Effects of PM2.5 Exposure in Different Air Quality Grades on Daily Outpatient Visits for Childhood Asthma in Shijiazhuang,China

正Asthma is a common chronic inflammatory disorder that is more prevalent in children than in adults.China has seen an increasing prevalence of childhood asthma in recentdecades~([1]).Earlier studies have shown that air particulate matter (PM),particularly fine particulate matter(PM2.5)~([2]),is an important factor triggering childhood asthma. Since nationalPM_(2.5)data were nota vailabl euntil 2013,     

Ambient fine particulate matter and cardiopulmonary health risks in China

In China, the level of ambient fine particulate matter (PM2.5) pollution far exceeds the air quality standards recommended by the World Health Organization. Moreover, the health effects of PM2.5 exposure have become a major public health issue. More than half of PM2.5-related excess deaths are caused by cardiopulmonary disease, which has become a major health risk associated with PM2.5 pollution. In this review, we discussed the latest epidemiological advances relating to the health effects of P...     

大气悬浮颗粒物所致气道黏液高分泌的研究进展

近年来随着我国社会经济的迅猛发展以及城市化的进程加快,空气污染也日益受到关注.以空气质量及能见度下降为特征的大气灰霾现象主要由悬浮颗粒物(particulate matter,PM)造成.     

细颗粒物在慢性阻塞性肺疾病炎症反应中的作用

<正>国内大城市频频出现的阴霾天气引起社会对其主要成分之一——细颗粒物(particulate matter,PM2.5)的广泛关注。流行病学资料显示PM2.5对呼吸系统疾病尤其是慢性阻塞性肺疾病(简称慢阻肺)的患病率、急性加重住院率以及日死亡风险的增加均有关。本文通过检索Pubmed、万方、维普数据库等,查阅近14年(2000~2014年)国内外文献,     

Health effects of airborne particulate matter trace elements

The effects of airborne particulate matter （PM） trace elements on health are widely concerned nowadays. Many achievements have been made while many unknowns exist. This article reports the recent research progresses, describes the effects of exposure to PM trace elements on health epidemiological evidence, toxicology findings, and raises some questions for future studies.     

Interaction between ambient particles and ozone and its effect on daily mortality

Objective To examine the effect of particulate matter （PM） less than 10 microns in diameter （PM10） and ozone （O3） on daily mortality in Shanghai, China. Methods A generalized additive model with penalized spline function was used to observe the acute effect of PM10 and O3 on daily mortality. Results Higher PM10 significantly increased the effect of 03 on total mortality, and O3 also increased the effect of PM10 although the estimated increment was statistically insignificant. Conclusion Our findings provide further evidence for the effect of PM10 and O3 on daily mortality.     

PM2.5引起炎性反应与氧化应激的研究现状

<正>近年来,城市雾霾无疑已成为我国面临的一个难题,影响着人们的出行和健康,其重要有害成分当属PM2.5颗粒。PM2.5无疑已成为全世界的一个棘手的问题。PM2.5(fine particulate matter)是指空气动力学直径≤2.5μm的颗粒物,是空气中各种气态污染物经化学反应产生的二次粒子。其体表面积大,所吸附的重金属、多环芳烃等有害成分多。颗粒物被吸入后沉积于肺泡,其中有些成分可以通过血气交换直接     

Atmospheric Particulate Matter 2.5(PM2.5) Induces Cell Damage and Pruritus in Human Skin

<正>With the accelerated rate of urbanization in recent years, air pollution has become an environmental problem that requires urgent resolution, almost all of the world’s population exposed to pollution on a daily basis. Among the various air pollutants, the excessive dispersion and suspension of particulate matter(PM) in the air,     

