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LNT in Milward v. Acuity Specialty Products Group

September 28th, 2013

Professor Edward J. Calabrese previously has written about the shadowy origins of the linear no threshold (LNT) model of cancer causation.  See The Dubious Origins of the Linear No Threshold Model of Carcinogenesis (Jan. 10, 2013).  Recently, Calabrese has deepened his historical scholarship with two additional, interesting articles. See “Toxicologist Says NAS Panel ‘Misled the World’ When Adopting Radiation Exposure Guidelines” (Aug. 13, 2013).

These articles, now available online, are important tools in the work chest of lawyers who litigate health effect claims.  Edward J. Calabrese, “How the US National Academy of Sciences misled the world community on cancer risk assessment: new findings challenge historical foundations of the linear dose response,” 87 Arch. Toxicol. (2013) (in press); Edward J. Calabrese, “Origin of the linearity no threshold (LNT) dose–response concept,” 87 Arch. Toxicol. 1621 (2013). Professor Calabrese illuminates the exaggerations and ipse dixit in the origins of the linear-no threshold model, first applied to radiogenic cancers, and later to human carcinogenesis more generally.

On remand from the First Circuit, the trial judge in Milward, now the Hon. Douglas Woodlock, faced a renewed Rule 702 motion directed to Milward’s specific causation expert witnesses.  Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013). Plaintiffs attempted to invoke the dubious LNT concept to argue that benzene should be in the “differential” for ascertaining the specific cause of Mr. Milward’s APL. In performing a careful Rule 702 analysis, Judge Woodlock rule that, “[t]o the extent Butler [Milward’s expert witness] seeks to establish specific causation based on the argument that any level of benzene is sufficient to cause leukemia—a so-called “no safe level,” “no threshold,” or “linear” model—her opinion is inadmissibly unreliable.”  Id. at *8.

In recognizing Dr. Butler’s reliance upon LNT concepts in civil litigation as unreliable, Judge Woodlock followed the lead of other courts, within the First Circuit, which have previously rejected expert witness opinion testimony founded upon the LNT model.  See, e.g., Whiting v. Boston Edison Co., 891 F.Supp. 12, 25 (D.Mass.1995) (“[t]he linear non-threshold model cannot be falsified, nor can it be validated. To the extent that it has been subjected to peer review and publication, it has been rejected by the overwhelming majority of the  scientific community. It has no known or potential rate of error. It is merely an hypothesis.” ); Sutera v. Perrier Group of America Inc., 986 F.Supp. 655, 666 (D.Mass.1997) (“Accordingly, although there is evidence that one camp of scientists … believes that a non-linear model is appropriate basis for predicting the risks of low-level exposures to benzene, there is no scientific evidence that the linear no-safe threshold analysis is an acceptable scientific technique used by experts in determining causation in an individual instance.”).  Strong precedent outside the First Circuit also supports Judge Woodlock’s holding.  See Allen v. Pennsylvania Eng’g Corp., 102 F.3d 194, 198 (5th Cir.1996); Henricksen v. ConocoPhillips Co., 605 F.Supp. 2d 1142, 1166 (E.D.Wash.2009) (“[Plaintiffs’ expert witness’s] theory that any amount of exposure more than negligible should be considered substantial risk factor for AML flies in the face of the scientific literature reviewed and other expert testimony in this case that there is a threshold or dose below which you do not see a statistically significant risk of developing AML.”); In re W.R. Grace & Co. 355 B.R. 462, 476 (Bankr. D. Del. 2006) (the “no threshold model . . . flies in the face of the toxicological law of dose-response . . . doesn’t satisfy Daubert, and doesn’t stand up to scientific scrutiny”); Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814, 853–54 (W.D. Tex. 2005) (even accepting the linear, no-threshold model for uranium mining and cancer, it is not enough to show exposure, you must show causation as well). See also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1244 (11th Cir. 2005) (“in evaluating the reliability of the experts’ opinions on general causation, it would help to know how much additional risk for heart attack or ischemic stroke Metabolife consumers have over the risks the general population faces”). National Bank of Commerce v. Assoc. Milk Producers, 22 F. Supp. 2d 942, 960 (E.D. Ark. 1998), aff’d, 191 F.3d 858 (8th Cir.1999). See generally Federal Judicial Center, Reference Manual on Scientific Evidence, at 643 n. 28 (3d ed.2011).

The district court in Milward held that because Dr. Butler “did not and could not quantify a threshold exposure level for benzene, Milward cannot posit that his cumulative exposure level crossed a relevant threshold.” Milward, 2013 WL 4812425, at 8.  In addressing Milward’s reliance upon LNT, Judge Woodlock rejected three specious arguments, which frequently recur in Rule 702 litigation.

First, the district saw through the argument that the claimed benzene-APL LNT model was good science because the United States Environmental Protection Agency (EPA) relies upon it.  The EPA applies the LNT model for benzene

“due to uncertainty about the shape of the dose-response curve below 40 ppm-years.”

Id. at 8[1]. The district court recognized that the EPA’s reasoning was a “classic example of a cautious prophylactic administrative rule” that “does not support the reliability of the linear, no-threshold model in establishing specific causation.”  Id.  In so ruling, the Milward district court joins a long line of courts that have distinguished administrative rulemaking from civil litigation standards for causation.  See, e.g., Allen v. Pa. Eng’g Corp., 102 F.3d 194, 198 (5th Cir. 1996)(“This methodology results from the preventive perspective that the agencies adopt in order to reduce public exposure to harmful substances. The agencies’ threshold of proof is reasonably lower than that appropriate in tort law, which traditionally makes more particularized inquiries into cause and effect.”)

Second, the Milward district court also saw through plaintiffs’ argument that the First Circuit’s embrace of its “weight of the evidence” general causation approach, which appears to enjoy support among federal bureaucrats, required approval of plaintiffs’ attempt to use a LNT prophylactic or precautionary approach. Milward, 649 F.3d at 18 & n. 9.  Plaintiffs have the burden of showing reliability of the LNT model, and the EPA’s acknowledged uncertainty about the model for benzene was an insuperable barrier to their success.  Milward, 2013 WL 4812425, at 8 & n.4.

Third, the district court rejected Dr. Butler’s attempt to “bait and switch,” by pointing to a study on hematotoxicity as opposed to carcinogenicity.  Butler argued that there was “no clear evidence of a threshold below which benzene does not cause hematotoxicity in humans.”[2] The court recognized that the study referred to the lack of a hematotoxicity threshold for low average doses of benzene. Hematotoxicity is not necessarily induction of APL; nor was the lack of clear evidence for a threshold evidence against a threshold.

Even in the regulatory realm, the LNT model is losing traction.  See Chlorine Chemistry Council v. EPA, 206 F.3d 1286, 1287 (D.C. Cir. 2000) (invalidating EPA regulation under the Safe Drinking Water Act, when the EPA persisted in using an LNT model, after it had concluded that chloroform, a contaminant in drinking water from chlorination exerted a “a nonlinear mode of carcinogenic action”).  In the scientific realm, researchers can merely watch in amazement at the “political science” that proceeds under a mistaken, outdated model of carcinogenesis.  See, e.g., Brant A. Ulsh, “Checking the Foundation: Recent Radiobiology and the Linear No-Threshold Theory,” 99 Health Physics 747 (2010) (“However, a large and rapidly growing body of radiobiological evidence indicates that cell and tissue level responses to this damage, particularly at low doses and/or dose-rates, are nonlinear and may exhibit thresholds. To the extent that responses observed at lower levels of biological organization in vitro are predictive of carcinogenesis observed in vivo, this evidence directly contradicts the assumptions upon which the microdosimetric argument is based.”); Bernard L. Cohen, “The Linear No-Threshold Theory of Radiation Carcinogenesis Should Be Rejected,” 13 J. Am. Physicians & Surgeons 70, 75 (2008) (“The conclusion from the evidence reviewed in this paper and more extensively elsewhere is that the linear-no threshold theory (LNT) fails very badly in the low-dose region, grossly overestimating the risk from low-level radiation. This means that the cancer risk from the vast majority of normally encountered radiation exposures is much lower than given by usual estimates, and may well be zero or even negative.”); Maurice Tubiana, Ludwig E. Feinendegen, Chichuan Yang, and Joseph M. Kaminski, “The Linear No-Threshold Relationship Is Inconsistent with Radiation Biologic and Experimental Data,” 251 Radiology 13, 13, 15-16, 18 (2009) (noting that LNT model is obsolete in view of known upregulation of cellular protective mechanisms against cancer; “LNT was a useful model half a century ago. But current radiation protection concepts should be based on facts and on concepts consistent with current scientific results and not on opinions. Preconceived concepts impede progress; in the case of the LNT model, they have resulted in substantial medical, economic, and other societal harm.”).


[1] The court EPA Office of Research and Development, Carcinogenic Effects of Benzene: An Update, at 38–39 (April 1998).

[2] Dr. Butler cited Richard B. Hayes, et al., “Benzene and Lymphohemaptopoietic Malignancies in Humans,” 40 Am. J. Indus. Med. 117, 120 (2001).

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Differential Diagnosis in Milward v. Acuity Specialty Products Group

September 26th, 2013

Graffiti on the bathroom wall in the building that housed my undergraduate college’s philosophy department:

How does a philosopher treat constipation?

By using iterative disjunctive syllogism.

The joke is that this variety of syllogism is nothing other than reasoning by the process of elimination.

A or B or C

~A

B or C

~B

∴C

The syllogism works as a valid form of argument if the premises are all true.  So, if we start with three possible causes, A, B, and C, and we know that one or more of them caused an outcome, then we might proceed by the process of elimination to show that we can rule out all the others but the alleged cause.  The first line of the syllogism is true if at least one of the disjuncts is true.  As we rule out particular disjuncts upon learning that they are in fact false, we are left we a smaller set of disjuncts.  If we can proceed until we are left with the disjunct of interest, we may actually have succeeded in identifying a cause in fact of the particular case.

