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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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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.

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Daubert Bewigged

September 11th, 2013

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.

McIvor argues that British judges have failed to engage with epidemiologic evidence, and have relegated epidemiologic evidence to a status inferior to clinical evidence, even when testifying clinicians have little to offer the fact finder.  If the be-wigged judges have done this shame on them, but McIvor suggests that a pre-trial hearing is necessary to address the proper (and improper) range of methodologies and inferences:

“The very fact that methodologically problematic evidence can end up before a trial court is indicative of the need for a pre-trial admissibility test for scientific evidence in UK civil law. Such a test would afford the court an opportunity to evaluate the scientific reliability of any epidemiological evidence that the parties wish to introduce at trial.”

McIvor at 22.  In advancing this recommendation, McIvor expands upon a recent Law Commission recommendation for what she describes as “a pre-trial admissibility test for scientific evidence in criminal litigation, similar to that which is used in the USA.”  McIvor at 32 (citing Law Commission, Expert Evidence in Criminal Proceedings in England and Wales (Law Comm’n No. 325, 2011)).

This recommendation and discussion, however, are confusing and perhaps confused.  The test in the United States is not a pre-trial test, although a party may ask for a determination in advance, either in conjunction with a motion for summary judgment, or to limit the evidentiary display at trial.   Nonetheless, objections to expert witness opinion testimony can certainly be made at trial.  Indeed, if the pre-trial motion is denied, the moving party may well have to renew its objection at trial in any event.

MacIvor’s recommendation is puzzling for other reasons.  First, most civil cases are tried to the bench, and the need to challenge the expert opinion pre-trial is certainly less pressing.  Lengthy, methodological challenges are virtually impossible before a jury but they would be made in front of the presiding judge, in any event.  Second, having recommended the pre-trial procedure, and the substantive standard for reliability and validity, McIvor proceeds to tell us that it [the Daubert standard] has “proven to be a rather controversial test in practice.”  Id. at 32 n.84 (citing no less of an authority than Carl Cranor, Toxic Torts: Science, Law and the Possibility of Justice 62-90 ( 2006)).  Cranor is hardly an unbiased, reliable source, but if McIvor accepts his pronouncements, her recommendation is hard to understand.  Third, McIvor gives us an example of a class of cases, which at first blush, suggest that judges on the other side of the Atlantic just do not understand science.  In McTear v. Imperial Tobacco, [2005] 2 SC 1, the trial judge, Lord Nimmo Smith, ruled in favor of a tobacco company in a lung cancer personal injury case.  His ruling was largely based upon a rejection of the epidemiologic evidence, which McIvor suggests is unreasonable, but then tells us that the rejection might have resulted from the plaintiffs’ reliance upon reports without the benefit of an epidemiologist to explain and teach the trial judge about the meaning of the evidence.

Indeed, McIvor tells us that Lord Nimmo Smith complained in his opinion that he had not been:

“‘sufficiently instructed by the expert evidence about this discipline’ to be able to form his own judgment of the evidence. This was not an unreasonable point, at least as regards the issue of individual causation.”

McIvor at 32 (quoting Lord Nimmo Smith).  Well, it does suggest that the good Lord may have been a stubborn Scot, who was not going to give any weight to the common wisdom, but rather insist that the plaintiff make his case in court.  Even McIvor goes on to characterize the plaintiff’s counsel’s strategy as “unwise, in hindsight.”  Id.

Rule 702 is an extremely important part of the law of evidence in federal courts, and in many state courts.  The U.K. would do well to adopt it, with allowance for the very different role of judges in civil cases on the other side of the Atlantic.

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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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THE COUNCIL FOR EDUCATION AND RESEARCH ON TOXICS

July 9th, 2013

When the Milward case hit the U.S. Court of Appeals for the First Circuit, it attracted the attentions of an amicus, the Council for Education and Research on Toxics (CERT).  I had never heard of CERT before, and the amicus brief filed by CERT was rather sketchy on the nature of the organization.

A bit of research on CERT revealed the following.  It is a non-profit California corporation, EIN: 42-1571530, founded in 2003.  CERT has a business address at:

401 E Ocean Blvd., Ste. 800, Long Beach, California 90802-4967

And a telephone number:  1-877-TOX-TORT

CERT’s mission statement? Furthering scientific understanding of toxins.

Plaintiffs’ lawyer Ralph Metzger is noted as the contact person for CERT.

Given its phone number and its contact person, one might think that its mission statement was “furthering legal positions on toxins.”

But wait; it gets better.  Ralphael Metzger, at the same Long Beach, California, address is the attorney for CERT on its amicus brief in Milward!

The potential conflicts grow deeper and wider.  Metzger has represented CERT, which shares at least his offices, if not his alter ego, in lawsuits including CERT v. Brad Berry Co., Ltd., No. BC461182 (Cal. Super. Ct., Los Angeles County, Cent. Dist., filed May 9, 2011), and CERT v. Starbucks Corp., BC435759 (L.A. Super. Ct., filed April 13, 2010).

CERT has sued McDonald’s and Burger King over its claim that their french fries contained high levels of acrylamide, a chemical “known” to the State of California to cause cancer. CERT has sued Chemtura on claims that the company’s chemical fire-preventive products, known as PBDEs, cause injuries to wildlife and humans.

Although not definitive, it seems that CERT’s mission is not exactly scientific, and the description of its interests in its Milward brief just a tad misleading.

