Background PM2.5 and O3 are the main air pollutants in China, and inflammation of the respiratory system is one of their main toxic effects. Cyclic RNAs are involved in many pathophysiological processes, but their relationship to the combined exposure to PM2.5 and O3 has not yet been investigated. Objective To elucidate the biological function played by hsa\_circ\_0001495 in the induction of 16HBE cellular inflammation by combined exposure to PM2.5 and O3. Method Detection of cell survival after 24h exposure of 16HBE cells to a combination of PM2.5 and O3 by CCK8. RT-qPCR and ELISA were used to detect inflammatory factors in 16HBE cells after co-exposing to PM2.5 and O3. CircRNA was screened using high throughput sequencing and bioinformatics analysis approaches. RNaseR experiments were carried out to verify the circular RNA properties of the circRNAs. Cytoplasmic-nuclear subcellular localisation assays and fish assays were used to verify the distribution of circRNAs in the nucleus versus the cytoplasm of the cell. To validate functions related with circRNA,RT-qPCR and ELISA were employed. Result Combined exposure to PM2.5 and O3 resulted in decreased cell viability.Combined exposure to PM2.5 and O3 resulted in 16HBE inflammation. High throughput sequencing and RT-qPCR results showed that the expression of hsa\_circ\_0001495 was significantly downregulated in 16HBE exposed to PM2.5 and O3 in combination. Hsa\_circ\_0001495 is not easily digested by RNaseR enzymes and has the properties of a circular RNA. Hsa\_circ\_0001495 is expressed in the cytoplasm as well as in the nucleus, but its distribution is predominantly in the cytoplasm. Conclusion In 16HBE cells, combined exposure to PM2.5 and O3 can induce an inflammatory response.hsa\_circ\_0001495 plays an inhibitory role in the inflammatory response of 16HBE cells that can be induced by combined exposure to PM2.5 and O3. ### Competing Interest Statement We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.

Background: Studies have shown that fine particulate matter (PM2.5) remains a significant problem in developing countries and plays a critical role in the onset and progression of respiratory illnesses. Circular RNAs (circRNAs) are involved in many pathophysiological processes,but their relationship to PM2.5 pollution is largely unexplored.Objectives: To elucidate the functional role of hsa_circ_0000992 in PM2.5-induced inflammation in a human bronchial epithelial cell line (16HBE) and to clarify whether the competing endogenous RNA (ceRNA) mechanism is involved in the interrelationships between hsa_circ_0000992 and hsa-miR-936 and the inflammatory signaling pathways.Methods: Detection of inflammatory factors in 16HBE cells exposed to PM2.5 by RT-qPCR and ELISA.High throughput sequencing and bioinformatics analysis methods were used to screen circRNA.The bioinformatics analysis method western blotting and dual-luciferase reporter gene system were used to verify mechanisms associated with circRNA.Results: PM2.5 cause inflammation in the 16HBE cells. High throughput sequencing and RT-qPCR result revealed that the expression of hsa_circ_0000992 was markedly up-regulated in 16HBE exposed to PM2.5. The binding sites between hsa_circ_0000992 and hsa-miR-936 was confirmed by dual-luciferase reporter gene system.Western blotting and RT-qPCR showed that hsa_circ_0000992 can interact with hsa-miR-936 to regulate AKT serine/ threonine kinase 3(AKT3),thereby activating the PI3K/AKT pathway and ultimately promoting the expression of interleukin (IL)-1 beta and IL-8. Conclusion: PM2.5 can induce the inflammatory response in 16HBE cells by activating the PI3K/AKT pathway. The expression of hsa_circ_0000992 increased when PM2.5 stimulated 16HBE cells,and the circRNA could then regulate the inflammatory response.Hsa_circ_0000992 regulates the hsa-miR-936/AKT3 axis through the ceRNA mechanism,thereby activating the PI3K/AKT signaling pathway,increasing the expression of cellular inflammatory factors,and promoting PM2.5-induced respiratory inflammation.

