The essence of a failure-to-warn claim is that (1) a manufacturer knows, or should know, about a harmful aspect of its product, (2) which knowledge is not appreciated by customers, (3) the manufacturer fails to warn adequately of this known harm, and (4) the manufacturer’s failure to warn causes the plaintiff to sustain the particular harm of which the manufacturer had knowledge, actual or constructive.
There are myriad problems with the assessing the knowledge component in failure-to-warn claims. Some formulations impute to manufacturers the knowledge of an expert in the field. First, which expert’s claim to knowledge counts for or against the existence of a duty? The typical formulation begs the question which expert’s understanding will control when experts in the field disagree. Second, and equally problematic, knowledge has a temporal aspect. There are causal relationships we “know” today, which we did not know in times past. This temporal component becomes even more refractory for failure-to-warn claims results when the epistemic criteria for claims of knowledge change over time.
In the early 20th century, infectious disease epidemiology, with its reliance upon Koch’s postulates. dominated the model of causation used in public and scientific discourse. The very nature of Koch’s postulates made the identification of a specific pathogen necessary to the causation of a specific disease. Later in the first half of the 20th century, epidemiologists and clinicians came to realize that the specific pathogen may be necessary but not sufficient for inducing a particular infectious disease. Still there was some comfort in having causal associations predicated upon necessary relationships. Clinicians and clinical scientists did not have to worry too much about probability theory or statistics.
The development of causal models in which the putative cause was neither necessary nor sufficient for bringing about the outcome of interest was a substantial shock to the system. In the absence of a one-to-one specificity, scientists had to account for confounding variables, in ways that they had not done so previously. The implications for legal state-of-the-art defenses could not be more profound. In the first half of the 20th century, case reports and series were frequently seen as adequate for suggesting and establishing causal relationships. By the end of the 1940s, scientists were well aware of the methodological inappropriateness of relying upon case reports and series, and the need for analytical epidemiologic studies to support causal claims.
Several historians of science have addressed the changing causal paradigm, which ultimately would permit and even encourage scientists to identify causal associations, even when the exposures studied were neither necessary nor sufficient to bring about the end point of interest. In 2011, Mark Parascandola, while he was an epidemiologist in the National Cancer Institute’s Tobacco Control Research Branch, wrote an important history of this paradigm shift and its implications in epidemiology.[1] His paper should be required reading for all lawyers who work on “long-tail” litigation, involving claims that risks were known to manufacturers even before World War II.
In Parascandola’s history, epidemiology and clinical science focused largely on infectious diseases in the early 20th century, and as a result, causal association was seen through the lens of Koch’s postulates with its implied model of necessary and sufficient conditions for causal attribution. Not until after World War II did “risk factor” epidemiology emerge to address the causal role of exposures – such as tobacco smoking – that were neither necessary nor sufficient for causing an outcome of interest.[2]
The shift from infectious to chronic diseases, such as cancer and cardiovascular disease, occurred in the 1950s, and brought with it, acceptance of a different concepts of causation, which involved stochastic events, indeterminism, multi-factorial contributions, and confounding of observations by independent but correlated causes. The causal criteria for infectious disease were generally unhelpful in supporting causal claims of chronic diseases.
Parascandola characterizes the paradigm shift as a “radical change,” influenced by developments in statistics, quantum mechanics, and causal theory.[3] Edward Cuyler Hammond, an epidemiologist with the American Cancer Society, for example, wrote in 1955, that:
“[t]he cause of an effect has sometimes been defined as a single factor which antecedes, which is necessary, and which is sufficient to produce the effect. Clearly this definition is inadequate for the study of biologic phenomena, which are produced by a complex pattern of environmental conditions interacting with the highly complex and variable make-up of living organisms.”[4]
The shift in causal models within epidemiologic thinking and research introduced new complexity with important practical implications. Gone was the one-to-one connection between pathogens (or pathogenic exposures) and specific diseases. Specificity was an important victim of the new model of causation. Causal models had to account for multi-factorial contributions to disease.[5] Confounding, the correlation between exposures of interest and other exposures that were truly driving the observations, became a substantial threat to validity. The discerning lens of analytical epidemiology was able to identify tobacco smoking as a cause of lung cancer only because of the large increased risks, ten-fold and greater, observed in multiple studies. There were no competing but independent risks of that magnitude, at hand, which could eliminate or reverse the observed tobacco risks.
