细颗粒物(PM_(2.5))主要组分模拟溶液对发光细菌的光抑制分析

为明确NH_4~+、 NO_3~-、SO_4~(2-)及金属等组分在水溶性提取液对发光细菌的光抑制过程中所起的作用,参照PM_(2.5)样品提取液浓度,模拟配制与3级以上PM_(2.5)样品提取液中主要组分:硫酸盐、硝酸盐、氨盐相同浓度的溶液,同时选取与PM_(2.5)可溶性提取液发光抑制率相关性较强的铅、锌,配制不同浓度级别模拟溶液,测试各单一组分对发光细菌的发光抑制率及其混合溶液对发光细菌的联合影响效应。基于毒性单位法(TU)、相加指数法(AI)和混合毒性指数法(MTI)评价了混合体系联合影响的作用类型。结果表明,与3~6级PM_(2.5)可溶性提取液中硫酸氨、硫酸氢氨、硝酸氨、硫酸锌和硝酸铅浓度相同的模拟溶液对发光细菌的发光没有抑制作用。不同的评价方法对PM_(2.5)主要组分混合体系联合效应评价结果具有较好的一致性,硫酸氨、硝酸氨、硫酸氢氨混合溶液中,对发光细菌的光抑制均为硫酸氢氨的独立作用,硫酸锌与硝酸铅的混合体系,锌和铅对发光细菌的联合影响效应表现为协同,硫酸氨、硝酸氨、硫酸氢氨与硫酸锌、硝酸铅的多元混合体系呈现协同作用。     

天然提取物抗PM2.5诱导A549细胞凋亡的作用

采集北京城区大气可吸人颗粒物中的细颗粒物(PM25),用其对人肺腺癌A549细胞染毒,探讨PM25对细胞增殖的毒性和诱导细胞凋亡的作用,并且考察了加入不同浓度的红豆越橘提取物和竹叶提取物对其的抗性作用.实验采用MTT法检测细胞增殖作用,采用Annexi V-FITC/PI双染法和流式细胞仪检测细胞凋亡.结果显示:PM2...     

大气中细颗粒物对肺癌细胞A549迁移和侵袭作用的影响

采集大连城区大气中可吸入性细颗粒物(PM_(2.5)),研究其对肺癌A549细胞迁移、黏附和侵袭力的影响,利用明胶酶谱法检测细胞分泌的基质金属蛋白酶活性,利用Western blot法测定A549细胞中转移相关蛋白的表达。结果表明,在无明显细胞毒性浓度下,PM_(2.5)可增加A549细胞的迁移速率;细胞与细胞外基质的黏附率增加;细胞侵袭实验结果表明PM_(2.5)可增加A549细胞穿透基底膜的能力;用明胶酶谱法检测发现PM_(2.5)可使A549细胞分泌的基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)活性增强。转移相关蛋白——细胞钙粘蛋白-N(N-cadherin)的表达量升高,而钙粘蛋白-E(E-cadherin)的表达量下降,实验结果表明,PM_(2.5)可增强A549细胞的侵袭性,大气中的可吸入性颗粒可能导致肺癌转移发生率增加。     

大气细颗粒物对小鼠T淋巴细胞亚群的影响

大气颗粒物对肺免疫系统有潜在毒性作用,打破免疫系统平衡,大气颗粒物成分中危害首当其冲的是大气细颗粒物(PM_(2.5)),为研究大气细颗粒物引起的机体T淋巴细胞中Th1/Th2免疫失衡方向。本研究通过免疫组化实验方法检测暴露后小鼠肺组织中T淋巴细胞的表达,进一步采用流式细胞术检测大气细颗粒物气管滴注后小鼠肺脏淋巴细胞中Th1/Th2比例。暴露组小鼠肺组织免疫组化研究结果提示浸润细胞区有大量的CD4~+T细胞,中高剂量暴露组小鼠肺组织中淋巴细胞亚群Th1/Th2比例向Th1偏移。大气细颗粒物影响免疫失衡,使T淋巴细胞向Th1漂移。     