In the syllogistic argument above, we must be able to show that A and B are false before we can then conclude that C is true.

In differential etiology, we start with known causes, exposures or conditions that are known to be capable of causing a disease or disorder.  We do not know whether the potential causes were actually in play in a given case.  If we can use this syllogistic reasoning to conclude that the defendant’s product was a cause of the of the plaintiff’s harm, we might actually have shown specific causation in a reliable fashion.  If, however, we cannot proceed to a conclusion that unequivocally includes the defendant’s product, we are left with an indeterminate outcome, and the plaintiff must take nothing.

The Milward case was recently back in the news.  On remand from the First Circuit, the district judge, now the Hon. Douglas Woodlock, faced a renewed Rule 702 motion directed to Milward’s specific causation expert witnesses.  Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013).

Judge Woodlock wryly commented upon the First Circuit’s ignoring the statutory mandate of Rule 702, by its embracing caselaw that predated the 2000 statutory amendment of the Rule:

“While a 2000 amendment to Fed.R.Evid. 702 codified a rigorous reliability test, the Daubert line of cases has been read by the First Circuit as “demand[ing] only that the proponent of the evidence show that the expert’s conclusion has been arrived at in a scientifically sound and methodologically reliable fashion.” Ruiz–Troche v. Pepsi Cola of Puerto Rico Bottling Co., 161 F.3d 77, 85 (1st Cir.1998). “So long as an expert’s scientific testimony rests upon good grounds based on what is known, it should be tested by the adversarial process, rather than excluded for fear that jurors will not be able to handle the scientific complexities.” Milward, 639 F.3d at 15 (internal quotation and citation omitted).”

Milward, at *3.  After noting the statute’s “rigorous reliability test,” and the First Circuit’s having  diluted the statutory standard by drawing from pre-statute caselaw, Judge Woodlock got down to the business of gatekeeping, by examining the facts of record before him.

The defense’s first challenge was to Milward’s industrial hygienist’s opinion that quantified his benzene exposure.  The industrial hygienist, James Stewart, estimated Milward’s benzene exposure, both total and from individual products.  The defense challenge was interesting, given that plaintiffs have challenged defendants’ use of similar exposure recreations to advance apportionments that will defeat joint and several liability.  The district court denied the defense challenge, and turned its attention to the specific causation issue, which proved to be a good example of patho-epistemology .

The plaintiffs relied upon Dr. Sheila Butler, who was board certified in occupational medicine, pathology, and hematology, to opine that Brian Milward’s exposure was responsible for causing his Acute Promyelocytic Leukemia (“APL”), a rare subtype of Acute Myeloid Leukemia (“AML”). Butler’s opinion was simple if not simpistic:

“there is a ‘reasonable medical probability that there is a direct causal association between Mr. Milward’s APL and his excessive occupational exposure to benzene containing substances’ based primarily on

(1) the fact that his exposure to benzene preceded his development of APL, and

(2) a survey of studies showing increased AML risk following low average dose exposures to benzene.”

Milward at *6.

Simplistic and simply wrong. Butler had equated exposure and some risk, unquantified, with specific causation, an empty and unsupported assertion.  Judge Woodlock did not dignify this subjective opinion with further discussion, but turned his attention to Butler’s “differential diagnosis” analysis by which Butler claimed to have eliminated other potential causes of Milward’s APL such that she could say that benzene was a specific cause.

The district court started from the premise that so-called differential diagnosis is useful and accepted for assessing causation. Id. at *7 (citing Baker v. Dalkon Shield Claimants Trust, 156 F.3d 248, 253 (1st Cir.1998).  For some reason, however, the court emphasized that the differential etiology was particularly appropriate when the expert witness’s opinion lacks a foundation of epidemiologic studies or a “well-established threshold exposure levels at which disease occurs.”  The district court did not explain what it possibly could have meant by this emphasis, and I doubt that there is any basis for the court’s statement.

The real issue in Milward, on remand, was whether Dr. Butler applied the differential etiology in a reliable manner.  The defense argued that Dr. Butler failed to rule out competing risk factors, Milward’s prior smoking, and his morbid obesity, as causes of Milward’s APL.  The court dismissed this challenge with the recognition that plaintiffs might still prevail if Milward’s disease resulted from either benzene and smoking or benzene, smoking, and obesity. Sadly, the court did not address the quality or quantity of the evidence for smoking, or for obesity, and APL; nor did it address the magnitude of the associations that were being claimed by the defense, or by the plaintiffs.  The court did not explore the evidentiary base for the defense assertion that smoking or obesity causes APL such that it should be in the first line of the iterative disjunctive syllogism.

The problem, of course, was not the plaintiffs’ failure to rule out obesity or smoking, but their failure to rule out the unknown factors, which account for the solid majority of APL cases.  Indeed, in the first round of Rule 702 briefings and hearings, plaintiffs’ expert witness, Dr. Martin Smith, opined that between 70 and 80 percent of APL cases are idiopathic; that is, they have no known cause.  Id. at *7.  The syllogism thus becomes very difficult because one proposition in the first line of the argument is that the cause is unknown, and the plaintiff cannot arrive at the conclusion that his APL was caused by benzene unless and until he provides reliable evidence that more likely than not, his APL disease was not caused by one or more of the unknown causes.  In other words, plaintiffs must show that the APL was not a background case that would have occurred regardless of occupational benzene exposure, and perhaps regardless of occupational exposure with obesity and smoking.  Judge Woodlock, relying heavily upon the Restatement (Third) of Torts expressed the matter this way:

“When a disease has a discrete set of causes, eliminating some number of them significantly raises the probability that the remaining option or options were the cause-in-fact of the disease.  Restatement (Third) of Torts: Phys. & Emot. Harm § 28, cmt. c(4) (2010) (‘The underlying premise [of differential etiology] is that each of the[] known causes is independently responsible for some proportion of the disease in a given population.  Eliminating one or more of these as a possible cause for a specific plaintiff’s disease increases the probability that the agent in question was responsible for that plaintiff’s disease.’). The same cannot be said when eliminating a few possible causes leaves not only fewer possible causes but also a high probability that a cause cannot be identified. Id. (‘When the causes of a disease are largely unknown … differential etiology is of little assistance’.).”

In the face of this irrefutable logic of this part of comment c, Butler argued that she had “ruled out” idiopathic APL by “ruling in” benzene.  Of course, benzene had to be postulated as a general cause in order for it to be placed into the first line of the syllogism, but Butler’s assertion about ruling in benzene as a specific cause is truly an ipse dixit, a non sequitur, and a petitio principii, all rolled into one opinion.  After all, the APL case may have arisen out of benzene exposure and the unknown causes, or only the unknown (idiopathic) causes.  Butler cannot rule in benzene until she rules out idiopathic causes as the sole specific causes in this case. To be fair, the prevalence of idiopathic cases cited by Martyn Smith might be lower in a population with heavy benzene exposure, assuming Smith’s general causation were true, but again, such an acknowledgment would only raise the question of what the prevalence of idiopathic cases is in a population of exposure that looked like Mr. Milward’s.

Dr. Butler argued that Martyn Smith had previously ruled in benzene, but that was only as a general cause that can then be represented as one disjunct in the first line of the syllogism.  Here Judge Woodlock identified another gap between Smith’s general causation opinion and Dr. Butler’s attempt to use Smith’s opinion to place benzene into the differential etiology for Mr. Milward.  On this remand, the plaintiffs had to show that “the levels of exposure that are hazardous to human beings generally as well as the plaintiff’s actual level of exposure.” Id. (citing Westberry v. Gislaved Gummi AB, 178 F.3d 257, 263-64 (4th Cir.1999) (talcum powder undisputedly could cause sinus problems, and plaintiff was exposed at levels known to be causative).  The court suggested that Milward had not yet shown that exposure at the levels he experienced could cause APL.  Of course, even if Milward sustained cumulative exposures capable of causing APL, this fact sufficed only to place benzene into the differential diagnosis, and it did not advance the iterative disjunctive syllogism to a conclusion of either a single or multiple disjuncts that included benzene.

Judge Woodlock did a good job of saving the First Circuit from the notoriety of its general causation decision in the Milward case. The new trial court decision is a strong reminder that risk does not equal causation.  Differential etiology cannot rule out idiopathic cause(s) as the sole specific cause of a plaintiff’s disease unless there is a fingerprint of causation that makes the risk identifiable as a cause in a specific case.  Such a fingerprint or biomarker was apparently absent in the Milward case.  Similarly, the differential etiology might rule out putative specific causes on a probabilistic basis if the idiopathic cases made up a small number of all the cases in relation to the number of cases that arise from the exposure that is the subject of the litigation.

The Milward decision joins other soundly decided differential diagnosis cases coming out of the First Circuit.  See, e.g., Plourde v. Gladstone, 190 F. Supp. 2d 708, 722-723 (D. Vt. 2002) (excluding testimony where expert failed to rule out causes of plaintiff’s illness other than exposure to herbicides); Whiting v. Boston Edison Co., 891 F. Supp. 12, 21 n.41 (D. Mass. 1995) (noting that differential diagnosis cannot be used to support conclusion of specific causation when 90% disease cases are idiopathic).

But lest anyone get too comfortable with the notion that this issue has been mastered by the federal judiciary, keep in mind that there are some really poorly reasoned cases out there. See, e.g., Allen v. Martin Surfacing, 263 F.R.D. 47, 56 (D. Mass. 2008) (admitting general and specific causation testimony to be tested by adversary process, rather than excluded altogether, despite paucity of epidemiologic evidence and general acceptance that there are no known causes of amyotrophic lateral sclerosis).

