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61,005 resultsShowing papers similar to Tracing the cellular consequences of polyethylene microplastics: senescence and apoptosis in A549 and Raw 264.7 macrophage cells
ClearMicroplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling
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.
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
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
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.
99 The Relative Toxicity and Bioreactivity of Ambient Microplastic Pollution to Human Alveolar Lung Epithelial Cells with and Without Urban PM2.5
This lab study exposed human lung cells to microplastic particles (polypropylene and polyamide) at sizes found in real-world air pollution, finding that both types caused cell death while urban air pollution particles (PM2.5) triggered inflammatory responses instead. The two types of harm worked through different mechanisms and didn't reliably combine when mixed, suggesting that microplastics in inhaled air pose a distinct and understudied risk to the respiratory system beyond conventional air pollution.
Sub-acute polyethylene microplastic inhalation exposure induced pulmonary toxicity in wistar rats through inflammation and oxidative stress
Researchers exposed rats to airborne polyethylene microplastics through inhalation for 28 days and found significant signs of lung damage. The exposed animals showed increased inflammation markers, elevated oxidative stress, and tissue changes in the lungs compared to controls. The study provides evidence that breathing in microplastic particles from degraded plastic bags and bottles may cause pulmonary toxicity.
Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells
Researchers found that microplastic exposure accelerates aging in fat tissue by triggering cellular senescence (a state where cells stop dividing and release inflammatory signals) in both mice and cell cultures. The microplastics accumulated in fat tissue, increased markers of aging and inflammation, and disrupted the normal development of new fat cells. These findings suggest that chronic microplastic exposure could contribute to age-related metabolic problems and obesity-related diseases in humans.
Impact of Degradation of Polyethylene Particles on Their Cytotoxicity
Researchers found that degradation of polyethylene particles altered their cytotoxicity, with weathered and fragmented PE showing different toxic effects on cells compared to pristine particles, suggesting environmental aging changes microplastic health risks.
Impact of nanoplastics emitted from incineration of polyethylene plastic on THP-1 macrophage viability and immune function
Researchers assessed whether nanoparticles emitted during the incineration of high-density polyethylene affect human lung macrophage viability and immune function. They found that HDPE incineration nanoparticles significantly reduced THP-1 macrophage viability and impaired immune responses, raising concerns about inhalation exposure at waste incineration sites.
Evaluation of potential toxicity of polyethylene microplastics on human derived cell lines
Researchers tested the toxic effects of two sizes of polyethylene microplastics on human cell lines representing different tissue types. They found that microplastic exposure triggered inflammatory responses and caused cellular damage, with effects varying depending on particle size and cell type. The findings suggest that microplastics commonly encountered in everyday life could pose health risks when they interact with human tissues.
The effect of microplastics on human lung cell lines
Researchers exposed three human lung cell lines—non-tumor WI-38, and tumor A549 and H1299—to polystyrene microspheres of 1.5 µm, 5 µm, and 10 µm diameters at concentrations of 1–1000 µg/mL. All cell lines showed increased proliferation at the highest concentrations and smallest particle sizes, with expression changes in cell cycle regulators AKT1, SMG1, and Caspase-9 suggesting complex size- and concentration-dependent cellular mechanisms.
Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence
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.
Atmospheric microplastic and nanoplastic: The toxicological paradigm on the cellular system
This review examines how airborne microplastics and nanoplastics affect human cells after being inhaled into the lungs. Because these particles are tiny and lightweight, they can penetrate deep into lung tissue and potentially enter the bloodstream. Studies on human cell lines show that inhaled plastic particles can cause inflammation, oxidative stress, and DNA damage, raising concerns about long-term respiratory and systemic health effects.
Chronic lung tissue deposition of inhaled polyethylene microplastics may lead to fibrotic lesions
In a mouse study, inhaled polyethylene microplastics accumulated in lung tissue over 90 days of repeated exposure, causing chronic inflammation, immune changes, and early signs of lung scarring (fibrosis). Even at the lowest doses, the microplastics triggered inflammatory cell buildup and thickening of lung walls. These findings suggest that long-term breathing of airborne microplastics could lead to permanent lung damage, which is concerning given rising levels of plastic particles in indoor and outdoor air.