全氟辛烷磺酸钾(PFOS)和纳米氧化锌(Nano-ZnO)单独与联合暴露对斑马鱼胚胎的氧化损伤和细胞凋亡的影响

探讨全氟辛烷磺酸钾(PFOS)和纳米氧化锌(Nano-Zn O)复合暴露对斑马鱼机体氧化损伤和细胞凋亡的影响。将斑马鱼胚胎暴露于PFOS(0、0.4、0.8和1.6 mg·L-1)、Nano-Zn O(0、12.5、25和50 mg·L-1)、PFOS+Nano-Zn O(0、0.4+12.5、0.8+25和1.6+50 mg·L-1)溶液中6天后,检测相关的酶活性变化(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(Gpx)、脂质过氧化物(MDA)、半胱氨酸蛋白酶(Caspase-3和Caspase-9)和与细胞凋亡相关基因(Bax,p53和Bcl-2)表达情况。结果表明:PFOS和Nano-Zn O单独与复合暴露均可造成斑马鱼胚胎的氧化损伤和细胞凋亡,但复合暴露组的氧化损伤和细胞凋亡程度明显大于单独暴露组。在PFOS和Nano-Zn O单独和复合暴露组中,随着处理浓度的升高,SOD、Gpx、Caspase-3和Caspase-9酶的活性显著升高。而CAT酶活性随着处理浓度的升高抑制作用显著。PFOS与Nano-Zn O复合暴露组与单独暴露组相比,Bax和p53表达显著上调,而Bcl-2表达显著下调。因此,在实验浓度范围内,等毒性配比1:1条件下,推测NanoZn O可以增强PFOS对斑马鱼胚胎的氧化损伤和细胞凋亡毒性。     

Cd~(2+)暴露对斑马鱼肝脏和卵巢抗氧化和免疫系统的影响及蓝LED光预暴露的保护作用

本研究探讨了急性镉暴露(Cd~(2+))对斑马鱼抗氧化和免疫系统的影响及蓝LED光源(LDB)预暴露的缓解作用。斑马鱼均分为2组,分别用白炽灯和LDB处理4周(辐照度为0.9 W·m-2)。4周后每组再分为2个小组,分别在白炽灯下用0和0.97 mg·L~(-1)Cd~(2+)的水体处理4 d。结果表明:Cd~(2+)暴露导致肝脏和卵巢丙二醛(MDA)和一氧化氮(NO)含量的显著升高。在肝脏中,Cd~(2+)暴露下调了铜锌超氧化物歧化酶(Cu/Zn-SOD)和过氧化氢酶(CAT)的酶活和m RNA表达水平,上调了环氧化酶2(COX-2)和诱导型一氧化氮合酶(i NOS)的表达和酶活。在卵巢中,Cd~(2+)导致Cu/Zn-SOD和CAT的表达,CAT、COX-2和i NOS的酶活显著升高。在卵巢中,LDB预暴露可显著缓解Cd~(2+)引起的MDA和NO含量、Cu/Zn-SOD的表达、CAT的表达和酶活、COX-2和i NOS的酶活的升高。在肝脏中,LDB预暴露不能影响Cd~(2+)引起的MDA和NO含量的升高,但是显著缓解了Cd~(2+)引起的Cu/Zn-SOD和CAT表达和酶活的下降和COX-2和i NOS表达的升高。在这些过程中,核转录相关因子2(Nrf2)和核转录因子-κB(NF-κB)与其目标基因的表达及其抑制因子Kelch样ECH联合蛋白1(Keap1a和Keap1b)和抑制蛋白激酶(IκBαa和IκBαb)显示了紧密的关联性。综上结果表明,斑马鱼急性Cd~(2+)暴露后,机体处于氧化应激状态,导致肝脏和卵巢氧化性损伤和炎症的产生,而LDB预暴露能够改善机体这种不利状态。这个过程可能分别涉及Nrf2和NF-κB诱导的抗氧化和免疫系统。     

