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

California Actos Decision Embraces Relative-Risk-Greater-Than-Two Argument

July 28th, 2015

A recent decision of the California Court of Appeal, Second District, Division Three, continues the dubious state and federal practice of deciding important issues under cover of unpublished opinions. Cooper v. Takeda Pharms. America, Inc., No. B250163, 2015 Cal. App. Unpub. LEXIS 4965 (Calif. App., 2nd Dist., Div. 3; July 16, 2015). In Cooper, plaintiff claimed that her late husband’s bladder cancer was caused by defendant’s anti-diabetic medication, Actos (pioglitazone). The defendant moved to strike the expert witness testimony in support of specific causation. The trial judge expressed serious concerns about the admissibility of plaintiff’s expert witnesses on specific causation, but permitted the trial to go forward. After a jury returned its verdict in favor of plaintiff, the trial court entered judgment for the defendants, on grounds that the plaintiff lacked admissible expert witness testimony.

Although a recent, large, well-conducted study[1] failed to find any meaningful association between pioglitazone and bladder cancer, there were, at the time of trial, several studies that suggested an association. Plaintiff’s expert witnesses, epidemiologist Dr. Alfred Neugut and bladder oncologist Dr. Norm Smith interpreted the evidence to claim a causal association, but both conceded that there were no biomarkers that allowed them to attribute Cooper’s cancer to pioglitazone. The plaintiff also properly conceded that identifying a cause of the bladder cancer was irrelevant to treating the disease. Cooper, 2015 Cal. App. Unpub. LEXIS 4965, at *13. Specific causation was thus determined by the so-called process of differential etiology, with the ex ante existence of risk substituting for cause, and using risk exposure in the differential analysis.

The trial court was apparently soured on Dr. Smith’s specific causation assessment because of his poor performance at deposition, in which he demonstrated a lack of understanding of Cooper’s other potential exposures. Smith’s spotty understanding of Cooper’s actual and potential exposures and other risks made any specific causation assessment less than guesswork. By the time of trial, Dr. Smith and plaintiff’s counsel had backfilled the gaps, and Smith presented a more confident analysis of Cooper’s exposures and potentially competing risks.

Cooper had no family history of bladder cancer, no alcohol consumption, and no obvious exposure to occupational bladder carcinogens. His smoking history would account for exposure to a known bladder carcinogen, cigarette smoke, but Cooper’s documented history was of minor tobacco use, and remote in time. Factually, Cooper’s history was suspect and at odds with his known emphysema. Based upon this history, along with their causal interpretation of the Actos bladder cancer association, and their quantitative assessment that the risk ratio for bladder cancer from Actos was 7.0 or higher for Mr. Cooper (controlled for covariate, potential confounders), the plaintiff’s expert witnesses opined that Actos was probably a substantial factor in causing Mr. Cooper’s bladder cancer. The court did not examine the reasonableness of Dr. Smith’s risk ratios, which seem exorbitant in view of several available meta-analyses.[2]

The court stated that under the applicable California law of “substantial factor,” the plaintiff’s expert witness, in conducting a differential diagnosis, need not exclude every other possible cause of plaintiff’s disease “with absolute certainty.” Cooper, at *41-42. This statement leaves unclear and ambiguous whether the plaintiff’s expert witness must (and did in this case) rule out other possible causes with some level of certitude less than “absolute certainty,” such as reasonable medical certainty, or perhaps reasonable probability. Dr. Smith’s testimony, as described, did not attempt to go so far as to rule out smoking as “a cause” of Cooper’s bladder cancer; only that the risk from smoking was a lower order of magnitude than that for Actos. In Dr. Smith’s opinion, the discrepancy in magnitude between the risk ratios for smoking and Actos allowed him to state confidently that Actos was the most substantial risk.

