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Updated: Aug 18, 2026

Split-and-pool Synthesis and Characterization of Peptide Tertiary Amide Library
Published on: June 20, 2014
Objective:
Current federal regulations of potentially carcinogenic environmental chemicals are based on the assumption that risks for humans can be extrapolated from the effects of chronic high-dose exposure of rodents. It is assumed that all chemicals induce cancer by a genotoxic mechanism (direct interaction with DNA) and that humans metabolize chemicals by the same pathways as the test rodents. Trichloroethylene, a former medicine, is now regulated because of rodent studies. Its major metabolite, chloral hydrate, widely used as a sedative in both adults and children, is in danger of being banned by comparable studies. This paper assesses the safety of chloral hydrate.
Design:
Analysis of the literature regarding the metabolic, toxicologic, and epidemiologic data on trichloroethylene and chloral hydrate.
Results:
The dose-response relationship for carcinogenesis of chloral hydrate and other chemicals in its metabolic breakdown pathway is nonlinear in rodents: very high doses given chronically, sufficient to cause cellular necrosis, are necessary for induction of malignancies. In addition, epidemiologic data on people exposed to substantial amounts of trichloroethylene (which is metabolized to chloral hydrate) show no increase in mortality or cancers.
Conclusions:
The assumptions underlying current regulatory practices for environmental chemicals are not applicable to the medicinal use of chloral hydrate. Instead, a threshold model is appropriate. The data do not suggest the need to ban chloral hydrate as a medicine; however, possible modifications in its use are suggested.
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