LNT in Milward v. Acuity Specialty Products Group

Professor Edward J. Calabrese previously has written about the shadowy origins of the linear no threshold (LNT) model of cancer causation.  See The Dubious Origins of the Linear No Threshold Model of Carcinogenesis (Jan. 10, 2013).  Recently, Calabrese has deepened his historical scholarship with two additional, interesting articles. SeeToxicologist Says NAS Panel ‘Misled the World’ When Adopting Radiation Exposure Guidelines” (Aug. 13, 2013).

These articles, now available online, are important tools in the work chest of lawyers who litigate health effect claims.  Edward J. Calabrese, “How the US National Academy of Sciences misled the world community on cancer risk assessment: new findings challenge historical foundations of the linear dose response,” 87 Arch. Toxicol. (2013) (in press); Edward J. Calabrese, “Origin of the linearity no threshold (LNT) dose–response concept,” 87 Arch. Toxicol. 1621 (2013). Professor Calabrese illuminates the exaggerations and ipse dixit in the origins of the linear-no threshold model, first applied to radiogenic cancers, and later to human carcinogenesis more generally.

On remand from the First Circuit, the trial judge in Milward, now the Hon. Douglas Woodlock, faced a renewed Rule 702 motion directed to Milward’s specific causation expert witnesses.  Milward v. Acuity Specialty Products Group, Inc., Civil Action No. 07–11944–DPW, 2013 WL 4812425 (D. Mass. Sept. 6, 2013). Plaintiffs attempted to invoke the dubious LNT concept to argue that benzene should be in the “differential” for ascertaining the specific cause of Mr. Milward’s APL. In performing a careful Rule 702 analysis, Judge Woodlock rule that, “[t]o the extent Butler [Milward’s expert witness] seeks to establish specific causation based on the argument that any level of benzene is sufficient to cause leukemia—a so-called “no safe level,” “no threshold,” or “linear” model—her opinion is inadmissibly unreliable.”  Id. at *8.

In recognizing Dr. Butler’s reliance upon LNT concepts in civil litigation as unreliable, Judge Woodlock followed the lead of other courts, within the First Circuit, which have previously rejected expert witness opinion testimony founded upon the LNT model.  See, e.g., Whiting v. Boston Edison Co., 891 F.Supp. 12, 25 (D.Mass.1995) (“[t]he linear non-threshold model cannot be falsified, nor can it be validated. To the extent that it has been subjected to peer review and publication, it has been rejected by the overwhelming majority of the  scientific community. It has no known or potential rate of error. It is merely an hypothesis.” ); Sutera v. Perrier Group of America Inc., 986 F.Supp. 655, 666 (D.Mass.1997) (“Accordingly, although there is evidence that one camp of scientists … believes that a non-linear model is appropriate basis for predicting the risks of low-level exposures to benzene, there is no scientific evidence that the linear no-safe threshold analysis is an acceptable scientific technique used by experts in determining causation in an individual instance.”).  Strong precedent outside the First Circuit also supports Judge Woodlock’s holding.  See Allen v. Pennsylvania Eng’g Corp., 102 F.3d 194, 198 (5th Cir.1996); Henricksen v. ConocoPhillips Co., 605 F.Supp. 2d 1142, 1166 (E.D.Wash.2009) (“[Plaintiffs’ expert witness’s] theory that any amount of exposure more than negligible should be considered substantial risk factor for AML flies in the face of the scientific literature reviewed and other expert testimony in this case that there is a threshold or dose below which you do not see a statistically significant risk of developing AML.”); In re W.R. Grace & Co. 355 B.R. 462, 476 (Bankr. D. Del. 2006) (the “no threshold model . . . flies in the face of the toxicological law of dose-response . . . doesn’t satisfy Daubert, and doesn’t stand up to scientific scrutiny”); Cano v. Everest Minerals Corp., 362 F. Supp. 2d 814, 853–54 (W.D. Tex. 2005) (even accepting the linear, no-threshold model for uranium mining and cancer, it is not enough to show exposure, you must show causation as well). See also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1244 (11th Cir. 2005) (“in evaluating the reliability of the experts’ opinions on general causation, it would help to know how much additional risk for heart attack or ischemic stroke Metabolife consumers have over the risks the general population faces”). National Bank of Commerce v. Assoc. Milk Producers, 22 F. Supp. 2d 942, 960 (E.D. Ark. 1998), aff’d, 191 F.3d 858 (8th Cir.1999). See generally Federal Judicial Center, Reference Manual on Scientific Evidence, at 643 n. 28 (3d ed.2011).