Having estimated the smoking-related increased risk to somewhere between 0 and 100%, with the Actos increased risk at 600% or greater, Dr. Smith was able to present an admissible opinion that Actos was a substantial factor. Of course, this all turns on the appellate court’s acceptance of risk, of some sufficiently large magnitude, as evidence of specific causation. In the Cooper court’s words:

“The epidemiological studies relied on by Dr. Smith indicated exposure to Actos® resulted in hazard ratios for developing bladder cancer ranging from 2.54 to 6.97.18 By demonstrating a relative risk greater than 2.0 that a product causes a disease, epidemiological studies thereby become admissible to prove that the product at issue was more likely than not responsible for causing a particular person’s disease. “When statistical analyses or probabilistic results of epidemiological studies are offered to prove specific causation . . . under California law those analyses must show a relative risk greater than 2.0 to be ‘useful’ to the jury. Daubert v. Merrell Dow Pharmaceuticals Inc., 43 F.3d 1311, 1320 (9th Cir.), cert. denied 516 U.S. 869 (1995) [Daubert II]. This is so, because a relative risk greater than 2.0 is needed to extrapolate from generic population-based studies to conclusions about what caused a specific person’s disease. When the relative risk is 2.0, the alleged cause is responsible for an equal number of cases of the disease as all other background causes present in the control group. Thus, a relative risk of 2.0 implies a 50% probability that the agent at issue was responsible for a particular individual’s disease. This means that a relative risk that is greater than 2.0 permits the conclusion that the agent was more likely than not responsible for a particular individuals disease. [Reference Manual on Scientific Evidence (Federal Judicial Center 2d ed. 2000) (“Ref. Manual”),] Ref. Manual at 384, n. 140 (citing Daubert II).” (In re Silicone Gel Breast Implant Prod. Liab. Lit. (C.D. Cal. 2004) 318 F.Supp.2d 879, 893; italics added.) Thus, having considered and ruled out other background causes of bladder cancer based on his medical records, Dr. Smith could conclude based on the studies that it was more likely than not that Cooper’s exposure to Actos® caused his bladder cancer. In other words, because the studies, to varying degrees, adjusted for race, age, sex, and smoking, as well as other known causes of bladder cancer, Dr. Smith could rely upon those studies to make his differential diagnosis ruling in Actos®—as well as smoking—and concluding that Actos® was the most probable cause of Cooper’s disease.”

Cooper, at *78-80 (emphasis in the original).

Of course, the epidemiologic studies themselves are not admissible, regardless of the size of the relative risk, but the court was, no doubt, speaking loosely about the expert witness opinion testimony that was based upon the studies with risk ratios greater than two. Although the Cooper case does not change California law’s facile acceptance of risk as a substitute for cause, the case does base its approval of plaintiff’s expert witness’s attribution as turning on the magnitude of the risk ratio, adjusted for confounders, as having exceeded two. The Cooper case leaves open what happens when the risk that is being substituted for cause is a ratio ≤ 2.0. Some critics of the risk ratio > 2.0 inference have suggested that risk ratios greater than two would lead to directed verdicts for plaintiffs in all cases, but this suggestion requires demonstrations of both the internal and external validity of the studies that measure the risk ratio, which in many cases is in doubt. In Cooper, the plaintiff’s expert witnesses’ embrace of a high, outlier risk ratio for Actos, while simultaneously downplaying competing risks, allowed them to make out their specific causation case.

[1] James D. Lewis, Laurel A. Habel, Charles P. Quesenberry, Brian L. Strom, Tiffany Peng, Monique M. Hedderson, Samantha F. Ehrlich, Ronac Mamtani, Warren Bilker, David J. Vaughn, Lisa Nessel, Stephen K. Van Den Eeden, and Assiamira Ferrara, “Pioglitazone Use and Risk of Bladder Cancer and Other Common Cancers in Persons With Diabetes,” 314 J. Am. Med. Ass’n 265 (2015) (adjusted hazard ratio 1.06, 95% CI, 0.89-1.26).

