大气PM2.5对自发性高血压大鼠心脏的急性毒作用

[目的]了解敏感个体急性暴露PM2.5可能出现的心脏损伤。[方法]12-13周龄的雄性自发性高血压 (spontaneous hypertension,SH)大鼠24只,随机分4组,其中3个实验组分别气管滴注不同浓度的PM2．5颗粒物悬浮液1．6、 8．0、40．0 mg/kg体重,对照组气管滴注生理盐水,连续染毒3 d。[结果]各组大鼠的心脏/体重比值相差不大。高浓度组与对照组相比,心脏生长转化园子β1(transforming growth factor-β1,TGF-β1)的mRNA表达明显升高(P<0．01)。心脏病理学改变随着染毒浓度的增加越加严重。[结论] PM2.5对SH大鼠心脏有一定的急性毒作用,并可引起心脏重构。     

Estimating effects of ambient PM(2.5) exposure on health using PM(2.5) component measurements and regression calibration

Most air pollution and health studies conducted in recent years have examined how a health outcome is related to pollution concentrations from a fixed outdoor monitor. The pollutant effect estimate in the health model used indicates how ambient pollution concentrations are associated with the health outcome, but not how actual exposure to ambient pollution is related to health. In this article, we propose a method of estimating personal exposures to ambient PM(2.5) (particulate matter less than 2.5 microm in diameter) using sulfate, a component of PM(2.5) that is derived primarily from ambient sources. We demonstrate how to use regression calibration in conjunction with these derived values to estimate the effects of personal ambient PM(2.5) exposure on a continuous health outcome, forced expiratory volume in 1 s (FEV(1)), using repeated measures data. Through simulation, we show that a confidence interval (CI) for the calibrated estimator based on large sample theory methods has an appropriate coverage rate. In an application using data from our health study involving children with moderate to severe asthma, we found that a 10 microg/m3 increase in PM(2.5) was associated with a 2.2% decrease in FEV(1) at a 1-day lag of the pollutant (95% CI: 0.0-4.3% decrease). Regressing FEV(1) directly on ambient PM(2.5) concentrations from a fixed monitor yielded a much weaker estimate of 1.0% (95% CI: 0.0-2.0% decrease). Relatively small amounts of personal monitor data were needed to calibrate the estimate based on fixed outdoor concentrations.     

核转录因子-kappa B在PM2.5染毒小鼠急性肺损伤中的作用

[目的]探讨核转录因子-kappa B（NF—κB）在PM2.5染毒小鼠急性肺损伤过程中的作用。[方法]采集上海市交通区PM2.5，设低（1.6mg／kg）、中（8．0mg／kg）、高（40mg／kg）浓度组和对照组，通过气管滴注染毒C57BL／6小鼠24h后，用RT—PCR方法对肺组织中肿瘤坏死因子α（TNF-α）、白细胞介素1（IL-1）、白细胞介素6（IL-6）、一氧化氮合酶（NOS）和NF-κB的基因表达水平进行检测，观察PM2.5染毒后各指标基因表达的改变情况。[结果]小鼠肺组织中TNF-α、IL-1、IL-6和NOS基因表达水平各染毒组均显著高于对照组（P〈0．01），并随着染毒浓度的增加而增加，NF—κB的基因表达水平与上述指标基因水平显著相关，相关系数均高于0．9（P〈0．01）。[结论]PM2.5能够引起小鼠肺组织中细胞因子和氧化酶基因水平表达增加，从而造成肺组织的免疫和氧化损伤，NF-κB在PM2.5引起急性肺损伤过程中可能起到重要的调节作用。     

