沙尘暴PM_(2.5)、PM_(10)对大鼠肺泡巨噬细胞吞噬功能的影响

目的　探讨了沙尘暴PM2 5、PM10 对大鼠肺泡巨噬细胞吞噬功能的影响。方法　沙尘暴颗粒物采集自北京市城区 ,细胞毒性测定用MTT法 ,巨噬细胞吞噬功能采用流式细胞法 ,以荧光标记的胶珠 (Latexbeads ,D =2 4 μm)来测定。 结果　MTT结果显示 ,随着染毒浓度的增加 ,巨噬细胞存活率逐渐减低 ,高剂量组约为对照的 85 %左右。流式细胞仪分析表明 ,各颗粒物染毒组细胞的平均荧光强度逐渐减弱 ,提示巨噬细胞摄入沙尘暴颗粒物后 ,其吞噬荧光胶珠的能力明显减低 ;另外各染毒组的平均侧向光散射强度 ,即摄入的总颗粒数 (沙尘暴颗粒 +荧光胶珠 )低于对照 ,提示巨噬细胞的吞噬功能受到了损伤。沙尘暴PM2 5的细胞毒性比相同浓度的PM10 大 ,对吞噬功能的损伤也更明显。结论　沙尘暴PM2 5、PM10 均能损伤大鼠肺泡巨噬细胞的吞噬功能 ,削弱其非特异性防御能力。     

济宁市某医学院医学生PM2.5相关知识知晓情况调查

目的了解医学生对PM2.5相关知识的知晓情况,探索PM2.5知晓情况的影响因素,为提高医学生的环保意识提供理论依据。方法 2012年6月采用整群抽样方法对济宁某医学院950名医学生进行问卷调查。结果调查950名医学生,对PM2.5的来源知晓率为89.10%,PM2.5加重呼吸系统炎症知晓率为85.84%,PM2.5使慢性病死亡率增加知晓率为84.04%。女生对PM2.5相关知识的知晓率一般高于男生（P〈0.05）,其中有关PM2.5的好发季节、PM2.5诱发心肌梗塞及PM2.5使慢性病死亡率增加等知识知晓情况差别有统计学意义（P〈0.05）。临床与预防专业的学生对PM2.5纳入空气质量监测、PM2.5影响胎儿发育的知晓率大于精神及其他专业（P〈0.05）。不同年级医学生对PM2.5称为细颗粒物、是一种严重污染物、纳入空气质量监测、加重呼吸系统炎症、引发高血压及增加慢性病死亡率等知识知晓情况差别有统计学意义（P〈0.05）。结论医学生对PM2.5相关知识的知晓率较高,但个别问题知晓率偏低。     

兰州市大气细颗粒物对大鼠肺泡巨噬细胞吞噬功能的影响

目的研究兰州市不同地区大气细颗粒物(PM2.5)对大鼠肺泡巨噬细胞吞噬功能的影响。方法于2005年12月15日—2006年2月15日,采集兰州市西固区、铁路局、草场街、夏官营大气PM2.5样本,测定其中的Fe、Mn、Ni、Pb、Cd金属含量。分别将4个地区的大气样本配置成7.5 mg/ml的PM2.5悬液0.2 ml,通过气管注入法经呼吸道对Wistar大鼠(n=8)染毒,测定大鼠肺泡巨噬细胞的吞噬率、吞噬指数。阴性对照组(n=8)进行气管灌注生理盐水,每只0.2 ml。结果与阴性对照组比较,4个染毒组巨噬细胞吞噬功能均显著下降,差异有统计学意义(P<0.01)。4个采样点中西固区大气PM2.5中金属元素的含量最高,大鼠巨噬细胞吞噬率和吞噬指数最低,分别为(74.2±1.31)%和1.041±1.06;夏官营大气PM2.5中金属含量最少,巨噬细胞吞噬率和吞噬指数最高,分别为(81.80±1.62)%和1.593±0.23。结论兰州市不同采样点大气PM2.5对大鼠巨噬细胞的吞噬率和吞噬指数的影响有差异。大鼠巨噬细胞的吞噬功能随着PM2.5中金属元素含量的增多而下降。     

