Risk assessments would seemingly be about assessing risks, but they are not. The Reference Manual on Scientific Evidence defines “risk” as “[a] probability that an event will occur (e.g., that an individual will become ill or die within a stated period of time or by a certain age).”[1] The risk in risk assessment, however, may be zero, or uncertain, or even a probability of benefit. Agencies that must assess risks and set “action levels,” or “permissible exposure limits,” or “acceptable intakes,” often work under great uncertainty, with inspired guesswork, using unproven assumptions.
The lawsuit industry has thus often embraced the false equivalence between agency pronouncements on harmful medicinal, environmental, or occupational exposures and civil litigation adjudication of tortious harms. In the United States, federal agencies such as the Occupational Safety and Health Administration (OSHA), or the Environmental Protection Agency (EPA), and their state analogues, regularly set exposure standards that could not and should not hold up in a common-law tort case.
Remarkably, there are state and federal court judges who continue to misunderstand and misinterpret regulatory risk assessments, notwithstanding efforts to educate the judiciary. The second edition of the Reference Manual on Scientific Evidence contained a chapter by the late Professor Margaret Berger, who took pains to point out the difference between agency assessments and the adjudication of causal claims in court:
[p]roof of risk and proof of causation entail somewhat different questions because risk assessment frequently calls for a cost-benefit analysis. The agency assessing risk may decide to bar a substance or product if the potential benefits are outweighed by the possibility of risks that are largely unquantifiable because of presently unknown contingencies. Consequently, risk assessors may pay heed to any evidence that points to a need for caution, rather than assess the likelihood that a causal relationship in a specific case is more likely than not.[2]
In March 2003, Professor Berger organized a symposium,[3] the first Science for Judges program (and the last), where the toxicologist Dr. David L. Eaton presented on the differences in the use of toxicology in regulatory pronouncements as opposed to causal assessments in civil actions. As Dr. Eaton noted:
“regulatory levels are of substantial value to public health agencies charged with ensuring the protection of the public health, but are of limited value in judging whether a particular exposure was a substantial contributing factor to a particular individual’s disease or illness.”[4]
The United States Environmental Protection Agency (EPA) acknowledges that estimating “risk” from low level exposures based upon laboratory animal data is fraught because of inter-specie differences in longevity, body habitus and size, genetics, metabolism, excretion patterns, genetic homogeneity of laboratory animals, dosing levels and regimens. The EPA’s assumptions in conducting and promulgating regulatory risk assessments are intended to predict the upper bound of theoretical risk, while fully acknowledging that there may be no actual risk in humans:
“It should be emphasized that the linearized multistage [risk assessment] procedure leads to a plausible upper limit to the risk that is consistent with some proposed mechanisms of carcinogenesis. Such an estimate, however, does not necessarily give a realistic prediction of the risk. The true value of the risk is unknown, and may be as low as zero.”[5]
The approach of the U.S. Food and Drug Administration (FDA) with respect to mutagenic impurities in medications provides an illustrative example of how theoretical and hypothetical risk assessment can be.[6] The FDA’s risk assessment approach is set out in a “Guidance” document, which like all such FDA guidances, describes itself as containing non-binding recommendations, which do not preempt alternative approaches.[7] The agency’s goal is devise a control strategy for any mutagenic impurity to keep it at or below an “acceptable cancer risk level,” even if the risk or the risk level is completely hypothetical.
The FDA guidance advances the concept of a “Threshold of Toxicological Concern (TTC),” to set an “acceptable intake,” for chemical impurities that pose negligible risks of toxicity or carcinogenicity.[8] The agency describes its risk assessment methodology as “very conservative,” given the frequently unproven assumptions made to reach a quantification of an “acceptable intake”:
“The methods upon which the TTC is based are generally considered to be very conservative since they involve a simple linear extrapolation from the dose giving a 50% tumor incidence (TD50) to a 1 in 10-6 incidence, using TD50 data for the most sensitive species and most sensitive site of tumor induction. For application of a TTC in the assessment of acceptable limits of mutagenic impurities in drug substances and drug products, a value of 1.5 micrograms (µg)/day corresponding to a theoretical 10-5 excess lifetime risk of cancer can be justified.”
For more potent mutagenic carcinogens, such as aflatoxin-like-, N-nitroso-, and alkyl-azoxy compounds, the acceptable intake or permissible daily exposure (PDE) is set lower, based upon available animal toxicologic data.
