johns-Manville Products Corporation: Revolution-or-Aberration in Products Liability,” 52 Fordham L. Rev. 786 (1984); J. Berman, “Beshada v. Johns-Manville Products Corp.: the function of state of the art evidence in strict products liability,” 10 Am. J. Law & Med. 93 (1984).

Bitten by the Dog That Didn’t Bark

There is a danger is saying too much, and, of course, in not saying the right thing. The New Jersey high Court recently addressed adverse inferences for expert witnesses not called at trial. Washington v. Perez, ___ N.J. ___ (2014). See Bruce D. Greenberg, “Failure to Call an Expert Witness to Testify,” (Sept. 12, 2014). The case was a relative simple vehicular injury case. The defense served two expert witness reports, but did not call either expert witness at trial. In his closing argument, the plaintiff’s lawyer focused on the defense’s uncalled expert witnesses, and went so far as to suggest that defense counsel had lied to the jury. On plaintiff’s request, the court issued an adverse inference charge, instructing the jury that if it reasonably thought defendants should have called Drs. Sharetts and Hayken, then it could infer from the defendants’ not having presented these witnesses, that the missing testimony would have been adverse to defendants’ position at trial. The jury awarded plaintiff substantial damages.

The trial court refused a motion for new trial, but the Appellate Division reversed and remanded for a new trial. Washington v. Perez, 430 N.J. Super. 121, 131 (App. Div. 2013) (holding that trial court had abused its discretion in giving the adverse inference charge). See David R. Kott & Edward J. Fanning Jr., “Adverse Inference for Failing To Call a Witness: What rules apply when a person with material knowledge of a case does not testify?” 212 N.J. Law Journal 783 (June 17, 2013) (reporting on the Appellate Division’s decision). Perhaps not knowing when to stop, plaintiff obtained review in the New Jersey Supreme Court, which then endorsed the Appellate Division’s decision, and held that the giving of the adverse inference charge was error.

As the Appellate Division explained, the kerfuffle started when the plaintiff’s counsel presented a videotaped deposition of plaintiff’s expert witness, Dr. Rosen. In the course of the deposition, Dr. Rosen testified:

“Q. And in both of those reports did Dr. Ha[y]ken indicate what traumatic event or what event he associated the herniated disc that we’ve spoken of and the radiculopathy that we’ve spoken of?

A. Dr. Ha[y]ken states in his report that he feels that the cervical herniated disc and radiculopathy are related to the accident of 12/20/06.”

The defense asked that this Q&A be redacted, and plaintiff’s counsel conceded that Dr. Hayken never so stated in his report. Judge Charles Little, sitting in Burlington County, however, took a “let it all in” approach, despite defense counsel’s statement that he did not plan upon calling Dr. Hayken, and so the elicited testimony would not have been appropriate rebuttal.

The trial judge’s error only compounded. During voir dire of the jury panel, defense counsel had identified his two expert witnesses, and in his opening statement, the defense counsel has told the jury that “the evidence will show that [plaintiff] was not injured in the accident … .” Plaintiff’s counsel ran with the admittedly false testimony of Dr. Rosen, pilloried defense counsel for not calling Dr. Hayken, and argued that Dr. Hayken would have supported the plaintiff’s case.

Despite the Appellate Division’s sure-footed handling of the case, the Supreme Court granted certification, and affirmed in a slip opinion over 40 pages long. Although it took a lot of words, at least in this instance the Court got to the decision right:

“an adverse inference charge should rarely be invoked to address the absence of an expert.”

Slip op. at 3.

Defense counsel had served reports of Drs. Sharetts and Hayken, on plaintiff’s counsel, with a disclaimer that the reports were not defendants’ adoptive admissions. Id. at 6. When objecting to Dr. Rosen’s testimony, defense counsel explained that he did not intend to call his expert witnesses, because plaintiff had failed to prove her case. Id. at 10. Later, however, he claimed that Dr. Hayken was unavailable. Id. at 12.

In any event, Rosen’s dodgy testimony, and the trial court’s equally dodgy awarding of an adverse inference charge, set defense counsel up for a pasting before the jury. After the summations, the trial court let on that it was unhappy with plaintiff’s closing argument that the defense had tried to hide evidence, and that it “should probably grant a new trial,” but the trial court incongruously and circularly denied the new trial because the defense did not present any expert witnesses. Id.

A large part of the bloat in the high court’s opinion is the Court’s exploration of missing witness instructions in civil and criminal cases, for fact and expert witnesses. Id. at 13-28. Given that the Court ultimately held that expert witnesses are different, it might have spared the reader a recitation of the law for fact witnesses. Two thirds into its opinion, the Court finally gets to expert witnesses, but attempts to resolve the conflicting case law and the claims in the case sub judice within the confines of its precedent in State v. Hill, 199 N.J. 545, 974 A.2d 403 (2009). Hill articulated a standard for the propriety of an adverse inference jury instruction in the face of a party’s failure or refusal to call a fact witness.

As the Supreme Court explains, and what we all know, expert witnesses are different. Slip op. at 30. Expert witnesses must be disclosed, and they are subject to heightened discovery in the form of interrogatories and depositions. Second, expert witnesses rarely are in exclusive possession of facts essential to the other side’s case. Id. at 31, 39. Somewhat puzzlingly, the Court offered that parties are not under any obligation to call an expert witnesses, unless their opinions are needed to satisfy an element of the claim or defense. Id. at 32. The same, however, could be said of fact witnesses.

Finally, and most importantly, Court acknowledged that there are “many strategic and practical reasons that may prompt a party who has retained an expert witness to decide not to present the expert’s testimony at trial.” Id. at 33. Expert witnesses are expensive; they are sometimes duplicative; and sometimes they are unavailable. Id. at 35.

According to the Supreme Court, expert witnesses are not generally under a party’s exclusive control, and there is no privilege in a testifying expert witness’s opinion. Id at 36-37. The Court thus suggested that expert witnesses are “available” to the party seeking the adverse inference. Id. at 37.

As with adverse inferences, the most interesting aspects of the Supreme Court’s decision in Washington v. Perez is what the Court did not say. The Court omitted a necessary discussion of how expert witness testimony is presented to a jury or a court, who may, as the finder of fact, accept some, all, or none of the opinion testimony. The party without the burden of proof is free to argue that the adversary’s expert witness was incredible, or that the witness conceded the most important points for the trial, and that calling yet another expert witness in opposition would have wasted the factfinder’s time, and the client’s money.

The availability argument raises the ethical concern of legal counsel attempting ex parte agreements with adversaries’ expert witnesses. And then there is the simple solution that plaintiff’s counsel did not need to elicit imaginary or phony concessions from Dr. Rosen about Dr. Hayken’s report; counsel could have taken Dr. Hayken’s deposition before trial, or during a short recess.

Perhaps even simpler yet, the Court could have (and should have) condemned the admission of Dr. Rosen’s concededly false testimony about what Dr. Hayken’s report stated. The exclusion of this testimony would taken away much of the rationale for plaintiff’s request for the adverse inference instruction.