气管滴注大气细颗粒物对大鼠的急性毒性

目的 探讨大气细颗粒物(PM2.5)对大鼠的急性毒性作用及其可能的作用机制.方法 将28只体重为280～310 g的雄性Wistar大鼠随机分为4组,即空白对照组、颗粒物低、中、高剂量组(7.5、15和30 mg/kg).采用一次性气管滴注染毒颗粒物,24h后处死动物,进行支气管肺泡灌洗液(BALF)细胞计数,并对BALF中总蛋白(TP)、乳酸脱氢酶(LDH)和炎性因子(IL-6、TNF-α)的水平进行测定.同时观察了不同染毒组大鼠血清中炎性因子(IL-6、TNF-α)和C-反应蛋白(CRP)的水平.结果 各染毒组大鼠BALF白细胞总数、中性粒细胞数、TP及TNF-α水平均较对照组高,差异均有统计学意义(P＜0.05或P＜0.001).与对照组比较,各染毒组大鼠血清IL-6和CRP水平升高,差异均有统计学意义(P＜0.05或P＜0.001);中、高剂量组TNF-α水平升高,差异均有统计学意义(均P＜0.05).结论 大气细颗粒物能引起染毒大鼠肺脏急性损伤和全身炎症,后者可能与其心血管系统损伤机制有关.     

Associations of Pregnancy Outcomes and PM2.5 in a National Canadian Study

Background

Numerous studies have examined associations between air pollution and pregnancy outcomes, but most have been restricted to urban populations living near monitors.

Objectives

We examined the association between pregnancy outcomes and fine particulate matter in a large national study including urban and rural areas.

Methods

Analyses were based on approximately 3 million singleton live births in Canada between 1999 and 2008. Exposures to PM_2.5 (particles of median aerodynamic diameter ≤ 2.5 μm) were assigned by mapping the mother’s postal code to a monthly surface based on a national land use regression model that incorporated observations from fixed-site monitoring stations and satellite-derived estimates of PM_2.5. Generalized estimating equations were used to examine the association between PM_2.5 and preterm birth (gestational age < 37 weeks), term low birth weight (< 2,500 g), small for gestational age (SGA; < 10th percentile of birth weight for gestational age), and term birth weight, adjusting for individual covariates and neighborhood socioeconomic status (SES).

Results

In fully adjusted models, a 10-μg/m³ increase in PM_2.5 over the entire pregnancy was associated with SGA (odds ratio = 1.04; 95% CI 1.01, 1.07) and reduced term birth weight (–20.5 g; 95% CI –24.7, –16.4). Associations varied across subgroups based on maternal place of birth and period (1999–2003 vs. 2004–2008).

Conclusions

This study, based on approximately 3 million births across Canada and employing PM_2.5 estimates from a national spatiotemporal model, provides further evidence linking PM_2.5 and pregnancy outcomes.

Citation

Stieb DM, Chen L, Beckerman BS, Jerrett M, Crouse DL, Omariba DW, Peters PA, van Donkelaar A, Martin RV, Burnett RT, Gilbert NL, Tjepkema M, Liu S, Dugandzic RM. 2016. Associations of pregnancy outcomes and PM_2.5 in a National Canadian Study. Environ Health Perspect 124:243–249; http://dx.doi.org/10.1289/ehp.1408995     

PM_(2.5)对小鼠脑组织急性氧化损伤的影响研究

目的探讨PM_(2.5)对小鼠脑组织的急性毒性效应。方法将SPF级雄性Balb/c小鼠48只随机分为6组:对照组(生理盐水组)、生理盐水+褪黑素组、4μg/d PM_(2.5)组、20μg/d PM_(2.5)组、100μg/d PM_(2.5)组、100μg/d PM_(2.5)+褪黑素组,每组8只。各染毒组分别以0.1、0.5、2.5 mg/ml PM_(2.5)溶液进行气道滴注,每只小鼠每天滴注40μl,连续7 d;生理盐水+褪黑素组、100μg/d PM_(2.5)+褪黑素组每天以1.0 mg/ml褪黑素灌胃,灌胃剂量为10 mg/(kg·d),连续7 d。检测脑组织中活性氧自由基(ROS)、丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测脑组织中白细胞介素-4(IL-4)的水平。结果 100μg/d PM_(2.5)组小鼠脑组织ROS、MDA、IL-4含量高于对照组,GSH含量低于对照组,差异均有统计学意义(P0.05或P0.01);20μg/d PM_(2.5)组小鼠脑组织MDA含量高于对照组,差异有统计学意义(P0.01)。100μg/d PM_(2.5)+褪黑素组小鼠脑组织ROS、MDA、IL-4含量低于100μg/d PM_(2.5)组,GSH含量高于100μg/d PM_(2.5)组,差异均有统计学意义(P0.05或P0.01)。结论 100μg/d PM_(2.5)气道滴注染毒可能对小鼠脑组织造成损伤,产生炎症反应,并通过氧化应激反应介导;褪黑素对PM_(2.5)引起的脑组织氧化损伤有一定的拮抗作用。     