Exposure assessment of particulate matter for susceptible populations in Seattle

In this article we present results from a 2-year comprehensive exposure assessment study that examined the particulate matter (PM) exposures and health effects in 108 individuals with and without chronic obstructive pulmonary disease (COPD), coronary heart disease (CHD), and asthma. The average personal exposures to PM with aerodynamic diameters < 2.5 microm (PM2.5) were similar to the average outdoor PM2.5 concentrations but significantly higher than the average indoor concentrations. Personal PM2.5 exposures in our study groups were lower than those reported in other panel studies of susceptible populations. Indoor and outdoor PM2.5, PM10 (PM with aerodynamic diameters < 10 microm), and the ratio of PM2.5 to PM10 were significantly higher during the heating season. The increase in outdoor PM10 in winter was primarily due to an increase in the PM2.5 fraction. A similar seasonal variation was found for personal PM2.5. The high-risk subjects in our study engaged in an equal amount of dust-generating activities compared with the healthy elderly subjects. The children in the study experienced the highest indoor PM2.5 and PM10 concentrations. Personal PM2.5 exposures varied by study group, with elderly healthy and CHD subjects having the lowest exposures and asthmatic children having the highest exposures. Within study groups, the PM2.5 exposure varied depending on residence because of different particle infiltration efficiencies. Although we found a wide range of longitudinal correlations between central-site and personal PM2.5 measurements, the longitudinal r is closely related to the particle infiltration efficiency. PM2.5 exposures among the COPD and CHD subjects can be predicted with relatively good power with a microenvironmental model composed of three microenvironments. The prediction power is the lowest for the asthmatic children.     

番茄红素对大气可吸入颗粒物致人肺成纤维细胞DNA损伤的保护作用

[目的]探讨大气粗颗粒物(PM10)、细颗粒物(PM2.5)对人肺成纤维细胞(HLF)增殖作用的影响和DNA链的损伤作用以及番茄红素的保护作用.[方法]采用细胞增殖试验(MTT)测定PM10、PM25以及番茄红素对HLF增殖作用.单细胞凝胶电泳法(SCGE)检测PM10、PM25对HLF DNA的损伤程度以及番茄红素对DNA损伤的保护作用.[结果]PM10、PM25均能抑制HLF的增殖,当颗粒物质量浓度为50μg/mL时,HLF的细胞存活率下降约10%,随着染毒剂量的增大细胞存活率进一步下降,具有明显的剂量一效应关系(P<0.01).同样质量浓度下比较,PM25对细胞增殖的抑制作用大干PM10;PM10和PM25均具有明显的DNA损伤作用,当PMs质量浓度仅为50μg/mL时,即能够引起细胞DNA损伤(P<0.01).且具有明显的剂量-反应关系(P<0.01),但PM25的损伤程度小于PM10;番茄红素可以有效地阻止由PM10、PM25导致的DNA损伤,浓度为25μmol/L的番茄红素即可明显减轻PMs对HLF造成的DNA损伤.[结论]PMs能抑制HLF的增殖、诱导HLF的DNA链断裂,番茄红素可以有效地减小PMs对HLF DNA造成的损伤.     

Comparison between different traffic-related particle indicators: elemental carbon (EC), PM2.5 mass,and absorbance

Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.     

