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Fine particulate matter (PM2.5) increases the risks of lung cancer. Epigenetics provides a new toxicology mechanism for the adverse health effects of PM2.5. However, the regulating mechanisms of PM2.5 exposure on candidate gene DNA methylation changes in the development of lung cancer remain unclear. Abnormal expression of the glutathione S transferase (GST) gene is associated with cancer. However, the relationship between PM2.5 and DNA methylation-mediated GST gene expression is not well understood. In this study, we performed GST DNA methylation analysis and GST-related gene expression in human A549 cells exposed to PM2.5 (0, 50, 100 µg/mL, from Taiyuan, China) for 24 h (n = 4). We found that PM2.5 may cause DNA oxidative damage to cells and the elevation of GSTP1 promotes cell resistance to reactive oxygen species (ROS). The Kelch-1ike ECH-associated protein l (Keap1)/nuclear factor NF-E2-related factor 2 (Nrf2) pathway activates the GSTP1. The decrease in the DNA methylation level of the GSTP1 gene enhances GSTP1 expression. GST DNA methylation is associated with reduced levels of 5-methylcytosine (5mC), DNA methyltransferase 1 (DNMT1), and histone deacetylases 3 (HDAC3). The GSTM1 was not sensitive to PM2.5 stimulation. Our findings suggest that PM2.5 activates GSTP1 to defend PM2.5-induced ROS and 8-hydroxy-deoxyguanosine (8-OHdG) formation through the Keap1/Nrf2 signaling pathway and GSTP1 DNA methylation. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the association between time restricted feeding (TRF) and different areas of cognitive function in the elderly in Chinese communities. This study consisted of 1353 community-dwelling Chinese older adults aged 60 years and older in Chongming area, Shanghai (563 males; the mean age, 73.38 ± 6.16 years). Mild cognitive impairment (MCI) and six different cognitive domains was assessed by the Chinese-version of Mini Mental State Examination (MMSE). Recording the eating time of each meal through oral inquiry to calculate the time window between the first meal and the last meal of the average day. Participants with an eating time window duration of more than 10 h were then identified, as well as those with eating time restricted to less than 10 h (TRF). Our study found that TRF may be associated with a higher incidence rate of cognitive impairment. TRF only limited the eating time window and did not change the frequency of participants' dietary intake. We used a linear regression model to study the association of TRF with cognitive function. After adjusting for confounding variables, the results showed that TRF was related to MMSE score (P < 0.001), "Orientation to place" (P < 0.001) and "Attention/calculation" (P < 0.001) functions. Among Chinese older community-dwellers, TRF was associated with a higher prevalence of CI and negatively correlated with the "Orientation to place" and "attention/calculation" functions. [ABSTRACT FROM AUTHOR]

• The catalyst activated PDS efficiently with high stability and generalizability. • The complexation of AL with RM favored the exposure of Fe active sites and adsorption of PDS. • The electron transfer pathway was the main pathway for PDS activation and SMZ degradation. • DFT demonstrated that Fe-active species are the primary site where electron transfer occurs. • T.E.S.T and biological experiments predicted lower toxicity of degradation intermediates. Advanced oxidation processes based on peroxydisulfate (PDS-AOPs) have been used for the remediation of organic wastewater. However, the mechanism for the generation of electron transfer sub-stable complexes in the metal–carbon/PDS system has not been fully elucidated. Herein, two environmental solid wastes were selected to synthesize a novel Fe-carbon catalyst (RM@KC 1:2 –800) using alkali lignin as the carrier and red mud (RM) as the iron source, and applied for peroxydisulfate (PDS) activation in sulfamethazine (SMZ) removal. The complexation of alkali lignin with RM favored the exposure of Fe active sites and adsorption of PDS. 97% of SMZ could be removed efficiently in the RM@KC 1:2 –800/PDS system, and the degradation efficiency remained at 80.81% after 5 cycles without metal leaching, which was suitable for a variety of natural water bodies. Combined with density functional theory (DFT) and other analyses confirmed that the electron transfer pathway is the main pathway for PDS activation and SMZ degradation. And the reactive Fe species were the active sites that contributed to the adsorption of PDS on the RM@KC 1:2 –800 surface to form sub-stable complexes (RM@KC-PDS*), whereby the electron transfer occurred. Surprisingly, the prediction of environmental toxicity of the degradation intermediates based on T.E.S.T software and biological experiments proved their environmental friendliness. Overall, this study follows the concept of "waste-to-waste" and proposes a strategy for a suitable and cost-effective Fe-carbon catalyst for large-scale production, while demonstrating its potential application in the treatment of organic wastewater. [ABSTRACT FROM AUTHOR]

Abstract Exposure to airborne fine particulate matter (PM 2.5) is associated with various adverse effects. However, the molecular mechanism involved in PM 2.5 -elicited energy metabolic reprogramming and the toxic chemical determinants within PM 2.5 are not well elucidated. In this study, nontargeted and targeted metabolomics research were conducted to investigate the overall metabolic changes and relevant toxicological pathways caused by Taiyuan winter total PM 2.5 and its water soluble and organic soluble fractions in human lung bronchial epithelial cells (BEAS-2B). The results showed that significant metabolome alterations in BEAS-2B cells were observed after the exposure of total PM 2.5 and its organic soluble fraction. Purine metabolism, arginine and proline metabolism, glutathione (GSH) metabolism, tricarboxylic acid (TCA) cycle and glycolysis were mainly affected. Along with a significant increase of reactive oxygen species (ROS), malondialdehyde (MDA), nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), obvious metabolic phenotype remodeling from oxidative phosphorylation to glycolysis was found in BEAS-2B cells treated with total PM 2.5 and its organic soluble fraction. Compared with water soluble fraction, organic soluble fraction was found to play the dominant role in PM 2.5 toxicity. Our study provided novel insights into the mechanism of PM 2.5 -elicited toxicity. Graphical abstract Unlabelled Image Highlights • Metabolomics was applied to study the toxic impacts of Taiyuan winter total PM 2.5 and its different fractions. • PM 2.5 majorly perturbed purine metabolism, arginine and proline metabolism and energy metabolism. • PM 2.5 induced cell energy metabolic reprogramming from oxidative phosphorylation to glycolysis. • Organic soluble fraction played the major role in PM 2.5 toxicity. [ABSTRACT FROM AUTHOR]

Abstract Carbon dots (CDs) have attracted much attention in a variety of fields owing to the diversified properties. However, the control of the structure and surface function of CDs are still urgent issues to be addressed for using it in specific application. Herein, the reduced state of carbon nanodots (R-CDs) has been produced through a convenient strategy by reduction of the pure carbon dots products, which was utilized as a good candidate of matrix for direct analysis of bisphenol (BP) analogs in negative-ion surface-assisted laser desorption/ionization time-of-flight mass spectrometry (SALDI-TOF MS). Due to the dominant hydroxyl groups on the surface of R-CDs, they were easier to absorb BPs through hydrogen bonding and van der Waals interactions, resulting in highly efficient detection of BPs. Meanwhile, compared with the organic matrix and raw carbon dots, the superior surface structure and properties of this R-CDs surface provide various advantages including low background noise, outstanding sensitivity and salt tolerance. This work opens a door for developing R-CDs as alternative substrate in SALDI-TOF MS for direct detection of small molecule pollutants. Graphical abstract fx1 Highlights • Reduced carbon nanodots (R-CDs) was used as a novel candidate for detection bisphenol analogs (BPs) in SALDI-TOF MS. • The R-CDs-assisted LDI MS exhibited low background noise, high sensitivity and salt tolerance in analysis of BPs. • This work provides a good alternative substrate to SALDI-TOF MS and expands the CDs’ new application scope. [ABSTRACT FROM AUTHOR]

A new atmospheric pressure gas chromatography-tandem mass spectrometry (APGC-MS/MS) was developed to simultaneously separate, identify and quantify 18 nitro-polyaromatic hydrocarbons (NPAHs) in air fine particulate matter (PM 2.5 ). Compared with traditional negative chemical ionization (NCI) or electron impact ionization (EI)-MS/MS methods, APGC-MS/MS equipped with an atmospheric pressure chemical ionization (APCI) source provided better sensitivity and selectivity for NPAHs analysis in PM 2.5 .18 NPAHs were completely separated, and satisfactory linear response (R 2  > 0.99), low instrumental detection limits (0.20–2.18 pg mL −1 ) and method detection limits (0.001–0.015 pg m −3 ) were achieved. Due to the reliable performance of the instrument, only minimal sample pretreatment is needed. It ensured the satisfactory method recovery (70%–120%) and qualified repeatability (RSD: 1.1%–17.2%), which met the requirement of trace analysis of NAPHs in the real environmental PM 2.5 . Using the developed method, the actual PM 2.5 samples collected from Taiyuan, China in both summer and winter were analyzed, and 17 NPAHs but 2-nitrofluorene were detected and quantified. According to the obtained NAPH concentration results, the generation mechanism of NPAHs in PM 2.5 and the effects on NPAHs formation caused by some ambient air pollutants were preliminarily discussed: secondary photochemical reaction might be the dominant source of NPAHs in PM 2.5 collected from Taiyuan in both summer and winter; ambient air pollutants (NO 2 , SO 2 , CO) had more contribution on the NPAHs secondary formation of PM 2.5 in winter. [ABSTRACT FROM AUTHOR]