BDE-47对人胚肾细胞HEK293的毒理效应及作用机制

2,2’,4,4’-四溴联苯醚(BDE-47)是生物体中含量最高且毒性最强的PBDEs之一,有关BDE-47对肾细胞的毒性及其作用机制的研究仍有待补充。选取3个剂量组(低:10-6mol·L-1、中:10-5mol·L-1、高:10-4mol·L-1)及溶剂对照组,研究了BDE-47对人胚肾细胞(HEK293)的细胞凋亡率及活性氧(ROS)水平的影响;并从分子水平对细胞氧化损伤、凋亡相关蛋白(APE1及p53)及凋亡相关基因m RNA(p53、Bax、Caspase 3、Caspase 8)的表达量进行测定。实验结果显示:与对照组相比,中、高剂量组细胞凋亡率显著增加(P0.05);ROS水平在中剂量组显著上升(P0.01);随BDE-47浓度的变化,APE1蛋白表达量与细胞ROS水平存在一致性;p53、Bax、Caspase 8 m RNA表达量与BDE-47的浓度间存在剂量-效应关系。结果表明,BDE-47可诱导HEK293细胞凋亡及氧化应激,APE1可能是细胞ROS升高与细胞凋亡间重要的中介因子;BDE-47可以通过影响Caspase 8及线粒体途径中p53及Bax的表达诱导细胞凋亡。     

运动及不同浓度PM2.5滴注对大鼠糖代谢部分酶活性的影响

为了探讨一次性递增负荷运动及不同浓度细颗粒物(PM2.5)暴露对大鼠己糖激酶(hexokinase,HK)-丙酮酸激酶(pyruvatekinase,PK)及异柠檬酸脱氢酶(isocitratedehydrogenase,IDH)活性影响的机制,将30只雄性Wistar SPF(Specific Pathogen Free,SPF)大鼠随机分为安静(QC)、运动对照组(EC)、低剂量PM2.5+运动组(LPE)、中剂量PM2.5+运动组(MPE)、高剂量PM2.5+运动组(HPE),采用一次性气管滴注染毒后进行递增负荷跑台训练,并通过酶联免疫法(enzyme-linked immunosorbent assay,ELISA)测定大鼠血清及肝脏组织HK,PK,IDH活性。结果表明,与安静组相比,运动对照组HK,PK酶活性下降,IDH活性升高,差异有统计学意义(p0.01)。和EC组相比,LPE,MPE,HPE组各组织中HK,PK,IDH活性均下降,差异有统计学意义(p0.05或p0.01)。实验表明,运动可以降低大鼠的HK,PK活性而增强IDH活性;随着浓度的增加,HK,PK,IDH活性与PM2.5暴露剂量具有相关性降低。     

大气颗粒物物理化学属性致病效应与损伤机制的研究进展

近些年,我国大气颗粒物所带来的健康问题越发突出,由此产生的环境疾病日益引起人们的广泛关注。大量的流行病学和毒理学研究发现,大气颗粒物能引起呼吸系统、心血管系统、神经系统、免疫系统等的损伤,造成新生儿出生缺陷,增加罹患癌症的风险,且与人群发病率和死亡率上升有关。但是由于大气颗粒物物化属性比较复杂,一种或几种损伤机制并不能完全解释其与致病效应的关系,因此具体的损伤机制目前还没有统一的说法,大气颗粒物物理化学属性与致病效应的关系仍在探索当中。本文从大气颗粒物的粒径、浓度、比表面积、来源、成分等基本属性入手,剖析其基本特点和可能影响健康的原因,探讨大气颗粒物通过氧化损伤途径诱导致病效应,并结合当前大气颗粒物健康影响研究现状提出在未来研究中应注重的相关内容。     

Mass concentrations and temporal profiles of PM10, PM2.5 and PM1 near major urban roads in Beijing