淄博市某城区大气PM2.5中苯并[a]芘的人群健康风险评估

目的了解淄博市某城区大气PM2.5及其附着的苯并[a]芘(BaP)的污染水平和人群健康风险。方法于2016年9月一2017年8月用大气采样器采集淄博市某城区大气PM2.5样品,分别检测大气PM2.5质量浓度和BaP浓度,并对其进行人群健康风险评估。结果淄博市某城区大气PM2.5的质量浓度范围为(11.3~905)μg/m3年均浓度为131μg/m3;PM2.5中BaP浓度范围为(0.03-27.0)ng/m^3,年均浓度为6.09 ng/m^3;BaP对(05)岁儿童、(617)岁儿童和成人终生致癌超额危险度分别为0.85×10^-6、0.98×10^-6和3.50×10^-6;采暖期PM2.5浓度、BaP浓度、成人及儿童的终生致癌超额危险度均分别高于非采暖期。结论2016年9月一2017年8月的监测期间,淄博市某城区大气PM2.5和PM2.5中BaP平均浓度超标,BaP的终生致癌风险,成人高于儿童采暖期高于非采暖期,但均处于可接受水平。     

Spatial and seasonal distribution of aerosol chemical components in New York City: (2) road dust and other tracers of traffic-generated air pollution

We describe spatial and temporal patterns of seven chemical elements commonly observed in fine particulate matter (PM) and thought to be linked to roadway emissions that were measured at residential locations in New York City (NYC). These elements, that is, Si, Al, Ti, Fe, Ba, Br, and black carbon (BC), were found to have significant spatial and temporal variability at our 10 residential PM(2.5) sampling locations. We also describe pilot study data of near-roadway samples of both PM(10-2.5) and PM(2.5) chemical elements of roadway emissions. PM(2.5) element concentrations collected on the George Washington Bridge (GWB) connecting NYC and New Jersey were higher that similar elemental concentration measured at residential locations. Coarse-particle elements (within PM(10-2.5)) on the GWB were 10-100 times higher in concentration than their PM(2.5) counterparts. Roadway elements were well correlated with one another in both the PM(2.5) and PM(10-2.5) fractions, suggesting common sources. The same elements in the PM(2.5) collected at residential locations were less correlated, suggesting either different sources or different processing mechanisms for each element. Despite the fact that these elements are only a fraction of total PM(2.5) or PM(10-2.5) mass, the results have important implications for near-roadway exposures where elements with known causal links to health effects are shown to be at elevated concentrations in both the PM(2.5) and PM(10-2.5) size ranges.     

沙尘暴细颗粒物致大鼠肺泡巨噬细胞DNA损伤

[目的]探讨沙尘暴和正常天气细颗粒物(PM2.5)及其水提取物和有机提取物对大鼠肺泡巨噬细胞的细胞毒性和DNA的损伤作用。[方法]沙尘暴和正常天气PM2.5于2004年3月采集自甘肃省武威市和内蒙古自治区包头市。细胞毒性用四甲基偶氮唑盐(MTT)分析法观察,细胞DNA损伤用单细胞凝胶电泳(SCGE)技术检测。[结果]沙尘暴和正常天气PM2.5及其水提取物和有机提取物均对大鼠肺泡巨噬细胞产生一定的细胞毒性,且随剂量的增大而增强;然而,沙尘暴与正常天气之间除了包头沙尘暴PM2.5有机提取物之外,余差异均无显著性。正常天气PM2.5和沙尘暴PM2.5水提取物和有机提取物均可引起细胞DNA损伤,且随剂量增加而损伤增大;正常天气PM2.5比沙尘暴PM2.5水提取物和有机提取物对细胞DNA损伤作用更大。不论正常天气PM2.5还是沙尘暴PM2.5,其有机提取物对DNA的损伤作用均比水提取物作用更强,表明PM2.5中引起DNA损伤的主要化学物是有机化合物种类。武威与包头两城市工业水平不同,大气污染程度不同,但两地沙尘暴PM2.5及其水提取物和有机提取物对细胞DNA的损伤作用,在两地之间并无明显差异。[结论]正常天气PM2.5和沙尘暴PM2.5及其水提取物和有机提取物均可引起DNA损伤,且正常天气PM2.5的损伤作用更强;然而不同地方沙尘暴PM2.5毒性作用未见差异,推测其所含遗传毒性化学物可能类似。     