1-Nitropyrene (1-NP) is a mutagenic and carcinogenic pollutant very widespread in the environment. However, the relative investigations on genotoxicity, oxidative stress and metabolic enzymes in lungs of mammalian caused by 1-NP have not been fully established. In this study, the 1-NP solutions at 3 dosages (1.0 × 10 −5 , 4.0 × 10 −5 and 1.6 × 10 −4 mg/kg body weight) were respectively given to rats by the intratracheal instillation. The responses of 1-NP on DNA damage and repair, oxidative stress and metabolism biomarkers in rat lungs after exposure to 1-NP were measured. The results showed 1-NP at three dosages induced obvious DNA strand breaks, 8-OH-dG formation and DNA-protein cross-link in rat lungs compared with the control. Higher dosage 1-NP (4.0 × 10 −5 and 1.6 × 10 −4 mg/kg body weight) greatly activated DNA repair gene OGG1 and inhibited MTH1 and XRCC1 expressions, and they significantly elevated the levels of GADD153, heme oxygenase-1 and malondialdehyde and decreased SOD activity, accompanied by the increases of CYP450, CYP1A1, CYP1A2 and GST levels. These results suggested the genotoxicity of 1-NP might rely on 1-NP-caused DNA damage and its combined effects on the suppression of DNA repair and the enhancement of oxidative stress and metabolic enzyme activity. [ABSTRACT FROM AUTHOR]

Currently, microplastic pollution is more serious and complicates the toxic effects of other co-existing pollutants in the environment. However, the effect and mechanism of biodegradable plastics on the growth and metabolism of probiotic remain unclear. This work selected Bacillus amyloliquefaciens as model bacterium for a three-day exposure experiment to probe the issues. The results showed that 100 mg/L polylactic acid microplastics (PLA MPs) (3–4 mm, flake shape) caused oxidative damage to cell membranes, disrupted cell wall composition and inhibited cell growth by 21.2–27.5 %. The toxicity was not simply additive or synergistic effects when PLA MPs (100 mg/L) and copper ions (10 mg/L) coexisted. PLA MPs did not significantly increase the toxicity of copper to bacteria, instead triggered some mechanisms to resist the toxicity of copper. The bacteria formed spores to resist PLA MPs, while the copper ions toxicity was weaken by chelation and efflux. It is worth noting that copper ions instead increased the expression of genes related fengycin and iturin then improving the bacteriostatic activity of the probiotic. This paper deeply analyzes the toxicity mechanism of combined pollution on Bacillus amyloliquefacien, and also provides new perspective for helping to inhibit pathogenic bacteria under biodegradable microplastics and metal stress. [Display omitted] • Paper discussed the toxicity of biodegradable microplastics and copper on probiotic. • Polylactic acid microplastics still had a certain toxicity to bacteria. • The toxicity of combined pollutants was not simple synergistic or additive effects. • Pollutants might instead improve the bacteriostatic effect of inoculants. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) and sulfur dioxide (SO2) are 2 common air pollutants, but their toxicological effects of coexposure are still not fully clear. In this study, SO2 exposure (5.6 mg/m³) couldn't cause obvious inflammatory responses in rat lungs. The PM2.5 exposure (1.5 mg/kg body weight) increased inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and some inflammation damage. Importantly, SO2 and PM2.5 (1.5, 6.0, and 24.0 mg/kg) coexposure induced pathological and ultrastructural damage and raised inflammatory cells in BALF compared with the control. Also, they significantly elevated the levels of proinflammatory cytokines, adhesion molecule, and nitric oxide (NO) and promoted the gene expression of nuclear factor kappa B (NF-κB), phosphorylated p38 (p-p38), and Toll-like receptor 4 (TLR4) in rat lungs treated with higher dose of PM2.5 (6.0 and 24.0 mg/kg) plus SO2 relative to the control or SO2 group, along with the decreased inhibitor of NF-κBa and increased inhibitor of NFκB kinase β expressions. The changes in the inflammatory markers in the presence of PM2.5 plus SO2 were not significant compared with the PM2.5 group. The results indicated that inflammatory injury and pathological and ultrastructural damage in rat lungs exposed to PM2.5 plus SO2 were involved in TLR4/p38/NF-κB pathway activation accompanied by oversecretion of proinflammatory cytokine, adhesion molecule, and NO. It provides more useful evidence to understand the possible toxicological mechanism that PM2.5 and SO2 copollution exacerbate lung disease. [ABSTRACT FROM AUTHOR]

Lignin exhibits some antioxidant and UV protection due to its large number of phenolic hydroxyl and methoxy groups, which can be used in the field of sun protection. However, its complex macromolecular structure, high polydispersity, low solubility and deep coloration limit their development in the sunscreen field. In this work, we purified and separated lignin by solvent fractionation so that its phenolic hydroxyl content could be retained or even increased without modification. Consequently, by controlling environmental factors, lignin rapidly self-assembles into nanospheres without changing its structure, which not only achieves the standard of light-colored lignin but also meets the requirement of high sunscreen performance. It was measured that the lignin nanospheres formed by this method could meet more than 90% of UV blocking, especially for ultraviolet (UVA) fragments, when mixed with commercially available creams. It not only promotes the application of lignin in the field of sun protection, realizes the sustainable development of lignin, but also alleviates the problem of solid waste treatment and disposal. [Display omitted] • Lignin fractions with different molecular weight, functional groups and solubility were obtained by solvent fractionation. • The union of solvent fractionation and self-assembly avoids the modification of lignin and promotes the synthesis of NPs. • Lignin sunscreens block UV rays up to 90% or more, especially for the UVA portion. • Compared with other methods for reducing lignin color rendering, it is simpler and environmentally friendly. • 30g of bamboo chips can meet the synthesis demand of sunscreen and realize the resource utilization of solid waste. [ABSTRACT FROM AUTHOR]

Epidemiological studies suggested that ambient fine particulate matter (PM 2.5 ) exposure was associated with cardiovascular disease. However, the underlying mechanism, especially the mitochondrial damage mechanism, of PM 2.5 -induced heart acute injury is still unclear. In this study, the alterations of mitochondrial morphology and mitochondrial fission/fusion gene expression, oxidative stress, calcium homeostasis and inflammation in hearts of rats exposed to PM 2.5 with different dosages (0.375, 1.5, 6.0 and 24.0 mg/kg body weight) were investigated. The results indicated that the PM 2.5 exposure induced pathological changes and ultra-structural damage in hearts such as mitochondrial swell and cristae disorder. Furthermore, PM 2.5 exposure significantly increased specific mitochondrial fission/fusion gene (Fis1, Mfn1, Mfn2, Drp1 and OPA1) expression in rat hearts. These changes were accompanied by decreases of activities of superoxide dismutase (SOD), Na + K + -ATPase and Ca 2+ -ATPase and increases of levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) as well as levels of pro-inflammatory mediators including TNF-α, IL-6 and IL-1β in rat hearts. The results implicate that mitochondrial damage, oxidative stress, cellular homeostasis imbalance and inflammation are potentially important mechanisms for the PM 2.5 -induced heart injury, and may have relations with cardiovascular disease. [ABSTRACT FROM AUTHOR]

Exposure to sulfur dioxide (SO2) increases asthma risk. Inflammatory and immune responses are typical in asthma disease. The exact effect of SO2 on modulation of the inflammatory and immune responses in asthmatic rats remains unclear. Objectives Here we sought to investigate the molecular mechanisms underlying the NF-κB inflammatory pathway and the Th1/Th2 imbalance in asthmatic rats exposed to SO2. Methods Male Wistar rats were challenged by ovalbumin (OVA) or SO2 alone or together, and then mRNA and protein levels of some inflammatory and immune genes were measured. NF-κB nuclear translocation was analyzed. Bronchoalveolar lavage (BAL), inflammatory cell counts and histopathologic examination were performed. Results (1) OVA plus SO2 induced abnormal pathological changes and inflammatory responses in lung relative to exposure to OVA alone; (2) showing NF-κB nuclear translocation and activation through up-regulating IKKβ mRNA and protein expression and down-regulating IκBα expression in the presence of OVA or OVA plus SO2; (3) OVA plus SO2 significantly raised TNF-α and IL-6 levels in BALF compared with the OVA group; (4) SO2 markedly elevated IL-4 levels and decreased IFN-γ levels in BALF in the asthmatic rats, stimulating IgE generation which was closely related to inhibiting the expression of Foxp3, a specific marker of regulatory T cells. Conclusions SO2 affects the airway inflammatory and immune responses of the asthmatic rats and enhances the susceptibility to OVA by aggravating inflammatory responses in lungs, up-regulating pro-inflammatory cytokine expression, and causing the Th1/Th2 imbalance, which might contribute to the increased risk of asthma disease. [ABSTRACT FROM AUTHOR]

