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Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling
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Researchers found that four common types of microplastics all caused premature aging (senescence) in human lung cells by increasing harmful reactive oxygen species, and that an antioxidant treatment could partially reverse this effect. When PVC microplastics were introduced into mouse lungs, the animals showed reduced physical function, increased body-wide inflammation, and accumulation of aged cells, suggesting that inhaling microplastics could accelerate lung aging.
Microplastics (MPs) are environmental pollutants and can be inhaled by humans to threaten health. The lung tissue, responsible for the gas exchange between the body and the environment, is vulnerable to MPs exposure. However, from the perspective of cellular senescence, the effect of MPs on lung cells and tissues has not yet been deeply dissected. In this study, we reported that all the four typical MPs exhibited the significant biological effects in term of inducing senescence of human lung derived cells A549 and BEAS-2B in vitro. We further found that polyvinyl chloride (PVC) increased the reactive oxygen species (ROS) level in A549 cells and that PVC-induced senescent characteristics could be largely reversed by antioxidant treatment. Importantly, intratracheal instillation of PVC MPs in mice could effectively impair their physical function, induce the increased systemic inflammation level, cause the accumulation of senescent cells. Our study demonstrates that MPs induce senescence in human lung epithelial cells and mouse lungs by activating ROS signaling, and provides new insight into the potential pathogenesis of MPs on lung diseases.
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This review summarizes existing lab research on tiny plastic particles and cell ageing processes. Studies found effects on cell energy production, DNA, and inflammation signals, with strongest evidence for mitochondrial problems and cell senescence, but most used high doses and short exposures, so links to human ageing remain unconfirmed.
The reactive oxygen species as pathogenic factors of fragmented microplastics to macrophages
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Researchers tested how fragment-shaped microplastics from polypropylene and polystyrene affect different human cell types and found that immune cells called macrophages were the most vulnerable. The toxicity was driven by the microplastics' ability to generate reactive oxygen species (ROS), and interestingly, weathered plastics were less toxic because environmental aging made them better at binding protective proteins. The study suggests that macrophages are a primary target cell for ingested microplastics and that oxidative stress is a key mechanism of their toxicity.
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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.
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