Exposure to polycyclic aromatic hydrocarbon (PAH) nanoparticles may contribute to cardiotoxic effects of hydrocarbon-based pollution. Phenanthrene (Phen), comprised of three fused benzene rings, is relatively abundant in polluted air and water. It is lipophilic and can access and accumulate in human tissue via skin and mucus membranes. Phen is a constituent PAH of crude oil spills and has been shown to increase ventricular action potential duration of fish ventricular myocytes; this action is associated with inhibition of the rapid delayed rectifier K+-current (Brette et al, 2017). Ether-à-go-go Related Gene encoded potassium channels mediate IKr in multiple species including human and are known to exhibit marked susceptibility to pharmacological blockade (Hancox et al, 2008). Human and fish ERG sequences are identical at the known drug binding region of the channel. The purpose of this study was to determine the propensity or otherwise of Phen to inhibit human ERG-encoded (hERG) potassium channels. Whole-cell patch-clamp recordings were made at room temperature from HEK 293 cells stably expressing recombinant hERG channels. Data are presented mean ± SEM. Computational docking was performed using a recent Cryo-EM structure of hERG (Wang and MacKinnon, 2017). A conventional voltage-step protocol, comprised of a 2-second depolarization to +20 mV from -80 mV, followed by repolarization to −40 mV to elicit hERG current (IhERG) tails, was applied in control solution and during exposure to Phen. Five different concentrations between 1 µM and 50 µM were tested, with at least 5 replicates per concentration. Phen was found to inhibit IhERG with a half-maximal inhibitory concentration (IC50) of 16.8 ± 1.7 µM, Hill slope: 1.0 ± 0.1. A modified version of the standard protocol incorporated test depolarizations to a range of voltages. IhERG tail inhibition by 10 µM Phen varied significantly with test voltage over the range evaluated (-40 to +60 mV; p<0.0001, one-way ANOVA; n=16 cells). Phen also shifted half maximal activation voltage (V0.5) for IhERG by -10.1 ± 0.9 mV. Use of an envelope of tails protocol showed that the extent of Phen inhibition of IhERG increased with duration of activating voltage command (to +20 mV). These results indicate that Phen inhibits hERG channels at micromolar levels and that this effect is contingent on the channel gating. In docking simulations Phen could readily be accommodated within the hERG channel pore; its small size means it may be able to interact within the pore in multiple binding configurations. We conclude that phenanthrene exerts inhibitory effects on the hERG potassium channel.