Exposure to 2-amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine (PhIP), a typical example of heterocyclic amine compounds, increases colon cancer risk. Seabuckthorn (SBT) seed oil is a biologically active substance extracted from seeds of wildHippophae rhamnoides L. Here, we sought to investigate the toxicological mechanisms underlying oxidative stress and cancer-related gene expression in the rat colons as well as the protective effect of SBT seed oil against colonic oxidative damage. Our results showed that PhIP significantly decreased the anti-oxidative enzyme activities whereas increased the malondialdehyde (MDA) contents, protein carbonyl (PCO) levels and DNA-protein cross-links (DPC) coefficients in the rat colons compared with the solvent-control group. Moreover, PhIP activated expression of c-fos and c-jun and inhibited p16 and Rb expression. Additionally, SBT seed oil plus PhIP significantly improved antioxidant markers and reduced the levels of MDA, PCO and DPC compared to those in rats exposed to PhIP alone. These data indicated that PhIP could induce oxidative stress and abnormal alterations of cancer-related gene expression in the rat colons while SBT seed oil may be beneficial because of its ability to alleviate the PhIP-induced oxidative damage to the rats. [ABSTRACT FROM AUTHOR]

Abstract: 2-Amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine (PhIP) is one of the most abundant heterocyclic amines (HCAs) generated from overcooking meat at high temperatures. To understand the possible mechanism of PhIP-associated stomach cancer, the effects of PhIP on morphology, oxidative stress, gene expression of c-fos, c-jun and p16 in rat stomachs were investigated. The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) PhIP (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and glutathioneperoxidase (GPx) activities, while increased catalase (CAT) activity compared with the control. With the elevated doses of PhIP, malondialdehyde (MDA) contents, protein carbonyl (PCO) contents and DNA–protein crosslinks (DPC) coefficients were significantly raised in a dose-dependent manner; (3) PhIP at the doses of 10mg/kg and/or 15mg/kg significantly inhibited p16 mRNA and protein expression, whereas enhanced c-fos and c-jun expression relative to control. The data indicated that PhIP could cause stomach injury, oxidative stress in rat stomachs as well as the activation of c-fos and c-jun and inactivation of p16, which may play a role in the pathogenesis of PhIP-associated stomach cancer. [Copyright &y& Elsevier]

Abstract: Sulfur dioxide (SO2) is a common gaseous pollutant. It is also, however, endogenously generated from sulfur-containing amino acids. Recent studies have demonstrated that rat blood pressure can be lowered by SO2-exposure in vivo and that vasodilation caused by SO2 at low concentrations (<450μM) is endothelium-dependent in rat aorta. However, effects of SO2 on nitric oxide synthase (NOS) and nitric oxide (NO) production have not been previously studied in rat aorta. The objective of the present study is to assess the effects of acute (10min) and prolonged (2h) stimulation with different concentrations of SO2 on NO/cGMP pathway in isolated rat aorta. The results show that: (1) the acute and prolonged pretreatments with SO2 produced an inhibition of vasoconstrictions induced by norepinephrine. (2) SO2 potentiated activity of endothelial nitric oxide synthase (eNOS), but not of induced NOS (iNOS). (3) SO2 could increase expression of eNOS gene on the transcription and translation levels in rat aorta. (4) SO2 enhanced NO formation in aortic tissue. (5) The level of cGMP in rat aorta was increased by SO2 and no change of cAMP. These findings led to the conclusion: there were acute and prolonged effects of SO2 on the NO/cGMP signalling pathway; and SO2 could upregulate the eNOS–NO–cGMP pathway and at least partly by which the SO2 might cause vasodilation and inhibition to vasoconstriction. [ABSTRACT FROM AUTHOR]

Inhibition of cell apoptosis is an increasingly important factor in modulating airway inflammation in asthma, which is related to environmental pollutants. To investigate the effects of sulfur dioxide (SO2) on the mRNA and protein expressions of apoptosis-related genes in lungs from asthmatic rats, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (2 ppm) inhalation alone or together. Examinations were performed 24 h after the last treatment. The mRNA and protein levels of p53, bax, and bcl-2 were analyzed in lungs using real-time reverse transcription-polymerase chain reaction (RT-PCR) assay and Western blot analysis, respectively. The results indicated that increases of bcl-2 or decreases of p53 and bax mRNA and protein levels were not significant in lungs of rats exposed to SO2 alone, compared with controls, but elevated or reduced levels of these genes appeared in lungs of asthmatic rats exposed to SO2 plus OVA, compared with controls, suggesting that SO2 exposure could result in OVA-induced increases or decreases of transcription and translation levels of these apoptosis-related genes in rat lungs, and may have relations to airway inflammation in asthma. The regulation mechanism of apoptosis in asthma disease exposure to SO2 needs further study. [ABSTRACT FROM AUTHOR]

Abstract: Sulfur dioxide (SO2) is a common air pollutant, and inhaled SO2 in airway epithelium easily forms its soluble derivatives in vivo (bisulfite and sulfite), which are toxic to the respiratory system and related to the exacerbation of asthma. In order to study the possible asthmatic molecular mechanism of SO2 and its derivatives, the dose-response and time-response relationships of SO2 derivatives on gene expressions of some asthma-related genes in human bronchial epithelial cells (BEP2D) were investigated. The mRNA and protein levels of EGF, EGFR, ICAM-1 and COX-2 were analyzed in BEP2D cells using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, radio-immunoassay (RIA) method and Western blot analysis, respectively. The results showed that SO2 derivatives caused the dose-dependent inductive expressions of four gene mRNA and protein in BEP2D cells. Moreover, SO2 derivatives significantly increased the mRNA and protein levels at 0, 0.5, 1, 4 and 24h post-exposure, along with the highest inductions at 0.5h post-exposure for EGFR and COX-2 and at 4h post-exposure for EGF and ICAM-1. It was suggested that SO2 derivatives could increase the expressions of EGF, EGFR, ICAM-1 and COX-2 on the transcription and translation levels in BEP2D cells, and result in mucus over-production and inflammation responses. This might be one of the possible mechanisms that SO2 aggravates asthma disease. [Copyright &y& Elsevier]

Abstract: Asthma is a chronic inflammatory disease characterized by infiltration and activation of various inflammatory cells and mucus secretion. To investigate the effects of SO2 on the expressions of asthma related-genes, male Wistar rats were challenged by ovalbumin (OVA) or SO2 (2ppm) inhalation alone or together. Bronchoalveolar lavage and histopathologic examination were performed 24h after the last treatment. The mRNA and protein levels of MUC5AC and ICAM-1 were analyzed in lungs and tracheas using real-time reverse transcription-polymerase chain reaction (real-time RT-PCR) assay, immunohistochemistry method and Western blot analysis, respectively. Exposure to OVA or to OVA plus inhaled SO2 significantly caused increases of the mRNA and protein levels of MUC5AC and ICAM-1 in lungs and tracheas of rats compared with the control (P <0.05 or P <0.01), but the increases of mRNA and protein levels after SO2 inhalation were not statistically significant. Exposure to OVA plus inhaled SO2 significantly not only induced the mRNA and protein expressions of these genes, but also induced the infiltration of inflammatory cells in lungs and tracheas and the increase of the numbers of inflammatory cells in bronchoalveolar lavage fluids (BALF), versus exposure to OVA alone. Meanwhile, a synergistic effect on the pathological changes between SO2 and OVA was observed in lungs after SO2 and OVA exposure. These results suggested that SO2 could increase the expressions of MUC5AC and ICAM-1 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms that SO2 pollution aggravates asthma disease. [Copyright &y& Elsevier]