The limits of the “process of elimination” approach has been addressed by some scientific organizations, such as the Teratology Society, in the particularly demanding context of determining a cause for a child’s congenital malformation:

“Biologic plausibility includes a consideration of alternative explanations for the outcome in an individual plaintiff. For example, if a plaintiff has a birth defect syndrome caused by a known genetic disorder, chemical exposure becomes implausible as a cause of the abnormality in that particular individual. The consideration of alternative explanations is sometimes misused by expert witnesses to mean that failure to find an alternative explanation for an outcome is proof that the exposure at issue must have caused the outcome. A conclusion that an exposure caused an outcome is, however, based on positive evidence rather than on lack of an alternative explanation.”

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

A brief, partial survey of differential etiology cases is set out below.

SECOND CIRCUIT

McCullock v. H.B. Fuller Co., 61 F.3d 1038, 1044 (2d Cir. 1995) (defining differential etiology as an analysis “which requires listing possible causes, then eliminating all causes but one”)

Prohaska v. Sofamor, S.N.C., 138 F. Supp. 2d 422, 439 (W.D.N.Y. 2001) (excluding expert’s opinion and granting summary judgment where expert “was unable to rule out, to a reasonable degree of medical certainty, [plaintiff’s] pre-existing condition, scoliosis, as a current cause of her pain”)

Zwillinger v. Garfield Slope Hous. Corp., 1998 WL 623589, at *20 (E.D.N.Y. Aug. 17, 1998) (excluding testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s immunotoxicity syndrome)

THIRD CIRCUIT

Magistrini v. One Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 608-610 (D.N.J. 2002) (excluding testimony of expert who sought to testify that dry cleaning fluid caused leukemia, but failed to rule out smoking as an alternative cause), aff’d, 68 F. App’x 356 (3d Cir. 2003)

In re Paoli R.R. Yard PCB Litig., 2000 WL 274262, at *5 (E.D. Pa. March 1, 2000) (expert’s opinion should be excluded “because she failed to rule out alternative causes” of plaintiff’s injuries)

Kent v. Howell Elec. Motors, 1999 WL 517106, at * 5 (E.D. Pa. July 20, 1999) (excluding expert testimony and granting summary judgment because expert could “not rule out reasonable alternative theories of what caused the retaining ring to fail”);

O’Brien v. Sofamor, 1999 WL 239414, at *5 (E.D. Pa. Mar. 30, 1999) (excluding expert’s testimony and granting summary judgment where plaintiff “offer[ed] no evidence that [plaintiff’s experts] performed a differential diagnosis, or even considered other potential causes” of plaintiff’s back condition)

Schmerling v. Danek Med., Inc., 1999 WL 712591, at *9 (E.D. Pa. Sept. 10, 1999) (excluding expert’s testimony and granting summary judgment on the grounds that expert’s failure to rule out alternative causes “alone warrants a determination that the expert’s methodology is unreliable”);

Turbe v. Lynch Trucking Inc., 1999 WL 1087026, at *6 (D.V.I. Oct. 7, 1999) (excluding expert’s testimony where expert “expressed awareness of obvious alternative causes” yet “did not investigate any other possible causes”);

Reiff v. Convergent Technologies, 957 F. Supp. 573, 582-83 (D.N. J. 1997) (excluding expert’s testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s carpal tunnel syndrome)

Rutigliano v. Valley Bus. Forms, 929 F. Supp. 779, 787 (D.N.J. 1996) (excluding expert’s testimony and granting summary judgment where the “record is replete with evidence, including [the expert’s] own admissions, that [plaintiff’s] symptoms could be attributable to medical conditions other than formaldehyde sensitization”)

Diaz v. Matthey, Inc., 893 F. Supp. 358, 376-377 (D.N.J. 1995) (excluding testimony and granting summary judgment where expert failed to rule out alternative causes for plaintiff’s asthma) (Irenas, J.)

Wade-Greaux v. Whitehall Labs., Inc., 874 F. Supp. 1441 (D.V. I.), aff’d, 46 F.3d 1120 (3d Cir. 1994) (excluding testimony of expert who failed to rule out alternative causes of plaintiff’s birth defects)

FOURTH CIRCUIT

Westberry v. Gislaved Gummi AB, 178 F.3d 257, 262-263 (4th Cir. 1999) (“Differential diagnosis, or differential etiology, is a standard scientific technique of identifying the cause of a medical problem by eliminating the likely causes until the most probable one is isolated”)

Shreve v. Sears, Robuck & Co., 166 F. Supp. 2d 378, 397-98 (D. Md. 2001) (excluding testimony where expert failed to rule out other causes of plaintiff’s injury other than an alleged defect in snow thrower)

Fitzerald v. Smith & Nephew Richards, Inc., 1999 WL 1489199 (D. Md. Dec. 30, 1999) (excluding expert’s testimony and granting summary judgment where expert “failed to rule out what could have been another cause of [plaintiff’s] condition”)

Aldridge v. Goodyear Tire & Rubber Co., 34 F. Supp. 2d 1010, 1024 (D. Md. 1999), vacated on other grounds, 223 F.3d 263 (4th Cir. 2000) (excluding testimony of plaintiffs’ experts where they “failed to adequately address possible alternative causes of plaintiffs’ illnesses”)

Oglesby v. General Motors Corp., 190 F.3d 244, 250 (4th Cir. 1999) (affirming exclusion of testimony where “as a matter of logic, [the expert witness] could not eliminate other equally plausible causes” of cracked plastic inlet);

Driggers v. Sofamor, S.N.C., 44 F. Supp. 2d 760, 765 (M.D.N.C. 1998) (excluding expert’s testimony and granting summary judgment where “expert failed to rule out other possible causes of [plaintiff’s back] pain”);

Higgins v. Diversey Corp., 998 F. Supp. 598, 603 (D. Md. 1997), aff’d, 135 F.2d 769 (4th Cir. 1998) (excluding expert’s testimony that the accidental inhalation of a bleach caused plaintiff’s injuries, where expert “admit[ted] that he [could] not rule out several other possible causes”)

FIFTH CIRCUIT

Michaels v. Avitech, Inc., 202 F.3d 746, 753 (5th Cir. 2000) (excluding testimony when “plaintiff’s experts wholly fail[ed] to address and rule out the numerous other potential causes” of an aircraft disaster)

Black v Food Lion, Inc, 171 F3d 308 (5th Cir 1999) (expert witness, purporting to use a differential diagnosis, testified that plaintiff’s slip in the supermarket caused fibromyalgia, which is largely idiopathic) (“This analysis amounts to saying that because [the physician] thought she had eliminated other possible causes of fibromyalgia, even though she does not know the real ‘cause,’ it had to be the fall at Food Lion. This is not an exercise in scientific logic but in the fallacy of post-hoc propter-hoc reasoning, which is as unacceptable in science as in law.”)

Conger v. Danek Med., Inc., 1998 WL 1041331, at *5-6 (N.D. Tex. Dec. 14, 1998) (excluding expert’s testimony and granting summary judgment when expert “had not attempted to rule out [other potential sources] as causes for [plaintiff’s back] pain”);

Leigh v. Danek Med., Inc., 1998 WL 1041329, at *4-5 (N.D. Tex. Dec. 14, 1998) (excluding expert’s testimony and granting summary judgment where expert failed to rule out alternative causes of plaintiff’s back pain)

Bennett v. PRC Public Sector, 931 F. Supp. 484, 492 (S.D. Tex. 1996) (excluding testimony of expert who failed to consider and rule out alternative causes of plaintiff’s repetitive motion disorders)

SIXTH CIRCUIT

Nelson v. Tennessee Gas Pipeline Co., 1998 WL 1297690, at *6 (W.D. Tenn. Aug. 1, 1998) (excluding testimony of expert who “failed to engage in adequate techniques to rule out alternative causes and offers no good explanation as to why his opinion is nevertheless reliable in light of other potential causes of the alleged injuries”);

Downs v. Perstorp Components, 126 F. Supp. 2d 1090, 1127 (E.D. Tenn. 1999) (excluding expert testimony as to whether exposure to chemicals caused plaintiff’s injuries where expert failed to rule out alternative causes)

EIGHTH CIRCUIT

Jisa Farms, Inc. v. Farmland Indus., No. 4:99CV3294, 2001 U.S. Dist. LEXIS 26084 (D. Neb. 2001)

Thurman v. Missouri Gas Energy, 107 F. Supp. 2d 1046, 1058 (W.D. Mo. 2000) (expert’s opinion “that the pipeline failed because of corrosion” was excluded and summary judgment granted where expert reached the conclusion “without eliminating other causes”)

Bruzer v. Danek Med., Inc., 1999 WL 613329, at *8 (D. Minn. Mar. 8, 1999) (excluding expert’s testimony and granting summary judgment where expert did “not attempt to rule out any alternative potential causes for [plaintiff’s] continuing and increasing [back] pain”)

National Bank of Commerce v. Assoc. Milk Producers, 22 F. Supp. 2d 942, 963 (E.D. Ark. 1998), aff’d, 191 F.3d 858 (8th Cir.1999) (excluding testimony and granting summary judgment where expert did “not successfully rule out other possible alternative causes” for cancer)

TENTH CIRCUIT

In re Breast Implant Lit., 11 F. Supp. 2d 1217, 1234 (D. Colo. 1998) (excluding expert testimony where expert failed to “explain what alternative causes he considered, or how he ruled out other possible causes” of plaintiffs’ auto- immune disease)

Stover v. Eagle Products, 1996 WL 172972, at *11 (D. Kan. Mar. 19, 1996) (excluding testimony of expert who “[did] not explain in any meaningful detail how he [was] able to exclude the numerous multiple alternative causes” of injury to plaintiff’s dogs)

ELEVENTH CIRCUIT

Rink v. Cheminova, Inc., 400 F.3d 1286, 1295 (11th Cir. 2005) (“[I]n the context of summary judgment . . . differential diagnosis evidence by itself does not suffice for proof of causation.”)