Pulmonary deposition of particles in welders: on-site measurements

The authors used integrating nephelometers to demonstrate the feasibility of measuring particulate matter with a diameter of 2.5 microm (PM2.5) in the breathing zone and PM2.5 mass deposition in the airways of 6 welders at their place of work. The authors also measured stationary PM2.5 measurements. The between-subject variation in deposition of PM2.5 mass was approximately 1/3 of the within-subject variation. Smokers had a significantly higher total respiratory system deposition than nonsmokers. The PM2.5 deposition for a given amount of exhaled air was dependent on PM2.5 concentration levels. The estimated total amount of PM2.5 deposited in the respiratory system of the subjects was approximately 1 mg/day.     

Ambient gas concentrations and personal particulate matter exposures: implications for studying the health effects of particles

BACKGROUND: Data from a previous study conducted in Baltimore, MD, showed that ambient fine particulate matter less than 2.5 mum in diameter (PM2.5) concentrations were strongly correlated with corresponding personal PM2.5 exposures, whereas ambient O3, NO2, and SO2 concentrations were weakly correlated with their personal exposures to these gases. In contrast, many of the ambient gas concentrations were reasonable surrogates of personal PM2.5 exposures. METHODS: Personal multipollutant exposures and corresponding ambient air pollution concentrations were measured for 43 subjects living in Boston, MA. The cohort consisted of 20 healthy senior citizens and 23 schoolchildren. Simultaneous 24-hour integrated PM2.5, O3, NO2, and SO2 personal exposures and ambient concentrations were measured. All PM2.5 samples were also analyzed for SO4 (sulfate). We analyzed personal exposure and ambient concentration data using correlation and mixed model regression analyses to examine relationships among (1) ambient PM2.5 concentrations and corresponding ambient gas concentrations; (2) ambient PM2.5 and gas concentrations and their respective personal exposures; (3) ambient gas concentrations and corresponding personal PM2.5 exposures; and (4) personal PM2.5 exposures and corresponding personal gas exposures. RESULTS: We found substantial correlations between ambient PM2.5 concentrations and corresponding personal exposures over the course of time. Additionally, our results support the earlier finding that summertime gaseous pollutant concentrations may be better surrogates of personal PM2.5 exposures (especially personal exposures to PM2.5 of ambient origin) than they are surrogates of personal exposures to the gases themselves. CONCLUSIONS: Particle health effects studies that include both ambient PM2.5 and gaseous concentrations as independent variables must be analyzed carefully and interpreted cautiously, since both parameters may be serving as surrogates for PM2.5 exposures.     

PM10和PM2.5与人类健康效应关系的研究进展

悬浮在空气中的颗粒物,按其空气动力学直径的大小,可分为PM10和PM2.5。2006年,WHO推荐用PM2.5代替PM10作为空气颗粒物浓度的指标。大气颗粒物（PM2.5）中主要包含有机碳、元素碳及碳酸盐碳。建筑扬尘、土壤尘、民用污染（燃煤）和交通污染（机动车尾气排放）为主要来源。北京、上海、西安日PM2.5和PM10日超标浓度皆较高。风速与春季和冬季的PM2.5质量浓度之间呈负相关,PM2.5质量浓度随空气相对湿度增加而增大,相对湿度与PM2.5质量浓度之间有正相关;温度与PM2.5质量浓度之间则无明显相关性。大气PM2.5浓度的升高会引起全死因疾病死亡率、心血管疾病死亡率的增加。大气PM2.5浓度的升高与心血管疾病有关。建议采取加大环境污染企业的治理力度,此外应该降低大城市汽车数量。     

