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Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells
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Researchers exposed human lung epithelial cells (A549) and macrophages (Raw 264.7) to sub-500 nm polyethylene microplastics and found dose-dependent induction of cellular senescence and apoptosis. The results suggest that PE microplastic inhalation could contribute to premature lung cell aging and airway inflammation.
The pervasive accumulation of plastic waste has led to widespread microplastics (MPs) pollution, raising concerns about potential human health impacts. Among these, polyethylene microplastics (PEMPs) are one of the most commonly encountered due to their prevalence in consumer products and the environment. This study investigates the cytotoxic and senescence-inducing effects of PEMPs (≤500 nm) on two cell models, A549 lung epithelial cells and Raw 264.7 macrophages. This study specifically examines cells exposed to varying concentrations of PEMPs (50-500 μg/mL), and key indicators of cellular stress were assessed, including viability, reactive oxygen species (ROS) generation, mitochondrial dysfunction, LDH release, apoptosis, and senescence. Our findings indicate that exposure to PEMPs significantly reduced cell viability and increased ROS production and mitochondrial damage in a dose- and time-dependent manner. At higher concentrations (500 μg/mL), both cell lines demonstrated that PEMPs induce apoptosis and senescence, with A549 cells showing early senescence morphology as early as 24 h post-exposure. These findings confirm the potential of PEMPs to disrupt cellular homeostasis and accelerate aging-related processes. Overall, the study reinforces the urgency of curbing plastic pollution and exploring its association with age-related pathologies and chronic health conditions.
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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.
In vitro effects of aged low-density polyethylene micro(nano)plastic particles on human airway epithelial cells.
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Aged low-density polyethylene (LDPE) micro(nano)plastic particles were found to damage human airway epithelial cells in vitro, causing oxidative stress, inflammation, and cytotoxicity at relevant concentrations. UV-weathered LDPE particles were more toxic than unaged counterparts, highlighting the importance of environmental aging in assessing airborne MP health risks.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
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A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
Polyethylene Micro/Nanoplastics Exposure Induces Epithelial–Mesenchymal Transition in Human Bronchial and Alveolar Epithelial Cells
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When human lung cells were exposed to polyethylene micro- and nanoplastics (the most common type of plastic pollution), the cells underwent a transformation called epithelial-mesenchymal transition, where they changed shape, reorganized their internal structure, and gained increased ability to migrate. This cellular change is a known early step in both lung fibrosis and cancer development, suggesting that inhaling polyethylene plastics could contribute to serious lung diseases.
Micro- and Nanoplastics as Potential Chronic Abiotic Stressors: Cellular Senescence, Hallmarks of Ageing, and an Oxidative–Mitochondrial–Inflammatory Framework
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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.
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