In addition to the CERT, the other amici joining the brief include:

Nicholas A. Ashford,
Nachman Brautbar,
David C. Christiani,
Richard W. Clapp,
James Dahlgren,
Devra Lee Davis,
Malin Roy Dollinger,
Brian G. Durie,
David A. Eastmond,
Arthur L. Frank,
Frank H. Gardner,
Peter L. Greenberg,
Robert J. Harrison,
Peter F. Infante,
Philip J. Landrigan,
Barry S. Levy,
Melissa A. McDiarmid,
Myron Mehlman,
Ronald L. Melnick,
Mark Nicas,
David Ozonoff,
Stephen M. Rappaport,
David Rosner,
Allan H. Smith,
Daniel Thau Teitelbaum,
Janet Weiss, and
Luoping Zhang

An interesting bunch; eh?  Page two of the amicus brief tells us that:

“None of the amici has any financial or other similar interest in the outcome of this lawsuit. Amici appear on their own behalf to inform this Court of the substantial medical knowledge and understanding of leukemia arising from exposure to benzene.”

That’s probably true for the Milward case itself, but more interesting for what the disclosure does not say.  Many of the amici have testified frequently in toxic tort cases, and several have been excluded by the straightforward application of Rule 702 or its state counterparts.  Some have lost income as a result of judicial gatekeeping, and most have seen their advocacy science curtailed by such gatekeeping.

Appendix I to the brief provides further information on the amici, but there is no mention of their testimonial adventures, their financial stake in expert witnessing, or their political or positional commitments.

I suppose from CERT you get CERT-i-tude, a certain kind of attitude.

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Sympathy for the Diablo — Peppermint Barry vs Spicy Seafood Pasta

June 12th, 2013

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

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

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

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

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

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

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

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

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

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

The Material Safety Data Sheet Ploy

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

The Treating Physician Echo

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

Pasta and Peppermints

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

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

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

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

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

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State of the Art — Tasing in the Dark

June 11th, 2013

In American product liability litigation, there are two causation requirements:  warnings causation and factual causation.  The law imposes a duty to warn of risks, and the alleged failure to warn must have some connection with the plaintiff’s use of the product in such a way as to have caused him harm.  If an adequate warning, whatever that is, would have protected plaintiff from the harm, then there is the requisite nexus between the alleged failure to warn and plaintiff’s harm.

The product must also, however, be a factual cause of the harm.  For instance, a really scary warning that promised death and destruction might have kept the plaintiff from using the product, but still, the product itself must have caused the harm, for the plaintiff to satisfy the factual causation requirement.

The history of the last 50 years or so of American products liability law has been a narrative of unending assault on causation, both with respect to warnings causation, and to medical or factual causation.  Plaintiffs have sought to dilute, eliminate, create presumptions for, and shift the burden of proof of, both causation requirements.

The duty to warn arises, understandably, when the seller or manufacturer has knowledge that the product can cause harm, and the buyer lacks this knowledge.  For various reasons, sloppiness, ideology, or advocacy, some writers neglect the requirement that the buyer must lack the knowledge of the danger.  Quod vanum et inutile est, lex non requirit.  The law does not require what is vain and useless.  This principle of equity and law still informs the law of product liability, through doctrines and rules such as sophisticated user and sophisticated intermediary.

The duty to warn was traditionally couched in terms of a duty to impart knowledge, actual or constructive, or a connection between a foreseeable use of the product and a serious harm.  The plaintiffs’ bar’s war on causation has sought to lower the epistemic standard for both warning and factual causation.  There are too many cases to cite for the proposition that sellers must warn of potential risks as well as actually known or knowable risks.  This erosion would be harmless but for the similar erosion in standards of medical or factual causation, and the attempts to abandon meaningful standards of expert witness causation opinions.

It is thus refreshing to see the Ninth Circuit hold that California’s law of duty to warn applies to only to known or knowable risks.  Last year, the Court of Appeals held that a Taser manufacturer had no duty to warn of the risk that repeated shocks administered by its products could lead to death by inducing metabolic acidosis, given the state of the art at the time the product was manufactured. In Rosa v. Taser International, Inc., 684 F.3d 941 (9th Cir. 2012) , the Rosa’s son died after being “tased” by police officers.  The autopsy report attributed death to ventricular arrhythmia, caused by Michael Rosa’s having used methamphetamine, along with the police’s use of Tasers.  Expert witnesses postulated the mechanism of causation between tasing and death was metabolic acidosis, which consists of increased lactic acid levels, which in turn increased the risk of cardiac arrest.

The Rosas sued Taser International, Inc., the manufacturer of the “stun guns” on theories of strict liability and negligent failure to warn the purchasers, the police, of the dangers of the product.  (They did not sue the meth manufacturer or retailer.) The Rosas argued that Taser had a duty to warn of any risk, “no matter how unsubstantiated,” even if based upon speculative or conjectural statements, or inadequate studies.  Id. at 946.  The Court Appeals decisively rejected a duty to warn on this inconclusive evidentiary display.

The Ninth Circuit held that California law conditions the duty to warn on a high epistemic standard of knowledge, actual or constructive.  Id. at 946.  The manufacturer must warn of a “particular risk … known or knowable in light of the generally recognized and prevailing best scientific and medical knowledge available at the time of manufacture and distribution.” Id. (quoting from Conte v. Wyeth, Inc., 168 Cal.App.4th 89, 85 Cal.Rptr.3d 299, 310 (2008) (emphasis added by the Circuit Court).

Noting that the California courts have not articulated epistemological principles for knowledge of hazards that must find their way into warnings, the court, in Rosa, noted some accepted considerations.  First, ignorance is not a defense. ‘‘[A] manufacturer is held to the knowledge and skill of an expert in the field; it is obliged to keep abreast of any scientific discoveries and is presumed to know the results of all such advances.’’ Id. at 946 (citing Carlin v. Superior Court, 13 Cal.4th 1104, 56 Cal. Rptr.2d 162, 920 P.2d 1347, 1351 n. 3 (1996)).

Second, a manufacturer need not warn of “every report of a possible risk, no matter how speculative, conjectural, or tentative.” Id. (internal citations omitted).  A duty to warn of every possible risk would have the counter-productive result of diluting the effect of specific warnings of real risks, by “inundat[ing the public] indiscriminately with notice of any and every hint of danger.” Id.

