An estimated 4.2 million premature deaths worldwide are attributed to air pollution, primarily through increased cardiovascular (CV) morbidity and mortality. Studies have found particulate matter (PM), a subgroup of pollutants, including polyaromatic hydrocarbons (PAHs) are associated most strongly with CV disease (CVD), due to the ability of these smaller particles to enter the systemic circulation. Studies in fish have shown PAHs, such as phenanthrene (Phe), can directly alter CV electrophysiology, including prolonged action potential duration (APD) and QT interval, reduced heart rate (HR), reduced contractility and changes in underlying ionic currents. This level of detailed mechanistic investigation is lacking in mammalian models. Using the mouse model, the current study found exposure to even a single pollutant, Phe, can alter cardiac electrophysiology. Acute exposure (15 minutes) to Phe led to a significant reduction in HR and prolongation of the RR interval both ex-vivo (25uM Phe, 16% reduction in HR, P=0.022, n=5) using the isolated heart preparation and in-vivo (50ug/kg Phe, 10% reduction in HR, P=0.0043, n=7) using electrocardiographs recorded from anaesthetised mice, suggesting Phe has some direct effects on the heart, which are unaffected by peripheral factors. Wild-type mice (10-weeks) were exposed to a lower dose of Phe (30ug/kg, n=8) or vehicle only (DMSO, n=6) for a 14-day period, followed by in-vivo electrocardiograph recording and tissue collection. PQRST intervals were calculated for all animals; a significant prolongation of the QTc and P-wave duration was observed in Phe treated animals (P<0.05), suggesting the pro-arrhythmic effects of Phe previously seen in fish, may also occur in mammals. Furthermore, the weight of hearts treated with Phe was significantly higher than animals treated with vehicle only (P=0.004), this could indicate a hypertrophic response, however further molecular analysis is needed to confirm this. This study is the first to show direct effects of Phe on the CV system (CVS) of mice, both in the absence and presence of peripheral factors. This study is also the first to investigate prolonged exposure to Phe in mice, showing actions on both cardiac electrophysiology and potentially structure. More detailed electrophysiological, and long-term exposure studies combined with RNA and protein analysis of tissue are needed to investigate the full effects of Phe and reveal novel mechanisms of action. Ambient PM is now ranked 5th in the global mortality risk factor list and as the global levels of pollution continue to rise, studies like ours will help manage and mitigate this avoidable cause of disease and death.