FDCC Quarterly Addresses "General Causation"
The Federation of Defense and Corporate Counsel has released the Fall 2003 issue of the FDCC Quarterly, which includes an article by William O. Dillingham, Patrick J. Hagan, and Rodrigo E. Salas, entitled Blueprint for General Causation Analysis in Toxic Tort Litigation.
The article is indeed a fair blueprint of standard defense arguments for challenging causation, many of which center on the uses and abuses of epidemiological data. But all in all, the article is more an aspirational portrayal of the law that defense counsel might prefer, than it is a neutral portrayal of the law as it stands.
Here is how the defense blueprint works. An analytical distinction is first drawn between "general" and "specific" (or "individual") causation. "General causation" involves the general capacity of some given toxic agent to cause harm in humans. "Specific" causation involves the question whether an exposure to that agent was indeed the cause in fact of a given plaintiff's injury. This analytical distinction once drawn, it is next demanded that general and specific causation be separately proved. It is then insisted that proof of general causation be undertaken through reliance on epidemiological studies. And, in some versions of the blueprint, it is urged, finally, that the only probative epidemiological evidence would be studies showing that exposures to the relevant toxin, at relevant levels, double the incidence of the relevant health effect in the exposed population.
Volumes could be written on how the controversy over this blueprint has played out in the courts. Here we will mention only three difficulties with it.
First, the fact that the elements of some claim can be parsed into logically component parts does not always warrant the inference that separate proof for each component is necessary or even feasible. Consider wire fraud. For me to use my phone to commit wire fraud, it's logically necessary that the phone be in sound working order. That is, it must possess the generic capacity to transmit communications between humans. It is also logically necessary, of course, that the phone be used to transmit a specific fraudulent message. Yet despite the logical necessity that both conditions be satisfied before wire fraud can be made out, no one supposes that the phone's generic operability must be proved separately from its use to transmit a particular fraudulent message on some particular occasion. Factfinders can infer its generic operability from evidence showing its use on a particular day to make a specific call. This analogy does hold in some toxic tort cases -- particularly in cases where the immediacy of temporal association provides strong evidence, by itself, of a causal effect. See, e.g., Bonner v. ISP Techs., Inc., 259 F.3d 924 (8th Cir. 2001).
Second, even where separate proof of general causation is offered, it is unrealistic, for a host of reasons, to expect that peer-reviewed epidemiological research will be universally available. The reasons include the dubious ethical propriety of exposing human populations to suspected toxins for research purposes, as well as the sheer impracticality of conducting anticipatory epidemiological studies for every potential toxin. The FDCC authors say epidemiological evidence should be the "linchpin" of general causation analysis, but courts have routinely rejected the contention that epidemiology is categorically required. See, e.g., Rider v. Sandoz Pharms. Corp., 295 F.3d 1194 (11th Cir. 2002).
Third, even where epidemiology is available and pertinent, care must be exercised to avoid conflating general and specific causation -- as does the proposal, still advanced by some in the defense bar, that only epidemiological evidence showing a doubling of population risk should be counted as proof that exposure to a toxin caused any given plaintiff's health condition. This proposal is often rested on the notion that only a doubling of risk would satisfy the "more likely than not" burden of persuasion -- a fallacious proposition for several reasons, including its spurious equation of evidentiary likelihood with statistical measures. It is equally spurious to equate "statistical significance" with epidemiological findings showing a relative risk of 2.0 or greater, as the authors of the FDCC article do. Courts have generally declined to impose any such "doubling of risk" test in the toxic tort setting. See, e.g., In re Hanford Nuclear Reservation Litig., 292 F.3d 1124 (9th Cir. 2002).
The article is indeed a fair blueprint of standard defense arguments for challenging causation, many of which center on the uses and abuses of epidemiological data. But all in all, the article is more an aspirational portrayal of the law that defense counsel might prefer, than it is a neutral portrayal of the law as it stands.
Here is how the defense blueprint works. An analytical distinction is first drawn between "general" and "specific" (or "individual") causation. "General causation" involves the general capacity of some given toxic agent to cause harm in humans. "Specific" causation involves the question whether an exposure to that agent was indeed the cause in fact of a given plaintiff's injury. This analytical distinction once drawn, it is next demanded that general and specific causation be separately proved. It is then insisted that proof of general causation be undertaken through reliance on epidemiological studies. And, in some versions of the blueprint, it is urged, finally, that the only probative epidemiological evidence would be studies showing that exposures to the relevant toxin, at relevant levels, double the incidence of the relevant health effect in the exposed population.
Volumes could be written on how the controversy over this blueprint has played out in the courts. Here we will mention only three difficulties with it.
First, the fact that the elements of some claim can be parsed into logically component parts does not always warrant the inference that separate proof for each component is necessary or even feasible. Consider wire fraud. For me to use my phone to commit wire fraud, it's logically necessary that the phone be in sound working order. That is, it must possess the generic capacity to transmit communications between humans. It is also logically necessary, of course, that the phone be used to transmit a specific fraudulent message. Yet despite the logical necessity that both conditions be satisfied before wire fraud can be made out, no one supposes that the phone's generic operability must be proved separately from its use to transmit a particular fraudulent message on some particular occasion. Factfinders can infer its generic operability from evidence showing its use on a particular day to make a specific call. This analogy does hold in some toxic tort cases -- particularly in cases where the immediacy of temporal association provides strong evidence, by itself, of a causal effect. See, e.g., Bonner v. ISP Techs., Inc., 259 F.3d 924 (8th Cir. 2001).
Second, even where separate proof of general causation is offered, it is unrealistic, for a host of reasons, to expect that peer-reviewed epidemiological research will be universally available. The reasons include the dubious ethical propriety of exposing human populations to suspected toxins for research purposes, as well as the sheer impracticality of conducting anticipatory epidemiological studies for every potential toxin. The FDCC authors say epidemiological evidence should be the "linchpin" of general causation analysis, but courts have routinely rejected the contention that epidemiology is categorically required. See, e.g., Rider v. Sandoz Pharms. Corp., 295 F.3d 1194 (11th Cir. 2002).
Third, even where epidemiology is available and pertinent, care must be exercised to avoid conflating general and specific causation -- as does the proposal, still advanced by some in the defense bar, that only epidemiological evidence showing a doubling of population risk should be counted as proof that exposure to a toxin caused any given plaintiff's health condition. This proposal is often rested on the notion that only a doubling of risk would satisfy the "more likely than not" burden of persuasion -- a fallacious proposition for several reasons, including its spurious equation of evidentiary likelihood with statistical measures. It is equally spurious to equate "statistical significance" with epidemiological findings showing a relative risk of 2.0 or greater, as the authors of the FDCC article do. Courts have generally declined to impose any such "doubling of risk" test in the toxic tort setting. See, e.g., In re Hanford Nuclear Reservation Litig., 292 F.3d 1124 (9th Cir. 2002).
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