TORTINI

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

Matrixx Unloaded

March 29th, 2011

In writing for a unanimous Court in Matrixx Initiatives, Inc. v. Siracusano, Justice Sotomayor wandered far afield from the world of pleading rules to flyblow the world of expert witness jurisprudence.  How and why did this happen?  Why did Matrixx invoke the concept of statistical significance to counter case reports of adverse events? Did Matrixx oversell its scientific position, thereby handing Justice Sotomayor an opportunity to unravel decades of evolution of law on the admissibility of expert witness opinion testimony?  Inquiring minds want to know.

Still, whatever the occasion for the obiter dicta, Court’s pronouncements on expert witnesses are stunning for their irrelevance and questionable scholarship:

“We note that courts frequently permit expert testimony on causation based on evidence other than statistical significance. See, e.g., Best v. Lowe’s Home Centers, Inc., 563 F. 3d 171, 178 (6th Cir 2009); Westberry v. Gislaved Gummi AB, 178 F. 3d 257, 263–264 (4th Cir. 1999) (citing cases); Wells v. Ortho Pharmaceutical Corp., 788 F. 2d 741, 744–745 (11th Cir. 1986). We need not consider whether the expert testimony was properly admitted in those cases, and we do not attempt to define here what constitutes reliable evidence of causation.”

Id. at 12.  What is remarkable about this passage is that the first two cases cited involved differential etiology or diagnosis to assess specific causation, not general causation.  As most courts have recognized, this assessment strategy requires that general causation has already been established. See, e.g., Hall v. Baxter Healthcare, 947 F. Supp. 1387 (D. Ore. 1996).

The citation to the third case, Wells, is noteworthy because the case has nothing to do with adverse event reports or statistical significance.  Wells involved a claim of birth defects caused by the use of spermicidal jelly contraceptive, which had been the subject of several studies, one of which at least yielded a statistically significant increase in detected birth defects over what was expected.  Wells v. Ortho Pharmaceutical Corp., 615 F. Supp. 262 (N.D.Ga. 1985), aff’d and rev’d in part on other grounds, 788 F.2d 741 (11th Cir.), cert. denied, 479 U.S.950 (1986).  Wells could thus hardly be an example of a case in which there was a judgment of causation based upon a scientific study that lacked statistical significance in its findings. Of course, finding statistical significance is just the beginning of assessing the causality of an association; Wells was notorious for its poor assessment of all the determinants of scientific causation.

The citation to Wells is thus remarkable because the Wells decision was rightly and widely criticized for its failure to evaluate the entire evidentiary display, as well as for its failure to rule out bias and confounding in the studies relied upon by the plaintiff.  See , e.g., James L. Mills and Duane Alexander, “Teratogens and ‘Litogens’,” 15 New Engl. J. Med. 1234 (1986); Samuel R. Gross, “Expert Evidence,” 1991 Wis. L. Rev. 1113, 1121-24 (1991) (“Unfortunately, Judge Shoob’s decision is absolutely wrong. There is no scientifically credible evidence that Ortho-Gynol Contraceptive Jelly ever causes birth defects.”). See also Editorial, “Federal Judges v. Science,” N.Y. Times, December 27, 1986, at A22 (unsigned editorial);  David E. Bernstein, “Junk Science in the Courtroom,” Wall St. J. at A 15 (Mar. 24,1993) (pointing to Wells as a prominent example of how the federal judiciary had embarrassed American judicial system with its careless, non-evidence based approach to scientific evidence). A few years later, another case in the same judicial district against the same defendant for the same product resulted in the grant of summary judgment.  Smith v. Ortho Pharmaceutical Corp., 770 F. Supp. 1561 (N.D. Ga. 1991) (supposedly distinguishing Wells on the basis of more recent studies).

Perhaps the most remarkable aspect of the Court’s citation to Wells is that the case, and all it stands for, was overruled sub silentio by the Supreme Court’s own decisions in Daubert, Joiner, Kumho Tire, and Weisgram.  And if that did not kill the concept, then there was the simple matter of a supervening statute:  the 2000 amendment of Rule 702, of Federal Rules of Evidence.

Citing a case as jurisprudentially dead and discredited as Wells could have been sloppy scholarship and lawyering.  The principle of charity, however, suggests it was purposeful, and that is a frightful prospect.

Courts and Commentators on the Use of Relative Risks to Infer Specific Causation

March 18th, 2011

Below, I have collected some of the case law and commentary 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 his or her disease or injury.


Radiation

Johnston v. United States, 597 F. Supp. 374, 412, 425-26 (D. Kan. 1984)

Allen v. United States, 588 F. Supp. 247 (1984), rev’d on other grounds, 816 F.2d 1417 (10th Cir. 1987)

In re TMI Litig., 193 F.3d 613, 629 (3d Cir. 1999)(rejecting “doubling dose” trial court’s analysis), amended, 199 F.3d 158 (3d Cir. 2000)

In re Hanford Nuclear Reservation Litig., 1998 WL 775340, at *8 (E.D.Wash. Aug. 21, 1998), rev’d, 292 F.3d 1124, 1136-37 (9th Cir. 2002)


Swine Flu- GBS Cases

Cook v. United States, 545 F. Supp. 306, 308 (N.D. Cal. 1982)(“Whenever the relative risk to vaccinated persons is greater than two times the risk to unvaccinated persons, there is a greater than 50% chance that a given GBS case among vaccinees of that latency period is attributable to vaccination, thus sustaining plaintiff’s burden of proof on causation.”)

