The African clawed frog (Xenopus laevis) is sensitive to pyrene exposure during early development

Toxicity of pyrene, a tetracyclic polyaromatic hydrocarbon (PAH), is poorly understood. Pyrene deposition in air, soil, and water results primarily from fossil fuel combustion. Pyrene is also abundant in cigarette smoke. PAHs cross the placenta; urinary 1‐hydroxypyrene (1‐HP) levels, a measure of PAH (and pyrene) exposure, are higher in pregnant smokers and their newborns than in nonsmokers and their newborns. Children in urban and industrial settings excrete more 1‐HP than those from rural areas. It is clear that developing humans are exposed to PAHs, including pyrene, both in utero and postnatally. To better understand how this abundant contaminant may affect development, we exposed the embryos of X. laevis , an important model of vertebrate development, to pyrene. Exposure to 5–10 ppm (25–49 μM) pyrene from stage 10.5–42 (~96 hrs) resulted in 90–100% mortality 48 hrs after their return to control conditions, while exposure to 0.1–1 ppm had no effect. Pyrene‐induced mortality may be stage‐specific. We observed 30% mortality in embryos exposed to 5 ppm until stage 18, a rate in contrast to the 90–100% mortality of embryos exposed to stage 24 or beyond. In addition, pyrene exposure induced edema at all doses (0.1–10 ppm). Based on these findings, further characterization of the toxicity of this common pollutant is warranted and potential health risks to humans assessed. (Supported by NH‐INBRE grant 1P20RR030360‐01)