Abstract

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition shaped by both genetic and environmental factors. While genetic studies have identified monogenic and polygenic contributions to ASD, growing evidence suggests that environmental exposures can modulate genetic susceptibility. Among these, bisphenol A (BPA), a widely studied endocrine-disrupting chemical, has drawn attention due to its ability to cross the blood-brain barrier and placenta. BPA can influence neurodevelopment through epigenetic modifications, mitochondrial dysfunction, and oxidative stress. Elevated BPA levels have been detected in serum and urine of individuals with ASD, correlating with altered gene expression in brain regions critical for cognition and behavior. Experimental models indicate that BPA exposure disrupts neuronal viability, synaptic connectivity, and neurotransmitter regulation, potentially exacerbating ASD-like phenotypes in genetically predisposed individuals. This review explores the interaction between genetic risk factors and environmental toxins, particularly BPA, in ASD pathogenesis. By integrating findings from epidemiological studies, molecular analyses, and animal models, we highlight the need for further research into gene-environment interactions to refine ASD risk assessment and therapeutic strategies.