Mass concentrations of PM₁₀, PM_2.5 and PM₁ were measured near major roads in Beijing during six periods: summer and winter of 2001, winter of 2007, and periods before, during and after the 2008 Beijing Olympic Games. Since the control efforts for motor vehicles helped offset the increase of emissions from the rapid growth of vehicles, the averaged PM_2.5 concentrations at roadsides during the sampling period between 2001 and 2008 fluctuated over a relatively small range. With the implementation of temporary traffic control measures during the Olympics, a clear “V” shaped curve showing the concentrations of particulate matter and other gaseous air pollutants at roadsides over time was identified. The average concentrations of PM₁₀, PM_2.5, CO and NO decreased by 31.2%, 46.3%, 32.3% and 35.4%, respectively, from June to August; this was followed by a rebound of all air pollutants in December 2008. Daily PM₁₀ concentrations near major roads exceeded the National Ambient Air Quality Standard (Grade II) for 61.2% of the days in the non-Olympic periods, while only for 12.5% during the Olympics. The mean ratio of PM_2.5/PM₁₀ near major roads remained relatively stable at 0.55 (±0.108) on non-Olympic days. The ratio decreased to 0.48 (±0.099) during the Olympics due to a greater decline in fine particles than in coarse-mode PM. The ratios PM₁/PM_2.5 fluctuated over a wide range and were statistically different from each other during the sampling periods. The average ratios of PM₁/PM_2.5 on non-Olympic days were 0.71.     

川南四座城市PM2.5化学组分污染特征及其源解析

为探究川南地区大气气溶胶中化学组分与来源特征,于2015年9月—2016年8月在四川盆地南部4个典型代表城市(泸州、内江、宜宾、自贡)采集了226个PM_2.5样品,对PM_2.5的质量浓度和主要化学组分(水溶性离子和碳质组分)进行测定,并利用颗粒物源解析受体模型对PM_2.5来源进行解析.结果表明:川南地区PM_2.5日均浓度为46.4—68.0μg·m^-3,均高于国家环境空气质量标准年均PM_2.5限值(35.0μg·m^-3).OC、EC和水溶性二次离子(SO₄^2-、NO₃-和NH₄+)分别占PM_2.5质量的15.7%—22.8%、4.2%—6.4%和28.6%—55.8%.PM_2.5及其主要化学组分浓度有显著的季节变化,即冬季浓度显著高于其他季节,夏季浓度最低.泸州除夏季外,其他季节SO₄2-、NO₃-同源性较好;其他城市在冬季,SO₄2-、NO₃-同源性较好.NH₄+主要存在形式为NH₄NO₃、(NH₄)2SO₄、NH₄HSO₄.OC、EC来源复杂,主要为机动车源、煤燃烧源和生物质燃烧源.川南地区PM_2.5的来源主要受8种因子影响,按总体贡献排序依次为:二次硫酸盐、生物质燃烧、工业源、二次硝酸盐、机动车源、煤燃烧、道路尘埃和建筑尘埃.此外,相比较而言,机动车源贡献在泸州市较凸显,煤燃烧源贡献在宜宾市较凸显.     

体育场馆内PM2.5的环境行为与急性毒理效应对运动大鼠免疫指标的影响

通过气管滴注法建立运动大鼠非暴露式损伤模型,以研究体育场馆内不同浓度PM_(2.5)污染对运动大鼠免疫指标的影响。实验选取32只雄性Wistar SPF(specific pathogen free, SPF)大鼠,随机分为运动对照组(EC)、高剂量运动组(30 mg·kg~(-1))(HPE)、中剂量运动组(15 mg·kg~(-1))(MPE)、低剂量运动组(7.5 mg·kg~(-1))(LPE),采用一次性气管滴注染毒后进行递增负荷跑台训练,通过酶联免疫法(ELISA)测定大鼠血清和肺泡灌洗液(BALF)中克拉拉细胞蛋白(CC16)、超敏C反应蛋白(hs-CRP)、大鼠单核细胞趋化蛋白-1(MCP-1)、大鼠巨噬细胞炎症蛋白1α(MIP-1α)和中性粒细胞弹性蛋白酶(NE)的表达水平。与EC相比,LPE、MPE和HPE中MCP-1、MIP-1α和hs-CRP表现出剂量相关性升高,NE和CC16则呈剂量相关性降低,差异均有统学意义。研究表明,PM_(2.5)气管滴注可以对急性运动大鼠的免疫系统功能造成一定程度的损伤。     

