Bisphenol A is a monomer that is polymerized to manufacture polycarbonate plastic food wrappings and it is detectable in the blood of human populations in developed countries. It has reached public attention due to its presence in food and beverages following leaching from plastic containers. Bisphenol A was shown in animal and in vitro studies to have estrogenic effects. Data link bisphenol A exposure to a variety of diseases including miscarriage, and cardiovascular syndromes. Objective: To assess the influence of Bisphenol A on the human heart voltage-gated sodium channel Nav1.5. Methods: hNav1.5 was expressed in HEK293t cells and whole-cell patch clamp experiments were performed. Results: We show that Bisphenol A reduces the peak sodium current through hNav1.5 from a holding potential of -120 mV with an EC50 of ~50 mM. This concentration is considerably higher than has been found in beverages from plastic bottles. Compared to other known sodium channel blockers such as local anesthetics at equivalent concentrations, blocking efficacy of Bisphenol A is approximately ten-fold higher. Bisphenol A shifts steady-state fast inactivation to more hyperpolarized potentials, whereas voltage-dependence of activation is unaffected. As with local anesthetics, bisphenol A binds preferentially to the inactivated state. The association time constant, as determined by a single exponential fit of peak current decline induced by 30 mM bisphenol A is approximately 14 times faster than that induced by 300 mM lidocaine. Conclusion: We have determined that bisphenol A has blocking effects on hNav1.5 sodium currents that are more pronounced than those of known blockers, such as lidocaine or lamotrigine.