STATE COURT CASES

Blanchard v. Goodyear Tire & Rubber Co.,  2011 Vt. 85, 30 A.3d 1271 (2011) (holding that plaintiff’s claim that his NHL was caused by benzene was not reliably supported by differential diagnosis when a large percentage of NHL cases have no known cause)

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Bradford Hill on Statistical Methods

September 24th, 2013

I am indebted to the article by Dr. Frank Woodside and Allison Davis on the so-called Bradford Hill criteria, for reminding me about the distorted view that some plaintiffs’ counsel advance in litigation about Bradford Hill’s view of statistical testing.  Frank C. Woodside, III & Allison G. Davis, “The Bradford Hill Criteria: The Forgotten Predicate,” 35 Thomas Jefferson L. Rev. 103 (2013).  Dr. David Schwartz has also written an insightful blog post on Bradford Hill.  See David Schwartz, “5 Reasons to Apply the Bradford Hill Criteria in Your Next Case” (Sept. 20, 2013).

Here is where Bradford Hill postulates the position of a research question before his famous nine factors come into the analysis:

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

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

The starting point, before the Bradford Hill nine factors come into play, requires a “clear-cut” association, which is “beyond what we would care to attribute to the play of chance.”  What is “clear-cut” association?  The most reasonable interpretation of Bradford Hill is that the starting point is an association that is not the result of chance, bias, or confounding.

I parted company with Woodside and Davis over whether Bradford Hill was somehow dismissive of the role of assessing chance in explaining an association.  In acknowledging any validity in the plaintiffs’ interpretation of Bradford Hill’s 1965 paper, Woodside and Davis, do an injustice, in my view, to Bradford Hill’s careful articulation of his position.

The starting position, quoted above, seems very clear, but Woodside and Davis note that later on in his speech, Bradford Hill suggested that tests of significance do not contribute to proof of the hypothesis.  Bradford Hill’s actual words are, however, fairly precise:

“No formal tests of significance can answer those questions. Such tests can, and should, remind us of the effects that the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that they contribute nothing to the ‘proof’ of our hypothesis.”

Bradford Hill at 299.

Plaintiffs’ counsel sometimes argue that this passage means that significance testing contributes “nothing” to proving the hypothesis, but this ignores two key points.  First, the argument ignores where in the text the passage occurs:  after Bradford Hill’s discussion of the nine factors.  Bradford Hill’s statement can be understood only as a reflection back on the nine factors.  The phrase “those questions” refers back to the nine factors, and this is the limitation that Bradford Hill is placing upon “formal tests of significance.” The starting point, before the nine factors are examined, is, after all, a “clear-cut” association, “beyond what we would care to attribute to the play of chance.”

Second, plaintiffs’ counsel’s argument ignores the clear meaning of the “[b]eyond that” phrase.  Beyond what?  Well, the limited role is nothing other than quantifying the play of chance in the observed results.  This role is hugely important, and of course, is incorporated into the starting point before the nine factors are examined.  In modern analyses, the role of random variability would actually be explored in the analysis of the exposure-outcome gradient, and perhaps in some of the other nine factors as well.  Bradford Hill implied that a statistically significant association was a preliminary step, after which the really hard work began.

It would be unfair to Bradford Hill to read into his statement much about “strict” testing versus a more flexible inferential approach in selecting or interpreting a Type I error rate.  By the time he presented his Presidential Address to the Royal Society of Medicine in 1965, much fur had flown in the disputes between Neyman and Fisher.  Resolving Bradford Hill’s view on the dispute is not a pressing issue because on either account, the quantification of the p-value is an extremely important step in evaluating scientific data.

In his textbook on medical statistics, Bradford Hill expands on the role of statistical analysis in medicine:

“Are simple methods of the interpretation of figures only a synonym for common sense or do they involve an art or knowledge which can be imparted? Familiarity with medical statistics leads inevitably to the conclusion that common sense is not enough. Mistakes which when pointed out look extremely foolish are quite frequently made by intelligent persons, and the same mistakes, or types of mistakes, crop up again and again. There is often lacking what has been called a ‘statistical tact, which is rather more than simple good sense’. That tact the majority of persons must acquire (with a minority it is undoubtedly innate) by a study of the basic principles of statistical method.”

Austin Bradford Hill, Principles of Medical Statistics at 2 (4th ed. 1948) (emphasis in original).

Even in this early work though, Bradford Hill acknowledges the limits of statistical methods:

“It is a serious mistake to rely upon the statistical method to eliminate disturbing factors at the completion of the work.  No statistical method can compensate for a badly planned experiment.”

Id. at 4 (emphasis in original).  That statistical method cannot save a poorly planned experiment (or observational study) does not, however, imply that statistical methods are not needed to interpret a properly planned experiment or study.

In the summary section of the first chapter, Bradford Hill removes any doubt about his view of the importance, and the necessity, of statistical methods:

“The statistical method is required in the interpretation of figures which are at the mercy of numerous influences, and its object is to determine whether individual influences can be isolated and their effects measured.”

Id. at 10 (emphasis added).

Posted in Causation, Scientific Evidence | Comments Off on Bradford Hill on Statistical Methods

Do English Judges Diss Epidemiology?

September 13th, 2013

As noted the other day, Claire McIvor, a senior lecturer, at the Birmingham Law School, has published an interesting U.K. perspective on the use of epidemiologic and statistical evidence in health-outcome litigation. See “Debunking some judicial myths about epidemiology and its relevance to UK tort law,” in 21 Med. Law Rev. (2013), in press.

Ms. McIvor criticizes one case in particular for what she argues is an inappropriate dismissal of epidemiologic evidence as presented by an epidemiologist. Novartis Grimsby Ltd. v. Cookson, [2007] EWCA Civ 1261.

The pursuer, Cookson, worked for Novartis Grimsby, at its factory that manufactured dyes, including azo dyes, from 1964, until 2001, when he developed bladder cancer.  Cookson also chose to be exposed to various carcinogens as a personal lifestyle; he smoked cigarettes, 1/2 to one pack per day, for about 20 years, before quitting around 1980.

Cookson sued Novartis on allegations that he was overexposed to various aromatic amines[1], some of which are known to cause bladder cancer.  Novartis had previously paid such claims, but it contested Mr. Cookson’s case because of its belief that his workplace exposures had not been excessive, and that his past smoking habit more likely explained his cancer.  Both sides called physician expert witnesses, urologists, who both agreed that smoking and the aromatic amines could cause bladder cancer, but disagreed as to what caused Mr. Cookson’s disease.

Given the contest on causation, the two urologists agreed that the input of an epidemiologist, jointly instructed, would be helpful.  Now how quaint is that, for both sides to agree upon an expert witness?  Most lawyers in the United States would think it malpractice to engage in such a practice.

Professor Ray Cartwright, an epidemiologist who had published on the causes of bladder cancer, was the jointly instructed witness. A PubMed search for articles written by Cartwright on bladder cancer is set out below, and suggests that he was an appropriate choice, ex ante, at any rate.

Cartwright reviewed the epidemiologic literature, including some of his own studies. Cartwright’s report disappointed the plaintiff, however, when he opined that the workplace aromatic amine exposure was slight and posed only a low risk compared to the smoking. In assessing Cookson’s workplace exposure, Cartwright relied upon the exposure estimates of the parties’ industrial hygienists, and based his causal attribution upon an assessment that exposures were low.  Later, when plaintiff’s counsel showed that Cartwright misinterpreted some of the exposure data, Cartwright revised his report, but maintained that Cookson’s cancer was caused by smoking.

Professor Cartwright’s misstep on exposure probably diminished the strength of his opinion in the eyes of the trial judge, who ruled for the plaintiff.  Ms. McIvor seems to believe that this ruling improperly elevated clinical testimony over epidemiologic testimony, and credited “personalized probabilities” of the plaintiff’s testifying urologist, who attributed the cancer 20–25% to smoking, versus 70–75% to workplace exposures, and who opined that the workplace more than doubled the risk level that Cookson would have had had he never worked at the Novartis factory.  Novartis Grimsby Ltd. at 48.

Novartis appealed, on grounds that included an allegation of error in equating fact of exposure with causation of the bladder cancer.  Speaking for a unanimous England and Wales Court of Appeal, Lady Justice Smith dismissed the appeal, including its challenge to the medical causation issues.  Contrary to Ms. McIvor, however, the appellate court’s decision gave due weight to the epidemiologist, but found that the epidemiologic evidence was accessible to, and interpretable by, the clinicians. Although neither the appellate decision nor McIvor reviewed the actual epidemiologic evidence, several studies suggest that the relative risks for benzidine-derived dyes are greater than for smoking, and especially the risk for former smokers.  The judicial decision flowed not from improvidently dismissing epidemiologic evidence, or testimony by an epidemiologist, but from relying upon epidemiologic evidence marshaled by the plaintiff, through his urologist.[2]

Both sides agreed that smoking could cause bladder cancer, but they also had to agree that the risk of bladder cancer wanes after smoking cessation. Unfortunately, the Court of Appeal did not review the evidence, but the Surgeon General’s Reports note that cessation reduces risk by half after only a few years.  Wynder and Stellman (1977) and Wynder and Goldsmith (1977) suggest that the risk returns to baseline after 15 years of abstinence.  A study by Cartwright himself suggested the return to baseline in six years, although other studies (by Iscovich; Howe; Vineis; Hartge; and Burch) suggested an initial decline, followed by a persistent increased risk even beyond 15 years of abstinence.

Lady Justice Smith declared herself perplexed by these data, which seemed to be at odds with the notion that bladder cancer develops after 20 or more years latency:

“I myself have found it hard to understand how the passage of time after stopping smoking could result in a reduced risk of developing the disease if the aetiology of the disease is that the cancer begins at the time of exposure but does not manifest itself until later. However, as I have said, this issue was not fully explored in evidence and both experts agreed that the risk of developing bladder cancer from smoking decreased after smoking ceased.”

Novartis Grimsby Ltd. at 45.