Parascandola notes that in the 1950s, the criteria for causal assessment were in flux and the subject of debate:
“Previous informal rules or guides for inference, such as Koch’s postulates, were not adequate to identify partial causes of chronic disease based on a combination of epidemiologic and laboratory evidence.”[6]
As noted above, the legal implications of Parascandola’s historical analysis are hugely important. Scientists and statisticians were scrambling to develop appropriate methodologies to accommodate the changed causal models and causal criteria. Mistakes were made along the way as the models and criteria changed. In Sir Richard Doll’s famous 1955 study of lung cancer among asbestos factory workers, the statistical methods were surprisingly primitive to modern epidemiology. Even more stunning was that Sir Richard failed to incorporate smoking histories and accounting for confounding from smoking before reaching a conclusion that lung cancer was associated with long-term asbestos factory work that had induced asbestosis.[7]
Not until the lae 1950s and early 1960s did statisticians develop multivariate models to help assess potential confounding.[8] Perhaps the most cited paper in epidemiology was published by Nathan Mantel (the pride of the Brooklyn Hebrew Orphan Asylum) and William Haenszel in 1959. Its approach to stratification of sample analyses was further elaborated upon by the authors and others all through the 1960s and into the 1970s.[9]
Similarly, the evolution of criteria for causal attribution based upon risk factor epidemiology required decades of discussion and debate. Reasonably well defined criteria did not emerge until the mid-1960s, with the famous Public Health Service report on smoking and lung cancer,[10] and Sir Austin Bradford Hill’s famous after-dinner talk to the Royal Society of Medicine.[11]
Several years before Parascandola published his historical analysis, three historians of science published a paper with a very similar thesis.[12] These authors noted that there was, indeed, a legitimate controversy over whether tobacco smoking caused lung cancer, in the 1950s early 1960s, as the mechanistic Koch’s postulates gave way to the statistical methods of risk-factor epidemiology. The historians’ paper observed that by the 1950s, infectious diseases such as tuberculosis were in retreat, and the public health community’s focus was on chronic diseases such as lung cancer. The lung cancer controversy of the 1950s pushed scientists to revise their conceptions of causation ,[13] and ultimately led to the strengthening of, and legitimizing, the field of epidemiology.[14] The growing acceptance of epidemiologic methods for identifying causes, neither necessary nor sufficient, pushed aside the attachment to Koch’s postulates and the skepticism over statistical reasoning.
Interestingly, this historians’ paper was funded completely by the Rollins Public Health of Emory University. Two of the authors had been sought out by a recruiting agency for the tobacco industry, but fell out with the agency and the tobacco companies when they realized that they could not support the litigation goals. In a footnote, the authors emphasized that their factual analysis and argument contradicted the industry’s desired defense.[15]
Reaching back even farther in time, there is the redoubtable Irving John Selikoff, who wrote in 1991:
“We are inevitably bound by the knowledge of the time in which we live. An example may be given. During the 1930s and 194Os, random instances of lung cancer occurring among workers exposed to asbestos were reported and attention was called to these by the collection of cases both in registers and in review papers. With the continued growth of the asbestos industry, it was deemed wise to epidemiologically examine the proposed association. This was done in an elegant, innovative, well-considered study by Richard Doll, a study which any one of us would have been proud to report in 1955.”[16]
What is ironic is that Dr. Selikoff had testified for plaintiffs’ counsel as an expert witness specifically on state of the art, or the question of when defendants should have known and warned that asbestos caused lung cancer.[17] Dr. Selikoff ultimately withdrew from testifying, in large part because his views on this matter were not particularly helpful to plaintiffs.
The shift in causal criteria, and rejection of case reports and case series, can be seen in the suggestion, in the 1930s, of a few pathologists who contended that silicosis caused lung cancer. The few scientists who made this causal claim relied upon heavily upon anecdotal and uncontrolled necropsy series.[18]
After World War II, these causal claims fell into disrepute as not properly supported by valid scientific methodology. Dr. Madge Thurlow Macklin, a female pioneer in clinical medicine and epidemiology,[19] and one the early adopters of statistical methodology in her work, debunked the causal claims:
“If silicosis is being considered as a causative agent in lung cancer, the control group should be as nearly like the experimental or observed group as possible in sex, age distribution, race, facilities for diagnosis, other possible carcinogenic factors, etc. The only point in which the control group should differ in an ideal study would be that they were not exposed to free silica, whereas the experimental group was. The incidence of lung cancer could then be compared in the two groups of patients.
