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Nanoplastics, an emerging contaminant, pose risks to fetal neural development, transferring from mother to offspring via placenta and breast milk. Assessing these risks, hippocampal CA3 samples from nanopolystyrene-exposed rat offspring were proteomically analyzed. Findings revealed reduced expression of neural developmental proteins (KIF21A, STMN2, DMTN, DLG1) and increased inhibitory proteins (PZP, α-2M, FN1, SERPINA1, ALOX15) in the hippocampus. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted ferroptosis enrichment, validated by significantly expressed ALOX15 and TF proteins. These alterations suggest nanopolystyrene's potential contribution to cognitive deficits and neurodevelopmental disorders, emphasizing its hazardous impact on neural development. This study provides novel insights into nanopolystyrene's risks. [ABSTRACT FROM AUTHOR]

As a new type of environmental pollutant, microplastics have been increasingly receiving attention for their impact on human health. Current research indicates that microplastics can enter the human body through various routes and exert neurotoxic effects. This article reviews the types, sources, and exposure pathways of microplastics, with a focus on the neurotoxic effects and potential mechanisms of microplastic exposure at different life stages in humans (fetal, infant, adult, and elderly). This review provides a comprehensive understanding of the neurotoxicity of microplastic exposure and its implications for human health risk assessment and effective prevention strategies. [ABSTRACT FROM AUTHOR]

Rapid social and industrial development has resulted in an increasing demand for fossil fuel energy, which increases particulate matter (PM) pollution. In this study, we employed a simple one-step electrospinning technique to fabricate polysulfone (PSF) fiber membranes for PM filtration. A 0.3 g/mL polymer solution with an N,N-dimethylformamide:tetrahydrofuran volume ratio of 3:1 yielded uniform and bead-free PSF fibers with a diameter of approximately 1.17 μm. The PSF fiber membrane exhibited excellent hydrophobicity and mechanical properties, including a tensile strength of 1.14 MPa and an elongation at break of 116.6%. Finally, the PM filtration performance of the PSF fiber membrane was evaluated. The filtration efficiencies of the membrane for PM2.5 and PM1.0 were approximately 99.6% and 99.2%, respectively. The pressure drops were 65.0 and 65.2 Pa, which were significantly lower than those of commercial air filters. Using this technique, PSF fiber membrane filters can be easily fabricated over a large area, which is promising for numerous air filtration systems. [ABSTRACT FROM AUTHOR]

Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants. [ABSTRACT FROM AUTHOR]

Polystyrene (PS) and di-(2-ethylhexyl) phthalate (DEHP) exist widely in the environment. However, their distribution in organisms remains unclear. We used three sizes (50 nm, 500 nm, and 5 μm) of PS and DEHP to study the distribution and accumulation of PS, DEHP, and mono(2-ethylhexyl) phthalate (MEHP) in mice and nerve cell models (HT22 and BV2 cells) and their potential toxicity. Results showed that PS entered the blood of mice, and the distribution of different particle sizes in different tissues was different. After the combined exposure to PS and DEHP, PS carried DEHP, which significantly increased the DEHP content and MEHP content and the highest content of MEHP was in the brain. With the decrease in PS particle size, the contents of PS, DEHP, and MEHP in the body increased. The levels of inflammatory factors were increased in the serum of the PS or/and DEHP group. In addition, 50 nm polystyrene can carry MEHP into nerve cells. These results suggest for the first time that PS and DEHP combined exposure can induce systemic inflammation, and the brain is an important target organ of PS and DEHP combined exposure. This study may serve as a reference for further evaluation of the neurotoxicity induced by combined exposure to PS and DEHP. [ABSTRACT FROM AUTHOR]

Extensive environmental pollution by microplastics has increased the risk of human exposure to plastics. However, the biosafety of polypropylene microplastics (PP-MPs), especially of PP particles < 10 μm, in mammals has not been studied. Thus, here, we explored the mechanism of action and effect of exposure to small and large PP-MPs, via oral ingestion, on the mouse intestinal tract. Male C57BL/6 mice were administered PP suspensions (8 and 70 μm; 0.1, 1.0, and 10 mg/mL) for 28 days. PP-MP treatment resulted in inflammatory pathological damage, ultrastructural changes in intestinal epithelial cells, imbalance of the redox system, and inflammatory reactions in the colon. Additionally, we observed damage to the tight junctions of the colon and decreased intestinal mucus secretion and ion transporter expression. Further, the apoptotic rate of colonic cells significantly increased after PP-MP treatment. The expression of pro-inflammatory and pro-apoptosis proteins significantly increased in colon tissue, while the expression of anti-inflammatory and anti-apoptosis proteins significantly decreased. In summary, this study demonstrates that PP-MPs induce colonic apoptosis and intestinal barrier damage through oxidative stress and activation of the TLR4/NF-κB inflammatory signal pathway in mice, which provides new insights into the toxicity of MPs in mammals. [ABSTRACT FROM AUTHOR]