One way to avoid the request for adverse inference instructions is to announce, say the day before resting, that you have decided not to call an expert witness and that you have released that witness to testify for anyone calling him. This announcement should place the onus on your adversary to ask for time to ask for, or compel, the attendance of the witness. This procedure also preserves the integrity of the process by making clear that your adversary is not free to contact your expert witness until you give permission.

Irving Selikoff – Media Plodder to Media Zealot

September 9th, 2014

Some historians note that Selikoff was “consistently demonized as a media zealot.” See Jock McCulloch & Geoffrey Tweedale, Shooting the messenger: the vilification of Irving J. Selikoff,” 37 Internat’l J. Health Services 619, 619 (2007).

McCulloch and Tweedale’s narrative is incomplete, incoherent and internally inconsistent. Selikoff was not the “messenger” of any novel information. McCulloch and Tweedale’s narrative turns upon a misconception that the dangerousness of asbestos to end users was somehow not known before Dr. Irving Selikoff publicized it with his work in 1964. Sir Richard Doll had published almost a decade earlier on asbestosis and lung cancer. Richard Doll, “Mortality from Lung Cancer in Asbestos Workers,”  12 Br. J. Indus. Med. 81 (1955). Selikoff’s publication, with its inadequate smoking histories, and lack of stratification for asbestosis, was not a significant advance over Doll’s work. With respect to mesothelioma, J. Christopher Wagner and colleagues published their work on mesothelioma among persons exposed to crocidolite, blue asbestos, in South Africa, over a decade before Selikoff published on asbestos. See J. Christopher Wagner, C.A. Sleggs, and Paul Marchand, “Diffuse pleural mesothelioma and asbestos exposure in the North Western Cape Province,” 17 Br. J. Indus. Med. 260 (1960); J. Christopher Wagner, “The discovery of the association between blue asbestos and mesotheliomas and the aftermath,” 48 Br. J. Indus. Med. 399 (1991).

And for asbestosis among insulators, the United States Navy was out in front of Selikoff, although the Navy was less generous in sharing its knowledge with its vendors.  Before Selikoff published on an asbestosis hazard among insulation workers, the United States Navy published an account in 1962, in which it acknowledged that working conditions were at times unsafe, and led to asbestosis among workers. Capt. H.M. Robbins & William T. Marr, “Asbestosis,” 19 Safety Review 10 (1962) (noting that asbestos dust counts of 200 million particles per cubic foot were not uncommon during insulation ripouts onboard naval vessels). Of course, the asbestosis hazard was known and understood by the asbestos insulators themselves, as can be seen in the union publication, Asbestos Worker, from 1930 on[1]. Anonymous, “The Pulmonary Asbestos Menace,” 9(9) The Asbestos Worker (1930). What was lacking in Selikoff’s work was a demonstration that asbestosis was occurring at exposures below the threshold limit value in place in the 1950s and much of the 1960s.

Second, Selikoff did use media, labor unions, federal agencies, and even industry to fund and advance his research agenda. Public fear worked to his advantage, and Selikoff overstated and exaggerated risk predictions to advance legislation and regulations he favored. See Richard Doll & Richard Peto, “The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today,” 66 J. Nat’l Cancer Inst. 1191 (1981). McCulloch and Tweedale never address this reality in their hagiographic narrative.

Although McCulloch and Tweedale focus on historical papers on Selikoff’s unusual path to becoming a physician, they do not address the other issues raised by Selikoff’s career, such as his testimonial adventures on behalf of workers, his lack of disclosure of his income from testifying in his publications, and his conspiratorial efforts to influence key judges in asbestos litigation by inviting them to a one-sided, ex parte conference in New York.

Interestingly, there is some evidence that Selikoff was not a “natural” as a media zealot; the skills were acquired, perhaps through his testimonial adventures in the late 1950s and 1960s. Selikoff’s early efforts at talking to the media showed him to be a “clumsy and plodding” presenter. The following 1955 article provides a contemporaneous account of Selikoff’s media efforts:

“Medical Horizons,” Broadcasting * Telecasting at 14 (Nov. 21, 1955)

“THE DRAMATIC and increasingly successful fight against tuberculosis managed to become a dull story indeed as told on Medical Horizons (ABC-TV), live documentary series showing present-day progress being made by doctors and drugs.

The Nov. 14 offering had narrator Don Goddard, complete with hand mike, making a tour of Seaview Hospital, Staten Island, N.Y., where he talked with Dr. Edward Robitzek and Dr. Irving Selikoff, pioneering physicians at the noted TB clinic. Lines intended to reflect spontaneity instead came out as clumsy and plodding from Mr. Goddard and the two medical men.”

[1] Of course, there is much coyness about acknowledging the risk and hazard information contained in union publications. See, e.g., Theer v. Philip Carey Co., 259 N.J. Super. 40, 44-45, 611 A.2d 148 (1992) (noting that plaintiff was a union insulation worker who received Asbestos Worker, but did not recall risk communications in his own union publication until the 1970s), rev’d, 133 N.J. 610, 628 A.2d 724 (1993); Skonberg v. Owens-Corning Fiberglas Corp., 576 N.E.2d 28, 30, 215 Ill. App.3d 735 (1991) (noting that plaintiff had received the Asbestos Worker magazine and read it regularly, but somehow managed to miss the information about cancer hazards). Defendants have been known to embrace Selikoff’s work because it coincided with the advent of their product warning labels, labels that were mostly the creation of the Restatement (Second) of Torts, and innovations in strict product liability. Selikoff’s claims of novelty helped support state-of-the-art defenses.

 

The Funding Effect in Science and in Law

September 8th, 2014

In some circles, the mere mention that a study or a paper was sponsored by an oil company is sufficient to discredit its findings, methods, and analyses, on the merits. For instance, in Exxon Shipping Co. v. Baker, 554 U.S. 471, 501 (2008), the Supreme Court struck down a $2.5 billion punitive damage award.  Justice Souter, writing for the Court in a 5-3 decision, observed that:

“We are aware of no scholarly work pointing to consistency across punitive awards in cases involving similar claims and circumstances.17

In his now infamous footnote 17, Justice Souter explained:

“The Court is aware of a body of literature running parallel to anecdotal reports, examining the predictability of punitive awards by conducting numerous ‛mock juries’, where different ‛jurors’ are confronted with the same hypothetical case. See, e.g., C. Sunstein, R. Hastie, J. Payne, D. Schkade, W. Viscusi, Punitive Damages: How Juries Decide (2002); Schkade, Sunstein, & Kahneman, Deliberating About Dollars: The Severity Shift, 100 Colum. L.Rev. 1139 (2000); Hastie, Schkade, & Payne, Juror Judgments in Civil Cases: Effects of Plaintiff’s Requests and Plaintiff’s Identity on Punitive Damage Awards, 23 Law & Hum. Behav. 445 (1999); Sunstein, Kahneman, & Schkade, Assessing Punitive Damages (with Notes on Cognition and Valuation in Law), 107 Yale L.J. 2071 (1998). Because this research was funded in part by Exxon, we decline to rely on it.”

Somehow it escaped Justice Souter’s attention that some of the investigators (Sunstein, Viscusi, Kahneman, et al.) in the papers were outstanding scientists and scholars. The mere funding disclosure gave Justice Souter the excuse to avoid any hard thinking and intellectual engagement with the merits of these papers.

