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For your delectation and delight, desultory dicta on the law of delicts.

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 P_L and P_U that are random variables based on the sample data. Thus, a confidence interval (P_L, P_U) 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 P_L and P_U.”

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.

Posted in Causation, Rule 702, statistical evidence | Comments Off on Woodside & Davis on the Bradford Hill Considerations

EPA Research on Ultrafine Particulate Matter

June 26th, 2013

White Hat Bias

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

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

Reynolds quoted one scientist as saying that:

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

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

White-Hat Bias & Black-Hat Ethics

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

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

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

The PM Chamber

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

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

The “Subject”

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

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

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

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

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

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

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

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

The Whole Truth

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

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

EPA – Hoisted With Its Own Petard

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

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

“I accused EPA of either: (1) conducting unethical human experimentation or exaggerating the dangers of fine airborne particulate matter (PM_2.5). It must be one or the other; it can’t be neither, according to EPA’s own documents.”

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

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

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

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

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

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

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

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

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

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

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

Sympathy for the Diablo — Peppermint Barry vs Spicy Seafood Pasta

June 12th, 2013

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

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

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

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

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

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

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

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

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

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

The Material Safety Data Sheet Ploy

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

The Treating Physician Echo

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

Pasta and Peppermints

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

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

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

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

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

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

The Mt. Sinai Catechism

June 7th, 2013

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

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

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

Id. at 481.

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

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

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

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

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

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

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

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

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

“Rationale

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

Objectives

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

Methods

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

Measurements and Main Results

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

Conclusions

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

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

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

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

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

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The Doubling Dose

June 5th, 2013

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

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

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

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

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

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

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

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

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

See Reference Manual on Scientific Evidence on Relative Risk Greater Than Two For Specific Causation Inference (April 25, 2015), for the updated the case law on the issue of using relative and attributable risks to satisfy plaintiff’s burden of showing, more likely than not, that an exposure or condition caused a plaintiff’s disease or injury.

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Landrigan v. The Celotex Corporation, Revisited

June 4th, 2013

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

Specific causation has been, and remains, the soft underbelly of the toxic tort world, at least for those cases not involving so-called signature diseases. A priori assessments of risk do not necessarily translate into post-exposure, post-diagnosis attributions of outcome to exposure. Put simply, risk is not cause. Guinn v AstraZeneca Pharms. LP, 602 F.3d 1245, 1255 (11th Cir. 2010) (“An expert, however, cannot merely conclude that all risk factors for a disease are substantial contributing factors in its development. The fact that exposure to a substance may be a risk factor for a disease does not make it an actual cause simply because the disease developed.”) Unless there is a “fingerprint of causation,” what scientists would call a completely specific biomarker, then specific causation opinions are mostly guesswork.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Id. at 1271.

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

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

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

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

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

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

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

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

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Two Schools of Thought

May 25th, 2013

In litigation of claims of professional malpractice, the “two schools of thought doctrine” is a complete defense. Jones v. Chidester, 531 Pa. 31, 40, 610 A.2d 964 (1992).

As explained by the Pennsylvania Supreme Court, physicians may defend against claims that they deviated from the standard of care, or of professional malpractice, by adverting to support for their treatment by a minority of professionals in their field:

“Where competent medical authority is divided, a physician will not be held responsible if in the exercise of his judgment he followed a course of treatment advocated by a considerable number of recognized and respected professionals in his given area of expertise.”

Id. at 40. See also Fallon v. Loree, 525 N.Y.S.2d 93, 93 (N.Y. App. Div. 1988) (“one of several acceptable techniques”); Dailey, “The Two Schools of Thought and Informed Consent Doctrine in Pennsylvania,” 98 Dickenson L. Rev. 713 (1994); Douglas Brown, “Panacea or Pandora’ Box: The Two Schools of Medical Thought Doctrine after Jones v. Chidester,” 44 J. Urban & Contemp. Law 223 (1993).