Long-term Exposure to PM2.5 and Incidence of Acute Myocardial Infarction

Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI).Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM_2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI.Results: An interquartile range (IQR) increase in area PM_2.5 (0.59 μg/m³) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM_2.5 (area + local, 1.05 μg/m³) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11).Conclusions: Residential exposure to PM_2.5 may best be represented by a combination of area and local PM_2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.     

Chronic Fatigue in a Population-Based Study of Gulf War Veterans

Fatigue has been associated with illness in veterans of the Gulf War; however, few studies have confirmed self-reported fatigue by using clinical evaluation, and symptomatic veterans have not been evaluated with established criteria for Chronic Fatigue Syndrome (CFS). The authors describe the frequency and clinical characteristics of CFS in a sample of veterans residing in the northwestern United States. The sample was selected randomly from U.S. Department of Defense databases of troops deployed to southwest Asia during the Gulf War. The selected individuals were invited to participate in a clinical case-control study of unexplained illness. Of 799 survey respondents eligible for clinical evaluation, 178 had fatigue symptoms. Of the 130 veterans who were evaluated clinically, 103 had unexplained fatigue, and 44 veterans met the 1994 U.S. Centers for Disease Control criteria for CFS. In this population, the authors estimated a minimum prevalence of any unexplained fatigue to be 5.1%, and of CFS to be 2.2%. The estimated prevalence was greater among females than among males. Cases were similar to healthy controls, as determined by laboratory tests and physical findings. In comparison to several clinical studies of CFS patients, the authors of this study found a lower proportion of veterans who reported a sudden onset of symptoms (19%) vs. a gradual onset (50%). Although it has previously been suggested that veterans of the Gulf War suffer from higher rates of chronic fatigue than the general population, the study results described herein–on the basis of clinical examination of a population-based sample of veterans–actually indicate that an increased rate may indeed exist. Gulf War veterans with unexplained fatigue should be encouraged to seek treatment so that the impact of these symptoms on overall quality of life can be reduced.     

西安市大气PM_（2.5）污染与城区居民死亡率的关系

目的定量评价西安大气PM2.5污染对城区居民每日疾病死亡率的影响。方法以大气PM2.5浓度为自变量,以总死亡,呼吸系统疾病,心血管疾病,中风,慢性阻塞型肺部疾病,冠心病,下呼吸道感染等疾病为因变量,进行了单因素泊松回归分析。结果单变量分析结果表明：除PM2.5对下呼吸道感染死亡率的影响无显著意义以外,与其它各种疾病死亡率之间的正相关关系均有显著意义。暴露-反应关系模型显示：PM2.5浓度每升高100μg/m3,总死亡、呼吸系统疾病、心血管疾病、冠心病、中风、COPD的死亡率分别增加4.08%,8.32%,6.18%,8.32%,5.13%,7.25%。结论大气PM2.5浓度的升高会引起相应疾病死亡率的增加。     

