Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to atmospheric PM2.5 exposure

In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter (PM_2.5) can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function. The results indicate that PM_2.5 inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation, thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice. Furthermore, excessive reactive oxygen species generation was involved in the impairment. Interestingly, these alterations were partially reversed after exposure to PM_2.5 ended. These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM_2.5 inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.     

Spatiotemporal trends of PM2.5 and its major chemical components at urban sites in Canada

To evaluate the effectiveness of emission control regulations designed for reducing air pollution, chemically resolved PM_2.5 data have been collected across Canada through the National Air Pollution Surveillance network in the past decade. 24-hr time integrated PM_2.5 collected at seven urban and two rural sites during 2010-2016 were analyzed to characterize geographical and seasonal patterns and associated potential causes. Site-specific seven-year mean gravimetric PM_2.5 mass concentrations ranged from 5.7 to 9.6 µg/m³. Seven-year mean concentrations of SO₄^2?, NO₃^?, NH₄⁺, organic carbon (OC), and elemental carbon (EC) were in the range of 0.68 to 1.6, 0.21 to 1.5, 0.27 to 0.71, 1.1 to 1.9, and 0.37 to 0.71 µg /m³, accounting for 10.8%-18.1%, 3.7%-16.7%, 4.7%-7.4%, 18.4%-21.0%, and 6.4%-10.6%, respectively, of gravimetric PM_2.5 mass. PM_2.5 and its five major chemical components showed higher concentrations in southeastern Canada and lower values in Atlantic Canada, with the seven-year mean ratios between the two regions being on the order of 1.7 for PM_2.5 and 1.8-7.1 for its chemical components. When comparing the concentrations between urban and rural sites within the same region, those of SO₄^2? and NH₄⁺ were comparable, while those of NO₃^?, OC, and EC were around 20%, 40%-50%, and 70%-80%, respectively, higher at urban than rural sites, indicating the regional scale impacts of SO₄^2? and NH₄⁺ and effects of local sources on OC and EC. Monthly variations generally showed summertime peaks for SO₄^2? and wintertime peaks for NO₃^?, but those of NH₄⁺, OC, and EC exhibited different seasonality at different locations.     

An integrative analysis of miRNA and mRNA expression in the brains of Alzheimer's disease transgenic mice after real-world PM2.5 exposure

Fine particulatematter (PM2.5) is associated with increased risks of Alzheimer’s disease (AD),yet the toxicologicalmechanisms of PM2.5 promoting AD remain unclear. In this study,wildtype and APP/PS1 transgenic mice (AD mice) were exposed to either filtered air (FA) or PM2.5 for eight weeks with a real-world exposure system in Taiyuan, China (mean PM2.5 concentration in the cage was 61 μg/m3). We found that PM2.5 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 PM2.5 exposure were screened.Using RT-qPCR, seven DEmiRNAs (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 PM2.5-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 PM2.5- elevated pro-inflammatory cytokine levels and PM2.5-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising miRNA andmRNA biomarkers and potentialmiRNA-mRNA interaction networks of PM2.5-promoted AD.     

铜陵市冬春季PM10和PM2.5中元素特征及来源分析

目的了解铜陵市颗粒物中的元素特征和主要来源。方法选择2014年冬季和春季的部分时段,在铜陵市国家环境空气监测站——新民污水处理厂(工业区)采集PM_(10)和PM_(2.5)样品,使用X射线荧光光谱(XRF)法进行元素的定量测试。采样期间,冬季的空气质量以良和中、轻度污染为主;春季以中度和重度污染天气为主,采样期间出现了明显的重污染。结果 PM_(2.5)和PM_(10)中S和Si元素的浓度均比其余元素高,P和Cu元素的浓度远低于其余元素。空气污染的指数越高,Fe、Mg、Al、Si则更易富集在PM_(10)上,而K、Cu、Na、Cl、S元素更易富集在PM_(2.5)上,Ca和P这两种元素在PM_(10)和PM_(2.5)上的富集程度相当。空气颗粒物中,富集最多的元素是K,其次为Fe和Mg;元素Cu、K、Cl在PM_(10)中的富集程度要高于PM_(2.5)。结论扬尘(包括地面扬尘和建筑尘)是PM_(10)的最大来源,其次是开采矿山和燃烧生物质,燃煤、炼铜等工企业排放贡献最小;对于PM_(2.5)而言,最大的来源是风沙、扬尘和开采矿山,其次是燃煤、燃烧生物质和其他的工企业排放,炼铜的贡献最小。     