Clearly though, it was not helpful to have Cartwright contradicted by the data in his own study.  Although the higher aromatic amine exposures occurred early in the plaintiff’s work career, Cookson continued to have some exposure up until the time of his diagnosis in 2001.  Professor Cartwright may well have been further undermined by the lack of any “time windows” in the occupational epidemiology, which would have supported a similar argument of declining risk from the more intense occupational exposure in the 1960’s.  The absence of such evidence for benzidine, compared with the evidence of latency and post-cessation declining risk for smoking, clearly hurt the employer’s case.  This imbalance in the evidence clearly helps to explain and support the courts’ rejection of Cartwright’s testimony.

Given the epidemiologic evidence, it is not at all clear that the plaintiff’s testifying urologist’s opinion that smoking contributed 25%-30%, whereas aromatic amines contributed 70%-75%, was merely a subjective or personal probability.  Smoking is associated with a two- to three-fold increase in risk in prospective studies, but Cookson was 20 years post-cessation.  His aromatic amine dyestuff exposure, which carries a much higher relative risk for bladder cancer, continued through till the end of his work tenure.  See “Dyes metabolized to benzidine,” in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans Volume 100F (WHO 2012).

Cookson’s bladder cancer might have been a “background” case, or a result of both smoking and aromatic amine exposure, or a result of one or the other contested causes.  There appeared to be no serious evidence of synergy.  Given the studies at issue, the plaintiff’s testifying urologist’s opinion may well have been a reasoned analysis of the epidemiologic evidence.  The epidemiologist’s opinion, on the other hand, was clearly undermined by the facts of smoking cessation, and an initial error in exposure estimation.  Novartis’ counsel argued that Cartwright was the “real expert” on the issue of attribution, but Cartwright’s opinion was lacking important foundational facts, and there was no argument that Mr. Barnard, the plaintiff’s urologist, had erred in interpreting the epidemiologic data.  Novartis Grimsby Ltd. at 56.  The real “expert” was in the data, and there was no showing (at least in the published opinion) that the clinician, Mr. Barnard, misunderstood or distorted the epidemiologic data.  In this respect, the Novartis Grimsby case is very different from the Milward case, in which a plaintiff’s toxicologist mistreated, misanalyzed, and misrepresented epidemiologic studies on benzene.

Lady Justice Smith rejected the appellant’s criticism of the trial judge’s weighting Mr. Barnard’s opinion over Professor Cartwright’s:

“The proposition that a clinician is not capable of fully understanding the published epidemiological literature on the causation of a condition within his own specialty seems unsustainable and would, I think, surprise many clinicians and epidemiologists. In my view, it was clear from his detailed reports on causation that Mr. Barnard was familiar with the published work and he was also able to discuss it intelligently when giving evidence. The Recorder was plainly of that view. As for the suggestion that Mr. Barnard was too ready to assume that working for the appellant created an increased risk, this was a good ‘jury point’ but, if it did not appeal to the Recorder, that was an end to it.”

Novartis Grimsby Ltd. at 57.

Although Ms. McIvor is correct to be concerned with the court’s eager over-generalization about the ability of clinicians to understanding of epidemiologic studies, there was little suggestion that Mr. Barnard had tripped up, and there was a good deal to suggest that Professor Cartwright’s opinion was lacking on essential issues.  Admittedly, this impression may have been created by selective reporting by the Court of Appeal.  I have not seen the record or the briefs, but Ms. McIvor has not cited anything from those sources.

Mr. Barnard, the plaintiff’s urologist, further testified that the “occupational exposure had more than doubled the risk due to smoking.”  Novartis Grimsby Ltd. at 53.  The Court of Appeal thus found it easy to affirm the verdict that Cookson had shown that his workplace exposure was the “but for” cause of his cancer.  Of course, the Court of Appeal here accepted evidence of risk and relative risk as showing causation, a dubious proposition. Novartis Grimsby Ltd. at 67. And the Court of Appeal, distinguishing a pneumoconiosis case, further pronounced that the bladder cancer injury was “indivisible,” and thus not capable of an apportionment because neither exposure could be said to make the disease more severe.  The Court could have said, if it yielded to its own risk as causation rationale, that both exposures made the cancer more likely, and the occupational exposure contributed to this overall risk three times as much as the plaintiff’s smoking.  In Justice Lady Smith’s words:

“The natural inference to draw from the finding of fact that the occupational exposure was 70% of the total is that, if it had not been for the occupational exposure, the respondent would not have developed bladder cancer. In terms of risk, if occupational exposure more than doubles the risk due to smoking, it must, as a matter of logic, be probable that the disease was caused by the former.”

Novartis Grimsby Ltd. at 74.

The Court of Appeal’s opinion was thus consistent with its own commitment to the conflation of risk with causation, a conflation that may well be objectionable, but does not seem to be the basis for Ms. McIvor’s objections to the Novartis decision.  Of course, a remand with directions to apportion would have a perfectly logical and consistent result with the insistence that risk be substituted for causation in supporting the verdict below.

Publications of Professor Cartwright on Bladder Cancer from National Library of Medicine Database

1: Subramonian K, Cartwright RA, Harnden P, Harrison SC. Bladder cancer in patients with spinal cord injuries. BJU Int. 2004 Apr;93(6):739-43. PubMed PMID: 15049983.

2: Cartwright RA. Bladder cancer screening in the United Kingdom. J Occup Med. 1990 Sep;32(9):878-80. PubMed PMID: 2074512.

3: Cuzick J, Babiker A, De Stavola BL, McCance D, Cartwright R, Glashan RW. Palmar keratoses in family members of individuals with bladder cancer. J Clin Epidemiol. 1990;43(12):1421-6. PubMed PMID: 2147716.

4: Philip PA, Fitzgerald DL, Cartwright RA, Peake MD, Rogers HJ. Polymorphic N-acetylation capacity in lung cancer. Carcinogenesis. 1988 Mar;9(3):491-3. PubMed PMID: 3345587.

5: Cartwright RA. Screening workers exposed to suspect bladder carcinogens. J Occup Med. 1986 Oct;28(10):1017-9. PubMed PMID: 3772536.

6: Boyko RW, Cartwright RA, Glashan RW. Bladder cancer in dye manufacturing workers. J Occup Med. 1985 Nov;27(11):799-803. PubMed PMID: 4067684.

7: Cartwright RA, Philip PA, Rogers HJ, Glashan RW. Genetically determined debrisoquine oxidation capacity in bladder cancer. Carcinogenesis. 1984 Sep;5(9):1191-2. PubMed PMID: 6467507.

8: Cartwright RA, Glashan RW. Palmar keratoses and bladder cancer. Lancet. 1984 Mar 10;1(8376):563. PubMed PMID: 6142276.

9: Cartwright RA, Adib R, Appleyard I, Glashan RW, Gray B, Hamilton-Stewart PA, Robinson M, Barham-Hall D. Cigarette smoking and bladder cancer: an epidemiological inquiry in West Yorkshire. J Epidemiol Community Health. 1983

Dec;37(4):256-63. PubMed PMID: 6655413; PubMed Central PMCID: PMC1052920.

10: Cartwright RA, Adib R, Appleyard I, Glashan RW, Richards B, Robinson MR, Sunderland E, Barham-Hall D. ABO, MNSs and rhesus blood groups in bladder cancer. Br J Urol. 1983 Aug;55(4):377-81. PubMed PMID: 6411162.

11: Cartwright RA, Adib R, Appleyard I, Coxon JG, Glashan RW, Richards B, Robinson MR, Sunderland E, Barham-Hall D. Ten genetic polymorphisms in bladder cancer. J Med Genet. 1983 Apr;20(2):112-6. PubMed PMID: 6221102; PubMed Central PMCID: PMC1049011.

12: Cartwright RA. Historical and modern epidemiological studies on populations exposed to N-substituted aryl compounds. Environ Health Perspect. 1983 Mar;49:13-9. PubMed PMID: 6339220; PubMed Central PMCID: PMC1569142.

13: Cartwright RA, Robinson MR, Glashan RW, Gray BK, Hamilton-Stewart P, Cartwright SC, Barham-Hall D. Does the use of stained maggots present a risk of bladder cancer to coarse fishermen? Carcinogenesis. 1983;4(1):111-3. PubMed PMID: 6821882.

14: Cartwright RA, Glashan RW, Rogers HJ, Ahmad RA, Barham-Hall D, Higgins E, Kahn MA. Role of N-acetyltransferase phenotypes in bladder carcinogenesis: a pharmacogenetic epidemiological approach to bladder cancer. Lancet. 1982 Oct 16;2(8303):842-5. PubMed PMID: 6126711.

15: Garner RC, Mould AJ, Lindsay-Smith V, Cartwright RA, Richards B. Mutagenic urine from bladder cancer patients. Lancet. 1982 Aug 14;2(8294):389. PubMed PMID: 6124790.

16: Cartwright R. Occupational bladder cancer and cigarette smoking in West Yorkshire. Scand J Work Environ Health. 1982;8 Suppl 1:79-82. PubMed PMID: 7100861.

17: Glashan RW, Cartwright RA. Occupational bladder cancer and cigarette smoking  in West Yorkshire. Br J Urol. 1981 Dec;53(6):602-4. PubMed PMID: 7317749.

18: Cartwright RA, Gadian T, Garland JB, Bernard SM. The influence of malignant cell cytology screening on the survival of industrial bladder cancer cases. J Epidemiol Community Health. 1981 Mar;35(1):35-8. PubMed PMID: 7264531; PubMed Central PMCID: PMC1052117.

19: Cartwright RA, Adib R, Glashan R, Gray BK. The epidemiology of bladder cancer in West Yorkshire. A preliminary report on non-occupational aetiologies. Carcinogenesis. 1981;2(4):343-7. PubMed PMID: 7273315.

20: Cartwright RA, Glashan RW, Gray B. Survival of transitional cell carcinoma cases in 2 Yorkshire centres. Br J Urol. 1980 Dec;52(6):497-9. PubMed PMID: 7459578.