Highlights: What are the main findings? OMPM exposure induced lung lesions and PF in rats. What is the implication of the main finding? OMPM exposure induced PF via TGF-β1/Smad3 and TGF-β1/p38 MAPK signaling pathways. OMPM exposure induced fibrotic phenotypes in the BEAS-2B cell line. OMPM exposure activated the differentiation of the HFL-1 cell line. OMPM exposure led to the BEAS-2B cell line being able to induce the differentiation of the HFL-1 cell line. Oil-mist particulate matter (OMPM) refers to oily particles with a small aerodynamic equivalent diameter in ambient air. Since the pathogenesis of pulmonary fibrosis (PF) has not been fully elucidated, this study aims to explore the potential molecular mechanisms of the adverse effects of exposure to OMPM at different concentrations in vivo and in vitro on PF. In this study, rats and cell lines were treated with different concentrations of OMPM in vivo and in vitro. Sirius Red staining analysis shows that OMPM exposure could cause pulmonary lesions and fibrosis symptoms. The expression of TGF-β1, α-SMA, and collagen I was increased in the lung tissue of rats. The activities of MMP2 and TIMP1 were unbalanced, and increased N-Cadherin and decreased E-Cadherin upon OMPM exposure in a dose-dependent manner. In addition, OMPM exposure could activate the TGF-β1/Smad3 and TGF-β1/MAPK p38 signaling pathways, and the differentiation of human lung fibroblast HFL-1 cells. Therefore, OMPM exposure could induce PF by targeting the lung epithelium and fibroblasts, and activating the TGF-β1/Smad3 and TGF-β1/MAPK p38 signaling pathways. [ABSTRACT FROM AUTHOR]

Background: Exposure to heavy metals during pregnancy is an important risk factor for adverse birth outcomes. We aimed to investigate the current heavy metal exposure levels in cord blood from healthy pregnant women residing in the Huaihe River Basin, China, and examined the association between heavy metal levels and dietary habits and lifestyle factors. In this study, we measured the exposure levels of five heavy metals in the umbilical cord blood from 350 healthy pregnant women and administered 350 self-reported questionnaires regarding the general characteristics and dietary habits of those women. Methods: This study was undertaken in Shenqiu county, Henan province, which is in the area of the Huai River Basin, in a cohort of pregnant women and newborn babies in 2013–2014. We recruited a sample of 1000 pregnant women among those receiving prenatal examination, measured the real individual newborn exposure to heavy metals in serum by ICP-MS, collected information regarding the pregnant women with a questionnaire survey and obtained data on environmental quality from environmental protection agencies and the available literature. We estimated the daily individual exposure to heavy metals of all the 1000 participants throughout the pregnancy and recorded their birth outcomes after delivery. Then we analyzed the association between birth outcome and individual exposure to heavy metals. Results: 54 newborn children had birth defects. The geometric means of cord blood levels of As, Cd, Cr, Pb and Hg were measured at 0.92 ± 1.01 ng mL−1, 0.11 ± 0.17 ng mL−1, 4.57 ± 5.02 ng mL−1, 3.37 ± 3.81 ng mL−1 and 0.89 ± 1.69 ng mL−1 for subjects (n = 54) who gave birth to infants with birth defects and 0.43 ± 0.88 ng mL−1, 0.52 ± 3.86 ng mL−1, 1.94 ± 2.92 ng mL−1, 4.38 ± 4.96 ng mL−1 and 0.43 ± 0.91 ng mL−1 for subjects (n = 296) with healthy infants, respectively. The contents of all five heavy metals in the whole blood of both of these two groups were higher than the reference values of the Chinese general population (P < 0.001). Conclusions: The occurrence of birth defects was 15.4% in this cohort, and was correlated to exposure of parents to environments containing heavy metal contaminants in Shenqiu county in the Huai River Basin. The heavy metal exposure situation of the investigated population had serious effects in terms of reproductive defects in children. The specific link between newborn defects and environmental heavy metal contaminants suggested that contamination in pregnant women persisted over time, and that the exposure may have a long term effect. [ABSTRACT FROM AUTHOR]