To study whether sulfur dioxide (SO 2 ) can enter into the different organs of mice exposed to SO 2 , the sulfite contents in brains, hearts, and lungs from male mice were determined by high-performance liquid chromatography with fluorescence detection (HPLC-FD). After reduction and precolumn derivation of tissue homogenates of brains, hearts, and lungs from mice, the mixture was centrifuged, and 5µl of the resulting supernatant was directly injected into HPLC; the mobile phase consisted of methanol–phosphoric acid (12:88, v/v), and for the fluorescence detection ? EX 392 nm and? EM —479 nm were used. The standard curve was linear in the range from 0.126 µg/ml to 126 µg/ml; the minimal detectable concentration was 0.04µg/ml (S/N = 3), the average methodological recoveries were from 97% to 101%, and the within-day and between-day precisions were less than 9%. These results showed that sulfite contents in all organs tested from mice in the SO 2 -exposed groups were significantly increased (p .92) compared with the control groups. These results indicated SO 2 could transform into sulfite in vivo after inhalation, and could distribute into lung and other organs such as brain and heart. These results offered a support for the viewpoint that SO 2 is a systemic toxic agent. [ABSTRACT FROM AUTHOR]

The atmosphere's fine particulate matter (PM2.5) can enter the liver through the circulatory system, leading to hepatic inflammation and fibrosis. As a non-flavonoid polyphenolic compound, resveratrol (RES) has anti-oxidant, anti-inflammatory and hepatoprotective effects, but the molecular mechanisms of liver fibrosis induced by PM2.5 exposure are still limited. In this study, we established an in vitro cell model to investigate the intervention effect of RES with different concentrations (5 and 20 μmol/mL) on mouse hepatic stellate cells (mHSCs) injury induced by PM2.5 (100 μg/mL). We determined the cell viability in mHSCs after treatment with PM2.5 or/and RES for 24 h. We investigated the intracellular oxidative stress by detecting the changes in reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) levels. We also measured the protein expressions of fibrosis-related genes (α-SMA, Collagen I and Collagen III) and key genes (SIRT1, NF-κB, NLRP3, Cleaved-Caspase1, IL-1β) in the NLRP3 pathway in mHSCs exposed to PM2.5 with or without RES. The results showed that (1) PM2.5 has cytotoxic effects on mHSCs, whereas RES (5 μmol/L and 20 μmol/L) inhibited PM2.5-induced cytotoxicity and LDH leakage; (2) RES effectively reduces ROS and MDA production caused by PM2.5 while concurrently enhancing SOD levels, thereby improving cellular anti-oxidant capacity; (3) the expression of α-SMA, Collagen I and Collagen III were notably downregulated in the PM2.5 plus RES treatment group compared to the PM2.5-exposed group; (4) RES significantly increased SIRT1 expression and decreased the expression of NF-κB, NLRP3, Cleaved-Caspase1 and IL-1β in mHSCs exposure to PM2.5 compared to the PM2.5 group. These results demonstrate that RES can up-regulate SIRT1 and mitigate PM2.5-induced fibrosis by suppressing oxidative stress in mHSCs and the SIRT1/NF–κB/NLRP3 pathway activated by PM2.5. [ABSTRACT FROM AUTHOR]

To realize high-precision and high-frequency unattended site calibration and detection of satellites, automatic direction adjustment must be implemented in mirror arrays. This paper proposes a high-precision automatic calibration model based on a novel point light source tracking system for mirror arrays. A camera automatically observes the solar vector, and an observation equation coupling the image space and local coordinate systems is established. High-precision calibration of the system is realized through geometric error calculation of multipoint observation data. Moreover, model error analysis and solar tracking verification experiments are conducted. The standard deviations of the pitch angle and azimuth angle errors are 0.0176° and 0.0305°, respectively. The root mean square errors of the image centroid contrast are 2.0995 and 0.8689 pixels along the x- and y-axes, respectively. The corresponding pixel angular resolution errors are 0.0377° and 0.0144°, and the comprehensive angle resolution error is 0.0403°. The calculated model values are consistent with the measured data, validating the model. The proposed point light source tracking system can satisfy the requirements of high-resolution, high-precision, high-frequency on-orbit satellite radiometric calibration and modulation transfer function detection. [ABSTRACT FROM AUTHOR]

• Modes of natural and industrial degradation of lignin are reviewed. • The changes of lignin structure and properties by organic solvent extraction and ionic liquid isolation are reviewed. • Organic solvent extraction can retain the inherent structure of lignin to the greatest extent and exploit native activity. • The types of products vary with the types of ionic liquids. • The challenges of lignin separation methods and the future development of ionic liquids are reviewed. The complex interlacing structure among cellulose, hemicellulose and lignin and the unique properties of lignin itself limit the value-added utilization of the lignin. As the "upstream" process of biorefinery, lignin separation technology is very important for lignin conversion into high-value materials. However, it is not easy to extract lignin with relatively complete structure without affecting performance from biomass raw materials. Notably, most of reviews regarding lignin focus on its degradation. The extraction or separation methods are not introduced in detail, and the effects of these methods on raw materials or lignin have not been reported. Herein, this paper critically reviews the changes in physicochemical properties and structure of lignin caused by several mild organic solvent extraction methods and new ionic liquids which has been widely used in recent years. Furthermore, the application and potential economic benefits of these lignin are summarized. These methods promote the effective utilization of lignin, which is no longer limited to heat energy, but also alleviates the solid waste disposal problem caused by lignin as waste stream. Finally, perspectives on the future research on the lignin separation, depolymerization and application are highlighted. This review may provide an insight for the development of bio-refining technology. [ABSTRACT FROM AUTHOR]

Atmospheric fine particulate matter exposure (PM 2.5) can increase the incidence and mortality of heart disease, and raise the risk of fetal congenital heart defect, which have recently drawn much attention. In this study, C57BL/6 mice were exposed to PM 2.5 (approximately equivalent to 174 μg/m3) by intratracheal instillation during the gestation. After birth, 10 weeks old offspring mice were divided into four groups: male exposed group (ME), female exposed group (FE), male control group (MC), female control group (FC). The pathological injury, pro-inflammatory cytokines, histone acetylation levels, and expressions of GATA-binding protein 4 (GATA4) and downstream genes were investigated. The results showed that exposure to PM 2.5 in utero increased pathological damage and TNF-α and IL-6 levels in hearts of offspring mice, and effects in ME were more serious than FE. Notably, GATA4 protein levels in hearts in ME were significantly lower than that of MC, accompanied by down-regulation of histone acetyltransferase (HAT)-p300 and up-regulation of histone deacetylase-SIRT3. As GATA4 downstream genes, ratios of β-MHC gene expression to α-MHC significantly raised in ME relative to the MC. Results of chromatin immunoprecipitation (ChIP)-qPCR assay found that binding levels of acetylated histone 3 lysine 9 (H3K9ac) in GATA4 promoter region in the hearts of ME or FE were markedly decreased compared with their corresponding control groups. It suggested that maternal exposure to PM 2.5 may cause cardiac injury in the offspring, heart damage of male mice was worse than female mice, in which process HAT-p300, H3K9ac, transcription factor GATA4 may play an important regulation role. Image 1 • PM 2.5 exposure in utero caused heart injury and inflammation in offspring mice. • GATA4 expression decline along with p300 down-regulation and SIRT3 up-regulation. • Binding levels of H3K9ac in GATA4 promoter region were related to GATA4 expression. • Gender differences of mouse heart damage after PM 2.5 exposure in utero exist. [ABSTRACT FROM AUTHOR]

[Display omitted] The coexistence of antibiotic resistance genes (ARGs) and antibiotic-resistant bacteria (ARB) in the environment poses a potential threat to public health. In our study, we have developed a novel advanced oxidation process for simultaneously removing ARGs and ARB by two types of iron and nitrogen-doped biochar derived from rice straw (FeN-RBC) and sludge (FeN-SBC). All viable ARB (approximately 108 CFU mL−1) was inactivated in the FeN-RBC/ peroxymonosulfate (PMS) system within 40 min and did not regrow after 48 h even in real water samples. Flow cytometry identified 96.7 % of dead cells in the FeN-RBC/PMS system, which verified the complete inactivation of ARB. Thorough disinfection of ARB was associated with the disruption of cell membranes and intracellular enzymes related to the antioxidant system. Whereas live bacteria (approximately 200 CFU mL−1) remained after FeN-SBC/PMS treatment. Intracellular and extracellular ARGs (tetA and tetB) were efficiently degraded in the FeN-RBC/PMS system. The production of active species, primarily •OH, SO 4 •- and Fe (IV), as well as electron transfer, were essential to the effective disinfection of FeN-RBC/PMS. In comparison with FeN-SBC, the better catalytic performance of FeN-RBC was mainly ascribed to its higher amount of pyridine-N and Fe0, and more reactive active sites (such as C O group and Fe-N sites). Density functional theory calculations indicated the greater adsorption energy and Bader charge, more stable Fe-O bond, more easily broken O O bond in FeN-RBC/PMS, which demonstrated the stronger electron transfer capacity between FeN-RBC and PMS. To encapsulate, our study provided an efficient and dependable method for the simultaneous elimination of ARGs and ARB in water. [ABSTRACT FROM AUTHOR]

