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

Goodman v Viljoen – Subterfuge to Circumvent Relative Risks Less Than 2

June 6th, 2014

Back in March, I wrote about a “Black Swan” case, in which litigants advanced a Bayesian analysis to support their claims. Goodman v. Viljoen, 2011 ONSC 821 (CanLII), aff’d, 2012 ONCA 896 (CanLII), leave appeal den’d, Supreme Court of Canada No. 35230 (July 11, 2013).

Goodman was a complex medical practice case in which Mrs. Goodman alleged that her obstetrician, Dr. Johan Viljoen, deviated from the standard of care by failing to prescribe antenatal corticosteroids (ACS) sufficiently in advance of delivery to reduce the risks attendant early delivery for her twin boys, of early delivery. Both boys developed cerebral palsy (CP). The parties and their experts agreed that the administration of ACS reduced the risks of respiratory distress and other complications of pre-term birth, but they disputed the efficacy of ACS to avoid or diminish the risk of CP.

According to the plaintiffs, ACS would have, more probably than not, prevented the twins from developing cerebral palsy, or would have diminished the severity of their condition. Dr. Viljoen disputed both general and specific causation. Evidence of general causation came from both randomized clinical trials (RCTs) and observational studies.

Limitations Issue

There were many peculiar aspects to the Goodman case, not the least of which was that the twins sued Dr. Viljoen over a decade after they were born. Dr. Viljoen had moved his practice in the passage of time, and he was unable to produce crucial records that supported his account of how his staff responded to Mrs. Goodman’s telephone call about signs and symptoms of labor. The prejudice to Dr. Viljoen illustrates the harshness of broad tolling statutes, the unfairness of which could be reduced by requiring infant plaintiffs to give notice of their intent to sue, even if they wait until the age of majority before filing their complaints.

State of the Art Issue

Dr. Viljoen suffered perhaps a more serious prejudice in the form of hindsight bias that resulted from the evaluation of his professional conduct by evidence that was unavailable when the twins were born in 1995. The following roughly contemporaneous statement from the New England Journal of Medicine is typical of serious thinking at the time of the alleged malpractice:

“Antenatal glucocorticoid therapy decreases the incidence of several complications among very premature infants. However, its effect on the occurrence of cystic periventricular leukomalacia, a major cause of cerebral palsy, remains unknown.”

Olivier Baud, Laurence Laurence Foix l’Hélias, et al., “Antenatal Glucocorticoid- Treatment and Cystic Periventricular Leukomalacia in Very Premature Infants,” 341 New Engl. J. Med. 1190, 1190 (1999) (emphasis added). The findings of this observational study illustrate some of the difficulties with the claim that Dr. Viljoen failed to prevent an avoidable consequence of pre-term delivery:

“Our results suggest that exposure to betamethasone but not dexamethasone is associated with a decreased risk of cystic periventricular leukomalacia.”

Id. at 1194. Results varied among various corticosteroids, among doses, among timing regimens. There hardly seemed enough data in 1995 to dictate a standard of care.

Meta-Analysis Issues

Over ten years after the Goodman twins were born, the Cochrane collaboration published a meta-analysis that was primarily concerned with the efficacy of ACS for lung maturation. Devender Roberts & Stuart R Dalziel “Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth,” Cochrane Database of Systematic Reviews Issue 3. Art. No. CD004454 (2006). The trials included mostly post-dated the birth of the twins, and the alleged malpractice. The relevance of the trials to address the causation of CP in infants who experienced periventricular leukomalacia (PVL) was hotly disputed, but for now, I will gloss over the external validity problem of the Cochrane meta-analysis.

The Cochrane Collaboration usually limits its meta-analyses to the highest quality evidence, or RCTs, but in this instance, the RCTs did not include CP in its primary pre-specified outcomes. Furthermore, the trials were generally designed to ascertain short-term benefits from ACS, and the data in the trials were uncertain with respect to longer-term outcomes, which may have been ascertained differentially. Furthermore, the trials were generally small and were plagued by sparse data. None of the individual trials was itself statistically significant at the 5 percent level. The meta-analysis did not show a statistically significant decrease in CP from ACS treatment. The authors reported:

“a trend towards fewer children having cerebral palsy (RR 0.60, 95% CI 0.34 to 1.03, five studies, 904 children, age at follow up two to six years in four studies, and unknown in one study).”

Id. at 8 (emphasis added).

The Cochrane authors were appropriately cautious in interpreting the sparse data:

“Results suggest that antenatal corticosteroids result in less neurodevelopmental delay and possibly less cerebral palsy in childhood.”

Id. at 13-14 (emphasis added).

The quality of the trials included in the Cochrane meta-analysis varied, as did the trial methodologies. Despite the strong clinical heterogeneity, the Cochrane authors performed their meta-analysis with a fixed-effect model. The confidence interval, which included 1.0, reflected a p-value of 0.065, but that p-value would have certainly increased if a more appropriate random-effects model had been used.

Furthermore, the RCTs were often no better than observational studies on the CP outcome. The RCTs here perhaps should not have been relied upon to the apparent exclusion of observational epidemiology.

Relative Risk Less Than Two

There is much to be said about the handling of statistical significance, the Bayesian analysis, the arguments about causal inference, but for now, let us look at one of the clearest errors in the case: the inference of specific causation from a relative risk less than two. To be sure, the Cochrane meta-analysis reported a non-statistically significant 40% decrease, but if we were to look at this outcome in terms of the increase in risk of CP from the physician’s failure to administer ACS timely, then the risk ratio would be 1.67, or a 67% increase. On either interpretation, fewer than half the cases of CP can be attributed to the failure to administer ACS fully and timely in the case.

The parties tried their case before Justice Walters, in St. Catherines, Ontario. Goodman v. Viljoen, 2011 ONSC 821 (CanLII). Justice Walters recognized that specific causation was essential and at the heart of the parties’ disagreement:

“[47] In order to succeed, the plaintiffs must establish that the failure to receive a full course of ACS materially affected the twins’ outcome. That is, they must establish that “but for” the failureto receive a full course of ACS, the twins would not have suffered from the conditions they now do, or that the severity of these afflictions would have been materially reduced.