Perhaps the two schools doctrine is an interesting anomaly that harkens back to a legal epistemology founded in authority rather than evidence. In the law of expert witnesses, the criterion for admissibility of opinion has shifted from “general acceptance” to epistemic warrant, but malpractice law still allows custom and practice to dictate the standard of care. The two schools doctrine ameliorates the practice of basing standard of care on authoritative, non-evidence based practices and opinions. If standards of care were truly evidence based, then there might still be situations in which the available evidence was inconclusive between two approaches to patient care. In situations of inconclusive evidence between two approaches, the two schools doctrine would provide a defense.

Products Liability

In products liability cases, failure-to-warn theories are often predicated upon claims that defendants should have known of a risk of harm posed by their products. Plaintiffs will cite past pronouncements made by authors as evidence that the harm was “known” to others, and thus the defendants should have known of the harm, and thus should have warned about the harm. This species of claiming often takes place, however, without any analysis whether the past pronouncements were made with good and adequate scientific bases.

If products liability law persists in treating past, putative knowledge uncritically, then it should, at least, allow defendants to defend on the ground that there were contrary pronouncements made. Juries should be told that the existence of contrary pronouncements from a respectable minority of writers is a complete defense. The two schools of thought doctrine should thus be given wider play in tort law than just professional malpractice. Products liability should honor the basic underlying principle of malpractice law that the opinions of even a respected minority of experts fully answers the claim of negligence. The existence of the contrary opinions should bar punitive damage claims altogether.

Consider what happens in the typical failure to warn case. The plaintiff goes trash picking through the dustbin of medical history to find some prescient writer who argued that the product in question causes disease. Defendant points to other authors who disputed the relationship. The court instructs the jury that they may find defendant negligent for failing to warn if they believe the plaintiffs’ evidence. The jury makes its decision, thoroughly infected with hindsight bias.

This scenario is unsatisfactory and unduly restrictive. Applying the two schools of thought doctrine, the court should instruct the jury to find for the plaintiff only if there was not a considerable number of recognized and respected professionals and experts, who had opined that the product caused the specific injury in question. The existence of such a minority should defeat claims for punitive damages as a matter of law.

United States v. Harkonen

On May 7, 2013, the Ninth Circuit of the United States Court of Appeals denied, Dr. Harkonen’s petition for rehearing in United States v. Harkonen. No data or analyses were false or fabricated in the Harkonen case. The government’s prosecution was predicated on a statistical orthodoxy that is opposed by a large number of recognized and respected statisticians. This fact would have been a complete defense to a claim of professional negligence. The two schools doctrine should completely bar a prosecution for fraud.

Remarkably, expert witnesses commonly testify to causal associations on lesser evidence than Dr. Harkonen relied upon in a press release for his judgment of causal efficacy, but the trial court believed the jury could infer scienter and falsity from conversations between an “orthodox” statistician and Dr. Harkonen about the propriety of drawing a casual inference from a given dataset.

Perhaps civil litigants should start counterclaiming for fraud when they receive expert witness reports.

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Asbestos Litigation Blues

May 22nd, 2013

Mr. Curtis Geatz alleges that he has mesothelioma as a result of asbestos exposure, including exposure to crocidolite from having smoked Kent Micronite filtered cigarettes for nine months, in 1955-56. Geatz v. Benjamin Moore & Co., File No. 62CV124946, Minn. D. Ct. for Ramsey Cty. (2d Jud. Dist.). See “Lorillard Executive Admits Asbestos Once Included in Kent Filters” (April 23, 2013) (misleadingly suggesting that testimony about filter content was something other than very old news).

Crocidolite is clearly the most potent cause of mesothelioma. In a published cohort study of workers at Hollingsworth & Vose, a company that made the filters for the Kent cigarette, over 15 percent of all deaths were due to mesothelioma. James Talcott, et al., “Asbestos-Associated Diseases in a Cohort of Cigarette-Filter Workers,” 321 New Engl. J. Med. 1220 (1989).

Despite the high potency of crocidolite in causing mesothelioma, the late Irving Selikoff worked hard to advance his opinion that all asbestos fiber types were comparable. Selikoff also propagandized the view that crocidolite was not widely used in the United States, although he and his colleagues documented the use of “blue” fiber at Johns-Manville factories in the United States. See “Selikoff and the Mystery of the Disappearing Amphiboles” (Dec. 10, 2010).