• PM 2.5 triggers mitochondrial morphological and function damage of H9c2 cells. • MiR-421/SIRT3 pathway regulates cardiac mitochondrial dynamics imbalance after PM 2.5 treatment. • MiR-421 inhibitor and resveratrol protect PM 2.5 -induced mitochondrial damage. Fine particulate matter (PM 2.5) exposure is associated with cardiovascular disease (CVD) morbidity and mortality. Mitochondria are sensitive targets of PM 2.5 , and mitochondrial dysfunction is closely related to the occurrence of CVD. The epigenetic mechanism of PM 2.5 -triggered mitochondrial injury of cardiomyocytes is unclear. This study focused on the miR-421/SIRT3 signaling pathway to investigate the regulatory mechanism in cardiac mitochondrial dynamics imbalance in rat H9c2 cells induced by PM 2.5. Results illustrated that PM 2.5 impaired mitochondrial function and caused dynamics homeostasis imbalance. Besides, PM 2.5 up-regulated miR-421 and down-regulated SIRT3 gene expression, along with decreasing p-FOXO3a (SIRT3 downstream target gene) and p-Parkin expression and triggering abnormal expression of fusion gene OPA1 and fission gene Drp1. Further, miR-421 inhibitor (miR-421i) and resveratrol significantly elevated the SIRT3 levels in H9c2 cells after PM 2.5 exposure and mediated the expression of SOD2, OPA1 and Drp1, restoring the mitochondrial morphology and function. It suggests that miR-421/SIRT3 pathway plays an epigenetic regulatory role in mitochondrial damage induced by PM 2.5 and that miR-421i and resveratrol exert protective effects against PM 2.5 -incurred cardiotoxicity. [Display omitted] [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) is a common pollutant, and its health risk has attracted much attention. Studies have shown that PM2.5 exposure is associated with liver disease. The composition of PM2.5 is complex, and its hepatotoxic effects and lipid metabolism process are not well understood. In this study, we detected the concentrations of PM2.5 and its components (metals and polycyclic aromatic hydrocarbon (PAHs)) in the winter in Taiyuan, Shanxi Province, China, from 2017 to 2020 and then assessed the health risks. We also investigated the effects of different components (whole particles (WP), water-soluble particles (WSP), organic particles (OP)) of PM2.5 on the cytotoxicity and lipid metabolism in human liver cell line (HepG2) after 24 h of treatment. The changes in cytotoxicity indexes (LDH, IL-6, reactive oxygen species (ROS)) and lipids (triglyceride (TG), free fatty acid (FFA)) were measured after 24 h. The mRNA expression of lipid metabolism-related factors (SREBP1, CD36, MTTP) was determined by real-time quantitative RT-qPCR. Finally, the correlation between metals and PAHs with higher PM2.5 content in 4 years and biomarkers was analyzed. The results showed that: (1) The PM2.5 pollution was severe in Taiyuan during winter in 2017 and the subsequent four years. The calculation results of the metal enrichment factor (EF) value and PAHs characteristic ratio of PM2.5 showed that PM2.5 pollution sources differed in different years. (2) Exposure to metals and PAHs in PM2.5 did not cause a non-carcinogenic risk. Metals had no cancer risk, while PAHs inhaled in PM2.5 in 2017 and 2018 had a potential cancer risk. The atmospheric PM2.5 pollution in Taiyuan has had a downward trend, but the PAHs in the PM2.5 of 2017–18, when the pollution is relatively serious, have a potential carcinogenic risk. (3) WP, OP and WSP inhibited cell survival rate from 2017 to 2020, and OP had higher cytotoxicity at the same concentration. (4) WP, OP and WSP increased the levels of LDH, IL-6, TNF-α, ROS, MDA, TG and FFA, and inhibited SOD activity in a dose-effect relationship. The organic components in PM2.5 are more toxic to HepG2 cells and affect the expression of lipid metabolism-related factors at the transcriptional level. (5) The mRNA expressions of factors related to lipid synthesis, uptake, oxidation and output were up-regulated after treatment with PM2.5 and its components, suggesting a lipid metabolism disorder. (6) The biomarkers were associated with certain metals (Zn, Pb, Cu and Cr) and PAHs in PM2.5. These suggested that PM2.5- and PM2.5-bound organic matter caused HepG2 cytotoxicity and affected lipid metabolism. [ABSTRACT FROM AUTHOR]

[Display omitted] Structural information of grassland changes on the Tibetan Plateau is essential for understanding alterations in critical ecosystem functioning and their underlying drivers that may reflect environmental changes. However, such information at the regional scale is still lacking due to methodological limitations. Beyond remote sensing indicators only recognizing vegetation productivity, we utilized multivariate data fusion and deep learning to characterize formation-based plant community structure in alpine grasslands at the regional scale of the Tibetan Plateau for the first time and compared it with the earlier version of Vegetation Map of China for historical changes. Over the past 40 years, we revealed that (1) the proportion of alpine meadows in alpine grasslands increased from 50% to 69%, well-reflecting the warming and wetting trend; (2) dominances of Kobresia pygmaea and Stipa purpurea formations in alpine meadows and steppes were strengthened to 76% and 92%, respectively; (3) the climate factor mainly drove the distribution of Stipa purpurea formation, but not the recent distribution of Kobresia pygmaea formation that was likely shaped by human activities. Therefore, the underlying mechanisms of grassland changes over the past 40 years were considered to be formation dependent. Overall, the first exploration for structural information of plant community changes in this study not only provides a new perspective to understand drivers of grassland changes and their spatial heterogeneity at the regional scale of the Tibetan Plateau, but also innovates large-scale vegetation study paradigm. [ABSTRACT FROM AUTHOR]

Abstract A new method for the determination of 19 polyaromatic hydrocarbons (PAHs) and 12 hydroxy-polyaromatic hydrocarbons (OHPAHs) in fine particulate matter (PM 2.5) was developed using atmospheric pressure gas chromatography-tandem mass spectrometry (APGC-MS/MS). Better sensitivity was achieved by APGC-MS/MS than conventional liquid chromatography or gas chromatography coupled with mass spectrometry. The method detection limits (< 0.4 pg m−3 for PAHs and < 0.076 pg m−3 for OHPAHs), recoveries (67.7–120%), repeatability (RSD of 0.9–19.1%) and linearity (R2 > 0.99) were obtained for the analysis of PM 2.5 samples. The content profile of 19 PAHs and 12 OHPAHs were successfully obtained in 55 PM 2.5 samples collected from two major Chinese megacities, Taiyuan and Guangzhou, in both summer and winter by this method. Based on the concentrations, possible emission sources for the pollutants were also identified. Graphical abstract fx1 Highlights • APGC-MS/MS achieved lower LODs of 19 PAHs and 12 OHPAHs in PM 2.5 than previous method. • 19 PAHs and 12 OHPAHs in PM 2.5 all could be detected by APGC-MS/MS. • Pollution characteristics of PAHs/OHPAHs in PM 2.5 were obtained based on determined concentrations. [ABSTRACT FROM AUTHOR]

PM 2.5 aggravated brain pathological injury and inflammatory responses in of AD mice. PM 2.5 increased Aβ−42 expression and induced neurotransmitter imbalance in AD mice. Selected miRNAs and genes have potential regulatory roles in brain of PM 2.5 -AD mice. Predicted signal pathways are significant in clarifying mechanism of PM 2.5 -caused AD. Fine particulate matter (PM 2.5) is associated with increased risks of Alzheimer's disease (AD), yet the toxicological mechanisms of PM 2.5 promoting AD remain unclear. In this study, wild-type and APP/PS1 transgenic mice (AD mice) were exposed to either filtered air (FA) or PM 2.5 for eight weeks with a real-world exposure system in Taiyuan, China (mean PM 2.5 concentration in the cage was 61 µg/m3). We found that PM 2.5 exposure could remarkably aggravate AD mice's ethological and brain ultrastructural damage, along with the elevation of the pro-inflammatory cytokines (IL-6 and TNF-α), Aβ-42 and AChE levels and the decline of ChAT levels in the brains. Based on high-throughput sequencing results, some differentially expressed (DE) mRNAs and DE miRNAs in the brains of AD mice after PM 2.5 exposure were screened. Using RT-qPCR, seven DE miRNAs (mmu-miR-193b-5p, 122b-5p, 466h-3p, 10b-5p, 1895, 384–5p, and 6412) and six genes (Pcdhgb8, Unc13b, Robo3, Prph, Pter, and Tbata) were evidenced the and verified. Two miRNA-target gene pairs (miR-125b-Pcdhgb8 pair and miR-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/AChE pairs) were demonstrated that they were more related to PM 2.5 -induced brain injury. Results of Gene Ontology (GO) pathways and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways predicted that synaptic and postsynaptic regulation, axon guidance, Wnt, MAPK, and mTOR pathways might be the possible regulatory mechanisms associated with pathological response. These revealed that PM 2.5 -elevated pro-inflammatory cytokine levels and PM 2.5 -altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising miRNA and mRNA biomarkers and potential miRNA-mRNA interaction networks of PM 2.5 -promoted AD. [Display omitted]. [ABSTRACT FROM AUTHOR]

