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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]

Non-coding RNAs appear to be involved in the regulation of the nervous system. However, no competing endogenous RNA (ceRNA) network related to PM 2.5 damage in the hippocampal function has yet been constructed. Herein, we used whole-transcriptome sequencing technology to systematically study the ceRNA network in rat hippocampi after PM 2.5 exposure. We identified 100 circRNAs, 67 lncRNAs, 28 miRNAs, and 539 mRNAs and constructed the most comprehensive ceRNA network to date, to our knowledge. Gene Ontology and KEGG analyses showed that the network molecules are involved in synapses, neural projections, and neural development and involve signal pathways such as the synaptic vesicle cycle. Finally, the expression of the differentially expressed RNAs confirmed by quantitative real-time PCR was consistent with the sequencing data. This study systematically dissected the ceRNA atlas related to cognitive memory function in the hippocampal tissue of PM 2.5 -exposed rats for the first time, to our knowledge, and promotes the development of potential new treatments for cognitive impairment. Unlabelled Image • The exposure of PM 2.5 can destroyhippocampal tissue and cognitive function of rats. • The most comprehensive ceRNA networks were identified and constructed by whole transcriptome sequencing for the first time. • GO and KEGG analysis showed the network are involved in process related to cognitive. • These results could provide a potential therapeutic target of cognitive dysfunction after PM 2.5 exposure. [ABSTRACT FROM AUTHOR]

Previous studies have shown that early-life exposure to fine particulate matter (PM2.5) is associated with an increasing risk of autism spectrum disorder (ASD), however, the specific sensitive period of ASD is unknown. Here, a model of dynamic whole-body concentrated PM2.5 exposure in pre- and early-postnatal male offspring rats (MORs) was established. And we found that early postnatal PM2.5 exposed rats showed more typical ASD behavioral characteristics than maternal pregnancy exposure rats, including poor social interaction, novelty avoidance and anxiety disorder. And more severe oxidative stress and inflammatory responses were observed in early postnatal PM2.5 exposed rats. Moreover, the expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) was down-regulated and the ratios of p-PI3K/PI3K and p-AKT/AKT were up-regulated in early postnatal PM2.5 exposed rats. This study suggests that early postnatal exposure to PM2.5 is more susceptible to ASD-like phenotype in offspring than maternal pregnancy exposure and the activation of PI3K-AKT signaling pathway may represent underlying mechanisms. • Early postnatal PM2.5 exposure induced more pronounced ASD-like phenotype in male offspring rats than maternal exposure. • Early postnatal period may be a sensitive window for PM2.5 to trigger autism spectrum disorder development. • PM2.5 exposure caused neuroinflammation and reduced anti-inflammatory melatonin levels in offspring rat brains. • PI3K-AKT pathway activation may link developmental PM2.5 exposure and autism spectrum disorder pathogenesis. [ABSTRACT FROM AUTHOR]

Exposure to fine atmospheric particulate matter (PM) is known to induce lung inflammation and injury; however, the way in which sophisticated endogenous lung repair and regenerative programs respond to this exposure remains unknown. In this study, we established a whole-body mouse exposure model to mimic real scenarios. Exposure to fine PM (PM with an aerodynamic diameter ≤ 2.5 µm [PM 2.5 ]; mean 1.05 mg/m3) for 1-month elicited inflammatory infiltration and epithelial alterations in the lung, which were resolved 6 months after cessation of exposure. Immune cells that responded to PM 2.5 exposure mainly included macrophages and neutrophils. During PM 2.5 exposure, alveolar epithelial type 2 cells initiated rapid repair of alveolar epithelial mucosa through proliferation. However, the reparative capacity of airway progenitor cells (club cells) was impaired, which may have been related to the oxidative production of neutrophils or macrophages, as suggested in organoid co-cultures. These data suggested that the pulmonary toxic effects of short-term exposure to fine atmospheric PM at a certain dosage could be overcome through tissue reparative mechanisms. [Display omitted] • Short-term whole-body PM 2.5 exposure induces transient lung inflammation and injury. • Lung stromal, endothelial, epithelial, and immune cells respond to PM 2.5 exposure. • Airway and alveolar progenitor cells show differential response to PM 2.5 exposure. • Neutrophils and macrophages impair functions of airway progenitor cells. [ABSTRACT FROM AUTHOR]