In Mr. Geatz’s case, Lorillard moved for summary judgment on grounds that crocidolite fibers in the cigarettes plaintiff smoked were not a substantial contributing factor of his mesothelioma. The trial court denied Lorillard’s motion, apparently on the strength of unidentified exhibits attached to an attorney affidavit (Tiffany Dickenson).

Mr. Geatz’ claim is not implausible on its face, but the trial court’s refusal of Lorillard’s motion for summary judgment is a conclusory black box. It may be right or wrong, but it fails to describe the defendant’s evidence or arguments as to why potent crocidolite in the Kent filter could not have been a substantial factor, or the plaintiffs’ evidence as to why the jury should be allowed to say otherwise. Lorillard may have argued that the fibers did not leave the filter, or that the exposure would have been too low, even to the extremely potent crocidolite fiber. Apparently there was no threshold issue of admissibility of each side’s expert witnesses, but still, the scientific issues, the plaintiffs, and the defendants deserve some explanation of the court’s decision.

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As They WOE, So No Recovery Have the Reeps

May 22nd, 2013

Late last year, Justice York excluded Dr. Shira Kramer’s WOE-ful opinion that gasoline fumes from an alleged fuel-line leak caused Sean Reep to be born with cerebral palsy. Reeps v. BMW of North America, LLC, 2012 NY Slip Op 33030(U), N.Y.S.Ct., Index No. 100725/08 (New York Cty. Dec. 21, 2012) (York, J.). Kramer’s opinion was a parody of science, pieced together from case reports, animal studies, and epidemiologic studies that looked at exposures utterly unlike that of Mrs. Reep’s exposure.

Justice York saw through the charade. The animal studies were largely exonerative. The case reports were of birth defects quite different from those sustained by Sean Reeps. The epidemiologic studies were of different chemicals or chemicals at levels very different from those experienced by Mrs. Reeps. Plaintiffs’ expert witnesses ignored established principles of teratology in claiming late-term birth defects to have been causally related to early term exposures. Plaintiffs’ expert witnesses gave a convincing presentation of how not to do science, and why judicial gatekeeping is necessary. See “New York Breathes Life into Frye Standard – Reeps v. BMW” (Mar. 5, 2013).

Justice York clearly articulated that the “plaintiff’s burden to prove the methodology applied to reach the conclusions will not be rejected by specialists in the field.” Reeps, slip op. at 11. The trial court recognized that under the New York state version of Frye, the court must determine whether plaintiffs’ expert witnesses are faithfully applying a methodology, such as the Bradford Hill criteria, or whether they are they are “pay[ing] lip service to them while pursuing a completely different enterprise.” Id. Justice York recognized that the court must examine a proffered opinion to determine whether it “properly relates existing data, studies or literature to the plaintiff’s situation, or whether, instead, it is connected to existing data only by the ipse dixit of the expert.” Id. (internal quotations omitted).

Plaintiffs were unhappy with Justice York’s decision, and their counsel moved for reconsideration, positing only 15 supposed errors or misunderstandings in the opinion. On May 10, the trial court denied the motion for reconsideration and further explicated the scientific deficiencies of plaintiffs’ witnesses’ opinions.

The trial court was unimpressed:

“In general, attorney for plaintiffs misrepresents the substance of this court’s Decision. The court did not prefer conclusions of defendants’ experts to that of plaintiffs – disagreement among experts is to be expected, since causation analysis involves professional judgment in interpreting data and literature. An expert opinion is precluded when it is reached in violation of generally accepted scientific principles. The court determined that Drs. Kramer and Frazier did not follow generally accepted scientific methodology.”

Reeps, 2013 NY Slip Op 31055(U) at 2 (Opinion on Motions to Reargue, to Renew, and for Oral Hearing) (May 10, 2013).

The court noted that the plaintiffs’ witnesses’ novel claim that low-level gasoline vapor inhalation causes birth defects, a claim that had escaped the attention of all other scientists and regulatory agencies, cried out for judicial intervention. Id. at 3.