水泥窑PM2.5排放特性及其PAHs风险分析

采用荷电低压颗粒物撞击器(ELPI)、便携式PM2.5采样器和稀释系统,对国内3家新型干法水泥生产厂(5条生产线)的水泥窑(包括窑头和窑尾)进行现场采样,分析水泥窑排放PM2.5的质量浓度、粒数浓度及其中的多环芳烃(PAHs)浓度,对呼吸致癌风险进行评价.结果表明:从粒数浓度分析,PM2.5中70%以上为PM0.33,这部分颗粒物主要是由气化凝结形成的.各采样点排放的PAHs主要以二环和三环的低环PAHs为主.第3个水泥厂窑头排放的PAHs含量最高,而且苯并[a]芘(BaP)超过国家所规定的8ng/m3标准限值,同时其呼吸致癌风险水平为4.46×10-4,高于可接受致癌风险水平的上限,需要有效处理.     

江苏省2014年上半年颗粒物PM2.5、PM10污染特征分析研究

根据2014年1月1日～6月30日江苏省13地级市监测PM2.5,PM10的数据,分析其污染特征.结果表明:全省PM2.5和PM10污染较严重,全省PM2.5,PM10超标率都分别达到78.33％,66.11％以上,尤其是细颗粒物的污染占主导地位;PM2.5/PM10的比值范围达到0.461 9～0.687 2,全省PM2.5和PM10之间存在显著的线性关系;PM2.5,PM10浓度时空分布特征为PM2.5:1月＞3月＞2月＞5月＞6月＞4月,PM10:1月＞5月＞3月＞6月＞2月＞4月;苏北＞苏中＞苏南.     

我国PM2.5的污染状况和污染特征

对中国大气中PM2.5的污染状况和污染特征进行了综述和分析,其中包括我国PM2.5质量浓度的时间、空间污染特征、来源解析以及与PM10的关系.     

Cause of PM2.5 pollution during the 2016-2017 heating season in Beijing, Tianjin, and Langfang, China

To investigate the cause of fine particulate matter(particles with an aerodynamic diameter less than 2.5 um,PM2.5) pollution in the heating season in the North China Plain(specifically Beijing,Tianjin,and Langfang),water-soluble ions and carbonaceous components in PM_2.5were simultaneously measured by online instruments with 1-hr resolution,from November 15,2016 to March 15,2017.The results showed extreme severity of PM_2.5 pollution on a regional scale.Secondary inorganic io...     

南京市空气中颗粒物PM10、PM2.5污染水平

 为了初步调查南京市空气中颗粒物PM10、PM2.5的污染水平,于2001年冬、春、秋3季在南京市的5个典型城市功能区,用大流量采样器收集了50个样品.结果表明,南京市PM10、PM2.5的污染很严重,超标率分别为72%和92%,最大超标倍数达到6.3和9.0,而且对人体健康危害更大的PM2.5占PM10的大部分,约为68%,应引起公众和相关职能部门的高度重视.     

上海冬季公共交通出行PM1污染暴露特征

使用DustTrakTM-II-8530粉尘仪对上海市居民出行的典型公共交通出行(地铁和公交车)的PM1暴露水平进行了平行监测,以了解其暴露特征.结果表明,公交车和地铁出行的单程平均PM1暴露浓度分别为(0.079±0.067)mg/m3和(0.065±0.056)mg/m3;交通工具内的暴露浓度低于户外步行的暴露浓度,尤其是地铁车厢内.公交车和地铁出行的单程暴露剂量分别为(0.028±0.024)mg和(0.034±0.033)mg.公交车出行的暴露剂量主要来源于车内,其贡献率达52.2%;地铁出行的暴露剂量主要来源于地面步行段(42.4%)及进站候车(44.2%).2种出行方式之间的暴露剂量和暴露浓度相对大小的不同表明,空气污染对公众健康影响的分析需要综合考虑出行方式和呼吸速率等的影响.     

