Schachtman Law

TORTINI

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

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).

Posted in Scientific Evidence | Comments Off on High, Higher, Highest Quality Research Act

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.

Posted in Causation | Comments Off on Asbestos Litigation Blues

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.

Posted in Causation, Expert Witnesses, Frye, Scientific Evidence | Comments Off on As They WOE, So No Recovery Have the Reeps

Where Are They Now? Marc Lappé and the Missing Data

May 19th, 2013

The recrudescence of silicone “science” made me wonder where some of the major players in the silicone litigation are today. Some of the plaintiffs’ expert witnesses were characters who gave the litigation “atmosphere.”

Marc Alan Lappé was an experimental pathologist, who testified frequently for plaintiffs in toxic exposure cases. He founded an organization, The Center for Ethics & Toxics (CETOS), to serve as platform for his advocacy activities. Lappé was a new-age scientist, and an author of popular books on toxic everything: Chemical Deception: The Toxic Threat to Health and the Environment, and Against the Grain: Biotechnology and the Corporate Takeover of Your Food. When the silicone-gel breast implant litigation went viral, or immunologic, Lappé was embraced by the silicone sisters and their lawyers as one of their leading immunology guys. Lappé, a revolutionary, obliged and produced another pop science classic: Marc Lappé, The Tao Of Immunology: A Revolutionary New Understanding Of Our Body’s Defenses (1997).

Lappé jumped in to the silicone litigation early. He supported autoimmune claims, as well as the dubious claim that polyurethane-covered breast implants caused or accelerated breast cancer. Livshits v. Natural Y Surgical Specialties, Inc., 1991 WL 261770 (S.D.N.Y. Nov. 27, 1991). In depositions and in trial testimony, Lappé was combative and evasive, but when he wanted to be clear, he could be clear enough:

“It’s my opinion that silicone directly or indirectly can precipitate an activated immune state in such women that can lead to an autoimmune condition.”

Lappé Dep. 44:19-22 (Aug. 21, 1995), in Roden v. Medical Engineering Corp., No. 94-02-103, in District Court of Wise County, Texas, 271st Judicial District.

Plaintiffs also offered Lappé as an ethicist, in what was an obvious attempt to turn personal injury cases into passion plays and to raise the emotional temperature of the court rooms. Plaintiffs were able to get away with such nonsense in some state court cases, but the federal judges generally would not abide expert witnesses on ethics. See, e.g., Switzer v. McGhan Medical Corp., CV 94-P-14229-S, Transcript at 96-98, N.D. Ala. (Jan. 4, 1996) (Pointer, J.) (noting that Lappé would not be permitted to testify that the defendant’s conduct was unethical or unconscionable). Ironically, Lappé would become ensnared by an article, the publication of which was surrounded in ethical controversy.

Although Lappé had some experience in experimental immunology, he had no background in silicone. Undaunted, he set about to publish a work of science fiction. Marc Lappé, “Silicone-reactive disorder: a new autoimmune disease caused by immunostimulation and superantigens,” 41 Medical Hypotheses 348 (1993). Lappé went on to find some researchers with whom he could join forces, and in 1993, he and his co-authors published an article based upon what was ostensibly bench research on silicone immunology. Alas, Lappé did not really know the other authors, who were pitching their immunological screening test to plaintiffs’ support groups and to plaintiffs’ lawyers. Lappé signed up as a co-author without knowing the authors’ marketing plan, and without ever having seen the underlying data and statistical analyses. Given his credentials as a bioethicist, the lapse was remarkable. Lappé learned only through his involvement as an expert witness that his coauthors had been warned by the Food and Drug Administration about unlawful marketing of their “test,” and that some of his co-authors were involved in litigation against Bristol-Myers Squibb. Although the article was clearly intended to support both the marketing of the test, the litigation that would have benefited his coauthors directly, as well as Lappé’s testimonial adventures, the article contained no conflict of interest disclosures. Laurence Wolf, Marc Lappé, Robert Peterson, and Edward Ezrailson, “Human immune response to polydimethylsiloxane (silicone): screening studies in a breast implant population,” 7 Faseb J. 1265 (1993).

Lappé was an advocate, but he was not stupid. The late Chuck Walsh took some of Lappé’s early depositions in the breast implant litigation, and pressed him on whether he had seen or had access to the underlying data. Lappé Dep. Roden at 94:4 -21 (Aug. 21, 1995). Lappé also acknowledged that he had been unaware that the data presented in the published paper was truncated from the data originally obtained in the study. Id. at 108:19 – 109:7. Lappé bristled, as well he should, at these challenges to his ethical bona fides. He apparently requested the underlying data on more than one occasion, but his colleagues would not share the data with him:

Question: I want to ask you, did you ever get the basic raw data?

Answer: That was asked and answered as recently as three weeks ago. And the same answer applies today: No. I had asked for it. It was not give[n] to me. I have asked for it again. It’s not been given to me.

Lappé Dep. at 172:9-14 (Mar. 21, 1996), in Wolf v. Surgitek, Inc., No. 92-60186, 113th Judicial District, District Court of Harris County, Texas.

In early 1998, before Judge Pointer’s neutral expert witnesses delivered their reports in the multi-district proceedings, I traveled to Gualala, California, to take Lappé’s deposition in Page v. Bristol-Myers Squibb Co., No. JCCP-2754-03740, California Superior Court, County of San Diego (Jan. 19, 1998). I recall the little coastal town of Gualala well. The hotel, restaurant, and even the deposition room were infested with fruit flies, no doubt because pesticides were banned under Lappé’s influence. When I asked Lappé whether he had changed his views in any way, he gracefully backed away from his previous testimony:

“I believe that the current evidence, the weight of evidence suggests that the antibodies that are formed in women, perhaps in excess of their background levels for IGG antibody, may not have a specificity towards silicone itself as an antigen but may bind preferentially to silicone and therefore given nonspecific binding results such as those as the Emerald Labs detected in their plate bioassay. I think their evidence does not presently weigh in favor of considering silicone by itself as an antigen.”

Lappé Dep. Wolf at 100: 5-18. Later that year, 1998, Tim Pratt extracted further concessions from Lappé, in a Mississippi case. Lappé acknowledged that the MDL court’s neutral expert witnesses had done a “reasonably good job,” and that he agreed with them that there was not consistent evidence to support the claim that silicone caused autoimmune disease. Lappé Dep. at 26:1-9 (Dec. 17, 1998), in Brassell v. Medical Engineering Corp., Case No. 251-96-1074 CIV, Hinds County Circuit Court, Mississippi.

The litigation faded away, and so did Lappé. He died in 2005. Douglas Martin, “Marc Lappé, 62, Dies; Fought Against Chemical Perils,” N.Y. Times (May 21, 2005). Few other expert witnesses for silicone plaintiffs had the intellectual integrity to confess error. I hope he has found his missing data.

Posted in Expert Witnesses, Scientific Evidence, Underlying Data | Comments Off on Where Are They Now? Marc Lappé and the Missing Data

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.

Posted in Causation, Scientific Evidence | Comments Off on Biopersistant Silicone

The opinions, statements, and asseverations expressed on Tortini are my own, or those of invited guests, and these writings do not necessarily represent the views of clients, friends, or family, even when supported by good and sufficient reason.