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61,005 resultsShowing papers similar to Lung inflammation from repeated airway exposure to washing-machine lint microfibers may be linked to phagocytosis dysfunction: Possible effects on mtDNA replication
ClearInhalation of dust accumulated on personal computer fans in the office may cause pathological effects by disrupting the metabolic activity of alveolar macrophages
Researchers collected dust from personal computer fans in offices and found it contained various types of microplastics and non-protein particles. When mice were exposed to this dust over 90 days, they developed lung inflammation, foamy macrophages, mitochondrial damage, and collagen fiber formation in lung and heart tissues. The study suggests that inhaling office dust containing microplastics may disrupt metabolic activity in lung cells and contribute to respiratory and cardiovascular effects.
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.
Polypropylene 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.
Inhaled Microplastics Inhibit Tissue Maintenance Functions of Pulmonary Macrophages
Researchers found that inhaled microplastics accumulate in lung macrophages, the immune cells responsible for cleaning and maintaining lung tissue, and significantly impair their normal functions. The microplastic-laden macrophages showed reduced ability to perform tissue maintenance tasks that are essential for lung health. The study provides evidence that breathing in microplastics could compromise the lung's built-in defense and repair systems, with potential implications for respiratory health.
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.
Polypropylene 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.
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.
Inhalable textile microplastic fibers impair lung repair
Inhalable textile microplastic fibers were tested in a lung repair model, with results showing that fibers significantly impaired alveolar epithelial healing and disrupted normal lung tissue regeneration. The study provides mechanistic evidence linking inhaled plastic fibers to lung damage, relevant to occupational and ambient air exposure scenarios.
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.
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.
Inhalable Textile Microplastic Fibers Impair Airway Epithelial Differentiation
Researchers exposed lung cells and mice to textile microplastic fibers (nylon and polyester) and found that nylon fibers significantly impaired airway cell growth and development. The damage came from chemicals leaching out of the nylon rather than the physical fibers themselves, and the effects persisted even after exposure ended. This is relevant because textile fibers are one of the most common types of microplastics people inhale daily.
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.
Inhalable textile microplastic fibers impair lung repair
Human and murine lung organoid experiments showed that nylon microfibers, but not polyester fibers, impaired airway organoid growth and development, with the damage driven by leached components rather than physical obstruction, raising concerns for lung health during early development.
Human airway organoids and microplastic fibers: A new exposure model for emerging contaminants
Researchers used human airway organoids, an advanced lab model that mimics real lung tissue, to study the effects of microplastic fibers released from household clothes dryers. While the fibers did not stop organoid growth, they reduced the expression of a gene important for airway cell function and became physically embedded within the growing tissue. The study suggests that inhaled microplastic fibers could have long-term implications for lung tissue repair and establishes organoids as a valuable model for studying airborne plastic contamination.
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.
Microplastic-Induced Macrophage Dysfunction Drives Lung Tumor Progression through Glutathione Imbalance
Researchers found that microplastics trigger a cascade of immune dysfunction in macrophages through toll-like receptor signaling, leading to disrupted glutathione metabolism and macrophage cell death via ferroptosis. In tumor-bearing mice, orally ingested microplastics accumulated in the lungs and remodeled the immune microenvironment over time, with increased infiltration of inflammatory macrophages and impaired lymphocyte function accompanying greater tumor burden.
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.
Microplastics as environmental modifiers of lung disease
This review examines growing evidence that inhaled microplastics may contribute to lung diseases including asthma, pulmonary fibrosis, and chronic obstructive pulmonary disease. Researchers found that different plastic types, sizes, and weathering states can trigger inflammation, oxidative stress, and cellular changes in lung tissue, suggesting microplastics may act as environmental modifiers that worsen respiratory conditions.
Respiratory Toxicity of Microplastics: Mechanisms, Clinical Outcomes, and Future Threats
This review examined the mechanisms by which inhaled airborne microplastics cause respiratory harm, including inflammation, oxidative stress, fibrosis, and impaired mucociliary clearance. The authors also discuss emerging evidence linking microplastic inhalation to worsening asthma, COPD, and potentially lung cancer.
Exposure and inhaling of microplastics: An evidence of cause of cancer
This review examined the evidence linking microplastic inhalation to cancer risk, covering how inhaled MPs accumulate in the lungs, trigger chronic inflammation, oxidative stress, and DNA damage, and may contribute to lung carcinogenesis. The authors identified microplastic inhalation as an underappreciated occupational and environmental cancer risk.
Respiratory Toxicity of Microplastics: Mechanisms, Clinical Outcomes, and Future Threats
This review summarized the respiratory toxicity of airborne microplastics, covering their sources, the routes by which they penetrate deep into lung tissue, and the range of clinical outcomes from chronic inflammation to potential malignancy. The authors warn that inhalation exposure represents an underappreciated and growing public health threat.
Inhaled tire-wear microplastic particles induced pulmonary fibrotic injury via epithelial cytoskeleton rearrangement
Researchers investigated the health effects of inhaling tire-wear microplastic particles in mice and found that exposure caused lung fibrosis and restricted breathing function. The study identified that the particles triggered rearrangement of the structural framework in lung cells, leading to scarring and tissue damage through epigenetic mechanisms. These findings suggest that airborne tire-wear particles, a common but understudied pollutant, may pose a significant risk to respiratory health.
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.