北京不同污染天气PM_(2.5)和PM_(10)染毒对大鼠生理病理参数的影响

为探讨北京不同污染天气大气可吸入颗粒物PM_(10)和细颗粒物PM_(2.5)污染对雄性大鼠血常规、氧化损伤、炎症反应和肺组织的影响,将64只雄性8周龄Wistar大鼠随机分为8组,分别为2个对照组(空白组和生理盐水组)和6个染毒组(清洁、雾霾及沙尘暴3种不同天气的PM_(10)染毒组和PM_(2.5)染毒组),每组8只。用2015年3月—5月在北京南海子麋鹿苑采集的清洁、雾霾和沙尘暴3种不同天气的PM_(10)和PM_(2.5)制备悬液,分别采用气管滴入PM_(10)和PM_(2.5)悬液作为染毒组,空白对照组不做任何处理,生理盐水对照组采用气管滴注生理盐水。急性染毒24 h后处死大鼠。采集血液测定18个血常规指标,分析肺泡灌洗液(BALF)中转化生长因子-β1(TGF-β1)、乳酸脱氢酶(LDH)、总抗氧化能力(T-AOC)、白介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)的含量,并在高倍显微镜下观察肺组织和气管病理形态变化。同时,对PM_(10)和PM_(2.5)中的水溶性离子、有机碳/元素碳、16种多环芳烃和7种重金属等元素进行了测定,并分析了各组分与大鼠生理病理指标的相关性。结果表明:清洁、沙尘暴天气的PM_(10)和雾霾天气的PM_(2.5)急性染毒导致大鼠白细胞系参数即免疫力显著下降。污染天气颗粒物染毒后大鼠BALF氧化炎症因子的改变表明呼吸系统受到感染:沙尘暴和清洁天的PM_(10)染毒均显著提高了TGF-β1,雾霾PM_(10)染毒后IL-6和LDH有一定程度升高。3种天气颗粒物染毒对肺和气管造成的组织病理伤害各有特点,但PM_(2.5)伤害程度普遍大于PM_(10)。染毒颗粒物粒径大小,其化学成分类别、浓度是造成大鼠血常规指标变化、氧化炎症反应和组织学病变的可能原因。     

Diverse bacterial populations of PM2.5 in urban and suburb Shanghai,China

• Urban aerosols harbour diverse bacterial communities in Shanghai. • The functional groups were associated with nitrogen, carbon, and sulfur cycling. • Temperature, SO₂, and wind speed were key drivers for the bacterial community. Airborne bacteria play key roles in terrestrial and marine ecosystems and human health, yet our understanding of bacterial communities and their response to the environmental variables lags significantly behind that of other components of PM_2.5. Here, atmospheric fine particles obtained from urban and suburb Shanghai were analyzed by using the qPCR and Illumina Miseq sequencing. The bacteria with an average concentration of 2.12 × 10³ cells/m³, were dominated by Sphingomonas, Curvibacter, Acinetobacter, Bradyrhizobium, Methylobacterium, Halomonas, Aliihoeflea, and Phyllobacterium, which were related to the nitrogen, carbon, sulfur cycling and human health risk. Our results provide a global survey of bacterial community across urban, suburb, and high-altitude sites. In Shanghai (China), urban PM_2.5 harbour more diverse and dynamic bacterial populations than that in the suburb. The structural equation model explained about 27%, 41%, and 20%–78% of the variance found in bacteria diversity, concentration, and discrepant genera among urban and suburb sites. This work furthered the knowledge of diverse bacteria in a coastal Megacity in the Yangtze river delta and emphasized the potential impact of environmental variables on bacterial community structure.     

