Atrazine is a commonly used herbicide in the United States that is reported to contaminate drinking water sources. Studies indicate atrazine adversely impacts the neuroendocrine and reproductive systems, and that it may be a potential carcinogen. The current maximum contaminant level in drinking water is 3 parts per billion (ppb); however, levels higher than 3 ppb are often reported. Ongoing studies in our laboratory are investigating the immediate and latent adverse health outcomes associated with a developmental atrazine exposure and identifying the genetic and epigenetic mechanisms of toxicity using the zebrafish model system. MicroRNAs (miRNAs) are epigenetic regulators that posttranscriptionally control the translation of mRNA. A preliminary study indicated expression of miR-126, a miRNA associated with angiogenesis and tumorigenesis, to be altered following an embryonic atrazine exposure. To further investigate the developmental expression of miR-126 in zebrafish, quantitative PCR (qPCR) was used to profile expression throughout embryogenesis. Expression of miR126 was developmental time point specific with significant peaks in expression at 36, 60, and 72 hours postfertilization (hpf). The deregulation of miR-126 by atrazine was also tested using qPCR. Zebrafish embryos exposed to 0.3, 3, or 30 ppb of atrazine were compared to a control treatment at all six developmental time points. While a dose-response trend in upregulation at 36 hpf and in down-regulation at 48 hpf was observed, a significant increase in expression was only observed at 60 hpf in embryos exposed to 30 ppb atrazine. This study is providing a greater understanding of an epigenetic mechanism of atrazine toxicity