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20 resultsShowing papers similar to Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
ClearInternalization and toxicity: A preliminary study of effects of nanoplastic particles on human lung epithelial cell
Researchers studied the effects of polystyrene nanoplastic particles on human lung cells and found that the particles were internalized by the cells and caused dose-dependent toxicity. The nanoplastics triggered oxidative stress, inflammation, and disrupted normal cell function. The findings suggest that inhaling airborne nanoplastics may pose risks to respiratory health.
Uptake of Breathable Nano- and Micro-Sized Polystyrene Particles: Comparison of Virgin and Oxidised nPS/mPS in Human Alveolar Cells
Researchers found that environmentally aged (oxidised) nano- and microplastics were rapidly taken up by human lung cells and caused significantly greater DNA damage, oxidative stress, and mitochondrial impairment compared to pristine particles, highlighting the heightened health risks of weathered airborne plastics.
Unveiling the Pulmonary Toxicity of Polystyrene Nanoplastics: A Hierarchical Oxidative Stress Mechanism Driving Acute–Subacute Lung Injury
Researchers investigated the pulmonary toxicity of polystyrene nanoplastics smaller than 100 nm in lung epithelial cells and macrophages, finding that exposure triggered a hierarchical oxidative stress mechanism that drove acute to subacute lung injury through lipid peroxidation and inflammation.
Polystyrene microplastic particles: In vitro pulmonary toxicity assessment
Researchers tested the effects of polystyrene microplastics on human lung cells in the laboratory and found that the particles triggered inflammation and oxidative stress. The microplastics also weakened the protective barrier function of lung tissue by depleting key structural proteins. The study suggests that inhaling microplastics may increase the risk of respiratory problems by damaging the lung's natural defenses.
In vitro evaluation of nanoplastics using human lung epithelial cells, microarray analysis and co-culture model
Researchers tested polystyrene nanoplastics on two types of human lung cells and found that the particles caused cell damage, oxidative stress, and inflammation-related gene changes at relatively low concentrations. Using a co-culture model that mimics the lung's layered structure, they showed that nanoplastics can trigger immune responses even in cells not directly exposed. The study suggests that inhaled nanoplastics may pose respiratory health risks through both direct toxicity and inflammatory signaling.
Polystyrene nanoparticles induce DNA damage and apoptosis in HeLa cells
Researchers exposed human HeLa cells to polystyrene nanoplastics — particles smaller than 100 nm — and found that even short exposures at low concentrations caused DNA damage, abnormal cell division, and signs of cell death including apoptosis and necrosis. The results suggest nanoplastics can directly damage human cell DNA, raising concerns about the health implications of everyday nanoplastic exposure.
Small Particles, Big Problems: Polystyrene nanoparticles induce DNA damage, oxidative stress, migration, and mitogenic pathways predominantly in non-malignant lung cells
Researchers exposed non-malignant and malignant lung cells as well as lung organoids to polystyrene micro- and nanoplastics at two sizes and measured DNA damage, oxidative stress, and cell migration. Non-malignant cells showed greater sensitivity than cancer cells, with the smaller 0.25 µm particles inducing more oxidative damage and migration at lower concentrations.
Hazard Assessment of Polystyrene Nanoplastics in Primary Human Nasal Epithelial Cells, Focusing on the Autophagic Effects
Researchers exposed primary human nasal epithelial cells to polystyrene nanoplastics of two sizes and found that the smaller particles caused more significant cellular changes, including activation of autophagy pathways. The nanoplastics triggered oxidative stress and altered cell processes related to waste recycling within cells. The study highlights the potential health risks of inhaling airborne nanoplastics, an exposure route that remains understudied.
Toxic effects of polystyrene nanoplastics on MDA-MB-231 breast cancer and HFF-2 normal fibroblast cells: viability, cell death, cell cycle and antioxidant enzyme activity
Researchers exposed human breast cancer cells and normal skin cells to polystyrene nanoplastics and found that smaller particles at higher concentrations caused significant cell death through apoptosis (programmed cell death) and reduced the cells' ability to defend against oxidative damage. The dose- and size-dependent toxicity suggests that nanoplastics small enough to enter cells are more biologically harmful than larger particles.
Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Photoaging of polystyrene microspheres causes oxidative alterations to surface physicochemistry and enhances airway epithelial toxicity
Researchers aged polystyrene microplastics with UV light and then tested their effects on human lung cells. They found that UV-weathered particles caused more pronounced biological responses than fresh ones, including cell cycle disruption, altered cell shape, and impaired wound healing. The study suggests that environmental aging of airborne microplastics may increase their potential to harm respiratory tissues.
Polystyrene nanoplastics induce pulmonary oxidative stress and programmed cell death through the cGAS-STING-NLRP3 pathway
Researchers exposed mice to polystyrene nanoplastics through nasal administration and studied the resulting lung damage over seven days. They found that the nanoplastics triggered oxidative stress, programmed cell death, and inflammatory responses in lung tissue through activation of the cGAS-STING-NLRP3 signaling pathway. The study provides evidence that inhaled nanoplastics can cause acute lung injury through specific molecular mechanisms involving both apoptosis and pyroptosis.
Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells
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.
Inhalation exposure to polystyrene nanoplastics induces chronic obstructive pulmonary disease-like lung injury in mice through multi-dimensional assessment
Mice that inhaled polystyrene nanoplastics developed lung damage resembling chronic obstructive pulmonary disease (COPD), including reduced breathing function, inflammation, and oxidative stress that worsened with longer exposure. The study found that nanoplastics caused this damage by disrupting mitochondria and triggering a type of cell death called ferroptosis, suggesting that breathing in airborne nanoplastics could increase the risk of serious lung disease.
Exposure of Human Lung Cells to Polystyrene Microplastics Significantly Retards Cell Proliferation and Triggers Morphological Changes
When human lung cells were exposed to polystyrene microplastics in the lab, cell growth slowed dramatically and their shape changed noticeably, even though the cells did not die outright. The 1-micrometer particles were taken up inside the cells, suggesting that inhaled microplastics could physically enter lung tissue. This is the first study to show that airborne microplastics can simultaneously slow human cell growth and alter cell structure, raising concerns about long-term respiratory health effects.
Unmodified Polystyrene Nanoparticles Induce Inflammatory and Oxidative Stress Responses in Human Lung Epithelial Cells
Exposure of human lung epithelial cells to unmodified polystyrene nanoparticles (60 nm) at concentrations as low as 50 µg/mL reduced cell viability by about 50% and triggered expression of inflammatory genes including IL-6 and CXCL10. These results suggest that nanoplastic particles reaching the respiratory tract could provoke lung inflammation, raising concerns about the health consequences of inhaling airborne nanoplastics.
Toxic effects of nanoplastics with different sizes and surface charges on epithelial-to-mesenchymal transition in A549 cells and the potential toxicological mechanism
Researchers exposed human lung cells to polystyrene nanoplastics of different sizes and surface charges and found they triggered a process called epithelial-to-mesenchymal transition, which is associated with the early stages of lung fibrosis. Smaller particles and those with positive surface charges caused the strongest effects, activating oxidative stress and inflammatory pathways. The study suggests that inhaled nanoplastics could contribute to respiratory health risks by promoting tissue scarring in the lungs.
Effects of Atmospheric Aging on the Respiratory Toxicity of Polystyrene Nanoplastic Particles
Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding that oxidized particles significantly elevated inflammatory gene expression (IL-8, TNF-α, IL-6) compared to fresh particles, demonstrating that environmental aging enhances respiratory toxicity.
Effects of Atmospheric Aging on the Respiratory Toxicityof Polystyrene Nanoplastic Particles
Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding significantly elevated expression of inflammatory genes IL-8, TNF-α, and IL-6 compared to fresh nanoplastics, demonstrating that environmental aging increases respiratory toxicity.
Cytotoxicity analysis of polystyrene nanoplastics in the bronchial epithelial cell line BEAS-2B
Researchers exposed bronchial epithelial cells to europium-doped polystyrene nanoplastics to assess cytotoxicity in a model of the human airway. The nanoplastics caused dose-dependent cell death and inflammatory signaling, supporting concerns about respiratory health effects from inhaled plastic particles.