Exposure to PM 2.5 can aggravate the occurrence and development of bronchial asthma and fibrosis. Here, we investigated the differences in bronchial injury caused by different exposure modes of PM 2.5 (high concentration intermittent exposure and low concentration continuous exposure), and the mechanism of macrophage activation and respiratory immune imbalance induced by PM 2.5 , leading to bronchial asthma and airway fibrosis using animal and cell models. A "PM 2.5 real-time online concentrated animal whole-body exposure system" was used to conduct PM 2.5 respiratory exposure of Wistar rats for 12 weeks, which can enhance oxidative stress in rat bronchus, activate epithelial cells and macrophages, release chemokines, recruit inflammatory cells, release inflammatory factors and extracellular matrix, promote bronchial mucus hypersecretion, inhibit the expression of epithelial cytoskeletal proteins, destroy airway barrier, and induce asthma. Furthermore, PM 2.5 induced M2 polarization in lung bronchial macrophages through JAK/STAT and PI3K/Akt signaling pathways, and compared with low concentration continuous exposure, high concentration intermittent exposure of PM 2.5 could regulate significantly higher expression of TIPE2 protein through promoter methylation of TIPE2 DNA, thereby activating PI3K/Akt signaling pathway and more effectively inducing M2 polarization of macrophages. Additionally, activated macrophages release IL-23, and activated epithelial cells and macrophages released TGF-β1, which promoted the differentiation of Th17 cells, triggered the Th17 dominant immune response, and activated the TGF-β1/Smad2 signaling pathway, finally causing bronchial fibrosis. Moreover, when the total amount of PM 2.5 exposure was equal, high concentration-intermittent exposure was more serious than low concentration-continuous exposure. In vitro experiments, the co-culture models of PM 2.5 with BEAS-2B, WL-38 and rat primary alveolar macrophages further confirmed that PM 2.5 could induce the macrophage activation through oxidative stress and TIPE2 DNA methylation, and activate the TGF-β1/Smad2 signaling pathway, leading to the occurrence of bronchial fibrosis. [Display omitted] • PM 2.5 exposure activated macrophages and epithelial cells to induce airway fibrosis. • PM 2.5 exposure triggered respiratory immune imbalance through Th17 cells activation. • PM 2.5 -induced above toxic effects was induced by oxidative stress mechanism. • PM 2.5 High-dose intermittent exposure is more harm than low-dose continuous exposure. • The difference between different exposure modes was related to TIPE2 DNA methylation. [ABSTRACT FROM AUTHOR]

The molecular mechanisms of PM 2.5 exposure in the male reproductive system, have scarcely been studied. Here, we demonstrate the possible relationship and molecular mechanisms between endoplasmic reticulum stress (ERS), oxidative stress, and reproductive toxicity caused by PM 2.5. A "PM 2.5 real-time online concentrated animal whole-body exposure system" was employed to expose male Wistar rats to PM 2.5 for 12 weeks, which could induce sperm quality decline, apoptosis, inflammation, oxidative stress, ERS, and histopathological damage in the testis. In vitro study on cultured primary testicular spermatogonia and Leydig cells confirmed that treatment with PM 2.5 (0–320 μg/mL) for 24 h decreased cell survival rate, increased reactive oxygen species, lactate dehydrogenase and 8-hydroxydeoxyguanosine levels, induced DNA damage, ERS and apoptosis, and inhibit the secretion and synthesis of testosterone in Leydig cells. These results clarified that ERS pathways triggered by oxidative stress could significantly induce CHOP and caspase-12 activation, which are significantly associated with cell apoptosis. However, oxidative stress and ERS inhibitors significantly inhibited the occurrence of these injuries. In conclusion, PM 2.5 triggers the ERS pathway and induces DNA damage in rat testicular cells through oxidative stress, ultimately leading to cellular apoptosis. Furthermore, high-concentration intermittent inhalation was more harmful than low-concentration continuous inhalation when the total mass of PM 2.5 exposure was the same. [Display omitted] • PM 2.5 can cause reproductive toxicity in male Wistar rats. • PM 2.5 can cause DNA damage and ERS in male rat germ cells through oxidative stress. • PM 2.5 can activate ERS-mediated CHOP and Caspase-12 apoptosis pathways. • PM 2.5 can activate the DNA damage-mediated mitochondrial apoptosis pathway. • High-dose PM 2.5 intermittent exposure is more toxic than low-dose continuous exposure. [ABSTRACT FROM AUTHOR]

[Display omitted] • Long-term exposure to PM 2.5 can induce pulmonary fibrosis via the degradation of Caveolin-1. • PM 2.5 can reduce Caveolin-1 protein by ERS induced-autophagy to activate TGF-β1/Smad3 pathway. • PM 2.5 can promote Caveolin-1 interact with the TGF-β1 type Ⅱ receptor. • High-dose PM 2.5 intermittent exposure is more toxic than low-dose continuous exposure. Air pollution is highly associated with respiratory diseases. However, the influence and mechanism of particulate matter with aerodynamic equal to or less than 2.5 μm (PM 2.5) in lung homeostasis remain unclear. Herein, we demonstrated the induction of pulmonary fibrosis (PF) by PM 2.5 exposure. The animal model showed that PM 2.5 exposure could activate the oxidative stress and inflammation response, promoting epithelial-mesenchymal transition and accumulation of collagen, high expression of pro-fibrotic factors, and pathological characteristics of fibrosis. The proteomic analysis indicated that PM 2.5 exposure decreased the expression of caveolin-1 (Cav-1), and many differential proteins were enriched in the TGF-β1/Smad, endoplasmic reticulum stress (ERS) and autophagy pathways. Combining in vivo and in vitro experiments, it was found that PM 2.5 exposure could reduce Cav-1 protein levels and activate TGF-β1/Smad3 signaling pathways through ERS and autophagy pathways, thereby inducing cell apoptosis and promoting pulmonary fibrosis. However, inhibiting ERS could alleviate the occurrence of autophagy, and blocking the autophagy system could increase the level of Cav-1 protein and inhibit TGF- β 1/Smad3 signaling pathway to improve pulmonary fibrosis. Therefore, we demonstrated that the exposure of PM 2.5 could enhance the ERS induced-autophagy-mediated Cav-1 degradation, thus activating the TGF-β1/Smad3 axis to promote pneumonocytes apoptosis and overproduction of extracellular matrix (ECM), finally aggravating PF. Moreover, our findings revealed that intermittent exposure to high doses of PM 2.5 was more toxic than continuous exposure to low dose. [ABSTRACT FROM AUTHOR]