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Associations of Fecal Microplastics with Oxidative Damage and Cardiopulmonary Function: Evidence from a Pilot Study
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Researchers conducted a pilot study measuring microplastic levels in the feces of 16 male college students and assessed associations with oxidative stress markers and cardiopulmonary function. The study found that higher fecal microplastic levels were associated with increased oxidative damage biomarkers, providing early evidence that microplastic exposure in humans may be linked to oxidative stress and potential cardiopulmonary effects.
The ubiquity of microplastics (MPs) in the environment has raised significant concerns, yet their potential impacts on human health are not fully elucidated. This study aimed to quantify human exposure to MPs in feces and evaluate their associations with oxidative stress and cardiopulmonary function. A panel study was conducted in 16 male college students with three-round visits. Fecal MPs were quantified using infrared micro-spectroscopy, and health effects were assessed through urinary biomarkers of oxidative damage (MDA and 8-OHdG) and cardiopulmonary function tests. Associations between MP exposure and health outcomes were analyzed using linear mixed-effect models. We found that fecal MP amount across 48 samples from 16 participants showed high intra-individual variation and poor reproducibility (ICCs < 0.4). MPs in feces were predominantly identified as sheets and fragments in the 100-200 μm size range, with polyamide (PA), polyester, polyethylene (PE), and polypropylene as the primary polymer types. Significant relationships were observed between fecal MP amount and oxidative damage biomarkers. Each one-unit increase in MPs corresponded to a 0.827 increase in MDA (95% CI: 0.116, 1.54) and a 1.11 increase in 8-OHdG (95% CI: 0.235, 1.98), with fibrous shapes and specific polymers (PE and PA) being the primary drivers. No significant associations were found between MP exposure and lung function or blood pressure. These findings indicated that MP exposure was significantly linked to increased oxidative damage, highlighting a pressing public health concern regarding their subclinical biological effects.
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Polyethylene Microplastics Disrupt Cardiopulmonary Homeostasis via Oxidative Stress, Inflammatory Crosstalk, and Mitochondrial Dysfunction in Wistar Rats
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Male Wistar rats orally dosed with polyethylene microplastics for 28 days showed elevated cardiac and pulmonary injury biomarkers, suppressed antioxidant defenses, inhibited mitochondrial TCA cycle enzymes, and disrupted respiratory chain complexes, indicating simultaneous heart and lung damage through shared oxidative and inflammatory pathways. The study suggests that routine microplastic ingestion may impose systemic cardiopulmonary stress, with organ-specific dose-response differences suggesting the lungs may be particularly sensitive.
Association Between Microplastic Exposure and Cognitive Function Decline
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Researchers detected PET and polypropylene microplastics in blood, urine, and feces of study participants and found a significant association between higher microplastic concentrations in biological fluids and greater cognitive function decline, particularly among those with the highest exposure levels.
The influence of microplastics on hypertension-associated cardiovascular injury via the modulation of gut microbiota
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Researchers found that people with high blood pressure had more microplastics in their stool samples than healthy individuals, and feeding microplastics to mice raised their blood pressure and caused heart damage. The harm was linked to changes in gut bacteria, and a high-fiber diet or antibiotics helped reduce the damage. This study suggests microplastic exposure may worsen heart and blood pressure problems by disrupting the gut microbiome.
Sub-acute polyethylene microplastic inhalation exposure induced pulmonary toxicity in wistar rats through inflammation and oxidative stress
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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.
Acute Toxicity Assessment of Orally Administered Microplastic Particles in Adult Male Wistar Rats
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Researchers gave adult male rats a single oral dose of microplastics made from PET water bottles and found that even this one-time exposure altered markers of liver, heart, and kidney function. Higher doses also reduced food intake and increased signs of oxidative stress, which is cell damage caused by harmful molecules. This study suggests that even brief microplastic exposure could trigger early changes in organ function, raising questions about the cumulative effect of daily human exposure through food and water.
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