[2] See, e.g., R.M. Turner, et al., “Thiazolidinediones and associated risk of bladder cancer: a systematic review and meta-analysis,” 78 Brit. J. Clin. Pharmacol. 258 (2014) (OR = 1.51, 95% CI 1.26-1.81, for longest cumulative duration of pioglitazone use); M. Ferwana, et al., “Pioglitazone and risk of bladder cancer: a meta-analysis of controlled studies,” 30 Diabet. Med. 1026 (2013) (based upon 6 studies, with median follow-up of 44 months, risk ratio = 1.23; 95% CI 1.09-1.39); Cristina Bosetti, “Cancer Risk for Patients Using Thiazolidinediones for Type 2 Diabetes: A Meta-Analysis,” 18 The Oncologist 148 (2013) (RR = 1.64 for longest exposure); Shiyao He, et al., “Pioglitazone prescription increases risk of bladder cancer in patients with type 2 diabetes: an updated meta-analysis,” 35 Tumor Biology 2095 (2014) (pooled hazard ratio = 1.67 (95% C.I., 1.31 – 2.12).

Ramazzini Serves Courtroom Silica Science Al Dente

July 25th, 2015

Collegium Ramazzini styles itself as an “independent, international academy.” The Collegium Ramazzini was founded in 1982, by the late Irving Selikoff and others to serve as an advocacy forum for their pro-compensation and aggressive regulation views on social and political issues involving occupational and environmental health.

The Collegium is a friendly place where plaintiffs’ expert witnesses, consultants, and advocates never have to declare their conflicts of interest.[1] Last year, in October 2014, the Collegium conducted a conference on silica health issues, entitled “Silica Three Hundred Years Later: Occupational Exposure, Medical Monitoring, and Regulation.”

The silica session was chaired by Christine Oliver, one of plaintiff’s key expert witnesses in Allen v. Martin Surfacing, 263 F.R.D. 47 (D. Mass. 2009). SeeBad Gatekeeping or Missed Opportunity – Allen v. Martin Surfacing” (Nov. 30, 2012). The purported goal of the session was

“to shine a light on silica as a persistent and dangerous threat to the health of exposed workers worldwide,” focusing on the following issues:

“1) Occupational silica exposures, new and old;

2) silica as a recognized human lung carcinogen and its interaction with other lung carcinogens such as tobacco smoke;

3) the role of silica and silicosis in tuberculosis;

4) issues relevant to medical surveillance of silica-exposed workers as set forth in OSHA’s proposed silica standard;

5) the role of the US Government in protecting the health of silica-exposed workers; and

6) international variability in addressing the threat to worker health posed by silicosis.”

Recently, the Collegium updated its website to provide PDF files of some of the conference presentations:

Carol H. Rice, “Silica – old, new and emerging uses result in worker exposure

Arthur L. Frank, “Silica as a lung carcinogen

Rodney Ehrlich, “Silica in the head of the snake. Silica, gold mining, and tuberculosis in southern Africa

Christine Oliver, “Medical surveillance for silica-related disease: the Collegium responds to OSHA’s proposed rulemaking,”

Gregory R. Wagner, “US Government role in recognizing, reducing, and regulating silica risk: 80 years and counting

Sverre Langard, “Silicosis 300 years after Ramazzini: Eradication in some countries, increased incidence in others

A poster session chaired by Melissa McDiarmid and Carol Rice, revealingly titled “Sustainable Work 2020 – an advocacy platform for Horizon 2020,” followed. Casey Bartrem asked whether “Asbestos-induced lung cancer in Germany: is the compensation practice in accordance with the epidemiological findings?” Odds are that this presentation was a brief for greater compensation. Xaver Baur of Germany, presented on the “Ethics in the applied sciences: The challenge of preventing corporate influence over public health regulation,” but remarkably no one presented on the challenge of preventing the litigation and compensation industry’s influence over public health regulation.