This necessity is often ignored; and a ‘random’ control group is obtained for comparison on the assumption that any group taken at random is a good group for comparison. Fallacious results based on such studies are discussed briefly.”[20]
Macklin’s advice sounds like standard-operating procedure today, but in the 1940s, it was viewed as radical and wrong by many physicians and clinical scientists.
Of course, the change over time in the knowledge of, and techniques for, diagnostic methods, quantitative measurements, and disease definitions also affect litigated issues. The change in epistemic standards and causal criteria, however, fundamentally changed legal standards for tort liability. The shift from deterministic models of necessary and sufficient causation to risk factor causation had, and continues to have, enormous ramifications for the legal adjudication of questions concerning when companies, held to the knowledge of an expert in the field, should have started to warn about the risks created by their products. Mind the gap!
[1] Mark Parascandola, “The epidemiologic transition and changing concepts of causation and causal inference,” 64 Revue d’histoire des sciences 243 (2011).
[2] Id. at 245.
[3] Id. at 248.
[4] Id. at 252, citing Edward Cuyler Hammond, “Cause and Effect,” in Ernest L. Wynder, ed., The Biologic Effects of Tobacco (1955).
[5] Id. at 257.
[6] Id.
[7] Richard Doll, “Mortality from Lung Cancer in Asbestos Workers,” 12 Brit. J. Indus. Med. 81 (1955).
[8] See Parascandola at 258.
[9] Nathan Mantel & William Haenszel, “Statistical aspects of the analysis of data from retrospective studies of disease,” 22 J. Nat’l Cancer Instit. 19 (1959). See Mervyn Susser, “Epidemiology in the United States after World War II: The Evolution of Technique,” 7 Epidemiology Reviews 147 (1985).
[10] Surgeon General, Smoking and health : Report of the Advisory Committee to the surgeon general of the Public Health Service, PHS publication No. 1103 (1964).
[11] Austin Bradford Hill, “The Environment and Disease: Association or Causation?” 58 Proc. Royal Soc’y Med. 295, 295 (1965).
[12] Colin Talley, Howard I. Kushner & Claire E. Sterk, “Lung Cancer, Chronic Disease Epidemiology, and Medicine, 1948-1964,” 59 J. History Med. & Allied Sciences 329 (2004) [Talley]. Parascandola appeared not to have been aware of this article; at least he did not cite it.
[13] Id. at 374.
[14] Id. at 334.
[15] Id. at 329.
[16] Irving John Selikoff, “Statistical Compassion,” 44 J. Clin. Epidemiol. 141S, 142S (1991) (internal citations omitted) (emphasis added).
[17] “Selikoff and the Mystery of the Disappearing Testimony,” (Dec. 3, 2010). See also Peter W.J. Bartrip, “Irving John Selikoff and the Strange Case of the Missing Medical Degrees,” 58 J. History Med. 3, 27 & n.88-92 (2003) (quoting insulator union President Andrew Haas, as saying “[w]e all owe a great debt of thanks for often and expert testimony on behalf of our members … .” Andrew Haas, Comments from the General President, 18 Asbestos Worker (Nov. 1972)).
[18] See, e.g., Max O. Klotz, “The Association Silicosis & Carcinoma of Lung 1939,” 35 Cancer Research 38 (1939); C.S. Anderson & J. Heney Dible, “Silicosis and carcinoma of the lung,” 38 J. Hygiene 185 (1938).
[19] Barry Mehler, “Madge Thurlow Macklin,” from Barbara Sicherman and Carl Hurd Green, eds., Notable American Women: The Modern Period 451-52 (1980); Laura Lynn Windsor, Women in Medicine: An Encyclopedia 134 (2002).
[20] Madge Thurlow Macklin, “Pitfalls in Dealing with Cancer Statistics, Especially as Related to Cancer of the Lung,” 14 Diseases Chest 525 532-33, 529-30 (1948). See also “History of Silica Litigation – the Lung Cancer Angle,” (Feb. 3, 2019); “The Unreasonable Success of Asbestos Litigation,” (July 25, 2015); “Careless Scholarship about Silica History,” (July 21, 2014) (discussing David Egilman); “Silicosis, Lung Cancer, and Evidence-Based Medicine in North America,” (July 4, 2014).
