Triclosan (TCS) is an antimicrobial agent found in personal care products that has become prevalent in surface waters. TCS readily bioaccumulates within aquatic organisms, and has been found to be toxic to fish. In larval fishes, exposure to TCS disrupts a variety of developmental processes, impairs hatching success, and causes pericardial edema. In mammals, TCS exposure disrupts excitation-contraction-coupling in cardiac cells, which is associated with reductions in cardiac output. Here, we examine the impacts of TCS on heart function to better understand potential risks that TCS may pose to wild fish. Zebrafish were exposed to 0, 0.4, 40, and 400 μg TCS/L from 8 to 120 h postfertilization via static waterborne exposure with daily renewal. We examined the incidence of pericardial edema, and the impacts on heart structure and heart function. While incidence of pericardial edema increased following exposure to ≥40 μg TCS/L and the structure of the heart was altered, cardiac output was only reduced following exposure to 400 μg TCS/L. A small but significant proportion of embryos showed increased incidence of regurgitation following exposure to ≥0.4 μg TCS/L. Our findings suggest that acute exposure to TCS has the potential to cause subtle cardiac toxicity in developing fish, and further evaluation of the risks TCS pose to wild fish and human health is needed.
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