Cardiovascular diseases (CVDs) are one of the leading the cause of deaths globally and in UK, costing an estimated 9 billion pounds to UK’s healthcare system. This burden is further amplified with established detrimental health effects of air pollution and its strong correlation with CVDs such as cardiac arrhythmias and stroke (1). Phenathrene (Phe), an important component of air pollution, is a 3 ringed poly-aromatic hydrocarbon (PAH) that binds to the surface of fine particulate matter (PM2.5). Previous studies show proarrhythmic effects of Phe on the heart of various marine fishes via the inhibition of IKr current leading to action potential (AP) prolongation (2). The rapid delayed rectifier K+ current, IKr, participates in phase 3 repolarisation of ventricular APs; it also plays a key protective role against premature stimuli late in repolarization and early diastole by mediating fast transient outward currents in response to premature ventricular beats. The aim of this study was to investigate the cardiotoxic effects of Phe using whole-cell patch-clamp in zebrafish (D. rerio) ventricular cardiomyocytes. Firstly, we show significant potency in inhibition of zebrafish IKr peak-tail current by Phe with an IC50 value of 2.7 ± 0.1 µM and a Hill slope (nH) of 0.6 ± 0.09 (n=6-9; N=3), along with increased channel deactivation kinetics. Further to this, we examined the effects of Phe on the protective IKr current envelope in zebrafish ventricular cardiomyocytes. A paired ventricular AP-like command waveform protocol was used to elicit transient outward currents in absence and presence of 3 µM Phe. Significant inhibition of approximately 60% of peak transient current was observed in presence of 3 µM Phe (n=7-8; N=3). Surprisingly, when Phe was tested on ventricular action potential (AP) elicited at 0.5 Hz through whole-cell patch current clamp recording, it significantly shortened action potential duration (APD90) at both 3 µM (by 20%; n=4; N=2; p<0.05, paired t-test) and 10 µM Phe (by 41% ms; n=4; N=2; p<0.05, paired t-test). Phe (10 µM) exhibited significant (40%) inhibition of ICaL currents (n=10; N=4; p<0.05, paired t-test) elicited using a double-pulse protocol with potassium free solutions, in the presence of 0.5 µM TTX. In these experiments Phe abbreviated AP duration, likely due to ICaL inhibition, whilst reducing the protective effect of IKr to premature stimulation. This combination of effects may abbreviate refractoriness and increase susceptibility to certain arrhythmia triggers such as premature ventricular beats/contractions.