The important divide between regulatory practice and the litigation of causal claims in civil actions arises from the theoretical nature of the risk assessment enterprise. The FDA acknowledges, for instance, that the acceptable intake is set to mark “a small theoretical increase in risk,” and a “highly hypothetical concept that should not be regarded as a realistic indication of the actual risk,” and thus not an actual risk.[9] The corresponding hypothetical or theoretical risk to the acceptable intake level is clearly small when compared with the human’s lifetime probability of developing cancer (which the FDA states is greater than 1/3, but probably now approaches 40%).
Although the TTC concept allows a calculation of an estimated “safe exposure,” the FDA points out that:
“exceeding the TTC is not necessarily associated with an increased cancer risk given the conservative assumptions employed in the derivation of the TTC value. The most likely increase in cancer incidence is actually much less than 1 in 100,000. *** Based on all the above considerations, any exposure to an impurity that is later identified as a mutagen is not necessarily associated with an increased cancer risk for patients already exposed to the impurity. A risk assessment would determine whether any further actions would be taken.”
In other words the FDA’s risk assessment exists to guide agency action, not to determine a person’s risk or medical status.[10]
As small and theoretical as the risks are, they are frequently based upon demonstrably incorrect assumptions, such as:
- humans are as sensitive as the most sensitive species;
- all organs are as sensitive as the most sensitive organ of the most sensitive species;
- the dose-response in the most sensitive species is a simple linear relationship;
- the linear relationship runs from zero exposure and zero risk to the exposure that yields the so-called TD50, the exposure that yields tumors in 50% of the experimental animal model;
- the TD-50 is calculated based upon the point estimate in the animal model study, regardless of any confidence interval around the point estimate;
- the inclusion, in many instances, of non-malignant tumors as part of the assessment of the TD50 exposure;
- there is some increased risk for any exposure, no matter how small; that is, there is no threshold below which there is no increased risk; and
- the medication with the mutagenic impurity was used daily for 70 years, by a person who weights 50 kg.
Although the FDA acknowledges that there may be some instances in which a “less than lifetime level” (LTL) may be appropriate, it places the burden on manufacturers to show the appropriateness of higher LTLs. The FDA’s M7 Guidance observes that
“[s]tandard risk assessments of known carcinogens assume that cancer risk increases as a function of cumulative dose. Thus, cancer risk of a continuous low dose over a lifetime would be equivalent to the cancer risk associated with an identical cumulative exposure averaged over a shorter duration.”[11]
Similarly, the agency acknowledges that there may be a “practical threshold,” as result of bodily defense mechanisms, such as DNA repair, which counter any ill effects from lower level exposures.[12]
“The existence of mechanisms leading to a dose response that is non-linear or has a practical threshold is increasingly recognized, not only for compounds that interact with non-DNA targets but also for DNA-reactive compounds, whose effects may be modulated by, for example, rapid detoxification before coming into contact with DNA, or by effective repair of induced damage. The regulatory approach to such compounds can be based on the identification of a No-Observed Effect Level (NOEL) and use of uncertainty factors (see ICH Q3C(R5), Ref. 7) to calculate a permissible daily exposure (PDE) when data are available.”
Expert witnesses often attempt to bootstrap their causation opinions by reference to determinations of regulatory agencies that are couched in similar language, but which use different quality and quantity of evidence than is required in the scientific community or in civil courts.
Supreme Court
Industrial Union Dep’t v. American Petroleum Inst., 448 U.S. 607, 656 (1980) (“OSHA is not required to support its finding that a significant risk exists with anything approaching scientific certainty” and “is free to use conservative assumptions in interpreting the data with respect to carcinogens, risking error on the side of overprotection, rather than underprotection.”).
Matrixx Initiatives, Inc. v. Siracusano, 563 U.S. 27, 131 S.Ct. 1309, 1320 (2011) (regulatory agency often makes regulatory decisions based upon evidence that gives rise only to a suspicion of causation)
First Circuit
Sutera v. Perrier Group of America, Inc., 986 F. Supp. 655, 664-65, 667 (D. Mass. 1997) (a regulatory agency’s “threshold of proof is reasonably lower than that in tort law”; “substances are regulated because of what they might do at given levels, not because of what they will do. . . . The fact of regulation does not imply scientific certainty. It may suggest a decision to err on the side of safety as a matter of regulatory policy rather than the existence of scientific fact or knowledge. . . . The mere fact that substances to which [plaintiff] was exposed may be listed as carcinogenic does not provide reliable evidence that they are capable of causing brain cancer, generally or specifically, in [plaintiff’s] case.”); id. at 660 (warning against the danger that a jury will “blindly accept an expert’s opinion that conforms with their underlying fears of toxic substances without carefully understanding or examining the basis for that opinion.”). Sutera is an important precedent, which involved a claim that exposure to an IARC category I carcinogen, benzene, caused plaintiffs’ leukemia. The plaintiff’s expert witness, Robert Jacobson, espousing a “linear, no threshold” theory, and relying upon an EPA regulation, which he claimed supported his opinion that even trace amounts of benzene can cause leukemia.
