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61,005 resultsShowing papers similar to Repeated inhalation exposure to polystyrene nanoplastics induced sustained pulmonary injury and fibrosis in mice.
ClearMulti-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics
Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
Microplastics and nanoplastics, emerging pollutants, increased the risk of pulmonary fibrosis in vivo and in vitro: A comparative evaluation of their potential toxicity effects with different polymers and size
Researchers compared the lung toxicity of microplastics and nanoplastics made from polystyrene, polyethylene, and polypropylene in mice and human lung cells. They found that all particle types induced signs of pulmonary fibrosis, inflammation, and tissue remodeling, with polystyrene nanoplastics causing the most severe effects. The study suggests that smaller nanoplastic particles and certain polymer types may pose greater risks to lung health.
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.
Size-Dependent Pulmonary Toxicity and Whole-Body Distribution of Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
Researchers exposed mice to airborne micro- and nanoplastic particles through normal breathing over an extended period and found the highest accumulation in the lungs, followed by the blood and spleen. Surprisingly, the larger 1-micrometer microplastics caused more severe lung damage than the smaller 80-nanometer particles, triggering inflammation, cell death, and scarring. These findings highlight that breathing in airborne plastic particles poses real health risks, with particle size playing an important role in the type of damage caused.
Deleterious effects of microplastics and nanoplastics on rodent lungs: a systematic review
This systematic review summarizes research on how inhaled micro- and nanoplastics affect the lungs in animal studies. The findings show these particles can cause lung inflammation, tissue damage, and immune responses, suggesting that breathing in airborne microplastics may pose real risks to respiratory health.
Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice
This mouse study found that inhaling polystyrene microplastics caused serious lung damage, including inflammation, cell death, and scar tissue buildup. Smaller microplastics (1-5 micrometers) caused more harm than larger ones, and the damage worsened with longer exposure. The study identified a specific immune pathway (TLR2/NF-kB) through which inhaled microplastics trigger lung injury, raising concerns about the respiratory effects of airborne microplastics on humans.
Inhaled polystyrene nanoparticles may cause fibrotic lesions via immune dysregulation and energy metabolism disturbance
Mice received polystyrene nanoparticles via pharyngeal instillation for 90 days and were assessed for local lung and systemic toxicity. The nanoparticles accumulated in lungs and hearts, caused immune dysregulation, disrupted energy metabolism, and induced fibrotic lesions at higher doses, suggesting that chronic inhalation of nanoplastics may contribute to pulmonary fibrosis.
Polystyrene nanoplastics induced lung injury in mice: Insights into lung metabolic disorders
Researchers exposed mice to polystyrene nanoplastics through the airway and found that the particles caused lung inflammation and tissue damage. Using metabolomics analysis, they discovered that the nanoplastics disrupted multiple metabolic pathways in lung tissue, with surface-modified particles causing more severe effects. The study provides evidence that inhaled nanoplastics can alter lung metabolism in ways that may contribute to respiratory health problems.
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.
Size-Dependent PulmonaryToxicity and Whole-Body Distributionof Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
Researchers used a whole-body inhalation exposure system to chronically expose male mice to polystyrene micro- and nanoplastics at environmental concentrations and tracked particle distribution and lung toxicity. Nanoplastics (80 nm) showed greater tissue transport than microplastics (1 µm), with highest accumulation in lungs followed by blood and spleen, and both sizes disrupted oxidative balance and antioxidant defenses.
Realistic Nanoplastics Induced Pulmonary Damage via the Crosstalk of Ferritinophagy and Mitochondrial Dysfunction
Researchers created realistic nanoplastics by mechanically breaking down bulk plastic rather than using lab-made particles, and found that inhaling these particles caused significant lung damage in mice through iron-related cell death and mitochondrial dysfunction. PVC nanoplastics were the most harmful of the four types tested, and all were more toxic than commonly used lab-standard polystyrene spheres, suggesting previous studies may have underestimated the lung health risks of airborne nanoplastics.
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.
Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice
Researchers administered polystyrene microplastics directly into the lungs of mice and found that the particles induced pulmonary fibrosis by triggering oxidative stress and activating the Wnt signaling pathway. The microplastics caused damage to the lung lining cells and promoted the buildup of scar tissue in lung tissue. The study provides evidence that inhaled microplastics may contribute to serious respiratory conditions by driving fibrotic changes in the lungs.
Analysis of Biodistribution and in vivo Toxicity of Varying Sized Polystyrene Micro and Nanoplastics in Mice
This study found that smaller plastic particles spread more widely through the bodies of mice and caused more organ damage than larger ones, particularly in the liver, kidneys, and heart. Nanoplastics (under 1 micrometer) were especially concerning because they crossed biological barriers more easily than microplastics. The results suggest that the tiniest plastic particles in our environment may pose the greatest health risks.