[48] Not surprisingly, this was the most contentious issue at trial and the court heard a good deal of evidence with respect to the issue of causation.”

One of the defendant’s expert witnesses, Robert Platt, a professor of statistics at McGill University School of Medicine, testified, according to Justice Walters:

“[144] Dr. Platt also stated that the absolute risk in and of itself does not tell us anything about what might have happened in a specific case absent clinical and mechanistic explanations for that specific case.”

The plaintiffs’ expert witnesses apparently conceded the point. Professor Andrew Willan, a statistician, testifying for the plaintiffs, attempted to brush Platt’s point aside by suggesting it would render clinical research useless, but that was hardly the point. Platt embraced clinical research for what it could show about the “averages” in a sample of the population, even if we cannot discern causal efficacy retrospectively in a specific patient:

“[133] Dr. Willan also responded to Dr. Platt’s criticism that it was impossible to determine the distribution of the effect across the population. Professor Willan felt this issue was a red herring, and if it were valid, it would render most clinical research useless. There is really no way of knowing who will benefit from a treatment and who will not. Unless there are reasons to believe otherwise, it is best to apply the population average effect to each person.”

Although Willan labeled Platt’s point as cold-blooded and fishy, he ultimately concurred that the population average effect should be applied to each person in the absence of evidence of risk being sequestered in a subgroup.

A closer look at Willan’s testimony at trial is instructive. Willan acknowledged, on direct examination, that the plaintiffs were at increased risk, even if their mother had received a full course of ACS. All he would commit to, on behalf of the plaintiffs, was that their risk would have been less had the ACS been given earlier:

“All we can say is that there’s a high probability that that risk would be reduced and that this is probably the best estimate of the excess risk for not being treated and I would say that puts that in the 70 percent range of excess risk and I would say the probability that the risk would have been reduced is into the 90 percentage points.”

Notes of Testimony of Andrew Willan at 62 (April 6, 2010). The 90 percentage points reference here was Willan’s posterior probability that the claimed effect was real.

On cross-examination, the defense pressed the point:

Q. What you did not do in this, in this report, is provide any quantification for the reduction in the risk, true?

A. That’s correct.

Notes of Testimony of Andrew Willan at 35 (April 9, 2010)

Q. And you stated that there is no evidence that the benefits of steroids is restricted to any particular subgroup of patients?

A. I wasn’t given any. I haven’t seen any evidence of that.

Id. at 43.

Q. And what you’re suggesting with that statement, is that the statistics should be generally, should be considered by the court to be generally applicable, true?

A. That’s correct.

Id. at 44.

Q. But given your report, you can’t offer assistance on the clinical application to the statistics, true?

A. That’s true.

Id. at 46.

With these concessions in hand, defense counsel elicited the ultimate concession relevant to the “but for” standard of causation:

Q. And to do that by looking at an increase in risk, the risk ratio from the data must achieve 2 in order for there to be a 50 percent change in the underlying data, true?

A. Yeah, to double the risk, the risk ratio would have to be 2, to double the risk.

Id. at 63.

* * *

Q. So, none of this data achieves the threshold of a 50 percent change in the underlying data, whether you look at it as an increase in risk or …

A. Sure.

Q …. a decrease in risk …

A. Yeah.

Id. at 66.

Leaping Inferences

The legal standard for causation in Canada is the same counterfactual requirement that applies in most jurisdictions in the United States. Goodman v. Viljoen, 2011 ONSC 821 (CanLII), at ¶14, 47. The trial court well understood that the plaintiffs’ evidence left them short of showing that their CP would not have occurred but for the delay in administering ACS. Remarkably, the court permitted the plaintiffs to use non-existing evidence to bridge the gap.

According to Dr. Max Perlman, plaintiffs’ expert witness on neonatology and pediatrics, CP is not a dichotomous condition, but a spectrum that is manifested on a continuum of signs and symptoms. The RCTs relied upon had criteria for ascertaining CP and including it as an outcome. The result of these criteria was that CP was analyzed as a binary outcome. Dr. Perlman, however, held forth that “common sense and clinical experience” told him that CP is not a condition that is either present or not, but rather presented on a continuum. Id. at [74].

Without any evidence, Perlman testified that when CP is not avoided by ACS, “it is likely that it is less severe for those who do go on to develop it.” Id. [75]. Indeed, Perlman made the absence of evidence a claimed virtue; with all his experience and common sense, he “could not think of a single treatment which affects a basic biological process that has a yes or no effect; they are all on a continuum.” Id. From here, Perlman soared to his pre-specified conclusion that “that it is more likely than not that the twins would have seen a material advantage had they received the optimal course of steroids.” Id. at [76].

Perlman’s testimony is remarkable for inventing a non-existing feature of biological evidence: everything is a continuum. Justice Walters could not resist this seductive testimony:

“[195] The statistical information is but one piece of the puzzle; one way of assessing the impact of ACS on CP. Notably, the 40% reduction in CP attributable to ACS represents an all or nothing proposal. In other words, 93.5% of the time, CP is reduced in its entirety by 40%. It was the evidence of Dr. Perlman, which I accept, that CP is not a black and white condition, and, like all biological processes, it can be scaled on a continuum of severity. It therefore follows that in those cases where CP is not reduced in its entirety, it is likely to be less severe for those who go on to develop it. Such cases are not reflected in the Cochrane figure.

[196] Since the figure of 40% represents an all or nothing proposal, it does not accurately reflect the total impact of ACS on CP. Based on this evidence, it is a logical conclusion that if one were able to measure the total effect of ACS on CP, the statistical measure of that effect would be inflated beyond 40%.

[197] Unfortunately, this common sense conclusion has never and can never be tested by science. As Dr. Perlman testified, such a study would be impossible to conduct because it would require pre-identification of those persons who go on to develop CP. Furthermore, because the short term benefits of ACS are now widely accepted, it would be unethical to withhold steroids to conduct further studies on long term outcomes.”