In re Neurontin Mktg., Sales Practices, and Prod. Liab. Litig., 612 F. Supp. 2d 116, 136 (D. Mass. 2009) (‘‘It is widely recognized that, when evaluating pharmaceutical drugs, the FDA often uses a different standard than a court does to evaluate evidence of causation in a products liability action. Entrusted with the responsibility of protecting the public from dangerous drugs, the FDA regularly relies on a risk-utility analysis, balancing the possible harm against the beneficial uses of a drug. Understandably, the agency may choose to ‘err on the side of caution,’ … and take regulatory action such as revising a product label or removing a drug from the marketplace ‘upon a lesser showing of harm to the public than the preponderance-of-the-evidence or more-like-than-not standard used to assess tort liability’.’’) (internal citations omitted)
Whiting v. Boston Edison Co., 891 F. Supp. 12, 23-24 (D. Mass. 1995) (criticizing the linear no-threshold hypothesis, common to regulatory risk assessments, because it lacks any known or potential error rate, and it cannot be falsified as would any scientific theory)
Second Circuit
Wills v. Amerada Hess Corp., No. 98 CIV. 7126(RPP), 2002 WL 140542 (S.D.N.Y. Jan. 31, 2002), aff’d, 379 F.3d 32 (2d Cir. 2004) (Sotomayor, J.). In this Jones Act case, the plaintiff claimed that her husband’s exposure to benzene and polycyclic aromatic hydrocarbons on board ship caused his squamous cell lung cancer. Plaintiff’s expert witness relied heavily upon the IARC categorization of benzene as a “known” carcinogen, and an “oncogene” theory of causation that claimed there was no safe level of exposure because a single molecule could induce cancer. According to the plaintiff’s expert witness, the oncogene theory dispensed with the need to quantify exposure. Then Judge Sotomayor, citing Sutera, rejected plaintiff’s no-threshold theory, and the argument that exposure that exceeded OHSA permissible exposure level supported the causal claim.
Mancuso v. Consolidated Edison Co., 967 F. Supp. 1437, 1448 (S.D.N.Y. 1997) (“recommended or prescribed precautionary standards cannot provide legal causation”; “[f]ailure to meet regulatory standards is simply not sufficient” to establish liability)
In re Agent Orange Product Liab. Litig., 597 F. Supp. 740, 781 (E.D.N.Y. 1984) (Weinstein, J.) (“The distinction between avoidance of risk through regulation and compensation for injuries after the fact is a fundamental one.”), aff’d in relevant part, 818 F.2d 145 (2d Cir.1987), cert. denied sub nom. Pinkney v. Dow Chemical Co., 484 U.S. 1004 (1988). Judge Weinstein explained that regulatory action would not by itself support imposing liability for an individual plaintiff. Id. at 782. “A government administrative agency may regulate or prohibit the use of toxic substances through rulemaking, despite a very low probability of any causal relationship. A court, in contrast, must observe the tort law requirement that a plaintiff establish a probability of more than 50% that the defendant’s action injured him.” Id. at 785.
In re Ephedra Prods. Liab. Litig., 393 F. Supp. 2d 181, 189 (S.D.N.Y. 2005) (improvidently relying in part upon FDA ban despite “the absence of definitive scientific studies establishing causation”)
Third Circuit
Gates v. Rohm & Haas Co., 655 F.3d 255, 268 (3d Cir. 2011) (affirming the denial of class certification for medical monitoring) (‘‘plaintiffs could not carry their burden of proof for a class of specific persons simply by citing regulatory standards for the population as a whole’’).
In re Schering-Plough Corp. Intron/Temodar Consumer Class Action, 2009 WL 2043604, at *13 (D.N.J. July 10, 2009)(“[T]here is a clear and decisive difference between allegations that actually contest the safety or effectiveness of the Subject Drugs and claims that merely recite violations of the FDCA, for which there is no private right of action.”)