大气颗粒物对肺部微生态的影响及在慢性阻塞性肺疾病发病中的作用

正大气颗粒物(particulate matter,PM)是指空气中悬浮的混合污染物,包括烟雾、灰尘、固体或液体的复杂混合物,以及多种生物成分,主要来源于自然现象(如沙尘暴)、工业生产、生物燃料使用和交通相关活动。大气PM的暴露与多种疾病的患病率和死亡率有着明显的相关性[1-2]。流行病学研究表明,大气PM暴露显著增加呼吸系统疾病的患病风险[3-5],我们发现这在慢性阻塞性肺疾病(简称慢阻肺)上表现得尤为明显[6-7],而减少PM暴露的浓度能够改善慢阻肺患者的肺功能和减少急性发作[8]。鉴于大气PM暴露是慢阻肺发病的重要危险因素,因此研究PM在慢阻肺发病中的机制就显得尤为重要及迫切,目前对于PM暴露致慢阻肺发病的研究主要集中在炎症机制方面[9-12],但随着近年来对肺部     

Gamma-linolenic Acid from a Blue-Green alga Spirulina platensis Might Alleviate PM2.5 Induced Damages in A549 Cells

<正>With the rapid progress of urbanization,atmospheric fine particulate matter with an aerodynamic diameter of less than 2.5μm (PM_2.5)has attracted increasing concern because of its hazardous effects as an air pollutant on human health^[1].Epidemiological studies have shown that PM2.5 has adverse effects on the respiratory,     

大气细颗粒物对人支气管上皮细胞的活性抑制和炎性作用

目的：研究大气细颗粒物(fine particulate matter,PM2.5)对人支气管上皮细胞活性的影响及其炎性作用。 方法：用PM2.5采样器采集上海地区大气PM2.5样本,扫描电镜观察PM2.5形态特征。将人支气管上皮细胞BEAS-2B暴露 于不同浓度(0,50,100,200,400,800 μg/mL)的PM2.5 12,24,48 h,细胞活力检测试剂盒(cell counting kit-8, CCK-8)法检测PM2.5暴露对细胞活性的影响。实时定量PCR(quantitative real-time PCR,qRT-PCR)检测细胞粒细胞-巨噬 细胞集落刺激因子(granulocyte-macrophage colony stimulating factor,GM-CSF)和TNF-α mRNA的表达,Western印迹检测 GM-CSF和TNF-α蛋白的表达。结果：扫描电镜观察发现,PM2.5形态多样,大小不一,直径大多等于或小于2.5 μm。 与同时间点未暴露组比较,各暴露组(50~800 μg/mL)细胞活性呈不同程度的下降,差异具有统计学意义(P<0.05)。与 未暴露组比较,暴露于100,400或800 μg/mL PM2.5 24 h后,GM-CSF和TNF-α mRNA和蛋白表达水平明显升高(P<0.05), 且PM2.5暴露浓度越高,GM-CSF和TNF-α的mRNA和蛋白升高水平越显著。结论：大气PM2.5可引起人支气管上皮细胞 的炎症反应,降低细胞活性,这可能与PM2.5促发和加重支气管肺部炎性疾病有关。     

Relationship between Ambient Fine Particles and Ventricular Repolarization Changes and Heart Rate Variability of Elderly People with Heart Disease in Beijing,China

Objective To explore the effects of particulate matters less than 2.5 μm in aerodynamic diameter (PM 2.5) on heart repolarization/depolarization and heart rate variability (HRV). Methods We conducted a panel study for elderly subjects with heart disease in Beijing from 2007 to 2008. PM 2.5 was measured at a fixed station for 20 h continuously each day while electrocardiogram (ECG) indexes of 42 subjects were also recorded repeatedly. Meteorological data was obtained from the China Meteorological Data Sharing Service System. A mixed linear regression model was used to estimate the associations between PM 2.5 and the ECG indexes. The model was adjusted for age, body mass index, sex, day of the week andmeteorology. Results Significant adverse effects of PM 2.5 on ECG indexes reflecting HRV were observed statistically and the strongest effect of PM 2.5 on HRV was on lag 1 day in our study. However, there were no associations between PM 2.5 and ECG indexes reflecting heart repolarization/depolarization. Additionally, the effects of PM 2.5 on subjects with hypertension were larger than on the subjects without hypertension. Conclusion This study showed ambient PM 2.5 could affect cardiac autonomic function of the elderly people with heart disease, and subjects with hypertension appeared to be more susceptive to the autonomic dysfunction induced by PM 2.5.     

