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61,005 resultsShowing papers similar to Polypropylene microplastic exposure leads to lung inflammation through p38-mediated NF- κB pathway due to mitochondrial damage
ClearPolypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage
This study found that polypropylene nanoplastics, one of the most common types of plastic particles, can cause lung inflammation by damaging mitochondria (the energy-producing parts of cells) and triggering inflammatory signaling pathways. These findings suggest that breathing in tiny plastic particles could contribute to lung disease through a specific chain of cellular damage.
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.
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.
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.
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.
Investigation of pulmonary inflammatory responses following intratracheal instillation of and inhalation exposure to polypropylene microplastics
Rats exposed to polypropylene microplastics through both inhalation and direct lung delivery developed inflammatory responses in their lungs, including increased immune cells and tissue changes. Even at relatively low concentrations, the microplastics triggered pulmonary inflammation, supporting concerns that breathing in airborne microplastics could contribute to respiratory health problems in humans.
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.
Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38 MAPK/p65 NF‐κB Signaling Pathway
Researchers found that exposure to PET microplastics induced liver fibrosis in mice through oxidative stress and activation of the p38 MAPK/p65 NF-kB signaling pathway. The study suggests that PET microplastics, which are frequently detected in both environmental samples and human tissues, may contribute to liver damage through inflammatory and oxidative mechanisms.
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.
Investigation of Pulmonary Inflammatory Responses Following Intratracheal instillation of and Inhalation exposure to Polypropylene Microplastics
Researchers conducted short-term pulmonary toxicity studies by exposing mice to polypropylene microplastics via intratracheal instillation and inhalation, finding dose-dependent inflammatory responses in lung tissue that confirm inhalation as a significant exposure route of concern.
Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway
After mice inhaled polystyrene microplastics, the particles spread to the brain, liver, kidneys, spleen, and other organs within days, triggering widespread inflammation through a specific immune signaling pathway called TLR/NF-kB. These findings suggest that breathing in microplastics could cause inflammatory damage across multiple organ systems in the body.
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.
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 secondary microplastic on the respiratory system of BALB/c mice
Researchers exposed BALB/c mice to secondary microplastics derived from environmentally weathered plastic and assessed respiratory system effects. Secondary MPs caused greater pulmonary inflammation and oxidative stress than virgin particles, suggesting that real-world aged plastics carry higher respiratory toxicity risks than pristine particles used in most laboratory studies.
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.
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.
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.
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.
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.
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.
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.
Lung hazards of microplastics and their toxicological mechanisms
This review summarizes eight key mechanisms by which microplastics cause lung injury, including oxidative stress, inflammation, DNA damage, and disruption of the immune response. Researchers explain how the small size and large surface area of microplastics allow them to evade respiratory clearance and deposit deep in lung tissue. The study provides a comprehensive framework for understanding how inhaled microplastics may contribute to respiratory health problems.
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.
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.