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61,005 resultsShowing papers similar to Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage
ClearPolypropylene microplastic exposure leads to lung inflammation through p38-mediated NF- κB pathway due to mitochondrial damage
Researchers found that instilling polypropylene microplastic particles into mouse lungs caused dose-dependent increases in inflammatory cell counts, reactive oxygen species, and pro-inflammatory cytokines, with lung tissue analysis revealing the particles triggered inflammation via mitochondrial damage activating the p38-mediated NF-kB signaling pathway.
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.
Nanoplastics Penetrate Human Bronchial Smooth Muscle and Small Airway Epithelial Cells and Affect Mitochondrial Metabolism
When human lung cells were exposed to 25 and 50 nanometer polystyrene nanoplastics in the lab, the particles penetrated both airway lining cells and the smooth muscle cells underneath, including cells from asthmatic donors. The nanoplastics disrupted the cells' energy-producing mitochondria, impairing both normal oxygen-based metabolism and backup energy pathways -- demonstrating a direct mechanism by which inhaled nanoplastics could harm respiratory health.
A particle of concern: explored and proposed underlying mechanisms of microplastic-induced lung damage and pulmonary fibrosis
This paper explores how inhaled microplastics may cause lung damage and scarring (pulmonary fibrosis) through several biological pathways. The research identifies signaling pathways that could be targeted for future treatments to reduce microplastic-induced lung damage. This is relevant to human health because people regularly breathe in airborne microplastic particles.
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.
Mitochondrial stress response in lung cells triggered by the inhaled nanoplastics
This review focuses on how inhaled nanoplastic particles affect mitochondrial function in lung cells, including the activation of stress responses, disruption of energy production, and triggering of cell death pathways. Researchers found that because of their extremely small size, nanoplastics can penetrate deep into lung tissue and interact directly with cellular components in ways larger particles cannot. The study highlights the lungs as a particularly vulnerable site for nanoplastic-related health effects.
A Review on Polypropylene Microplastics and Respiratory Toxicity
This review of existing research shows that tiny plastic particles from polypropylene (a common plastic used in food containers and clothing) can get into our lungs when we breathe and cause harmful inflammation. Studies on animals and cells found that these microplastics damage lung tissue and trigger the body's immune system, potentially leading to breathing problems. While scientists have now detected these plastic particles in human lungs, more research is needed to fully understand the long-term health risks for people.
Metabolomics Reveal Nanoplastic-Induced Mitochondrial Damage in Human Liver and Lung Cells
Researchers exposed normal human liver and lung cells to 80-nanometer plastic particles and found that the nanoplastics damaged mitochondria, the energy-producing structures inside cells, without causing widespread cell death. Using metabolomics analysis, they identified specific disruptions to energy metabolism and lipid processing pathways in both cell types. This study reveals a subtle but important way that nanoplastics could impair organ function in humans by disrupting cellular energy production.
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.
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.
Impact of Micro- and Nanoplastics on Mitochondria
This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
Multi-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.
Intratracheal Administration of Polystyrene Micro(nano)plastics with a Mixed Particle Size Promote Pulmonary Fibrosis in Rats by Activating TGF-β1 Signaling and Destabilizing Mitochondrial Dynamics and Mitophagy in a Dose- and Time-Dependent Manner.
SD rats exposed to mixed polystyrene micro(nano)plastics via intratracheal administration at escalating doses over time developed pulmonary fibrosis and mitochondrial dysfunction, with severity linked to dose. The findings demonstrated a clear biological pathway connecting inhaled microplastic exposure to lung injury.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
Inhaled microplastics and lung health: Immunopathological effects and disease implications
This review examines the molecular mechanisms by which inhaled microplastics damage lung health, focusing on oxidative stress, inflammation, and immune disruption. Researchers found that microplastics trigger reactive oxygen species production, deplete antioxidants, impair mitochondrial function, and compromise immune defenses in lung tissue. The evidence indicates that microplastics may also act as carriers for other toxic pollutants, amplifying respiratory health risks.
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.
The Effect of Subchronic Polyethylene Microplastic Exposure on Pulmonary Fibrosis Through Pro-Inflammatory Cytokines TNF-α and IL-1β in Wistar Rats
This animal study found that breathing in polyethylene microplastics over several weeks led to lung scarring (pulmonary fibrosis) in rats by triggering inflammatory immune responses. The results suggest that chronic inhalation of airborne microplastics could contribute to serious lung damage in humans, since we breathe in thousands of plastic particles daily.
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.
Effects of true-to-life PET nanoplastics using primary human nasal epithelial cells
Researchers exposed human nasal cells to nanoplastics made from real PET water bottles and found that the particles were absorbed into cells and triggered oxidative stress. The nanoplastics also disrupted mitochondrial function and activated the cell's autophagy cleanup pathway. Since the nose is the first barrier encountered when breathing in airborne plastic particles, these findings suggest that nasal tissues may be particularly vulnerable to nanoplastic exposure.
Silent invaders: the role of MPs on epithelium inflammation and damage in airway diseases
This review examines how inhaled microplastics and nanoplastics interact with airway epithelial surfaces and trigger inflammatory, oxidative, and structural changes that may contribute to respiratory diseases. The study describes how these particles activate key inflammatory pathways such as NF-kB and PI3K/Akt/mTOR, potentially worsening conditions like asthma and COPD through enhanced barrier dysfunction, oxidative stress, and disrupted tissue repair.
Nasal instillation of polystyrene nanoplastics induce lung injury via mitochondrial DNA release and activation of the cyclic GMP-AMP synthase-stimulator of interferon genes-signaling cascade
Researchers showed that inhaled polystyrene nanoplastics trigger lung fibrosis and inflammation in mice by inducing mitochondrial DNA release into the cytoplasm, which activates the cGAS-STING innate immune signaling pathway — a discovery that identifies a specific molecular mechanism linking nanoplastic inhalation to pulmonary injury.
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.
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.
Breathing under siege: a narrative review on the potential biological mechanisms linking micro- and nanoplastic exposure to lung diseases
This narrative review examines how inhaled micro- and nanoplastics from indoor and outdoor air — including from synthetic textiles and face masks — can trigger lung inflammation, oxidative stress, and fibrosis, and outlines proposed mechanisms linking plastic inhalation to respiratory disease.