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.
Characterization of microparticles derived from waste plastics and their bio‐interaction with human lung A549 cells
Researchers characterized secondary microplastics derived from waste plastics and studied their interaction with human lung cells, finding that irregularly shaped particles from real-world plastic waste induced different biological responses than the uniform spheres typically used in laboratory studies.
122 Elucidating the Impact of Inhaled Micro-, Nanoplastics (MNPs) from Surgical Face Masks In Vitro
This in vitro study tested whether polypropylene particles shed from surgical face masks can harm human lung cells, finding that aerosolized mask-derived microplastics caused dose-dependent cell death, increased inflammatory markers (IL-1β, IL-6, IL-8), and early signs of DNA damage. The results suggest that breathing particles released from plastic masks represents a real hazard to the respiratory system, though more research is needed to establish real-world exposure levels.
Detrimental effects of microplastic exposure on normal and asthmatic pulmonary physiology
Researchers exposed both healthy and asthmatic mice to airborne microplastics and found significant lung inflammation, immune activation, and increased mucus production in both groups. Microplastic particles were taken up by immune cells called macrophages, and gene analysis revealed changes in immune response, cellular stress, and cell death pathways. The study suggests that inhaling microplastics may worsen respiratory health in both normal and vulnerable populations.
Potential toxicity of micro- and nanoplastics in primary bronchial epithelial cells of patients with chronic obstructive pulmonary disease
Researchers investigated how micro- and nanoplastics affect lung cells taken from patients with chronic obstructive pulmonary disease (COPD), a condition that already impairs breathing. The study aimed to determine whether plastic particle exposure poses additional toxic risk to people whose airways are already compromised.
The regulation of circRNA_kif26b on alveolar epithelial cell senescence via miR-346-3p is involved in microplastics-induced lung injuries
Researchers found that inhaled polystyrene microplastics caused lung damage in rats by accelerating the aging of cells lining the air sacs, through a specific molecular pathway involving circular RNA. The microplastics triggered inflammation, fibrosis, and premature cell aging in lung tissue over a 35-day exposure period. The study reveals a new mechanism by which inhaled microplastics may contribute to lung injury.
Temporal Trend in Accumulation of Microplastics in Decedent Human Lungs
Researchers compared lung tissue samples from people who died in 1991 and 2024 and found that microplastic presence increased from 19% to 77% of individuals over that period, with the number of particles per gram of tissue also rising significantly. The polymer composition shifted from predominantly polyethylene to a more diverse mix including PET and PVC, and lung samples containing microplastics showed greater signs of inflammation and fibrosis.
Micro- and nano-plastics induce inflammation and cell death in human cells.
Human cell cultures exposed to micro- and nano-plastics (MNPLs) showed elevated inflammation markers and cell death, with effects varying by particle type and concentration. The study developed a novel extraction and staining technique to identify individual plastic types in complex mixtures, advancing methods for assessing human cellular toxicity.
The Effect of Subacute Exposure to Low-Density Polyethylene (LDPE) Microplastics on Oxidative Stress and Membrane Damage in Alveolar Macrophage Cells of Rattus Norvegicus Wistar Strain
Researchers exposed rat alveolar macrophage cells to low-density polyethylene microplastics via inhalation and measured oxidative stress (F2-isoprostanes) and membrane damage markers. Subacute microplastic inhalation increased oxidative stress indicators and membrane damage in lung immune cells, suggesting that inhaled plastic particles impair the lungs' front-line defenses.
Micro- and Nanoplastic-Induced Respiratory Disease and Dysfunction: A Scoping Review
A systematic scoping review of 68 studies found that inhaled micro- and nanoplastics are detected in human lung tissue and associated with pulmonary inflammation, fibrosis, and impaired lung function, though most evidence comes from occupational settings and in vitro experiments.