Fine particulate matter (PM2.5) pollution increases the risk of respiratory diseases and death, and apoptosis is an important factor in the occurrence of respiratory diseases caused by PM2.5 exposure. In addition, circular RNAs (circRNAs) can interact with proteins and widely participate in physiological and pathological processes in the body. The aim of this study was to investigate the mechanism of circRNA and protein interaction on PM2.5-induced apoptosis of human bronchial epithelial cells (16HBE) in vitro. In this study, we exposed human bronchial epithelial cells to a PM2.5 suspension with different concentration gradients for 24 h. The results showed that apoptosis of 16HBE cells after PM2.5 treatment was accompanied by cell proliferation. After exposure of PM2.5 to 16HBE cells, circRNAs related to apoptosis were abnormally expressed. We further found that the expression of hsa_circ_0002854 increased with the increase in exposure concentration. Functional analysis showed that knocking down the expression of hsa_circ_0002854 could inhibit apoptosis induced by PM2.5 exposure. We then found that hsa_circ_0002854 could interact with MAPK1 protein and inhibit MAPK1 phosphorylation, thus promoting apoptosis. Our results suggest that hsa_circ_0002854 can promote 16HBE apoptosis due to PM2.5 exposure, which may provide a gene therapy target and scientific basis for PM2.5-induced respiratory diseases.

The deficiency of effective biomarker for the toxic effects of water pollutants greatly limits the application of biological monitoring. This study aimed to investigate the possibility of circulating exosomes of indigenous fish acting as biomarker for the ecotoxicity effect of water environment. The Helong Reservoir in Guangzhou, China, was chosen as the investigating field, of which the water quality belongs to Class V (2013) (GB 3838-2002, China). The clean drinking water source of the upper reaches of the Liuxihe Reservoir was selected as the control. Indigenous fishes including Oreochromis niloticus (Nile tilapia), Labeo rohita (Rohu), Carassius auratus (Crucian carp) were sampled during the period from July 2020 to April 2021. Circulating exosomes of fish samples were isolated by using ultracentrifugation, characterized with transmission electron microscopy (TEM) and quantified by using bicinchoninic acid (BCA) assay. Oxidative stress, DNA and chromosome damage in liver, kidney, brain, gill and blood of fish samples were measured. The results showed that there were significant differences in superoxide dismutase (SOD) activity, glutathione (GSH) and malondialdehyde (MDA) contents, DNA and chromosome damage in fish samples between the Helong Reservoir and the control. Interestingly, there were also significant differences in circulating exosome levels of fish samples between them. Our data suggested that circulating exosome level of indigenous fish may be a novel biomarker for the ecotoxicity effects of water environment.

为探讨黄龙带水库浮游生物现状及水质情况,于2021年2—5月对黄龙带水库进行环境流行病学调查采样,分析其浮游生物的种类组成和丰度;通过Shannon-Wiener多样性指数和Pielou均匀度指数对水质进行综合评价.结果表明:本次调查共采集到黄龙带水库浮游植物6门30种,其优势藻类为绿藻门;浮游动物13属15种,以轮虫门为主.浮游植物和浮游动物丰度分别为10.00×105 ind./L和413 ind./L.黄龙带水库浮游生物Shannon-Wiener多样性指数大于3;浮游植物和浮游动物Pielou均匀度指数分别为0.67和0.94.黄龙带水库浮游生物多样性较高,水质综合评价结果为清洁贫营养型.

