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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Nanoplastics Sign in to save

Nanoplastics: An emerging environmental concern in age-related diseases

Environmental Pollution 2025 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Saugat Shiwakoti, Bikalpa Dhakal, Yejoo Ok, Yejoo Ok, Dal-Seong Gong, Ju-Young Ko, Pil-Gon Kim, Min–Ho Oak

Summary

This review examines the growing body of evidence linking nanoplastics to aging and age-related conditions. Researchers found that nanoplastics can disrupt key molecular pathways involved in inflammation, oxidative stress, and cellular damage that are central to the aging process. The study suggests that chronic nanoplastic exposure may accelerate biological aging, raising concerns about long-term health effects as environmental plastic pollution continues to increase.

Body Systems

The global demand for plastics has increased in recent years, with annual production exceeding 400 million tons. Despite their versatility and economic advantages, plastics pose severe environmental challenges due to inadequate waste management, with only 9 % being recycled. The rest accumulate in the environment, leading to widespread plastic pollution and the emergence of nanoplastics (NPs), plastic particles smaller than 0.1 μm. Their persistence in ecosystems, air, and water sources has raised significant ecological and health concerns. Beyond environmental concerns, NPs have been found in human tissues, with growing evidence linking them to adverse biological effects. Of particular concern is their role in aging and age-related diseases. Their ability to disrupt molecular pathways involved in DNA damage, mitochondrial function, and immune responses further implicates them in premature aging. Moreover, the interaction of NPs with cellular machinery can alter critical signaling pathways, such as p53 and p16INK4a/Rb, which regulate cell cycle progression and genomic integrity. Dysregulation of these pathways by NPs may drive cellular senescence, an irreversible growth arrest state contributing to tissue dysfunction and age-related pathologies. This review specifically highlights the mechanistic links between NPs exposure, cellular senescence, and biological aging, offering a novel and timely perspective on how NPs may contribute to age-related pathologies. It aims to examine recent researches on NPs in relation to senescence and aging, providing insights into their mechanistic impact at cellular and systemic levels. By analyzing emerging evidence on their role in senescence and aging, this study highlights potential health risks and underscores the urgent need for further investigations and regulatory measures to mitigate their long-term consequences.

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