Thymic involution produced by diesel exhaust particles and their constituents in mice

Epidemiological studies suggest that diesel exhaust particles (DEP) contribute to an increase in allergic diseases. To assess the effects of DEP on the central immune system, mice were exposed to DEP by intraperitoneal (IP) administration. Exposure to DEP resulted in severe thymic involution accompanied by a reduction in the number of thymocytes, especially in cortical CD4⁺CD8⁺ double positive and double negative subsets. Core carbon particles associated with a mixture of chemical compounds in DEP did not appear to be responsible for the DEP-induced thymic involution because carbon graphite does not affect neither the number nor the CD4/CD8 profile of thymocytes. Extraction of DEP by ether, acidic and basic solvents showed that several independent fractions including the neutral ether fraction, which contains polycyclic aromatic hydrocarbons (PAH), induced thymic involution. Among major PAH components of DEP, benzo[b]fluoranthene (BbF), benzo[a]pyrene (BaP), and benzo[k]fluoranthene (BkF) were very potent inducers of thymic involution at an ED50 of less than 100?ng per mouse body. Nonetheless, DEP treatment of mice with targeted disruption of genes encoding the aryl hydrocarbon receptor (AHR), AHR nuclear translocator (ARNT), or microsomal epoxide hydolase (mEH) indicated that DEP produced thymic involution even in the absence of PAH-induced AHR/ARNT signal transduction or mEH-mediated PAH catabolism. On the other hand, BaP-mediated thymic involution was completely dependent on AHR, partially dependent on ARNT in T cells, and independent of mEH. These results indicate that DEP-induced thymic involution is mediated both by PAH-AHR/ARNT-dependent and -independent mechanisms.     

出生前后全氟辛烷磺酸（PFOS）暴露对大鼠额叶皮质中IGF-Ⅰ、IGF-ⅠR和IGFBP-2 mRNA水平的影响

为研究出生前后不同时期全氟辛烷磺酸(PFOS)暴露对大鼠仔鼠额叶皮质胰岛素样生长因子-Ⅰ(IGF-Ⅰ)、胰岛素样生长因子-Ⅰ受体(IGF-ⅠR)和胰岛素样生长因子结合蛋白-2(IGFBP-2)mRNA水平的影响,将28只受孕Wistar大鼠按3:2:2的比例随机分到对照(C)、低剂量(L)和高剂量(H)组中,从妊娠第0天开始分别自由摄食含0、7.2、14.4mg·kg-(1以饲料中的PFOS计)的粉末状饲料进行连续染毒至出生后28天.采用交叉哺育的方法建立出生前后均不暴露(CC)、仅出生前暴露(LC和HC)、仅出生后暴露(CL和CH)、出生前后均暴露(LL和HH)于PFOS的动物模型.采用半定量RT-PCR法检测各组仔鼠额叶皮质IGF-Ⅰ、IGF-ⅠR和IGFBP-2mRNA水平的变化.结果表明,对照组仔鼠额叶皮质IGF-Ⅰ、IGFBP-2mRNA在PD14时处于较高水平,而在PD1和PD28时水平较低;IGF-ⅠRmRNA在PD1时只处于较低水平,随年龄的增加而逐渐升高.在PD1时,暴露组仔鼠IGF-Ⅰ、IGF-ⅠR、IGFBP-2mRNA水平显著高于对照组(p<0.05).在PD14时,除LC组仔鼠IGF-ⅠRmRNA水平显著高于对照组之外,其余各暴露组仔鼠3者mRNA水平均显著低于对照组(p<0.01).此外,出生后暴露PFOS组的仔鼠额叶皮质IGF-Ⅰ、IGFBP-2mRNA水平降低程度比出生前暴露PFOS组仔鼠更高.在PD28时,暴露组仔鼠IGF-Ⅰ、IGF-ⅠRmRNA水平显著低于对照组(p<0.01),而IGFBP-2mRNA水平与对照组之间的差异无显著性(p>0.05).出生前后不同时期暴露PFOS导致大鼠仔鼠额叶皮质IGF-Ⅰ、IGF-ⅠR和IGFBP-2mRNA水平变化,为PFOS发育神经毒性的研究提供了一定的线索.     

