Schachtman Law

TORTINI

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

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

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?

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The Mt. Sinai Catechism

June 7th, 2013

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

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

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

Id. at 481.

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

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

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

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

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

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

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

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

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

“Rationale

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

Objectives

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

Methods

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

Measurements and Main Results

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

Conclusions

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

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

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

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

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

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

Irving Selikoff and the Right to Peaceful Dissembling

June 5th, 2013

Among concerned writers on corporate conflicts of interest, it is a commonplace that industrial sponsors of epidemiologic and other research selectively publish studies favorable to their positions in litigation and regulatory controversies. In my experience, most companies are fairly scrupulous about publishing the studies they funded. If there is a correlation in industry funding and outcome, it is largely the result of corporate funding being directed to areas in which weak or corrupt politically motivated, public-interested scientists have already published studies with dubious results. Common sense suggests that a fair test of the their claims will result in exonerative results.

It is also a commonplace that academic and public-spirited researchers will not have similar motives to suppress unfavorable results. Again, in my experience, the opposite is true. Consider that paragon of public-interested, political scientist, the late Dr. Irving Selikoff. During the course of discovery in the Caterinnichio case, I obtained manuscripts of two studies that Selikoff and his colleague, Bill Nicholson, prepared, but never published. One study examined the mortality, and especially the cancer mortality, of workers at a Johns-Manville asbestos product manufacturing plant in New Jersey. William J. Nicholson& Irving J. Selikoff, “Mortality experience of asbestos factory workers; effect of differing intensities of asbestos exposure”(circa 1988).

Selikoff’s failure to publish this manuscript on the Manville plantworkers is curious given his tireless and repeated republication of data from his insulator cohort. For those familiar with Selikoff’s agenda, the failure to publish this paper appears to have an obvious goal: suppress the nature and extent of Johns Manville’s use of crocidolite asbestos in its products:

“[O]ther asbestos varieties (amosite, crocidolite, anthophyllite) were also used for some products. In general, chrysotile was used for textiles, roofing materials, asbestos cements, brake and friction products, fillers for plastics, etc.; chrysotile with or without amosite for insulation materials; chrysotile and crocidolite for a variety of asbestos cement products.”

Id. The suppression of studies obviously takes place outside the world of commercial or industrial interests. See “Selikoff and the Mystery of the Disappearing Amphiboles.”

There was yet another studied never published by Selikoff, his work, again with Bill Nicholson, on the mortality of shipyard workers at the Electric Boat Company, in Groton, Connecticut. Irving Selikoff & William Nicholson, “Mortality Experience of 1,918 Employees of the Electric Boat Company, Groton, Connecticut January 1, 1967 – June 30, 1978” (Jan. 27, 1984) [cited below as Electric Boat].

Many of the asbestos cases that worked their way through the legal system in the 1980s and 1990s were filed by shipyard workers. Most of these shipyard workers were not insulators, but claimed asbestos bystander exposure from work near insulators. Invariably, the expert witnesses for these shipyard worker plaintiffs relied upon risk data from the Selikoff of asbestos insulators, even though Selikoff himself cautioned against using the insulator data for non-insulators:

“These particular figures apply to the particular groups of asbestos workers in this study. The net synergistic effect would not have been the same if their smoking habits had been different; and it probably would have been different if their lapsed time from first exposure to asbestos dust had been different or if the amount of asbestos dust they had inhaled had been different.”

Selikoff, et al., “Asbestos Exposure, Cigarette Smoking and Death Rates,” 330 Ann. N.Y. Acad. Sci. at 487 (1979).

Having access to Selikoff’s shipyard worker data would have been extremely useful to the fact-finding process, because these data failed to support the cancer projections used by testifying expert witnesses. Selikoff and Nicholson pointed out that about 50% of the Electric Boat shipyard workers had X-ray abnormalities Electric Boat at 2. (This finding must be interpreted in the darkness of Selikoff’s documented propensity to overread chest X-rays for asbestos findings. Rossiter, “Initial repeatability trials of the UICC/ Cincinnati classification of the radiographic appearances of pneumoconioses.” 29 Brit. J. Indus. Med. 407 (1972) (reporting IJS’s readings as among the most extreme outliers in a panel of pulmonary and radiology physicians; showing that IJS films were read as showing abnormal profusion of small, irregular densities up to twice as often as the most reliable readers in the study.)).

Selikoff’s unpublished Electric Boat study cautioned that the mortality data reflected short duration and latency, and that the full extent of asbestos-related manifestations had not been reached. Electric Boat at 3. This assertion was not really borne out by the data. Selikoff’s paper reported the following observed and expected data for lung cancer:

Years from onset of employment	10-14	15-19	20-24	25-29	30+	TOTAL
OBSERVED	4	23.3	15	3	4	35
EXPECTED	1.3	17.7	8.1	4.7	5.1	25.9

The study is primitive even by then contemporary standards. There is no control for smoking; and no data on smoking habits. There is no data on radiation exposure. (Electric Boat built nuclear submarines.) No p-values or confidence intervals are supplied; nor are any estimates of trends included.