The Rosas relied upon four peer-reviewed articles to argue that Taser had a duty to warn. Id. at 497. The Ninth Circuit looked past the fact of mere publication and peer review, to the actual nature and content of the relied-upon articles.  Some of the publications did not address stun guns, but two did, although in speculative ways.  See Raymond Fish & Leslie A. Geddes, “Effects of Stun Guns and Tasers,” 358 The Lancet 687 (2001).  The second publication was a Department of Defense report, which predated Michael Rosa’s death, but was not generally available until after his death.  John M. Kenny, et al., Human Effects Advisory Panel, Report of Findings Sticky Shocker Assessment (1999).  The court doubted whether such a report, unavailable to defendant, could be the predicate for defendant’s duty warn.  In any event, the content of the 1999 report was itself speculative, and merely concluded that  “deaths following Taser[] use may be due to acidosis.” Kenny at 31. The report did not state a causal conclusion, and it qualified its dataset as limited by small size.  Kenny at 32.

Taser added relevant warnings, six years after Michael Rosa’s death, and the Rosas sought to capitalize upon the warnings as admissions of some sort.  Id. at 948.  The Court of Appeals rebuffed this argument, not only on the basis of subsequent remedial measure, but also on the basis of “state of the art,” which requires that the evidence of the harm, which forms the basis for the duty to warn, be known or knowable at the time of marketing of the product.  Id.

In Rosa, the available evidence that might constitute “knowledge” of a harm shifted between the time of injury, and the time of litigation.  In latent disease litigation, the shift in evidence can be extreme, and hence the importance of “state of the art” as a limit to the duty to warn.

Can the evidence for a knowledge claim regress?  If what was in the medical literature at some earlier time turned out to be false later, then it would seem that it was never “knowledge” in the first place.  Still, plaintiffs would likely rely upon the older apparent knowledge to claim that it created a duty to warn.  For instance, in asbestos litigation, plaintiffs have claimed, since the late 1970s, that asbestos exposure causes gastrointestinal (GI) cancer.  The plaintiffs’ claims were supported  by Dr. Selikoff and his cadre of Mt. Sinai testifying physicians and scientists, and many textbooks and review articles stated, without qualification, that asbestos caused GI cancer.  In 2006, however, the Institutes of Medicine convened a committee to review non-pulmonary cancers and asbestos, and concluded that the studies, accumulated over 35 years since Dr. Selikoff’s ipse dixit, did not support a conclusion that asbestos causes colorectal cancer.  Institute of Medicine of the National Academies, Asbestos: Selected Health Effects (2006).  If the claim is unsupported in 2006, it was not established at times past, despite the assertions of plaintiffs and their partisan expert witnesses in litigation, and in publications.

Another example of the uneven path of knowledge is the claim that silica causes lung cancer.  Early writers suggested this hypothesis on the basis of flawed evidence, but the claim came to be rejected when astute authors realized that the lung cancer mortality experience of uranium miners was determined by their exposure to ionizing radiation, not to silica.  Starting in the 1980s, however, a group of advocate scientists started to press for recognition of silica itself as a lung carcinogen, and these scientists narrowly succeeded, by a deeply divided vote, in an IARC working group vote in 1996.  This IARC classification put crystalline silica into category I, but the rationale for this classification was soon thereafter shown to be lacking.  See Patrick A. Hessel, John F. Gamble, J. Bernard L. Gee, Graham Gibbs, Francis H.Y. Green, W. Keith C. Morgan, and Brooke T. Mossman, “Silica, Silicosis, and Lung Cancer: A Response to a Recent Working Group Report,” 42 J. Occup. Envt’l Med. 704 (2000).  A seller of crystalline silica should, under the Rosa case, be well within its rights not to warn of a risk of lung cancer.  The reality is that the litigation system is way too uncertain and even capricious, leading most companies to have warned of lung cancer “risk” from the mid-1980s, forward.

What is encouraging about Rosa is its implicit recognition that the Rule 702 factors for reliable scientific opinion are very much in play when evaluating historical scientific opinion, which is asserted to be the basis for a duty to warn.  The more typical “state of the art” decisions simply pass over validity and reliability of historical statements and conclusions, with a grand gesture that everything published serves to provide “notice” of a potential hazard.  This usual approach begs the question, however, whether there was a sound basis for a conclusion that the product was known to cause the harm alleged in the pending case.  The scientific nature of the historical determination may mean that historians, lacking in scientific credentials, will be inappropriate witnesses to support historical claims of knowledge of risks.  The Rosa court’s insistence upon historical study and conclusion validity and correctness requires a careful review of the historical epistemic claim in view of the full historical and contemporary record.

In the Rosa case itself, the claim of failure to warn failed as a result of a fair analysis of the extant evidence for the claim at the time of marketing of the Taser. The post-marketing shift in the epistemic basis for the failure-to-warn claim was irrelevant to the Rosas’ case.  Perhaps the warnings vel non on the methamphetamine used by Michael Rosa would have been a better predicate for the lawsuit?

Posted in Historian Testimony, Rule 702 | Comments Off on State of the Art — Tasing in the Dark

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

Cranor’s Defense of Milward at the CPR’s Celebration

May 12th, 2013

THE RISE OF THE UBER-EXPERT

One of the curious aspects of the First Circuit’s decision in Milward was the court’s willingness to tolerate a so-called weight of the evidence (WOE) assessment of a causal issue by toxicologist Martyn Smith, when much of the key evidence did not involve toxicology.  In defending WOE, Professor Cranor argues that scientists (such as those in an International Agency for Research on Cancer (IARC) working group) evaluate evidence from different lines of research into a single, evaluative judgment of the likelihood of causation.  The lines of evidence may involve animal toxicology, cell biology, epidemiology or other disciplines:

“In drawing conclusions from the data to a theory or explanation, it is necessary for scientists to evaluate the quality of different lines of evidence, to integrate them and to assess what conclusion the lines of evidence most likely supports and how well they do so in comparison with alternative explanations.”