Padgett v. United States, 553 F. Supp. 794, 800 – 01 (W.D. Tex. 1982) (“From the relative risk, we can calculate the probability that a given case of GBS was caused by vaccination. . . . [A] relative risk of 2 or greater would indicate that it was more likely than not that vaccination caused a case of GBS.”);

Manko v. United States, 636 F. Supp. 1419, 1434 (W.D. Mo. 1986)(relative risk of 2, or less, means exposure not the probable cause of disease claimed), aff’d in relevant part, 830 F.2d 831 (8th Cir. 1987)


IUD Cases – Pelvic Inflammatory Disease

Marder v. G.D. Searle & Co., 630 F. Supp. 1087, 1092 (D.Md. 1986) (“In epidemiological terms, a two-fold increased risk is an important showing for plaintiffs to make because it is the equivalent of the required legal burden of proof—a showing of causation by the preponderance of the evidence or, in other words, a probability of greater than 50%.”), aff’d mem. on other grounds sub nom. Wheelahan v. G.D.Searle & Co., 814 F.2d 655 (4th Cir. 1987)(per curiam)


Bendectin cases

Lynch v. Merrill-National Laboratories, 646 F.Supp. 856 (D. Mass. 1986)(granting summary judgment), aff’d, 830 F.2d 1190, 1197 (1st Cir. 1987)(distinguishing between chances that “somewhat favor” plaintiff and plaintiff’s burden of showing specific causation by “preponderant evidence”)

DeLuca v. Merrell Dow Pharm., Inc., 911 F.2d 941, 958-9 (3d Cir. 1990)

Daubert v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1321 (9th Cir.)(“Daubert II”)(holding that for epidemiological testimony to be admissible to prove specific causation, there must have been a relative risk for the plaintiff of greater than 2) (“For an epidemiological study to show causation under a preponderance standard . . . the study must how that children whose mothers took Bendectin are more than twice as likely to develop limb reduction birth defects as children whose mothers did not.”), cert. denied, 516 U.S. 869 (1995)

DePyper v. Navarro, 1995 WL 788828 (Mich. Cir. Ct. Nov. 27, 1995)

Oxendine v. Merrell Dow Pharm., Inc., 1996 WL 680992 (D.C. Super. Ct. Oct. 24, 1996)

Merrell Dow Pharms., Inc. v. Havner, 953 S.W.2d 706, 716 (Tex. 1997) (holding, in accord with the weight of judicial authority, “that the requirement of a more than 50% probability means that epidemiological evidence must show that the risk of an injury or condition in the exposed population was more than double the risk in the unexposed or control population”); id. at at 719 (rejecting isolated statistically significant associations when not consistently found among studies)


Silicone Cases

Hall v. Baxter Healthcare, 947 F.Supp. 1387, 1392, 1397, 1403-04 (D. Ore. 1996)(discussing relative risk of 2.0)

Pick v. American Medical Systems, Inc., 958 F. Supp. 1151, 1160 (E.D.La. 1997) (noting, in penile implant case, that “any” increased risk suggests that the exposure “may” have played some causal role)

In re Breast Implant Litigation, 11 F. Supp. 2d 1217, 1226 -27 (D. Colo. 1998)(relative risk of 2.0 or less shows that the background risk is at least as likely to have given rise to the alleged injury)

Barrow v. Bristol-Myers Squibb Co., 1998 WL 812318 (M.D. Fla. Oct. 29, 1998)

Allison v. McGhan Med. Corp., 184 F.3d 1300, 1315n.16, 1316 (11th Cir. 1999)(affirming exclusion of expert testimony based upon a study with a risk ratio of 1.24; noting that statistically significant epidemiological study reporting an increased risk of marker of disease of 1.24 times in patients with breast implants was so close to 1.0 that it “was not worth serious consideration for proving causation”; threshold for concluding that an agent more likely than not caused a disease is 2.0, citing Federal Judicial Center, Reference Manual on Scientific Evidence 168-69 (1994))

Grant v. Bristol-Myers Squibb, 97 F. Supp. 2d 986, 992 (D. Ariz. 2000)

Pozefsky v. Baxter Healthcare Corp., No. 92-CV-0314, 2001 WL 967608, at *3 (N.D.N.Y. August 16, 2001) (excluding causation opinion testimony given contrary epidemiologic studies; noting that sufficient epidemiologic evidence requires relative risk greater than two)

In re Silicone Gel Breast Implant Litig., 318 F. Supp. 2d 879, 893 (C.D. Cal. 2004)

Norris v. Baxter Healthcare Corp., 397 F.3d 878 (10th Cir. 2005) (discussing but not deciding specific causation and the need for relative risk greater than two; no reliable showing of general causation)

Barrow v. Bristol-Meyers Squibb Co., 1998 WL 812318, at *23 (M.D. Fla., Oct. 29, 1998)

Minnesota Mining and Manufacturing v. Atterbury, 978 S.W.2d 183, 198 (Tex.App. – Texarkana 1998) (noting that “[t]here is no requirement in a toxic tort case that a party must have reliable evidence of a relative risk of 2.0 or greater”)


Asbestos

Washington v. Armstrong World Indus., Inc., 839 F.2d 1121 (5th Cir. 1988)(affirming grant of summary judgment on grounds that there was insufficient evidence that plaintiff’s colon cancer was caused by asbestos)

Lee v. Johns Manville Corp., slip op. at 3, Phila. Cty. Ct. C.P., Sept. Term 1978, No. 88 (123) (Oct. 26, 1983) (Forer, J.)(entering verdict in favor of defendants on grounds that plaintiff had failed to show that his colo rectal cancer had been caused by asbestos exposure after adducing evidence of a relative risk less than two)

Primavera v. Celotex Corp., Phila. Cty. Ct. C.P., December Term, 1981, No. 1283 (Bench Op. of Hon. Berel Caesar, (Nov. 2, 1988) (granting compulsory nonsuit on the plaintiff’s claim that his colorectal cancer was caused by his occupational exposure to asbestos)

