Nanoplastics as Epigenetic Disruptors: A Biochemical Review of Environmental Pollutants and Gene Regulation

Nanoplastics (NPLs), emerging environmental contaminants, have been found to perturb cellular homeostasis through biochemical and epigenetic mechanisms. Due to their small size and high surface reactivity, NPLs can pierce biological systems where they induce oxidative stress, inflammation, and endocrine disruption. Recent studies propose that NPLs have the ability to alter DNA methylation patterns, histone changes, and non-coding RNA expression, leading to persistent alterations in gene regulation. Such epigenetic changes correlate with the development of cancer, neurological diseases, and metabolic disorders with possible heritable effects crosswise through generations. In spite of rising evidence, considerable deficiencies remain in current research, especially regarding human epidemiological experiments and standardized detection assays. Lack of longitudinal experiments with accredited biomarkers limits our data about chronic exposure as well as transgenerational impacts. Multi-omics approaches, such as transcriptomics, proteomics, and metabolomics, hold viable methodologies to establish molecular pathways induced by NPLs. Integration of biochemical data with environmental toxicity is critical to enable accurate risk assessment as well as policy construction. Our review highlights an imperative for interdisciplinary collaboration to address the complex health and environmental implications of nanoplastics. Improvement of detection technologies, standardizing exposure protocols, and incorporating epigenetic endpoints into regulatory protocols are critical steps to reduce NPLs' molecular legacy.