Doubly unfortunate, because Perlman’s argument was premised on a counterfactual assumption. Many biological phenomena are dichotomous. Pregnancy, for instance, does not admit of degrees. Disease states are frequently dichotomous, and no evidence was presented that CP was not dichotomous. Threshold effects abound in living organisms. Perlman’s argument further falls apart when we consider that the non-experimental arm of the RCTs would also have had additional “less-severe” CP cases, with no evidence that they occurred disproportionately in the control arms of these RCTs. Furthermore, high-quality observational studies might have greater validity than post-hoc RCTs in this area, and there have been, and likely will continue to be, such studies to attempt better understanding of the efficacy of ACS, as well as differing effects among the various corticosteroids, doses, and patterns of administration.

On appeal, the Justice Walters’ verdict for plaintiffs was affirmed, but over a careful, thoughtful dissent. Goodman v. Viljoen, 2012 ONCA 896 (CanLII) (Doherty, J., dissenting). Justice Doherty caught the ultimate futility of Dr. Perlman’s opinion based upon non-existent evidence: even if there were additional sub-CP cases in the treatment arms of the RCTs, and if they occurred disporportionately more often in the treatment than in the placebo arms, we are still left guessing about the quantitative adjustment to make to the 40% decrease, doubtful as it was, which came from the Cochrane review.

Posted in Causation, Scientific Evidence, statistical evidence | Comments Off on Goodman v Viljoen – Subterfuge to Circumvent Relative Risks Less Than 2

Recrudescence of Traumatic Cancer Claims

June 4th, 2014

In 1991, Peter Huber, discussing traumatic cancer claims, wrote:

“After years of floundering in the junk science morass of traumatic cancer, judges slowly abandoned sequence-of-events logic, turned away from the sympathetic speculations of family doctors, and struggled on to the higher and firmer ground of epidemiology and medical science. Eventually, the change of heart among appellate judges was communicated back down to trial judges and worker’s compensation boards, and traumatic cancer went into almost complete remission.”

Peter W. Huber, Galileo’s Revenge: Junk Science in the Courtroom 55-56 (1991).

With the advent of Daubert and meaningful gatekeeping of expert witness opinion testimony, the traumatic cancer claims did recede. For a while. Plaintiffs’ counsel, and stalwart opponent of epistemic standards for scientific claims in court, Kenneth Chesebro attacked Huber’s précis of the traumatic cancer law and science. Kenneth J. Chesebro, “Galileo’s Retort: Peter Huber’s Junk Scholarship,” 42 Am. Univ. L. Rev. 1637 (1993). Defenses of the dubious science continue to appear, although mostly in non-peer-reviewed publications.[1]

One of the more disturbing implications of the West Virginia Supreme Court’s decision in Harris v. CSX Transportation, Inc., 232 W.Va. 617, 753 S.E.2d 275 (2013), was the Court’s reliance upon its own, recent approval of traumatic cancer claims. The Harris Court cited, with approval, a 2002 traumatic cancer case, State ex rel. Wiseman v. Henning, 212 W.Va. 128, 569 S.E.2d 204 (2002). The Wiseman case involved a specious claim that a traumatic rib injury caused multiple myeloma, a claim at odds with scientific method and observation. The West Virginia Supreme Court blinked at the challenge to the physician expert witness who advanced the causal claim in Wiseman; and in Harris, the Court made clear that blinking is what trial courts should do when confronted with methodological challenges to far-fetched causal opinions.

A couple of years ago, the New York Times ran an article about traumatic cancer. C. Claiborne Ray, “Injury and Insult” (Nov. 5, 2012), responding to the question “Is it possible for cancer to develop as a result of an injury?” Here is how Times science reporter responded:

A. “It’s a common myth that injuries can cause cancer,” the American Cancer Society says on its Web site. Until the 1920s, some doctors believed trauma did cause cancer, “despite the failure of injury to cause cancer in experimental animals.” But most medical authorities, including the cancer society and the National Cancer Institute, see no such link. The more likely explanation, the society suggests, is that a visit to the doctor for an injury could lead to finding an existing cancer.

Other possibilities are that scar tissue from an old trauma could look like a cancerous lesion and that an injured breast or limb would be more closely watched for cancer to develop.

Ms. Ray went on to note a published study, in which would-be myth-busters presented observational data purportedly showing a relationship between physical injury and subsequent breast cancer. The paper cited by Ms. Ray was a report on a small case-control study done by investigators at the Department of Geography, Lancaster University. See Jan Rigby, et al., “Can physical trauma cause breast cancer?” 11 Eur. J. Cancer. Prev. 307 (2002). The study consisted of 67 breast cancer cases and 134 controls, matched on age, family history, age of menarche, parity, age at first birth, and menopausal status.

Not surprisingly, considering its small size, the Rigby study reported no statistically significant differences for several factors known to be associated with breast cancer: social class, education, residence, smoking and alcohol consumption. Although lacking power to detect differences of known risk factors, this study turned up a large, statistically significant association between physical trauma and breast cancer:

“Women with breast carcinoma were more likely to report physical trauma to the breast in the previous 5 years than were the controls (odds ratio (OR) 3.3, 95% confidence interval (CI) 1.3-10.8, P < 0.0001).”

* * * * *

“More likely to [self-]report” hardly implies causation, but the authors jumped not only to a causal explanation but to a causal conclusion:

* * * * *

“In conclusion, recall bias is an unlikely explanation for these results in view of the nature and severity of physical trauma. Models of epithelial cell generation indicate that a causal link between physical trauma and cancer is plausible. A latent interval between cancer onset and presentation of under 5 years is also plausible. The most likely explanation of the findings is that physical trauma can cause breast cancer.”

Rigby at 307.