You won’t find any cutting-edge science in the linked slides, but you will find some interesting revelations. Sverre Langard’s presentation makes the dramatic point that silicosis has been declining, despite the hand waving of OSHA Administrator David Michaels, and the histortions of Rosner and Markowitz. Consider Langard’s slide, based upon CDC data:

CDC Siicosis vs Asbestosis Mortality Over Time

And consider the admissions of Arthur Frank, veteran plaintiffs’ expert witness, who acknowledged that:

“until very recently it [silica] was not recognized as a carcinogen.”

True to form, Dr. Frank blamed Selikoff and his other teachers at Mt. Sinai Hospital in New York City, where he trained:

“At Mount Sinai I did not get trained that silica was a carcinogen”

Well, even a scurry of blind squirrels sometimes find their nuts!

[1][1] Some of the names on the list of Fellows and Emeritus Fellows reads like a “Who’s Who” of testifying expert witnesses, consultants, and advocates for the litigation industry:

Henry A. Anderson, Barry Castleman, David C. Christiani, Carl F. Cranor, Devra Lee Davis , John M. Dement, Arthur Frank, Bernard D. Goldstein, Howard Frumkin, Lennart Hardell, Peter F. Infante, Joseph LaDou, Philip Landrigan, Richard A. Lemen, Barry S. Levy, Roberto G. Lucchini, Steven B. Markowitz, Myron A. Mehlman, Ronald L. Melnick, Donna Mergler, Albert Miller, Franklin E. Mirer, Herbert L. Needleman, L. Christine Oliver, David M. Ozonoff, Carol H. Rice, Kenneth D. Rosenman, Sheldon W. Samuels, Ellen K. Silbergeld, Peter D. Sly, Martyn Thomas Smith, Colin L. Soskolne, Leslie Thomas Stayner, Daniel T. Teitelbaum, Laura Welch

The Unreasonable Success of Asbestos Litigation

July 25th, 2015

In asbestos litigation, the plaintiffs’ bar has apparently invented a perpetual motion machine that feeds on outrage that will never run out. Still, lawyers who have not filled their wallets with legal fees from asbestos cases sometimes attempt to replicate the machine. For the most part, the imitators have failed.

What accounts for the unreasonable success of asbestos litigation? Unlike pharmaceutical litigation, exposure does not require a prescription. Although asbestos insulators and applicators experienced the most exposure, other trades and occupations worked with, or near, asbestos materials. Anecdotal testimony of exposure suffices in almost every case. Add para-occupational exposure, and the sky’s the limit for the class of potential plaintiffs. See Lester Brickman, “Fraud and Abuse in Mesothelioma Litigation,” 88 Tulane L. Rev. 1071 (2014); Peggy Ableman, “The Garlock Decision Should be Required Reading for All Trial Court Judges in Asbestos Cases,” 37 Am. J. Trial Advocacy 479, 488 (2014).

Then there is the range of diseases and disorders attributable to asbestos. Excessive exposure to asbestos minerals cause non-malignant pleural plaques and thickening, as well as lung fibrosis, asbestosis. Some asbestos minerals cause mesothelioma, and despite a differential in potency among some of the minerals (between amosite and crocidolite), the general and specific causation of mesothelioma is often uncontested. Furthermore, lung cancer in the presence of asbestosis may be the result of interaction of asbestos exposure and cigarette smoking. Plaintiffs’ counsel and The Lobby have expanded the list of attributable diseases to include non-pulmonary cancers, only to find some defendants willing to pay money on these claims as well.

In addition to the ease of claiming, or manufacturing, exposure, and the willing cooperation of the occupational medical community in supporting medical causation, asbestos litigation is a lightning rod for moral outrage in the courtroom. Plaintiffs claim that “industry” knew about the hazards of asbestos, including its carcinogenicity, long before warnings appeared. Defending the knowledge claim requires nuanced explanation of shifting standards for establishing causality as epidemiology developed and was applied to putative asbestos-related cancer outcomes, as well as changing views about the latencies of asbestos-related diseases.