Source apportionment studies for particulates (PM10) in Kozhikode,South Western India using a combined receptor model

In the present work, source apportionment studies were carried out for particulate matter – one among the significant pollutants as addressed by The National Ambient Air Quality Standards. Advantages and disadvantages of each receptor model were addressed using a combined receptor model which integrates Factor Analysis (FA), Positive Matrix Factorisation (PMF) and Chemical Mass Balance (CMB). Verification of the approach was done using sets of synthetic data as well as field data from Kozhikode. Sampling was carried out in National Institute of Technology, Calicut for a period of over 26 days with 24-hour sampling. The sampling gave an average PM concentration value in the range of 29.174–129.176 µg m^?3. Studies using field data revealed five dominant sources and their contributions obtained from CMB and PMF were compared. Soil dust (contribution from CMB: 18%; contribution from PMF: 16%), marine aerosol (17%; 25%), construction and aggregate processing (46%; 11%), garden waste combustion (18%; 45%), and vehicular exhaust (1%; 3%) were major contributors in the site under study. The outcomes of the study integrated with the support of local authorities and by the acceptance of residents can definitely curb the pollution levels in the site under the study.     

改进型重组基因酵母TR-GRIP1检测化合物甲状腺激素干扰活性

应用酵母双杂交技术构建重组TR(甲状腺激素受体)基因酵母,用以检测类/抗甲状腺激素化合物及环境样品的甲状腺激素干扰活性. 提取并纯化含有TR基因的酵母表达质粒pGBT9-TR以及含有TR共激活因子GRIP1基因的酵母表达质粒pGAD424-GRIP1,将pGBT9-TR和pGAD424-GRIP1同时转化至酵母细胞Y187,以营养缺陷型培养基(SD/-Trp/-Leu)筛选阳性菌落,构建TR-GRIP1双杂交酵母. 考察该酵母与天然甲状腺激素——T₃(三碘甲状腺原氨酸)的结合情况,确定最佳暴露时间,建立剂量－效应关系曲线. 结果表明:TR-GRIP1双杂交酵母能够与T₃结合诱导β-半乳糖苷酶活性,选择暴露时间为2 h,T₃诱导酶活性的EC₅₀值为1.1×10-7 mol/L;构建的重组基因酵母TR-GRIP1提供了检测化合物甲状腺激素干扰活性的新方法.      

大气颗粒物源解析受体模型优化技术研究

针对大气颗粒物来源解析技术存在的2大问题:二次有机碳(SOC)对CMB模型的影响及源与受体不匹配程度对源成分谱共线性的影响,给出了解决方案.对于SOC影响的问题,提出从受体的角度扣除SOC,对CMB模型进行修正,降低SOC的影响;对于共线性问题,提出了PCA/MLR-CMB复合模型,复合模型首先进行PCA/MLR的解析,降低受体中未知源的影响,使得纳入CMB模型中的源和受体匹配程度大大提高,从而使得共线性源类能够得到理想的结果.     

成都市区夏季大气挥发性有机物污染特征及来源解析

2019年6~9月在成都市区对挥发性有机物（VOCs）进行在线观测,研究夏季VOCs浓度水平、变化特征、臭氧生成贡献（OFP）及来源贡献.结果表明,成都市区夏季TVOCs（总挥发性有机物）平均质量浓度为112.66 μg·m^-3,烷烃（29.51%）和卤代烃（23.23%）为主要组分;VOCs日变化峰值主要出现在上午10：00~11：00,受城市机动车、油气挥发和工业排放影响;夏季VOCs的OFP贡献中芳香烃贡献率（42.7%）最高,其次为烯烃（27.4%）,关键活性物种为间/对-二甲苯、乙烯、丙烯、邻-二甲苯、异戊烷、环戊烷和丙烯醛等;使用PMF受体模型进行来源解析表明,移动源为成都市区夏季VOCs的主要贡献源,贡献率为34%,其次为工业源（17%）和油气挥发（14%）,溶剂使用源和天然源分别贡献11%和13%.因此,机动车和工业排放为成都市区VOCs的重点控制源,同时溶剂使用及油气挥发等污染源的管控也不可忽视.     

