Opinion ID: 513179
Heading Depth: 3
Heading Rank: 1

Heading: Evidence of Developmental Toxicity

Text: 77 EPA based its finding as to developmental toxicity on several factors, none of which has been rebutted successfully by CMA. First, one study (the Ritter Study) reported that EHA caused an increased incidence of fetal malformations. J.A. 233-36. Another (the Hazelton Laboratories Study) illustrated adverse effects on fetuses of laboratory animals. Proposed Test Rule, 50 Fed.Reg. at 20,682. It is true that EPA described the Ritter Study as not being state-of-the-art and thus inappropriate for assessing human risk. Final Test Rule, 51 Fed.Reg. at 40,320. The Agency noted flaws with the Hazelton Laboratories Study. Id. at 40,321. EPA noted at the same time, however, that the studies, flawed as they concededly were, raise[d] sufficient concern about developmental toxicity to warrant testing. Id. at 40,320. In a statutory structure that calls for a testing rule precisely where there are insufficient data and experience on which to base a conclusion as to toxicity, 15 U.S.C. Sec. 2603(a)(1)(A)(ii), the existence of such studies surely provides the basis for demanding testing in order to assess risk conclusively. Cf. Ausimont, 838 F.2d at 97 ([i]f no doubt existed, testing would not be required). 78 Secondly, the agency found that EHA is structurally similar to valproic acid, which has been shown to cause harm to the developing embryo. Proposed Test Rule, 50 Fed.Reg. at 20,681-82. CMA describes the EPA inference of toxicity drawn from these facts as speculative and debatable. CMA Br. 48. But Congress explicitly contemplated that EPA would base test rules on comparisons among structurally similar chemicals. See H.R.Rep. No. 1341, supra, at 17. It is true that CMA criticized the studies done on valproic acid. J.A. 105-08. But EPA responded with its own analysis of those points. J.A. 307-11. Again, while it recognized that existing studies were inconclusive, EPA maintained that they were sufficient to raise enough concern to merit conducting new studies that would be more adequate. J.A. 308. Cf. Ausimont, 838 F.2d at 96 (characterizing similar arguments by industry as highlight[ing] the need for testing). 79 The statutory standard requires EPA to correlate the suspected toxicity of a substance with the suspected level of exposure. We find that the Agency had a more-than-theoretical basis for suspecting that the toxicity of EHA, even in rare or single doses of 60 milligrams per kilogram of body weight, sufficed to present an unreasonable risk of injury to health. 80 Sufficient evidence existed as to single-dose toxicity. The Ritter Study found evidence of developmental toxicity in test animals after single doses of EHA. Final Test Rule, 51 Fed.Reg. at 40,320. Another study (the Nau Study) showed that chemicals structurally similar to EHA cause fetal effects in test animals in single doses. Id. at 40,321; J.A. 291, 292. Single-dose toxicity is considered by EPA to be a possibility with developmental toxicants generally. Guidelines for the Health Assessment of Suspect Developmental Toxicants, 51 Fed.Reg. 34,028, 34,037 (1986). 81 The evidence, moreover, provided sufficient grounds for concern as to single doses in the suspected amount of real-world exposure, 60 milligrams of EHA per kilogram of body weight. The Ritter and Nau Studies involved exposing test animals to substance amounts 10 to 30 times those expected to occur to EHA workers. 22 These large-dose exposures caused high incidence of fetal toxicity; in one study, a non-exposed control group experienced 4.4 percent incidence of fetal toxicity while exposed animals experienced 71.1 percent in cidence of fetal toxicity. Final Test Rule, 51 Fed.Reg. at 40,320. While conceding that large-dose testing does not necessarily provide precise information for predicting toxicity at small dosage levels, EPA pointed out that a no-observed-effect level for EHA has never been found. Id. at 40,321. EPA reasonably maintained, therefore, that the high-dosage studies provided a rational basis for requiring tests to study the effects of EHA at lower dosages. Indeed, as our examination of the legislative history made clear, section 4 of TSCA authorizes issuance of test rules in the absence of adequate information to reasonably predict health effects. Were we to deem the high-dosage studies an insufficient basis for a test rule, EPA would be unable to react to the potential dangers of a chemical substance until either the Agency conducted government-funded studies at the expected real-world dosage level or private researchers fortuitously happened to publish such studies. The aim of TSCA was to make producers and users of chemical substances assume the costs of testing, so long as a more-than-theoretical basis existed for finding the presence of an unreasonable risk of injury to health. We are persuaded that EPA's finding of potential developmental toxicity is supported by substantial evidence.