Grassis v. Johns-Manville Corp., 248 N.J.Super. 446, 455-56, 591 A.2d 671, 676 (App. Div. 1991)

Landrigan v. Celotex Corp., 127 N.J. 404, 419, 605 A.2d 1079 (1992)

Caterinicchio v. Pittsburgh Corning Corp., 127 N.J. 428, 605 A.2d 1092 (1992)

In re Joint E. & S. Dist. Asbestos Litig., 758 F. Supp. 199 (S.D.N.Y. 1991), rev’d sub nom. Maiorano v. Owens Corning Corp., 964 F.2d 92 (2d Cir. 1992)

Maiorana v. National Gypsum, 827 F. Supp. 1014, 1043 (S.D.N.Y. 1993), aff’d in part and rev’d in part, 52 F.3d 1122, 1134 (2d Cir. 1995)

Jones v. Owens-Corning Fiberglas Corp., 288 N.J. Super. 258, 266, 672 A.2d 230, 235 (App. Div. 1996)

Keene Corp. v. Hall, 626 A.2d 997 (Md. Spec. Ct. App. 1993)(laryngeal cancer)

In re W.R. Grace & Co., 355 B.R. 462, 483 (Bankr. D. Del. 2006) (requiring showing of relative risk greater than two to support property damage claims based on unreasonable risks from asbestos insulation products).


Pharmaceutical Cases

Ambrosini v. Upjohn, 1995 WL 637650, at *4 (D.D.C. 1995)

Ambrosini v. Labarraque, 101 F.3d 129, 135 (D.C. Cir. 1996)(Depo-Provera, birth defects)

Miller v. Pfizer, 196 F. Supp. 2d 1062, 1079 (D. Kan. 2002) (acknowledging that most courts require a showing of RR > 2, but questioning their reasoning), aff’d, 356 F. 3d 1326 (10th Cir. 2004)

Smith v. Wyeth-Ayerst Laboratories Co., appears to recognize that risk and cause are distinct concepts. 278 F. Supp. 2d 684, 691 (W.D.N.C. 2003) (“Epidemiologic data that shows a risk cannot support an inference of cause unless (1) the data are statistically significant according to scientific standards used for evaluating such associations; (2) the relative risk is sufficiently strong to support an inference of ‘more likely than not’; and (3)  the epidemiologic data fits the plaintiff’s case in terms of exposure, latency, and other relevant variables.”)

Burton v. Wyeth-Ayherst Laboratories, 513 F. Supp. 2d 719 (N.D. Tex. 2007)

In re Bextra and Celebrex Marketing Sales Practices and Prod. Liab. Litig., 524 F. Supp. 2d 1166, 1172 (N.D. Calif. 2007)(observing that epidemiologic studies “can also be probative of specific causation, but only if the relative risk is greater than 2.0, that is, the product more than doubles the risk of getting the disease”)

In re Viagra Products Liab. Litigat., 572 F. Supp. 2d 1071, 1078 (D. Minn. 2008)(noting that some but not all courts have concluded relative risks under two support finding expert witness’s opinion to be inadmissible).


Toxic Tort Cases

In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 785, 836 (E.D.N.Y. 1984) (“A government administrative agency may regulate or prohibit the use of toxic substances through rulemaking, despite a very low probability of any causal relationship.  A court, in contrast, must observe the tort law requirement that a plaintiff establish a probability of more than 50% that the defendant’s action injured him. … This means that at least a two-fold increase in incidence of the disease attributable to Agent Orange exposure is required to permit recovery if epidemiological studies alone are relied upon.”), aff’d 818 F.2d 145, 150-51 (2d Cir. 1987)(approving district court’s analysis), cert. denied sub nom. Pinkney v. Dow Chemical Co., 487 U.S. 1234 (1988)

Sanderson v. Int’l Flavors & Fragrances, Inc., 950 F. Supp. 981, 998 n. 17,  999-1000, 1004 (C.D.Cal.1996) (more than a doubling of risk is required in case involving aldehyde exposure and claimed multiple chemical sensitivities)

Wright v. Willamette Indus., Inc., 91 F.3d 1105 (8th Cir. 1996)(“Actions in tort for damages focus on the question of whether to transfer money from one individual to another, and under common-law principles (like the ones that Arkansas law recognizes) that transfer can take place only if one individual proves, among other things, that it is more likely than not that another individual has caused him or her harm.  It is therefore not enough for a plaintiff to show that a certain chemical agent sometimes causes the kind of harm that he or she is complaining of.  At a minimum, we think that there must be evidence from which the factfinder can conclude that the plaintiff was exposed to levels of that agent that are known to cause the kind of harm that the plaintiff claims to have suffered. See Abuan v. General Elec. Co., 3 F.3d at 333.  We do not require a mathematically precise table equating levels of exposure with levels of harm, but there must be evidence from which a reasonable person could conclude that a defendant’s emission has probably caused a particular plaintiff the kind of harm of which he or she complains before there can be a recovery.”)