环境和人体中氯代/溴代多环芳烃的研究进展——污染来源、分析方法和污染特征

氯代/溴代多环芳烃（Cl/Br-PAHs）是一类具有与二噁英和多环芳烃（PAHs）相似结构和致癌效应的新兴持久性毒害污染物,其环境行为归趋和潜在风险受到了高度重视.本研究以"Cl-PAH*" OR "Br-PAH*" OR "H-PAH*" OR "chlorinated PAH*" OR "brominated PAH*" OR "halogenated PAHs" OR "chlorinated polycyclic aromatic hydrocarbon*" OR "brominated polycyclic aromatic hydrocarbon*" OR "halogenated polycyclic aromatic hydrocarbon*"为主题对Web of Science核心合集数据库进行了检索,并着重对环境/人体中Cl/Br-PAHs污染来源、污染特征和分析方法的研究进展进行了综述.结果表明：截止2021年1月,环境/人体中Cl/Br-PAHs的相关文献共计225篇.这些研究表明：Cl/Br-PAHs主要来源于废弃物焚烧、汽车尾气排放、金属冶炼、电子垃圾拆解等热过程和光化学反应过程;目前已在全球各类环境介质中被检出,并表现出持久存在性、长距离迁移性和生物可利用性;Cl/Br-PAHs被证实具有与其母体PAHs相似甚至更强的毒性,但目前对其形成机理和环境行为尚不明确,也尚未有统一有效且精准的分析方法,已报道的化合物种类十分有限,总体研究处于起步阶段.结合目前Cl/Br-PAHs的研究现状和存在的问题,今后应在其高通量精准筛查分析、源排放指纹识别追溯、环境迁移转化行为及潜在风险上开展研究.     

大气中挥发性有机化合物(VOCs)的人为来源研究

在2002年春、夏、秋、冬四季对环境大气中挥发性有机化合物的组成和变化规律进行了研究,在此基础上运用CMB8.0受体模型对各类污染源进行了源解析,得到受体点各人为污染源的年平均贡献率分别为:汽车尾气62%,汽油挥发9%,石油液化气10%,涂料6%,石油化工6%,未知源6%.对不同物种贡献的分析显示,环境大气中的乙烯、苯和甲苯等化合物主要来自于汽车尾气的排放,异戊烷来自于汽油的挥发,石油液化气、涂料、石油化工分别对大气中的异丁烷、正己烷和2,4-二甲基戊烷贡献量最大.     

工频磁场诱导人FL细胞膜EGF的受体聚簇及噪声磁场的干预

为了研究50Hz工频磁场对人源细胞膜表皮生长因子(epidermal growth factor,EGF)的受体聚簇现象的可能诱导作用及噪声磁场的干预,将人羊膜细胞FL(human amniotic cells)分别用EGF、不同强度(0.05、0.1、0.2、0.4mT)工频磁场、噪声磁场、工频磁场和噪声磁场叠加的复合场处理15 min后,用间接免疫荧光染色法标记,并用激光共聚焦显微镜观察细胞膜表皮生长因子(EGF)的受体的聚簇现象.结果表明,0.1、0.2、0.4mT工频磁场辐照FL细胞15 min可诱导细胞膜EGF的受体发生聚簇,但0.05mT工频磁场辐照时,细胞膜不出现EGF受体的明显聚簇.0.2mT噪声磁场则不能诱导细胞膜EGF受体的聚簇;当0.2mT噪声磁场与0.1、0.2mT工频磁场叠加后,可抑制工频磁场诱导的细胞膜EGF受体聚簇,但不能完全抑制0.4mT工频磁场诱导的细胞膜EGF受体聚簇.研究结果表明,一定强度的工频磁场能诱导细胞膜EGF受体的聚簇;其作用阈值在0.05～0.1mT之间;噪声磁场对工频磁场诱导膜受体聚簇的干预作用存在剂量-效应关系.