富集因子判定大气可吸入颗粒物元素污染来源研究方法初探

本文利用分析速度快、线性范围宽、能够多元素同时分析的电感耦合等离子体发射光谱（ICP-AES）分析技术、采用微波消解的方法检测大气颗粒物PM10样品膜中的元机元素含量,用富集因子法探讨了某地春季大气可吸入颗粒物中元素的富集程度,判断出自然与人为污染来源,对大气可吸入颗粒物的研究方法进行了初步的探讨,为相应的治理措施提供了科学的依据。     

徐州市大气颗粒物PM_(10)与PM_(2.5)污染水平分析

在徐州市的7个典型城市功能区采集大气颗粒物样品,对PM_(10)和PM_(2.5)的污染水平进行了分析。结果表明,徐州市PM_(10)和PM_(2.5)的污染较严重,超标率分别为26.3%和31.2%;空间上,工业区和交通居住混合区污染严重;时间上,污染水平呈现为冬季春季秋季夏季;PM_(2.5)在PM_(10)中的比重大于粗颗粒物,约占58%,应重视对其监测与治理。     

北京市城乡结合部大气可吸入颗粒物中正构烷烃的分析

分不同季节采集分析北京市城乡结合部的大气可吸入颗粒物。用气相色谱-质谱技术分析了北京市城乡结合部大气可吸入颗粒物中饱和烃组分,检测出C11～C37的正构烷烃及其它烃类化合物。正构烷烃分布主要可分为3种类型:前峰型、后峰型、单峰型。利用地球化学的相关参数,同时结合正构烷烃的分布特征,对正构烷烃的污染来源进行分析。前峰型,主要来源于汽车尾气和化石燃料燃烧。后峰型,主要来源于植物蜡。单峰型,既有植物蜡的输入,也有尾气和化石燃料燃烧的输入。对正构烷烃在不同季节大气可吸入颗粒物中分布情况的比较,表明正构烷烃分布随季节有较明显的变化。     

佛山禅城区大气可吸入颗粒物污染特征及其影响因素分析

通过对佛山禅城区5个测点大气中5种粒径的可吸入颗粒物密度进行测定,指出可吸入颗粒物的日变化、季节变化以及空间分布特征,并在分析其影响因素及主要来源的基础上,提出了一些防治对策和建议。     

超声提取高效液相色谱法测定大气可吸入颗粒物PM10中的四种多环芳烃

建立了以甲醇-水为流动相,高效液相色谱法同时测定大气可吸入颗粒物PM10中四种多环芳烃化合物的方法。方法用中流量TH-16A四通道采样器,石英纤维滤膜采集大气颗粒物样品,以甲醇为溶剂,超声波提取样品;用甲醇-水作流动相进行高效液相色谱分离,荧光检测器检测。采用优化的分离和测定条件对四种多环芳烃化合物苯并(b)荧蒽、苯并(k)荧蒽、苯并(a)芘、苯并[ghi]芘进行加标回收率和精密度实验,回收率范围为86%~93%,相对标准偏差分别为2.0%~6.2%。     

燃烧源可吸入颗粒物声波团聚研究进展与展望

燃烧过程是大气可吸入颗粒物PM10的重要来源,控制燃烧源PM10排放已引起广泛关注,目前技术发展的主要途径是设置预处理阶段使细颗粒凝并成较大颗粒后用常规除尘设备脱除,外加声场可使PM10团聚长大;从声波团聚的宏观效果及微观机理试验2个方面对可吸入颗粒物声波团聚研究现状进行了述评,分析了声波团聚存在的主要问题及其今后需继续进行的研究方向,并介绍了作者的初步研究结果。     

光催化防治燃烧源可吸入颗粒物可行性及存在问题分析

依据气相、固相光催化特性、燃烧源一次、二次可吸入颗粒物PM10的形成机理等研究成果,对应用光催化技术防治燃烧源PM10的可行性及存在问题加以分析;指出在光催化-热催化耦合新技术降解一次PM10的气相有机前体物及PM10中可溶性有机组分SOF、室温光催化氧化二次有机气溶胶SOA及其气相前体物等方面有一定的可行性,但由于存在光催化剂的失活,紫外光强的衰减,废气中SO2、NOx的影响,SOF、SOA降解速率慢及光催化过程主要发生在催化剂表面等原因,目前,欲应用光催化技术有效解决燃烧源PM10的污染问题尚有一定难度.     

喷淋塔内可吸入颗粒物的脱除与凝结增长特性

引言 可吸入颗粒物是一种重要的大气污染物,其对人类健康和大气环境带来极大危害[1-2].在当前以燃用化石燃料为主的能源结构和与日俱增的能源消耗形势下,燃烧源的排放成为可吸入颗粒物的一个重要来源[3],主要原因是目前电站及工业生产中的除尘设备,如电除尘器、过滤除尘器等虽然已达到很高的水平,但对可吸入颗粒物的脱除效率却较低,使得大量颗粒排放到大气中.     

