91桃色

Abstract

Epigenetic toxicology plays a crucial role in understanding how environmental exposures during critical developmental periods influence long-term health outcomes. The Developmental Origins of Health and Disease (DOHaD) hypothesis suggests that early-life environmental factors, including exposure to toxicants, can induce persistent epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNA regulation. These alterations can dysregulate gene expression, predisposing individuals to chronic diseases such as metabolic disorders, cardiovascular diseases, neurodevelopmental impairments, and cancers later in life. Common environmental toxicants, including endocrine-disrupting chemicals (EDCs), heavy metals, air pollutants, and persistent organic pollutants (POPs), have been linked to epigenetic changes that impact fetal programming and disease susceptibility. Understanding the mechanisms by which toxicant-induced epigenetic alterations contribute to disease risk is essential for developing early biomarkers of exposure, preventive strategies, and targeted interventions. This review explores the latest advancements in epigenetic toxicology within the DOHaD framework, highlighting key toxicants, mechanisms, health implications, and future research directions.