Evidence of risk is not evidence of causation. It never has been; it never will be. Risk and causation are distinct concepts. Processes, events, or exposures may be risks; that is, they may be capable of causing an outcome of interest. Risk, however, is an ex ante concept. We can speak of a risk only before the outcome of interest has occurred. After its occurrence, we are interested in what caused the outcome.
Before the tremendous development of epidemiology in the decades after World War II, most negligence and products liability cases involved mechanistic conceptions of causation. Juries and courts considered claims of causation that conceptually were framed in the manner of billiard balls hitting one another until the final, billiard-of-ball of interest, went into the pocket. Litigants and courts did not need to consider statistical evidence when considering whether a saw dismembered a plaintiff, or even whether chronic asbestos exposure caused inflammation and scarring in the lungs of workers. In some instances, judicial efforts to cast causation as a mechanistic process smack of quackery. Claims that blunt trauma caused malignant tumors at the site of the trauma, within days or weeks of the impact, come to mind as an example of magical thinking that plagued courts and juries in a era that was short on scientific gatekeeping, and long on deferring to clinical judgment, empty of meaningful scientific support. See, e.g., Baker v. DeRosa, 413 Pa. 164, 196 A.2d 387 (1964)(holding that question whether car accident caused tumor was for the jury).
The advent of epidemiologic evidence introduced an entirely different class of claims, ones that were based upon stochastic concepts of causation. The exposure, event, or process that was a putative cause had a probabilistic element to its operation. The putative cause exercised its contribution to the outcome through a random process, which left changed the frequency of the harmful outcome in those who encountered the exposure. In addition, the outcome that resulted from the “putative cause” was frequently indistinguishable from those outcomes that arose spontaneously or from other causes in the environment or from normal human aging. Discerning which risks (or “putative causes”) operated in a given case of chronic human disease (such cancer, cardiovascular disease, autoimmune disease) became a key issue for courts and litigants’ expert witnesses. The black box of epidemiology, however, sheds little or no light on the issue, and no other light source was available.
Today, expert witnesses, typically for plaintiffs, equate risk with causation. Because risk is an ex ante concept, the inference from risk to causation is problematic. In rare instances, the risk is absolute under the circumstances of the plaintiff’s manifestation, such that the outcome can be tied to the exposure that created the risk. In most cases, however, there will have been other competing risks, which alone could have operated to produce the outcome of which the plaintiff complains. In toxic tort litigation, we frequently see a multiplicity of pre-existing risks for a chronic disease that is prevalent in the entire population. When claimants attempt to show causation for such outcomes by epidemiologic evidence, the inference of causation from a particular prior risk is typically little more than a guess.
One well-known epidemiologist explained the limits of inferences with respect to stochastic causation:
“An elementary but essential principal that epidemiologists must keep in mind is that a person may be exposed to an agent and then develop disease without there being any causal connection between exposure and disease.” ****
“In a courtroom, experts are asked to opine whether the disease of a given patient has been caused by a specific exposure. This approach of assigning causation in a single person is radically differentfrom the epidemiologic approach, which does not attempt to attribute causation in any individual instance. Rather, the epidemiologic approach is to evaluate the proposition that the exposure is a cause of the disease in a theoretical sense, rather than in a specific person.”
Kenneth Rothman, Epidemiology: An Introduction 44 (Oxford 2002)(emphasis added).
Another epidemiologist, who wrote the chapter in the Federal Judicial Center’s Reference Manual on Scientific Evidence, on epidemiology, put the matter thus:
“Epidemiology answers questions about groups, whereas the court often requires information about individuals.”
Leon Gordis, Epidemiology 3d ed. (Philadelphia 2004)(emphasis in original). Accord G. Friedman, Primer of Epidemiology 2 (2d ed. 1980 (epidemiologic studies address causes of disease in populations, not causation in individuals); Sander Greenland, “Relation of the Probability of Causation to Relative Risk and Doubling Dose: A Methodologic Error that Has Become a Social Problem,” 89 Am. J. Pub. Health1166, 1168 (1999)(“[a]ll epidemiologic measures (such as rate ratios and rate fractions) reflect only the net impact of exposure on a population”); Joseph V. Rodricks & Susan H. Rieth, “Toxicological Risk Assessment in the Courtroom: Are Available Methodologies Suitable for Evaluating Toxic Tort and Product Liability Claims?” 27 Regulatory Toxicol. & Pharmacol. 21, 24-25 (1998)(noting that a population risk applies to individuals only if all persons within the population are the same with respect to the influence of the risk on outcome).
These cautionary notes are important reminders of the limits of epidemiologic method. What these authors miss is that there may be no other principled way to connect one pre-existing risk, among several, to an outcome that is claimed to be tortious. As the young, laconic Wittgenstein wrote:
“Wovon man nicht sprechen kann, darüber muß man schweigen.”
L. Wittgenstein, Tractatus Logico-Philosophicus, Proposition 7 (1921)(translated by Ogden as “Whereof one cannot speak, thereof one must be silent”). Unfortunately, expert witnesses in legal proceedings sometimes do not feel the normative force of Wittgenstein’s Proposition 7, and they speak without restraint. As a contemporary philosopher explained in a more accessible idiom,
“Bullshit is unavoidable whenever circumstances require someone to talk without knowing what he is talking about. Thus the production of bullshit is stimulated whenever a person’s obligations or opportunities to speak about some topic exceed his knowledge of the facts that are relevant to that topic.”
Harry Frankfurt, On Bullshit 63 (Princeton University Press 2005).