Despite Selikoff’s assertion that the follow-up period was not sufficiently long to capture asbestos-related malignancies, the data tell a different story. The lung cancer Obs./Exp. ratios are increased for 10-14 years, and for 15-19 years, and so these risk ratios reflect that the cohort likely had non-asbestos-related risks for lung cancer, which risks are at work before the cohort entered the lagged period in which they might have elevated asbestos-related risks. Although the numbers are smaller for the time intervals that involve more than 20 years from first employment, the observed numbers and risk ratios of lung cancers hardly suggests very much in terms of an occupational asbestos risk.

These data were obtained only because Bill Nicholson often served as an expert witness for plaintiffs in personal injury actions. When he did so in New Jersey, he was subject to fairly broad discovery obligations, and thus I was able to obtain his unpublished studies. Otherwise, the public and the scientific community learned only what Selikoff selectively disclosed in media interviews. See Samuel G. Freedman, “Worker’s suit over asbestos at Groton shipyard to open” New York Times (Jan. 19, 1982) (noting the 50% prevalence finding, but not the mortality data).

Posted in Data Sharing, Scientific Evidence, Scientific Misconduct, Underlying Data | Comments Off on Irving Selikoff and the Right to Peaceful Dissembling

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.

Posted in Causation, Expert Witnesses, Scientific Evidence | Comments Off on The Doubling Dose

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

Styles of Judicial Opinion Writing

May 28th, 2013

Not Enough Original Words

You copy a little,
But not too much.
Some people say it’s degrading.

In Cojocaru v. British Columbia Women’s Hospital and Health Centre, the Supreme Court of Canada confronted an interesting question whether a litigant may challenge an adverse judgment on grounds that the trial judge plagiarized from the plaintiffs’ submissions. Cojocaru (May 24, 2013).

In this complex medical malpractice case, the trial court issued its written judgment in 368 paragraphs, of which only 47 were discernibly original. The overwhelming majority of the paragraphs, 321, were plagiarized from the plaintiffs’ submissions, without attribution. The Supreme Court agreed that this degree of plagiarism raises a serious question whether the trial judge’s judgment should be set aside as not a truly independent evaluation of the facts and law. Id. at para. 10-11.

The Court proceeded to note that trial court judgments are “entitled” to a presumption of integrity and impartiality. The defendants argued that any such presumption was vaporized by the “the extent of the copying, the quality of the copying, the lack of attribution for the copying, the nature of the case and the failure to fulfill the basic functions of reasons for judgment.” Id. at para. 52.

Although acknowledging that the trial court had copied over 87% of its judgment from the plaintiffs’ briefs, the Supreme Court held that the defendants had failed to rebut the presumption of judicial integrity and impartiality. Id. at para. 73. Judicial plagiarism is, according to the Supreme Court, “a longstanding and accepted practice.” Id. at para 30. The Court, however, acknowledged that excessive plagiarism “may raise problems.” Id.

The Supreme Court rejected the notion that judges should express themselves in their own language, and that their reasons should be their “original” work product. Id. at 31. Copying, according to the Court, does not mean that plagiarist judges have failed to think about and resolve the issues before them. Id.

The Court conceded that it was not “best practice for judges to bulk up their judgments with great swaths of borrowed material.” If the carried the copying to excess (presumably much greater than 87%), the copying “may raise problems.”

Rules and prohibitions against plagiarism do not apply to judges, say the Canadian Supreme Court judges. Id. at para. 32. According to the high court, lack of originality is a virtue in a system that depends upon precedent. “Judges are not selected, and are only rarely valued, because of their gift for original expression.” Id. (quoting, with attribution, thankfully, Simon Stern, “Copyright Originality and Judicial Originality” 63 Univ. Toronto L. J. 1 (2013)).

The Supreme Court cited precedential support of its judgment that judges are too busy to think and write in their own words. See id. at para. 37, 38 (citing English v. Emery Reimbold & Strick Ltd., [2002] EWCA Civ 605, [2002] 3 All E.R. 385 (holding that copying does not invalidate a court’s decision); id. at para. 41 (citing United States v. El Paso Natural Gas Co., 376 U.S. 651, 656 (1964) (noting that when trial judge “adopt[s] verbatim” the findings of fact submitted by counsel, “[t]hose findings, though not the product of the workings of the … judge’s mind, are formally his; they are not to be rejected out-of-hand, and they will stand if supported by evidence”).

The majority of the intermediate appellate court, the Court of Appeal, had held that the extent and nature of the plagiarism was “cogent evidence” of lack of the trial judge’s judicial integrity. Although the Supreme Court rejected the conclusion that the trial judge had failed to make an independent decision, the Supreme Court did display some original, independent thought in upholding the defendants’ assignments of error. The Supreme Court reversed the judgment for plaintiffs on the merits. Id. at para. 76.