臭氧和细颗粒物暴露对大鼠心脏自主神经系统和系统炎症的影响

目的探讨臭氧(O3)和大气细颗粒物(PM2.5)暴露对大鼠心脏自主神经系统和系统炎症的影响以及二者之间是否存在关联。方法 48只Wistar大鼠随机分为8组。PM2.5低、中、高剂量单独暴露组为每只动物分别经气管滴注0.2、0.8和3.2mg的细颗粒物。O3和PM2.5联合暴露低、中、高剂量组为大鼠预先暴露于0.8ppm的臭氧4h,然后再气管滴注PM2.50.2、0.8和3.2mg。O3单独暴露组为只吸入暴露4h臭氧,对照组为气管滴注生理盐水,每周暴露2次,共3周。末次暴露24h后,测定血压,同时记录心电图。测定血清中TNF-α、IL-6和CRP。取右心室进行HE染色病理分析。结果 PM2.5单独暴露和联合暴露组中心率变异性(HRV)指标与对照组比较有显著变化。O3单独暴露仅引起低频成分(LF)显著增加。心率只有在联合暴露组有明显降低。血压在联合暴露组和高剂量PM2.5组有明显上升。TNF-α和IL-6在PM2.5单独暴露和联合暴露组均有上升趋势。CRP在PM2.5单独和联合暴露组均表现出明显的剂量-效应关系。IL-6、TNF-α和CRP与HRV之间显著相关。病理学检查发现,PM2.5暴露组有颗粒物的沉积和心肌炎症。结论 O3可增强由PM2.5暴露引起的大鼠心脏自主神经系统紊乱和炎症反应。     

深圳市某区中小学教室可吸入颗粒物现况评价

目的了解深圳市某区中小学教室空气可吸入颗粒物状况,为改善中小学教学环境卫生状况提供科学依据。方法分层抽取深圳市某区19所中小学114个教室,采用DUSTMATE环境粉尘仪对PM 10,PM 2.5,PM 1.0进行检测。结果 PM 10最大值为0.418mg/m3,超出国家标准1.79倍;PM 2.5最大值为0.142 mg/m3,超出美国EPA新标准3.06倍;PM 1.0最大值为0.056 mg/m3。工业区中小学教室PM 10,PM 2.5,PM 1.0含量高于商业区和居民区,差异均有统计学意义(P值均<0.05)。小学教室PM 10、PM 2.5合格率均高于中学教室;教室PM 10,PM 2.5含量随着楼层增加而下降,差异均有统计学意义(P值均<0.05)。结论深圳市某区中小学教室颗粒物PM 10,PM 2.5,PM 1.0污染情况严重,应引起高度重视并采取综合控制措施。     

室内颗粒物污染对儿童哮喘的影响

目的探讨室内大气PM_(10)、PM_(2.5)、PM1污染对儿童哮喘的影响。方法采用1∶1成组病例-对照研究,于2015年10月—2016年5月对石河子市80名哮喘儿童和80名健康对照儿童进行问卷调查与室内颗粒物浓度检测,分析儿童哮喘的危险因素。结果两组合计160名儿童的室内PM_(10)、PM_(2.5)、PM1浓度范围分别为26.57~507.30、12.66~159.00、4.53~77.08μg/m~3,其中PM_(10)超标率为61.9%,PM_(2.5)超标率为6.9%。病例组室内空气中的PM_(10)、PM_(2.5)、PM1浓度中位数均高于对照组,差异有统计学意义(P0.01)。多因素logistic回归分析结果显示,儿童有过敏史(OR=5.171)、有环境烟草烟雾(ETS)暴露(OR=2.429)、PM_(2.5)浓度高于中位数(OR=3.459)是儿童哮喘的危险因素,母乳喂养(OR=0.454)是儿童哮喘的保护因素,均有统计学意义(P0.05)。结论儿童有过敏史、ETS暴露和PM_(2.5)暴露可能增加儿童哮喘风险,同时应提倡母乳喂养,以保护儿童呼吸系统健康。     

