Increased occurrence of reproductive disorders has raised concerns regarding the impact of endocrine disrupting chemicals (EDCs) on reproductive health especially when such exposure occurs during fetal life. Prenatal testosterone (T) treatment leads to growth retardation, postnatal hypergonadotropism, compromised estradiol positive feedback, polycystic ovaries and infertility in the adult. Prenatal dihydrotestosterone treatment failed to affect ovarian morphology or estradiol positive feedback suggesting that effects of prenatal T may be facilitated via conversion of T to estradiol, thus raising concerns regarding fetal exposure to estrogenic EDCs. This study tested if fetal exposure to methoxychlor (MXC) or bisphenol A (BPA) would disrupt cyclicity in the ewe. Suffolk ewes were administered MXC (n = 10), BPA (n = 10) (5 mg/kg/day s.c in cotton seed oil) or the vehicle (C; n = 16) from days 30 to 90 of gestation. On day 60 of treatment, maternal MXC concentrations in fat tissue and BPA in blood averaged 200 µg/g fat and 37.4 ± 3.3 ng/mL, respectively. Birth weights of BPA offspring were lower (P < 0.05) relative to C. There was no difference in the time of puberty between groups. BPA females were hypergonadotropic during early postnatal life and ended their breeding season later compared with C. Characterization of cyclic changes following synchronization with PGF2 in 5C, 6 MXC and 6 BPA females found that the onset of the LH surge was delayed in MXC (P < 0.05) and the LH surge magnitude severely dampened (P < 0.05) in BPA sheep. These findings suggest that prenatal BPA and MXC exposure have long-term differential effects on a variety of reproductive endocrine parameters that could impact fertility.