The world of philosophy provides another example. Massimo Pigliucci is professor of philosophy at the City University of New York, and a frequent commentator on junk science. Pigliucci, Nonsense on Stilts: How to Tell Science from Bunk (2010). In railing against positions taken by a so-called “think tank,” the Competitive Enterprise Institute, Professor Pigliucci felts compelled to note, on almost every mention, that the Institute is partially funded by Exxon-Mobil, and so its pronouncements should be discounted. See, e.g., id. at 156.

Chris Prandoni, a contributor to Forbes, recently published a story about a Senate investigation into the “funding effect” of various environmentalist organizations. Chris Prandoni, “Senate Committee Report Details Environmentalists’ Inner Workings,” (July 30, 2014). Prandoni notes that the environmental movement has morphed into a billion-dollar industry, with funding by many one-percenters. The minority staff of the United States Senate Committee on Environment and Public Works (EPW) has issued a report entitled The Chain of Command: How a Club of Billionaires and Their Foundations Control the Environmental Movement and Obama’s EPA (July 30, 2014), which documents how a “Billionaires’ Club” funds many, if not most, of the environmental non-government organizations and their media and grassroots activities.

The Committee report also describes how many scientists and leaders from the funded organizations have entered the “revolving door” of the Obama Administration’s agencies. The Committee might have expanded its focus to include organizations such as the Project on Scientific Knowledge and Public Policy (SKAPP), a pass-through organization for the plaintiffs’ bar, a/k/a the litigation industry. SKAPP was formerly headed by David Michaels, now head of OSHA. SeeSKAPP a Lot” (April 30, 2010).

Other organizations that front for the interests of wealthy lawyers seeking to expand the largesse of the tort system include the Council for Education and Research on Toxics (“CERT”), and the Center for Progressive Reform. See Milward Symposium Organized By Plaintiffs’ Counsel and Witnesses” (Feb. 16, 2013).

The Senate Committee report highlights the hypocrisy of some critics of the Supreme Court’s recent decision in, Citizens United v. FEC, 130 S. Ct. 876 (2010), which held that the First Amendment prohibits governmental restrictions of corporations’ independent political expenditures. The hypocritical criticism lay in denouncing the political expenditures and speech of corporations, as corrupted by the wealth and motivations of the speakers, while turning blind eyes from huge expenditures by wealthy self-styled public interest groups through think tanks and non-governmental organizations. Even foreign governments have joined in the spending spree. See Eric Lipton, Brooke Williams & Nicolas Confessore, “Foreign Powers Buy Influence at Think Tanks,” N.Y. Times (Sept. 6, 2014).

Perhaps it is time to follow the data as ardently as we follow the money?

Frank Advocacy on Welding Health “Effects”

September 1st, 2014

Arthur L. Frank is a professor and the chair of Drexel University School of Public Health’s program in Environmental and Occupational Health. Frank testifies fairly extensively for plaintiffs in asbestos litigation. See, e.g., Frank Affidavit. He also has testified for plaintiffs in manganese fume litigation brought by welders, although he has no specialty training in movement disorder neurology.

Although Arthur Frank has testified for plaintiffs in asbestos cases, he does not appear to comply with professional association disclosure of conflicts, when he presents on asbestos issues. See, e.g.,More Hypocrisy Over Conflicts of Interest” (Dec. 4, 2010). The same disregard for conflict disclosures seems to hold for his work on welding health outcomes.

Last year, in September 2013, Frank presented a poster at the 11th Inhaled Particles XI (IPXI) conference, organized by the British Occupational Hygiene Society (BOHS). Frank’s poster was entitled,Health Effects of Welding Fumes,” although the poster reported only a cross-sectional study without controls from Qingdao City, China. Frank provided no conflict-of-interest disclosure in the poster. Arthur Frank, Huanqiang Zhang, and Chunsheng Xu, “Health Effects of Welding Fumes,” Inhaled Particle XI Conference, Nottingham, U.K. (Sept. 2013). His current C.V., available online, reports this as an abstract from the Inhaled Articles conference. One does not need an epidemiologic study to see how scientists could choke on this article if inhaled.

Frank’s study was based upon an anonymous questionnaire to 505 steel welders, at state-owned, foreign-funded, and privately owned companies, in Qingdao City, China. No industrial hygiene exposure measurements or use of personal respiratory protection is reported. No physical examinations are reported. No statistical tests are reported. Frank reported a “symptom” of unsteady gait/difficulty walking of 1%, but he and his Chinese colleagues did not report whether this 1% had musculo-skeletal or neurological problems. The former would be fairly common among tradesmen such as welders whose work often puts them at risk of traumatic injury.

According to Frank, a “striking” finding was an 18% prevalence hand tremor among those working at least 15 years, with lower prevalence reported for less than 5 years (4%), at 5 years (3%), and at 10 years (5%). Frank offered no explanation of how these prevalence rates were ascertained in a cross-sectional questionnaire based study; nor did Frank offer any qualification as to whether these hand tremors were rest or action tremor, bilateral or unilateral, or of any particular kind. Notwithstanding the severe limitations of this “study,” Frank offers a conclusion that “[m]anganese from inhaled particles from welding fumes cause serious outcomes in welders. Welding fumes also cause other health effects. Workplace hygiene correlates with health outcome.”

Shortly after the Inhaled Particles conference, a colleague reported that Frank had testified in an asbestos case that he had submitted a “manganese in welding” manuscript to the Annals of Industrial Hygiene, which is the journal of the (BOHS). To date, no article by Frank has appeared in this, or any, journal.

Perhaps the only interesting aspect of this little cross-sectional study, based upon self-reported symptoms, is that workers employed by the communist state report a higher rate of symptoms than those employed by privately owned companies. More evidence that worker illness, if any there should be, is not necessarily the result of the “profit motive” of private corporations. The abstract also shows that at some scientific conferences, anything goes with respect to conflicts-of-interest disclosures and shameless advocacy.

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.

Peer Review, PubPeer, PubChase, and Rule 702 – Candles in the Ear

August 28th, 2014

In deciding the Daubert case, the Supreme Court identified several factors to assess whether “the reasoning or methodology underlying the testimony is scientifically valid and of whether that reasoning or methodology properly can be applied to the facts in issue.” One of those factors was whether the proffered opinion had been “peer reviewed” and published. Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579, 593-94 (1993). The Court explained the publication factor:

“Another pertinent consideration is whether the theory or technique has been subjected to peer review and publication. Publication (which is but one element of peer review) is not a sine qua non of admissibility; it does not necessarily correlate with reliability, and in some instances well-grounded but innovative theories will not have been published. Some propositions, moreover, are too particular, too new, or of too limited interest to be published. But submission to the scrutiny of the scientific community is a component of ‘good science,’ in part because it increases the likelihood that substantive flaws in methodology will be detected. The fact of publication (or lack thereof) in a peer reviewed journal thus will be a relevant, though not dispositive, consideration in assessing the scientific validity of a particular technique or methodology on which an opinion is premised.”

