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61,005 resultsShowing papers similar to Co-exposure to polystyrene microplastics and di-(2-ethylhexyl) phthalate aggravates allergic asthma through the TRPA1-p38 MAPK pathway
ClearCo-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.
Co-exposure of polystyrene nanoplastics and ozone synergistically induced airway inflammation: Evidence and biomarkers screening
Researchers discovered that co-exposure to airborne polystyrene nanoplastics and ozone in mice caused significantly worse airway inflammation than either pollutant alone, with the two acting synergistically. They identified specific metabolic pathways and genes involved in the inflammatory response, providing potential biomarkers for monitoring this type of combined exposure. The findings suggest that breathing in nanoplastics alongside common air pollutants like ozone may pose amplified respiratory health risks.
Co-exposure to microplastics enhances the allergenic potentials of house dust mite allergen Der p 1
This study found that polystyrene microplastics can make common house dust mite allergens more potent, increasing allergic reactions. The microplastics changed the shape of the allergen protein, boosting its ability to trigger immune responses and worsening airway inflammation in mice. This research suggests that indoor microplastic pollution could be contributing to the rising rates of allergies and asthma by making existing allergens more harmful.
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.
Gut-lung axis: a novel mechanism involving microbiota dysbiosis-coordinated PLA2-TRPV1 neuroimmune crosstalk in nanoplastic-induced asthma exacerbation
Researchers found that inhaled polystyrene nanoplastics worsen asthma in mice by triggering a chain reaction involving gut bacteria disruption, nerve-immune signaling, and airway inflammation, revealing a gut-lung connection where plastic particles in the body can amplify respiratory disease through multiple biological pathways at once.
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.
Mechanisms of exacerbation of Th2-mediated eosinophilic allergic asthma induced by plastic pollution derivatives (PPD): A molecular toxicological study involving lung cell ferroptosis and metabolomics
Researchers found that mice exposed to polystyrene microplastics combined with a common plastic additive (dibutyl phthalate) developed significantly worse allergic asthma symptoms, including increased airway inflammation driven by a specific type of immune response. The microplastics triggered a form of cell death called ferroptosis in lung cells, which amplified the allergic reaction. Treatment with an iron-binding drug provided relief, suggesting potential therapeutic approaches for people with asthma who are exposed to plastic pollution.
Impact of Microplastic Exposure on Airway Inflammation in an Acute Asthma Murine Model
Mouse experiments found that microplastic exposure worsened inflammatory responses in healthy lungs but did not further aggravate airway inflammation in mice with pre-existing asthma, suggesting the lung's response to microplastics depends on baseline immune state.
Combined Enterohepatic Toxicity of Polystyrene Microplastics and Di(2-ethylhexyl) Phthalate in Mice: Gut Microbiota-Dependent Synergistic Effects
Researchers investigated the combined toxicity of polystyrene microplastics and the plasticizer DEHP in mice, focusing on gut-liver axis effects. They found that co-exposure worsened harmful outcomes compared to either pollutant alone, with gut microbiota playing a key mediating role in the synergistic toxicity. The study suggests that microplastics and their associated chemical additives may interact to amplify health risks through disruption of the gut-liver connection.
Mechanisms underlying Th2-dominant pneumonia caused by plastic pollution derivatives (PPD): A molecular toxicology investigation that encompasses gut microbiomics and lung metabolomics
In a mouse study, exposure to dibutyl phthalate (a plastic additive) and polystyrene microplastics for five weeks caused pneumonia-like lung damage, increased oxidative stress, and triggered inflammation. The researchers found that these plastic pollution byproducts caused a specific type of immune response that leads to eosinophilic inflammation in the airways, connected through the gut-lung axis. The findings suggest that everyday exposure to plastic-derived chemicals and particles could contribute to respiratory disease.
Combined ecotoxicity of polystyrene microplastics and Di-(2-ethylhexyl) phthalate increase exposure risks to Mytilus coruscus based on the bioaccumulation, oxidative stress, metabolic profiles, and nutritional interferences
Researchers exposed hard-shelled mussels to a common plastic additive (DEHP) and polystyrene microplastics together, and found that the microplastics increased how much DEHP accumulated in the animals' digestive organs. The combined exposure disrupted the mussels' antioxidant defenses and altered their metabolic processes more than either pollutant alone. The study suggests that microplastics can amplify the harmful effects of chemical pollutants in marine organisms.