上海市A城区大气PM_(10)、PM_(2.5)污染与居民日死亡数的相关分析

目的　探讨大气颗粒物污染对人群健康的影响。方法　采用Poisson广义相加模型对上海市A城区大气PM1 0 、PM2 5的日平均污染浓度与居民日死亡数进行相关回归分析 ,并控制了时间长期趋势、气象、季节、一周日效应混杂因素的影响。结果　当大气PM1 0 、PM2 5浓度上升 10 μg m3时 ,总死亡数分别上升 0 5 3%(0 2 2 %～ 0 85 % )、0 85 % (0 32 %～ 1 39% )。结论　大气粗细颗粒物污染具有潜在的急性人群健康危害。     

Incidence and Short-term Mortality From Perforated Peptic Ulcer in Korea: A Population-Based Study

Background

Perforated peptic ulcer (PPU) is associated with serious health and economic outcomes. However, few studies have estimated the incidence and health outcomes of PPU using a nationally representative sample in Asia. We estimated age- and sex-specific incidence and short-term mortality from PPU among Koreans and investigated the risk factors for mortality associated with PPU development.

Methods

A retrospective population-based study was conducted from 2006 through 2007 using the Korean National Health Insurance claims database. A diagnostic algorithm was derived and validated to identify PPU patients, and PPU incidence rates and 30-day mortality rates were determined.

Results

From 2006 through 2007, the PPU incidence rate per 100 000 population was 4.4; incidence among men (7.53) was approximately 6 times that among women (1.24). Incidence significantly increased with advanced age, especially among women older than 50 years. Among 4258 PPU patients, 135 (3.15%) died within 30 days of the PPU event. The 30-day mortality rate increased with advanced age and reached almost 20% for patients older than 80 years. The 30-day mortality rate was 10% for women and 2% for men. Older age, being female, and higher comorbidity were independently associated with 30-day mortality rate among PPU patients in Korea.

Conclusions

Special attention should be paid to elderly women with high comorbidity who develop PPU.Key words: peptic ulcer perforation, incidence, mortality, population     

Chronic PM2.5 exposure and risk of infant bronchiolitis and otitis media clinical encounters

Chronic particulate matter less than 2.5 μm in diameter (PM_2.5) exposure can leave infants more susceptible to illness. Our objective is to estimate associations of the chronic PM_2.5 exposure with infant bronchiolitis and otitis media (OM) clinical encounters. We obtained all first time bronchiolitis (n = 18,029) and OM (n = 40,042) clinical encounters among children less than 12 and 36 months of age, respectively, diagnosed from 2001 to 2009 and two controls per case matched on birthdate and gestational age from the Pregnancy to Early Life Longitudinal data linkage system in Massachusetts. We applied conditional logistic regression to estimate odds ratios (OR) and confidence intervals (CI) per 2-μg/m³ increase in lifetime average satellite based PM_2.5 exposure_. Effect modification was assessed by age, gestational age, frequency of clinical encounter, and income. We examined associations between residential distance to roadways, traffic density, and infant bronchiolitis and OM risk. PM_2.5 was not associated with infant bronchiolitis (OR = 1.02, 95% CI = 1.00, 1.04) and inversely associated with OM (OR = 0.97, 95% CI = 0.95, 0.99). There was no evidence of effect modification. Compared to infants living near low traffic density, infants residing in high traffic density had elevated risk of bronchiolitis (OR = 1.23, 95% CI = 1.14, 1.31) but not OM (OR = 0.98, 95% CI = 0.93, 1.02) clinical encounter. We did not find strong evidence to support an association between early-life long-term PM_2.5 exposure and infant bronchiolitis or OM. Bronchiolitis risk was increased among infants living near high traffic density.     

