Lin Ruei-Hong, Chen Hao-Ting, Lee I-Ta, Vo Thi-Thuy-Tien, Wang Yung-Li
National Keelung Senior High School, Keelung City 205001, Taiwan.
School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei City 11031, Taiwan.
Life (Basel). 2025 Sep 16;15(9):1449. doi: 10.3390/life15091449.
Microplastics (MPs) and nanoplastics (NPs) have emerged as ubiquitous environmental contaminants that pose significant threats to human health, with multiple exposure pathways (e.g., ingestion and inhalation) contributing to systemic exposure. Although growing evidence highlights their biological effects, the underlying mechanisms by which these particles induce cellular dysfunction remain incompletely understood. This review synthesizes current knowledge on the MPs/NPs-induced cellular toxicity mechanisms, including investigations into cellular uptake pathways, disruption of molecular signaling, oxidative stress, inflammatory responses, and genotoxic effects. MPs/NPs contamination can arise from consumer products and clinical procedures, with estimated Daily Microplastic Emission (DME)-based national totals (India) ranging from ~0.36 to 74 billion particles/day across oral-care product categories. At the cellular level, MPs and NPs trigger interconnected toxicological cascades, including impaired endocytosis, mitochondrial dysfunction, chronic inflammation, genotoxicity, endoplasmic reticulum (ER) stress, and accelerated cellular senescence. These mechanisms act in concert to compromise epithelial barrier integrity. Overall, MPs/NPs present substantial risks to health through multiple interconnected pathways. Local and systemic effects are plausible across exposed tissues which may also serve as a gateway for systemic distribution by these contaminants. These findings highlight the urgent need for coordinated global efforts, including restrictions on intentionally added MPs, improvements in product design, development of advanced removal technologies, and implementation of clinical prevention strategies.
微塑料（MPs）和纳米塑料（NPs）已成为普遍存在的环境污染物，对人类健康构成重大威胁，多种暴露途径（如摄入和吸入）导致全身暴露。尽管越来越多的证据凸显了它们的生物学效应，但这些颗粒诱导细胞功能障碍的潜在机制仍未完全了解。本综述综合了目前关于MPs/NPs诱导细胞毒性机制的知识，包括对细胞摄取途径、分子信号传导破坏、氧化应激、炎症反应和遗传毒性作用的研究。MPs/NPs污染可能源于消费品和临床程序，基于每日微塑料排放量（DME）估算的印度全国总量，在各类口腔护理产品中范围约为每天0.36亿至740亿个颗粒。在细胞水平上，MPs和NPs引发相互关联的毒理学级联反应，包括内吞作用受损、线粒体功能障碍、慢性炎症、遗传毒性、内质网（ER）应激和细胞衰老加速。这些机制共同作用，损害上皮屏障的完整性。总体而言，MPs/NPs通过多种相互关联的途径对健康构成重大风险。在暴露组织中，局部和全身效应都有可能发生，这些组织也可能成为这些污染物全身分布的通道。这些发现凸显了全球协调努力的迫切需要，包括限制故意添加的MPs、改进产品设计、开发先进的去除技术以及实施临床预防策略。