Rowe v. E.I. DuPont de Nemours & Co., Civ. No. 06-1810 (RMB), 2008 U.S. Dist. LEXIS 103528, *46-47 (D.N.J. Dec. 23, 2008) (rejecting reliance upon regulatory findings and risk assessments in which “the basic goal underlying risk assessments . . . is to determine a level that will protect the most sensitive members of the population.”) (quoting David E. Eaton, “Scientific Judgment and Toxic Torts – A Primer in Toxicology for Judges and Lawyers,” 12 J.L. & Pol’y 5, 34 (2003) (“a number of protective, often ‘worst case’ assumptions . . . the resulting regulatory levels . . . generally overestimate potential toxicity levels for nearly all individuals.”)
Soldo v. Sandoz Pharms. Corp., 244 F. Supp. 2d 434, 543 (W.D. Pa. 2003) (finding FDA regulatory proceedings and adverse event reports not adequate or helpful in determining causation; the FDA “ordinarily does not attempt to prove that the drug in fact causes a particular adverse effect.”)Wade-Greaux v. Whitehall Laboratories, Inc., 874 F. Supp. 1441, 1464 (D.V.I.) (“assumption[s that] may be useful in a regulatory risk-benefit context … ha[ve] no applicability to issues of causation-in-fact”), aff’d, 46 F.3d 1120 (3d Cir. 1994)
O’Neal v. Dep’t of the Army, 852 F. Supp. 327, 333 (M.D. Pa. 1994) (administrative risk figures are “appropriate for regulatory purposes in which the goal is to be particularly cautious [but] overstate the actual risk and, so, are inappropriate for use in determining” civil liability)
Fourth Circuit
Dunn v. Sandoz Pharmaceuticals Corp., 275 F. Supp. 2d 672, 684 (M.D.N.C. 2003) (FDA “risk benefit analysis” “does not demonstrate” causation in any particular plaintiff).
Meade v. Parsley, No. 2:09-cv-00388, 2010 U.S. Dist. LEXIS 125217, * 25 (S.D.W. Va. Nov. 24, 2010) (‘‘Inasmuch as the cost-benefit balancing employed by the FDA differs from the threshold standard for establishing causation in tort actions, this court likewise concludes that the FDA-mandated [black box] warnings cannot establish general causation in this case.’’)
Rhodes v. E.I. du Pont de Nemours & Co., 253 F.R.D. 365, 377 (S.D. W.Va. 2008) (rejecting the relevance of regulatory assessments, which are precautionary and provide no information about actual risk).
Fifth Circuit
Moore v. Ashland Chemical Co., 126 F.3d 679, 708 (5th Cir. 1997) (holding that expert witness could rely upon a material safety data sheet (MSDS) because mandated by the Hazard Communication Act, 29 C.F.R. § 1910.1200), vacated 151 F.3d 269 (5th Cir. 1998) (affirming trial court’s exclusion of expert witness who had relied upon MSDS).
Johnson v. Arkema Inc., 685 F.3d 452, 464 (5th Cir. 2012) (per curiam) (affirming exclusion of expert witness who upon regulatory pronouncements; noting the precautionary nature of such statements, and the absence of specificity for the result claimed at the exposures experienced by plaintiff)
Allen v. Pennsylvania Eng’g Corp., 102 F.3d 194, 198-99 (5th Cir. 1996) (“Scientific knowledge of the harmful level of exposure to a chemical, plus knowledge that the plaintiff was exposed to such quantities, are minimal facts necessary to sustain the plaintiffs’ burden in a toxic tort case”; regulatory agencies, charged with protecting public health, employ a lower standard of proof in promulgating regulations than that used in tort cases). The Allen court explained that it was “also unpersuaded that the “weight of the evidence” methodology these experts use is scientifically acceptable for demonstrating a medical link. . . . Regulatory and advisory bodies. . .utilize a “weight of the evidence” method to assess the carcinogenicity of various substances in human beings and suggest or make prophylactic rules governing human exposure. This methodology results from the preventive perspective that the agencies adopt in order to reduce public exposure to harmful substances. The agencies’ threshold of proof is reasonably lower than that appropriate in tort law, which traditionally makes more particularized inquiries into cause and effect and requires a plaintiff to prove that it is more likely than not that another individual has caused him or her harm.” Id.
