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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]

Neutral mucin is purplish red, and acidic mucin is blue; the tissues and cells containing both neutral and acidic mucins show different degrees of purple. The values are the means ± SDs (normalized amounts of AB-PAS and immunohistochemistry, I n i = 3; intestinal-barrier-related protein level, I n i = 5). In Section 2.2, Animals and Experimental Design, in the first paragraph, lines 3-5, we make the following correction: "All animal experiments were approved by the Experimental Animal Welfare Ethics Committee of the Tianjin Institute of Environmental and Operational Medicine, IACUC approval code AMMS-04-2021-014.". [Extracted from the article]

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]

Tungsten trioxide nanoparticles (WO3 NPs) have shown increasing promise in biological and biomedical fields in recent years. However, their possible hazards, especially the adverse effects related to their sizes on human health and environment, are still yet poorly understood. In this study, we compared the hepatotoxicity in mice induced by WO3 nanorods of two different lengths (125−200 nm and 0.8−2 μm) via intraperitoneal injection, and explored the protective role of melatonin, an antioxidant, against the hepatotoxicity. The results showed that 10 mg/kg/day of shorter WO3 nanorods could cause obvious hepatic function impairment, histopathological lesions, and significant enhancement in levels of oxidative stress and inflammation in mouse liver. However, similar effects were found only in the 20 mg/kg/day longer WO3 nanorods–treated mice, and these adverse effects were attenuated by pretreatment with melatonin. These findings indicate that WO3 nanorods can exert hepatotoxicity in mice in a dose- and length-dependent manner, and that shorter WO3 nanorods cause more severe hepatotoxicity than their longer counterparts. Melatonin could serve as an effective protective agent against the longer WO3 nanorods–induced hepatotoxicity by decreasing the oxidative stress level. This study is important for determining the environmental and human health risks of exposure to WO3 NPs and their size-dependent toxicity, and provides an appealing strategy to avoid the adverse effects. [ABSTRACT FROM AUTHOR]

Ultrafine particles (UFPs) referred to particular matters with aerosol diameter less than 100 nm. Because of the lightweight and small size, UFPs have become an occupational inhalation risk. The UFPs will be accumulated in the deep lung through inhalation, and then reach into all the organs via circulation system; some UFPs even stay in the brain. As previous study reported, UFPs exposure is usually associated with cardiovascular disease, such as atherosclerosis (AS). In our study, we tried to understand how acute UFP exposure caused the biological dysregulation in atherosclerosis. Acute exposure of UFPs were applied to mice for 6 consecutive days, mice were sacrificed after 3, 5, 7, and 10 days post-exposure. Aorta and serum were collected for histological and biomarkers analysis. Mice aortic adventitial fibroblasts (MAFs) were isolated from mice and used to further study to understand the mechanism of UFPs induced atherosclerosis. Compared to the untreated control, the inflammation responses and nitrate stress were observed after acute exposure of UFPs, with increased IL-6, MCP-1, p47phox, and 3-NT levels in the mice serum. Besides, upregulation of microRNAs: miR-301b-3p and Let-7c-1-3p, and their downstream target: Smad2, Smad3, and TGFβ1 were also observed in mouse aorta after acute exposure of UFPs. Similar results were identified in vitro as well. Acute exposure of UFPs induced the systematic nitrate stress and inflammation responses, along with the changes of vascular permeability. Dysregulated miRNAs and TGFβ/Smads signaling pathway indicated the higher risk of atherosclerosis/vasculature remodeling when exposed to UFPs. [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]

Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is one of the widely used organophosphorus flame retardants (OPFRs), which are regarded as suitable substitutes for brominated flame retardants (BFRs). Previously, we have validated the toxicity of TDCIPP in PC12 cells owing to the induced alterations in GAP43, NF-H, CaMK2a/2b, and tubulin α/β proteins; however, limited information is currently available on the toxicity and mechanism of TDCIPP. In the present study, cytotoxicity effects were evaluated by exposing PC12 cells to different concentrations of TDCIPP (0-50 μM) for 4 days. To explore the possible mechanisms through which cytotoxicity is induced, changes in intracellular [Ca2+]i levels and the activation of calmodulin dependent protein kinase 2 (CaMK2), c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases (ERK1/2), and p38 mitogen-activated protein kinases (MAPK) pathways were evaluated. Furthermore, PC12 cells were pretreated with CaMK2 inhibitor KN93 to investigate the relationship between TDCIPP-induced phosphorylation of CaMK2 and activation of JNK, ERK1/2, and p38 MAPK pathways. Our results indicate that TDCIPP-induced toxicity might be associated with the overload of [Ca2+]i levels, increased phosphorylation of CaMK2, and activation of the JNK, ERK1/2, and p38 MAPK pathways, the lattermost of which was further demonstrated to be partially elicited by the CaMK2 phosphorylation. [ABSTRACT FROM AUTHOR]