2011年秋季广州城区大气PM2.5微观形貌和粒度分布

利用高分辨率扫描电镜加能谱仪(SEM-EDX)和图像数据分析技术对2011年秋季广州市中心大气PM2.5的微观形貌和粒度分布特征进行研究,系统获得3种典型颗粒(矿物、烟尘集合体和燃煤飞灰)和其它未知颗粒的数量-粒度分布和体积-粒度分布数据.结果表明,PM2.5颗粒数量-粒度分布峰值落在0.1~0.2μm之间,属于积聚模态中含有气相反应产物的凝结亚模态.3种典型颗粒对PM2.5的数量和体积贡献均为矿物>>烟尘集合体>飞灰.矿物主要分布在0.1~0.3μm范围内,所占数量百分比为41.97%,其中0.1~0.2μm范围内矿物占比高达26.42%,是影响PM2.5颗粒整体分布的主要因素.不同采样时段(上午、下午、晚上)和下雨前后PM2.5颗粒的粒度分布特征基本一致,但晚上和下雨后小于0.1μm的颗粒比例有明显减少趋势.     

不同混合基体改进剂在涂钼石墨管测定细颗粒物中锡的应用研究

细颗粒物(PM2.5)是目前环境相关研究的焦点对象之一,但如何客观有效的分析检测细颗粒物的金属组分,却缺乏相关国家标准规范支撑,对应研究亦鲜见报道.利用美国PE公司AAnalyst600型石墨炉原子吸收仪进行实验,研究几种不同混合基体改进剂在涂钼石墨管石墨炉原子吸收法测定细颗粒物(PM2.5)中锡的影响,发现利用硝酸钯-钼酸铵混合溶液为基体改进剂测定锡,方法的相对标准偏差为1.8%~4.5%,空白回收率为95.4%~97.8%,实际样品回收率为87.3%~98.5%.能够满足国家实验室分析质控要求.适用于细颗粒物中微量锡的测定.     

广州市区公交车站PM_(2.5)与CO暴露水平研究

用便携式颗粒物浓度测定仪(DustTrak Model8520)和CO测定仪(Q-Trak Model8551),于2008年9月至2009年1月对广州市区11个代表性公交车站的PM2.5和CO暴露水平进行了测定。结果表明,公交车站7:00～19:00时间段PM2.5的平均浓度范围为206～348μg/m3,总体均值达288μg/m3,显示公交车站PM2.5污染问题突出;CO平均浓度范围1.5～4.0mg/m3,总体平均2.8mg/m3,有六个站点平均浓度超过了我国环境空气质量标准限值(4.0mg/m3或3.2mg/m3)。大多数站点工作日与非工作日PM2.5与CO水平差异不大,部分站点则受车流量和客流量变化影响呈现差异。同一站点PM2.5日变化特征不如CO明显,一次污染物CO变化受交通高峰影响呈双峰特征,而PM2.5水平影响因素复杂,一般白天较低,夜晚21:00出现峰值。不同站点CO与车流量未见显著相关性,表明车流量并不是决定公交站点CO水平的唯一因素,而扩散条件及公交车排放可能也是重要影响因素;与CO不同,不同站点PM2.5与车流量表现出显著相关(p0.05),可能侧面反映路面扬尘对公交车站PM2.5水平的影响和贡献。     

贵州农村冬季不同燃料燃烧产生的室内外PM_(2.5)研究

为了解贵州农村家庭冬季不同燃料燃烧产生的室内外PM2.5污染状况及其产生与变化规律,2011年11月～2012年2月间选择燃煤村寨水城县A村、烧柴村寨从江县B村和沼气推广示范村寨贵阳市乌当区C村各1户,每户设置厨房、卧室和室外3个监测点,进行连续5天PM2.5小时浓度和日均浓度的监测。结果表明:贵州农村室内因冬季燃烧不同燃料,产生的PM2.5浓度水平差异较大,但3户室内外空气中PM2.5的浓度大部分高于GB 3095—2012《环境空气质量标准》中PM2.5日均浓度限值75μg/m3,其中燃煤的A村室内PM2.5的浓度水平最高;厨房PM2.5的浓度,燃煤的家庭>燃柴的家庭>燃沼气的家庭,表明沼气是相对最为清洁的能源;而厨房与卧室相比,燃煤家庭和燃柴家庭厨房PM2.5平均小时浓度均高于卧室的PM2.5平均小时浓度,表明厨房应是室内主要的因燃料引起的环境空气污染区域;B村室外环境空气中PM2.5日均浓度高于其卧室中PM2.5日均浓度,表明除燃料燃烧本身引起的室内环境空气污染外,改善室外环境空气质量也是不容忽视的重要方面。     