交通污染相关PM_(2.5)亚急性染毒对大鼠免疫功能的影响

目的建立交通污染相关PM_(2.5)大鼠亚急性染毒模型,研究其对大鼠肺泡巨噬细胞吞噬功能、体液免疫和细胞免疫功能的影响。方法将24只雄性SD大鼠随机分为4组,即对照组(生理盐水组)及低、中、高剂量PM_(2.5)染毒组(剂量分别为1.5、6、24 mg/kg)。采用气管内滴注PM_(2.5)混悬液的方式对大鼠进行染毒,隔天染毒1次,共染毒6次。采用中性红比色法测定肺泡巨噬细胞吞噬功能,MTT法检测T淋巴细胞增殖功能,ELISA法测定血清中IgG、IgM、IgA水平。结果大鼠肺泡巨噬细胞的吞噬功能随着染毒剂量的增加而下降,24 mg/kg PM_(2.5)染毒组大鼠的肺泡巨噬细胞吸光度(OD值)低于1.5 mg/kg PM_(2.5)组,差异有统计学意义(P0.05)。大鼠脾脏T淋巴细胞增殖功能随着染毒剂量的增加而下降,各剂量PM_(2.5)染毒组大鼠刺激指数(SI)均低于对照组,差异有统计学意义(P0.05)。大鼠血清IgG、IgM、IgA水平随着染毒剂量的增加而降低,6、24 mg/ml PM_(2.5)染毒组大鼠血清IgG水平低于对照组,1.5、6、24 mg/ml PM_(2.5)染毒组血清IgM、IgA水平低于对照组,差异均有统计学意义(P0.05)。结论交通污染相关PM_(2.5)可能抑制大鼠的肺泡巨噬细胞吞噬功能、细胞免疫功能和体液免疫功能。     

杭州市大气PM2.5污染状况及其细胞毒性

目的研究杭州市春夏季大气细颗粒物(PM2.5)的污染状况及其细胞毒性。方法采用PM10 PM2.5-2型颗粒物采样器和重量法收集2005年春季(4—5月)和夏季(7—8月)大气PM2.5样本,采样地点位于杭州市中心。选择WI-38人胚肺细胞株,将春季和夏季大气PM2.5样本分别以25、50、100、200、500μg/ml染毒细胞24 h,并以等量三蒸水为溶剂对照组,采用克隆形成率法测定PM2.5的细胞毒性。结果以2006年美国EPA新颁布的大气环境质量PM2.5标准(0.035 mg/m3)为参考,杭州市春、夏两季超标天数百分率分别为96.7%和90.0%;以1997年颂布的标准(0.065 mg/m3)为参考,分别为33.3%和20.0%。春季大气PM2.5样本染毒细胞,染毒剂量为25、50、100、200、500μg/ml,相对克隆形成率分别为99.6%,96.2%,85.0%,73.8%和54.6%;夏季大气PM2.5样本染毒细胞,染毒剂量为25、50、100、200、500μg/ml相对克隆形成率分别为97.0%,96.9%,88.0%,83.0%和64.7%;相对克隆形成率随着处理剂量的增加而递减...     

太原市采暖期前后交通路口PM2.5污染状况分析

目的了解山西省太原市采暖期前后交通路口细颗粒物(PM2.5)污染状况及其影响因素,为交通环境PM2.5污染防治提供依据。方法以太原市康乐街路口为监测点,2010年10—11月连续采样,采用质量法测定PM2.5浓度,记录气温、气压、风速和车流量。结果10月和11月交通路口PM2.5的平均日浓度分别为0.137、0.162 mg/m³,均高于2006年美国环境保护局(EPA)新颁布的PM2.5标准(0.035 mg/m³),其超标百分率分别为100%和96.7%;采暖前PM2.5浓度低于采暖后浓度(P<0.01);早晨、中午和下午PM2.5浓度差异无统计学意义;细颗粒物的浓度与风速、温度和气压呈负相关,与车流量呈正相关。结论太原市交通路口PM2.5污染严重,其浓度受到风速、温度、气压和车流量的影响,应对之加强治理。     