Daubert, 509 U.S. at 593-94 (internal citations omitted). See, e.g., Lust v. Merrell Dow Pharms., Inc., 89 F. 3d 594, 597 (9th Cir. 1996) (affirming exclusion of Dr. Alan Done, plaintiffs’ expert witness in Chlomid birth defects case, in part because of the lack of peer review and publication of his litigation-driven opinions); Hall v. Baxter Healthcare Corp., 947 F. Supp. 1387, 1406 (1996)  (noting that “the lack of peer review for [epidemiologist] Dr. Swan’s theories weighs heavily against the admissibility of Dr. Swan’s testimony”).

Case law since Daubert has made clear that peer review is neither necessary nor sufficient for the admissibility of an opinion. United States v. Mikos, 539 F.3d 706, 711 (7th Cir. 2008) (noting that the absence of peer-reviewed studies on subject of bullet grooving did not render opinion, based upon FBI database, inadmissible); In re Zoloft Prods. Liab. Litig. MDL No. 2342; 12-md-2342,  2014 U.S. Dist. LEXIS 87592; 2014 WL 2921648 (E.D. Pa. June 27, 2014) (excluding proffered testimony of epidemiologist Anick Bérard for arbitrarily selecting some point estimates and ignoring others in published studies).

As Susan Haack has noted, “peer review” has taken on mythic proportions in the adjudication of expert witness opinion admissibility.  Susan Haack, “Peer Review and Publication: Lessons for Lawyers,” 36 Stetson L. Rev. 789 (2007), republished in Susan Haack, Evidence Matters: Science, Proof, and Truth in the Law 156 (2014). Peer review, at best, is a weak proxy for the study validity, which is what is really needed in judicial proceedings. Proxies avoid the labor of independent, original thought, and so they are much favored by many judges.

In the past, some litigants oversold peer review as a touchstone of reliable, admissible expert witness testimony only to find that some very shoddy opinions show up in ostensibly peer-reviewed journals. SeeMisplaced Reliance On Peer Review to Separate Valid Science From Nonsense” (Aug. 14, 2011). Scientists often claim that science is “self-correcting,” but in some areas of research, there are few severe tests and little critical review, and mostly glib confirmations from acolytes.

Letters to the editor are sometimes held out as a remedy to peer-review screw ups, but such letters, which are not themselves peer reviewed, are subject to the whims of imperious editors who might wish to silence the views of those who would be critical of their judgment in publishing the article under discussion. Most journals have space only for a few letters, and unpopular but salient points of view can go unreported. Many scientists will not write letters to the editors, even when the published article is terribly wrong in its methods, data analyses, conclusions, or discussion.  Letters to the editor are often frowned upon in academic circles as not advancing affirmative research and scholarship agenda.

Letters to the editor often must be sent within a short time window of initial publication, often too short for busy academics to analyze a paper carefully and comment.  Furthermore, letters  and are often limited to a few hundred words, which length is often inadequate to develop a careful critique or exposition of the issues in the paper.  Moreover, such letters suffer from an additional procedural problem:  authors are permitted a response, and the letter writers are not permitted a reply. Authors thus get the last word, which they can often use to deflect or diffuse important criticisms.  The authors’ response can be sufficiently self-serving and misleading, with immunity from further criticism, that many would-be correspondents abandon the project altogether. See, e.g., PubPeer – “Example case showing why letters to the editor can be a waste of time” (Oct. 8, 2013).

Websites and blogs provide for dynamic content, with the potential for critical reviews that can be identified by search engines. See, e.g., Paul S. Brookes, “Our broken academic journal corrections system,” PSBLAB: Cardiac Mitochondrial Research in the Lab (Jan. 14, 2014). Mostly, the internet holds untapped potential for analysis, discussion, and debate on published studies.  To be sure, some journals provide “comment fields,” on their websites, with an opportunity for open discussion.  Often, full critiques must be developed and presented elsewhere. See, e.g., Androgen Study Group, “Letter to JAMA Asking for Retraction of Misleading Article on Testosterone Therapy” (Mar. 25, 2014).

PubPeer

Kate Yandell, in TheScientist, reports on the creation of PubPeer a few years ago, as a forum for post-publication review and discussion published scientific papers. Kate Yandell, “Concerns Raised Online Linger” (Aug. 25, 2014).  Billing itself as an “online journal club,” PubPeer has pointed out potentially serious problems, some of which have led to retractions and corrections. Another internet site of interest is PubChase, which monitors discussion of particular articles, as well as generating email alerts and recommendations for related articles.

One journal editor has taken notice and given notice that he will not pay attention to post-publication peer review.  Eric J. Murphy, the editor in chief of Lipids, posting a comment at PubPeer, illustrates that there will be a good deal of resistance to post-publication open peer review, out of the control of journal editors:

“As an Editor-in-Chief of a society journal, I have never examined PubPeer nor will I do so. First, there is the crowd or group mentality that may over emphasize some point in an irrational manner.  Just as using the marble theory of officiating is bad, one should never base a decision on the quantity of negative or positive comments. Second, if the concerned individual sent an e-mail or letter to me, then I would be duty bound to examine the issue.  It is not my duty to monitor PubPeer or any other such site, but rather to respond to queries sent to me.  So, with regards to Hugh’s point, I don’t support that position at all.

Mistakes happen, although frankly we try to limit these mistakes and do take steps to prevent publishing papers with FFP, it does happen.  Also, honest mistakes happen in science all the time, so[me] of these result in an erratum, while others go unnoticed by editors and reviewers.  In such a case, someone who does notice should contact the editor to put them on notice regarding the issue so that it may be resolved.  Resolution does not necessarily mean correction, but rather the editor taking a close look at the situation, discussing the situation with the original authors, and then reaching a decision.  Most of the time a correction will be made, but not always.”

Murphy’s comments are remarkable.  PubPeer provides a forum for post-publication comment, but it hardly requires editors, investigators, and consumers of scientific studies to evaluate published works by “nose counts” of favorable and unfavorable comments.  This is not, and never has been, a democratic enterprise.  Somehow, we might expect Murphy and others to evaluate the comments, on the merits, not on their prevalence.  Murphy’s declaration that he is duty-bound to investigate and evaluate letters or emails sent to him about published articles is encouraging, but the editors’ ability to ratify publication, in the face of a private communication, without comment to the scientific community, strips the community of making a principled decision on its own.  Murphy’s way, which seems largely the way of contemporary scientific publishing, ignores the important social dimension of scientific debate and resolution of issues.  Leaving control of the discussion in the hands of the editors who approved and published studies may be asking too much of editors. Nemo iudex in causa sua.

PubPeer has already tested the limits of free speech. Kate Yandell, “PubPeer Threatened with Legal Action” (Aug. 19, 2014). A scientist whose works were receiving unfavorable attention on PubPeer threatened a lawsuit.  Let’s hope that scientists can learn to be sufficiently thick skinned that there can be open discourse of the merits of their research, their data, and their conclusions.

Pritchard v. Dow Agro – Gatekeeping Exemplified

August 25th, 2014

Robert T. Pritchard was diagnosed with Non-Hodgkin’s Lymphoma (NHL) in August 2005; by fall 2005, his cancer was in remission. Mr. Pritchard had been a pesticide applicator, and so, of course, he and his wife sued the deepest pockets around, including Dow Agro Sciences, the manufacturer of Dursban. Pritchard v. Dow Agro Sciences, 705 F.Supp. 2d 471 (W.D.Pa. 2010).