大气可吸入颗粒物对环境和人体健康的危害

本文介绍了大气可吸入颗粒物 PM10（空气动力学直径小于或等于10（μm）的基本特性及污染现状。阐述了可吸入颗粒物对环境产生的严重影响;依据国内外流行病学研究的结果,概述了可吸入颗粒物对人体呼吸系统、心血管系统、神经系统、生殖系统等造成的较为广泛的损害。同时,也指出了我国进行大气可吸入颗粒物研究的意义。     

印染污泥脱水车间PM_(10)与PM_(2.5)质量浓度分析

夏秋两季对两个典型的污泥脱水车间(CY和HT)采集大气颗粒样品,对PM_(10)与PM_(2.5)质量浓度进行分析。结果表明,通风性较差的HT点的PM_(10)与PM_(2.5)污染严重,超过《环境空气质量标准》(GB3095-2012)规定2至3倍;颗粒物浓度季节变化规律:秋季夏季;PM_(2.5)/PM_(10)比值在0.5以上,表明颗粒物以PM_(2.5)为主;CY点通风好,利于室内颗粒物排放;HT点通风差,不利于室内颗粒物排放。HT点应改善通风设备,保障工人生命健康安全。     

Inter- and Intra-Community Variability in Continuous Coarse Particulate Matter (PM10-2.5) Concentrations in the Los Angeles Area

Continuous coarse particulate matter (CPM, PM _10?2.5 ) concentrations were measured hourly at three different sites in the Los Angeles area from April 2008 through May 2009 as part of a larger study of the characteristics and toxicology of CPM. Mean hourly concentrations calculated seasonally ranged from less than 5 μg m ^–3 to near 70 μg m ^–3 at the three sites depending upon the CPM source variability and prevailing meteorology. Different diurnal concentration profiles were observed at each site. Correlation analysis indicates that CPM concentrations can generally be explained by wind-induced road dust re-suspension, particularly in drier seasons. CPM concentrations between the sites were not appreciably correlated and metrics used to assess variability between the sites—the coefficients of divergence—indicated that CPM concentrations were heterogeneous. The relative CPM contribution to observed PM ₁₀ concentrations varied by season and between sites. Additional concurrent CPM data available within a few km of the three sites indicate that intra-community variability can be on the same order as that observed for inter-community variability, although a similar analysis using PM ₁₀ data yielded reduced heterogeneity. The results indicate that accurate exposure assessment to CPM in the Los Angeles area requires measurements of CPM concentrations at different sites with higher temporal resolution than a single daily mean value.     

Emission of Particulate Matter 2.5 (PM2.5) from Sewage Sludge Incinerators in Japan

Because fine particulate matter ≤2.5 µm in diameter (PM2.5) causes health problems, PM2.5 emissions are of concern. However, little research on stationary sources has been conducted. To determine the concentration and filtration behavior of PM2.5, dust was collected from five fluid-bed sewage sludge incinerators (SSIs) sorted by particle size using cascade impactors. The average PM2.5 concentration was 0.00014–4.8 mg/Nm³. The total estimated amount of PM2.5 emissions from the SSIs for all plants in Japan was 0.96–8.9 tons/year. Since the SSIs with dry Electrostatic Precipitators (EP) contributed 75–99% of the total emissions, replacing dry EPs with bag filters would significantly reduce the PM2.5 emissions from SSI.     

大气颗粒物PM2.5化学组分分析方法概述

大气细颗粒物PM2.5中化学组分的分析方法做了简要的介绍,PM2.5的化学组分主要包括水溶性离子、无机元素、有机碳和元素碳,并分析了各种方法的优缺点,以便于在研究中选取更简单有效的方法,并展望了PM2.5中组分的研究前景.     

Nucleotide Excision Repair Pathway Activity Is Inhibited by Airborne Particulate Matter (PM10) through XPA Deregulation in Lung Epithelial Cells

Airborne particulate matter with a diameter size of ≤10 µm (PM₁₀) is a carcinogen that contains polycyclic aromatic hydrocarbons (PAH), which form PAH–DNA adducts. However, the way in which these adducts are managed by DNA repair pathways in cells exposed to PM₁₀ has been partially described. We evaluated the effect of PM₁₀ on nucleotide excision repair (NER) activity and on the levels of different proteins of this pathway that eliminate bulky DNA adducts. Our results showed that human lung epithelial cells (A549) exposed to 10 µg/cm² of PM₁₀ exhibited PAH–DNA adducts as well as an increase in RAD23 and XPD protein levels (first responders in NER). In addition, PM₁₀ increased the levels of H4K20me2, a recruitment signal for XPA. However, we observed a decrease in total and phosphorylated XPA (Ser196) and an increase in phosphatase WIP1, aside from the absence of XPA–RPA complex, which participates in DNA-damage removal. Additionally, an NER activity assay demonstrated inhibition of the NER functionality in cells exposed to PM₁₀, indicating that XPA alterations led to deficiencies in DNA repair. These results demonstrate that PM₁₀ exposure induces an accumulation of DNA damage that is associated with NER inhibition, highlighting the role of PM₁₀ as an important contributor to lung cancer.     

