Wf. Heydens et al., SUBCHRONIC, DEVELOPMENTAL, AND GENETIC TOXICOLOGY STUDIES WITH THE ETHANE SULFONATE METABOLITE OF ALACHLOR, Fundamental and applied toxicology, 33(2), 1996, pp. 173-181
The ethane sulfonate (ESA) metabolite of the herbicide alachlor is for
med 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 as
sessment. ESA did not induce chromosomal effects in a mouse bone marro
w micronucleus assay following acute administration. Administration of
ESA to rats in drinking water at concentrations of 200, 2000, and 10,
000 ppm for 91 days elicited biologically significant indications of t
oxicity only at the high-dose level (1002 mg/kg/day). The observed res
ponses 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 mic
roscopic lesions. ESA did not produce any adverse effects in pregnant
rats or their offspring even at 1000 mg/kg/day, the highest dose teste
d. These findings show that the subchronic and developmental toxicity
of ESA are low. Furthermore, comparison of results from studies with a
lachlor and its metabolite shows that the toxicity of ESA is substanti
ally lower. Margins of exposure for ESA range from 133,824 to 2,573,52
9 even using worst-case estimates of exposure, indicating that the met
abolite poses little risk of producing adverse effects at the very low
levels occasionally encountered. These results and accompanying analy
ses support the conclusion that ESA is not of toxicological concern. (
C) 1996 Society of Toxicology