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Papers
1,247 resultsMicroplastics in the bloodstream can induce cerebral thrombosis by causing cell obstruction and lead to neurobehavioral abnormalities
Researchers discovered that microplastics in the bloodstream can cause blood clots in the brain by getting swallowed by immune cells that then block tiny blood vessels. These blockages reduced blood flow and caused neurological problems in mice. This reveals a new way microplastics may harm the brain, not by crossing into brain tissue directly, but by disrupting blood circulation.
Polylactic Acid Micro/Nanoplastic Exposure Induces Male Reproductive Toxicity by Disrupting Spermatogenesis and Mitochondrial Dysfunction in Mice
Even so-called "eco-friendly" biodegradable plastic (polylactic acid, or PLA) was found to cause reproductive harm in male mice. After breaking down in the digestive system, tiny PLA nanoparticles crossed into the testes and damaged sperm quality, mitochondria (the energy producers in cells), and hormone levels. This challenges the assumption that biodegradable plastics are safe and highlights potential risks to male fertility.
Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
Polystyrene micro- and nanoplastics caused spermatogenesis disorders in mice by disrupting mitochondrial dynamics, triggering excessive mitochondrial fission that activated both apoptosis and pyroptosis pathways in testicular tissue. Nanoplastics caused mitochondrial DNA to leak into the cytoplasm, activating the cGAS-STING inflammatory pathway — a mechanism confirmed by rescue experiments with a mitochondrial fission inhibitor.
Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage
In mouse and cell studies, polystyrene nanoplastics at doses near real-world human exposure levels caused miscarriage by blocking the movement of placental cells needed for a healthy pregnancy. The nanoplastics triggered a cellular recycling process called autophagy that broke down key proteins required for placental cell migration and invasion.
Features, Potential Invasion Pathways, and Reproductive Health Risks of Microplastics Detected in Human Uterus
Researchers found microplastics in the uterine lining of 22 women, identifying common plastics like polyamide, polyurethane, and PET in sizes ranging from 2 to 200 micrometers. In mouse experiments, microplastic exposure led to reduced fertility, abnormal offspring sex ratios, and significant uterine inflammation. These findings raise serious concerns about the potential impact of microplastic contamination on female reproductive health and pregnancy outcomes.
The effects of heavy metal exposure on brain and gut microbiota: A systematic review of animal studies
This systematic review of 16 animal studies found evidence that heavy metal exposure disrupts gut microbiota composition, which may in turn affect brain function through the gut-brain axis. Lead was the most studied metal, and the findings suggest that environmental contaminant-induced gut dysbiosis could mediate neurotoxic effects, a mechanism that may also apply to microplastic exposure.
Identification of microplastics in human tear fluid and meibum: Implications for dry eye disease pathogenesis
For the first time, researchers confirmed the presence of microplastics in human tear fluid and the oily secretions of the eyelid glands (meibum), with polyethylene being the most common type found. Higher polyethylene levels correlated with worse dry eye disease symptoms. In lab and mouse experiments, polyethylene exposure damaged eye surface cells and triggered inflammation, suggesting airborne microplastics may contribute to dry eye disease.
Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage
In a mouse study, polystyrene nanoplastics accelerated the development of colon cancer linked to inflammatory bowel disease by disrupting fat metabolism and causing DNA damage in intestinal cells. The nanoplastics also altered gut bacteria and increased intestinal inflammation, suggesting that plastic particle exposure could worsen outcomes for people already at risk for colon cancer.
Exposure to polyethylene terephthalate micro(nano)plastics exacerbates inflammation and fibrosis after myocardial infarction by reprogramming the gut and lung microbiota and metabolome
Researchers found that PET microplastics and nanoplastics, one of the most common plastic types found in human coronary blood, worsen heart damage after a heart attack. The plastic particles activated an inflammatory pathway (NLRP3) and disrupted the balance of gut and lung bacteria, leading to chronic inflammation and increased scarring of heart tissue. These findings suggest that plastic pollution exposure may make recovery from heart attacks more difficult.
Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs
Researchers found that polystyrene nanoplastics disrupt the gut lining in mice by altering tiny RNA molecules that control the production of protective proteins in the intestinal barrier. The nanoplastics also caused an imbalance in gut bacteria, creating a chain reaction where damaged gut cells release particles that further weaken the intestinal barrier and change the microbiome.
Incorporation of polylactic acid microplastics into the carbon cycle as a carbon source to remodel the endogenous metabolism of the gut
Researchers discovered that gut bacteria can break down so-called biodegradable PLA microplastics and incorporate the carbon into their own metabolism, fundamentally altering the gut's energy balance. This process reduced beneficial short-chain fatty acids that fuel gut lining cells and caused decreased appetite and weight loss in mice, suggesting that biodegradable plastics may not be as harmless inside the body as assumed.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.