广州市学龄儿童在校期间PM2.5暴露水平评价

采用便携式大气颗粒物采样器(MiniVol)和便携式颗粒物检测仪(pDR-1500)在2010年3月底至4月初对广州市某小学的室内外细颗粒物(PM2.5)浓度进行了监测,并对学龄儿童在校期间活动模式进行了跟踪调查,评价了学龄儿童在校期间PM2.5暴露水平.结果显示该小学室内外日均PM2.5浓度范围为25.1~145.9μg/m3,室内PM2.5浓度略低于室外,两者呈明显的正相关关系(R2=0.65);室内实时PM2.5浓度结果表明非假期与假期存在差异.使用离子色谱分析了PM2.5的阴离子成分,其中NO3-和SO42-占阴离子成分总量的73%~95%.研究显示道路交通源是采样地点PM2.5主要来源之一.学龄儿童在校期间单位体重PM2.5日均潜在暴露水平为7.6μg/(kg×d),个体日均潜在暴露水平为246.8μg/d.     

金昌市PM2.5及PM10短期暴露对成人血压水平的影响

为探索西北地区颗粒物(PM)短期暴露对人群血压(BP)水平的影响,基于金昌队列研究平台,收集甘肃省金昌市2011~2017年颗粒物污染数据及队列人群血压测量数据,在调整相关混杂因素基础上,采用线性混合效应模型分析PM_2.5和PM₁₀短期暴露对收缩压(SBP)、舒张压(DBP)、平均动脉压(MAP)、脉压(PP)和Mid-BP (SBP和DBP的均值)的影响.结果显示,随着PM_2.5浓度的增加,人群SBP,MAP,PP和Mid-BP均呈上升趋势,该效应值分别在累积滞后05,03,07和05d最大.随着PM₁₀浓度的增加,5种BP指标也均呈上升趋势,效应最大值均出现在累积滞后07d.PM_2.5和PM₁₀对BP产生的影响分别在吸烟和男性人群中更为显著.此外,沙尘天气和气态污染物(SO₂和NO₂)对PM-BP效应存在一定的修饰作用.因此,在该队列人群中,PM_2.5和PM₁₀短期暴露对人群血压具有一定影响,吸烟者和男性人群可能是颗粒物影响血压效应的易感人群.     

Adverse effects of triclosan on kidney in mice: Implication of lipid metabolism disorders

Triclosan (TCS) is a ubiquitous antimicrobial used in daily consumer products. Previous reports have shown that TCS could induce hepatotoxicity, endocrine disruption, disturbance on immune function and impaired thyroid function. Kidney is critical in the elimination of toxins, while the effects of TCS on kidney have not yet been well-characterized. The aim of the present study was to investigate the effects of TCS exposure on kidney function and the possible underlying mechanisms in mice. Male C57BL/6 mice were orally exposed to TCS with the doses of 10 and 100 mg/(kg•day) for 13 weeks. TCS was dissolved in dimethyl sulfoxide (DMSO) and diluted by corn oil for exposure. Corn oil containing DMSO was used as vehicle control. Serum and kidney tissues were collected for study. Biomarkers associated with kidney function, oxidative stress, inflammation and fibrosis were assessed. Our results showed that TCS could cause renal injury as was revealed by increased levels of renal function markers including serum creatinine, urea nitrogen and uric acid, as well as increased oxidative stress, pro-inflammatory cytokines and fibrotic markers in a dose dependent manner, which were more significantly in 100 mg/(kg•day) group. Mass spectrometry-based analysis of metabolites related with lipid metabolism demonstrated the occurrence of lipid accumulation and defective fatty acid oxidation in 100 mg/(kg•day) TCS-exposed mouse kidney. These processes might lead to lipotoxicity and energy depletion, thus resulting in kidney fibrosis and functional decline. Taken together, the present study demonstrated that TCS could induce lipid accumulation and fatty acid metabolism disturbance in mouse kidney, which might contribute to renal function impairment. The present study further widens our insights into the adverse effects of TCS.