The Rigby study is a valuable demonstration of how malleable researchers can be in discovering plausible explanations for their data. The authors fail to discuss the natural history of breast carcinoma, such as tumor doubling time, which would make their five-year window decidedly implausible. The Rigby paper also demonstrates how strident researchers can be in claiming that they have produced a study that has eliminated bias in observational research, when they have barely scratched the surface of bias or confounding. Magical thinking is not the exclusive domain of lawyers.

Until reading the Harris and Wiseman cases, I had thought that the legal system had graduated from the “mythology” of traumatic cancer cases.[2] To be sure, in the past, any number of physicians have supported traumatic cancer claims, in print and in the courtroom.[3] Some authors attempted to put some rational limits on the extent of the traumatic cancer claims.[4] By 1947, at least, the trauma theory was criticized in leading texts.[5] In 1974, the Mayo Clinic published a review that emphasized the lack of experimental evidence to support the claim that uncomplicated trauma causes cancer.[6] The law review literature attempted to make sense of the compensation-frenzied courts, without much success.[7]

Many cases from most jurisdictions have approved traumatic cancer claims. Some are set out below. Some courts heroically resisted the pro-compensation Zeitgeist, usually on case-specific evidentiary issues.[8]

In New York, judges seem to be well aware that post hoc ergo propter hoc is a fallacy. Cassano v. Hagstrom, 5 N.Y.2d 643, 159 N.E.2d 348, 187 N.Y.S.2d 1 (1959) (affirming dismissal of case based because of plaintiffs’ attempt to use fallacious reasoning in the form of “post hoc ergo propter hoc”); Holzberg v. Flower & Fifth Ave. Hosps., 39 AD 2d 526 (N.Y. 1st Dep’t 1972). Still, the New York courts struggled with traumatic cancer claims, and appeared to oscillate wildly without clear guidance on whether or to what extent the courts could reject specious claiming supported by speculative or unreliable expert witness opinion testimony.[9] Given the current hostility to gatekeeping of expert witness opinion, a recrudescence of traumatic cancer claims is likely.

Opinions Approving Causation in Traumatic Cancer Cases

California

Santa Ana Sugar Co. v. Industrial Accid. Comm’n, 170 P. 630, 630 (Cal. Dist. Ct. App. 1917)

Colorado

Canon Reliance Coal Co. v. Indus. Comm’n, 72 Colo. 477, 211 P. 868, 869-70 (1922) (cancer caused by being hit on cheek with a lump of coal)

Georgia

National Dairy Prods. Corp. v. Durham, 154 S.E.2d 752, 753-54 (Ga. Ct. App. 1967)

Kentucky

Louisville Ry v. Steubing’s Adm’r, 136 S.W. 634, 634 (Ky. Ct. App. 1911)

Louisiana

Reed v. Mullin Wood Co., 274 So. 2d 845, 846-47 (La. Ct. App. 1972), cert. denied, 275 So. 2d 729, 791 (La. 1973);

Thompson v. New Orleans Ry. & Light Co., 83 So. 19, 20 (La. 1919)

Michigan

Wilson v. Doehler-Jarvis Div. of Nat’l Lead Co., 353 Mich. 363, 91 N.W.2d 538, 539-40 (1958) (blow to lip caused cancer)

Mooney v. Copper Range RR, 27 N.W.2d 603, 604 (Mich. 1947)

Minnesota

Daly v. Bergstedt, 267 Minn. 244, 126 N.W.2d 242, 247–48 (1964) (affirming jury finding of causation between traumatic leg fracture and breast cancer; six physicians testified against causation; one stated cancer “could” result from trauma; imagining that scientific and legal standards of causation differ)

Pittman v. Pillsbury Flour Mills, Inc., 48 N.W.2d 735, 736 (Minn. 1951)

Hertz v. Watab Pulp & Paper Co., 237 N.W. 610, 611 (Minn. 1931)

Austin v. Red Wing Sewer Pipe Co., 163 Minn. 397, 204 N.W. 323, 323-24 (Minn. 1925) (cancer developed one year after worker was hit in the face with coal)

Gaetz v. City of Melrose, 193 N.W. 691, 692 (Minn. 1923)

Missouri

Vitale v. Duerbeck, 338 Mo. 536, 92 S.W.2d 691, 695 (1936)

New Hampshire

Jewell v. Grand Trunk Ry, 55 N.H. 84 (1874) (reversing traumatic cancer verdict on other grounds)

New Mexico

White v. Valley Land Co., P.2d 707, 708-10 (N.M. 1957)

Ohio

Hanna v. Aetna Ins., 24 Ohio Misc. 27, 52 Ohio Op. 2d 316, 259 N.E.2d 177, 177-79 (Ohio Mun. Ct. Dayton 1970)(breast lump found three months after car accident)

Glenn v. National Supply, 129 N.E.2d 189, 190-91 (Ohio Ct. App. 1954)

Oregon

Devine v. Southern Pacific Co., 207 Or. 261, 295 P.2d 201 (1956) (holding that physician’s testimony as to “probable” causation between shoulder fracture and lung cancer was sufficient; jury verdict for plaintiff reversed on other grounds).

Pennsylvania

Baker v. DeRosa, 413 Pa. 164, 196 A.2d 387, 389–90 (Pa. 1964)

Menarde v. Philadelphia Transp. Co., 376 Pa. 497, 103 A.2d 681, 684(1954) (the fact that breast cancer was found in the same place as the injury-caused bruise helped establish causation);

Southern S.S. Co. v. Norton, 41 F. Supp. 103 (E.D. Pa. 1940) (trauma to skull and lower back held to have caused lung cancer)

Tennessee

Koehring-Southern & Am. Mut. Ins. Co. v. Burnette, 464 S.W.2d 820, 821 (Tenn. 1970)

Boyd v. Young, 193 Tenn. 272, 246 S.W.2d 10, 10 (Tenn. 1951)

Rhode Island

Valente v. Bourne Mills, 77 R.I. 274, 278-79, 75 A.2d 191, 193-94 (1950) (adopting house of cards position in which any rational inference suffices even if not supported by expert medical opinion)

Emma v. A.D. Julliard & Co., 75 R.I. 94, 63 A.2d 786, 787-89 (R.I. 1949)(plaintiff had malignant tumor removed from her breast seven weeks after being hit with a can of juice)

Texas

Traders & General Insur. Co. v. Turner, 149 S.W.2d 593, 597-98 (Tex. Civ. App. 1941) (testicular cancer)

Virginia

Ellis v. Commonwealth Dep’t of Highways, 28 S.E.2d 730, 731-32, 735 (Va. 1944) (accepting post-hoc reasoning “[f]acts prevail over possibilities or probabilities”)

Winchester Milling Corp. v. Sencindiver, 138 S.E. 479, 480-81 (Va. 1927)

[1] See, e.g., Melvin A. Shiffman, Can Trauma Cause or Accelerate the Growth of Cancer? Forensic Examiner 6 (Fall 2004).