Every once in a while, plaintiffs’ and defense counsel[1], the media[2], the academy[3], and the insurance industry[4] ask whether “silica” is the next asbestos. Although the prospects have been, and remain, dim, plaintiffs’ counsel continue to try to build their litigation palace on sand, with predictably poor results. See Kimberley A. Strassel, “He Fought the Tort Bar — and Won,” Wall St. J. (May 4, 2009).

There are many serious disanalogies between asbestos and silica litigation. One glaring difference is the inability to summon any outrage over suppressed or nondisclosed knowledge of alleged silica cancer hazards. The silica cancer state of the art, written by those who are lionized in the asbestos litigation – Hueper, Schepers, and Hardy, along with NIOSH and the Surgeon General, all appropriately denied or doubted silica as a cause of lung cancer. See below. When the IARC shifted its views in the 1990s, under the weight of determined advocacy from some partisans in the occupational medicine community, and with the help from some rather biased reviews, industry promptly warned regardless of the lack of scientific support for the IARC’s conclusion. The manufacturing of faux consensus and certainty on silica and lung cancer is an important counter to the incessant media stories about the manufacturing of doubt on topics such as climate change.

[1] Robert D. Chesler, James Stewart, and Geoffrey T. Gibson, “Is Silica the Next Asbestos?” 176 N.J.L.J. 1 (June 28, 2004); Mark S. Raffman, “Where Will Silica Litigation Go?” 1 LJN Silica Legal News 1 (2005); Chris Michael Temple, “A Case for Why Silica Litigation Is Not the ‘Next Asbestos’,” LJN Product Liability Law & Strategy (2004).

[2] Jonathan D. Glater, “Suits on Silica Being Compared To Asbestos Cases,” N.Y. Times (Sept. 6, 2003).

[3] Michelle J. White, “Mass Tort Litigation: Asbestos,” in Jürgen Georg Backhaus, ed., Encyclopedia of Law and Economics 1 (2014); Melissa Shapiro, “Is Silica the Next Asbestos? An Analysis of the Silica Litigation and the Sudden Resurgence of Silica Lawsuit Filings,” 32 Pepperdine L. Rev. 4 (2005).

[4]Is silica the new asbestos?The Actuary (2005).

Historical Statements – – State-of-the-Art

Maxcy, ed., Rosenau Preventive Medicine and Hygiene 1051 (N.Y., 7th ed. 1951) (“Thus, there is no evidence that lung cancer is related in any way to silicosis.”)

May Mayers, “Industrial Cancer of the Lungs,” 4 Compensation Medicine 11, 12 (1952) (“Nevertheless, silicosis is not, apparently associated with, or productive of, lung cancer, whereas asbestosis very probably is.”) (Chief, Medical Unit, Division of Industrial Hygiene and Safety Standards, N.Y. Dep’t of Labor)

Geritt Schepers, “Occupational Chest Diseases,” Chap. 33, p. 455, ¶3, in A. Fleming, et al., eds., Modern Occupational Medicine (Phila. 2d ed. 1960) (“Lung cancer, of course, occurs in silicotics and is on the increase. Thus far, however, statistical studies have failed to reveal a relatively enhanced incidence of pulmonary neoplasia in silicotic subjects.”)

Spencer, Pathology of the Lung (1962) (“Silicosis and lung cancer inhaled silica, unlike asbestos, does not predispose to the development of lung cancer.”)

Wilhelm Hueper, Occupational and Environmental Cancers of the Respiratory System at 2-6 (N.Y. 1966) (“The bulk of the available epidemiologic evidence on the association of silicosis and lung cancer supports the view of a mere coincidental role of silicosis in this combination. *** From the evidence on hand, it appears that a well advanced silicosis does not seem to furnish a favorable soil for the development of cancer of the lung.”) (chief of the National Cancer Institute)

Harriet L. Hardy, “Current Concepts of Occupational Lung Disease of Interest to the Radiologist,” 2 Sem. Roentgenology 225, 231-32 (1967) (“cancer of the lung is not a risk for the silicotic. It is a serious risk following asbestos exposure and for hematite, feldspar, and uranium miners. This means that certain dusts and ionizing radiation alone or perhaps with cigarette smoke act as carcinogens.”)