PM2.5和PM1O监测数据“倒挂”成因浅析

针对PM2.5和PM10在线监测过程中出现的“数据倒挂”现象进行成因分析,并提出对应的改进和保障措施,确保给出有效而高质量的PM 2.5监测数据.     

环境空气监测中颗粒物异常的特征及原因分析

根据合肥市范围内环境空气自动监测点位的PM10与PM2.5数据,分析了不同监测仪器组合下的PM10与PM2.5监测数据异常情况。结果表明:当PM10采用振荡天平法时,PM10与PM2.5的倒挂率较高;冬季和夏季异常现象发生率明显高于其他季节;PM10与PM2.5在线监测数据异常的概率受方法、仪器、数据采集频率等影响。     

广州市黄埔区降水的化学特征及来源解析

以2006年广州市黄浦区降水样品监测资料为基础对广州市工业区降水的化学特征进行了分析,结果表明黄浦区降水样品pH值分布范围在3．56—6．41,雨量加权平均值为4．44。降水的酸雨频率为94．6％,降水中的主要阴离子为SO4^2-和NO3-,分别占阴离子总量的50．6％和29．8％;主要阳离子是Ca2＋和NH4＋分别占阳离子总量的52．6％和30．5％。相对酸度（FA）计算结果表明约有67．6％的降水酸度被碱性成分的Ca2＋和NH4＋中和。此外,利用富集系数方法,计算了降水中重要离子的来源,结果表明SO4^2-和NO3-主要来源于人类活动,而Ca2＋和K＋主要来源于岩石／土壤风化。     

A Macrophage-Based Method for the Assessment of the Reactive Oxygen Species (ROS) Activity of Atmospheric Particulate Matter (PM) and Application to Routine (Daily-24 h) Aerosol Monitoring Studies

Both short- and long-term exposure to particulate matter (PM) air pollution have been demonstrated to cause increases in cardiovascular disease, cancer, and respiratory disorders. Although the specific mechanisms by which exposure to PM cause these affects are unclear, significant evidence has accumulated to suggest that PM exposure leads to increased inflammation as the result of excessive production of reactive oxygen species (ROS) in critical cell types. In order to better understand how real-world PM exposure causes adverse health effects, there is a need to efficiently integrate metrics of PM toxicity into large scale air monitoring and health effects/epidemiology studies. Here we describe a rapid, inexpensive, method that can be employed to assess the potential of sub-mg masses of PM to generate oxidative stress in alveolar macrophage cells. Importantly, the approach is compatible with routine daily PM sampling programs such as those administered by EPA (Speciation trends network (STN), IMPROVE network, PM2.5 mass monitoring network), allowing for multiple samples to be assessed simultaneously with low volumes and brief exposure periods. We apply the method to a set of water extracts of daily PM2.5 samples (25–350 μ g PM mass) collected in the Denver-Metro area. Variations in the magnitude of the ROS response observed between the samples were only partially explained by differences in mass loading, with the highest levels of ROS being observed in samples collected during the summer months. This assay provides a very useful tool that can be coupled with detailed chemical analysis and statistical models to work towards the goal of attributing PM toxicity to specific real-world chemical sources.     

Particulate Matter (PM10) Promotes Cell Invasion through Epithelial–Mesenchymal Transition (EMT) by TGF-β Activation in A549 Lung Cells

Air pollution presents a major environmental problem, inducing harmful effects on human health. Particulate matter of 10 μm or less in diameter (PM₁₀) is considered an important risk factor in lung carcinogenesis. Epithelial–mesenchymal transition (EMT) is a regulatory program capable of inducing invasion and metastasis in cancer. In this study, we demonstrated that PM₁₀ treatment induced phosphorylation of SMAD2/3 and upregulation of SMAD4. We also reported that PM₁₀ increased the expression and protein levels of TGFB1 (TGF-β), as well as EMT markers SNAI1 (Snail), SNAI2 (Slug), ZEB1 (ZEB1), CDH2 (N-cadherin), ACTA2 (α-SMA), and VIM (vimentin) in the lung A549 cell line. Cell exposed to PM₁₀ also showed a decrease in the expression of CDH1 (E-cadherin). We also demonstrated that expression levels of these EMT markers were reduced when cells are transfected with small interfering RNAs (siRNAs) against TGFB1. Interestingly, phosphorylation of SMAD2/3 and upregulation of SMAD induced by PM₁₀ were not affected by transfection of TGFB1 siRNAs. Finally, cells treated with PM₁₀ exhibited an increase in the capacity of invasiveness because of EMT induction. Our results provide new evidence regarding the effect of PM₁₀ in EMT and the acquisition of an invasive phenotype, a hallmark necessary for lung cancer progression.