Foodborne and airborne polyethersulfone nanoplastics respectively induce liver and lung injury in mice: Comparison with microplastics
Researchers compared the effects of polyethersulfone micro and nanoplastics when consumed through food versus inhaled through air in mice. Eaten particles mainly damaged the liver by disrupting gut bacteria and metabolism, while inhaled particles primarily harmed the lungs. Nanoplastics caused more damage than microplastics in both cases, suggesting that the smallest plastic particles we breathe and eat may pose the greatest health risks.
Systematic toxicity evaluation of polystyrene nanoplastics on mice and molecular mechanism investigation about their internalization into Caco-2 cells
Researchers fed mice polystyrene nanoplastics (about 100 nm) for 28 days and found the particles accumulated in multiple organs including the spleen, lungs, kidneys, intestines, testes, and brain. The nanoplastics caused cell death, inflammation, and tissue damage in these organs, as well as disrupted fat metabolism and blood cell counts. This study demonstrates that ingested nanoplastics can spread throughout the body and cause widespread harm, raising concerns about long-term human exposure.
Oropharyngeal Administration of Polystyrene Microplastics Induces Profibrotic and Oxidative Changes in Murine Lung Tissue
Researchers investigated the early lung effects of inhaled polystyrene microplastics in mice over a 21-day exposure period. While overall fibrosis scores did not reach statistical significance in this short timeframe, they observed significant macrophage infiltration, active particle uptake by immune cells, and upregulation of oxidative stress and fibrosis-related molecular markers. The findings suggest that microplastic inhalation triggers early immune and oxidative responses that may precede lung tissue remodeling.
Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice
Researchers tested the lung toxicity of three common plastic types -- polypropylene, polystyrene, and polyethylene -- in mice by exposing them to microplastic fragments. The study assessed how these inhaled microplastic particles from everyday plastics affect lung health, which is relevant since humans regularly breathe in airborne microplastics.
Acute exposure to polystyrene nanoplastics induces unfolded protein response and global protein ubiquitination in lungs of mice
Mice exposed to polystyrene nanoplastics through their airways showed signs of cellular stress in lung tissue, including activation of the unfolded protein response (a defense mechanism cells use when proteins are damaged) and increased protein breakdown. The effects were dose-dependent, with higher nanoplastic doses causing more cellular distress. This research reveals a specific mechanism by which inhaled nanoplastics could damage lung cells, raising concerns about airborne microplastic exposure.
Pulmonary toxicity of polymethyl methacrylate nanoplastics via intratracheal intubation in mice
Researchers exposed mice to polymethyl methacrylate nanoplastics through inhalation over 28 days to study their lung effects. The exposed mice experienced weight loss, nanoplastic accumulation in the lungs, increased inflammatory cell counts, and elevated inflammatory cytokines. The findings demonstrate that inhaling these common nanoplastics can induce lung inflammation, tissue damage, and changes in protein and RNA expression.
Nanopolystyrene Translocation and Fetal Deposition After Acute Lung Exposure During Late-Stage Pregnancy
Nanopolystyrene particles inhaled by pregnant mice during late pregnancy crossed into the bloodstream and deposited in fetal tissues. This finding raises concern that airborne nanoplastics could pose a risk to fetal development, especially given growing human exposure to plastic particles in indoor and outdoor air.
In vivo toxicity assessment of microplastics in Balb/C mice : study of inhalation exposure and its inflammatory effects
Researchers examined the in vivo toxicity of inhaled microplastics in Balb/C mice, studying pulmonary inflammation, oxidative stress, and systemic effects following repeated inhalation exposure. The study found dose-dependent lung inflammation and evidence of particle translocation to other organs.
Nanopolystyrene translocation and fetal deposition after acute lung exposure during late-stage pregnancy
Researchers exposed pregnant mice to nanoscale polystyrene particles through inhalation and tracked where the particles traveled. They found that the nanoplastics crossed from the lungs into the bloodstream and accumulated in both placental and fetal tissues, confirming that inhaled plastic nanoparticles can reach developing offspring during pregnancy.
Inhalation of nanoplastics in the mouse model: Tissue bio-distribution and effects on the olfactory system
Mice that inhaled polystyrene nanoplastics for one week accumulated the particles in their brains, lungs, fat tissue, and testicles. Although the particles cleared from most tissues within a month, the mice suffered lasting damage to their sense of smell, with reduced brain cell function and signs of inflammation in the olfactory region. This is the first study to show that inhaled nanoplastics can impair the sense of smell and trigger long-term brain changes, even after the particles are gone.