Micro-nanoplastics pollution and mammalian fertility: A systematic review and meta-analysis
This meta-analysis of 79 studies across five mammalian species found that micro- and nanoplastics cause reproductive toxicity in a concentration-dependent manner, particularly at high doses. Polystyrene was the most studied polymer, and most research focused on male fertility in mice, leaving a significant gap in knowledge about effects on food-producing animals that could serve as vectors for human exposure.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Size-dependent internalization of polystyrene microplastics as a key factor in macrophages and systemic toxicity
Researchers systematically tested how the size of polystyrene microplastics affects their uptake and toxicity in immune cells and mice. Smaller particles (0.5 micrometers) were taken up much more readily by immune cells and caused more damage, including mitochondrial dysfunction and cell death, compared to larger 5-micrometer particles. In living mice, smaller microplastics accumulated more in organs and caused broader changes in blood and metabolic markers, confirming that particle size is a key factor in microplastic toxicity.
Microplastics exacerbate ferroptosis via mitochondrial reactive oxygen species-mediated autophagy in chronic obstructive pulmonary disease
Researchers found that microplastics worsen chronic obstructive pulmonary disease (COPD) by triggering a chain reaction in lung cells: the plastics damage mitochondria (the cell's energy centers), which produces harmful molecules that activate a self-destructive process called autophagy-dependent ferroptosis. Lung tissue from COPD patients contained significantly higher concentrations of polystyrene microplastics than healthy controls. When scientists blocked this destructive pathway in mice, it reduced the excessive inflammation and prevented COPD flare-ups caused by microplastic exposure.
Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology
Scientists found that polystyrene nanoplastics can travel from the gut to the brain along nerve pathways and worsen Parkinson's disease in mice. The nanoplastics accelerated the clumping of alpha-synuclein, a protein central to Parkinson's, which triggered brain inflammation, damaged mitochondria, and impaired the cellular cleanup system. Mice exposed to both nanoplastics and the disease protein showed progressive physical and motor decline resembling Parkinson's symptoms.
Hazard assessment of airborne and foodborne biodegradable polyhydroxyalkanoates microplastics and non-biodegradable polypropylene microplastics
A mouse study compared biodegradable PHA plastic particles to conventional polypropylene microplastics and found both types caused harm to the lungs, liver, and gut when inhaled or eaten. However, the biodegradable PHA particles caused notably less damage than polypropylene, suggesting that while biodegradable plastics are not harmless, they may pose lower health risks than traditional plastics.
Size-Dependent Pulmonary Toxicity and Whole-Body Distribution of Inhaled Micro/Nanoplastic Particles in Male Mice from Chronic Exposure
Researchers exposed mice to airborne micro- and nanoplastic particles through normal breathing over an extended period and found the highest accumulation in the lungs, followed by the blood and spleen. Surprisingly, the larger 1-micrometer microplastics caused more severe lung damage than the smaller 80-nanometer particles, triggering inflammation, cell death, and scarring. These findings highlight that breathing in airborne plastic particles poses real health risks, with particle size playing an important role in the type of damage caused.
Combined toxicity of polystyrene microplastics and perfluorobutane sulfonate on mouse liver: Impact on lipid metabolism and gut-liver axis disruption
This study examined what happens when mice are exposed to both polystyrene microplastics and PFBS (a type of "forever chemical") at the same time. The combination caused significantly worse liver damage than either pollutant alone, disrupting fat metabolism and triggering gut bacteria imbalances that further harmed the liver through the gut-liver connection. These findings are concerning because microplastics can absorb PFAS chemicals in the environment, meaning people may often be exposed to both together.
Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
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.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
In a mouse study, tiny nanoplastics (30-50 nanometers) that were swallowed reached the brain and caused memory problems by activating the brain's immune cells, called microglia, which triggered inflammation. This is concerning because it shows that nanoplastics small enough to be found in everyday products like cosmetics could cross into the brain and impair cognitive function.
Polystyrene microplastics impair the functions of cultured mouse Leydig (TM3) and Sertoli (TM4) cells by inducing mitochondrial-endoplasmic reticulum damage
Lab experiments showed that polystyrene microplastics damaged two key types of testicular cells in mice -- Leydig cells that produce testosterone and Sertoli cells that support sperm development -- by harming their mitochondria (the cell's energy centers) and stressing the endoplasmic reticulum. These findings suggest that microplastic exposure could contribute to male reproductive problems by disrupting hormone production and sperm development at the cellular level.