The court also rebuffed the claim that plaintiffs’ witnesses, Shira Kramer and Linda Frazier, had followed the Bradford Hill guidelines:

“These guidelines are employed only after a study finds an association to determine whether that association reflects a true causal relationship.”

Id. at 5 (quoting Federal Judicial Center, National Research Council, Reference Manual on Scientific Evidence at 598-599 (3d ed. 2011)) (emphasis in the original). Kramer and Frazier never got off the dime with the Bradford Hill guidelines.

In considering the plaintiffs’ motions, the trial court also had occasion to revisit the assertion that “weight of the evidence” (WOE) substituted for, or counted as, a scientific basis for a conclusion of causality:

“The metaphorical use of the term is, if nothing else, ‘a colorful way to say the body of evidence we have examined and judged using a method we have not described but could be more or less inferred from a careful between-the-lines reading of our paper’.”

Id. at 5 (quoting Douglas Weed, “Weight of Evidence: A Review of Concept and Methods,” 25 Risk Analysis 1545, 1546-47 (2005).

Unmoved by the sophistical hand waving, the court emphasized that Kramer and Frazier had confused “suggestive” evidence with “conclusions,” and they had misrepresented the meaning and significance of threshold limit values. All in all, a convincing demonstration of the need for, and the judicial competence to carry out, gatekeeping of expert witness opinion testimony.

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Biopersistant Silicone

May 18th, 2013

From the late 1980’s until the late 1990’s, a cadre of public health zealots waged war against various silicone medical devices, but especially against silicone gel breast implants. Their charge was that silicone degraded in vivo to silica, and that it caused autoimmune disease. Their supposed method: weight of the evidence.

I recall sitting next to Professor Carl Cranor at a meeting in Washington, D.C. When the subject of silicone gel breast implants came up, he started trash talking the exonerative epidemiology. When I introduced myself and told him that I represented one of the defendants in that litigation, he got up and moved. Thankfully.

In 1999, the Institute of Medicine issued its consensus report that debunked the plaintiffs’ attempts to draw a causal connection between silicone and autoimmune disease. Stuart Bondurant, et al., Safety of Silicone Breast Implants (1999). The phrases “weight of the evidence” or “weight of evidence” are never mentioned in the report, over 500 pages long.

Recently, the silicone plaintiffs’ causal theory has resurfaced. There has been no new important evidence, but with the scientific community’s attention drawn elsewhere, some old zealots and some new have wandered back into the field to recycle the claims and hypotheses that consumed lawyers and scientists in the last century.

Last year saw a review by Yehuda Shoenfeld and his Israeli colleagues, who describe a “new” syndrome that manifests with various immune-system disturbances. These authors call their syndrome ASIA (autoimmune syndrome induced by adjuvant). M. Lidar, N. Agmon-Levin, P. Langevitz, and Y. Shoenfeld, “Silicone and scleroderma revisited,” 21 Lupus 121 (2012).

Shoenfeld, who has dabbled with this theory for 20 years, acknowledges that the epidemiologic studies fail to support the ASIA notion. Despite the lack of support from controlled, observational studies, these authors proceed to describe “the mechanisms by which silicone may mediate autoimmunity in general, as well as the evidence for causal associations with more specific autoimmune syndromes in general, and scleroderma in particular.” Id. at 121.

Last month, an article was published online with a collection of case reports from the Netherlands. Jan Tervaert & R. M. Kappel, “Silicone implant incompatibility syndrome (SIIS):A frequent cause of ASIA (Shoenfeld’s syndrome),” 56 Immunologic Research (2013), published online, April 2013. The authors employ Shoenfeld’s criteria for ASIA, and postulate a causal relationship between silicone implants and the syndrome in 32 cases.

This month, the assault has stepped up. Yehuda Shoenfeld, “Video Q&A: what is ASIA? An interview with Yehuda Shoenfeld,” 11 BMC Medicine 118 (2013). The video of Dr. Shoenfeld is also available for those who may find it hard to believe that article has found its way into print.

Silicone. It never goes away.

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