[2] See Manasco v. Insurance Co. of State of Pennsylvania, 89 S.W.3d 239 (Tex. App. Texarkana 2002) (affirming denial of benefits to worker who claimed head injury caused brain tumor; citing to epidemiological studies that failed to show an association between trauma and brain tumors).

[3] See, e.g., George R. Parsons, “Sufficiency of Proof in Traumatic Cancer Cases,” 2 Tort & Med. Year Book 335 (1962); Stoll & Crissey, “Epithelioma from Single Trauma,” 62 N.Y. St. J. Med. 496 (Feb. 15, 1962); Wilhelm C. Hueper, Trauma and Cancer (1959); Arden R. Hedge, “Can a Single Injury Cause Cancer?” 90 Calif. Med. 55 (1959); R. Crane, “The Relationship of a Single Act of Trauma to Subsequent Malignancy,” in Alan R. Moritz & David S. Helberg, eds., Trauma and Disease 147 (1959); Shields Warren, M.D., “Minimal criteria required to prove causation of traumatic or occupational neoplasms,” Ann. Surgery 585 (1943); Bishop, “Cancer, Trauma, and Compensation,” 32 So. Med. J. 302 (1939); Knox, “Trauma and Malignant Tumors, 26 Am. J. Surg. 66, 69-70 (1934); William B. Coley & Norman L. Higinbotham, “Injury as a causative factor in the development of malignant tumors,” 98 Ann. Surg. 991 (1933); Wainwright, “Single Trauma, Carcinoma and Workman’s Compensation,” 5 Am. J. Surg. 433 (1928); Alson R. Kilgore & Curtis E. Smith, “Industrial liability for cancer,” 25 Calif. & Western Med. 70 (1926); Charles Phelps, “The relation of trauma to cancer formation,” 51 Ann. Surgery 609 (1910).

[4] James Ewing, “Modern Attitudes Toward Traumatic Cancer,” 19 Arch. Path. 690, 692 (1935); James Ewing, “The Relation of Trauma to Malignant Tumors,” Am. J. Surg. 30, 31-34 (Feb. 1926).

[5] See, e.g., James A. Tobey, Public Health Law 321 (3ed 1947) (“Although there is little, if any, scientific evidence to prove conclusively that malignant growths such as carcinoma, sarcoma, and other forms of cancer are ever caused by single blows, wounds, injuries, or other forms of trauma, the courts have awarded damages in a number of instances to persons who have developed cancers following single injuries.”) (internal citations omitted).

[6] George R. Monkman, Gregg Orwoll & John C. Ivins, “Trauma and Oncogenesis,” 49 Mayo Clinic Proc. 157 (1974).

[7] The trauma theory of carcinogenesis was discussed and questioned in several law review articles. See, e.g., Orrin E. Tilevitz, “Judicial Attitudes Towards Legal and Scientific Proof of Cancer Causation,” 3 Colum. J. Envt’l L. 344 (1977); Donald J. Ladanyi, “Impact Trauma As ‘Legal Cause’ of Cancer,” 20 Cleveland State L. Rev. 409 (1971); Theodore Dyke, “Traumatic Cancer?” 15 Clev.-Marshall L. Rev. 472 (1966); Jerry G. Elliott, “Traumatic cancer and ‘an old misunderstanding between doctors and lawyers’,” 13 U. Kan. L. Rev. 79 (1964); Comment, Sufficiency of Proof in Traumatic Cancer: A Medico-Legal Quandary, 16 Ark. L. Rev. 243 (1962); Comment, “Sufficiency of Proof in Traumatic Cancer Cases,” 46 Cornell L.Q. 581 (1961); Adelson, Injury and Cancer, 5 Western Res. L. Rev. 150 (1954).

[8] State Compensation Ins. Fund v. Kindig, 445 P.2d 72 (Colo. 1968) (head injury held not to have caused leukemia 68 days later); Slack v. C.L. Percival Co., 198 Iowa 54, 199 N.W. 323, 326 (1924) (anticipating Daubert by rejecting expert witness opinion that was “wholly in the realm of conjecture, speculation, and surmise”); Ortner v. Zenith Carburetor Co., 207 Mich. 610, 175 N .W. 122 (1919) (holding that 30 months was too long for a claim that accident that crushed worker’s fingers caused blood poisoning and penile cancer); Stordahl v. Rush Implement Co., 417 P.2d 95 (Mont. 1966) (rejecting traumatic causation of malignant tumor); Tonkovich v. Dep’t of Lab. & Indus., 31 Wash. 2d 220, 195 P.2d 638 (1948) (injury to foot held not to have caused abdominal cancer)