Nanomaterials have been widely used in a number of applications; however, these nanomaterials may potentially be risky for human health, particularly for the respiratory system. In this study, we used a mouse asthma model to study whether graphene oxide (GO), a promising carbonaceous nanomaterial with unique physicochemical properties, aggravates allergic asthma via the oxidative stress pathway. Mice were sensitized with ovalbumin (OVA) to trigger immune reactions, while vitamin E (Ve) was administered as an antioxidant. Our results showed that GO aggravated OVA-induced allergic asthma in mice, as suggested by increased reactive oxygen species (ROS), elevated total immunoglobulin E (IgE), upregulated Th2 response, and the aggravation of allergic asthma symptoms, such as airway remolding, collagen deposition with mucus hypersecretion, and airway hyperresponsiveness (AHR). The administration of Ve dramatically attenuated all of the above effects. In conclusion, Ve showed anti-allergic properties in antagonizing the exacerbation of allergic asthma induced by GO, providing a new possibility for the treatment of allergic asthma. [ABSTRACT FROM AUTHOR]

Growing concern has been raised over the potential hazard of nanoparticles (NPs) on human health from ambient particulate air pollution. Silicon dioxide (SiO) NPs are one of the most widely used nanoparticles in many sectors of industry. Research on NPs has focused mainly on their toxicity in organs. Meanwhile, NPs are present in the air year-round, but are more serious in winter. Thus, the aim of this study was to evaluate the inflammatory response to SiO NPs using in vivo test systems. The composition of particulate matter is complicated; however, elemental silicon accounts for a significant proportion. Cold exposure can induce many kinds of systemic reactions. Thus, the second aim of this study was also to evaluate the combined effect of NPs and cold exposure on human health. There is little research on the combined effects of nanoparticles and cold on inflammation. Sprague-Dawley rats were randomly divided into four groups: those exposed to SiO NPs by intratracheal instillation, those exposed to at 4 °C 4 h/day for 4 weeks, a combined SiO NPs and cold exposure group, and a control group. Inflammatory cell infiltration in the lungs was mainly observed after exposure to SiO NPs or cold. Hematoxylin and eosin staining revealed that inflammation of the lungs was more serious in the combined group. In the white adipose tissue and brown adipose tissue of the combined groups, the mRNA expressions of pro-inflammatory cytokines were upregulated. In conclusion, SiO NPs combined with cold exposure induced a stronger systemic inflammatory response, accompanied by more serious health hazards. [ABSTRACT FROM AUTHOR]

Concern has been growing over the potential hazard of nanoparticles to human health because of increasing ambient particulate air pollution. Much research has been performed on the toxicology of nanoparticles to organs. Meanwhile, particles floating in air, particularly in winter, are more serious. Thus, the purpose of this study was to evaluate the effect of nanoparticles and cold on human health. There is little research on the effects of nanoparticles on energy metabolism. The composition of particulate matter is complicated; however, silicon in particles accounts for a significant proportion. Adipose tissue is the main organ that produces heat and maintains the body temperature in a cold environment. White adipose tissue (WAT) stores energy in the form of triacylglycerol, whereas brown adipose tissue (BAT) dissipates energy in the form of heat to maintain the body temperature. This article presents the effect of air ultra-particles and cold on the WAT and BAT. In vivo, Sprague-Dawley rats were divided into four groups: exposed to the same deposited doses of silicon dioxide (SiO2) nanoparticles (NPs) by intratracheal instillation or/and cold exposure at 4 °C, 4 h per day for four weeks. Cold exposure induced weight loss and WAT browning, as indicated by pathology, transmission electron microscopy (TEM), upregulated mRNA levels of BAT and WAT specific genes and molecular switches. Intratracheal instillation of nano-SiO2 induced a slowdown in metabolism, weight gain and inhibited WAT browning, as indicated by the downregulated mRNA levels of BAT and WAT marker genes and molecular switches. This study provided direct evidence that SiO2 NPs might inhibit the effect of cold-induced white/brown adipose tissue changes in plasticity and metabolism. [ABSTRACT FROM AUTHOR]