目的 探究环状RNAhsa_circ_0087960 在PM2.5 致人脐静脉内皮细胞(HUVEC)氧化损伤中的作用.方法 采集广州大气PM2.5 制备成细胞染毒液.0、25、50、75 μg/ml PM2.5 染毒液暴露HUVEC细胞 24 h,检测氧化应激指标超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GPX)活力和丙二醛(MDA)含量.利用circRNA高通量测序技术和生物信息学分析筛选出差异表达的 circRNA,实时荧光定量 PCR 法(RT-qPCR)验证测序结果.利用小干扰 RNA(siRNA)抑制hsa_circ_0087960 的表达水平,PM2.5(75 μg/ml)暴露 24 h,检测SOD和GPX活力.结果 PM2.5 染毒HUVEC后,SOD和GPX活力降低,MDA含量升高;RT-qPCR验证测序结果证明hsa_circ_0087960 在PM2.5 致HUVEC细胞氧化损伤中异常高表达,与PM2.5 存在剂量-效应关系(r=0.95,P＜0.05);抑制hsa_circ_0087960 后PM2.5(75 μg/ml)染毒 24 h,阳性转染组HUVEC的SOD和GPX活力高于阴性对照组(P＜0.05),且与无PM2.5 处理的阴性对照组差异无统计学意义(P＞0.05).结论 在PM2.5 致HUVEC细胞产生氧化损伤中,hsa_circ_0087960 具有促进作用,而抑制hsa_circ_0087960 具有提高甚至恢复抗氧化物酶活力的作用,从而在一定程度上抑制PM2.5 对HUVEC产生的氧化损伤.

目的 探究环状RNAhsa_circ_0066367 在PM2.5 致人支气管上皮细胞(16HBE)炎症反应中的调控作用机制.方法 将 0、100 和 300 μg/ml浓度的PM2.5 染毒 16HBE细胞 48h后,用实时荧光定量PCR分析法检测细胞中IL-1β、IL-8 与hsa_circ_0066367 的表达.以RNase R酶处理验证hsa_circ_0066367 成环性.接着,利用RNA干扰技术沉默 16HBE细胞中hsa_circ_0066367,再联合暴露染毒于 300 μg/ml的PM2.5 后,使用RT-qPCR检测细胞内IL-1β与IL-8 的表达水平变化.同时,利用生物信息学方法预测hsa_circ_0066367可能结合的miRNA,及目标miRNAs的下游靶基因,并对下游靶基因进行功能富集分析,成功构建与PM2.5 致 16HBE炎症相关的circRNA-miRNA-mRNA的调控互作网络.结果 PM2.5 染毒 16HBE细胞后,细胞中炎症因子IL-1β、IL-8 与hsa_circ_0066367 表达量升高.沉默细胞内hsa_circ_0066367 表达水平后再经 PM2.5 染毒,16HBE 细胞中 IL-1β 与 IL-8 的 mRNA 表达水平下降.生物信息学预测软件分析发现hsa_circ_0066367 可能通过作为hsa-miR-1290 与hsa-miR-622 分子的"海绵"吸附体发挥其调控作用,GO功能和KEGG通路分析表明,hsa-miR-1290 与hsa-miR-622 分子的下游靶基因主要参与有丝分裂核膜分解、转录调控、蛋白质苏糖化等生物学进程,以及在ErbB信号通路、Wnt信号通路与MAPK信号通路等炎症相关通路中富集.结论 hsa_circ_0066367在PM2.5 染毒 16HBE细胞后发生异常高表达,并可能作为hsa-miR-1290 与hsa-miR-622 分子的"海绵"吸附体发挥其在PM2.5 染毒引起的 16HBE细胞炎症反应中的调控作用.