The principal active ingredient of Dursban is chlorpyrifos, along with some solvents, such as xylene, cumene, and ethyltoluene. Id. at 474.  Dursban was licensed for household insecticide use until 2000, when the EPA phased out certain residential applications.  The EPA’s concern, however, was not carcinogenicity:  the EPA categorizes chlorpyrifos as “Group E,” non-carcinogenetic in humans. Id. at 474-75.

According to the American Cancer Society (ACS), the cause or causes of NHL cases are unknown.  Over 60,000 new cases are diagnosed annually, in people from all walks of life, occupations, and lifestyles. The ACS identifies some risk factors, such as age, gender, race, and ethnicity, but the ACS emphasizes that chemical exposures are not proven risk factors or causes of NHL.  See Pritchard, 705 F.Supp. 2d at 474.

The litigation industry does not need scientific conclusions of causal connections; their business is manufacturing certainty in courtrooms. Or at least, the appearance of certainty. The Pritchards found their way to the litigation industry in Pittsburgh, Pennsylvania, in the form of Goldberg, Persky & White, P.C. The Goldberg Persky firm sued Dow Agro, and then put the Pritchards in touch with Dr. Bennet Omalu, to serve as their expert witness.  A lawsuit ensued.

Alas, the Pritchards’ lawsuit ran into a wall, or at least a gate, in the form of Federal Rule of Evidence 702. In the capable hands of Judge Nora Barry Fischer, Rule 702 became an effective barrier against weak and poorly considered expert witness opinion testimony.

Dr. Omalu, no stranger to lost causes, was the medical examiner of San Joaquin County, California, at the time of his engagement in the Pritchard case. After careful consideration of the Pritchards’ claims, Omalu prepared a four page report, with a single citation, to Harrison’s Principles of Internal Medicine.  Id. at 477 & n.6.  This research, however, sufficed for Omalu to conclude that Dursban caused Mr. Pritchard to develop NHL, as well as a host of ailments he had never even sued Dow Agro for, including “neuropathy, fatigue, bipolar disorder, tremors, difficulty concentrating and liver disorder.” Id. at 478. Dr. Omalu did not cite or reference any studies, in his report, to support his opinion that Dursban caused Mr. Pritchard’s ailments.  Id. at 480.

After counsel objected to Omalu’s report, plaintiffs’ counsel supplemented the report with some published articles, including the “Lee” study.  See Won Jin Lee, Aaron Blair, Jane A. Hoppin, Jay H. Lubin, Jennifer A. Rusiecki, Dale P. Sandler, Mustafa Dosemeci, and Michael C. R. Alavanja, “Cancer Incidence Among Pesticide Applicators Exposed to Chlorpyrifos in the Agricultural Health Study,” 96 J. Nat’l Cancer Inst. 1781 (2004) [cited as Lee].  At his deposition, and in opposition to defendants’ 702 motion, Omalu became more forthcoming with actual data and argument.  According to Omalu, the Lee study “the 2004 Lee Study strongly supports a conclusion that high-level exposure to chlorpyrifos is associated with an increased risk of NHL.’’ Id. at 480.

This opinion put forward by Omalu bordered on scientific malpractice.  No; it was malpractice.  The Lee study looked at many different cancer end points, without adjustment for multiple comparisons.  The lack of adjustment means at the very least that any interpretation of p-values or confidence intervals would have to modified to acknowledge the higher rate of random error.  Now for NHL, the overall relative risk (RR) for chlorpyrifos exposure was 1.03, with a 95% confidence interval, 0.62 to 1.70.  Lee at 1783.  In other words, the study that Omalu claimed supported his opinion was about as null a study as can be, with reasonably tight confidence interval that made a doubling of the risk rather unlikely given the sample RR.

If the multiple endpoint testing were not sufficient to dissuade a scientist, intent on supporting the Pritchards’ claims, then the exposure subgroup analysis would have scared any prudent scientist away from supporting the plaintiffs’ claims.  The Lee study authors provided two different exposure-response analyses, one with lifetime exposure and the other with an intensity-weighted exposure, both in quartiles.  Neither analysis revealed an exposure-response trend.  For the lifetime exposure-response trend, the Lee study reported an NHL RR of 1.01, for the highest quartile of chloripyrifos exposure. For the intensity-weighted analysis, for the highest quartile, the authors reported RR = 1.61, with a 95% confidence interval, 0.74 to 3.53).

Although the defense and the district court did not call out Omalu on his fantasy statistical inference, the district judge certainly appreciated that Omalu had no statistically significant associations between chloripyrifos and NHL, to support his opinion. Given the weakness of relying upon a single epidemiologic study (and torturing the data therein), the district court believed that a showing of statistical significance was important to give some credibility to Omalu’s claims.  705 F.Supp. 2d at 486 (citing General Elec. Co. v. Joiner, 522 U.S. 136, 144-46 (1997);  Soldo v. Sandoz Pharm. Corp., 244 F.Supp. 2d 434, 449-50 (W.D. Pa. 2003)).

Figure 3 adapted from Lee

Figure 3 adapted from Lee

What to do when there is really no evidence supporting a claim?  Make up stuff.  Here is how the trial court describes Omalu’s declaration opposing exclusion:

 “Dr. Omalu interprets and recalculates the findings in the 2004 Lee Study, finding that ‘an 80% confidence interval for the highly-exposed applicators in the 2004 Lee Study spans a relative risk range for NHL from slightly above 1.0 to slightly above 2.5.’ Dr. Omalu concludes that ‘this means that there is a 90% probability that the relative risk within the population studied is greater than 1.0’.”

705 F.Supp. 2d at 481 (internal citations omitted); see also id. at 488. The calculations and the rationale for an 80% confidence interval were not provided, but plaintiffs’ counsel assured Judge Fischer at oral argument that the calculation was done using high school math. Id. at 481 n.12. Judge Fischer seemed unimpressed, especially given that there was no record of the calculation.  Id. at 481, 488.

The larger offense, however, was that Omalu’s interpretation of the 80% confidence interval as a probability statement of the true relative risk’s exceeding 1.0, was bogus. Dr. Omalu further displayed his lack of statistical competence when he attempted to defend his posterior probability derived from his 80% confidence interval by referring to a power calculation of a different disease in the Lee study:

“He [Omalu] further declares that ‘‘the authors of the 2004 Lee Study themselves endorse the probative value of a finding of elevated risk with less than a 95% confidence level when they point out that ‘this analysis had a 90% statistical power to detect a 1.5–fold increase in lung cancer incidence’.”

Id. at 488 (court’s quoting of Omalu’s quoting from the Lee study). To quote Wolfgang Pauli, Omalu is so far off that he is “not even wrong.” Lee and colleagues were offering a pre-study power calculation, which they used to justify their looking at the cohort for lung cancer, not NHL, outcomes.  Lee at 1787. The power calculation does not apply to the data observed for lung cancer; and the calculation has absolutely nothing to do with NHL. The power calculation certainly has nothing to do with Omalu’s misguided attempt to offer a calculation of a posterior probability for NHL based upon a subgroup confidence interval.