21: Cartwright RA, Bernard SM, Glashan RW, Gray BK. Bladder cancer amongst dye users. Lancet. 1979 Nov 17;2(8151):1073-4. PubMed PMID: 91807.

22: Cartwright RA. Genetic association with bladder cancer. Br Med J. 1979 Sep 29;2(6193):798. PubMed PMID: 519209; PubMed Central PMCID: PMC1596415.

23: Williams DR, Cartwright RA. The esterase D polymorphism in patients with diabetes or carcinoma of the bladder and a matched sample of non-dono. Ann Hum Biol. 1978 May;5(3):281-4. PubMed PMID: 686669.

[1] α-naphthylamine, some of which was contaminated with β-napthylamine, benzidine, dianisidine and o-tolidine

[2] There was a suggestion that the plaintiff’s urologist had invoked his clinical experience in treating men from the factory with bladder cancer, but the courts did not seem to give dispositive weight to this irrelevant argument for causation. Novartis Grimsby Ltd. at 56.

Posted in Causation, Rule 702, Scientific Evidence | Comments Off on Do English Judges Diss Epidemiology?

Woodside & Davis on the Bradford Hill Considerations

August 23rd, 2013

Dr. Frank Woodside and Allison Davis have published an article on the so-called Bradford Hill criteria.  Frank C. Woodside, III & Allison G. Davis, “The Bradford Hill Criteria: The Forgotten Predicate,” 35 Thomas Jefferson L. Rev. 103 (2013).

Their short paper may be of interest to Rule 702 geeks, and students of how the law parses causal factors in litigation.

The authors argue that a “predicate” to applying the Hill criteria consists of:

  • ascertaining a clear-cut association,
  • determining the studies establishing the association are valid, and
  • satisfying the Daubert [1][sic] requirements.

Id. at 107.  Parties contending for a causal association often try to flyblow the need for statistical significance at any level, and argue that Bradford Hill did not insist upon statistical testing.  Woodside and Davis remind us that Bradford Hill was quite firm in insisting upon the need to rule out random variability as an explanation for an association:

“Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance.”

Id. at 105; see Hill, Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295 (1965).  The authors correctly note that the need for study validity is fairly implied by Bradford Hill’s casual expression about “perfectly clear-cut.”

Woodside and Davis appear to acquiesce in the plaintiffs’ tortured interpretation of Bradford Hill’s speech, on which statistical significance supposedly is unimportant.  Woodside & Davis at 105 & n.7 (suggesting that Bradford Hill “seemingly negates the second [the requirement of statistical significance] when he discounts the value of significance testing, citing Bradford Hill at 299).

Woodside and Davis, however, miss the heavy emphasis that Bradford Hill actually placed upon “tests of significance”:

“No formal tests of significance can answer those questions. Such tests can, and should, remind us of the effects that the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that they contribute nothing to the ‘proof’ of our hypothesis.”

Bradford Hill at 299.  Bradford Hill never says that statistical tests contribute nothing to proving an hypothesis; rather, his emphasis is on the insufficiency of statistical tests alone to establish causality.  Bradford Hill’s “beyond that” language clearly stakes out the preliminary, but necessary importance of ruling out the play of chance before proceeding to consider the causal factors.

Passing beyond their exegetical fumble, Woodside and Davis proceed to discuss the individual Bradford Hill considerations and how they have fared in the crucible of Rule 702.  Their discussion may be helpful to lawyers who want to track the individual considerations, and how they have treated, or dismissed, by trial courts charged with gatekeeping expert witness opinion testimony.

There is another serious problem in the Woodside and Davis paper.  The authors describe risk ratios and the notion of “confidence intervals”:

“A confidence interval provides both the relative risk found in the study and a range (interval) within which the risk would likely fall if the study were repeated numerous times.32 … As such, risk measures used in conjunction with confidence intervals are critical in establishing a perfectly clear-cut association when it comes to examining the results of a single study.35”

Woodside & Davis at 110.  The authors cite to the Reference Manual on Scientific Evidence (3d 2011), but they fail to catch important nuances of the definition of a confidence interval.  The obtained interval from a given study is not the interval within which the “risk would likely fall if the study were repeated… .”  Rather it is 95% of the many intervals, from the many repeated studies done on the same population, with the same sample size, which would capture the true risk.  As for the obtained interval, the true risk is either within it, or not, and no probability value attaches to the likelihood that the true value lies within the obtained interval.

It is a mystery why lawyers would bother to define something like the confidence interval, and then do it incorrectly.  Here is how Professors Finkelstein and Levin define the confidence interval in their textbook on statistics:

“A confidence interval for a population proportion P is a range of values around the proportion observed in a sample with the property that no value in the interval would be considered unacceptable as a possible value for P in light of the sample data.”

Michael Finkelstein & Bruce Levin, Statistics for Lawyers 166-67 (2d ed. 2001).   This text explains why and where Woodside and Davis went astray:

“It is the confidence limits PL and PU that are random variables based on the sample data. Thus, a confidence interval (PL, PU) is a random interval, which may or may not contain the population parameter P. The term “confidence” derives from the fundamental property that, whatever the true value of P, the 95% confidence interval will contain P within its limits 95% of the time, or with 95% probability. This statement is made only with reference to the general property of confidence intervals and not to a probabilistic evaluation of its truth in any particular instance with realized values of PL and PU.”

Id. at 167-71.

[1] Surely the time has come to stop referring to the Daubert factors and acknowledge that the Daubert case was just one small step in the maturation of evidence law.  The maturation consisted of three additional Supreme Court cases, many lower court cases, and a statutory revision to Federal Rule of Evidence 702, in 2000.  The Daubert factors hardly give due consideration to the depth and breadth of the law in this area.

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EPA Research on Ultrafine Particulate Matter

June 26th, 2013

White Hat Bias

Hyping environmental and so-called toxic risk has gone on so long that many Americans have no sense of the truth when it comes to the causal consequences of personal, occupational, and environmental exposures.  Recently, I listened to a lecture given by Judge Calibresi of the Second Circuit.  In the course of talking about regulatory prohibitions and tort-law incentives, he told of his visit to the late Professor Bickel, who had then just been diagnosed with brain cancer.  In his lecture, Judge Calibresi stated that he knew that Bickel’s brain cancer was caused by his smoking, and went on to muse whether banning smoking would have saved his friend’s life.  Judge Calibresi’s ruminations upon the nature of regulation and tort law were profound; his cursory hipshot about what caused his friend’s terminal illness, juvenile.

Some years ago, a science journalist published an account of how dire predictions of asbestos deaths had not come to pass.  Tom Reynolds, “Asbestos-Linked Cancer Rates Up Less Than Predicted,” 84 J. Nat’l Cancer Instit. 560 (1992)

Reynolds quoted one scientist as saying that:

“the government’s exaggeration of the asbestos danger reflects a 1970s’ Zeitgeist that developed partly in response to revelations of industry misdeeds.  ‘It was sort of the “in” thing to exaggerate … [because] that would be good for the environmental movement’….  ‘At the time it looked like you were wearing a white hat if you made these wild estimates. But I wasn’t sure whoever did that was doing all that much good.”

Id. at 562.  Reynolds’ quote captures the nature of “white-hat” bias, a form of political correctness applied to issues that really depend upon scientific method and data for their resolution.  Perhaps the temptation to overstate the evidence against a toxic substance is unavoidable, but it diminishes the authority and credibility of regulators entrusted with promulgating and enforcing protective measures.

White-Hat Bias & Black-Hat Ethics

I recently came across a disturbing article in the Environmental Health Perspectives, a peer-reviewed journal, supported by the National Institute of Environmental Health Sciences, National Institutes of Health, United States Department of Health and Human Services.  The article detailed a case report of an individual woman experimentally exposed to ultrafine particulate matter (PM 2.5) in a test chamber.  Andrew J. Ghio, Maryann Bassett, Tracey Montilla, Eugene H. Chung, Candice B. Smith, Wayne E. Cascio, and Martha Sue Carraway, “Case Report: Supraventricular Arrhythmia after Exposure to Concentrated Ambient Air Pollution Particles,” 120 Envt’l Health Perspect. 2275 (2012) [Ghio article].  There were no controls.

The point of the case report was that a person exposed to PM 2.5, experimentally, experienced a “cardiac event,” (atrial fibrillation or AFib) which resolved after cessation of exposure.  The experiment was conducted in a federal agency facility, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, North Carolina.

The authors stated that the experiment had the approval of the University of North Carolina School of Medicine Committee on the Protection of the Rights of Human Subjects. Given that the EPA has made extraordinary claims about the harmfulness of PM 2.5, including heart disease, lung disease, and cancers, and that there was no imaginable benefit to the subject from participating in the experiment, this experiment seemed dubious indeed.  The narrative of the case report, however, reveals even more disturbing information about the potential improprieties of the human experiment.

The PM Chamber

The human guinea pig was 58 years old.  Her age is significant. Although the authors claim that AFib is uncommon among those under 60, it does increase with age.  The human subject in the published experiment was close to the age at which AFib is no longer uncommon, and she was unwell to begin with.

The case report notes that the human subject had previously participated in the same exposure “protocol” without “complications.”  The report does not explain why this human subject was returning to the EPA center for being placed in a “chamber,” and being exposed sequentially to “filtered air and concentrated ambient particles (CAPs).” The implied suggestion is that she was a likely candidate to experience a “cardiac event” eventually from repeated exposures in the PM 2.5 chamber.

The “Subject”

The human subject was not well.  Although she was asymptomatic on the day of the experimental exposure to CAPs, she had a history of osteoarthritis and hypertension.  The latter condition was being treated with an angiotensin-converting enzyme inhibitor and a diuretic (10 mg. lisinopril and 12.5 mg. hydrochlorothiazide).  The subject had had surgeries for hernia repair, cholecystectomy, and knee arthroplasty. She was a little over 5 feet 6 inches tall, and obese, weighing over 230 pounds, with a 45 inch waist.