Raymond Parkes, Occupational Lung Disorders 192 (London 1974) (“Bronchial carcinoma occasionally occurs in silicotic lungs but there is no evidence of a causal relationship between it and silicosis; indeed the incidence of lung cancer in miners with silicosis is significantly lower than in non-silicotic males.”)

Kaye Kilburn, Ruth Lilis, Edwin Holstein, “Silicosis,” in Maxcy-Rosenau, Public Health and Preventive Medicine, 11th ed., at 606 (N.Y. 1980) (“Lung cancer is apparently not a complication of silicosis.”)

Robert Jones, “Silicosis,” Chap. 16, in W. Rom, et al., eds., Environmental and Occupational Medicine 205 (Boston 1983) (“The weight of epidemiologic evidence is against the proposition that silicosis carries an increased risk of respiratory malignancy.”)

W. Keith C. Morgan & Anthony Seaton, eds., Occupational Lung Diseases 266 (1984) (“It is generally believed that silicosis does not predispose to lung cancer. * * * On balance, it seems unlikely that silicosis itself predisposes to lung cancer.”)

1 Anderson’s Pathology at 910b (1985) (“There is no evidence that silica increases the risk of lung cancer, nor does it enhance tobacco induced carcinogenesis.”)

U.S. Dep’t of Health and Human Services, The Health Consequences of Smoking – Cancer and Chronic Lung Disease in the Workplace: A Report of the Surgeon General at 348, Chapter 8 “Silica‑Exposed Workers” (1985) (“the evidence does not currently establish whether silica exposure increases the risk of developing lung cancer in men.”)

J. Cotes & J. Steel, Work-Related Lung Disorders 156 (Oxford 1987) (“The inhalation of silica dust does not contribute to malignancy.”)

NIOSH Silicosis and Silicate Disease Committee, “Diseases Associated With Exposure to Silica and Non-fibrous Silicate Minerals,” 112 Arch. Path. & Lab. Med. 673, 707 (1988) (“Epidemiologic studies have been conducted in an effort to assess the role of silica exposure in the pathogenesis of lung cancer. *** Thus, the results are inconclusive … .”)

Arthur Frank, “Epidemiology of Lung Cancer, in J. Roth, et al., Thoracic Oncology, Chap. 2, at p. 8 (Table 2-1), 11 (Phila. 1989) (omitting silica from list of lung carcinogens) (“The question of the relationship of coal mining to the development of lung cancer has been frequently considered. Most evidence points to cigarette smoking among coal miners as the major causative factor in the development of lung cancer, and neither a recent84 nor a British study of lung cancer among coal miners has found any relationship to occupational exposure.”)

Canadian Judges’ Reference Manual on Scientific Evidence

July 24th, 2015

I had some notion that there was a Canadian version of the Reference Manual on Scientific Evidence in the works, but Professor Greenland’s comments in a discussion over at Deborah Mayo’s blog drew my attention to the publication of the Science Manual for Canadian Judges [Manual]. See “‘Statistical Significance’ According to the U.S. Dept. of Health and Human Services (ii),Error Statistics Philosophy (July 17, 2015).

The Manual is the product of the Canadian National Judicial Institute (NJI), which is an independent, not-for-profit group that is committed to educating Canadian judges. The NJI’s website describes the Manual:

“Without the proper tools, the justice system can be vulnerable to unreliable expert scientific evidence.

* * *

The goal of the Science Manual is to provide judges with tools to better understand expert evidence and to assess the validity of purportedly scientific evidence presented to them. …”

The Chief Justice of Canada, Hon. Beverley M. McLachlin, contributed an introduction to the Manual, which was notable for its frank admission that:

[w]ithout the proper tools, the justice system is vulnerable to unreliable expert scientific evidence.