See Carl F. Cranor, “Milward v. Acuity Specialty Products: Advances in General Causation Testimony in Toxic Tort Litigation,” PDF 3 Wake Forest J. L. & Policy 105, 117 (2013)[hereinafter cited as Cranor].

Presumably, the scientists will come to the table with the training, experience, and expertise appropriate to their discipline.  The curious aspect of Cranor’s defense is that Martyn Smith’s expertise did not encompass many of  the lines of research advanced, in particular, the epidemiologic.  Of course, in the real world of science, the assessment of the “lines” of evidence is conducted by scientists from the different, relevant disciplines.  In the make-believe world of courtroom science, the collaboration breaks down when a single expert witness, such as Smith, offers opinions outside his real expertise.  Because the law is not particularly demanding with respect to the extent and scope of expertise, Smith was able to hold forth not only on animal experiments, but on human epidemiologic studies.  The defense was able to show that Smith disregarded basic principles of epidemiology, but the First Circuit agreed with Cranor, that consideration of Smith’s disregard should be kicked down the road, to the jury for its consideration.

As a practical matter, in today’s world of highly specialized scientific disciplines, it is simply not possible for an expert witness to address evidence from all the fields needed to evaluate the multiple lines of evidence relevant to a causal issues.  We should rightfully be skeptical of a single expert witness who claims the ability to weigh disparate lines of evidence to synthesize a judgment of causation.  Of course, this is how science is practiced in a courtroom, not in a university.

REJECTION OF EVIDENCE HIERARCHY

Another salient feature of Cranor’s argument is his insistence that there is no hierarchy of evidence.  Cranor’s argument is ambiguous between rejecting a hierarchy of disciplines or a hierarchy within epidemiology itself .  Cranor never actually argues directly for a leveling of all types of epidemiologic studies, and as we will see, his one key citation (repeated three times) is for the hierarchy of disciplines:  epidemiology, molecular biology, genetics, pathology, and the like.

Clearly there are instances of causation determined without epidemiology.  The Henle-Koch postulates after all were developed to assess causation by infection biological organisms.  And in some instances, very suggestive evidence of viral causes of cancer has been attained before confirming epidemiologic evidence.  If there is a meaningful population attributable risk, however, epidemiology should be able to confirm the suspicions of virology or molecular biology.

Cranor repeatedly cites a meeting report of a workshop held in Washington, D.C., in 2003.  See also Michael Green, Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence 549, 564 (3d ed. 2011) (citing same meeting report).  Cranor’s citations and quotations misleadingly suggest that the report was an official function of the National Cancer Institute (NCI), and that the published report was an official pronouncement of the NCI.  Neither suggestion is true.

Cranor praises the Circuit’s Milward decision for adopting his argument and citing the meeting report for his claim that there is no hierarchy of evidence:

“Citing National Cancer Institute scientists, [the Circuit] also added that “[t]here should be no such hierarchy” of evidence for carcinogenicity as between epidemiological and some other kinds of evidence.100 These scientists and many distinguished scientific committees would not require epidemiological studies to support claims that a substance can cause adverse effects in humans or place certain other a priori constraints on evidence.101”

Cranor at 119 (citing Milward, at 17, citing Michele Carbone, et al., Modern Criteria to Establish Human Cancer Etiology, 64 Cancer Research 5518, 5522 (2004)).

Given the emphasis that Cranor places upon the Carbone article, it is worth taking a close look.  Carbone’s article was styled “Meeting Report.” See also Michelle Carbone, Jack Gruber, and May Wong, “Modern criteria to establish human cancer etiology,” 14 Semin. Cancer Biol. 397 (2004).  The article was a report of a workshop, not an official NCI publication.  The NCI hosted the meeting; the meeting was not sponsored by the NCI, and the published meeting report was not an official statement of the NCI.  Notably, the report appeared in Cancer Research as a paid advertisement, not in the Journal of the National Cancer Institute as a scholarly article.

In assessing the citation, readers should consider the authors of the meeting report.  Importantly, the discipline of epidemiology was not strongly represented; most of the chairpersons and scientists in attendance were pathologists, cell biologists, virologists, and toxicologists.  The authors of the meeting report reflect the interests and focus of the scientists in attendance.  The lead author was Michele Carbone, a pathologist at Loyola University Chicago.  Some may recognize Carbone as one of the proponents of Simian Virus 40 as a cause of mesothelioma, a hypothesis that has not fared terribly well in the crucible of epidemiologic science.  Other authors included:

George Klein, with the Microbiology and Tumor Biology Center, Karolinska Institute, in Stockholm,

Jack Gruber, a virologist with the Cancer Etiology Branch of the NCI, and

May Wong, a biochemist, with the NCI.

The basis of the citation to Carbone’s meeting report is an informal discussion session that took place at the meeting.  Those in attendance broke out into two groups, one chaired by Brook Mossman, a pathologist, and the other group chaired by Dr. Harald zur Hausen, a famous virologist who discovered the causal relationship between human papilloma virus and cervical cancer.

The meeting report included a narrative of how the two groups responded to twelve questions. Cranor’s citation to this article is based upon one sentence in Carbone’s report, about one of twelve questions:

“6. What is the hierarchy of state-of-the-art approaches needed for confirmation criteria, and which bioassays are critical for decisions: epidemiology, animal testing, cell culture, genomics, and so forth?

There should be no such hierarchy.  Epidemiology, animal, tissue culture and molecular pathology should be seen as integrating evidences in the determination of human carcinogenicity.”

