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ToxSci Advance Access published online on June 2, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi213
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Published by Oxford University Press 2005.
Received March 22, 2005
Accepted May 26, 2005

Reproductive and Developmental Toxicology

Adverse Effects of Prenatal Exposure to Atrazine During a Critical Period of Mammary Gland Growth

Jennifer L. Rayner 1, Rolondo R. Enoch 2, and Suzanne E. Fenton 3*

1 Department of Environmental Sciences and Engineering, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, 27599; Reproductive Toxicology Division, Office of Research and Development, National Health & Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, 27711
2 Reproductive Toxicology Division, Office of Research and Development, National Health & Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, 27711; Present Address: Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, CA 90048
3 Reproductive Toxicology Division, Office of Research and Development, National Health & Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, 27711

* To whom correspondence should be addressed.
Suzanne E. Fenton, E-mail: fenton.suzanne{at}epa.gov


  Abstract

Prenatal exposure to 100 mg/kg atrazine (ATR) delays mammary gland (MG) development in resulting female offspring of Long Evans rats. To determine if the fetal MG was sensitive to ATR effects during specific periods of development, timed-pregnant dams (N=8/group/block) were dosed for 3 or 7-gestation day (GD) intervals (GD13-15, 15-17, 17-19, or 13-19) with 100 mg ATR/kg/d or vehicle (C), and their offspring were evaluated for changes. MG taken from pups prenatally exposed to ATR displayed significant delays in epithelial development as early as PND 4 compared to C, with continued developmental delays at later time points that varied by time of exposure. However, the most persistent and severe delays were seen in the GD17-19 and GD13-19 ATR exposure groups, demonstrating statistically similar growth retardation. Because MG developmental deficits persisted into adulthood, we hypothesized that ATR-exposed animals may have difficulties nursing their young. Females exposed prenatally to either ATR (as defined) or C (N>4 litters/group) were bred and the resulting F2 offspring from GD17-19 and GD13-19 exposure groups were significantly smaller in BW than C. In a separate study, it was determined that ATR (25 to 100 mg/kg), delivered from GD15-19, did not decrease fetal body weights on GD20, even though the higher doses significantly decreased weight gain of the dosed dams. These data suggest that the consequences of brief ATR exposure, during a critical period of fetal MG development (GD17-19), are both delayed MG development of the offspring and inadequate nutritional support of F2 offspring, resulting in adverse effects on pup weight gain.

Keywords: atrazine; mammary gland; critical period; lactation.
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