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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 Reproductive & Development Sign in to save

Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence

Cells 2024 116 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 75 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Qing‐Xiang Amy Sang, Faiza Mahmud, Drishty B. Sarker, Jonathan A. Jocelyn

Summary

This review summarizes research showing that micro- and nanoplastics trigger oxidative stress, inflammation, and premature cell aging across many experimental models. These are the same biological processes linked to heart disease, brain disorders, and other age-related conditions. Particularly concerning, studies in animals show that plastic-related damage can be passed from parents to offspring, suggesting potential long-term generational health effects.

Microplastics and nanoplastics (MNPs) are ubiquitous environmental contaminants. Their prevalence, persistence, and increasing industrial production have led to questions about their long-term impact on human and animal health. This narrative review describes the effects of MNPs on oxidative stress, inflammation, and aging. Exposure to MNPs leads to increased production of reactive oxygen species (ROS) across multiple experimental models, including cell lines, organoids, and animal systems. ROS can cause damage to cellular macromolecules such as DNA, proteins, and lipids. Direct interaction between MNPs and immune cells or an indirect result of oxidative stress-mediated cellular damage may lead to increased production of pro-inflammatory cytokines throughout different MNP-exposure conditions. This inflammatory response is a common feature in the pathogenesis of neurodegenerative, cardiovascular, and other age-related diseases. MNPs also act as cell senescence inducers by promoting mitochondrial dysfunction, impairing autophagy, and activating DNA damage responses, exacerbating cellular aging altogether. Increased senescence of reproductive cells and transfer of MNPs/induced damages from parents to offspring in animals further corroborates the transgenerational health risks of the tiny particles. This review aims to provoke a deeper investigation into the notorious effects these pervasive particles may have on human well-being and longevity.

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