McDaniel v. CSX Transp., Inc., 955 S.W.2d 257, 264 (1997) (doubling of risk is relevant but not required as a matter of law)

Lofgren v. Motorola, 1998 WL 299925 *14 (Ariz. Super. 1998) (TCE, cancer)

Berry v. CSX Transp., Inc., 709 So. 2d 552 (Fla. D. Ct.App. 1998)(solvents, toxic encephalopathy)

Bartley v. Euclid, Inc., 158 F.3d 261 (5th Cir. 1998)

Magistrini v. One Hour Martinizing Dry Cleaning, 180 F. Supp. 2d 584, 591-92 (D.N.J.2002) (‘‘the threshold for concluding that an agent was more likely than not the cause of an individual’s disease is a relative risk greater than 2.0’’), aff’d, 68 F. App’x 356 (3d Cir. 2003)

Ferguson v. Riverside School Dist. No. 416, 2002 WL 34355958 (E.D. Wash. Feb. 6, 2002)(No. CS-00-0097-FVS)

Daniels v. Lyondell-Citgo Refining Co., 99 S.W.3d 722, 727 (Tex. App. – Houston [1st Dist.] 2003)

Graham v Lautrec Ltd., 2003 WL 23512133 (Mich. Cir. Ct., July 24, 2003)

Theofanis v. Sarrafi, 791 N.E.2d 38,48 (Ill. App. 2003)(reversing and granting new trial to plaintiff who received an award of no damages when experts testified that relative risk was between 2.0 and 3.0)(“where the risk with the negligent act is at least twice as great as the risk in the absence of negligence, the evidence supports a finding that, more likely than not, the negligence in fact caused the harm”).

Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814, 846 (W.D. Tex. 2005)(relative risk less than 3.0 represents only a weak association)

Mobil Oil Corp. v. Bailey, 187 S.W.3d 263, 268 (Tex. App. – Beaumont 2006)

Cook v. Rockwell Internat’l Corp., 580 F. Supp. 2d 1071, 1088-89 (D. Colo. 2006)

In re Lockheed Litig. Cases, 115 Cal. App. 4th 558 (2004), rev’d in part, 23 Cal. Rptr. 3d 762, 765 (Cal. App. 2d Dist. 2005), cert. dismissed, 192 P.3d 403 (Cal. 2007)

Watts v. Radiator Specialty Co., 990 So. 2d 143 (Miss. 2008)(“The threshold for concluding that an agent was more likely than not the cause of an individual’s disease is a relative risk greater than 2.0.”)

Henricksen v. Conocophillips Co., 605 F. Supp. 2d 1142, 1158 (E.D. Wash. 2009) (noting that under Circuit precedent, epidemiologic studies showing low-level risk may suffiicent to show general causation but are sufficient to show specific causation only if relative risk exceeds two) (excluding plaintiff‘s expert witness’s testimony because epidemiologic evidence iis “contradictory and inconsistent”)

George v. Vermont League of Cities and Towns, 2010 Vt. 1, 993 A.2d 367, 375 (2010)

City of San Antonio v. Pollock, 284 S.W.3d 809, 818 (Tex. 2009) (holding testimony admitted insufficient as matter of law).


ACADEMIC COMMENTATORS

Michael Dore, “A Commentary of the Use of Epidemiological Evidence in Demonstrating Cause-in-Fact,” 7 Harv. Envt’l L.Rev. 429, 431-40 (1983)

Bert Black & David E. Lilienfeld, Epidemiologic Proof in Toxic Tort Litigation, 52 Fordham L. Rev. 732, 767 – 69 (1984)

David E. Lilienfeld & Bert Black, “The Epidemiologist in Court,” 123 Am. J. Epidemiology 961, 963 (1986)(a relative risk of 1.5 allows an inference of attributable risk of 33%, which means any individual case is less likely than not to be causally related)

Powell, “How to Tell the Truth With Statistics: A New Statistical Approach to Analyzing the Bendectin Epidemiological Data in the Aftermath of Daubert v. Merrell Dow Pharmaceuticals,” 31 Houston L. Rev. 1241, 1310 (1994) (“The plaintiff who wishes to reach the jury on the issue of causation must submit a statistical analysis indicating that exposure to the drug in question more likely than not caused the birth defects in question.  To support a finding of causation, the meta-analysis summary odds ratio must exceed two.”)

Linda Bailey, et al., “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence at 121, 168-69 (Federal Judical Ctr. 1st ed. 1994) (“The threshold for concluding that an agent was more likely the cause of a disease than not is a relative risk greater than 2.0 … .  A relative risk greater than 2.0 would permit an inference that an individual plaintiff’s disease was more likely than not caused by the implicated agent.”)

Ben Armstrong & Gilles Theriault, “Compensating Lung Cancer Patients Occupationally Exposed to Coal Tar Pitch Volatiles,” 53 Occup. Envt’l Med. 160 (1996)

Philip E. Enterline, “Toxic Torts:  Are They Poisoning Scientific Literature?” 30 Am. J. Indus. Med. 121 (1996)

Joseph V. Rodricks & Susan H. Rieth, “Toxicological Risk Assessment in the Court:  Are Available Methodologies Suitable for Evaluating Toxic Tort and Product Liability Claims?,” 27 Reg. Toxicol. & Pharmacol. 21, 25-30 (1998)

Michael Green et al., “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence 333, 381, 383 (Federal Judicial Center ed., 2d ed. 2000), available at http://www.fjc.gov ( “[E]pidemiology addresses whether an agent can cause a disease, not whether an agent did cause a specific plaintiff’s disease.  * * *  Nevertheless, the specific causation issue is a necessary legal element in a toxic substance case. The plaintiff must establish not only that the defendant’s agent is capable of causing disease but also that it did cause the plaintiff’s disease.  Thus, a number of courts have confronted the legal question of what is acceptable proof of specific causation and the role that epidemiologic evidence plays in answering that question. This question is not a question that is addressed by epidemiology. Rather, it is a legal question a number of courts have grappled with.”) (“[t]he civil burden of proof is described most often as requiring the fact finder to believe that what is sought to be proved is more likely true than not true. The relative risk from epidemiologic studies can be adapted to this 50% plus standard to yield a probability or likelihood that an agent caused an individual’s disease.”)