大气颗粒物PM10和PM2.5对人肺成纤维细胞及其炎性因子分泌的影响

目的 探讨大气颗粒物PM10和PM2.5对人肺成纤维细胞及其分泌肿瘤坏死因子(TNF-a)、白细胞介素6(IL-6)和白细胞介素8(IL-8)的影响.方法 于冬季采暖期采集颗粒物样品PM10和PM2.5,实验细胞为传代培养的人肺成纤维细胞,用剂量分别为25、50、100、200μg/ml的PM10和PM2.5对人肺成纤维细胞染毒24 h.采用四甲基偶氮唑盐微量酶反应比色法测定细胞毒性;放射免疫法测定炎性因子TNF-a、IL-6和IL-8.结果 25、50、100、200μg/ml的PM10作用于人肺成纤维细胞24 h后产生一定的毒性作用,低剂量时刺激细胞增殖,高剂量时抑制细胞增殖,各浓度时细胞存活率分别为118.80%,120.47%,107.42%,95.97%.25、50、100、200μg,/ml的PM2.5作用24 h后亦对人肺成纤维细胞产生一定的毒性作用,亦表现为低剂量时刺激细胞增殖,高剂量时抑制细胞增殖,各浓度时细胞存活率分别为107.81%,101.48%,91.86%,81.35%.PM10和PM2.5能刺激人肺成纤维细胞分泌炎性因子TNF-a、IL-6和IL-8,尤其200μg,/ml浓度时与对照组相比,各炎性分子浓度差异有统计学意义(P<0.05).结论 大气颗粒物PM10和PM2.5对人肺成纤维细胞有一定毒性作用;PM10和PM2.5染毒24 h后能诱导人肺成纤维细胞分泌炎性因子TNF-a、IL-6、IL-8.     

大气细颗粒物污染监测及其遗传毒性研究

目的比较燃煤污染型城市(太原市)和燃煤与汽车尾气混合污染型城市(北京市)细颗粒物(PM2.5)污染水平并研究其遗传毒性。方法采用滤膜法采集太原市和北京市大气中细颗粒物,并用单细胞凝胶电泳法,以人肺泡上皮细胞(A549)作为靶细胞,测定细颗粒物对细胞DNA的损伤。结果北京市冬季大气中PM2.5为0.028～0.436mg/m3,太原市为0.132～0.681mg/m3。细颗粒物在5、50、200μg/ml浓度内染毒12h和24h均可引起人肺泡上皮细胞DNA损伤,与阴性对照组相比,其拖尾率和尾长差异均有显著性(P<0.05),且存在剂量-反应关系。结论细颗粒物具有一定程度的遗传毒性。     

北京市冬季住宅内PM_(2.5)暴露水平及室内外关系的研究

目的研究自然通风条件下大规模人群的住宅内PM_(2.5)浓度水平,探讨PM_(2.5)浓度的室内外关系,为评估室内PM_(2.5)暴露提供重要数据支撑和新的研究思路。方法于2013年12月1日—2014年2月28日(2013—2014冬季)在北京市某区开展大规模人群的时间-活动模式和空气污染暴露影响因素调查,基于调查数据及PM_(2.5)空气动力学特性建立住宅内PM_(2.5)的质量平衡模型,利用环境监测站点PM_(2.5)监测数据模拟住宅内PM_(2.5)浓度,计算室内外PM_(2.5)浓度比(I/O),并探讨PM_(2.5)室内外关系。结果本研究1 092个样本2013—2014冬季住宅内PM_(2.5)浓度范围为26~167μg/m~3,PM_(2.5)浓度的中位数为73μg/m~3,四分位数间距为34μg/m~3。室外PM_(2.5)浓度范围分别为0~33μg/m~3、34~65μg/m~3、66~129μg/m~3、≥130μg/m~3时,PM_(2.5)浓度I/O分别为1.75、1.05、0.76和0.63;随着室外PM_(2.5)浓度的增加,I/O呈减小趋势,且分布趋于集中。结论基于大规模人群的时间-活动模式和空气污染暴露影响因素调查建立质量平衡模型,可实现大规模人群室内PM_(2.5)浓度的连续模拟。     

