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Size-dependent toxicological effects of microplastics: A review

Ecotoxicology and Environmental Safety 2026 Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Guoliang Zhou, Jia Li, Jia Li, Ying Chen, Ying Chen, Yanfan Cui, Yujie Wang, Liping Zheng, Dalei Zhang, Tao Luo, Tao Luo

Summary

This review synthesizes evidence on how microplastic and nanoplastic particle size influences toxicity across major organ systems, including digestive, reproductive, cardiovascular, respiratory, and nervous systems. Researchers found a broadly consistent pattern in which smaller particles, particularly those under 10 micrometers and at the nanoscale, tend to elicit stronger adverse responses due to enhanced barrier crossing, cellular uptake, and oxidative stress.

Industrialization has accelerated plastic production and emissions, resulting in pervasive environmental plastic pollution. Plastic debris can fragment into microplastics (<5 mm) and nanoplastics, collectively referred to as microplastics and nanoplastics (MNPs). Beyond their ubiquity in ecosystems, MNPs have also been detected in human-relevant matrices (e.g., placenta and breast milk), intensifying concerns about potential organ-specific health risks. Although particle size is increasingly recognized as a critical determinant of MNP toxicity, a cross-system synthesis of size-dependent effects and their implications for risk assessment remains incomplete. This review integrates current evidence on size-associated toxicological outcomes across major organ systems, including the digestive, reproductive, urinary, cardiovascular, respiratory, and nervous systems. Across many experimental settings, a broadly consistent pattern emerges in which smaller MNPs, particularly sub-10 μm particles and nanoscale plastics, more often elicit stronger adverse responses than larger particles. This tendency is generally consistent with size-related internal fate and tissue delivery that enhance barrier crossing and cellular interactions, thereby promoting oxidative stress and immune or inflammatory activation and ultimately contributing to organ-level impairment and functional disruption. Future studies should adopt harmonized size classification and reporting, appropriate exposure metrics, environmentally relevant test materials, and long-term or low-dose designs, complemented by human-relevant biomonitoring, to strengthen size-resolved risk assessment while prioritizing monitoring and mitigation of the difficult-to-capture sub-10 μm fraction.

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