Impaired endometrial receptivity is a major bottleneck in pregnancy success and is associated with implantation failure. Exposure to endocrine disrupting chemicals (EDCs) has sparked much interest, due to their widespread use in consumer and industrial products. Triclosan (TSC) and Methylparaben (MeP) are commonly used antimicrobials and preservatives with known oestrogenic and endocrine disruptor effects. These chemicals are linked with infertile pathologies in both human and domestic species, posing a significant risk factor for endometrial function. Hence, this study aimed to determine if in vitro exposure to TSC and MeP would impact endometrial epithelial cell adhesive, proliferation and oestrogen responsive gene expression. To evaluate the functional impacts of EDC exposure, Ishikawa cells were treated for 24 hours with varying environmentally relevant concentrations of TSC or MeP at 0, 10, 250 and 1500nM found in humans. Cells were then subjected to xCELLigence real-time monitoring for 72 hours to investigate changes in their adhesive and proliferative capacity. In separate cultures, qRT-PCR was performed to investigate changes in oestrogen responsive gene targets (oestrogen receptor alpha, leukemia inhibitory factor receptor, homeobox A cluster and claudin 3) involved in endometrial remodelling and receptivity. Repeated measures analysis and area under the curve were employed to determine statistical differences in cellular adhesion and proliferation. Non-parametric analyses were used to identify changes in gene expression. No differences in epithelial cell adhesion or proliferation were detected for either chemical (n=3 replicates per chemical per concentration; P>0.1). Equally, no changes in gene expression relative to control were evident (P>0.1) using the current in vitro exposure paradigms. Further studies are required to verify these findings by exploring variations in in vitro conditions and alternative function measures to better elucidate the effects of chronic MeP and TSC exposure on endometrial function.