David W. Barnes, “Too Many Probabilities:  Statistical Evidence of Tort Causation,” 64 Law and Contemp. Problems 191, 206 (2001) (criticizing the uncritical use of a relative risk greater than two to signify the probability, but acknowledging that sometimes a credible, precise RR, greater than 1.0, will be too small to support specific causation, such as the RR of 1.24 seen in the Allison case)

Russellyn S. Carruth & Bernard D. Goldstein, “Relative Risk Greater than Two in Proof of Causation in Toxic Tort Litigation,” 41 Jurimetrics 195 (2001) (criticizing the use of a relative risk of two benchmark, but acknowledging that when a disease has multiple causes and a substantial base rate in the general population, “there is no objective means to determine if a particular person’s disease was caused by some other environmental exposure, or by a non-environmental cause.”)

Richard W. Clapp & David Ozonoff, “Environment and Health:  Vital Intersection or Contested Territory?” 36 Am. J. L. & Med. 189, 210 (2004)( incorrectly describing the meaning of a confidence interval:  “A relative risk of 1.8, with confidence interval of 1.3 to 2.9 could very likely represent a true relative risk greater than 2.0, and as high as 2.9 in 95 out of 100 repeated trials.”)

Erica Beecher-Monas, Evaluating Scientific Evidence 58, 67 (N.Y. 2007)(“No matter how persuasive epidemiological or toxicological studies may be, they could not show individual causation, although they might enable a (probabilistic) judgment about the association of a particular chemical exposure to human disease in general.”)(“While significance testing characterizes the probability that the relative risk would be the same as found in the study as if the results were due to chance, a relative risk of 2 is the threshold for a greater than 50 percent chance that the effect was caused by the agent in question.”)(incorrectly describing significance probability as a point probability as opposed to tail probabilities)

Andrew W. Jurs, “Daubert, Probabilities and Possibilities and the Ohio Solution:  A Sensible Approach to Relevance Under Rule 702 in Civil and Criminal Applications,” 41 Akron L. Rev. 609, 637 (2008)(acknowledging that relative risks less than 2.0 invite jury speculation about individual, specific causation)

Relative Risks and Individual Causal Attribution Using Risk Size

March 18th, 2011

The relative risk argument is simple.  A relative risk of 1.0 means that the rate of disease incidence or mortality is the same among the exposed and control populations.  A relative risk of 2.0 means that the incidence rate in the exposed population is twice that in the controls.  The existence of an observed rate among the non-exposed controls suggests that we are dealing with a disease of “ordinary life,” for which there is an expected rate of occurrence.  Most chronic diseases, such as cancer, autoimmune disease, cardiovascular diseases, fall into this category of diseases of ordinary life.

If a study of a disease that is prevalent in the general population, say colon cancer, is conducted in an exposed cohort of workers, say asbestos insulators, and the study finds a relative risk of 1.5, we would have to take several steps to assess the finding’s relevance in litigation.  First, this positive association would have to be evaluated for causality.  Bias and confounding would have to be ruled out as explaining the apparent increase in risk.  Furthermore, the association would have to be evaluated for various indicia of causality, such as consistency with other studies, dose-response relationship between exposure and outcome, biological plausibility and coherence, and support from experimental studies.  In the case of asbestos and colon cancer, the causal hypothesis has repeated failed to be supported by such evaluations, but even if we were to assume general causation, arguendo, we would be left without a way to infer causation in a given case.  If plaintiff supported his case with evidence or a relative risk of 1.5, we would have 50% more observed cases than expected.  So if the observed population was expected to experience 100 colon cancer cases over the observation period, a relative risk of 1.5 means that 150 such cases were observed, or 100 expected cases and 50 putative excess cases.  Alas, there is no principled way to tell an excess case from an expected case, and the odds favor the defense two to one that any given case arose from the expected population as opposed to the excess group.  As a probability, the probability that plaintiff’s case arose from the excess portion is 33%, well below what is needed to support a sustainable claim.  Again, this assumes many facts in plaintiff’s favor, such as a perfect epidemiologic study, without bias or confounding, and with consistency among the findings of similar studies.  (None of these assumptions is even close to satisfied for asbestos and colon cancer.)

In the Agent Orange litigation, Judge Weinstein implicitly recognized the problem that very large relative risks suggested that an individual case was likely to have been related to its antecedent risks.  Small relative risks suggested that any inference of specific causation from the antecedent risk was largely speculative, in the absence of some reliable marker of exposure-related causation. See In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 785, 817 (E.D.N.Y. 1984)(plaintiffs must prove at least a two-fold increase in rate of disease allegedly caused by the exposure), aff’d, 818 F.2d 145, 150-51 (2d Cir. 1987)(approving district court’s analysis), cert. denied sub nom. Pinkney v. Dow Chemical Co., 484 U.S. 1004  (1988); see also In re “Agent Orange” Prod. Liab. Litig., 611 F. Supp. 1223, 1240, 1262 (E.D.N.Y. 1985)(excluding plaintiffs’ expert witnesses), aff’d, 818 F.2d 187 (2d Cir. 1987), cert. denied, 487 U.S. 1234 (1988). 

Ever since Judge Weinstein embraced the relative risk of two, as an important benchmark to be exceeded if plaintiffs hoped to show specific causation, scientists who practice medicine for the redistribution of wealth have attacked the concept.  The challengers have urged that small relative risks, including relative risks of two or less, could suffice to support causal attribution in a given case, especially in the presence of relevant clinical findings.  The challengers, however been vague and evasive when it comes to identifying what are the relevant clinical findings and how they operate to show that the risk has actually operated to become part of the causal pathway that has led to the individual’s injury or disease.