In addition to her chronic hypertension, morbid obesity, and musculoskeletal disease, the subject also had a family and personal history of heart disease.  Her father had died from a myocardial infarction, at the age of 57.  Immediately before the experimental exposure, a Holter monitor showed evidence of increased supraventricular ectopy, with 157 ± 34 premature atrial contractions/hour.

The investigators do not tell us how the experimental exposure relates to typical urban exposures, or to EPA regulatory standards, guidelines, or recommendations.  About 23 minutes after exposure to CAPs started (filter weight, 112 μg/m3; particle number, 563,912/cc), the human subject developed a “nonsustained atrial fibrillation that quickly organized into atrial flutter.”  The woman remained asymptomatic, and her EKG showed that she spontaneously reverted to a normal sinus rhythm.

The investigators acknowledge that there are many risk factors for AFib, and that the subject had several of them: hypertension, obesity, and possibly family history.  The woman had a history of premature atrial contractions, which may have increased her risk for AFib.

Despite this rich clinical background, the authors claim, without apparently trying very hard, that there was no “obvious” explanation for the subject’s arrhythmia while in the chamber.  They argue, however, that the exposure to PM 2.5 was causal because the arrhythmia began in the chamber, and resolved when the subject was removed from exposure.  The argument is rather weak considering that the subject may have been stressed by the mere fact of placement in a chamber, or being wired up to monitors.  See, e.g., Luana Colloca, MD, PhD, and Damien Finniss, MSc Med., “Nocebo Effects, Patient-Clinician Communication, and Therapeutic Outcomes,” 307 J. Am. Med. Ass’n 567, 567 (2012). The authors of the PM 2.5 case report acknowledge that “coincident atrial fibrillation cannot be excluded,” but they fail to deal with the potentially transient nature of AFib.

Human experimentation requires a strong rationale in terms of helping the experimental participant.  What was the rationale for this human experiment?  Here is what the EPA investigators posit:

“Although epidemiologic data strongly support a relationship between exposure to air pollutants and cardiovascular disease, this methodology does not permit a description of the clinical presentation in an individual case. To our knowledge, this is the first case report of cardiovascular disease after exposure to elevated concentrations of any air pollutant.”

Ghio at 275. The authors seemed to be saying that we know that PM 2.5 causes cardiovascular disease, but we wanted to be able to describe a person in the throes of a cardiovascular event brought on by exposure. See also Andrew J. Ghio, Jon R. Sobus, Joachim D. Pleil, Michael C. Madden, “Controlled human exposures to diesel exhaust,” 142 Swiss Med. Weekly w13597 (2012).

The Whole Truth

The Ghio article mentions only the one woman who experienced the mild, transient AFib.  A reader might wonder whether she was the only test subject.  Why was she retested after a previously incident-free experience in the chamber? How many other people were subjected to this protocol?

What is remarkable is that the authors claim not only an “association,” but causality, in a totally uncontrolled experiment, and without ruling out chance, bias, or confounding.  The article is both deficient in scientific methodological rigor, and dubious on ethical principles.

EPA – Hoisted With Its Own Petard

What I did not realize when I read this experimental case report is that the article had been a cause célèbre of the anti-regulatory right.  The EPA had walked right onto an ethical landmine by first sponsoring this research, and then by relying upon it to support a regulatory report. Steven Milloy editorialized about the EPA research, followed by a FOIA investigation. In September 2012, a regulatory watchdog group filed a lawsuit to strike an EPA report, which was based in part upon the questionable research.

Milloy’s strategy was designed to impale the EPA on the horns of a dilemma:

“I accused EPA of either: (1) conducting unethical human experimentation or exaggerating the dangers of fine airborne particulate matter (PM2.5). It must be one or the other; it can’t be neither, according to EPA’s own documents.”

Steven Milloy, “Did Obama’s EPA relaunch Tuskegee experiments?” (April 24, 2012).  The EPA had branded diesel particulate, which was used in the experiments, as “carcinogenic” and “lethal,” even from short exposures.  Accordingly, if the EPA were sincere, it should have never conducted the experiment documented in Environmental Health Perspectives.  If the agency believed that PM 2.5 was innocuous, then it unethically exaggerated and overstated its dangers.

In course of his FOIA initiative, Milloy did obtain answers to some of the questions I had from reading the Ghio article.  There were apparently about 40 human subjects, who were subjected to PM 2.5 exposure in chambers fed by diesel exhaust or other sources.  The exposure levels were upwards of 20 times what the EPA labeled a “permissible” level.  Of course, the EPA is positionally committed to a “linear, no-threshold” model of carcinogenesis, which makes any exposure to a substance it “knows” to cause cancer ethically improper.

The information from the FOIA requests puts the Ghio article in an extremely bad light.  The human subject on whom the authors reported had run about 40 other people through their chamber without ill effect, but failed to mention these cases.  The consent forms and IRB documents show that the investigators were specifically interested in “vulnerable” patients, who had diabetes, asthma, etc.  The fair inference is that the investigators wanted to provoke an anecdote that would support their causal narrative, which they believed had already been established with epidemiologic evidence.  This seems like a scientific hat trick: bad science, bad ethics, and bad publication practice.

The lawsuit did not fare well.  Predictably, it foundered on the lack of final agency action, and the lack of standing.  On January 31, 2013, Judge Anthony J. Trenga dismissed the complaint, after having previously denied a temporary restraining order.  The American Tradition Institute Environmental Law Center v. U.S. EPA, Case 1:12-cv-01066-AJT-TCB (E.D. Va. 2013).  While legally correct, the opinion is blandly devoid of any sense of ethical concern.

From a brief search, there does not appear to be an appeal to the Fourth Circuit in the works.  Of course, there were no personal injuries alleged in the ATI lawsuit, and the human subject in the Ghio article has appeared not to have sued.  Despite the lack of legal recourse, the science “right” is up in arms over EPA duplicity.  In a recent publication, Milloy and a co-author, quote former EPA Administrator Lisa Jackson, at a congressional hearing:

“Particulate matter causes premature death. It’s directly causal to dying sooner than you should.”

When Representative, now Senator, Edward J. Markey asked, “How would you compare [the benefits of reducing airborne PM2.5] to the fight against cancer?” Jackson answered hyperbolically:

“If we could reduce particulate matter to healthy levels, it would have the same impact as finding a cure for cancer in our country.”

Steve Milloy & John Dale Dunn, “Environmental Protection Agency’s Air Pollution Research: Unethical and Illegal?” 17 J. Am. Phys. & Surg. 109 (2012) (quoting Jackson).  The FOIA and other background materials from this EPA posturing can be found on one of Milloy’s websites.

Sadly, I found the answers raised by the Ghio article only because of the anti-regulatory activism of Milloy and the American Tradition Institute.  The white-hat bias remains a potent force in regulatory agencies, and in scientific laboratories.

Posted in Causation, Scientific Misconduct, Underlying Data | Comments Off on EPA Research on Ultrafine Particulate Matter

Sympathy for the Diablo — Peppermint Barry vs Spicy Seafood Pasta

June 12th, 2013

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

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

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

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

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

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

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

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

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

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

The Material Safety Data Sheet Ploy

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

The Treating Physician Echo

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

Pasta and Peppermints

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

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

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

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

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

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Sympathy for the Diablo — Peppermint Barry vs Spicy Seafood Pasta

The Mt. Sinai Catechism

June 7th, 2013

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

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

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

Id. at 481.

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

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

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

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

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

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

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

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

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

“Rationale

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

Objectives

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

Methods

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

Measurements and Main Results

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

Conclusions

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

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

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

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

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

Posted in Causation, Conflicts of Interest, Expert Witnesses, Scientific Evidence | Comments Off on The Mt. Sinai Catechism

The Doubling Dose

June 5th, 2013

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

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

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

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

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

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

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

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

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

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

 

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Landrigan v. The Celotex Corporation, Revisited

June 4th, 2013

Old-fashioned torts presented few problems for attributing causation of the plaintiff’s harm.  Summers v. Tice, 33 Cal.2d 80, 199 P.2d 1 (1948), may have involved uncertainty about the shooter, but there was no doubt that a pellet from one of the two defendants’ guns hit the plaintiff and caused a legally recognized injury.

Specific causation has been, and remains, the soft underbelly of the toxic tort world, at least for those cases not involving so-called signature diseases.  A priori assessments of risk do not necessarily translate into post-exposure, post-diagnosis attributions of outcome to exposure.  Put simply, risk is not cause. Guinn v AstraZeneca Pharms. LP, 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.”) Unless there is a “fingerprint of causation,” what scientists would call a completely specific biomarker, then specific causation opinions are mostly guesswork.

Tobacco companies and others exploited this fact, in face of large relative risks of lung cancer among smokers, to maintain that these epidemiologic assessment were not probative of specific causation.  Andrew See, “Use of Human Epidemiology Studies in Proving Causation,” 67 Def. Couns. J. 478, 478 (2000) (“Epidemiology studies are relevant only to the issue of general causation and cannot establish whether an exposure or factor caused disease or injury in a specific individual.”); Melissa Moore Thomson, Causal Inference in Epidemiology: Implications for Toxic Tort Litigation, 71 N.C. L. Rev. 247, 255 (1992) (“statistic-based epidemiological study results should not be applied directly to establish the likelihood of causation in an individual plaintiff”); Michael Dore, Commentary on the Use of Epidemiological Evidence in Demonstrating Cause-in-Fact, 7 Harv. Envt’l L. Rev. 429, 433 (1983) (“Epidemiological evidence, like other generalized evidence, deals with categories of occurrences rather than particular individual occurrences. . . . Such evidence may help demonstrate that a particular event occurred, but only when accompanied by more specific evidence.”).  See, e.g., In re Fibreboard Corp.,893 F.2d 706, 712 (5th Cir.1990) (“It is evident that these statistical estimates deal only with general causation, for population-based probability estimates do not speak to a probability of causation in any one case; the estimate of relative risk is a property of the studied population, not of an individual’s case.” (emphasis in original; internal quotation omitted)).