细颗粒物(PM2.5)对大鼠心肌梗死和心肌组织中MG53蛋白表达的影响

目的 探讨细颗粒物(fine particulate matter,PM2.5)对SD大鼠心肌梗死(myocardial infraction,MI)的影响及心肌组织中Mitsugumin 53(MG53)蛋白表达的变化.方法 将40只体质量210～250 g的雄性SD大鼠分为假手术(Sham)组、MI组、Sham+ PM2.5组、MI+ PM2.5组(n=10).通过结扎左冠状动脉前降支建立心肌梗死模型.Sham+ PM2.5组及MI+ PM2.5组经气道滴灌PM2.5混悬液(10 mg/mL,40 μL/次,3次/周,共4周),Sham组及MI组同法滴灌等量PBS缓冲液作为对照.4周后观察各组大鼠肺组织病理变化、心肌梗死面积、心功能情况、大鼠生存率及心肌组织中MG53蛋白表达的变化.结果 HE染色显示气道滴灌PM2.5的大鼠肺组织可见细颗粒物沉积,表明滴灌成功.MI+PM2.5组与MI组大鼠相比,4周后心肌梗死面积明显增大[(17.78±2.13)％ vs(11.49±2.23)％,P＜0.05],射血分数(EF％)显著降低[(37.14±5.14)％ vs (47.13±4.09)％,P＜0.05],生存率下降,心肌梗死区MG53蛋白的表达也明显降低.结论 PM2.5会加重大鼠心肌梗死的程度,其原因可能与PM2.5抑制心肌受损的膜修复因子MG53蛋白的表达有关.     

短期暴露于不同剂量细颗粒物对哮喘小鼠气道炎症的影响

目的:观察短期暴露于不同剂量细颗粒物(fine particulate matter,PM2.5)对哮喘小鼠气道炎症的影响,并初步探索PM2.5影响哮喘小鼠气道炎症机制?方法:将40只Balb/c小鼠采用随机数字表法分为5组:对照组?卵清蛋白(ovalbumin,OVA)组?OVA+低剂量PM2.5(10 ?滋g)组?OVA+中剂量PM2.5(31.6 ?滋g)组和OVA+高剂量PM2.5(100 ?滋g)组?通过腹腔注射OVA致敏?雾化吸入OVA构建小鼠哮喘模型,第26?28?30天予以PM2.5滴鼻激发?第31天处死小鼠后观察HE染色观察各组小鼠肺组织病理变化?炎性细胞浸润情况,比较各组小鼠肺泡灌洗液(BALF)中细胞总数及分类计数;并通过ELISA方法检测各组小鼠肺泡灌洗液中IL-3?IL-14及血清IgE水平?结果:OVA+低剂量PM2.5组小鼠BALF中细胞总数?分类计数百分比及IL-4?IL-13水平与OVA组相比均无统计学差异(P > 0.05);而OVA+中剂量PM2.5组及OVA+高剂量PM2.5组较OVA组升高(P < 0.05)?OVA+低剂量PM2.5组和OVA+中剂量PM2.5组血清IgE与OVA组相比轻度升高,但无统计学差异 (P > 0.05);OVA+高剂量PM2.5组较OVA组升高(P < 0.05)?结论:中剂量PM2.5(31.6 ?滋g)和高剂量PM2.5(100 ?滋g)可进一步加重哮喘小鼠气道炎症;而低剂量PM2.5(10 ?滋g)对哮喘小鼠气道炎症无显著影响?     