Among the most vociferous of the challengers has been Professor Sander Greenland, of the University of California Los Angeles School of Public Health.  Greenland has published his criticisms of the inference of a probability of individual causation from the relative risk on many occasions.  See, e.g., Sander Greenland & James Robins, “Conceptual Problems in the Definition and Interpretation of Attributable Fractions,” 128 Am. J. Epidem. 1185 (1988); James Robins & Sander Greenland, “The Probability of Causation Under a Stochastic Model for Individual Risk,” 45 Biometrics 1125 (1989); James Robins & Sander Greenland, “Estimability and Estimation of Excess and Etiologic Fractions,” 8 Statistics in Medicine 845 (1989); James Robins & Sander Greenland, “Estimability and Estimation of Expected Years of Life Lost Due to a Hazardous Exposure,” 10 Statistics in Medicine 79 (1991); Jan Beyea & Sander Greenland, “The Importance  of Specifying the Underyling Biologic Model in Estimating the Probability of Causation,” 76 Health Physics 269 (1999; Sander Greenland, “Relation of Probability of Causation to Relative Risk and Doubling Dose:  A Methodologic Error That Has Become a Social Problem,” 89 Am. J. Pub. Health 1166 (1999); Sander Greenland & James Robins, “Epidemiology, Justice, and the Probability of Causation,” 40 Jurimetrics 321 (2000).

Greenland’s criticisms turn on various assumptions such as the risk may not be evenly distributed within the sampled population, or the causal mechanism may accelerate onset of disease in such a way as to leave the relative risk unchanged in the study under consideration.  Greenland is correct that it is important to have a clear causal model in mind when evaluating the possibility of causal attributions in the light of population studies and their measures of relative risk.  He is also correct that his clever assumptions, if true, could affect the reasonableness of claiming that a relative risk of two or less supports the defense position in many toxic tort cases.  Unfortunately, Greenland’s clever assumptions and his arguments prove too much, because in many, if not most, cases the causal model is not defined.  There is often no evidence to support the plaintiffs’ claims of acceleration, or of sequestration of risk within the sampled population, and certainly no basis for claiming that the plaintiff belongs to a subset of “vulnerable” exposed persons with a higher than average risk that is reflected in the study relative risk.  Without evidence to support Greenland’s various assumptions, even higher relative risks than 2.0, say risks in the range of 2.0 to 20.0, would be unhelpful to support a plaintiffs’ case.  We would be thrown back to the early case law that held that risk can never support individual attributions, and Judge Weinstein’s rather pragmatic pronouncement in Agent Orange would be thrown aside, to the benefit of defendants in toxic tort cases. 

Last year, the Vermont Supreme Court reaffirmed the continuing vitality of the relative risk argument, on the original pragmatic justification offered by Judge Weinstein in the Agent Orange cases.  George v. Vermont League of Cities and Towns, 2010 Vt. 1, 993 A.2d 367 (Vt. 2010).  Indeed, George may well have been one of the best, and the least unheralded, decisions of 2010.

Mr. George had been a fireman before he died of non-Hodgkin’s lymphoma (NHL).  In administrative workman’s compensation proceedings, the Commissioner ruled that widow failed to show a causal connection between firefighting and NHL, although there was an “association.” His widow appealed the denial of benefits.  On de novo review, the trial court excluded plaintiffs’ expert witnesses on Rule 702 grounds.  (Vermont law follows federal law on requiring relevance and reliability of expert witnesses’ opinions.) The case ended up before the Vermont Supreme Court, which had to review the trial court’s handling of the Rule 702 issues.

Several issues were at play.  The plaintiff had presented multiple expert witnesses, Drs. Tee Guidotti and James Lockey, who had presented general and/or specific causation opinions on firefighting and NHL.  These witnesses relied upon epidemiologic studies, some of which had been incorporated into a meta-analysis, and a so-called “weight of the evidence” methodology.

The Vermont Supreme Court recognized the limits of using epidemiology to resolve the specific causation question in George. The Court found the Texas Supreme Court’s treatment of this issue to be persuasive: 

“epidemiological studies can assist in demonstrating a general association between a substance and a disease or condition, but they cannot prove that a substance actually caused a disease or condition in a particular individual.”

Id. at 374 (relying upon and quoting from Merrell Dow Pharms., Inc. v. Havner, 953 S.W.2d 706, 715 (Tex.1997)).

The Court also quoted from, and relied upon, the pronouncement of the Federal Judicial Center’s Reference Manual, which explains that ‘‘epidemiology is concerned with the incidence of disease in populations and does not address the question of the cause of an individual’s disease.  This question, sometimes referred to as specific causation, is beyond the domain of the science of epidemiology.’’ Id. at 375 (quoting from M. Green et al., “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence 333, 381 (2d ed. 2000); footnote omitted in court’s quotation of this source).

Faced with the academic and judicial criticisms of using the relative risk (which is sometimes referred to as “effect size”), the Court recognized the pragmatic compromise between science and the needs of the legal system, embraced by using the relative risk as a benchmark showing for plaintiffs to make in toxic tort litigation:

“The trial court here adopted a relative risk factor of 2.0 as a benchmark, finding that it easily tied into Vermont’s ‘more likely than not’ civil standard and that such a benchmark was helpful in this case because the eight epidemiological studies relied upon by claimant’s experts reflected widely varying degrees of relative risk.”

 Id. at 375.

“Given claimant’s burden of proof, however, and the inherent limitations of epidemiological data in addressing specific causation, the trial court reasonably found the 2.0 standard to be a helpful benchmark in evaluating the epidemiological evidence underlying Dr. Guidotti’s opinion.”

Id. at 377.

“Mindful of this balance, we conclude that the trial court did not abuse its discretion in considering a relative risk greater than 2.0 as a reasonable and helpful benchmark under the circumstances presented here.”

 Id. at 378.