Given that there were epidemiologic studies available, Judge Fischer noted that expert witnesses were obligated to factor such studies into their opinions. See 705 F.Supp. 2d at 483 (citing Soldo, 244 F.Supp. 2d at 532).  Omalu sins against Rule 702 included his failure to consider any studies other than the Lee study, regardless of how unsupportive the Lee study was of his opinion.  The defense experts pointed to several studies that found lower NHL rates among exposed workers than among controls, and Omalu completely failed to consider and to explain his opinion in the face of the contradictory evidence.  See 705 F.Supp. 2d at 485 (citing Perry v. Novartis Pharm. Corp. 564 F.Supp. 2d 452, 465 (E.D. Pa. 2008)). In other words, Omalu was shown to have been a cherry picker. Id. at 489.

In addition to the abridged epidemiology, Omalu relied upon an analogy between the ethyl-toluene and other solvents that contained benzene rings and benzene itself to argue that these chemicals, supposedly like benzene, cause NHL.  Id. at 487. The analogy was never supported by any citations to published studies, and, of course, the analogy is seriously flawed. Many chemicals, including chemicals made and used by the human body, have benzene rings, without the slightest propensity to cause NHL.  Indeed, the evidence that benzene itself causes NHL is weak and inconsistent.  See, e.g., Knight v. Kirby Inland Marine Inc., 482 F.3d 347 (2007) (affirming the exclusion of Dr. B.S. Levy in a case involving benzene exposure and NHL).

Looking at all the evidence, Judge Fischer found Omalu’s general causation opinions unreliable.  Relying upon a single, statistically non-significant epidemiologic study (Lee), while ignoring contrary studies, was not sound science.  It was not even science; it was courtroom rhetoric.

Omalu’s approach to specific causation, the identification of what caused Mr. Pritchard’s NHL, was equally spurious. Omalu purportedly conducted a “differential diagnosis” or a “differential etiology,” but he never examined Mr. Pritchard; nor did he conduct a thorough evaluation of Mr. Pritchard’s medical records. 705 F.Supp. 2d at 491. Judge Fischer found that Omalu had not conducted a thorough differential diagnosis, and that he had made no attempt to rule out idiopathic or unknown causes of NHL, despite the general absence of known causes of NHL. Id. at 492. The one study identified by Omalu reported a non-statistically significant 60% increase in NHL risk, for a subgroup in one of two different exposure-response analyses.  Although Judge Fischer treated the relative risk less than two as a non-dispositive factor in her decision, she recognized that

“The threshold for concluding that an agent was more likely than not the cause of an individual’s disease is a relative risk greater than 2.0… . When the relative risk reaches 2.0, the agent is responsible for an equal number of cases of disease as all other background causes. Thus, a relative risk of 2.0 … implies a 50% likelihood that an exposed individual’s disease was caused by the agent. A relative risk greater than 2.0 would permit an inference that an individual plaintiff’s disease was more likely than not caused by the implicated agent.”

Id. at 485-86 (quoting from Reference Manual on Scientific Evidence at 384 (2d ed. 2000)).

Left with nowhere to run, plaintiffs’ counsel swung for the bleachers by arguing that the federal court, sitting in diversity, was required to apply Pennsylvania law of evidence because the standards of Rule 702 constitute “substantive,” not procedural law. The argument, which had been previously rejected within the Third Circuit, was as legally persuasive as Omalu’s scientific opinions.  Judge Fischer excluded Omalu’s proffered opinions and granted summary judgment to the defendants. The Third Circuit affirmed in a per curiam decision. 430 Fed. Appx. 102, 2011 WL 2160456 (3d Cir. 2011).

Practical Evaluation of Scientific Claims

The evaluative process that took place in the Pritchard case missed some important details and some howlers committed by Dr. Omalu, but it was more than good enough for government work. The gatekeeping decision in Pritchard was nonetheless the target of criticism in a recent book.

Kristin Shrader-Frechette (S-F) is a professor of science who wants to teach us how to expose bad science. S-F has published, or will soon publish, a book that suggests that philosophy of science can help us expose “bad science.”  See Kristin Shrader-Frechette, Tainted: How Philosophy of Science Can Expose Bad Science (Oxford U.P. 2014)[cited below at Tainted; selections available on Google books]. S-F’s claim is intriguing, as is her move away from the demarcation problem to the difficult business of evaluation and synthesis of scientific claims.

In her introduction, S-F tells us that her book shows “how practical philosophy of science” can counteract biased studies done to promote special interests and PROFITS.  Tainted at 8. Refreshingly, S-F identifies special-interest science, done for profit, as including “individuals, industries, environmentalists, labor unions, or universities.” Id. The remainder of the book, however, appears to be a jeremiad against industry, with a blind eye towards the litigation industry (plaintiffs’ bar) and environmental zealots.

The book promises to address “public concerns” in practical, jargon-free prose. Id. at 9-10. Some of the aims of the book are to provide support for “rejecting demands for only human evidence to support hypotheses about human biology (chapter 3), avoiding using statistical-significance tests with observational data (chapter 12), and challenging use of pure-science default rules for scientific uncertainty when one is doing welfare-affecting science (chapter 14).”

Id. at 10. Hmmm.  Avoiding statistical significance tests for observational data?!?  If avoided, what does S-F hope to use to assess random error?

And then S-F refers to plaintiffs’ hired expert witness (from the Milward case), Carl Cranor, as providing “groundbreaking evaluations of causal inferences [that] have helped to improve courtroom verdicts about legal liability that otherwise put victims at risk.” Id. at 7. Whether someone is a “victim” and has been “at risk” turns on assessing causality. Cranor is not a scientist, and his philosophy of science turns of “weight of the evidence” (WOE), a subjective, speculative approach that is deaf, dumb, and blind to scientific validity.

There are other “teasers,” in the introduction to Tainted.  S-F advertises that her Chapter 5 will teach us that “[c]ontrary to popular belief, animal and not human data often provide superior evidence for human-biological hypotheses.”  Tainted at 11. Chapter 6 will show that“[c]ontrary to many physicists’ claims, there is no threshold for harm from exposure to ionizing radiation.” Id.  S-F tells us that her Chapter 7 will criticize “a common but questionable way of discovering hypotheses in epidemiology and medicine—looking at the magnitude of some effect in order to discover causes. The chapter shows instead that the likelihood, not the magnitude, of an effect is the better key to causal discovery.” Id. at 13. Discovering hypotheses — what is that about? You might have thought that hypotheses were framed from observations and then tested.

Which brings us to the trailer for Chapter 8, in which S-F promises to show that “[c]ontrary to standard statistical and medical practice, statistical-significance tests are not causally necessary to show medical and legal evidence of some effect.” Tainted at 11. Again, the teaser raises lots of questions such as what could S-F possibly mean when she says statistical tests are not causally necessary to show an effect.  Later in the introduction, S-F says that her chapter on statistics “evaluates the well-known statistical-significance rule for discovering hypotheses and shows that because scientists routinely misuse this rule, they can miss discovering important causal hypotheses. Id. at 13. Discovering causal hypotheses is not what courts and regulators must worry about; their task is to establish such hypotheses with sufficient, valid evidence.