Di-(2-ethyl hexyl) phthalate induced oxidative stress promotes microplastics mediated apoptosis and necroptosis in mice skeletal muscle by inhibiting PI3K/AKT/mTOR pathway
Researchers investigated how the plastic additive DEHP and polystyrene microplastics affect skeletal muscle in mice, finding that combined exposure caused more severe oxidative stress and cell death than either substance alone. The study suggests that co-exposure triggers apoptosis and necroptosis in muscle tissue by inhibiting a key cellular signaling pathway involved in cell survival.
Polystyrene nanoparticles aggravate the adverse effects of di-(2-ethylhexyl) phthalate on different segments of intestine in mice
Researchers exposed mice to polystyrene nanoparticles and the plasticizer DEHP simultaneously, finding that co-exposure caused greater intestinal damage — including shorter villi, disrupted tight junctions, and reduced mucus coverage — than either contaminant alone, with gut microbiota alterations likely contributing to the enhanced toxicity.
Polystyrene particles induces asthma-like Th2-mediated lung injury through IL-33 secretion
Researchers found that inhaled polystyrene microplastic particles triggered asthma-like inflammation in the lungs of mice, with smaller particles causing more severe responses. The particles stimulated the release of IL-33, a signaling molecule that activates a specific type of immune response associated with allergic airway disease. The study identifies a potential mechanism by which airborne microplastics could contribute to respiratory inflammation.
Microplastics and di (2-ethylhexyl) phthalate synergistically induce apoptosis in mouse pancreas through the GRP78/CHOP/Bcl-2 pathway activated by oxidative stress
Researchers found that combined exposure to microplastics and the plasticizer DEHP synergistically induced pancreatic cell apoptosis in mice through oxidative stress activation of the GRP78/CHOP/Bcl-2 pathway, suggesting these co-occurring pollutants pose greater risk together than individually.
Polystyrene microplastics and di-2-ethylhexyl phthalate co-exposure: Implications for female reproductive health
When rats were exposed to both polystyrene microplastics and the common plasticizer DEHP together, they developed significantly more ovarian damage -- including increased cystic follicles, fibrosis, and hormone imbalance -- than from either substance alone. The combined exposure activated a specific signaling pathway (TGF-beta1/Smad3) linked to ovarian fibrosis and may increase the risk of polycystic ovary syndrome, raising concerns about real-world co-exposure in women.
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.
Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver
Mice exposed to microplastics, the plasticizer DEHP, or both together showed liver damage including oxidative stress, cell death, and disrupted metabolism. The combined exposure was worse than either pollutant alone, activating cancer-related genes and impairing the liver's ability to process fats and amino acids. Since DEHP is commonly found alongside microplastics in the environment, these findings suggest that real-world exposure to contaminated plastics could pose a greater liver health risk than previously estimated.
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.
Early clues and molecular mechanism involved in neurodegenerative diseases induced in immature mice by combined exposure to polypropylene microplastics and DEHP
Researchers exposed young mice to polypropylene microplastics combined with DEHP, a chemical commonly found in plastics, and observed significant brain damage including memory problems and damage to the hippocampus. The combined exposure was worse than either substance alone, showing additive or synergistic toxic effects on the developing brain. This is particularly concerning for young children, who are most commonly exposed to polypropylene products and may be more vulnerable to these neurotoxic effects.
Effects of microplastics on allergic airways and potential pathogenesis: a review
This review examines how microplastics, which can enter the body through breathing, eating, and skin contact, may affect allergic airway conditions. Researchers found evidence that microplastics can damage airway lining cells, disrupt the protective barrier of the respiratory tract, and trigger heightened airway reactivity. The study suggests that chronic microplastic exposure may worsen allergic airway inflammation, though more research is needed to fully understand the mechanisms involved.
Polystyrene nanoparticles enhance the adverse effects of di-(2-ethylhexyl) phthalate on male reproductive system in mice
Researchers investigated the combined reproductive toxicity of polystyrene nanoparticles and the plasticizer DEHP in male mice over 35 days. The study found that co-exposure to nanoparticles and DEHP produced enhanced adverse effects on sperm quality and testicular tissue compared to either substance alone, suggesting nanoplastics may amplify the endocrine-disrupting effects of plasticizers.
Cellular and molecular mechanisms of allergic asthma
Researchers reviewed the cellular and molecular mechanisms behind allergic asthma, finding that rising exposure to environmental pollutants — including microplastics — likely contributes to the disease's increasing prevalence, as pollutants disrupt airway barrier integrity and trigger immune responses that lead to chronic airway inflammation.
Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production
Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.