Carbone at 5522.  Considering the fuller context of the meeting and this report, there is nothing particularly surprising about this statement.  It is not clear that the full question and answer even remotely supports the weight that Cranor places upon it.  Clearly, Cranor’s quotations are unduly selective.  For instance, Cranor does not discuss the disagreement among those in attendance over criteria for different carcinogens:

“2. Should the criteria be the same for different agents (viruses, chemicals, physical agents, promoting agents versus initiating DNA-damaging agents)?

There were different opinions. Group 1 debated this issue and concluded that the current listing of criteria should remain the same because we lack sufficient evidence to develop a separate classification. Group 2 strongly supported the view that it is useful to separate the biological or infectious agents from chemical and physical carcinogens due to their frequently entirely different mode of action.”

Carbone at 5521.

Perhaps Cranor did not think a legal audience would be interested in the emphasis given to epidemiology.  The authors of the meeting report noted that the importance to epidemiology for general causation, but its limitations for determining specific causation:

“Concerning the respective roles of epidemiology and molecular pathology, it was noted that epidemiology allows the determination of the overall effect of a given carcinogen in the human population (e.g., hepatitis B virus and hepatocellular carcinoma) but cannot prove causality in the individual tumor patient.”

Carbone at 5518.  The report did not state that epidemiology was not necessary for confirmation of carcinogenicity in the species of interest (humans). The meeting report emphasized the need to integrate the findings of epidemiology and of molecular biology; it did not urge that epidemiology be ignored or disregarded:

“A general consensus was often reached on several topics such as the need to integrate molecular pathology and epidemiology for a more accurate and rapid identification of human carcinogens.”

Carbone at 5518.

“Ideally, before labeling an agent as a human carcinogen, it is important to have epidemiological, experimental animals, and mechanistic evidences (molecular pathology). Not all of the evidence is always available, and, at times, it may be prudent to identify a human carcinogen earlier rather than later.”

Carbone at 5519 (emphasis added).  Unlike Cranor, the authors of the meeting report distinguish between instance when they are acting on a scientific determination of causation, and a precautionary assessment that proceeds prudentially “as if” causation is determined.

Against this fuller context, Cranor’s characterization of the meeting report, and his limited citations and quotations can be seen to be misleading:

“The First Circuit wisely followed the Etiology Branch of the National Cancer Institute, which sponsored a workshop on cancer causation that concluded ‘there should be no . . . hierarchy’ among epidemiology, animal testing, cell culture, genomics, and so forth.164”

Cranor at 129.  The suggestion that the informal workshop statement represented the views of the Etiology Branch is bogus.  Not content to misrepresent twice, Cranor comes back for yet a third misleading citation to this report:

“A further conclusion, already noted, is that scientific experts in court should be permitted to rely upon all scientifically relevant evidence in nondeductive arguments to draw conclusions about causation.209 “There should be no such hierarchy” of evidence, as the Milward court put it, following scientists conducting a workshop at the National Cancer Institute.210 This decision stands as an important corrective to the views of some other appellate and district courts concerning the scientific foundation for expert testimony in toxic tort cases.”

Cranor at 135 (emphasis in original) (citing Carbone for a third time).  To see how misleading is Cranor’s suggestion that scientists should be permitted upon all scientific relevant evidence, consider the meeting report’s careful admonition about the lack of validity of some animal models and mechanistic research:

“Moreover, carcinogens and anticarcinogens can have different effects in different situations.  As shown by the example of addition of β-carotene in the diet, β-carotene has chemopreventive effects in many experimental systems, yet it appears to have increased the incidence of lung cancer in heavy smokers. Animal experiments can be very useful in predicting the carcinogenicity of a given chemical. However, there are significant differences in susceptibility among species and within organs in the same species, and differences in the metabolic pathway of a given chemical among human and animals could lead to error.”

Carbone at 5521.  Obviously relevance is conditioned upon validity, a relationship that is ignored, suppressed, and dismissed in Cranor’s article.

The devil, or the WOE, comes from with ignoring the details.

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Cranor’s Defense of Milward at the CPR’s Celebration

Professor Sanders’ Paen to Milward

May 7th, 2013

Deconstructing the Deconstruction of Deconstruction

Some scholars have suggested that the most searching scrutiny of scientific research takes place in the courtroom.  Barry Nace’s discovery of the “mosaic method” notwithstanding, lawyers rarely contribute new findings, which I suppose supports Professor Sanders’ characterization of the process as “deconstructive.”  The scrutiny of courtroom science is encouraged by the large quantity of poor quality opinions, on issues that must be addressed by lawyers and their clients who wish to prevail.  As philosopher Harry Frankfurt described this situation:

“Bullshit is unavoidable whenever circumstances require someone to talk without knowing what he is talking about.  Thus the production of bullshit is stimulated whenever a person’s obligations or opportunities to speak about some topic exceed his knowledge of the facts that are relevant to that topic.”

Harry Frankfurt, On Bullshit 63 (Princeton Univ. 2005).

This unfortunate situation would seem to be especially true for advocacy science that involves scientists who are intent upon influencing public policy questions, regulation, and litigation outcomes.  Some of the most contentious issues, and tendentious studies, take place within the realm of occupational, environmental, and related disciplines. Sadly, many occupational and environmental medical practitioners seem particularly prone to publish in journals with low standards and poor peer review.  Indeed, the scientists and clinicians who work in some areas make up an insular community, in which the members are the peer reviewers and editors of each other’s work.  The net result is that any presumption of reliability for peer-reviewed biomedical research is untenable.

The silicone gel-breast implant litigation provides an interesting case study of the phenomenon.  Contrary to post-hoc glib assessments that there was “no” scientific evidence offered by plaintiffs, the fact is that there was a great deal.  Most of what was offered was published in peer-reviewed journals; some was submitted by scientists who had some credibility and standing within their scientific, academic communities:  Gershwin, Kossovsky, Lappe, Shanklin, Garrido, et al.  Lawyers, armed with subpoenas, interrogatories, and deposition notices, were able to accomplish what peer reviewers could not.  What Professor Sanders and others call “deconstruction” was none other than a scientific demonstration of study invalidity, seriously misleading data collection and analysis, and even fraud.  See Hon. Jack B. Weinstein, “Preliminary Reflections on Administration of Complex Litigation” 2009 Cardozo L. Rev. de novo 1, 14 (2009) (describing plaintiffs’ expert witnesses in silicone litigation as “charlatans” and the litigation as largely based upon fraud).