Particle-bound PCDD/Fs in the atmosphere of an electronic waste dismantling area in China

Objective Particulate samples from the atmosphere in an electronic waste dismantling area were collected to investigate the levels and sources of polychlorinated dibenzo‐p‐dioxins and dibenzofurans (PCDD/Fs). Methods Particulate samples including total suspended particulates (TSP) and particulate matter <2.5 μm diameter (PM2.5) were collected on selected non‐rainy days in summer (Jul 10-12, 2006) and winter (Jan 11-13, 2007) from Fengjiang (FJ), an electronic waste (e‐waste) dismantling area in eastern Chin...     

颗粒物对气道上皮TLR2及其下游信号分子表达的影响

 目的  研究颗粒物(particulate matter, PM)暴露所致急性肺损伤的肺组织Toll样受体2 (Toll-like receptors 2, TLR2)及其下游分子的改变。方法  采用气管滴注PM小鼠模型, 将24只SPF级C57BL.6J雄性小鼠随机分成4组(每组6只):对照组、低浓度PM组、中浓度PM组和高浓度PM组。肺泡灌洗液(bronchoalveolar lavage fluid, BALF)细胞分类计数和肺组织苏木精-伊红染色评估肺损伤情况。免疫组化染色法(immunohistochemistry, IHC)观察TLR2在肺脏的表达情况。采用人支气管上皮细胞株BEAS-2B进行体外PM暴露研究, qRT-PCR、Western blot、流式细胞仪检测细胞TLR2及其下游信号分子的表达。结果  各PM暴露组小鼠BALF细胞总数增加, 中性粒细胞数量及构成比增加, 肺组织炎性损伤加重, IHC染色显示TLR2在气道上皮强表达。各PM暴露组支气管上皮细胞TLR2、MyD88 、IRAK1、RelA mRNA水平呈浓度梯度依赖上调表达, TLR2和p-NF-κB蛋白质水平增加。结论  PM所致急性肺损伤中, 肺组织尤其是气道上皮细胞TLR2表达明显上调。TLR2/MyD88/IRAK1/NF-κB信号通路在人支气管上皮细胞的激活可能介导PM所致肺组织的炎性损伤。      

论述PM2.5与心血管疾病的关联

<正>空气污染对健康的影响成为近年来国内外医学科研的主要议题。其中,细颗粒污染对心血管疾病的影响得到医学、环保以及社会工作者的共同关注。本篇文章将综合目前已获得的科研成果来阐述PM2.5与心血管疾病的发病率及死亡率的关系,其致病机理以及目前可行的防范措施。1背景介绍近年来,由于城市发展和现代化进程加快,空气污染对健康的影响成为医学科研的主要议题。空气污染物主要包括气态污染物和颗粒物(particulate matter,PM),而后者的致病性主要根据颗粒大小、成分、来源、溶解度、产生活性氧的能力来     

Airborne fine particulate matter induced pulmonary inflammation as well as oxidative stress in neonate rats

Background Airborne fine particulate matter （PM） can induce pulmonary inflammation which may adversely affect human health, but very few reports about its effect on the neonate rats are available. This study aimed to observe the potential impact and toxicity of fine PMs on the airway in neonate rats.Methods Pulmonary inflammation, cytotoxicity, histopathology, and antioxidants as well as oxidant products were assessed 24 hours after intratracheal instillation of fine PM consecutively for 3 days. Cytotoxicity of fine PM was measured in Hep-2 cells.Results Rats treated with high dose fine PM developed significant pulmonary inflammation characterized by neutrophiland macrophage infiltration. The inflammatory process was related to elevated level of TNF-α and prooxidant/antioxidant imbalance in the lung. Cytotoxicity studies performed in human epithelial cells indicated that high dose fine PM significantly reduced cell viability.Conclusion The study demonstrated acute exposure to fine PM induced airway inflammation as well as increased oxidative stress in addition to its direct toxic effect on airway epithelium cells.     