[9] See Dennison v. Wing, 279 App. Div. 494, 110 N.Y.S.2d 811, 813 (1952) (rejecting cancer claim when latency was two months on grounds that cancer took longer to develop); Sikora v. Apex Beverage Corp., 282 App. Div. 193, 196-97 (1953) (reversing judgment for plaintiff based upon jury’s finding that slip and fall accelerated breast cancer based upon lack of evidentiary support), aff’d, 306 N.Y. 917, 119 N.E.2d 601 (1954); Frankenheim v. B. Altman & Co., 13 Misc. 2d 1079, 1080-81, 177 N.Y.S.2d 2 (Bronx Cty. S.Ct. 1958) (granting motion to set aside verdict for plaintiff based upon traumatic cancer claim on grounds of insufficient evidence), app. dism’d, 8 App. Div. 2d 809 (First Dep’t 1959). But see McGrath v. Irving, 24 App. Div. 2d 236, 265 N.Y.S.2d 376 (1965) (affirming jury verdict based upon claim that plaintiff’s swallowing glass in car accident caused or accelerated development of laryngeal cancer); Mattfield v. Ward Baking Co., 14 App. Div. 2d 942, 221 N.Y.S.2d 224, 224 (1st Dep’t 1961) (affirming award for traumatic cancer based upon the “usual” conflicting expert witness testimony) Mattfield v. Ward Baking Co., 14 App. Div. 2d 942, 942 (1961) (affirming workman’s compensation award for “aggravation” of cancer, which resulted after “the usual conflict of medical opinion”); Pezzolanti v. Green Bus Lines, 114 App. Div. 2d 553, 553-54, 494 N.Y.S.2d 168, 169 (1985) (affirming workman’s compensation award for disability to wrist, which resulted from “trauma” of hitting pothole, which in turn injured asymptomatic wrist destabilized by pre-existing cancer).

Posted in Causation, Expert Witnesses, Rule 702, Scientific Evidence | Comments Off on Recrudescence of Traumatic Cancer Claims

Intellectual Due Process in West Virginia and Beyond

June 1st, 2014

Harris v. CSX Transportation

I have borrowed and modified the phrase “Intellectual Due Process” from earlier writers because of its obvious implications for the presentation, interpretation, synthesis, and evaluation of scientific evidence in court. See Scott Brewer, “Scientific Expert Testimony and Intellectual Due Process,” 107 Yale L. J. 1535 (1998). The major reason courts write opinions is to explain and justify their decisions to litigants, present and future, and to a wider audience of lawyers, scholars, and the general public. Judicial opinions involving scientific evidence, whether in legislation, regulation, or litigation must satisfy the societal need to explain and justify the acceptance and rejection of scientific claims. Despite a great deal of hand waving that law and science are somehow different, in the end, when courts describe their acceptance or rejection of scientific claims, they are addressing the same epistemic warrant that scientists themselves employ. Even a cursory review of the judicial output reveals an unsatisfactory state of affairs in which many courts mangle scientific and statistical evidence and inference. There is much that is needed to correct the problem.

One proposal would be to require that the parties file proposed findings of facts in connection with Rule 702 gatekeeping challenges. Courts should file detailed findings of facts that underlie their decisions to admit or to exclude expert witness opinion testimony. Another proposal would require courts to cite properly the scientific studies that they discuss in reaching a legal conclusion about sufficiency or admissibility. These are small steps, but ones that would help reduce the gross inaccuracies and the glib generalizations, while increasing the opportunity for public scrutiny and criticism.

We do not think anything is amiss with special courts for tax, patent, family law, national security, equity, or commercial matters. There is an even greater need for scientific skill, knowledge, and aptitude in a specialized science court. The time has come for special courts to hear cases involving scientific claims in health effects and other litigation.

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A decision of the West Virginia Supreme Court, late last year, illustrates the need for substantial reform of how claiming based upon “scientific evidence” is permitted and evaluated in court. Mrs. Harris sued the railroad for the wrongful death of her husband, who died of multiple myeloma. Mr. Harris had been exposed, in his railroad workplace, to diesel exhaust, which Mrs. Harris claimed caused his cancer. See Harris v. CSX Transportation, Inc., 232 W.Va. 617, 753 S.E.2d 275 (2013). The trial court excluded Mrs. Harris’s expert witnesses. Harris v. CSX Transportation, Inc., No. 12-1135, 2012 WL 8899119 (Cir. Ct. Marshall Cty., W.Va. Aug. 21, 2012).

1. The West Virginia Supreme Court reversed the trial court’s exclusion of witnesses on the basis of an asymmetrical standard of review, which would allow de novo review of trial court decisions to exclude expert witness opinions, but which would privilege trial court decisions to admit opinions by limiting appellate review to abuse of discretion. This asymmetry was, of course, the same dodge that the Third and Eleventh Circuits had used to keep the “gates open,” regardless of validity or reliability concerns, and the same dodge that the Supreme Court shut down in General Electric v. Joiner. A single judge dissented in Harris, Justice Loughry, who took the majority to task for twisting facts and law to get to a desired result.

2. The Harris Court cited a federal court case for dicta that “Rule 702 reflects an attempt to liberalize the rules governing the admissibility of expert testimony.” See Harris, 753 S.E.2d at 279 (citing and quoting from Weisgram v. Marley Co., 169 F.3d 514, 523 (8th Cir.1999). Remarkably, the Harris Court omitted reference to the United States Supreme Court’s unanimous affirmance of Weisgram, which saw Justice Ginsburg write that “[s]ince Daubert, moreover, parties relying on expert evidence have had notice of the exacting standards of reliability such evidence must meet.” Weisgram v. Marley Co., 528 U.S. 440, 442 (2000). The Harris Court’s lack of scholarship is telling.

3. Meta-analysis appeared to play a role in the case, but the judicial decisions in Harris fail to describe the proffered evidence. The majority in Harris noted that one of plaintiff’s expert witnesses, Dr. Infante, relied upon a meta-analysis referred to as “Sonoda 2001.” Harris, 753 S.E.2d at 309. Neither the Court nor the dissent cited the published meta-analysis in a way that would help an interested reader in finding the paper. One could imagine the hue and cry if courts cited judicial cases or statutes by short-hand names without providing enough information to access the relied upon source. In this case, a PubMed search reveals the source so perhaps the error is harmless. Tomoko Sonoda, Yoshie Nagata, Mitsuru Mori, Tadao Ishida & Kohzoh Imai, “Meta-analysis of multiple myeloma and benzene exposure,” 11. J. Epidemiol. 249 (2001). Still, the time has come for courts to describe and report the scientific evidence with the same care and detail that they would use in a car collision case.