Burst v. Shell Oil Co., C. A. No. 14–109, 2015 WL 3755953, *8 (E.D. La. June 16, 2015) (explaining Fifth Circuit’s rejection of regulatory “weight of the evidence” approaches to evaluating causation)
Sprankle v. Bower Ammonia & Chem. Co., 824 F.2d 409, 416 (5th Cir. 1987) (affirmed Rule 403 exclusion evidence of OSHA violations in claim of respiratory impairment in a non-employee who experienced respiratory impairment after exposure to anhydrous ammonia; court found that the jury likely be confused by regulatory pronouncements)
Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814, 825 (W.D. Tex. 2005) (noting that a product that “has been classified as a carcinogen by agencies responsible for public health regulations is not probative of” common-law specific causation) (finding that the linear no-threshold opinion of the plaintiffs’ expert witness, Malin Dollinger, lacked a satisfactory scientific basis)
Burleson v. Glass, 268 F. Supp. 2d 699, 717 (W.D. Tex. 2003) (“the mere fact that [the product] has been classified by certain regulatory organizations as a carcinogen is not probative on the issue of whether [plaintiff’s] exposure. . .caused his. . .cancers”), aff’d, 393 F.3d 577 (5th Cir. 2004)
Newton v. Roche Labs., Inc., 243 F. Supp. 2d 672, 677, 683 (W.D. Tex. 2002) (FDA’s precautionary decisions on labeling are not a determination of causation of specified adverse events) (“Although evidence of an association may … be important in the scientific and regulatory contexts…, tort law requires a higher standard of causation.”)
Molden v. Georgia Gulf Corp., 465 F. Supp. 2d 606, 611 (M.D. La. 2006) (“regulatory and advisory bodies make prophylactic rules governing human exposure based on proof that is reasonably lower than that appropriate in tort law”)
Sixth Circuit
Nelson v. Tennessee Gas Pipeline Co., 243 F.3d 244, 252-53 (6th Cir. 2001) (exposure above regulatory levels is insufficient to establish causation)
Stites v Sundstrand Heat Transfer, Inc., 660 F. Supp. 1516, 1525 (W.D. Mich. 1987) (rejecting use of regulatory standards to support claim of increased risk, noting the differences in goals and policies between regulation and litigation)
Mann v. CSX Transportation, Inc., case no. 1:07-Cv-3512, 2009 U.S. Dist. Lexis 106433 (N.D. Ohio Nov. 10, 2009) (rejecting expert testimony that relied upon EPA action levels, and V.A. compensation for dioxin exposure, as basis for medical monitoring opinions)
Baker v. Chevron USA, Inc., 680 F. Supp. 2d 865, 880 (S.D. Ohio 2010) (“[R]egulatory agencies are charged with protecting public health and thus reasonably employ a lower threshold of proof in promulgating their regulations than is used in tort cases.”) (“[t]he mere fact that Plaintiffs were exposed to [the product] in excess of mandated limits is insufficient to establish causation”; rejecting Dr. Dahlgren’s opinion and its reliance upon a “one-hit” or “no threshold” theory of causation in which exposure to one molecule of a cancer-causing agent has some finite possibility of causing a genetic mutation leading to cancer, a theory that may be accepted for purposes of setting regulatory standards, but not as reliable scientific knowledge)
Adams v. Cooper Indus., 2007 WL 2219212 at *7 (E.D. KY 2007).
Seventh Circuit
Wood v. Textron, Inc., No. 3:10 CV 87, 2014 U.S. Dist. LEXIS 34938 (N.D. Ind. Mar. 17, 2014); 2014 U.S. Dist. LEXIS 141593, at *11 (N.D. Ind. Oct. 3, 2014), aff’d, 807 F.3d 827 (7th Cir. 2015). Dahlgren based his opinions upon the children’s water supply containing vinyl chloride in excess of regulatory levels set by state and federal agencies, including the EPA. Similarly, Ryer-Powder relied upon exposure levels’ exceeding regulatory permissible limits for her causation opinions. The district court, with the approval now of the Seventh Circuit would have none of this nonsense. Exceeding governmental regulatory exposure limits does not prove causation. The con-compliance does not help the fact finder without knowing “the specific dangers” that led the agency to set the permissible level, and thus the regulations are not relevant at all without this information. Even with respect to specific causation, the regulatory infraction may be weak or null evidence for causation. (citing Cunningham v. Masterwear Corp., 569 F.3d 673, 674–75 (7th Cir. 2009)
Eighth Circuit