Indeed, some courts continue to uphold this extreme anti-probabilistic view, even when relative risks exceed 20, or more.  McTear v. Imperial Tobacco Ltd., [2005] CSOH 69, at ¶ 6.180 (Nimmo Smith, L.J.) (“epidemiological evidence cannot be used to make statements about individual causation… . Epidemiology cannot provide information on the likelihood that an exposure produced an individual’s condition. The population attributable risk is a measure for populations only and does not imply a likelihood of disease occurrence within an individual, contingent upon that individual’s exposure.

In past posts, I have addressed some misunderstandings and misrepresentations concerning the use of a priori risk to assessment of specific causation.  One of the more glaring examples of bad scholarship in this area comes in a text edited by Professor Joseph Gastwirth:

“The court in Landrigan v. Celotex Corp. (1992: 1087) arrived at a similar conclusion, finding that:

a relative risk of 2.0 is not so much a password to a finding of causation as one piece of evidence, among others, for the court to consider in determining whether the expert has employed a sound methodology in reaching his or her conclusion.”

Accordingly the court granted recovery for injuries alleged to have arisen as the result of exposure to asbestos, although the demonstrated relative risk was 1.5.

Sana Loue, “Epidemiological Causation in the Legal Context: Substance and Procedures,” in Joseph Gastwirth, ed., Statistical Science in the Courtroom 263, 277 (2000).

Now that is stunningly bad scholarship, from someone who is both a lawyer and a scientist. The New Jersey Supreme Court, in the cited case, reversed a directed verdict for the defendants, and remanded for reconsideration of the admissibility of the plaintiffs’ expert witnesses.  There was never even an opportunity for the Supreme Court to “grant recoveries.”  Indeed, Mrs. Landrigan never obtained a favorable verdict in her lawsuit.  After remand, she dismissed her action in the face of the daunting task faced by her expert witnesses.

The author of the chapter, Sana Loue, is a Professor and Director in the Department of Epidemiology and Biostatistics in the School of Medicine of Case Western Reserve University, Cleveland, Ohio. Dr. Loue holds doctoral degrees in epidemiology and medical anthropology, as well as a law degree.

Dr. Loue is not alone in misunderstanding the Landrigan case. Some of the confusion perhaps results from the New Jersey Supreme Court’s errant opinion.  Some language in the Supreme Court’s decision makes it seem that there was an objection to the admissibility of the plaintiff’s expert witnesses’ opinions.  There was none.  Unlike many gatekeeping decisions, the plaintiff had a full opportunity to be heard; the defendants moved for a directed verdict at the end of the plaintiff’s case.  In addressing the defendants’ motion, the trial court assumed, for the sake of argument, that asbestos can cause colorectal cancer.  General causation was, of course, contested, but the motion turned on whether there was evidence in the record that would support specific causation.  The trial court held that specific causation required expert witness opinion testimony, but that the testimony in the case failed to provide a basis on which a reasonable jury could conclude that Mr. Landrigan’s colorectal cancer was caused by his alleged occupational asbestos exposure.

The New Jersey Appellate Division affirmed in a published opinion.  579 A.2d 1268 (1990).  The Appellate Division’s decision is still worth reading, not only because it correctly decided the issues, but because it reports material facts that the Supreme Court chose to ignore.  First, the Appellate Division noted that the most that Mr. Landrigan had sustained in terms of respiratory effects from his occupational asbestos exposure was pleural thickening, which never caused him impairment in his lifetime.  Indeed, Mr. Landrigan never was aware of this radiographic change, which only an expert witness hired by plaintiff’s counsel could see.  Id. at 1269.  (Plaintiff’ pulmonary physician expert witness, Dr. Sokolowski, had failed his B-reader examination, but he was a favorite of the asbestos plaintiffs’ bar for his “liberal” readings of chest films.)

The Appellate Division also emphasized the record evidence that the cause of most cases of colon cancer was (and remains) unknown, and more important that Mr. Landrigan’s colorectal cancer was physically indistinguishable from almost all other cases of the disease.  Id. at 1270.  The plaintiff’s hired expert witnesses had only epidemiologic evidence of an increased risk of colorectal cancer among asbestos-exposed workers. Although most of the better conducted studies fail to support the claim of increased risk, Drs. Sokolowski and Wagoner, the plaintiff’s witnesses, relied upon Selikoff’s cohort study of insulation workers, and its mortality risk ratios.  Irving J. Selikoff, E. Cuyler Hammond, and Herbert Seidman, “Mortality Experience of Insulation Workers in the United States and Canada, 1943-1976,” 330 Ann. N.Y. Acad. Sci. 91, 103 (1979) (colorectal cancer risk ratio 1.55);  E. Cuyler Hammond, Irving J. Selikoff,  and Herbert Seidman, “Asbestos Exposure, Cigarette Smoking and Death Rates,” 330 Ann. N.Y. Acad. Sci. 473, 480 (1979) (colorectal cancer mortality ratios 1.59 to 1.81).

Mrs. Landrigan’s witnesses both relied upon evidence of an increased risk, while ignoring or dismissing studies that found no such risk, and upon what they claimed was an absence of risk factors, such as fatty diet, excessive alcohol consumption, family history, and prior bowel disease, in Mr. Landrigan.  The trial court, and the Appellate Division, realized that the reasoning that these witnesses advanced failed to support their conclusions, as a matter of science, logic, and law:

“Although not stated by Dr. Sokolowski in so many words, he seems to be saying that risk exposure equates with causation, a proposition which we find legally untenable.”

579 A.2d at 1270 (1990).  The hand waving about ruling out known risk factors left the most likely cause in plain view:  unknown:

“One cannot rule out the presence of other risk factors without knowing what those factors may be.”

Id. at 1271.

The New Jersey Supreme Court reversed and remanded the case for further inquiries into the reliability of the expert witnesses’ opinions.  Landrigan v. The Celotex Corp., 127 N.J. 404, 605 A.2d 1079 (1992).  Therese Keeley, the capable lawyer who tried the Landrigan case for the defense, had argued the appeal before the Appellate Division, but another lawyer, less familiar with the issues, argued for the defendant, in the Supreme Court.  The Supreme Court made much of the new lawyer’s concessions in oral argument:

“Defense counsel urges that the Appellate Division opinion may be read as requiring that an expert may not rely on an epidemiological study to support a finding of individual causation unless the relative risk is greater than 2.0. See 243 N.J.Super. at 457-59, 579 A.2d 1268. At oral argument before us, they agreed that such a requirement may be unnecessary. Counsel acknowledged that under certain circumstances a study with a relative risk of less than 2.0 could support a finding of specific causation. Those circumstances would include, for example, individual clinical data, such as asbestos in or near the tumor or a documented history of extensive asbestos exposure. So viewed, a relative risk of 2.0 is not so much a password to a finding of causation as one piece of evidence, among others, for the court to consider in determining whether the expert has employed a sound methodology in reaching his or her conclusion.”

Id. at 419.  Even so, these concessions, improvident as they might have been, would not permit the Supreme Court to resolve the case as it did.  There was nothing in the Landrigan case, however, which would count as a biomarker of individual causation, or as support for a claim that Mr. Landrigan’s exposure was so much heavier than average that his personal exposure put him on the dose-response curve at a point that corresponded to a relative risk greater than two.

Here is how the Supreme Court described Dr. Sokolowski’s attempted reasoning process:

“In the present case, Dr. Sokolowski began by reviewing the scientific literature to establish both the ability of asbestos to cause colon cancer and the magnitude of the risk that it would cause that result. Next, he assumed that decedent was exposed to asbestos and that his exposure, in both intensity and duration, was comparable to that of the study populations described in the literature. He then assumed that other known risk factors for colon cancer did not apply to decedent. After considering decedent’s exposure and the absence of those factors, Dr. Sokolowski concluded that decedent’s exposure more likely than not had been the cause of his colon cancer.”

Id. at 420-21, 1087-88.  The obvious fly in the ointment is simply that many people with no known risk factors for colon cancer develop the disease.  The assumption behind a cohort study is that all the risk factors are even balanced between the exposed and the unexposed cohorts, and so the relative risk reflects the role of the exposure in question.  Of course, this assumption is rarely true outside the context of a randomized clinical trial, and the Selikoff studies relied upon by plaintiff’s witnesses were particularly inept in controlling or accounting for confounding factors.  Assuming, however, that both the exposed and unexposed groups had the same proportion of men without “known” risk factors, then the most Sokolowski and Wagoner could say was that Mr. Landrigan’s risk of colorectal cancer had been increased by 55% or so, above that of the risk for men similarly situated but lacking occupational asbestos exposure.  This 55% increase was the basis for the Court’s observation that the attributable risk was about 35%.  What the Court left for another day was how, if at all, this evidentiary display could support a conclusion of specific causation.  The trial and intermediate appellate courts saw clearly that Sokolowski and Wagoner had utterly failed to support their specific causation opinions, but the Supreme Court was intent upon giving them another bite at the apple:

“Without limiting the trial court on remand, its assessment of Dr. Sokolowski’s testimony should include an evaluation of the validity both of the studies on which he relied and of his assumption that the decedent’s asbestos exposure was like that of the members of the study populations. The court should also verify Dr.  Sokolowski’s assumption concerning the absence of other risk factors. Finally, the court should ascertain if the relevant scientific community accepts the process by which Dr. Sokolowski reasoned to the conclusion that the decedent’s asbestos exposure had caused his cancer.”

Id. at 420, 1088.  The Court thus did not give plaintiff’s expert witnesses a free pass for trial number two.  When faced with the prospect of having to show that Sokolowski’s and Wagoner’s ipse dixit were reaccepted by the relevant scientific community, the plaintiff dismissed her case.

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Landrigan v. The Celotex Corporation, Revisited

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