 The Vermont Supreme Court was also clearly worried about how and why plaintiff’s expert witnesses selected some studies to include in their “weight of evidence” methodology.  Without an adequate explanation of selection and weighting criteria, the choices seemed like arbitrary “cherry picking.”  Id. at 389. This worry is amply justified.  Weight of the evidence methodology is notoriously vague and indeterminate; unless the criteria for weighting are pre-specified and rigorously followed, claims based upon this methodology may be little more than subjective preferences. See, e.g., Douglas L.Weed, “Weight of Evidence: A Review of Concept and Methods,” 25 Risk Analysis 1545 (2005). 

In part, plaintiff’s expert witnesses also relied upon a meta-analysis of observational studies that looked at NHL risk among firefighters.  The Court was concerned about the plaintiffs’ expert witnesses’ failure to explain selection and weighting of studies in the meta-analysis methodology.  This criticism may well be simply plaintiff’s witnesses’ failure to explain the methodology of a published study, which in turn may have properly used an acceptable methodology to provide a summary estimate of risk of NHL among firefighters.  The meta-analysis in question, however, appears to have found a summary risk estimate of 1.51, with a 95% confidence interval, 1.31-1.73.  G.K. LeMasters, et al., “Cancer risk among firefighters: a review and meta-analysis of 32 studies,” 48 J. Occup. Envt’l Med. 1189 (2006).  The plaintiff’s expert witnesses were thus relying upon a study that quantifying the increased risk at 51%, with an upper bound from sampling variability, at 73%.  To the extent that the plaintiff had succeeded in providing reliable evidence of increased risk, she had also succeeded in showing that a doubling, or more, of the risk for NHL was statistically unlikely.  This is hardly a propitious way to win a lawsuit.

Risk and Causation in the Law

March 16th, 2011

In “Risk ≠ Causation,” I discussed the lack of scientific basis for confusing and conflating risk and cause.  For many years, the law was in accord, and plaintiffs could not substitute evidence of risk for evidence of cause in fact.  Some of the case law is collected, below.  The law in this area was fairly stable until Judge Weinstein’s important decision in the Agent Orange litigation, where the court confronted the limitations of epidemiologic evidence to support conclusions about specific causation. Judge Weinstein implicitly recognized the problem that very large relative risks certainly suggested that an individual case was likely to have been related to its antecedent risks.  Small relative risks suggested that any inference of specific causation from the antecedent risk was largely speculative, in the absence of some reliable marker of exposure-related causation. See In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 785, 817 (E.D.N.Y. 1984)(plaintiffs must prove at least a two-fold increase in rate of disease allegedly caused by the exposure), aff’d, 818 F.2d 145, 150-51 (2d Cir. 1987)(approving district court’s analysis), cert. denied sub nom. Pinkney v. Dow Chemical Co., 484 U.S. 1004  (1988); see also In re “Agent Orange” Prod. Liab. Litig., 611 F. Supp. 1223, 1240 (E.D.N.Y. 1985)(excluding plaintiffs’ expert witnesses), aff’d, 818 F.2d 187 (2d Cir. 1987), cert. denied, 487 U.S. 1234 (1988). 

CASE LAW

Krim v. pcOrder.com, Inc., 402 F.3d 489 (5th Cir. 2005)(rejecting standing plaintiffs’ standing to sue for fraud absent a showing of actual tracing of sharings to the offending public offering; statistical likelihood of those shares having been among those purchased was insufficient to confer standing)

Howard v. Wal-Mart Stores, Inc., 160 F.3d 358, 359–60 (7th Cir. 1998) (Posner, C.J.)

Norman v. National Gypsum Co., 739 F. Supp. 1137, 1138 (E.D. Tenn. 1990)(statistical evidence of risk of lung cancer from asbestos and smoking was insufficient to show individual causation, without evidence of asbestos fibers in the plaintiff’s lung tissue)

Washington v. Armstrong World Industries, 839 F.2d 1121 (5th Cir. 1988)(affirming grant of summary judgment on grounds that statistical correlation between asbestos exposure and disease did not support specific causation)

Thompson v. Merrell Dow Pharm., 229 N.J. Super. 230, 244, 551 A.2d 177, 185 (1988)(epidemiology looks at increased incidences of diseases in populations) 

Johnston v. United States, 597 F.Supp. 374, 412, 425-26 (D.Kan. 1984)(although the probability of attribution increases with the relative risk, expert must still speculate in making an individual attribution; “a statistical method which shows a greater than 50% probability does not rise to the required level of proof; plaintiffs’ expert witnesses’ reports were “statistical sophistry,” not medical opinion)

Robinson v. United States, 533 F. Supp. 320, 330 (E.D. Mich. 1982)(finding for government in swine flu vaccine case; the court found that that the epidemiological evidence offered by the plaintiff was not probative, and that it “would reach the same result if the epidemiological data were entirely excluded since statistical evidence cannot establish cause and effect in an individual

Sulesky v. United States, 545 F. Supp. 426, 430 (S.D.W.Va. 1982)(swine flu vaccine GBS cases; epidemiological studies alone do not prove or disprove causation in an individual)

Olson v. Federal American Partners, 567 P.2d 710, 712 13 (Wyo. 1977)(affirming judgment for employer in compensation proceedings; cigarette smoking claimant failed to show that his lung cancer resulted from workplace exposure to radiation, despite alleged synergism between smoking and radiation).

Heckman v. Federal Press Co., 587 F.2d 612, 617 (3d Cir. 1977) (statistical data about a group do not establish facts about an individual).

