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Our studies suggested that prenatal exposure to the herbicide atrazine (ATR) could delay vaginal opening (VO) and mammary development in the offspring of Long–Evans (LE) rats. To evaluate ATR exposure parameters required for pubertal delays, including mammary gland development, we used cross-fostering to determine if effects were strictly dam-mediated (via milk) or a direct effect (transplacental) on the pups. Timed-pregnant LE rats (N = 20/treatment group) were gavaged on gestational days (GD) 15–19 with 100 mg ATR/kg body weight (BW) or vehicle (controls, C). On PND1, half of all litters were cross-fostered, creating four treatment groups: C-C, ATR-C, C-ATR, and ATR-ATR (dam-milk source, respectively). A significant delay in VO and increase in VO BW was seen only in the litters receiving milk from ATR-exposed dams. However, mammary glands of female offspring (two per dam) in all groups exposed to ATR (ATR-C, C-ATR, and ATR-ATR) displayed significant delays in epithelial development. These changes were detected as early as PND4 and stunted development was evident through PND40. Further, at all developmental stages examined, offspring in the ATR-ATR group exhibited the least developed glands. These delays in pubertal endpoints do not appear to be related to body weight or endocrine hormone concentrations. Our data suggest that the delay in VO of ATR-exposed offspring (C-ATR lactationally, ATR-ATR lactationally and in utero) is mediated via the dam [milk], whereas brief direct exposure to ATR in utero can cause delays in mammary gland development. Our data suggest that milk-derived factors (growth factors or hormones), in addition to transplacental exposure during mammary bud outgrowth, may be involved in ATR mode of action on delayed mammary gland development.