Glastetter v. Novartis Pharms. Corp., 107 F. Supp. 2d 1015, 1036 (E.D. Mo. 2000) (“[T]he [FDA’s] statement fails to affirmatively state that a connection exists between [the drug] and the type of injury in this case. Instead, it states that the evidence received by the FDA calls into question [drug’s] safety, that [the drug] may be an additional risk factor. . .and that the FDA had new evidence suggesting that therapeutic use of [the drug] may lead to serious adverse experiences. Such language does not establish that the FDA had concluded that [the drug] can cause [the injury]; instead, it indicates that in light of the limited social utility of [the drug for the use at issue] and the reports of possible adverse effects, the drug should no longer be used for that purpose.”) (emphasis in original), aff’d, 252 F.3d 986, 991 (8th Cir. 2001) (FDA’s precautionary decisions on labeling are not a determination of causation of specified adverse events; “methodology employed by a government agency results from the preventive perspective that the agencies adopt”)( “The FDA will remove drugs from the marketplace upon a lesser showing of harm to the public than the preponderance-of-the-evidence or the more-like-than-not standard used to assess tort liability . . . . [Its] decision that [the drug] can cause [the injury] is unreliable proof of medical causation.”), aff’d, 252 F.3d 986 (8th Cir. 2001)
Wright v. Willamette Indus., Inc., 91 F.3d 1105, 1107 (8th Cir. 1996) (rejecting claim that plaintiffs were not required to show individual exposure levels to formaldehyde from wood particles). The Wright court elaborated upon the difference between adjudication and regulation of harm:
“Whatever may be the considerations that ought to guide a legislature in its determination of what the general good requires, courts and juries, in deciding cases, traditionally make more particularized inquiries into matters of cause and effect. Actions in tort for damages focus on the question of whether to transfer money from one individual to another, and under common-law principles (like the ones that Arkansas law recognizes) that transfer can take place only if one individual proves, among other things, that it is more likely than not that another individual has caused him or her harm. It is therefore not enough for a plaintiff to show that a certain chemical agent sometimes causes the kind of harm that he or she is complaining of. At a minimum, we think that there must be evidence from which the factfinder can conclude that the plaintiff was exposed to levels of that agent that are known to cause the kind of harm that the plaintiff claims to have suffered. See Abuan v. General Elec. Co., 3 F.3d at 333. We do not require a mathematically precise table equating levels of exposure with levels of harm, but there must be evidence from which a reasonable person could conclude that a defendant’s emission has probablycaused a particular plaintiff the kind of harm of which he or she complains before there can be a recovery.”
Gehl v. Soo Line RR, 967 F.2d 1204, 1208 (8th Cir. 1992).
Nelson v. Am. Home Prods. Corp., 92 F. Supp. 2d 954, 958 (W.D. Mo. 2000) (FDA’s precautionary decisions on labeling are not a determination of causation of specified adverse events)
National Bank of Commerce v. Associated Milk Producers, Inc., 22 F. Supp. 2d 942, 961 (E.D.Ark. 1998), aff’d, 191 F.3d 858 (8th Cir. 1999)
Junk v. Terminix Internat’l Co., 594 F. Supp. 2d 1062, 1071 (S.D. Iowa 2008) (“government agency regulatory standards are irrelevant to [plaintiff’s] burden of proof in a toxic tort cause of action because of the agency’s preventative perspective”)
Ninth Circuit
Henrickson v. ConocoPhillips Co., 605 F. Supp. 2d 1142, 1156 (E.D. Wash. 2009) (excluding expert witness causation opinions in case involving claims that benzene exposure caused leukemia)
Lopez v. Wyeth-Ayerst Labs., Inc., 1998 WL 81296, at *2 (9th Cir. Feb. 25, 1998) (FDA’s precautionary decisions on labeling are not a determination of causation of specified adverse events)
In re Epogen & Aranesp Off-Label Marketing & Sales Practices Litig., 2009 WL 1703285, at *5 (C.D. Cal. June 17, 2009) (“have not been proven” allegations are an improper “FDA approval” standard; the FDA’s determination to require warning changes without establishing causation is established does not permit a court or jury, bound by common-law standards, to impose such a duty to warn when common-law causation requirements are not met).
In re Hanford Nuclear Reservation Litig., 1998 U.S. Dist. Lexis 15028 (E.D. Wash. 1998) (radiation and chromium VI), rev’d on other grounds, 292 F.3d 1124 (9th Cir. 2002).
Tenth Circuit
Hollander v. Shandoz Pharm. Corp., 95 F. Supp. 2d 1230, 1239 (W.D. Okla. 2000) (distinguishing FDA’s threshold of proof as lower than appropriate in tort law), aff’d in relevant part, 289 F.3d 1193, 1215 (10th Cir. 2002)
Mitchell v. Gencorp Inc., 165 F.3d 778, 783 n.3 (10th Cir. 1999) (benzene and CML) (quoting Allen, 102 F.3d at 198) (state administrative finding that product was a carcinogen was based upon lower administrative standard than tort standard) (“The methodology employed by a government agency “results from the preventive perspective that the agencies adopt in order to reduce public exposure to harmful substances. The agencies’ threshold of proof is reasonably lower than that appropriate in tort law, which traditionally makes more particularized inquiries into cause and effect and requires a plaintiff to prove it is more likely than not that another individual has caused him or her harm.”)