Crawford v. Industrial Comm’n, 23 Ariz. App. 578, 582-83, 534 P.2d 1077, 1078, 1082-83 (1975)(affirming an employee’s award of no compensation because he was exposed to disease producing conditions both on and off the job; a physician’s testimony, expressed to a reasonable degree of medical certainty that the working conditions statistically increased the probability of developing a disease does not satisfy the reasonable certainty standard)

Guenther v. Armstrong Rubber Co., 406 F.2d 1315, 1318 (3d Cir. 1969)(holding that defendant cannot be found liable on the basis that it supplied 75-80% of the kind of tire purchased by the plaintiff; any verdict based on this evidence “would at best be a guess”). 

In re King, 352 Mass. 488, 491 92, 225 N.E.2d 900, 902 (1967)(physician expert’s opinion that expressed a mathematical likelihood that claimant’s death was caused by his accident was legally insufficient to support a judgment)

Garner v. Heckla Mining Co., 19 Utah 2d 367, 431 P.2d 794, 796 97 (1967)(affirming denial of compensation to family of a uranium miner who had smoked cigarettes and had died of lung cancer; statistical evidence of synergistically increased risk of lung cancer among uranium miners is insufficient to show causation of decedent’s lung cancer, especially considering his having smoked cigarettes)

Mahoney v. United States, 220 F. Supp. 823, 840 41 (E.D. Tenn. 1963)(Taylor, C.J.)(holding that plaintiffs had failed to prove that their cancers were caused by radiation exposures, on the basis of their statistical, epidemiological proofs), aff’d, 339 F.2d 605, (6th Cir. 1964)(per curiam)

Kamosky v Owens-Illinois Co., 89 F. Supp. 561, 561-62 (M.D.Pa. 1950)(directing verdict in favor of defendant; statistical likelihood that defendant manufactured the bottle that injured plaintiff was insufficient to satisfy plaintiff’s burden of proof)

Sargent v. Massachusetts Accident Co., 307 Mass. 246, 250 (1940)(“It has been held not enough that mathematically the chances somewhat favor a proposition to be proved; for example, the fact that colored automobiles made in the current year outnumber black ones would not warrant a finding that an undescribed automobile of the current year is colored and not black, nor would the fact that only a minority of men die of cancer warrant a finding that a particular man did not die of cancer. The weight or preponderance of the evidence is its power to convince the tribunal which has the determination of the fact, of the actual truth of the proposition to be proved. After the evidence has been weighed, that proposition is proved by a preponderance of the evidence if it is made to appear more likely or probable in the sense that actual belief in its truth, derived from the evidence, exists in the mind or minds of the tribunal notwithstanding any doubts that may linger there.”)

Day v. Boston & Maine R.R., 96 Me. 207, 217–218, 52 A. 771, 774 (1902) (“Quantitative probability, however, is only the greater chance.  It is not proof, nor even probative evidence, of the proposition to be proved.  That in one throw of dice, there is a quantitative probability, or greater chance, that a less number of spots than sixes will fall uppermost is no evidence whatever that in a given throw such was the actual result.  Without something more, the actual result of the throw would still be utterly unknown.  The slightest real evidence would outweigh all the probability otherwise.”)

LEGAL COMMENTARY

Federal Judicial Center, Reference Manual on Scientific Evidence 337 (2d ed. 2000)( “A final caveat is that employing the results of group-based studies of risk to make a causal determination for an individual plaintiff is beyond the limits of epidemiology. Nevertheless, a substantial body of legal precedent has developed that addresses the use of epidemiologic evidence to prove causation for an individual litigant through probabilistic means, and these cases are discussed later in this reference guide.”)

Special Committee on Science and Law, “An Analysis of Proposesd Changes in Substantive and Procedural Law in Response to Perceived Difficulties in Establishing Whether or Not Causation Exists in Mass Toxic Tort Litigation,” The Record of the Ass’n of the Bar of the City of N.Y. 905, 916, 920 (1986)(epidemiologic evidence cannot answer causation issue, with “any certainty,” in the case of an individual claimant whose disease occurs “naturally” in unexposed people).

Dore, A Proposed Standard for Evaluating the Use of Epidemiological Evidence in Toxic Tort and Other Personal Injury Cases, 28 Howard L.J. 677, 692 (1985)(individual causation questions are beyond the competence of epidemiologists and the description of epidemiology)

E. Cleary, et al., eds., McCormick on Evidence § 209, at 646 & n.1 (3d ed. 1984)( “In and of itself, statistical analysis can never prove that some factor A causes some outcome B.  It can show that in a sample of observations, occurrences of B tend to be associated with those of A, and it can suggest that this statistical association probably would be observed for repeated samples.  But the association, even though “statistically significant,” need not be causal.  For instance, a third factor C could be causing both A and B.  Thus, over some time period, there may be a correlation between the number of people smoking cigarettes and the number of certain crimes committed, but if told that the population was growing rapidly during this time, no one would think that this proves that smoking causes crime.  Experimental design and some forms of statistical analysis can help control for the effects of other variables, but even these merely help formulate, confirm or refute theories about causal relationships.”)

Cong. Research Serv. Library of Cong., Report to the Subcommittee on Science, Research and Technology, “Review of Risk Assessment Methodologies,” 95th Cong., 1st Sess. 11 (Mar. 1983)(recognizing that epidemiologic predictions of disease incidence among groups can establish establishing statistical associations, but show specific causation) 

Solomons, “Workers’ Compensation for Occupational Disease Victims:  Federal Standards and Threshold Problems,” 41 Alb. L. Rev. 195, 201 (1977)(“suggesting that epidemiological showing a high probability of employment relatedness of lung cancer in an asbestos insulation worker, for example, would probably not establish causation in an individual claim.”) 

Estep, “Radiation Injuries and Statistics:  The Need for a New Approach to Injury Litigation,” 59 Mich. L. Rev. 259, 268-69 (1960)