Judicial Verbosity – Too Many Original Words

There is a tradition in New Jersey appellate cases to never issue a short, succinct opinion when a long one is at hand. Plaintiff Alison Rosenberg took Merck’s drug, Fosamax, for osteoperosis. After undergoing a tooth extraction, Rosenberg developed bone complications of her jaw. She claimed that she developed osteonecrosis of the jaw (ONJ), and that this condition was caused by her use of Fosamax, and by Merck’s negligent failure to warn that Fosamax causes ONJ. Rosenberg et al. v. Merck Sharp & Dohme Corp., No. A-5271-10T3, 2013 WL 1187916 (N.J. Super. Ct. App. Div. Mar. 25, 2013) (per curiam).

Merck defended and affirmatively sought to show that Rosenberg did not have ONJ. Its expert witness, Brent Ward, D.D.S., M.D., an expert in ONJ and in maxillofacial surgery, testified that Rosenberg suffered from osteomyelitis, not from ONJ.

At the end of the case, the trial judge instructed the jury to make findings:

“(1) whether plaintiff proved it was more likely than not that plaintiff had ONJ;

(2) whether plaintiff’s development of ONJ was a result of taking Fosamax; and

(3) whether Merck negligently failed to adequately warn about the risks of ONJ from Fosamax.”

The jury resolved the first question by finding that the plaintiff had not suffered from ONJ, and pursuant to the trial court’s instructions, ceased deliberations and notified the court of their final verdict, upon which judgment was entered. The jury thus never reached the questions about ONJ and Merck’s liability.

Rosenberg, et vir., appealed, contending that the trial judge erred in excluding evidence of Merck’s 2010 change in its warning label, which impeded her attempt to impeach Dr. Ward on the relationship between Fosamax and ONJ. The problem is that the excluded evidence was relevant only to an issue that the jury never reached. Somehow the New Jersey Appellate Division managed to draw out its per curiam opinion to eleven pages, in its own words.

Posted in Trial Procedure | Comments Off on Styles of Judicial Opinion Writing

High, Higher, Highest Quality Research Act

May 25th, 2013

“The High Quality Research Act” (HQRA), which has not been formally introduced in Congress, continues to draw attention. See “Clowns to the left of me, Jokers to the right.” Last week, Nature published an editorial piece suggesting that the HQRA is not much of a threat. Daniel Sarewitz, “Pure hype of pure research helps no one, ” 497 Nature 411 (2013).

Sarewitz suggests that “the problem” is the hype about the benefits of pure research and the let down that results from the realization that scientific progress is “often halting and incremental,” with much research not “particularly innovative or valuable.” Fair enough, but why is this Congress such an unsophisticated consumer of scientific research in the 21st century? How can it be a surprise that the scientific community engages in the same rent-seeking behaviors as do other segments of our society? Has it escaped Congress’s attention that scientists are subject to enthusiasms and group think, just like, … congressmen?

Still, Sarewitz believes that the HQRA bill is not particularly threatening to the funding of science:

“In other words, it’s not a very good bill, but neither is it much of a threat. In fact, it’s just the latest skirmish in a long-running battle for political control over publicly funded science — one fought since at least 1947, when President Truman vetoed the first bill to create the NSF because it didn’t include strong enough lines of political accountability.”

This sanguine evaluation misses the effect of the superlatives in the criteria for National Science Foundation funding:

“(1) is in the interests of the United States to advance the national health, prosperity, or welfare, and to secure the national defense by promoting the progress of science;

(2) is the finest quality, is ground breaking, and answers questions or solves problems that are of utmost importance to society at large; and

(3) is not duplicative of other research projects being funded by the Foundation or other Federal science agencies.”

HQRA Section 2(a) – (c). These superlatives set up most research proposals to fail because of the scientific community’s inability to predict in advance which studies will be truly “ground breaking” and will “answer questions .. that are of utmost importance….” Congressmen will thus be able selectively to target research grants to embarrass the NSF Director in public hearings. The Director will hardly be able to defend a particular grant with the assertion that, “well, we have many other grants that are also very fine, although not of the “finest quality”; we have other grants that are really important to society, but also not of the “utmost” importance.

Certainly, there is a good deal of wasted research funding, on grants that are frivolous. Directing funding to worthwhile research is not an easy task, but it almost certainly beyond the ken of congressional committees.

What the HQRA attempts to set up is not another layer of peer review by the NSF Director, but by Congress itself, with a line-item veto for research that offends particular Congressional sensibilities. Sarewitz is naive to believe that this bill poses little threat or change to the funding of science in the United States. The HQRA is a particularly serious threat, not to NSF funding of scientific research, but to the selection of grants that to be funded.

Congress should be looking at the NSF budget for waste, but the best way to ensure that the NSF triages funding of truly important research is to limit the funds appropriated. Contrary to the current wisdom, neither right nor left has a monopoly on stupidity when it comes to science. The history of federal funding of alternative medicine in this country (e.g., National Center for Complementary and Alternative Medicine (NCCAM), and previously the Office of Alternative Medicine.) illustrates all too well how ideological funding and Congressional “oversight” works. See, e.g., Eric Boyle, “The Politics of Alternative Medicine at the National Institutes of Health,” Federal History online 16 (2011).

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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.

Posted in Causation, Scientific Evidence | Comments Off on Two Schools of Thought

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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