ABSTRACT Microplastics and nanoplastics (MNPs) are common pollutants that engage with proteins, lipids, nucleic acids, and other biomolecules, damaging cell structure. This review goes beyond simply listing where MNPs are found to explore how they cause harm, detailing mechanisms such as oxidative stress, endocrine disruption, genotoxicity, protein misfolding, lipid membrane destabilization, and epigenetic changes. Propose an integrated mechanistic hypothesis connecting these processes via oxidative epigenetic feedback loops, size‐dependent organelle targeting, and pollutant corona effects, with potential implications for cellular aging and transgenerational outcomes. Emphasize dose–response alignment, ecological relevance, and the biological significance of reported concentrations. Identify key knowledge gaps, especially regarding chronic low‐dose exposures, co‐pollutant interactions, and protein corona dynamics. This framework aims to enhance risk assessment, regulatory strategies, and mitigation of MNP‐related ecological and human health risks.
Marycleopha et al. (2025) studied this question.