In re Breast Implant Litig., 11 F. Supp. 2d 1217, 1229 (D.Colo. 1998)
Johnston v. United States, 597 F. Supp. 374, 393-394 (D. Kan.1984) (noting that the linear no-threshold hypothesis is based upon a prudent assumption designed to overestimate risk; speculative hypotheses are not appropriate in determining whether one person has harmed another)
Eleventh Circuit
Rider v. Sandoz Pharmaceuticals Corp., 295 F.3d 1194, 1201 (11th Cir. 2002) (FDA may take regulatory action, such as revising warning labels or withdrawing drug from the market ‘‘upon a lesser showing of harm to the public than the preponderance-of-the-evidence or more-likely-than-not standard used to assess tort liability’’) (“A regulatory agency such as the FDA may choose to err on the side of caution. Courts, however, are required by the Daubert trilogy to engage in objective review of the evidence to determine whether it has sufficient scientific basis to be considered reliable.”)
McClain v. Metabolife Internat’l, Inc., 401 F.3d 1233, 1248-1250 (11th Cir. 2005) (ephedra) (allowing that regulators “may pay heed to any evidence that points to a need for caution,” and apply “a much lower standard than that which is demanded by a court of law”) (“[U]se of FDA data and recommendations raises a more subtle methodological issue in a toxic tort case. The issue involves identifying and contrasting the type of risk assessment that a government agency follows for establishing public health guidelines versus an expert analysis of toxicity and causation in a toxic tort case.”)
In re Seroquel Products Liab. Litig., 601 F. Supp. 2d 1313, 1315 (M.D. Fla. 2009) (noting that administrative agencies “impose[] different requirements and employ[] different labeling and evidentiary standards” because a “regulatory system reflects a more prophylactic approach” than the common law)
Siharath v. Sandoz Pharmaceuticals Corp., 131 F. Supp. 2d 1347, 1370 (N.D. Ga. 2001) (“The standard by which the FDA deems a drug harmful is much lower than is required in a court of law. The FDA’s lesser standard is necessitated by its prophylactic role in reducing the public’s exposure to potentially harmful substances.”), aff’d, 295 F.3d 1194 330 (11th Cir. 2002)
In re Accutane Products Liability, 511 F.Supp.2d 1288, 1291-92 (M.D. Fla. 2007)(acknowledging that regulatory risk assessments are not necessarily realistic in human populations because they are often based upon animal studies, and that the important differences between experimental animals and humans are substantial in various health outcomes).
Kilpatrick v. Breg, Inc., 2009 WL 2058384 at * 6-7 (S.D. Fla. 2009) (excluding plaintiff’s expert witness), aff’d, 613 F.3d 1329 (11th Cir. 2010)
District of Columbia Circuit
Ethyl Corp. v. E.P.A., 541 F.2d 1, 28 & n. 58 (D.C. Cir. 1976) (detailing the precautionary nature of agency regulations that may be based upon suspicions)
STATE COURTS
Arizona
Lofgren v. Motorola, 1998 WL 299925 (Ariz. Super. Ct. 1998) (finding plaintiffs’ expert witnesses’ testimony that TCE caused cancer to be not generally accepted; “it is appropriate public policy for health organizations such as IARC and the EPA to make judgments concerning the health and safety of the population based on evidence which would be less than satisfactory to support a specific plaintiff’s tort claim for damages in a court of law”)
Colorado
Salazar v. American Sterilizer Co., 5 P.3d 357 (Colo. Ct. App. 2000) (allowing testimony about harmful ethylene oxide exposure based upon OSHA regulations)
Georgia
Butler v. Union Carbide Corp., 712 S.E.2d 537, 552 & n.37 (Ga. App. 2011) (distinguishing risk assessment from causation assessment; citing the New York Court of Appeals decision in Parker for correctly rejecting reliance on regulatory pronouncements for causation determinations)
Illinois
La Salle Nat’l Bank v. Malik, 705 N.E.2d 938 (Ill. App. 3d) (reversing trial court’s exclusion of OSHA PEL for ethylene oxide), writ pet’n den’d, 714 N.E.2d 527 (Ill. 2d 1999)
New York
Parker v. Mobil Oil Corp., 7 N.Y.3d 434, 450, 857 N.E.2d 1114, 1122, 824 N.Y.S.2d 584 (N.Y. 2006) (noting that regulatory agency standards usually represent precautionary principle efforts deliberately to err on side of prevention; “standards promulgated by regulatory agencies as protective measures are inadequate to demonstrate legal causation.”
