Abstract

Endocrine-disrupting chemicals (EDCs) are widespread environmental contaminants capable of mimicking, 
antagonizing, or altering endogenous hormone signaling. Beyond classical toxicological endpoints, a growing body 
of evidence shows that EDCs induce epigenetic modifications - heritable changes in gene expression that do not 
involve alterations to DNA sequence. These include DNA methylation, histone modification, chromatin remodeling, 
and altered expression of non-coding RNAs. Such changes may persist across developmental stages and, in some 
cases, be transmitted across generations, amplifying health consequences long after initial exposure. This review 
synthesizes current knowledge of the mechanisms by which common EDCs such as bisphenols, phthalates, 
pesticides, heavy metals, and persistent organic pollutants exert epigenetic toxicity. We explore the molecular 
pathways implicated, highlight evidence from animal and human studies, and examine critical periods of 
susceptibility including fetal development, puberty, and gametogenesis. Particular attention is paid to 
transgenerational inheritance of altered epigenetic marks and the associated risks for endocrine, reproductive, 
neurodevelopmental, and metabolic disorders. Finally, we discuss methodological challenges, emerging biomarkers, 
and implications for risk assessment and regulatory policy. Understanding the interplay between EDC exposure and 
epigenetic programming provides a vital framework for preventing long-term and transgenerational health impacts 
in the Anthropocene.