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.