In re Bextra & Celebrex, 2008 N.Y. Misc. LEXIS 720, *20, 239 N.Y.L.J. 27 (2008) (characterizing FDA Advisory Panel recommendations as regulatory standard and protective measure).
Juni v. A.O. Smith Water Products Co., 48 Misc. 3d 460, 11 N.Y.S.3d 416, 432, 433 (N.Y. Cty. 2015) (“the reports and findings of governmental agencies [declaring there to be no safe dose of asbestos] are irrelevant as they constitute insufficient proof of causation”), aff’d, 32 N.Y.3d 1116, 116 N.E.3d 75, 91 N.Y.S.3d 784 (2018)
Ohio
Valentine v. PPG Industries, Inc., 821 N.E.2d 580, 597-98 (Ohio App. 2004), aff’d, 850 N.E.2d 683 (Ohio 2006).
Pennsylvania
Betz v. Pneumo Abex LLC, 44 A. 3d 27 (Pa. 2012).
Texas
Borg-Warner Corp., 232 S.W.3d 765, 770 (Tex. 2007)
Exxon Corp. v. Makofski, 116 S.W.3d 176, 187-88 (Tex. App. 2003) (describing “standards used by OSHA [and] the EPA” as inadequate for causal determinations)
[1] Michael D. Green, D. Michal Freedman, and Leon Gordis, “Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence 549, 627 (3d ed. 2011).
[2] Margaret A. Berger, “The Supreme Court’s Trilogy on the Admissibility of Expert Testimony,” in Reference Manual On Scientific Evidence at 33 (Fed. Jud. Center 2d. ed. 2000).
[3] Margaret A. Berger, “Introduction to the Symposium,” 12 J. L. & Pol’y 1 (2003). Professor Berger described the symposium as a “felicitous outgrowth of a grant from the Common Benefit Trust established in the Silicone Breast Implant Products Liability Litigation to hold a series of conferences at Brooklyn Law School.” Id. at 1. Ironically, that “Trust” was nothing more than the walking-around money of plaintiffs’ lawyers from the Silicone-Gel Breast Implant MDL 926. Although Professor Berger was often hostile the causation requirement in tort law, her symposium included some well-qualified scientists who amplified her point from the Reference Manual about the divide between regulatory risk assessment and scientific causal assessments.
[4] David L. Eaton, Scientific Judgment and Toxic Torts- A Primer in Toxicology for Judges and Lawyers, 12 J.L. & Pol’y 5, 36 (2003). See also Joseph V. Rodricks and Susan H. Rieth, “Toxicological risk assessment in the courtroom: are available methodologies suitable for evaluating toxic tort and product liability claims?” 27 Regul. Toxicol. & Pharmacol. 21, 27 (1998) (“The public health-oriented resolution of scientific uncertainty [used by regulators] is not especially helpful to the problem faced by a court.”)
[5] EPA “Guidelines for Carcinogen Risk Assessment” at 13 (1986).
[6] The approach is set out in FDA, M7 (R1) Assessment and Control of DNA Reactive (Mutagenic) Impurities in Pharmaceuticals to Limit Potential Carcinogenic Risk: Guidance for Industry (2018) [FDA M7]. This FDA guidance is essentially an adoption of the M7 document of the Expert Working Group (Multidisciplinary) of the International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use (ICH).
[7] FDA M7 at 3.
[8] FDA M7 at 5.
[9] FDA M7 at 5 (emphasis added).
[10] See Labeling of Diphenhydramine Containing Drug Products for Over-the-Counter Human Use, 67 Fed. Reg. 72,555, at 72,556 (Dec. 6, 2002) (“FDA’s decision to act in an instance such as this one need not meet the standard of proof required to prevail in a private tort action. . .. To mandate a warning or take similar regulatory action, FDA need not show, nor do we allege, actual causation.”) (citing Glastetter).
[11] FDA M7 at “Acceptable Intakes in Relation to Less-Than-Lifetime (LTL) Exposure (7.3).”
[12] FDA M7 at 12 (“Mutagenic Impurities With Evidence for a Practical Threshold (7.2.2)”).
