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Microplastic exposure and human health risks across the life cycle: a focus on reproduction, development, and aging

Frontiers in Cell and Developmental Biology 2026 Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Guosheng Liu, Xiao Liu, Guosheng Liu, Tian Shi, Shengyao Tang, Xia Huang Xia Huang Xiao Liu, Xiao Liu, Xiao Liu, Xiao Liu, Xia Huang

Summary

This review of existing research shows that tiny plastic particles called microplastics are now found everywhere in our environment and regularly enter our bodies through the food we eat, air we breathe, and things we touch. The evidence suggests these plastic particles may harm human health throughout our entire lives—potentially affecting fertility and pregnancy, interfering with child development, and possibly speeding up aging by damaging our cells. While more research is needed, this highlights why reducing plastic pollution matters for protecting human health at every life stage.

Microplastic pollution has emerged as a critical global environmental and public health challenge. These small plastic particles of diverse origins are ubiquitously distributed in aquatic, atmospheric, terrestrial, and food systems, entering the human body through ingestion, inhalation, and dermal contact, thereby creating complex lifelong exposure scenarios. Accumulating evidence indicates that microplastics (MPs) not only pose threats to key early-life stages—including reproductive health, pregnancy maintenance, fetal development, and child growth—but may also systematically accelerate the aging process and increase the risk of age-related diseases. This review provides a comprehensive synthesis of the physicochemical properties, environmental distribution, human exposure pathways, and life-cycle health impacts of MPs. It elaborates on their specific adverse effects on the reproductive system and their interference with fetal and child development. Furthermore, it delves into the core molecular mechanisms by which MPs drive cellular and tissue aging, primarily through the induction of mitochondrial dysfunction, oxidative stress, and chronic inflammation. The review also summarizes current research limitations concerning methodological standardization and epidemiological evidence, while outlining priority areas for future investigation. By integrating evidence across the life course, this review aims to establish a solid theoretical foundation for understanding the composite health risks of MPs, identifying vulnerable life stages, and informing the development of scientific prevention and intervention strategies.

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