Paging through the book reveals that a rhetoric that is thick and unremitting, with little philosophy of science or meaningful advice on how to evaluate scientific studies.  The statistics chapter calls out, and lo, it features a discussion of the Pritchard case. See Tainted, Chapter 8, “Why Statistics Is Slippery: Easy Algorithms Fail in Biology.”

The chapter opens with an account of German scientist Fritz Haber’s development of organophosphate pesticides, and the Nazis use of related compounds as chemical weapons.  Tainted at 99. Then, in a fevered non-sequitur and rhetorical flourish, S-F states, with righteous indignation, that although the Nazi researchers “clearly understood the causal-neurotoxic effects of organophosphate pesticides and nerve gas,” chemical companies today “claim that the causal-carcinogenic effects of these pesticides are controversial.” Is S-F saying that a chemical that is neurotoxic must be carcinogenic for every kind of human cancer?  So it seems.

Consider the Pritchard case.  Really, the Pritchard case?  Yup; S-F holds up the Pritchard case as her exemplar of what is wrong with civil adjudication of scientific claims.  Despite the promise of jargon-free language, S-F launches into a discussion of how the judges in Pritchard assumed that statistical significance was necessary “to hypothesize causal harm.”  Tainted at 100. In this vein, S-F tells us that she will show that:

“the statistical-significance rule is not a legitimate requirement for discovering causal hypotheses.”

Id. Again, the reader is left to puzzle why statistical significance is discussed in the context of hypothesis discovery, whatever that may be, as opposed to hypothesis testing or confirmation. And whatever it may be, we are warned that “unless the [statistical significance] rule is rejected as necessary for hypothesis-discovery, it will likely lead to false causal claims, questionable scientific theories, and massive harm to innocent victims like Robert Pritchard.”

Id. S-F is decidedly not adverting to Mr. Pritichard’s victimization by the litigation industry and the likes of Dr. Omalu, although she should. S-F not only believes that the judges in Pritchard bungled their gatekeeping wrong, she knows that Dr. Omalu was correct, and the defense experts wrong, and that Pritchard was a victim of Dursban and of questionable scientific theories that were used to embarrass Omalu and his opinions.

S-F promised to teach her readers how to evaluate scientific claims and detect “tainted” science, but all she delivers here is an ipse dixit.  There is no discussion of the actual measurements, extent of random error, or threats to validity, for studies cited either by the plaintiffs or the defendants in Pritchard.  To be sure, S-F cites the Lee study in her endnotes, but she never provides any meaningful discussion of that study or any other that has any bearing on chlorpyrifos and NHL.  S-F also cited two review articles, the first of which provides no support for her ipse dixit:

“Although mutagenicity and chronic animal bioassays for carcinogenicity of chlorpyrifos were largely negative, a recent epidemiological study of pesticide applicators reported a significant exposure response trend between chlorpyrifos use and lung and rectal cancer. However, the positive association was based on small numbers of cases, i.e., for rectal cancer an excess of less than 10 cases in the 2 highest exposure groups. The lack of precision due to the small number of observations and uncertainty about actual levels of exposure warrants caution in concluding that the observed statistical association is consistent with a causal association. This association would need to be observed in more than one study before concluding that the association between lung or rectal cancer and chlorpyrifos was consistent with a causal relationship.

There is no evidence that chlorpyrifos is hepatotoxic, nephrotoxic, or immunotoxic at doses less than those that cause frank cholinesterase poisoning.”

David L. Eaton, Robert B. Daroff, Herman Autrup, James Bridges, Patricia Buffler, Lucio G. Costa, Joseph Coyle, Guy McKhann, William C. Mobley, Lynn Nadel, Diether Neubert, Rolf Schulte-Hermann, and Peter S. Spencer, “Review of the Toxicology of Chlorpyrifos With an Emphasis on Human Exposure and Neurodevelopment,” 38 Critical Reviews in Toxicology 1, 5-6(2008).

The second cited review article was written by clinical ecology zealot[1], William J. Rea. William J. Rea, “Pesticides,” 6 Journal of Nutritional and Environmental Medicine 55 (1996). Rea’s article does not appear in Pubmed.

Shrader-Frechette’s Criticisms of Statistical Significance Testing

What is the statistical significance against which S-F rails? She offers several definitions, none of which is correct or consistent with the others.

“The statistical-significance level p is defined as the probability of the observed data, given that the null hypothesis is true.8

Tainted at 101 (citing D. H. Johnson, “What Hypothesis Tests Are Not,” 16 Behavioral Ecology 325 (2004). Well not quite; attained significance probability is the probability of data observed or those more extreme, given the null hypothesis.  A Tainted definition.

Later in Chapter 8, S-F discusses significance probability in a way that overtly commits the transposition fallacy, not a good thing to do in a book that sets out to teach how to evaluate scientific evidence:

“However, typically scientists view statistical significance as a measure of how confidently one might reject the null hypothesis. Traditionally they have used a 0.05 statistical-significance level, p < or = 0.05, and have viewed the probability of a false-positive (incorrectly rejecting a true null hypothesis), or type-1, error as 5 percent. Thus they assume that some finding is statistically significant and provides grounds for rejecting the null if it has at least a 95-percent probability of not being due to chance.

Tainted at 101. Not only does the last sentence ignore the extent of error due to bias or confounding, it erroneously assigns a posterior probability that is the complement of the significance probability.  This error is not an isolated occurrence; here is another example:

“Thus, when scientists used the rule to examine the effectiveness of St. John’s Wort in relieving depression,14 or when they employed it to examine the efficacy of flutamide to treat prostate cancer,15 they concluded the treatments were ineffective because they were not statistically significant at the 0.05 level. Only at p < or = 0.14 were the results statistically significant. They had an 86-percent chance of not being due to chance.16

Tainted at 101-02 (citing papers by Shelton (endnote 14)[2], by Eisenberger (endnote 15) [3], and Rothman’s text (endnote 16)[4]). Although Ken Rothman has criticized the use of statistical significance tests, his book surely does not interpret a p-value of 0.14 as an 86% chance that the results were not due to chance.

Although S-F previous stated that statistical significance is interpreted as the probability that the null is true, she actually goes on to correct the mistake, sort of:

“Requiring the statistical-significance rule for hypothesis-development also is arbitrary in presupposing a nonsensical distinction between a significant finding if p = 0.049, but a nonsignificant finding if p = 0. 051.26 Besides, even when one uses a 90-percent (p < or = 0.10), an 85-percent (p < or = 0.15), or some other confidence level, it still may not include the null point. If not, these other p values also show the data are consistent with an effect. Statistical-significance proponents thus forget that both confidence levels and p values are measures of consistency between the data and the null hypothesis, not measures of the probability that the null is true. When results do not satisfy the rule, this means merely that the null cannot be rejected, not that the null is true.”

Tainted at 103.

S-F’s repeats some criticisms of significance testing, most of which involve their own misunderstandings of the concept.  It hardly suffices to argue that evaluating the magnitude of random error is worthless because it does not measure the extent of bias and confounding.  The flaw lies in those who would interpret the p-value as the sole measure of error involved in a measurement.

