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61,005 resultsShowing papers similar to Co-exposure of polystyrene nanoplastics and ozone synergistically induced airway inflammation: Evidence and biomarkers screening
ClearCo-exposure to ozone and polystyrene nanoplastic exacerbates cognitive impairment and anxiety-like behavior by regulating neuronal pyroptosis in mice
Mice exposed to both ozone and polystyrene nanoplastics showed worse cognitive problems and anxiety-like behavior than those exposed to either pollutant alone. The combined exposure triggered a type of inflammatory cell death called pyroptosis in the brain's prefrontal cortex. This is concerning because people in polluted urban areas are routinely exposed to both ozone and airborne nanoplastics, and the combination may be more harmful to brain health than either one individually.
Synergistic pulmonary toxicity of resorcinol bis(diphenylphosphate) and microplastics: Integrated proteomics and metabolomics approach reveals oxidative stress-inflammatory crosstalk
Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
Combined toxicity evaluation of polystyrene nanoplastics and Nano-ZnO of distinctive morphology on human lung epithelial cells
Researchers tested how polystyrene nanoplastics combined with zinc oxide nanoparticles affect human lung cells, finding that the two pollutants interact differently depending on their shapes and concentrations. Zinc oxide primarily damaged cell membranes while nanoplastics mainly triggered oxidative stress and cell death, and their combined effects varied from additive to counteracting. This study is important because people are likely exposed to both nanoplastics and metal particles in polluted air, and understanding their combined effects is key to assessing real-world health risks.
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.
Polystyrene nanoplastics and benzo(a)pyrene synergistically induce lung fibrosis and inflammation via relaxin signalling in mice
Researchers exposed mice to polystyrene nanoplastics, benzo(a)pyrene, or their combination over 16 weeks and found that only combined exposure produced significant lung inflammation and fibrosis, with transcriptomic analysis identifying the Relaxin signaling pathway — acting through PI3K-AKT, MAPK, and calcium-dependent macrophage trap formation — as a key mediator of the synergistic toxicity.
Co-exposure to polystyrene microplastics and di-(2-ethylhexyl) phthalate aggravates allergic asthma through the TRPA1-p38 MAPK pathway
This mouse study found that polystyrene microplastics combined with DEHP, a common plastic additive, worsened allergic asthma symptoms more than either pollutant alone. The combination activated an inflammatory pathway called TRPA1-p38 MAPK in lung tissue, increasing airway inflammation and mucus production. The findings suggest that real-world exposure to microplastics carrying chemical additives could aggravate respiratory conditions like asthma.
Co-exposure to different sized polystyrene microplastics and benzo[a]pyrene affected inflammation in zebrafish andbronchial-associated cells
Researchers found that co-exposure to different sizes of polystyrene microplastics together with the carcinogen benzo[a]pyrene produced greater toxic effects in aquatic organisms than either pollutant alone. The study highlights the importance of studying microplastic interactions with other contaminants rather than treating them as isolated stressors.
Co-exposure to polystyrene nanoplastics and glyphosate exacerbates NETs-mediated pyroptosis by activating the NLRP3 inflammasome in mouse liver
Researchers found that co-exposing mice to polystyrene nanoplastics and the herbicide glyphosate caused significantly worse liver damage than either pollutant alone. The combined exposure triggered a chain of inflammatory events including immune cell infiltration, formation of neutrophil traps, and cell death in liver tissue, all driven by activation of a key inflammatory pathway called NLRP3. The study suggests that nanoplastics may amplify the harmful effects of common agricultural chemicals when they enter the body together.
Combined cytotoxicity of polystyrene nanoplastics and phthalate esters on human lung epithelial A549 cells and its mechanism
Researchers investigated the combined toxicity of polystyrene nanoplastics and common plasticizer chemicals (phthalate esters) on human lung cells. At lower nanoplastic concentrations, the particles actually reduced the toxicity of the plasticizers by adsorbing them, but at higher concentrations nanoplastics dominated and worsened overall cell damage. The study identified oxidative stress and inflammation as key mechanisms driving the combined toxic effects on lung tissue.
Compound effect and mechanism of oxidative damage induced by nanoplastics and benzo [a] pyrene
Researchers examined how polystyrene nanoplastics and a common environmental pollutant called benzo[a]pyrene work together to cause oxidative damage in earthworm cells. They found that the two contaminants had a synergistic toxic effect, with combined exposure producing significantly higher levels of cell-damaging reactive oxygen species than either pollutant alone. The study suggests that nanoplastics may enhance the harmful effects of other soil pollutants by altering how they interact with living cells.
Co-exposure to polyethylene microplastics and house dust mites aggravates airway epithelial barrier dysfunction and airway inflammation via CXCL1 signaling pathway in a mouse model
In a mouse model of asthma, co-exposure to inhaled polyethylene microplastics and house dust mite allergens caused worse airway inflammation than either pollutant alone. The microplastics damaged the airway lining and amplified allergic reactions through a specific inflammatory signaling pathway called CXCL1. This finding suggests that breathing in airborne microplastics could make allergies and asthma worse by helping allergens penetrate deeper into the lungs.