In this study, 123 PM2.5 filter samples were collected in Wuhan, Hubei province from December 2014 to November 2015. Water- soluble inorganic ions (WSIIs), elemental carbon (EC), organic carbon (OC) and inorganic elements were measured. Source apportionment and back trajectory was investigated by the positive matrix factorization (PMF) model and the hybrid single particle lagrangian integrated trajectory (HYSPLIT) model, respectively. The annual PM2.5 concentration was 80.5 ± 38.2 μg/m3, with higher PM2.5 in winter and lower in summer. WSIIs, OC, EC, as well as elements contributed 46.8%, 14.8%, 6.7% and 8% to PM2.5 mass concentration, respectively. SO42−, NO3− and NH4+ were the dominant components, accounting for 40.2% of PM2.5 concentrations. S, K, Cl, Ba, Fe, Ca and I were the main inorganic elements, and accounted for 65.2% of the elemental composition. The ratio of NO3−/SO42− was 0.86 ± 0.72, indicating that stationary sources play dominant role on PM2.5 concentration. The ratio of OC/EC was 2.9 ± 1.4, suggesting the existence of secondary organic carbon (SOC). Five sources were identified using PMF model, which included secondary inorganic aerosols (SIA), coal combustion, industry, vehicle emission, fugitive dust. SIA, coal combustion, as well as industry were the dominant contributors to PM2.5 pollution, accounting for 34.7%, 20.5%, 19.6%, respectively.

Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 mu M PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-Kappa B pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation.

了解广州市典型水库水环境因子与浮游生物生态学现状及其水质情况,为水质安全的预防和控制工作提供基础资料.于2021年2月至5月,对该市典型水库进行了现场环境流行病学现况调查.根据水库水环境的历史资料,有针对性地对8种环境因子进行了检测;分析水环境中浮游动物及浮游植物的构成及丰度;运用Shannon-Weaver指数法分析水环境中浮游生物的多样性;运用Pielou指数法分析水环境中浮游生物的均匀度;基于浮游生物的生态学现状,对水环境质量进行了初步评价.参照《地表水环境质量标准》(GB 3838—2002),8种环境质量指标符合Ⅱ类水质限值.本次调查共采集到浮游植物6门40种,丰度为26.67×105 ind./L,优势藻类为绿藻(37.5％)和蓝藻(30％);浮游动物共采集到17属25种,丰度为488 ind./L,优势种类为轮虫(64％);浮游植物Shannon-Weaver多样性指数为1.35;浮游动物Shannon-Weaver多样性指数为1.22;浮游植物Pielou均匀度指数为0.25;浮游动物Pielou均匀度指数为0.26.虽然该水库理化指标符合Ⅱ类水质限值,但浮游生物多样性指数及均匀度指数较低.本次调查暴露了水质理化指标的局限性,理化指标无法全面反映水质的生态健康状况.水质理化监测与生物监测的联合运用,在水环境质量的全面和客观评价中具有重要意义.

目的 探讨某市典型水库水质的生态毒理学效应,为地方水质安全防护措施的合理实施提供基础资料.方法 自2020年7月～2021年4月,通过环境流行病学现场调查,采集在某市典型水库库区及清洁对照组水源生长的野生鲫鱼、泰国鲮鱼以及尼罗罗非鱼样本;运用微核实验分析鱼血细胞的染色体损伤效应;运用单细胞凝胶电泳技术(single cell gel electrophoresis,SCGE)分析鱼血细胞及肝细胞的DNA损伤效应;采用试剂盒法检测鱼肝组织超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)和丙二醛(MDA)含量;运用鱼卵黄蛋白原(vitellogenin,VTG)ELISA试剂盒法检测鱼血浆VTG水平,分析水质的环境雌激素效应.结果 某市典型水库库区3种鱼类血细胞彗星尾部DNA含量及血细胞微核形成率明显高于清洁对照组鱼类(P＜0.05);典型水库库区3种鱼类肝组织SOD活性明显低于对照组(P＜0.05),GSH及MDA含量明显高于对照组(P＜0.05);典型水库库区尼罗罗非鱼血浆VTG水平明显高于对照组(P＜0.05),而鲫鱼、泰国鲮鱼血浆VTG水平差异无统计学意义(P＞0.05).结论 某市典型水库水质对库区野生鱼类可能具有一定的生态毒性效应.