Effects of Combined Exposure to Formaldehyde and PM2.5 on the Brain of Balb/c Mice Asthma Model

Epidemiological studies have shown that there is a link between asthma and brain damage,but toxicological studies have not fully confirmed yet,especially the effects of asthma on the brain. In this study,at first,we explore the effects of asthma on the brain through the establishment of an allergic asthma model. Then PM_(2.5),a typical outdoor air pollutant and formaldehyde,a typical indoor air pollutant were selected to be closer to the true environment and find whether there is any synergism between them. In this study,an ovalbumin( OVA)-sensitized mice asthma model was established. 30 male Balb/c mice were randomly divided into 5 groups:( 1) saline control group,( 2) OVA-sensitized group,( 3) OVA-combined with formaldehyde exposure group,( 4) OVA-combined with PM_(2.5) exposure group,( 5) Combination of OVA,formaldehyde and PM_(2.5) exposure group. The mice were inhaled with formaldehyde or/and instilled with PM_(2.5) from day 1 to 18. The mice asthma model was developed by OVA sensitization and challenge. The mice were sensitized with OVA+Al( OH)3( 5 mg OVA and 175 mg Al( OH)3 in 30 m L saline each time) or saline( 30 m L saline each time) by intraperitoneal injection on day 1,7 and 14.This was then followed by an aerosol challenge in 1% OVA( 30 min·d~(-1)) from day 19 to 25( 7 times) using an ultrasonic nebulizer. On the 26 th day,the organ coefficient of mice brain was counted,then the contents of oxidative stress of mice brain were measured,including reactive oxygen species( ROS),glutathione( GSH) and malondialdehyde( MDA),and the concentrations of NF-κB and interleukin-1β( IL-1β) were detected by using ELISA kits.Detection of interleukin-6( IL-6) was made with immunohistochemical method. Histological assay for brain was also conducted. In our results,all the OVA treated groups showed a significant increase of ROS and a significant decrease of GSH contents when compared with the control group. Except OVA-sensitized group,other OVA treated groups also showed a significant increase of MDA contents when compared with the control group,and MDA contents of OVA-sensitized group showed significant change when compared to the combined exposure group. In ROS and GSH,combined exposure showed some joint effect compared with single exposure. When OVA was applied in combination with formaldehyde and PM_(2.5),NF-κB was activated. And all the OVA treated groups showed increased levels of IL-1β and IL-6 compared with the control group. And the combined exposure showed an aggravated effect when compared with OVA-sensitized group. Histopathological observation of the hippocampus in mice brain clearly showed the difference of eosin( EO) stained neurons in the combined exposure group compared with the control group and OVA-sensitized group. The pyramidal neurons of the mice with allergic asthma exposed to formaldehyde and/or PM_(2.5) had been reduced in number,the cells were swollen and the dendrites had disappeared. Allergic asthma can cause damage to the brain through oxidative stress. Exposure to formaldehyde and PM_(2.5) will increase the damage caused by allergic asthma to the brain,which may be mediated by oxidative stress and NF-κB activation.This promotes the release of the inflammatory factors,resulting in increased inflammation.     

Modelling concentrations of airborne primary and secondary PM10 and PM2.5 with the BelEUROS-model in Belgium

The Eulerian Chemistry-Transport Model BelEUROS was used to calculate the concentrations of airborne PM₁₀ and PM_2.5 over Europe. Both primary as well as secondary particulate matter in the respirable size-range was taken into account. Especially PM_2.5 aerosols are often formed in the atmosphere from gaseous precursor compounds. Comprehensive computer codes for the calculation of gas phase chemical reactions and thermodynamic equilibria between compounds in the gas-phase and the particulate phase had been implemented into the BelEUROS-model. Calculated concentrations of PM₁₀ and PM_2.5 are compared to observations, including both the spatial and daily, temporal distribution of particulate matter in Belgium for certain monitoring locations and periods. The concentrations of the secondary compounds ammonium, nitrate and sulfate have also been compared to observed values. BelEUROS was found to reproduce the observed concentrations rather well. The model was applied to assess the contribution of emissions derived from the sector agriculture in Flanders, the northern part of Belgium, to PM₁₀- and PM_2.5-concentrations. The results demonstrate the importance of ammonia emissions in the formation of secondary particulate matter. Hence, future European emission abatement policy should consider more the role of ammonia in the formation of secondary particles.