北京市大气PM10和PM2.5对人肺成纤维细胞间隙连接通讯及连接蛋白的影响

[目的]探讨北京市大气颗粒物PM_(10)和PM_(2.5)对人肺成纤维细胞(HLF)间隙连接通讯(GJIC)及间隙连接蛋白(Cx43)的影响。[方法]颗粒物样品采自北京市城区采暖期,实验细胞为HLF。采用划痕染料标记示踪法(SLDT)测定HLF的GJIC的水平;蛋白免疫印迹(weslen bloting)法观察HLF细胞膜上Cx43的表达。[结果]细胞划痕实验结果显示,PM_(10)和PM_(2.5)均可抑制细胞间荧光扩散,抑制作用随剂量增高而增强;蛋白免疫印迹结果显示,PM_(10)和PM_(2.5)可使细胞膜Cx43表达减少,减少量随浓度的增高而增加。[结论]北京市大气颗粒物PM_(10)和PM_(2.5)能抑制HLF的GJIC,抑制的机制可能与Cx43表达抑制有关。     

Usual Gait Speed Independently Predicts Mortality in Very Old People: A Population-Based Study

ObjectivesIn older people, usual gait speed has been shown to independently predict mortality; however, less is known about whether usual gait speed is as informative in very old populations, in which prevalence of multimorbidity and disability is high. The aim of this study was to investigate if usual gait speed can independently predict all-cause mortality in very old people, and whether the prediction is influenced by dementia disorder, dependency in activities of daily living (ADL), or use of walking aids in the gait speed test.DesignProspective cohort study.SettingPopulation-based study in northern Sweden and Finland (the Umeå 85+/GERDA Study).ParticipantsA total of 772 participants with a mean age of 89.6 years, 70% women, 33% with dementia disorders, 54% with ADL dependency, and 39% living in residential care facilities.MeasurementsUsual gait speed assessed over 2.4 meters and mortality followed-up for 5 years.ResultsThe mean ± SD gait speed was 0.52 ± 0.21 m/s for the 620 (80%) participants able to complete the gait speed test. Cox proportional hazard regression analyses adjusted for potential confounders were performed. Compared with the fastest gait speed group (≥0.64 m/s), the hazard ratio for mortality was for the following groups: unable = 2.27 (P < .001), ≤0.36 m/s = 1.97 (P = .001), 0.37 to 0.49 m/s = 1.99 (P < .001), 0.50 to 0.63 m/s = 1.11 (P = .604). No interaction effects were found between gait speed and age, sex, dementia disorder, dependency in ADLs, or use of walking aids.ConclusionAmong people aged 85 or older, including people dependent in ADLs and with dementia disorders, usual gait speed was an independent predictor of 5-year all-cause mortality. Inability to complete the gait test or gait speeds slower than 0.5 m/s appears to be associated with higher mortality risk. Gait speed might be a useful clinical indicator of health status among very old people.     

大气颗粒物PM10和PM2.5中水溶性离子及元素分析

目的了解大气颗粒物PM10与PM2.5中水溶性离子及元素的主要组成及其浓度。方法在北京市城区设置1个采样点,于2006年6月16—18日和6月20—22日采集大气颗粒物PM10和PM2.5。采用离子色谱法测定PM10和PM2.5中8种水溶性离子(SO42-、NO3-、Cl-、NH4 、K 、Na 、Ca2 和Mg2 )的浓度;采用"酸提"法测定其中Ca、Mg、Al、As、Zn、Pb、Cu、V、Mn、Co、Fe、Se、Mo、Ni、Cr和Cd的浓度;采用"水提"法测定其中Zn、Pb、Cu、V、Mn、Co、Fe、Ni、Cr和Cd的浓度。结果PM2.5和PM10中8种水溶性离子平均质量浓度范围分别为0.44～9.16μg/m3和0.69～12.61μg/m3。PM2.5中SO42-和NO3-浓度分别占离子总浓度的30.2%和26.5%。PM10中SO42-和NO3-浓度分别占离子总浓度的29.7%和25.6%。PM2.5和PM10中,"酸提"元素平均质量浓度范围分别为1.06～6607.30ng/m3和1.92～12455.50ng/m3;"水提"元素平均质量浓度范围分别为0.31～189.80ng/m3和0.48～187.45ng/m3。结论水溶性离子是大气颗粒物的主要成分之一,值得关注。