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

• Published in: Environment international Vol. 185; p. 108489
• Main Authors: Jin, Wenhua, Zhang, Weibo, Tang, Hejing, Wang, Pengjie, Zhang, Yan, Liu, Siyuan, Qiu, Ju, Chen, Han, Wang, Lijuan, Wang, Ran, Sun, Yanan, Liu, Ping, Tang, Huan, Zhu, Yinhua
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.03.2024; Elsevier
• Subjects: Cellular senescence; Lung tissues; Microplastics; Polyvinyl chloride; Reactive oxygen species; Lung tissues; Reactive oxygen species; Microplastics; Polyvinyl chloride; Cellular senescence
• ISSN: 0160-4120; 1873-6750
• DOI: 10.1016/j.envint.2024.108489

[Display omitted] •The activity of four microplastics to induce cellular senescence was evaluated.•Polyvinyl chloride induced senescence of lung cells by activating ROS signaling.•Polyvinyl chloride caused the senescence and redox imbalance in mouse lung. 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.