4. A quick read shows that the Sonoda meta-analysis supports the dissent’s assessment:

“‘Dr. Infante testified on direct examination that Sonoda 2001 considered 8 case-control studies specific to engine exhaust and stated it concluded that diesel and non-diesel engine exhaust causes multiple myeloma.’ Yet, as the trial court found, ‘[o]n cross examination Dr. Infante acknowledged that none of the 8 papers included in the Sonoda meta-analysis mention diesel exhaust’.”

Harris, 753 S.E.2d at 309. The dissent would have been considerably more powerful had it actually adverted to the language of Sonoda 2001:

“These results suggested that benzene exposure itself was not likely to be a risk factor of MM [multiple myeloma]. It is thought that several harmful chemical agents in engine exhaust, other than benzene, could be etiologically related to the risk of MM. Further case-control studies on MM are needed to obtain more information about detailed occupational exposure to toxic substances.”

Sonoda at 249 (2001) (emphasis added). Contrary to Infante’s asseveration, Sonoda and colleagues never concluded that diesel exhaust causes multiple myeloma. The state of scholarship and “intellectual due process” makes it impossible to tell whether or not Dr. Infante was telling the truth or the Harris Court badly misunderstood the record. Either way, something must give.

The dissent went on to note that Dr. Infante conducted his own meta-analysis, which included studies that did not mention diesel exhaust. Harris, 753 S.E.2d at 309. The railroad complained that some of the studies were small and had limited power, but that is exactly why a meta-analysis would be appropriate. The more disturbing complaints were that the meta-analysis left out important studies, and that it included irrelevant studies of benzene exposure and myeloma, which raised insuperable problems of external validity.

5. A half empty glass that is always full. According to the Harris Court, the West Virginia shadow of Rule 702 is a rule of “admissibility rather than exclusion.” Harris, 753 S.E.2d at 279 (citing and quoting from In re Flood Litig. Coal River Watershed, 222 W.Va. 574, 581, 668 S.E.2d 203, 210 (2008), which in turn quoted a federal case, Arcoren v. United States, 929 F.2d 1235, 1239 (8th Cir. 1991), decided before the Supreme Court decided Daubert.) This is just silly hand waving and blatant partisanship. A rule that sets out criteria or bases for admissibility also demarcates the inadmissible.

6. Cherry Picking. Dr. Infante was permitted by the Harris Court to aggregate data from studies that did not observe diesel exposure, while he failed to include, or he deliberately excluded data from, a large, powerful, exonerative study conducted by scientists from the National Cancer Institute, the International Agency for Research on Cancer (IARC), and the Karolinska Institute. See Paolo Boffetta, Mustafa Dosemeci, Gloria Gridley, Heather Bath, Tahere Moradi and Debra Silverman, “Occupational exposure to diesel engine emissions and risk of cancer in Swedish men and women,” 12 Cancer Causes Control 365 (2001). Dr. Infante inexplicably excluded this study, which found a risk ratio for men exposed to diesel exhaust that was below one, 0.98, with a very narrow 95% confidence interval, 0.92-1.05. Boffetta at 368, Table 2.

7. The West Virginia articulated an incohorent definition of “reliable,” designed to give itself the ability to reject gatekeeping completely. Citing its earlier decision in Flood, the Court offered its own ipse dixit:

“The assessment of whether scientifically-based expert testimony is “reliable,” as that term is used in [Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), and Wilt v. Buracker, 191 W.Va. 39, 443 S.E.2d 196 (1993)], does not mean an assessment of whether the testimony is persuasive, convincing, or well-founded. Rather, assessing ‘reliability’ is a shorthand term of art for assessing whether the testimony is to a reasonable degree based on the use of knowledge and procedures that have been arrived at using the methods of science — rather than being based on irrational and intuitive feelings, guesses, or speculation. If the former is the case, then the jury may (or may not, in its sole discretion) ‘rely upon’ the testimony. In re Flood Litig., 222 W.Va. at 582 n. 5, 668 S.E.2d at 211 n. 5.”

Harris, 753 S.E.2d at 279-80. Surely, this is circular or vacuous or both. Opinions not “well-founded” will be ones that are based upon guesses or speculation. Opinions arrived at by the “methods of science” will be ones that have an epistemic warrant that will survive a claim that they are not “well-founded.”

8. The Harris Court evidenced its hostility to scientific evidence by dredging up one of its own decisions involving a multiple myeloma causation claim, State ex rel. Wiseman v. Henning, 212 W.Va. 128, 569 S.E.2d 204 (2002). Wiseman involved a specious claim that a traumatic rib injury caused multiple myeloma, a claim at odds with scientific method and observation:

“Some research has suggested that people in some jobs may have an increased risk of developing multiple myeloma because they are exposed to certain chemicals. But the International Agency for Research on Cancer (IARC) states that the evidence is limited overall. It has been suggested that people may have an increased risk if they work in the petrol or oil industry, farming, wood working, the leather industry, painting and decorating, hairdressing, rubber manufacturing or fire fighting. But there is no evidence to prove that any of these occupations carry an increased risk of myeloma.”

Cancer Research UK, “Myeloma risks and causes” (last visited May 28, 2014). Even the most non-progressive jurisdictions have generally eradicated specious claiming for trauma-induced cancers, but West Virginia has carved out a place second to none in its race to the bottom.