Some scientific publications are motivated almost exclusively by the goal of influencing regulatory or political action.  Consider the infamous meta-analysis by Nissen and Wolski, of clinical trials and heart attack among patients taking Avandia.  Steven Nissen & Kathy Wolski, “Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes,” 356 New Engl. J. Med. 2457 (2007). The New England Journal of Medicine rushed the meta-analysis into print in order to pressure the FDA to step up its regulation of post-marketing surveillance of licensed medications.  Later, better-conducted meta-analyses showed how fragile Nissen’s findings were.  See, e.g., George A. Diamond, MD, et al., “Uncertain Effects of Rosiglitazone on the Risk for Myocardial Infarction and Cardiovascular Death,” 147 Ann. Intern. Med. 578 (2007); Tian, et al., “Exact and efficient inference procedure for meta-analysis and its application to the analysis of independent 2 × 2 tables with all available data but without artificial continuity correction,” 10 Biostatistics 275 (2008).  Lawyers should not be shy about pointing out political motivations of badly conducted scientific research, regardless of authorship or where published.

On the other hand, lawyers on both sides of litigation are prone to attack on personal bias and potential conflicts of interest because these attacks are more easily made, and better understood by judges and jurors.  Perhaps it is these “deconstructions” that Professor Sanders finds overblown, in which case, I would agree.  Precisely because jurors have difficulty distinguishing between allegations of funding bias and validity flaws that render studies nugatory, and because inquiries into validity require more time, care, analysis, attention, and scientific and statistical learning, pretrial gatekeeping of expert witnesses is an essential part of achieving substantial justice in litigation of scientific issues.  This is a message that is obscured by the recent cheerleading for the Milward decision at the litigation industry’s symposium on the case.

Deconstructing Professor Sanders’ Deconstruction of the Deconstruction in Milward

A few comments about Professor Sanders’ handling of the facts of Milward itself.

The case arose from a claim of occupational exposure to benzene and an outcome known as APL (acute promyelocytic leukemia), which makes up about 10% of AML (acute myeloid leukemia).  Sanders argues, without any support, that APL is too rare for epidemiology to be definitive.  Sanders at 164.  Here Sanders asserts what Martyn Smith opined, and ignores the data that contradicted Smith.  At least one of the epidemiologic studies cited by Smith was quite large and was able to discern small statistically significant associations when present.  See, e.g., Nat’l Investigative Group for the Survey of Leukemia & Aplastic Anemia, “Countrywide Analysis of Risk Factors for Leukemia and Aplastic Anemia,” 14 Acta Academiae Medicinae Sinicae (1992).  This study found a crude odds ratio of 1.42 for benzene exposure and APL (M3). The study had adequate power to detect a statistically significant odds ratio of 1.54 between benzene and M2a.  Of course, even if one study’s “power” were low, there are other, aggregative strategies, such as meta-analysis, available.  This was not a credibility issue concerning Dr. Smith, for the jury; Smith’s opinion turned on an incorrect and fallacious analyses that did not deserve “jury time.”

The problem is, according to Sanders one of “power.”  In a lengthy footnote, Sander explains what “power” is, and why he believes it is a problem:

“The problem is one of power. Tests of statistical significance are designed to guard against one type error, commonly called Type I Error. This error occurs when one declares a causal relationship to exist when in fact there is no relationship, … . A second type of error, commonly called Type II Error, occurs when one declares a causal relationship does not exist when in fact it does. Id. The “power” of a study measures its ability to avoid a Type II Error. … Power is a function of a study’s sample size, the size of the effect one wishes to detect, and the significance level used to guard against Type I Error. …. Because power is a function of, among other things, the significance level used to guard against Type I errors, all things being equal, minimizing the probability of one type of error can be done only by increasing the probability of making the other. …  Formulae exist to calculate the power of case-control and cohort studies from 2 x 2 contingency table data. …

Because the power of any test is reduced as the incidence of an effect decreases, Type II threats to causal conclusions are particularly relevant with respect to rare events. Plaintiffs make a fair criticism of randomized trials or epidemiological cohort studies when they note that sometimes the studies have insufficient power to detect rare events. In this situation, case-control studies are particularly valuable because of their relatively greater power. In most toxic tort contexts, the defendant would prefer to minimize Type I Error while the plaintiffs would prefer to minimize Type II Error. Ideally, what we would prefer are studies that minimize the probability of both types of errors. Given the importance of power in assessing epidemiological evidence, surprisingly few appellate opinions discuss this issue. But see DeLuca v. Merrell Dow Pharm., Inc., 911 F.2d 941, 948 (3d Cir. 1990), which contains a good discussion of epidemiological evidence. The opinion discusses the two types of error and suggests that courts should be concerned about both. Id. Unfortunately, neither the district court opinion nor the court of appeals opinion in Milward discusses power.”

Sanders at 164 n.115 (internal citations omitted).

Sanders is one of the few law professors who almost manages to describe statistical power correctly.  Calculating and evaluating power requires pre-specification of alpha (our maximum tolerated Type I error), sample size, and an alternative hypothesis that we would want to be able to identify at a statistically significant level.  This much is set out in the footnote quoted above.