探讨广州市增塘水库浮游生物种群特征及水质现状,为水质安全监控提供基础资料.于2021年3—7月,运用环境流行病学现场调查采样方法,采集增塘水库浮游植物及浮游动物样本,分析其种群构成及丰度;采用Shannon-Weaver指数法分析水库浮游生物的多样性;采用Pielou指数法分析水库浮游生物的均匀度;基于上述指数对水库的水环境质量做出初步评价.本次调查共采集到浮游植物35种,隶属于5门27属.其中优势藻类为绿藻13种(37.15％),其次为蓝藻10种(28.57％);浮游植物丰度为29.00×105 ind./L,其中硅藻门的丰度最大,为13.05×105 ind./L.浮游动物共计14属19种,其中轮虫12种(63.16％),为优势种群,其次为桡足类5种(26.31％);浮游动物丰度为967 ind./L,其中轮虫丰度最大,为860 ind./L.浮游植物Shannon-Weaver H'为3.24,对应水质为清洁;浮游动物Shannon-Weaver H'为2.24,对应水质为轻度污染;浮游植物Pielou J'为0.63,对应水质为轻度污染;浮游动物Pielou J'值为0.53,对应水质为轻度污染.本次环境流行病学现场调查结果提示,广州市增塘水库水质目前处于轻度污染状态.

The present study was conducted to assess the genotoxic potential of water from the Helong Reservoir, which was designated as a strategic drinking water source by the Guangdong Provincial Government of China in October 2016. Four kinds of common indigenous fish samples (Labeo rohita, Cirrhinus molitorella, red tilapia, and Oreochromis niloticus) were collected at 6 sampling sites during the period from July to November 2020. Fish from the clean drinking water source of the upper reaches of the Liuxihe Reservoir in Guangzhou were collected as the control. Both the alkaline single cell gel electrophoresis assay and the micronucleus test were used to detect DNA damage and the micronucleus rate in erythrocytes of fish samples, respectively. The results indicated that there was a significant increase in comet tail length, Olive tail moment, and micronucleus rates of all fish samples compared with those of the control (p < 0.05). The order of sensitivity to DNA damage and micronucleus formation was Labeo rohita > Cirrhinus molitorella > red tilapia > Oreochromis niloticus. The results of the 2 kinds of experiments were in perfect agreement with each other. We conclude that there are obvious genotoxic effects from the water in the Helong Reservoir. As a strategic drinking water source, the safety of the Reservoir water quality should be considered. The local government should put the restoration of the Helong Reservoir water quality on the agenda as soon as possible. Environ Toxicol Chem 2021;40:1919-1927. © 2021 SETAC.

Kitchen emissions are mixed indoor air pollutants with adverse health effects, but the large-scale assessment is limited by costly equipment and survey methods. This study aimed to discuss the application of backpropagation (BP) neural network models in the assessment of kitchen emissions based on the exposure marker. A total of 3686 participants were recruited for the kitchen survey, and their sleep quality was measured by the Pittsburgh sleep quality index (PSQI). After excluding the confounders, 365 participants were selected to assess their urinary hydroxy polycyclic aromatic hydrocarbons (OH-PAHs) concentrations by ultra-high-performance liquid chromatography/tandem mass spectrometry. Two BP neural network models were then set up using the survey and detection data from the 365 participants and used to predict the total urinary OH-PAHs concentrations of all participants. The total urinary OH-PAHs and 1-hydroxy-naphthalene (1-OHNap) concentrations were significantly higher among the 365 participants with poor sleep quality (global PSQI score > 5; P < 0.05). Results from internal and external validation showed that our model has high credibility (model 2). Further, the participants with higher predicted total urinary OH-PAHs concentrations were associated with the global PSQI score of >5 (odds ratio (OR) = 1.284, 95% confidence interval (CI) = 1.082–1.525 for participants with predicted total urinary OH-PAHs concentrations of over 1.897 μg/mmol creatinine in model 1, and OR = 1.467, 95% CI = 1.240–1.735 for participants with predicted total urinary OH-PAHs concentrations of over 2.253 μg/mmol creatinine in model 2) after adjusting for the confounders. Findings suggest that the BP neural network model is suitable for assessing kitchen emissions, and the urinary OH-PAHs concentrations can be taken as the model outlay.