Exposure to fine particulate matter (PM 2.5 ) has a close association with respiratory damage. Vitamin c and quercetin have been documented to possess antioxidant and anti-inflammation properties. However, their potential protective effects against PM 2.5 -induced respiratory damage have not been evaluated yet. Hence, the study was aimed to investigate their protective effects and delineate the possible mechanisms. The results indicated that PM 2.5 depleted the cell viability of 16HBE cells, elevated reactive oxygen species (ROS) generation, and inhibited mitochondrial genes expressions, including fusion proteins Mfn1 and OPA1 , along with biogenesis markers SIRT1 and p53R2 . Additionally, the damage of mitochondrial morphology was observed upon PM 2.5 exposure using both JC-1 and MitoTracker Red staining. Expressions of mitochondrial respiratory chain genes including NDUFS2 and UQCRI1 were also attenuated by PM 2.5 exposure. Furthermore, PM 2.5 promoted the mRNA levels of NADPH oxidase and inflammation cytokines. However, the addition of vitamin c or quercetin strikingly antagonized the PM 2.5 -induced toxic effects. Collectively, these findings suggest that vitamin c and quercetin have repressive roles in respiratory oxidative damage incurred by PM 2.5 , which provide the theoretical basis about intervention and control of food nutrients on PM 2.5 -induced human adverse health. [ABSTRACT FROM AUTHOR]

Macrophyte rhizospheric dissolved organic matter (ROM) served as widespread abiotic components in aquatic ecosystems, and its effects on antibiotic residues and antibiotic resistance genes (ARGs) could not be ignored. However, specific influencing mechanisms for ROM on the fate of antibiotic residues and expression of ARGs still remained unclear. Herein, laboratory hydroponic experiments for water lettuce (Pistia stratiotes) were carried out to explore mutual interactions among ROM, sulfamethoxazole (SMX), bacterial community, and ARGs expression. Results showed ROM directly affect SMX concentrations through the binding process, while C O and N-H groups were main binding sites for ROM. Dynamic changes of ROM molecular composition diversified the DOM pool due to microbe-mediated oxidoreduction, with enrichment of heteroatoms (N, S, P) and decreased aromaticity. Microbial community analysis showed SMX pressure significantly stimulated the succession of bacterial structure in both bulk water and rhizospheric biofilms. Furthermore, network analysis further confirmed ROM bio-labile compositions as energy sources and electron shuttles directly influenced microbial structure, thereby facilitating proliferation of antibiotic resistant bacteria (Methylotenera, Sphingobium, Az spirillum) and ARGs (sul 1, sul 2, intl 1). This investigation will provide scientific supports for the control of antibiotic residues and corresponding ARGs in aquatic ecosystems. [Display omitted] • Amide and amino groups in ROM are main binding sites for sulfamethoxazole. • ROM bio-labile compositions are closely linked to microbial metabolisms. • ROM fractions favored the formation of rhizospheric biofilms. • SMX pressure stimulated the succession of bacterial community. • Rhizospheric biofilms offered favorable microenvironments for ARB development. [ABSTRACT FROM AUTHOR]

[Display omitted] • Lamellar cluster LDH in situ grew on the MIL-88A template. • Dispersed LDH covers stably activate PMS at wide circumneutral pH from 2.5 to 10.5. • Disequilibrium of hydrolysis-precipitation in limit pH caused catalysis declines. • ROSs reconfiguration and dissociable SMT reactivity were examined in limited pH. • Toxicity of structural rearrangements in sulfonamide moiety was revealed. The development of effective and reliable Fenton-like catalytic systems in circumneutral pH is a longstanding interest. Metal-organic framework derivatives become promising catalyst candidates due to high catalytic accessibility and structural flexibility, but their stability remains in doubt. Herein, a MIL-88A self-templating strategy to synthesize structurally decentralized FeCo-layered-double hydroxide (FeCo-LDH, M−FCL) was proposed. The well-constructed M−FCL 3 presented superior peroxymonosulfate (PMS) activation for nearly 100 % sulfamethazine (SMT) degradation within 15 min, which was virtually wobble-slight in the pH = 2.5 ∼ 10.5 range. The performance decrease at limiting pH was mainly ascribed to activity-blocked of M−FCL 3 by analyzing the involved reaction substrates and reactive oxygen species. In specific, the hydrolytic detachment or excessive aggregation of surface-active FeCo-LDH occurred at limiting pH with unbalanced hydrolysis-coprecipitation. Especially, theoretical calculations further exposed that the loss of dominated active Co site and the formation of inert SMT+ dissociating species were detrimental to the catalytic process in acidic environments. Nevertheless, the well-founded resistance of the constructed M−FCL 3 /PMS system to interference and its ability to operate for a long period proved its potential for application in near-neutral environments. This work raised concern for the variations of Fenton-like catalysis at limiting pH, promoting the application of MOF-derived LDH for environmental remediation. [ABSTRACT FROM AUTHOR]

A simple and rapid method that uses synthesized magnetic graphene composites as both an adsorbent for enrichment and as a matrix in MALDI-TOF MS analysis was developed for the detection of nitropolycyclic hydrocarbons (nitro-PAHs) in PM2.5 samples. Three nitro-PAHs were detected down to sub pg μL−1 levels based on calculations from an instrumental signal-to-noise better than 3, which shows the feasibility of using the new materials in MALDI-TOF MS as a potential powerful analytical approach for the analysis of nitro-PAHs in PM2.5 samples. [ABSTRACT FROM AUTHOR]

The aim of the study is to investigate chemical compositions of fine chalk dust particles (chalk PM 2.5 ) and examine their adverse effects on alveolar macrophages (AMs) in vitro . Morphologies and element concentrations of individual chalk particles were analyzed by using the quantitative energy-dispersive electron probe X-ray microanalysis (ED-EPMA). The oxidative response of AMs and the potential to generate nitric oxide (NO) by luminol-dependent chemiluminescence (CL) and nitrate reductase method were assessed 4 h following the treatment of AMs with differing dosages of fine chalk particles, respectively. Oxidative stress and cytotoxicity elicited by chalk PM 2.5 were also examined. The results showed that fine chalk particles were mainly composed of gypsum, calcite, dolomite and a little amount of organic adhesives. Exposure to chalk PM 2.5 at 100 μg mL −1 or 300 μg mL −1 significantly increased intracellular catalase, malondialdehyde, and NO levels and decreased superoxide dismutase level in AMs, leading to leakage of lactate dehydrogenase (LDH) and reduction of the cell viability. Furthermore, luminol-dependent CL from respiratory burst in AMs was enhanced. It was suggested that chalk PM 2.5 could make oxidative damages on AMs and result in cytotoxicity, being likely attributed to excessive reactive oxygen species or reactive nitrogen species induced by mixture of fine gypsum and calcite/dolomite particles. [ABSTRACT FROM AUTHOR]

[Display omitted] Heavy metal pollution in water bodies is a serious environmental problem continuously, which requires urgently seeking an efficient and cost-effective solution. Apatite as the most abundant phosphate on earth exhibits remarkable adsorption effect on heavy metals. Based on this, three kinds of apatite adsorbents were prepared in this study by titration co-precipitation method for the removal of heavy metals Pb (II) and Cd (II) from water. In the single system, the maximum adsorption capacity of hydroxyapatite (Hap), chlorapatite (Clap), and fluorapatite (Fap) for Pb (II) was 1597.16 mg/g, 1477.82 mg/g, and 1455.99 mg/g, for Cd (II) were Hap (107.18 mg/g), Clap (79.08 mg/g) and Fap (15.8 mg/g). Pb (II) was more competitive than Cd (II) in binary metal system. Apatite adsorbents mainly remove Pb (II) and Cd (II) from solution by dissolution precipitation, electrostatic attraction, surface complexation and ion exchange. The results of this study show that the three kinds of apatite adsorbents exhibited excellent adsorption performance for Pb (II), and also had a certain removal effect for Cd (II). Therefore, the three kinds of apatite have certain application prospects in heavy metal wastewater treatment. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to investigate the contamination levels of antibiotics and antibiotic resistance genes (ARGs) in the landfill leachates and their correlations with the bacteria. Methods and results: Using HPLC‐MS, quantitative PCR and high‐throughput sequencing, we measured the pollution levels of 14 antibiotics and 10 ARGs in the leachates of the landfill in Taiyuan, China, and analysed changes in the bacterial community and the correlations of bacteria with antibiotics and ARGs. The main results showed high levels of antibiotics (like enrofloxacin, pefloxacin and oxytetracycline) and ARGs (like sulfonamides, tetracycline, macrolides, quinolones and β‐lactam‐resistance genes) in the landfill leachates, along with higher diversity and richness of the bacteria. Some types of antibiotics had positive correlations with their corresponding ARGs. The dominant bacteria in the landfill leachates were Pseudomonas, Defluviitoga and Sulfurimonas, which correlated with the antibiotics and ARGs and might have potential effects on degrading them. Conclusions: Antibiotics and ARG pollution existed in the landfill leachates, while bacteria were closely associated with them. Significance and impact of the study: It will provide helpful information for the potential application of the bacteria in antibiotics and ARGs pollution control and landfill leachate management. [ABSTRACT FROM AUTHOR]