Sample size, however, is just one factor in the study’s variance, which is not in turn completely specified by sample size.  More important, Sanders’ invocation of power to evaluate the exonerative quality of a study has been largely rejected in the world of epidemiology.  His note that “[f]ormulae exist to calculate the power of case-control and cohort studies from 2 x 2 contingency table data” is largely irrelevant because power is mostly confined to sample size determinations before a study is conducted.  After the data are collected, studies are evaluated by their point estimates and their corresponding confidence intervals. See, e.g., Vandenbroucke, et al., “Strengthening the reporting of observational studies in epidemiology (STROBE):  Explanation and elaboration,” 18 Epidemiology 805, 815 (2007) (Section 10, sample size) (“Do not bother readers with post hoc justifications for study size or retrospective power calculations. From the point of view of the reader, confidence intervals indicate the statistical precision that was ultimately obtained.) (emphasis added). See also “Power in the Courts — Part Two” (Jan. 21, 2011).

Type II error is important in the evaluation of evidence, but it requires a commitment to a specific alternative hypothesis.  That alternative can always be set closer and closer to the null hypothesis of no association in order to conclude, as some plaintiffs’ counsel would want, that all studies lack power (except of course the ones that turn out to support their claims).  Sanders’ discussion of statistical power ultimately falters because claiming a lack of power without specifying the size of the alternative hypothesis is unprincipled and meaningless.

Sanders tells us that cohorts will have less power than case-control studies, but again the devil is in the details.  Case-control studies are of course relatively more efficient in studying rare diseases, but the statistical precision of their odds ratios will be given by the corresponding confidence intervals.

What is missing from Sanders’ scholarship is a simple statement of what the point estimates and their confidence intervals are.  Plaintiffs in Milward argued that epidemiology was well-nigh unable to detect increased risks of APL, but then they embraced epidemiology when Smith had manipulated and re-arranged data in published studies.

The Yuck Factor

One of the looming problems in expert witness gatekeeping is judicial discomfort and disability in recounting the parties’ contentions, the studies’ data, and the witnesses’ testimony.  In a red car/blue car case, judges are perfectly comfortable giving detailed narratives of the undisputed facts, and the conditions that give rise to discounting or excluding evidence or testimony.  In science cases, not so much.

Which brings us to the data manipulation conducted by Martyn Smith in the Milward case.  Martyn Smith is not an epidemiologist, and he has little or no  experience or expertise in conducting and analyzing epidemiologic studies.  The law of expert witnesses makes challenges to an expert’s qualifications very difficult; generally courts presume that expert witnesses are competent to testify about general scientific and statistical matters.  Often the presumption is incorrect.

In Milward, Smith claimed, on the one hand, that he did not need epidemiology to reach his conclusion, but on the other hand that “suggestive” findings supported his opinion.  On the third hand, he seemed to care enough about the epidemiologic evidence to engage in fairly extensive reanalysis of published studies.  As the district court noted,  Smith made “unduly favorable assumptions in reinterpreting the studies, such as that cases reported as AML could have been cases of APL.”  Milward v. Acuity Specialty Products Group, Inc., 664 F.Supp. 2d 137, 149 (D. Mass. 2009), rev’d, 639 F.3d 11, 19 (1st Cir. 2011), cert. denied sub nom. U.S. Steel Corp. v. Milward, 132 S. Ct. 1002 (2012).  Put less charitably, Smith made up data to suit his hypothesis.

The details of Smith’s manipulations go well beyond cherry picking.  Smith assumed, without evidence, that AML cases were APL cases.  Smith arbitrarily chose and rearranged data to create desirable results.  See Deposition Testimony of Dr. David Garabrant at 22 – 53, in Milward (Feb. 18, 2009).  In some studies, Smith discarded APL cases from the unexposed group, with the consequence of increasing the apparent association; he miscalculated odds ratios; and he presented odds ratios without p-values or confidence intervals.  The district court certainly was entitled to conclude that Smith had sufficiently deviated from scientific standards of care as to make his testimony inadmissible.

Regrettably, the district court did not provide many details of Smith’s reanalyses of studies and their data.  The failure to document Smith’s deviations facilitated the Circuit’s easy generalization that the fallacious reasoning and methodology was somehow invented by the district court.

The appellate court gave no deference to the district court’s assessment, and by judicial fiat turned methodological missteps into credibility issues for the jury.  The Circuit declared that the analytical gap was of the district court’s making, which seemed plausible enough if one read only the appellate decision.  If one reads the actual testimony, the Yuck Factor becomes palpable.

WOE Unto Bradford Hill

Professor Sanders accepts the appellate court’s opinion at face value for its suggestion that:

“Dr. Smith’s opinion was based on a ‘weight of the evidence’ methodology in which he followed the guidelines articulated by world-renowned epidemiologist Sir Arthur Bradford Hill in his seminal methodological article on inferences of causality.”

Sanders at 170 n.140 (quoting Milward, 639 F.3d at 17).

Sanders (and the First Circuit) is unclear whether WOE consists of following the guidelines articulated by Sir Arthur (perhaps Sir Austin Bradford Hill’s less distinguished brother?), or merely includes the guidelines as a larger process.  Not only was there no Sir Arthur, but Sir Austin’s guidelines are distinctly different from WOE in that they pre-specify the consideration to be applied.  No where does the appellate court give any meaningful consideration to whether there was an exposure-response gradient shown, or whether the epidemiologic studies consistently showed an association between benzene and APL.  Had the Circuit given any consideration to the specifics of the guidelines, it would have likely concluded that the district court had engaged in fairly careful, accurate gatekeeping, well within its discretion.  (If the standard were de novo review rather than “abuse of discretion,” the Circuit would have had to confront the significant analytical gaps and manipulations in Smith’s testimony.)  Futhermore, it is time to acknowledge that Bradford Hill’s “guidelines” are taken from a speech given by Sir Austin almost 50 years ago; they hardly represent a comprehensive, state-of-the-art set of guidelines for causal analysis in epidemiology today.

So there you have it.  WOE means the Bradford Hill guidelines, except that the individual guidelines need not be considered.  And although Bradford Hill’s guidelines were offered to evaluate a body of epidemiologic studies, WOE teaches us that we do not need epidemiologic studies, especially if they do not help to establish a plaintiffs’ claim.  Sanders at 168 & n.133 (citing Milward at 22-24).

