Endocrine disrupting chemicals (EDCs) are environmental contaminants that interfere with one or more aspects of hormone action. Exposure to EDCs during critical periods of life, often during discrete stages of development, can induce permanent changes to organs or increase the risk of disease later in life. The mammary gland is a dynamic organ that undergoes extensive changes in morphology and function throughout pregnancy, lactation, and involution. Following pregnancy, the mammary gland has important structural and functional changes that are distinct from a nulliparous female and are associated with a lifetime reduction in breast cancer risk. Estrogens play a key role in the mammary gland’s morphological transformation during early pregnancy, where estradiol binds to and activates estrogen receptor (ER). However, estradiol levels drop before lactation while ER expression remains relatively steady throughout lactation. Yet, few data address the vulnerability of the mammary gland during pregnancy and lactation to environmental estrogens or the long-term consequences these exposures pose for mammary gland health. We hypothesized that exposure to ER agonists during pregnancy and/or lactation could alter lactogenesis in the short term, while disrupting parity-induced changes in the long-term. To address EDC effects on lactation, we exposed mice to ethinyl estradiol (EE2) from the start of lactation to weaning and evaluated dams and pups for evidence of lactational deficiencies. Our results indicate that EE2 exposure reduced dam and pup weight throughout the lactation period and reduced overall ductal epithelial complexity. However, EE2 did not induce early involution suggesting that EE2 exposure likely reduces lactogenesis. To determine long-term changes in the mammary gland induced by EDC exposure, we exposed mice throughout pregnancy and lactation to one of three estrogenic chemicals (propylparaben, butyl benzyl phthalate, or EE2) followed by a 5-week wash-out period to ensure full involution before evaluating the mammary glands. We found that all exposures altered epithelial density, while PP and BBP altered steroid receptor signaling and reduced macrophage infiltration of the post-involution mammary gland. These results indicate that pregnancy and lactation are vulnerable to estrogenic EDC exposure and that exposures during these critical windows can produce long-term alterations in the parous mammary gland.