9. WOE. Not surprisingly, the Harris Court relied heavily on the First Circuit’s “weight of the evidence” end-run around the notion of epistemic warrant for scientific claims, citing Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11 (1st Cir.2011), cert. denied sub nom., U.S. Steel Corp. v. Milward, ___ U.S. ___, 2012 WL 33303 (2012). The Harris Court went on to conflate and confuse WOE with Bradford Hill, and cited a recent New York case that confidently saw through WOE hand waving, while ignoring its devasting critique of expert witnesses’ attempts to pass off WOE for scientific, epistemic warrant. Reeps ex rel. Reeps v. BMW of N. Am., LLC, No. 100725/08,

2013 WL 2362566, at *3, 2012 N.Y. Misc. LEXIS 5788; 2012 NY Slip Op 33030U (N.Y. Sup. Ct. May 10, 2013).

10. Link. Dr. Infante links a lot, even when his sources do not:

“Dr. Infante testified that the International Agency for Research on Cancer issued Technical Publication Number 42 in 2009, and that the publication stated that diesel exhaust exposures have been linked to multiple myeloma and leukemia.”

Harris, 753 S.E.2d at 294. The Harris Court neglected to give the title of the publication, which tells a different story. Identification of research needs to resolve the carcinogenicity of high-priority IARC carcinogens. The dissent was willing to go behind the conclusory and false characterization that Dr. Infante and plaintiff gave to this publication. Harris, 753 S.E.2d at 309. The trial court’s finding (and the dissent’s assertion) that the IARC Technical Publication 42 intended to express a research agenda, not to make a causation statement, seems unassailable. Furthermore, it appears to be precisely the sort of specious claim that a court should keep from a jury. The cited IARC source actually notes that the then current IARC classification of diesel exhaust was of inadequate evidence for human carcinogenicity, with a focus on lung cancer, and barely a mention of multiple myeloma.

11. The Benzene Connection. Plaintiffs’ expert witnesses, including Dr. Infante, argued that benzene was a component of diesel exhaust, and benzene caused multiple myeloma. This move ignored not only the lack of evidence to implicate benzene in the causation of multiple myeloma, but it also ignored the large quantitative differences between the benzene occupational exposure studies and the very small amounts of benzene in diesel exhaust. The Harris Court held that the trial court acted improperly by inquiring into and finding the following facts, which were “exclusively” for the jury:

“There is substantially more benzene in cigarette smoke than diesel exhaust.

Benzene is present only in trivial doses in diesel exhaust.

The hypothesis that diesel exhaust causes multiple myeloma is confounded by the fact that cigarette smoking does not.”

The Harris majority further chastised the trial court for adverting to the ten or so studies that failed to find a statistically significant association between benzene exposure and multiple myeloma. Harris, 753 S.E.2d at 305-06. This inquiry directly calls into question, however, Dr. Infante’s methodology.

If these facts, found by the trial court, were reasonably established, then Dr. Infante’s argument was less than bogus, and a major underpinning for inclusion of benzene studies in his meta-analysis was refuted. These are precisely the sort of foundational facts that must be part of an inquiry into the methodological grounds of an expert witness’s opinion.

12. The Harris Court confused “proving causation” with “showing a methodology that provides an epistemic warrant for concluding.” Harris, 753 S.E.2d at 300. The Harris Court asserted that the trial court exceeded its gatekeeping function by inquiring into whether Mrs. Harris’s expert witnesses “proved” causation. Harris, 753 S.E.2d at 300. Speaking of “proof of” or “proving” causation is an affectation of lawyers, who refer to their evidence as their “proofs.” Epidemiologic articles and meta-analyses do not end with quod erat demonstrandum. Beyond the curious diction, there is a further issue in the majority’s suggestion that the trial court set the bar too high in declaring that the plaintiff failed to “prove” causation. Even if we were to accept the continuous nature of strength of evidence for a causal conclusion, Dr. Infante and the other plaintiff’s witnesses, would be fairly low on the curve, and their lowly position must of necessity speak to the merits of the defense motion to exclude under Rule 702.

13. Purely Matters for Jury. The Harris Court criticized the trial court for conducting a “mini-trial,” which set out to “resolve issues that were purely matters for jury consideration.” Harris, 753 S.E.2d at 305. In holding that the matters addressed in the pre-trial hearing were “exclusively grist for the jury and which had no relevancy to the limited role the trial court had under the facts of this case,” the Harris Court displayed a profound disregard for what facts would be relevant for a challenge to the plaintiff’s expert witnesses’ methodology. Many of the facts found by the trial court were directly relevant to “general acceptance,” validity (internal and external) of studies relied upon, and reliability of reasoning and inferences drawn. Aside from the lack of general acceptance and peer review of the plaintiff’s claimed causal relationship, the proffered testimony was filled with gaps and lacunae, which are very much at issue in methodological challenges to an opinion of causality.

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The Harris case has taken its place next to Milward in the litigation industry’s arsenal of arguments for abandoning meaningful judicial supervision and gatekeeping of expert witness opinion testimony. See Andrew S. Lipton, “Proving Toxic Harm: Getting Past Slice and Dice Tactics,” 45 McGeorge L. Rev. 707, 731 (2014) (plaintiffs’ bar cheerleading for the Harris decision as “a lengthy and thoughtful analysis”, and for the Milward case as roadmap to evade meaningful judicial oversight). Not all was perfect with the trial court’s opinion. The defense seemed to have misled the court by asserting that “a difference between a case group and control group is not statistically significant then there is no difference at all.” See Respondent’s Brief at 5, Harris v. CSX Transportation, Inc., 2013 WL 4747999 (filed (Feb. 4, 2013) (citing App. 169, 228-230 (Shields) as having explained that the p-values greater than 0.05 do not support a causal association).

This is hardly true, and indeed, the lack of statistical significance does not lead to a claim that the null hypothesis of no association between exposure and outcome is correct. The defense, however, did not have a burden of showing the null to be correct; only that there was no reliable method deployed to reject the null in favor an alternative that the risk ratio for myeloma was raised among workers exposed to diesel exhaust.

Still, the trial court did seem to understand the importance of replication, in studies free of bias and confounding. Courts generally will have to do better at delineating what are “positive” and “negative” studies, with citations to the data and the papers, so that judicial opinions provide a satisfactory statement of reasons for judicial decisions.

Posted in Causation, Expert Witnesses, Meta-analysis, Rule 702, Scientific Evidence | Comments Off on Intellectual Due Process in West Virginia and Beyond