石家庄市大气颗粒物与儿童急性下呼吸道感染门诊量的时间序列分析

目的探讨石家庄市大气颗粒物(PM2.5和PM10)对儿童急性下呼吸道感染日门诊量的影响,为大气环境治理和儿童呼吸道感染的预防控制提供理论依据。方法应用Poison分布广义可加模型分析PM2.5和PM10对儿童急性下呼吸道感染日门诊量的影响进行(0-5)d的滞后分析及多污染物模型分析;计算颗粒物每增加10μg/m3,日门诊量增加的比值比。结果PM2.5在lag0 d、lag1 d和累积lag01 d^lag03 d对儿童急性下呼吸道感染日门诊量的影响具有统计学意义PM10在lag0 d^lag2 d和累积滞后lag01 d^lag05 d对儿童急性下呼吸道感染日门诊量的影响具有统计学意义;PM2.5在暴露当天、累积滞后1 d以及PM10在累积滞后1 d、2 d对日门诊量的影响最大PM2.5或PM10浓度每增加10μg/m3,儿童急性下呼吸道感染的日门诊量均增加0.35%。多污染物模型的分析结果显示PM2.5只有在引入SO2后模型才具有统计学意义,PM10在引入其他污染物后均具有统计学意义,但引入SO2后效应最大。结论石家庄市PM2.5和PM10度的增加会导致儿童急性下呼吸道感染的门诊量增加,且PM10的滞后效应较PM2.5强。     

Relationships of mortality with the fine and coarse fractions of long-term ambient PM10 concentrations in nonsmokers

In a cohort of 6338 California Seventh-day Adventists, we previously observed for males associations between long-term concentrations of particulate matter (PM) with an aerodynamic diameter less than 10 microm (PM10) and 15-year mortality due to all natural causes (ANC) and lung cancer (LC) listed as underlying causes of death and due to nonmalignant respiratory disease listed as either the underlying or a contributing (CRC) cause of death. The purpose of this analysis was to determine whether these outcomes were more strongly associated with the fine (PM2.5) or the coarse (PM2.5-10) fractions of PM10. For participants who lived near an airport (n=3769), daily PM2.5 concentrations were estimated from airport visibility, and on a monthly basis, PM2.5-10 concentrations were calculated as the differences between PM10 and PM2.5. Associations between ANC, CRC, and LC mortality (1977-1992) and mean PM10, PM2.5, and PM2.5-10 concentrations at study baseline (1973-1977) were assessed using Cox proportional hazards models. Magnitudes of the PM10 associations for the males of this subgroup were similar to those for the males in the entire cohort although not statistically significant due to the smaller numbers. In single-pollutant models, for an interquartile range (IQR) increase in PM10 (29.5 microg/m3), the rate ratios (RRs) and 95% confidence intervals (CI) were 1.15 (0.94, 1.41) for ANC, 1.48 (0.93, 2.34) for CRC, and 1.84 (0.59, 5.67) for LC. For an IQR increase in PM2.5 (24.3 microg/m3), corresponding RRs (95% CI) were 1.22 (0.95, 1.58), 1.64 (0.93, 2.90), and 2.23 (0.56, 8.94), and for an IQR increase in PM2.5-10 (9.7 microg/m3), corresponding RRs (95% CI) were 1.05 (0.92, 1.20), 1.19 (0.88, 1.62), and 1.25 (0.63, 2.49), respectively. When both PM25 and PM2.5-10 were entered into the same model, the PM2.5 estimates remained stable while those of PM2.5-10 decreased. We concluded that previously observed associations of long-term ambient PM10 concentration with mortality for males were best explained by a relationship of mortality with the fine fraction of PM10 rather than with the coarse fraction of PM10.