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Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling

Environment International 2024 77 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 70 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Wenhua Jin, Wenhua Jin, Weibo Zhang, Lijuan Wang, Wenhua Jin, Weibo Zhang, Hejing Tang, Lijuan Wang, Han Chen, Hejing Tang, Lijuan Wang, Huan Tang, Pengjie Wang, Yan Zhang, Lijuan Wang, Huan Tang, Huan Tang, Siyuan Liu, Han Chen, Ju Qiu, Yan Zhang, Han Chen, Huan Tang, Pengjie Wang, Lijuan Wang, Ran Wang, Yanan Sun, Huan Tang, Ping Liu, Huan Tang, Yinhua Zhu

Summary

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.

Polymers
Models
Study Type In vitro

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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