analysis of the described studies, including an assessment of the relationship of maternal toxicity to developmental toxicity and the strengths, limitations, and consistency of the various study results; (2) characterization of maternal toxicity (e.g., mild or severe) associated with the studies listed in Table 4-10 and use of consistent nomenclature (ppm or mg/m3) for listing tetrachloroethylene concentrations; (3) the scientific basis for selecting the Tinston (1994) and Carney et al. (2006) studies as supportive of an RfV; (4) the scientific rationale for selecting the Tinston (1994) study instead of the Carney et al. (2006) study for derivation of the comparative RfV; (5) information on the mode of action for tetrachloroethylene-induced developmental toxicity which addresses the apparent contradictions raised in the committee’s review that TCA may be the causative agent; and (6) characterization of the evidence for tetrachloroethylene-induced reproductive and developmental toxicity in animals based on EPA risk assessment guidelines. Stating explicitly whether the animal evidence is sufficient or insufficient for these important end points will help risk managers and others to more readily identify and protect against potential adverse health effects. It will also help to identify data gaps in the tetrachloroethylene database. In addition to revising the chapter, the committee also recommends that EPA consider conducting a bench-mark dose analysis and deriving an RfV based on the Carney et al. (2006) study in addition to, or instead of, the Tinston (1994) study. This will address the potential confounding effects of maternal toxicity at the 1,000 ppm exposure level observed in the Tinston (1994) study.