The Deepwater Horizon disaster drew global attention to the toxicity of crude oil and the potential for adverse health effects among spill responders and the numerous animals in the northern Gulf of Mexico. Crude oil from the spill released complex mixtures of polycyclic aromatic hydrocarbons (PAHs) into marine areas included pelagic spawning habitats for tunas, billfish, and other ecologically important top predators. PAH exposure of whole fishes during development and exposure to heart cells from adults, reveal the heart is vulnerable to oil-toxicity. However, the precise PAHs that cause cardiotoxicity, as well as the mechanisms underlying contractile dysfunction, are not known. Here we used electrophysiological and confocal microscopy techniques in tunas (Pacific bluefin tuna, Thunnus Orientalis, yellowfin tuna, Thunnus albacares) and Pacific mackerel (Scomber japonicus) to demonstrate that phenanthrene, a PAH with a benzene 3-ring structure , is the key compound disrupting cardiac function. Phenanthrene prolongs the action potential due to potassium channel blockade and decreases the amplitude of the cellular Ca2+ transients that drive force generation. Because there are many important environmental sources of phenanthrene in addition to petroleum based oil spills, including urban air pollution, our findings suggest that phenanthrene may be a major worldwide cause of vertebrate cardiac dysfunction.