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Microplastics and Nanoplastics in Human Health: Toxicological Mechanisms Involving Oxidative Stress, Endocrine Interference, and Inflammatory Responses
Summary
This review of existing research shows that tiny plastic particles from broken-down plastic waste can harm our bodies in three main ways: by damaging cells, disrupting hormones, and causing inflammation. These microscopic plastics are now everywhere in our environment - in the air we breathe, water we drink, and food we eat - and studies suggest they may contribute to health problems affecting our hearts, digestive system, and other organs. While scientists are still studying exactly how dangerous these particles are to humans, the evidence suggests we should be concerned about our constant exposure to plastic pollution.
The increasing prevalence of microplastics (MPs) and nanoplastics (NPs) in various environments has raised significant public health concerns worldwide. Defined as plastic particles smaller than 5 mm (MPs) and under 1 μm (NPs), they arise from both industrial manufacturing processes and the breakdown of larger plastic items. MPs and NPs are found in air, water, soil, and food systems, representing an unavoidable source of human exposure. This review synthesizes scientific research on the toxicological effects of MPs and NPs, focusing on three main biological mechanisms: oxidative stress, endocrine disruption, and inflammation. Experimental studies reveal that these plastic particles lead to increased production of reactive oxygen species, resulting in mitochondrial damage, lipid peroxidation, protein oxidation, and DNA injury. Such oxidative effects disrupt critical signaling pathways, including Nrf2, MAPKs, and toll-like receptor-associated pathways. Additionally, MPs and NPs can transport endocrine-disrupting chemicals like bisphenols and phthalates, which interfere with hormone synthesis and neuroendocrine regulation. The particles also trigger innate immune responses by enhancing inflammation through inflammasome activation and prolonged release of inflammatory mediators. The combination of oxidative stress, endocrine disruption, and chronic inflammation has been linked to continuous damage across multiple organ systems, including reproductive, gastrointestinal, hepatic, cardiovascular, and nervous systems. Despite accumulating experimental evidence, there are still considerable knowledge gaps regarding exposure levels, dose-response relationships, and the clinical impacts on humans, which are essential to address for effective risk assessment and regulatory policy development.