An evaluation of the feasibility of using cytogenetic damage as a biomarker for alachlor exposure

Alachlor is a widely used herbicide for which there is significant human ex posure, principally through groundwater contamination and inhalation. Becau se alachlor is purported to be carcinogenic and mutagenic, we initiated stu dies to determine if induced cytogenetic damage could be used as a biomarke r for exposure to this herbicide. Both isolated and whole blood human lymph ocytes were exposed to alachlor using several protocols. The lymphocytes we re cultured for analysis of sister chromatid exchange (SCE), chromosome abe rrations (CAs), micronuclei (MN) in cytochalasin B-induced binucleated cell s, and proliferation kinetics using the replicative index (RT). In addition , CD rats were injected with either 10 or 50 mg kg(-1) of alachlor, 2-chlor o-N-(2,6-diethylphenyl) acetamide (CDEPA) or 2,6-diethylanaline (DEA). Afte r 24 h, the peripheral blood lymphocytes were removed and cultured for SCE and RI analysis. Alachlor did induce a concentration-related increase in SC E in vitro, but neither it nor its metabolites (CDEPA or DEA) induced a sig nificant increase in SCEs or an alteration of RI in vivo. At the highest in vitro concentration tested, alachlor induced a statistically-significant i ncrease in MN, but no concomitant increase in CAs was seen. From analyses o f our data and the literature on alachlor clastogenicity and exposure level s, we concluded that cytogenetic damage may not be an adequately sensitive marker for evaluating human exposure to alachlor. (C) 1999 Elsevier Science B.V. All rights reserved.