N-乙酰半胱氨酸对PM2.5致大鼠睾丸毒性的保护作用

目的 探讨N-乙酰半胱氨酸(N-acetylcysteine,NAC)改善亚急性暴露于大气细颗粒物(particulate matter,PM)2.5致大鼠睾丸损伤的作用。 方法 30只 Wistar大鼠随机分为3组,分别为生理盐水对照组、PM2.5暴露组、PM2.5+N-乙酰半胱氨酸组。通过气管内滴注的方法进行染毒,每次剂量为5.0 mg/kg,每周染毒一次,共8周;NAC组在PM2.5染毒的基础上,通过灌胃方式连续给予150 mg·kg-1·d-1 NAC;生理盐水对照组通过气管内滴注同体积生理盐水（1 mL/kg）作为对照。造模后HE染色制作睾丸组织病理切片,TUNEL法检测睾丸凋亡情况,分光光度计法检测睾丸组织超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽（glutathione,GSH）、和丙二醛（malondialdehyde,MDA）指标,酶联免疫吸附测定（enzyme-linked immunosorbent assay,ELISA）法测定睾丸白细胞介素10(interleukin-10,IL-10)及睾酮水平。 结果 PM2.5暴露组和PM2.5+NAC组大鼠血清睾酮水平及睾丸组织GSH、SOD、IL-10水平均低于盐水对照组,睾丸组织MDA水平升高,PM2.5+NAC组睾酮水平及睾丸组织GSH、SOD、IL-10水平高于PM2.5组,睾丸组织MDA水平下降(P＜0.05)。在PM2.5暴露组中,曲精小管中多个细胞核表现出明显的深棕色染色,TUNEL阳性细胞的计数明显高于盐水对照组和PM2.5+NAC组(P＜0.05);而PM2.5+NAC组凋亡细胞数明显低于PM2.5组,但高于盐水对照组(P＜0.05)。PM2.5暴露组和PM2.5+NAC组睾丸细胞凋亡指数高于盐水对照组,PM2.5+NAC组低于PM2.5暴露组(P＜0.05)。 结论 PM2.5亚急性暴露可以造成大鼠睾丸组织病理损伤,诱导睾丸细胞凋亡,引起氧化炎症指标改变,而NAC作为一种抗氧化剂,可以明显改善上述损伤作用,对PM2.5致睾丸毒性作用具有拮抗作用。     

大气细颗粒物PM2.5对肺癌血管新生的影响

[目的]研究大气细颗粒物2.5(particulate matter2.5,PM2.5)对肺癌血管新生的影响。[方法]采集杭州大气PM2.5全颗粒物,对肺癌细胞A549进行染毒,CCK-8法观察PM2.5对肺癌A549细胞增殖的影响,选择50、100、150μg·m L~(-1)浓度的PM2.5染毒A549细胞24h,实时荧光定量PCR和Western blot检测血管内皮生长因子(vascular endothelial growth factor,VEGF)、基质金属蛋白酶-9(matrix metal proteinase-9,MMP-9)和缺氧诱导因子-1α(hypoxia-inducible factor-1α,HIF-1α)的m RNA和蛋白的表达。并建立人肺癌鸡胚移植瘤模型,用50、100、150μg·m L~(-1)的PM2.5染毒液处理肺癌移植瘤,测定PM2.5对血管数目和血管面积比值的影响。[结果]大于等于50μg·m 的PM2.5染毒后能促进A549细胞的增殖作用。与对照组比,PM2.5染毒A549细胞24h后VEGF、MMP-9与HIF-1α的m RNA和蛋白表达增加,并具有一定的量效关系。PM2.5染毒后肺癌鸡胚移植瘤模型新生血管数目和面积比高于对照组,差异有统计学意义(P0.05,P0.01)。[结论]PM2.5暴露能诱导肺癌中VEGF、MMP-9和HIF-1α基因的过表达,促进肺癌的血管新生,进而促使肺癌的发展。