S-F takes the criticisms of significance probability to be sufficient to justify an alternative approach: evaluating causal hypotheses “on a preponderance of evidence,47 whether effects are more likely than not.”[5] Here citations, however, do not support the notion that an overall assessment of the causal hypothesis is a true alternative of statistical testing, but rather only a later step in the causal assessment, which presupposes the previous elimination of random variability in the observed associations.

S-F compounds her confusion by claiming that this purported alternative is superior to significance testing or any evaluation of random variability, and by noting that juries in civil cases must decide causal claims on the preponderance of the evidence, not on attained significance probabilities:

“In welfare-affecting areas of science, a preponderance-of-evidence rule often is better than a statistical-significance rule because it could take account of evidence based on underlying mechanisms and theoretical support, even if evidence did not satisfy statistical significance. After all, even in US civil law, juries need not be 95 percent certain of a verdict, but only sure that a verdict is more likely than not. Another reason for requiring the preponderance-of-evidence rule, for welfare-related hypothesis development, is that statistical data often are difficult or expensive to obtain, for example, because of large sample-size requirements. Such difficulties limit statistical-significance applicability. ”

Tainted at 105-06. S-F’s assertion that juries need not have 95% certainty in their verdict is either a misunderstanding or a misrepresentation of the meaning of a confidence interval, and a conflation of two very kinds of probability or certainty.  S-F invites a reading that commits the transposition fallacy by confusing the probability involved in a confidence interval with that involved in a posterior probability.  S-F’s claim that sample size requirements often limit the ability to use statistical significance evaluations is obviously highly contingent upon the facts of case, but in civil cases, such as Pritchard, this limitation is rarely at play.  Of course, if the sample size is too small to evaluate the role of chance, then a scientist should probably declare the evidence too fragile to support a causal conclusion.

S-F also postulates that that a posterior probability rather than a significance probability approach would “better counteract conflicts of interest that sometimes cause scientists to pay inadequate attention to public-welfare consequences of their work.” Tainted at 106. This claim is a remarkable assertion, which is not supported by any empirical evidence.  The varieties of evidence that go into an overall assessment of a causal hypothesis are often quantitatively incommensurate.  The so-called preponderance-of-the-evidence described by S-F is often little more than a subjective overall assessment of weight of the evidence.  The approving citations to the work of Carl Cranor support interpreting S-F to endorse this subjective, anything-goes approach to weight of the evidence.  As for WOE eliminating inadequate attention to “public welfare,” S-F’s citations actually suggest the opposite. S-F’s citations to the 1961 reviews by Wynder and by Little illustrate how subjective narrative reviews can be, with diametrically opposed results.  Rather than curbing conflicts of interest, these subjective, narrative reviews illustrate how contrary results may be obtained by the failure to pre-specify criteria of validity, and inclusion and exclusion of admissible evidence. Still, S-F asserts that “up to 80 percent of welfare-related statistical studies have false-negative or type-II errors, failing to reject a false null.” Tainted at 106. The support for this assertion is a citation to a review article by David Resnik. See David Resnik, “Statistics, Ethics, and Research: An Agenda for Education and Reform,” 8 Accountability in Research 163, 183 (2000). Resnik’s paper is a review article, not an empirical study, but at the page cited by S-F, Resnik in turn cites to well-known papers that present actual data:

“There is also evidence that many of the errors and biases in research are related to the misuses of statistics. For example, Williams et al. (1997) found that 80% of articles surveyed that used t-tests contained at least one test with a type II error. Freiman et al. (1978)  * * *  However, empirical research on statistical errors in science is scarce, and more work needs to be done in this area.”

Id. The papers cited by Resnik, Williams (1997)[6] and Freiman (1978)[7] did identify previously published studies that over-interpreted statistically non-significant results, but the identified type-II errors were potential errors, not ascertained errors, because the authors made no claim that every non-statistically significant result actually represented a missed true association. In other words, S-F is not entitled to say that these empirical reviews actually identified failures to reject fall null hypotheses. Furthermore, the empirical analyses in the studies cited by Resnik, who was in turn cited by S-F, did not look at correlations between alleged conflicts of interest and statistical errors. The cited research calls for greater attention to proper interpretation of statistical tests, not for their abandonment.

In the end, at least in the chapter on statistics, S-F fails to deliver much if anything on her promise to show how to evaluate science from a philosophic perspective.  Her discussion of the Pritchard case is not an analysis; it is a harangue. There are certainly more readable, accessible, scholarly, and accurate treatments of the scientific and statistical issues in this book.  See, e.g., Michael B. Bracken, Risk, Chance, and Causation: Investigating the Origins and Treatment of Disease (2013).


[1] Not to be confused with the deceased federal judge by the same name, William J. Rea. William J. Rea, 1 Chemical Sensitivity – Principles and Mechanisms (1992); 2 Chemical Sensitivity – Sources of Total Body Load (1994),  3 Chemical Sensitivity – Clinical Manifestation of Pollutant Overload (1996), 4 Chemical Sensitivity – Tools of Diagnosis and Methods of Treatment (1998).

[2] R. C. Shelton, M. B. Keller, et al., “Effectiveness of St. John’s Wort in Major Depression,” 285 Journal of the American Medical Association 1978 (2001).

[3] M. A. Eisenberger, B. A. Blumenstein, et al., “Bilateral Orchiectomy With or Without Flutamide for Metastic [sic] Prostate Cancer,” 339 New England Journal of Medicine 1036 (1998).

[4] Kenneth J. Rothman, Epidemiology 123–127 (NY 2002).

[5] Endnote 47 references the following papers: E. Hammond, “Cause and Effect,” in E. Wynder, ed., The Biologic Effects of Tobacco 193–194 (Boston 1955); E. L. Wynder, “An Appraisal of the Smoking-Lung-Cancer Issue,”264  New England Journal of Medicine 1235 (1961); see C. Little, “Some Phases of the Problem of Smoking and Lung Cancer,” 264 New England Journal of Medicine 1241 (1961); J. R. Stutzman, C. A. Luongo, and S. A McLuckey, “Covalent and Non-Covalent Binding in the Ion/Ion Charge Inversion of Peptide Cations with Benzene-Disulfonic Acid Anions,” 47 Journal of Mass Spectrometry 669 (2012). Although the paper on ionic charges of peptide cations is unfamiliar, the other papers do not eschew traditional statistical significance testing techniques. By the time these early (1961) reviews were written, the association that was reported between smoking and lung cancer was clearly accepted as not likely explained by chance.  Discussion focused upon bias and potential confounding in the available studies, and the lack of animal evidence for the causal claim.

[6] J. L. Williams, C. A. Hathaway, K. L. Kloster, and B. H. Layne, “Low power, type II errors, and other statistical problems in recent cardiovascular research,” 42 Am. J. Physiology Heart & Circulation Physiology H487 (1997).

[7] Jennie A. Freiman, Thomas C. Chalmers, Harry Smith and Roy R. Kuebler, “The importance of beta, the type II error and sample size in the design and interpretation of the randomized control trial: survey of 71 ‛negative’ trials,” 299 New Engl. J. Med. 690 (1978).

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