Atrazine (ATZ), a widely utilized herbicide, is notable for its long environmental half-life and high solubility, raising significant concerns regarding its ecological and health impacts. While debates continue over its role as an endocrine disruptor, increasing attention has been directed toward its potential epigenetic effects. Utilizing the zebrafish model, a vertebrate with considerable genetic similarity to humans, provides valuable insights into how ATZ exposure may translate into human health risks. This review systematically examines the differential DNA methylation induced by ATZ's non-competitive inhibition of DNA methyltransferases, miRNA dysregulation resulting from mutations in miRNA processing enzymes, and the complex epigenetic interactions affecting histone modifications. Additionally, potential epigenetic biomarkers for ATZ exposure are proposed, which could advance targeted treatment strategies and improve health risk assessments. This synthesis of current understanding identifies knowledge gaps and guides future research towards a more comprehensive understanding of ATZ's epigenetic mechanisms.