Evidence that microplastics aggravate the toxicity of organophosphorus flame retardants in mice (Mus musculus)
Researchers co-exposed mice to polyethylene and polystyrene microplastics along with organophosphorus flame retardants for 90 days and found that microplastics aggravated the toxicity of the flame retardants. Evidence from biochemical markers and metabolomics indicated increased oxidative stress and metabolic disruption in co-exposed animals, suggesting microplastics may worsen the health effects of chemical pollutants they encounter in the environment.
Synergistic effects of microplastics and bioaerosols: emerging trends in urban air pollution complexification and public health implications
This review examines the emerging synergistic health risks of airborne microplastics and bioaerosols in urban environments. Researchers found that microplastics can serve as carriers for bacteria, fungi, and viruses, potentially prolonging pathogen survival and increasing human exposure through inhalation. The combined exposure may amplify respiratory inflammation and oxidative stress beyond what either pollutant causes individually, highlighting a growing concern for urban public health.
Polystyrene nanoplastics aggravate house dust mite induced allergic airway inflammation through EGFR/ERK-dependent lung epithelial barrier dysfunction
In mice with allergic asthma triggered by house dust mites, exposure to polystyrene nanoplastics significantly worsened airway inflammation and lung damage. The nanoplastics disrupted the protective barrier of lung cells by activating a specific signaling pathway (EGFR/ERK), allowing more allergens and immune cells to penetrate lung tissue. This finding suggests that airborne nanoplastics could make asthma and allergies worse for the millions of people who already suffer from these conditions.
Environmental relevant concentrations of polystyrene nanoplastics and lead co-exposure triggered cellular cytotoxicity responses and underlying mechanisms in Eisenia fetida
Researchers studied how polystyrene nanoplastics and lead, a toxic heavy metal, interact when earthworm immune cells are exposed to both simultaneously at environmentally realistic concentrations. The combined exposure caused more severe cell damage, oxidative stress, and inflammation than either pollutant alone. The findings suggest that nanoplastics can increase the harmful effects of heavy metals on soil organisms, raising concerns about the real-world impact of mixed contaminant exposure.
Combined exposure of polystyrene microplastics and benzo[a]pyrene in rat: Study of the oxidative stress effects in the liver
Researchers exposed rats to polystyrene microplastics and the carcinogen benzo[a]pyrene, both individually and in combination, to study oxidative stress in liver tissue. The combined exposure caused significantly more liver damage, inflammation, and oxidative stress than either pollutant alone. The study suggests that microplastics may amplify the harmful effects of environmental carcinogens when both are ingested together.
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.
Maternal polystyrene nanoplastics exposure during pregnancy induces obesity development in adult offspring through disrupting lipid homeostasis
Researchers found that maternal inhalation exposure to polystyrene nanoplastics during pregnancy induced obesity development in adult offspring of mice, suggesting in utero exposure to airborne nanoplastics programs metabolic dysfunction. The study linked prenatal nanoplastic exposure to increased adiposity and metabolic changes persisting into adulthood.
Toxic impacts of polystyrene nanoplastics and PCB77 in blunt snout bream: Evidence from tissue morphology, oxidative stress and intestinal microbiome
Researchers studied the combined toxicity of polystyrene nanoplastics and a persistent organic pollutant (PCB77) in freshwater fish. They found that co-exposure caused worse tissue damage, higher oxidative stress, and greater disruption to gut bacteria than either contaminant alone. The study highlights that microplastics can worsen the harmful effects of other environmental pollutants when organisms are exposed to both simultaneously.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Airborne polystyrene microplastics and nanoplastics induce nasal and lung microbial dysbiosis in mice
Researchers found that airborne polystyrene microplastics and nanoplastics can induce microbial dysbiosis in the nasal passages and lungs of mice. The study showed that both micro- and nanoplastics altered airway microbiota composition, with microplastics having a stronger influence on lung bacterial communities, suggesting that inhaled plastic particles may disrupt respiratory microbial balance.
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.
Effects of Atmospheric Aging on the Respiratory Toxicityof Polystyrene Nanoplastic Particles
Researchers exposed human bronchial epithelial cells to atmospherically aged polystyrene nanoplastics at an air-liquid interface, finding significantly elevated expression of inflammatory genes IL-8, TNF-α, and IL-6 compared to fresh nanoplastics, demonstrating that environmental aging increases respiratory toxicity.
Co-exposure to polystyrene nanoplastics and triclosan induces synergistic cytotoxicity in human KGN granulosa cells by promoting reactive oxygen species accumulation
Researchers found that when human ovarian cells are exposed to both nanoplastics and triclosan (a common antibacterial chemical) at the same time, the toxic effects are worse than either one alone. The combination triggered more cell damage, harmful oxygen molecules, and cell death than individual exposure. This matters because people are typically exposed to multiple pollutants simultaneously, and this synergy could have implications for female reproductive health.