What is WOE?

If WOE were not really the Bradford Hill guidelines, then what might it be? Attempting to draw a working definition of WOE from the Milward appellate decision, Sanders tell us that WOE requires looking at all the relevant evidence.  Sanders at 169.  Not much guidance there.  Elsewhere he tells us that WOE is “reasoning to the best explanation,” without explicating what such reasoning entails.  Sanders at 169 & n. 136 (quoting Milward at 23,“The hallmark of the weight of the evidence approach is reasoning to the best explanation.”).  This hardly tells us anything about what method Smith and his colleagues were using.

Sanders then tells us that WOE means the whole “tsumish.” (My word; not his.)  Not only should expert witnesses rely upon all the relevant evidence, but they should eschew an atomistic approach that looks (too hard) at individual studies.  Of course, there may be value in looking at the entire evidentiary display.  Indeed, a holistic view may be needed to show the absence of causation.  In many litigations, plaintiffs’ counsel are adept in filling up the courtroom with “bricks,” which do not fit together to form the wall they claim.  In the silicone gel breast implant litigation, plaintiffs’ counsel were able to pick out factoids from studies to create sufficient confusion and doubt that there might be a causal connection between silicone and autoimmune disease.  A careful, systematic analysis, which looked at the big picture, demonstrated that these contentions were bogus.  Committee on the Safety of Silicone Breast Implants, Institute of Medicine, Safety of Silicone Breast Implants (Wash. D.C. 1999) (reviewing studies, many of which were commissioned by litigation defendants, and which collectively showed lack of association between silicone and autoimmune diseases).  Sometimes, however, taking in the view of the entire evidentiary display may obscure what makes up the display.  A piece by El Anatsui may look like a beautiful tapestry, but a closer look will reveal it is just a bunch of bottle caps wired together.

Contrary to Professor Sanders’ assertions, nothing in the Milward appellate opinion explains why studies should be viewed only as a group, or why this view will necessarily show something greater than the parts. Sanders at 170.  Although Sanders correctly discerns that the Circuit elevated WOE from “perspective” to a methodology, there is precious little content to the methodology, especially if it permits witnesses to engage in all sorts of data shenanigans or arbitrary weighting of evidence.  The quaint notion that there is always a best explanation obscures the reality that in science, and especially in science that is likely to be contested in a courtroom, the best explanation will often be “we don’t know.”

Sanders eventually comes around to admit that WOE is perplexingly vague as to how the weighing should be done.  Id. at 170.  He also admits that the holistic view is not always helpful.  Id. at 170 & n.139 (the sum is greater than its parts but only when the combination enhances supportiveness of the parts, and the collective support for the conclusion at issue, etc.).  These concessions should give courts serious pause before they adopt a dissent from a Supreme Court case, that has been repeatedly rejected by courts, commentators, and ultimately by Congress in revising Rule 702.

WOE is Akin to Differential Diagnosis

The Milward opinion seems like a bottomless reserve of misunderstandings.    Professor Sanders barely flinches at the court’s statement that “The use of judgment in the weight of the evidence methodology is similar to that in differential diagnosis.”  Milward at 18.  See Sanders at 171.  Differential “diagnosis” requires previous demonstration of general causation, and proceeds by iterative disjunctive syllogism.  Sanders, and the First Circuit, somehow missed that this syllogistic reasoning is completely unrelated to the abductive inferences that may play a role in reaching conclusions about general causation.  Sanders revealingly tells us that “[e]xperts using a weight of the evidence methodology should be given the same wide latitude as is given those employing the differential diagnosis method.”  Sanders at 172 & n.147.  This counsel appears to be an invitation to speculate.  If the “wide latitude” to which Sanders refers means the approach of a minority of courts that allow expert witnesses to rule in differentials by speculation, and then rule them in by failing to rule out idiopathic cases, then Sanders’ approach is advocacy for epistemic nihilism.

The Corpuscular Approach

Professor Sanders seems to endorse the argument of Milward, as well as Justice Stevens’ dissent in Joiner, that scientists do not assess research by looking at the validity (vel non) of individual studies, and therefore courts should not permit this approach.  Sanders at 173 & n.15.  Neither Justice Stevens nor Professor Sanders presents any evidence for the predicate assertion, which a brief tour of IARC’s less political working group reports would show to be incorrect.

The rationale for Sanders (and Milward’s) reductionism of science to WOE becomes clear when Sanders asserts that “[p]erhaps all or nearly all critiques of an expert employing a weight of the evidence methodology should go to weight, not admissibility. Id. at 173 & n.155.  To be fair, Sanders notes that the Milward court carved out a “solid-body” of exonerative epidemiology exception to WOE.  Id. at 173-74.  This exception, however, does nothing other than placing a substantial burden upon the opponent of expert witness opinion to show that the opinion is demonstrably incorrect.  The proponent gets a free pass as long as there is no “solid body” of such evidence that shows he is affirmatively wrong.  Discerning readers will observe that maneuver simply shifts the burden of admissibility to the opponent,  and eschews the focus on methodology for a renewed emphasis upon general acceptance of conclusions.  Id.

Sanders also notes that other courts have seen through the emptiness of WOE and rejected its application in specific cases.  Id. at 174 & n.163-64 (citing Magistrini v. One Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 601-02 (D.N.J. 2002), aff’d, 68 F. App’x 356 (3d Cir. 2003), where the trial court rejected Dr. Ozonoff’s attempt to deploy WOE without explaining or justifying the mixing and matching of disparate kinds of studies with disparate results).  Sanders’ analysis of Milward seems, however, designed to skim the surface of the case in an effort to validate the First Circuit’s superficial approach.

 

Posted in Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Professor Sanders’ Paen to Milward

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