Background: The toxicological effects of fine particulate matter (PM2.5) on the cardiopulmonary and nervous systems have been studied widely, whereas the study of PM2.5 on systemic toxicity is not in-depth enough. Lipopolysaccharide (LPS) can cause multiple organ damage. The combined effects of co-exposure of PM2.5 plus LPS on the stomach, spleen, intestine, and kidney are still unclear. Purpose: This study was aimed to explore the toxicological effects of co-exposure of PM2.5 and LPS on the different organs of mice. Research Design and Study Sample Using a real-ambient PM2.5 exposure system and an intraperitoneal LPS injection mouse model, we investigated multiple organ damage effects on male BALB/c mice after co-exposure of PM2.5 plus LPS for 23 weeks in Linfen, a city with a high PM2.5 concentration in China. Data Collection: Eosin-hematoxylin staining, ELISA and the biochemical assay analysed the toxicological effects. Results: The pathological tissue injury on the four organs above appeared in mice co-exposed to PM2.5 plus LPS, accompanied by the body weight and stomach organ coefficient abnormality, and significant elevation of pro-inflammatory cytokines levels, oxidative stress in the spleen and kidney, and levels of kidney injury molecule (KIM-1) increase in the kidney. There were tissue differences in the pathological damage and toxicological effects on mice after co-exposure, in which the spleen and kidney were more sensitive to pollutants. In the PM2.5 + LPS group, the superoxide dismutase inhibition and catalase (CAT) activity promotion in the kidney or spleen of mice were significant relative to the PM2.5 group; the CAT and interleukin-6 (IL-6) levels in the spleen were raised considerably compared with the LPS group. Conclusions: These findings suggested the severity and sensitivity of multiple organ injuries in mice in response to PM2.5 plus LPS. [ABSTRACT FROM AUTHOR]

Simulation of fine particulate matter (PM 2.5) exposure is essential for evaluating adverse health effects. In this work, an ambient exposure system that mimicked real atmospheric conditions was installed in Taiyuan, China to study impacts of chronic PM 2.5 exposure on adult and aged mice as well as Sirtuin3 knockout (Sirt3 KO) mice and wild-type (WT) mice. The real-ambient exposure system eliminated the possible artificial effects caused from exposure experiments and maintained the physiochemical characteristics of PM 2.5. The case studies indicated that aged mice exhibited apparent heart dysfunction involving increased heart rate and decreased blood pressure after 17-week of real-ambient PM 2.5 exposure. Meanwhile, 15-week of real-ambient PM 2.5 exposure decreased the heart rate and amounts of associated catecholamines to induce heart failure in Sirt3 KO mice. Additionally, the increased pro-inflammatory cytokines and decreased platelet related indices suggested that inflammation occurred. The changes of biomarkers detected by targeted metabolomics confirmed metabolic disorder in WT and Sirt3 KO mice after exposed to real-ambient PM 2.5. These results indicated that the real-ambient PM 2.5 exposure system could evaluate the risks of certain diseases associated with air pollution and have great potential for supporting the investigations of PM 2.5 effects on other types of rodent models. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] Gestational exposure to PM 2.5 is associated with adverse postnatal outcomes. PM 2.5 can enter alveoli by using intratracheal instillation, even penetrate through lung cells into the blood circulation. Subsequently, they are transferred across the placenta and fetal blood brain barrier, causing the adverse birth outcomes of offspring. This study demonstrated that the gestational exposure resulted in cognitive and emotional disorders in female offspring although the offspring were not exposed to PM 2.5. Placental metabolic pathways modulated fetal brain development and played a pivotal role for maternal-placental-fetal interactions in the fetal programming of adult behavioral and mental disorders. Samples of fetus, offspring hippocampus and placenta from the mice exposed to PM 2.5 were investigated using a comprehensive approach including mass spectrometry-based lipidomics and three-dimensional imaging. The exposure induced the neuro-degeneration in hippocampus, impairment of placental cytoarchitecture, and reprogramming of lipidome, which might affect the modulation of maternal-fetal cross-talk and result in the behavior disorders of offspring. The variation of spatial distribution of lipids was profoundly affected in dorsal pallium and hippocampal formation regions of fetal brain, offspring hippocampus, as well as labyrinth and junctional zones of placenta. The abundance alteration of lipid markers associated with neurodegenerative diseases was validated in transgenic mouse model with Alzheimer's disease and human cerebrospinal fluid from patients with Parkinson's disease. The finding could help with the selection of more suitable heterogeneous-related substructures targeting PM 2.5 exposure and the exploration of PM 2.5 -induced toxicological effects on neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

• Graphene-based freestanding catalysts have renewed research interests. • Material and energy efficiencies are two important evaluation criteria for energy conversion and storage devices. • Surface and interface engineering can produce electronic conduction and active sites for energy storage devices. • Important synergy between different components can benefit capacitance performance. Next-generation energy storage methods are closely related to green recovery in the post-pandemic period and the future energy structure. Advanced graphene-based freestanding electrodes with highly tunable electronic structures and mechanical stability present superior electrochemical performance, which are among the most promising candidates for achieving efficient energy storage. However, the ever-increasing demand for energy has triggered significant room for the growth of material and energy efficiencies of graphene-based freestanding electrodes. Fortunately, their intrinsic reactivity can be improved by atomic-level tailoring of the surfaces and interfaces of electrodes. Therefore, there is an urgent need for researchers to grasp the relationship between the structure and electrochemical performance of graphene-based freestanding electrodes. In this review, we presented a focused discussion and multidimensional analysis of graphene-based freestanding electrodes, including the predictive design of valence electron structure, mechanistic understanding of conversion and storage, and performance evaluation in practical application. Moreover, future research aspects of the graphene-based freestanding electrodes are proposed. [ABSTRACT FROM AUTHOR]

The concentrations of ambient fine particulate matter (PM2.5) and its compositions in urban Taiyuan, China during a typical winter and summer time period in 2017 were measured to investigate the pollution characteristics, source apportionment and health risks assessment of PM2.5 pollution. The results demonstrated that the mean daily mass concentration of PM2.5 in winter (102.6 ± 6.2 μg/m3) was higher than that in summer (65.0 ± 17.2 μg/m3) during sampling. The relatively high concentrations of heavy metals (Zn, Pb, Cu, As, Ni, Cr and Cd), anion (SO42−, NO3−, Cl− and F−) and high-molecular-weight PAHs in PM2.5 were observed. The enrichment factors (EFs) values, special diagnostic ratios like ratios of NO3−/SO42− and individual PAHs concentration ratio showed that coal combustion and vehicle emissions were the major sources of PM2.5 pollution. Health risk assessment illustrated that mean hazard indices for non-cancer and cancer risk of all analyzed metals were within the safe range. However, inhalation exposure to PM2.5-bound PAHs had carcinogenic risk, while not indicating non-carcinogenic risk. Taken together, although PM2.5 pollution was alleviated to some extent, PM2.5 pollution in 2017 was still serious and PM2.5 was mainly originated from coal burning, especially, in which PM2.5-bound PAHs in Taiyuan may pose a potential health risk. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) exposure increases the risk of asthma. However, the effect of PM 2.5 exposure on liver metabolism in mice with asthma symptoms remains unclear. We established an ovalbumin (OVA)-induced asthma model in mice and divided the animals into four groups: control group (C), PM 2.5 exposure group (P), OVA-induced asthma group (O) and OVA-induced asthma PM 2.5 exposure group (OP). Gas chromatography-mass spectrometry (GC-MS) was used to identify the metabolite markers and related perturbed metabolic pathways in mouse liver tissue after PM 2.5 exposure. Multivariate analysis showed 9 and 12 potential metabolite markers in the P and OP groups, respectively, after PM 2.5 exposure that were significantly correlated with lipid peroxidation indices. PM 2.5 exposure perturbed 5 and 7 metabolic pathways in the P and OP groups, respectively. These metabolic pathways mainly involve the lipid metabolism, amino acid metabolism, carbohydrate metabolism, and nucleotide metabolism. These results highlight the potential to study PM 2.5 -triggered alterations via liver tissue in normal and OVA-induced asthmatic mice to gain a more realistic appraisal of the resulting early toxicity events. Additionally, these results revealed potential metabolite markers of early antioxidant defense events triggered by PM 2.5 and indicated that metabolite markers are more sensitive than antioxidant indicators. Image 1 • Metabolic disorders were observed in liver tissues of normal mice and OVA-induced asthma mice after PM 2.5 exposure. • After exposure to PM 2.5 , 9 and 12 metabolic markers were screened in normal mice and asthmatic mice, respectively. • Perturbed metabolic pathways mainly involved the metabolism of lipid, amino acid, carbohydrate, and nucleotide metabolism. • Metabolomics plays a significant role in exploring the toxicity mechanism of PM 2.5 in mouse liver. [ABSTRACT FROM AUTHOR]