Within the increasingly science-rich culture of the courtroom, the judiciary needs to discern ‘good’ science from ‘bad’ science, in order to assess expert evidence effectively and establish a proper threshold for admissibility. Judicial education in science, the scientific method, and technology is essential to ensure that judges are capable of dealing with scientific evidence, and to counterbalance the discomfort of jurists confronted with this specific subject matter.”

Manual at 14. These are laudable goals, indeed.

The first chapter of the Manual is an overview of Canadian law of scientific evidence, “The Legal Framework for Scientific Evidence,” by Canadian law professors Hamish Stewart (University of Toronto), and Catherine Piché (University of Montreal). Several judges served as peer reviewers.

The second chapter, “Science and the Scientific Method,” contains the heart of what judges supposedly should know about scientific and statistical matters to serve as effective “gatekeepers.” Like the chapters in the Reference Manual on Scientific Evidence, this chapter was prepared by a scientist author (Scott Findlay, Ph.D., Associate Professor of Biology, University of Ottawa) and a lawyer author (Nathalie Chalifour, Associate Professor of Law, University of Ottawa). Several judges, and Professor Brian Baigrie (University of Toronto, Victoria College, and the Institute for the History and Philosophy of Science and Technology) provided peer review. The chapter attempts to cover the demarcation between science and non-science, and between scientific and other expert witness opinion. The authors describe “the” scientific method, hypotheses, experiments, predictions, inference, probability, statistics and statistical hypothesis testing, data reliability, and related topics. A subsection of chapter two is entitled “Normative Issues in Science – The Myth of Scientific Objectivity,” which suggests a Feyerabend, post-modernist influence at odds with the Chief Justice’s aspirational statement of goals in her introduction to the Manual.

Greenland noted some rather cavalier statements in Chapter two that suggest that the conventional alpha of 5% corresponds to a “scientific attitude that unless we are 95% sure the null hypothesis is false, we provisionally accept it.” And he pointed elsewhere where the chapter seems to suggest that the coefficient of confidence that corresponds to an alpha of 5% “constitutes a rather high standard of proof,” thus confusing and conflating probability of random error with posterior probabilities. Some have argued that these errors are simply an effort to make statistical concepts easier to grasp for lay people, but the statistics chapter in the FJC’s Reference Manual shows that accurate exposition of statistical concepts can be made understandable. The Canadian Manual seems in need of some trimming with Einstein’s razor, usually paraphrased as “Everything should be made as simple as possible, but no simpler.[1] The razor should certainly applied to statistical concepts, with the understanding that pushing to simplify too aggressively can sometimes result in simplistic, and simply wrong, exposition.

Chapter 3 returns to more lawyerly matters, “Managing and Evaluating Expert Evidence in the Courtroom,” prepared and peer-reviewed by prominent Canadian lawyers and judges. The final chapter, “Ethics of the Expert Witness,” should be of interest to lawyers and judges in the United States, where the topic is largely ignored. The chapter was prepared by Professor Adam Dodek (University of Ottawa), along with several writers from the National Judicial Institute, the Canadian Judicial Council, American College of Trial Lawyers, Environment Canada, and notably, Joe Cecil & the Federal Judicial Center.

Weighing in at 228 pages, the Science Manual for Canadian Judges is much shorter than the Federal Judicial Center’s Reference Manual on Scientific Evidence. Unlike the FJC’s Reference Manual, which is now in its third edition, the Canadian Manual has no separate chapters on regression, DNA testing and forensic evidence, clinical medicine and epidemiology. The coverage of statistical inference is concentrated in chapter two, but that chapter has no discussion of meta-analysis, systematic review, evidence-based medicine, confounding, and the like. Perhaps there will soon be a second edition of the Science Manual for Canadian Judges.

[1] See Albert Einstein, “On the Method of Theoretical Physics; The Herbert Spencer Lecture,” delivered at Oxford (10 June 1933), published in 1 Philosophy of Science 163 (1934) (“It can scarcely be denied that the supreme goal of all theory is to make the irreducible basic elements as simple and as few as possible without having to surrender the adequate representation of a single datum of experience.”).

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