A creative combination of chitosan with polyacrylic acid (PAA) improves the acidity resistance of chitosan and increases its potential in the field of adsorption. In order to facilitate recovery, magnetic nanoparticles were incorporated in CS-PAA to obtain a magnetic-CS-PAA (MCS-PAA) nanocomposite. The physical and chemical characteristics of the composite adsorbent MCS-PAA were determined by SEM, TEM, FTIR, EDX, XRD, and XPS. This environmental-friendly, magnetic, composite adsorbent showed significantly better adsorption performance than those of the individual adsorbents alone. The maximal adsorption capacity was 204.89 mg/g according to the Langmuir isotherm model, when the concentration of Pb(II) was 100 mg/L at the equilibrium time of 70 min. The main adsorption mechanism was the complexation between the carboxyl, amino, and hydroxyl groups in MCS-PAA and Pb(II). Further, introduction of PAA also improved the acid resistance of CS. The new adsorbent MCS-PAA is thus expected to facilitate a wider range of applications for chitosan in the adsorption of Pb(II). (C) 2019 Elsevier B.V. All rights reserved.

目的 探讨长链非编码RNA(lncRNA)NONHSA T198249.1在PM2.5致人脐静脉内皮细胞(HUVECs)炎症反应的调控作用及其分子机制.方法 在广州地区采集大气PM2.5制备染毒液染毒HUVECs细胞,用实时荧光定量分析法(RT-qPCR)检测暴露不同浓度(25～75μg/ml)PM2.5染毒液染毒后,细胞炎症因子IL-1β、IL-8以及lncRNA NONHSA T198249.1 mRNA水平的变化.运用胞浆胞核分离试剂盒进行lncRNA NONHSA T198249.1亚细胞定位.应用pc-DNA NONHSA T198249.1转染HUVECs,检测过表达lncRNA NONHSA T198249.1后对75μg/ml PM2.5诱导HUVECs细胞炎症因子IL-1β、IL-8 mRNA水平的影响.结果 PM2.5可以诱导HUVECs中NONHSA T198249.1表达下调,且与染毒浓度存在剂量-效应关系(P＜0.05);过表达NONHSA T198249.1后用75 μg/ml PM2.5染毒,细胞炎症因子IL-1β、IL-8 mRNA的表达水平明显下降(P＜0.05).结论 LncRNA NONHSA T198249.1在PM2.5染毒的HUVECs中低表达,过表达lncRNA NONHSA T198249.1可以抑制IL-1β、IL-8的分泌,lncRNA NONHSA T198249.1可能在PM2.5致HUVECs细胞炎症反应中起抑制炎症的作用.

Several studies have demonstrated that PM2.5 inhalation is associated with an increased risk of cerebrovascular disease (CVD), in which inflammation plays an important role. The mechanisms of this disease are not fully understood to date. Long non-coding RNAs (lncRNAs) are involved in many pathophysiological processes, such as immune responses; however, their functions associated with inflammation are largely unexplored. High-throughput sequencing assay and obtained numerous lncRNAs that altered the expression in response to PM2.5 treatment in HUVECs. NONHSAT247851.1 was also identified, which was significantly up-regulated to control the expression of immune response genes. Mechanistically, the results indicated that NONHSAT247851.1 knockdown reduced the expression of IL1β. In study, we investigated NONHSAT247851.1 as a promoter in regulating immune response genes via binding with raf-1 to regulate the phosphorylation level of p65 protein in HUVECs. The data collected suggests that NONHSAT247851.1 regulates inflammation via interaction with raf-1 to control the inflammatory expression in PM2.5 exposure.