Microplastics pollution in environments has become a major concern and it has been proven to have adverse impacts on plants, so there is an urgent to find approaches to alleviate the detrimental effects of microplastics. In our study, we investigated the influence of polystyrene microplastics (PSMPs) on the growth, photosynthesis, and oxidative defense system changes of ryegrass, as well as the behavior of MPs at roots. Then three types of nanomaterials were applied to alleviate the adverse impact of PSMPs on ryegrass, which were nano zero-valent iron (nZVI), carboxymethylcellulose-modified-nZVI (C-nZVI) and sulfidated nZVI (S-nZVI), respectively. Our results suggested that PSMPs had significant toxicity to ryegrass, leading to decrease of shoot weight, shoot length and root length. Three nanomaterials regained the weight of ryegrass to a varying extent and made more PSMPs aggregate near roots. In addition, C-nZVI and S-nZVI facilitated the entrance of PSMPs into the root and promoted the chlorophyll a and chlorophyll b contents in leaves. Analysis of antioxidant enzymes and malondialdehyde content indicated that ryegrass coped well with the internalization of PSMPs, and all three types of nZVI could alleviate PSMPs-stress in ryegrass. This study elaborates the toxicity of MPs on plants and provides a novel insight into the fixing of MPs by plants and nanomaterials in environments, which needs to be further explored in future research. [Display omitted] • PSMPs decreased biomass, length and photosynthetic pigments of plants. • Three types of nZVI all alleviated the toxicity of PSMPs. • Three types of nZVI all promoted plant growth under exposure of PSMPs. • C-nZVI and S-nZVI facilitated the internalization of PSMPs. • S-nZVI might have a more alleviation on the oxidative stress when exposed to PSMPs. [ABSTRACT FROM AUTHOR]

A magnetic covalent organic framework nanomaterial (Fe3O4@COFs) served as an adsorbent for enrichment and a new matrix for SALDI-TOF-MS analysis of PAHs and their derivatives in PM2.5. The unique properties of Fe3O4@COFs in terms of high enrichment ability and matrix-free interference made it possible for sensitive analysis of low-concentration organic small-molecule pollutants in complex environmental samples. [ABSTRACT FROM AUTHOR]

Abstract The risk of development of asthma, a multi-faceted chronic disease, increases as a result of exposure to PM 2.5. However, the mechanism underlying asthma-related metabolic changes caused by PM 2.5 exposure is unclear. Here, we investigated the major metabolic changes, metabolic pathways involved, and underlying molecular mechanisms in mice with PM 2.5 exposure-induced asthma. Forty-eight adult female mice were randomly assigned to control (C), low concentration-PM 2.5 exposure: 0.50 mg kg−1 (L), medium concentration-PM 2.5 exposure: 1.58 mg kg−1 (M), and high concentration-PM 2.5 exposure: 4.98 mg kg−1 (H) groups. M and H groups presented significantly higher IL-4, IL-8, IL-1β, IL-5, IL-13, and OVA-specific IgE levels, and significantly lower IFN-γ levels, than the C group, as well as significantly increased eosinophil count and MUC5AC expression in the lung tissue. These findings indicate that exposure to medium and high concentrations of PM 2.5 induced asthma in mice. Statistical analyses identified 13 asthma-related major metabolites, which were analyzed by gas chromatography-mass spectrometry (GC-MS). Meta Mapp Software revealed 4 major metabolic pathways. PM 2.5 -induced ATP requirement and oxidative stress may perturb metabolic processes in asthma. The present findings increase our understanding of the toxic effect of PM 2.5 in the development of asthma and identify potentially useful biomarkers. Graphical abstract Image 1 Highlights • PM 2.5 induces asthma in mice. • GC-MS analysis identified 13 biomarkers in PM 2.5 -induced asthmatic mice. • Screening identified four metabolic pathways involved in the pathogenesis of asthma. • PM 2.5 regulates amino acid and purine metabolism by disrupting the TCA cycle. [ABSTRACT FROM AUTHOR]

Abstract Toxic chemicals such as flame retardants are associated with atmospheric fine particles (PM 2.5), which are an important pollutant in the world. In this study, a sensitive method using gas chromatography-tandem triple quadrupole mass spectrometry combined with ultrasonic-assisted extraction and multi-phase column purification was developed for simultaneously determination of 29 flame retardants including halogenated flame retardants (HFRs) and organophosphate flame retardants (OPFRs) in PM 2.5 samples. Extraction time, as well as the type and volume of elution solvent were optimized. The recoveries of all target flame retardants from PM 2.5 samples were in the range of 70%‒130%, with good repeatability and reproducibility (0.39%‒17.4%). The instrumental detection limits (IDLs) and method quantitation limits (MQLs) of HFRs were in the range of 0.004‒5.44 pg and 0.002‒2.52 pg m−3, while those of OPFRs were 0.003‒0.23 pg and 0.07‒5.41 pg m−3, respectively. The developed method has been successfully applied for analysis of target flame retardants in atmospheric PM 2.5 collected from the cities of Guangzhou and Taiyuan, China. HFRs were found at concentrations of 45.7‒1230 pg m−3 and 51.2‒82.3 pg m−3 in Guangzhou and Taiyuan. The concentrations of HFRs were lower than those of OPFRs, which were detected at concentrations of 6004‒49,800 pg m−3 and 16,741‒34,346 pg m−3 in Guangzhou and Taiyuan. Accordingly, the analytical method is robust and useful for further elucidating the contamination profiles of flame retardants in PM 2.5. Graphical abstract fx1 Highlights • A sensitive method for analysis of 17 HFRs and 12 OPFRs in PM 2.5 was developed. • MQLs of most OPFRs by GC-MS/MS were lower than the reported MQLs by GC-MS. • Good performance characteristics were obtained for all target flame retardants. • The method was successfully applied for analysis of PM 2.5 in different areas. [ABSTRACT FROM AUTHOR]

Abstract Exposure to ambient fine particulate matter (PM 2.5) is associated with neurodegenerative diseases. Mitochondrion is key to brain degeneration. However, the underlying mechanism of PM 2.5 -induced brain injury, especially mitochondrial damage, is still unclear. In this study, changes in mitochondrial dynamics, mitochondrial permeability transition pore (mPTP), mitochondrial DNA (mtDNA) and oxidative stress in human SH-SY5Y cells exposed to PM 2.5 at different concentrations (0, 25, 100, and 250 μg mL−1) were investigated. The results showed that PM 2.5 caused more mitochondrial swell, accompanied by the opening of mPTP and the decrease of ATP levels, mitochondrial membrane potential and mtDNA copy number in SH-SY5Y cells. PM 2.5 significantly enhanced the expression of mitochondrial fission/fusion genes (Drp1 and OPA1) and affected the gene expression of CypD, SIRT3, and COX Ⅳ in SH-SY5Y cells. Besides, PM 2.5 triggered the increase of cellular ROS, Ca2+ and Aβ-42 levels, inhibition of manganese-superoxide dismutase (SOD 2) activities, reduction of GSH levels GSH/GSSG ratio, and elevation of mitochondrial malondialdehyde contents. It suggests that mitochondrial dysfunction and oxidative stress are the potential mechanisms underlying PM 2.5 -induced brain nerve cell injury, which may be related to neurological diseases. Additionally, our study elucidated that PM 2.5 components trigger different cytotoxicity. Graphical abstract Image 1 Highlights • PM 2.5 induces mitochondrial morphological damage of SH-SY5Y cells. • PM 2.5 triggers mitochondrion permeability transition pore opening. • PM 2.5 reduces ATP, mitochondrial membrane potential and mtDNA copy number. • PM 2.5 -caused oxidative stress related to enhancement of ROS, SIRT3 and Aβ-42 levels. [ABSTRACT FROM AUTHOR]