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, are associated most strongly with CV disease (CVD); particularly due to the ability of smaller particles (PM2.5), such as polyaromatic hydrocarbons (PAHs), to cross the alveolar-blood barrier and enter the systemic circulation. Most research on PAHs is done in fish and there is a paucity of experimental evidence in mammalian models. The mouse model could prove a vital experimental tool to elucidate the molecular mechanisms underlying the CV effects of PAHs, such as Phenanthrene. Firstly, the mouse model allows the effect of PAH exposure on whole heart function, both ex-vivo and in-vivo, to be determined; preliminary studies show a reduction in heart rate from 348.5+/-15.51 bpm under control conditions to 288+/-5.63 bpm after 15 minute Phe exposure (P<0.022, n=3). Secondly, chronic exposure to PAHs can be studied in mice, this is important due to the ability of PAHs to bioaccumulate in tissue over time. Finally, the availability of mouse CVD models, allows the potential of PAH exposure to exacerbate existing disease to be studied.