The negative impacts of endocrine disruptors on health have predominantly been identified following chronic exposure to supra-physiological concentrations, while studies of acute exposure to physiological concentrations are less common. Bisphenol A (BPA), found in plastics, is linked to the incidence of obesity, and is thought to act via oestrogen receptor mediated pathways. However, the exact mechanisms and critical time of exposure remain uncertain. This study aimed to determine whether exposure of the early embryo to physiological concentrations of BPA affected embryo development, quality and metabolism. Bovine oocytes were matured in vitro, fertilised (d0) and cultured to d3 in ESOFaa. Eight-cell embryos (n=840) were cultured in groups of 15 in LSOFaa until d7 in the presence or absence of BPA or oestradiol 17β (0, 1 or 10ng/ml). On d7 embryo quality and development were evaluated prior to differential cell staining. Alternatively, between d6 and 7, embryos (n=50) were individually cultured in 4μl L-SOF containing BPA or oestradiol 17β (0, 1 or 10ng/ml) to measure glucose uptake and lactate production. All data were analysed by ANOVA. Neither BPA nor oestradiol affected (P>0.1) blastocyst rates, total, ICM or trophectoderm cell numbers when compared to control. Preliminary data suggests however, that BPA (10ng) and oestradiol (1 and 10ng) negatively impacts the percentage of expanded stage blastocysts, as well as the number of grade 1-2 embryos. Following exposure to high BPA, glucose uptake was substantially increased (P<0.01) compared with the control. No differences (P>0.1) in lactate production were evident between groups. In conclusion, even a brief exposure to physiological concentrations of BPA during early embryo development is sufficient to perturb embryo metabolism and quality. These subtle effects on embryo metabolism offer one potential mechanism by which BPA may adversely impact long-term health, although further studies are however required to identify the specific pathways responsible.