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The ethane sulfonate (ESA) metabolite of the herbicide alachlor is formed in soil by microbial action. The present studies were conducted to assess the toxicity of ESA and provide a base set of data for risk assessment. ESA did not induce chromosomal effects in a mouse bone marrow micronucleus assay following acute administration. Administration of ESA to rats in drinking water at concentration of 200, 2000, and 10,000 ppm for 91 days elicited biologically significant indications of toxicity only at the high-dose level (1002 mg/kg/day). The observed responses included decreases in body weights and food consumption as well as effects on clinical chemistry values. Many of the changes appeared to be due to decreased palatability of the drinking water. There were no ESA-induced gross pathology findings, organ weight changes, or microscopic lesions. ESA did not produce any adverse effects in pregnant rats or their offspring even at 1000 mg/kg/day, the highest dose tested. These findings show that the subchronic and developmental toxicity of ESA are low. Furthermore, comparison of results from studies with alachlor and its metabolite shows that the toxicity of ESA is substantially lower. Margins of exposure for ESA range from 133,824 to 2,573,529 even using worst-case estimates of exposure, indicating that the metabolite poses little risk of producing adverse effects at the very low levels occasionally encountered. These results and accompanying analyses support the conclusion that ESA is not of toxicological concern.

Subchronic, Developmental, and Genetic Toxicology Studies with the Ethane Sulfonate Metabolite of Alachlor