Previous studies demonstrated that tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) caused adverse effects on thyroid hormone (TH) imbalance in aquatic and avian organisms. This study focused on the effects of TDCIPP on thyroid function and hormone homeostasis in mammals. Pubertal female Sprague-Dawley rats were orally administered 50, 100, or 250 mg per kg per d of TDCIPP from postnatal day (PND) 22 to PND42 for 21 days. The serum triiodothyronine (T3) levels increased significantly at 250 mg per kg per d of TDCIPP. There were no significant differences in the body weight, serum thyroxine (T4) and free thyroxine (FT4) levels between the control and TDCIPP treated groups. There were significant dose-dependent increases in the mRNA and protein expression levels of genes related to drug metabolism (cytochrome-p450-3A1, CYP3A1) and TH clearance (udp-glucuronosyltransferase-1A6, UGT1A6) in the liver. Treatment with TDCIPP increased hepatic type 1 deiodinase (DIO1) mRNA at 250 mg per kg per d but down-regulated hepatic TH receptor beta (TRβ) mRNA expression. In addition, TDCIPP exposure induced slight thyroid follicular hyperplasia, and several genes involved in TH biosynthesis (NIS, TPO, Tg) were altered at 100 and 250 mg per kg per d of TDCIPP. Nevertheless, serum thyroid stimulating hormone (TSH) levels and the receptor (TSHr) mRNA significantly decreased at only the low dose group. Based on these results, we certified that TDCIPP disturbs the normal bioprocess on TH synthesis, biotransformation or clearance, and hepatic detoxification of pubertal female SD rats, causing thyroid function disorder. [ABSTRACT FROM AUTHOR]

Sidestream cigarette smoke, the major component of environmental tobacco smoke, is a complex and reactive aerosol. The particulate matter (PM) in sidestream smoke is one of the carriers of chemical constituents. However, particle size-dependent toxicological effects of PM are poorly understood. In this study, we evaluated the relationship between the PM size and in vitro cytotoxicity and mutagenicity of sidestream cigarette smoke. A NanoMoudi-II 125A was used to collect PM samples ranging from 10 nm to 10 μm. The in vitro toxicity of PM was evaluated using a neutral red cytotoxicity assay and Salmonella mutagenicity assay. The results showed that the cytotoxicity and mutagenicity of PM larger than 1 μm was significantly lower than PM sized 10 nm-1 μm. Furthermore, there was a noticeable trend that the smaller the size of the PM of sidestream cigarette smoke, the greater the toxicity. This study suggests that the toxicity of PM in sidestream cigarette smoke is size-dependent. [ABSTRACT FROM AUTHOR]

Environmental pollutants co-exist and exhibit interaction effects that are different from those associated with a single pollutant. As one of the more commonly manufactured nanomaterials, titanium dioxide nanoparticles (TiO-NPs) are most likely to bind to other contaminants in water. In this paper, we aimed to study the combined toxicological effects of TiO-NPs and bisphenol A (BPA) on organism. First, in vitro adsorption experiments were conducted to determine the adsorptive interaction between TiO-NPs and BPA. Second, zebrafish embryo toxicity tests were performed to monitor for changes in the toxicological effects associated with the two chemicals. The study results demonstrated that adsorptive interactions exist between the two chemicals and increased toxicity effects which included an advanced toxicological effect time, decreased survival, increased morphological abnormalities, and delayed embryo hatching. Also, we suggest that the mode of combined action has a synergistic effect. Based on this, we postulate that concomitant exposure to TiO-NPs and BPA increased BPA bioavailability and uptake into cells and organisms. Further studies are required to understand the mechanisms of interactions of this mixture. [ABSTRACT FROM AUTHOR]

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3-14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation. [ABSTRACT FROM AUTHOR]

This study mainly investigated the neurotoxicity induced by zinc oxide nanoparticle (ZnO NP) in different-aged mice and the interaction between age and ZnO NP exposure. Sixty adult and old male C57BL/6J mice were assigned to four groups based on a two-factor (age and ZnO NP exposure) design. Results showed that ZnO NPs (5.6 mg/kg, intraperitoneal) induced increased production of pro-inflammatory cytokines in the serum and the brain of mice. A synergistic reaction between aging and ZnO NP exposure occurred regarding serum interleukin 1 (IL-1) and interleukin 6 (IL-6). In the brain, increased oxidative stress level, impaired learning and memory abilities, and hippocampal pathological changes were identified, especially in old mice, following ZnO NP exposure. Then, a potential mechanism of cognitive impairment was examined. The contents of hippocampal cAMP response element binding protein (CREB), phosphorylated CREB, synapsin I, and cAMP were decreased in an age-dependent manner, and the most substantial decrease occurred in old mice treated with ZnO NPs. These findings demonstrated for the first time that aging and ZnO NP exposure synergistically influenced systemic inflammation, and indicated old individuals were more susceptible to ZnO NP-induced neurotoxicity. One of the mechanisms might due to the supression of cAMP/CREB signaling. [ABSTRACT FROM AUTHOR]