The district court in Milward held that because Dr. Butler “did not and could not quantify a threshold exposure level for benzene, Milward cannot posit that his cumulative exposure level crossed a relevant threshold.” Milward, 2013 WL 4812425, at 8.  In addressing Milward’s reliance upon LNT, Judge Woodlock rejected three specious arguments, which frequently recur in Rule 702 litigation.

First, the district saw through the argument that the claimed benzene-APL LNT model was good science because the United States Environmental Protection Agency (EPA) relies upon it.  The EPA applies the LNT model for benzene

“due to uncertainty about the shape of the dose-response curve below 40 ppm-years.”

Id. at 8[1]. The district court recognized that the EPA’s reasoning was a “classic example of a cautious prophylactic administrative rule” that “does not support the reliability of the linear, no-threshold model in establishing specific causation.”  Id.  In so ruling, the Milward district court joins a long line of courts that have distinguished administrative rulemaking from civil litigation standards for causation.  See, e.g., Allen v. Pa. Eng’g Corp., 102 F.3d 194, 198 (5th Cir. 1996)(“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.”)

Second, the Milward district court also saw through plaintiffs’ argument that the First Circuit’s embrace of its “weight of the evidence” general causation approach, which appears to enjoy support among federal bureaucrats, required approval of plaintiffs’ attempt to use a LNT prophylactic or precautionary approach. Milward, 649 F.3d at 18 & n. 9.  Plaintiffs have the burden of showing reliability of the LNT model, and the EPA’s acknowledged uncertainty about the model for benzene was an insuperable barrier to their success.  Milward, 2013 WL 4812425, at 8 & n.4.

Third, the district court rejected Dr. Butler’s attempt to “bait and switch,” by pointing to a study on hematotoxicity as opposed to carcinogenicity.  Butler argued that there was “no clear evidence of a threshold below which benzene does not cause hematotoxicity in humans.”[2] The court recognized that the study referred to the lack of a hematotoxicity threshold for low average doses of benzene. Hematotoxicity is not necessarily induction of APL; nor was the lack of clear evidence for a threshold evidence against a threshold.

Even in the regulatory realm, the LNT model is losing traction.  See Chlorine Chemistry Council v. EPA, 206 F.3d 1286, 1287 (D.C. Cir. 2000) (invalidating EPA regulation under the Safe Drinking Water Act, when the EPA persisted in using an LNT model, after it had concluded that chloroform, a contaminant in drinking water from chlorination exerted a “a nonlinear mode of carcinogenic action”).  In the scientific realm, researchers can merely watch in amazement at the “political science” that proceeds under a mistaken, outdated model of carcinogenesis.  See, e.g., Brant A. Ulsh, “Checking the Foundation: Recent Radiobiology and the Linear No-Threshold Theory,” 99 Health Physics 747 (2010) (“However, a large and rapidly growing body of radiobiological evidence indicates that cell and tissue level responses to this damage, particularly at low doses and/or dose-rates, are nonlinear and may exhibit thresholds. To the extent that responses observed at lower levels of biological organization in vitro are predictive of carcinogenesis observed in vivo, this evidence directly contradicts the assumptions upon which the microdosimetric argument is based.”); Bernard L. Cohen, “The Linear No-Threshold Theory of Radiation Carcinogenesis Should Be Rejected,” 13 J. Am. Physicians & Surgeons 70, 75 (2008) (“The conclusion from the evidence reviewed in this paper and more extensively elsewhere is that the linear-no threshold theory (LNT) fails very badly in the low-dose region, grossly overestimating the risk from low-level radiation. This means that the cancer risk from the vast majority of normally encountered radiation exposures is much lower than given by usual estimates, and may well be zero or even negative.”); Maurice Tubiana, Ludwig E. Feinendegen, Chichuan Yang, and Joseph M. Kaminski, “The Linear No-Threshold Relationship Is Inconsistent with Radiation Biologic and Experimental Data,” 251 Radiology 13, 13, 15-16, 18 (2009) (noting that LNT model is obsolete in view of known upregulation of cellular protective mechanisms against cancer; “LNT was a useful model half a century ago. But current radiation protection concepts should be based on facts and on concepts consistent with current scientific results and not on opinions. Preconceived concepts impede progress; in the case of the LNT model, they have resulted in substantial medical, economic, and other societal harm.”).

[1] The court EPA Office of Research and Development, Carcinogenic Effects of Benzene: An Update, at 38–39 (April 1998).

[2] Dr. Butler cited Richard B. Hayes, et al., “Benzene and Lymphohemaptopoietic Malignancies in Humans,” 40 Am. J. Indus. Med. 117, 120 (2001).

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