The disease burden from ambient air pollution is becoming increasingly apparent. Despite the lung being the first site of exposure for air pollution, numerous epidemiological studies show strong correlations between air pollution and cardiovascular disease. Inhaled particulate matter (PM) can interact directly with airway epithelia but the surface chemicals on PM, like polyaromatic hydrocarbons (PAH), are also known to exert a cardiovascular response. The focus of our current work is phenanthrene (Phe), a small 3-ringed member of the PAH family which is ubiquitous in air and water fossil fuel-based pollution. We have examined the mechanisms underlying the cardiotoxicity of Phe on the ion channels and intracellular Ca2+ cycling pathways in zebrafish ventricular myocytes. Data are presented as percentage mean ± SEM. Using whole-cell current clamp we find a significant shortening of action potential duration (APD) in presence of 10µM Phe, with APD50 and APD90 shortening by approximately 49% ± 6.4 and 41% ± 7.5 of control values, respectively (p<0.05, two-way ANOVA). This finding is in contrast to the prolongation of APD90 found in marine species at similar concentrations which was attributed to direct inhibition of erg (Ether-à-go-go Related) channel (Brette et al, 2017). However, during the current clamp experiments, subsequent application of 2µM E-4031, a selective inhibitor of erg channel, after 10µM Phe showed no further prolongation of APD90 indicating the block of erg channel. Whole-cell voltage clamp experiments confirmed inhibition of IKr tail-current following 10 µM Phe exposure (by 82% ± 2.6, p<0.05, unpaired t-test). Phe exposure also reduced the intracellular calcium transient amplitude in field stimulated zebrafish ventricular cardiomyocytes by 13 % (p<0.05; paired t-test) and doubled the rate of transient decay (p<0.05; paired t-test). This work indicates the disruptive effect of Phe on the zebrafish myocardial function and also reveals how variable susceptibility of outward and inward currents to PAH-based pollution can affect the electrical and contractile properties of the vertebrate heart.