A novel ethylenediaminetetraacetic acid (EDTA)-functionalized magnetic chitosan oligosaccharide and carboxymethyl cellulose (Fe3O4@CMCCOS-EDTA) nanocomposite adsorbent was successfully fabricated for Pb(II) adsorption. The adsorbent was characterized by Fourier transform infrared, and X-ray photoelectron spectroscopy was used to confirm successful EDTA modification and Pb(II) adsorption. Scanning electron microscopy, transmission electron microscopy, vibrating sample magnetometer, and thermogravimetric analysis were used to study the morphology and properties of magnetic particles. EDTA modification considerably improved the capacity of the adsorbent. The batch adsorption experiment results indicated that the pseudo-second-order (PSO) model and the Langmuir isotherm model reliably described the adsorption behavior. The maximum adsorption capacity (qm) for monolayer chemical adsorption was calculated to be 432.34 mg/g at the pH of 5 and temperature of 308 K. Notably, Fe3O4@CMCCOS-EDTA exhibited a high Pb(II) removal rate of ~100% using an initial metal ion solution of 100 mg/L and 200 mg/L.

目的 探讨暴露于我国环境空气质量二级浓度限值以内的大气环境对广州市大学生肺功能的短期影响.方法 在PM2.5浓度处于我国环境空气质量一级浓度限值内(对照日)和二级浓度限值内(暴露日)各检测1次广州市某大学49名在校学生的肺功能指标,包括用力肺活量(FVC)、1s用力呼气容积(FEV1)、最大呼气流量(PEF)和最大通气量(MVV),并检测血清炎症指标高敏C反应蛋白(hs-CRP)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平,分析肺功能及炎症指标与空气质量的关系.结果 暴露日与对照日之间的男性FVC、女性FVC、男性PEF、女性PEF、女性MVV水平均无明显差异(P＞0.05),而男性和女性FEV1水平均为暴露日高于对照日,男性MVV水平为对照日高于暴露日,差异均有统计学意义(P＜0.05).与对照日相比,暴露日血清炎症指标均有不同程度上升,hs-CRP、IL-1β、IL-6、TNF-α平均浓度分别较对照日增加36.5％,27.9％,13.2％,11.3％.结论 研究对象短期暴露于大气污染物可能对肺功能造成一定影响,其影响可能与大气污染物引起的机体炎症反应有关.

目的 探讨长链非编码RNA(lncRNA) AABR07008568.1在大气PM2.5诱导大鼠肺泡巨噬细胞(NR8383)炎症反应中的作用及其分子机制.方法 采集广州地区现场实时PM2.5样品制成混悬液用于后续实验的染毒,用0、200 μg/ml PM2.5染毒液暴露NR8383细胞24 h后,采用lncRNA高通量测序并结合生物信息学分析方法筛选出有差异表达的lncRNAs,使用实时荧光定量PCR分析法(RT-qPCR)验证测序结果.运用胞浆胞核亚细胞定位试剂盒检测AABR07008568.1在胞浆胞核的分布情况.采用RNA干扰(RNAi)技术敲低NR8383细胞中AABR07008568.1的表达水平,以RT-qPCR检测RNA干扰联合200 μg/ml PM2.5染毒液暴露NR8383细胞后IL-6的表达水平.用NFκB特异性抑制剂(BAY11-7082,10 μmol/L)处理细胞后检测AABR07008568.1的表达水平.结果 高通量测序和RT-qPCR结果显示,随着PM2.5暴露浓度的增加,AABR07008568.1表达量增高(P＜0.05).通过干扰AA BR07008568.1后发现siRNA1的转染效率最高,达到约60％(P＜0.05).敲低AABR07008568.1且联合PM2.5暴露后,与阴性对照(NC)组相比,siRNA1组中IL-6的表达水平降低,差异具有统计学意义(P＜0.05);NC+PM2.5组中的IL-6表达上调,差异具有统计学意义(P＜0.05).当使用NFκB特异性抑制剂阻断NFκB通路后,AABR07008568.1表达量下降(P＜0.05).结论 AABR07008568.1参与了NFκB通路的激活,但两者之间具体的调控机制尚需更深层次的探索.