大气PM_(2.5)的健康影响

大量流行病学研究表明 ,大气PM2 .5的暴露与人类健康危害之间存在持续的统计学相关性 ,大气PM2 .5对健康的潜在危害已受到国内外学者的普遍关注。本文综述了大气PM2 .5的来源和组成、对人体的危害及毒理学研究的初步进展     

妊娠期PM_(2.5)及其组分暴露对早产的影响

目的分析孕妇妊娠期细颗粒物(PM_(2.5))及其组分[有机碳(OC)、元素碳(EC)、铵盐(NH_(4)^(+))、硝酸盐(NO_(3)^(-))和硫酸盐(SO_(4)^(2-))]暴露对早产的影响。方法基于在北京市通州区妇幼保健院建立的前瞻性出生队列,通过问卷收集2018年3月至11月期间怀孕的4360名孕妇的人口学资料和生活方式等信息,通过医疗记录收集妊娠期合并症及新生儿分娩孕周、出生体重、性别等分娩信息。利用改进的多尺度空气质量(CMAQ)模型评估孕妇妊娠期的PM_(2.5)及其组分暴露情况。使用Cox比例风险回归模型分析妊娠期PM_(2.5)及其组分暴露对早产的影响。结果本研究共209名(4.8%)孕妇早产。校正孕妇年龄、教育水平、工作情况、民族、产次、孕前是否超重肥胖、孕早期吸烟及饮酒、妊娠期合并症、新生儿性别等混杂因素后,妊娠期PM_(2.5)、OC、EC、NH_(4)^(+)、NO_(3)^(-)、SO_(4)^(2-)每增加一个四分位间距,早产发生风险分别增加至1.499倍(95%CI:1.340~1.678)、1.469倍(95%CI:1.324~1.629)、1.153倍(95%CI:1.082~1.228)、1.518倍(95%CI:1.350~1.707)、1.700倍(95%CI:1.470~1.965)、1.507倍(95%CI:1.332~1.705)。结论妊娠期PM_(2.5)及其组分暴露会导致早产风险增加。研究结果为阐明PM_(2.5)及其组分暴露对早产风险的影响提供流行病学证据,同时为促进PM_(2.5)防控标准的制定提供科学依据。     

大气PM2.5的健康影响

大量流行病学研究表明,大气PM2.5的暴露与人类健康危害之间存在持续的统计学相关性,大气PM2.5对健康的潜在危害已受到国内外学的普遍关注。本综述了大气PM2.5的来源和组成、对人体的危害及毒理学研究的初步进展。     

127 大气PM2.5的健康影响

大量流行病学研究表明,大气PM25的暴露与人类健康危害之间存在持续的统计学相关性,大气PM25对健康的潜在危害已受到国内外学者的普遍关注.本文综述了大气PM2.5的来源和组成、对人体的危害及毒理学研究的初步进展.     

大气PM_(2.5)中重金属研究进展

近年来大气PM_(2.5)污染及其危害受到全球关注,我国污染现状尤其严重。作为重要的大气污染物成分,PM_(2.5)富集的重金属对生态环境和人体健康有较大威胁。该文分析总结了我国大气PM_(2.5)中重金属的研究现状,包括污染水平、时空分布特征、来源解析、化学形态、生物有效性和毒理健康效应等方面,提出了现阶段研究的不足,并对今后大气颗粒物污染及其成分研究进行展望,以利于环境空气质量的合理评价及其标准完善,为大气污染防治决策提供科学依据。     

江苏四城市PM_(2.5)中多环芳烃室外呼吸暴露健康风险评估

目的分析比较江苏省四城市PM_(2.5)中多环芳烃的污染水平和特征,评估其健康风险。方法对南京、无锡、徐州、镇江5个监测点2016年1-12月PM_(2.5)中16种多环芳烃进行分析,并在监测点周围选择4 813名≥18岁成人居民开展室外暴露时间调查,用苯并[a]芘致癌当量浓度、人群终身致癌超额危险度评价大气多环芳烃经室外呼吸暴露途径的人群健康风险。结果 PAHs年平均浓度由高到低分别为徐州(28.94±38.17)ng/m~3、无锡(16.70±14.85)ng/m~3、镇江(12.21±11.09)ng/m~3、南京化工园区(9.36±8.34)ng/m~3、南京江宁(6.25±5.86)ng/m~3,PAHs构成以4~6环为主,有一定的季节变化,1月和12月最高,主要来源于燃煤和机动车燃油的混合污染。居民平均室外暴露时间2.34~5.28h/d,南京化学工园区、南京江宁、无锡、徐州、镇江大气PAHs污染室外呼吸暴露途径所致成人的终身致癌超额危险度分别为1.6×10~(~(-6))、1.1×10~(-6)、3.0×10~(-6)、6.5×10~(-6),1.2×10~(-6)。结论 2016年南京、无锡、徐州、镇江大气PM_(2.5)中PAHs污染室外呼吸暴露途径所致成人的终身致癌超额危险度高于可接受水平,存在一定的致癌风险。     

大气PM_(2.5)有机提取物暴露对BEAS-2B细胞因子表达的影响

目的通过观察人支气管上皮细胞(BEAS-2B)株释放IL-8I、L-1β、SICAM-1等的变化,探讨PM2.5有机提取物(EOM)对气道上皮细胞的炎性损伤作用;并研究BEAS-2B损伤后释放的炎症因子诱导T淋巴细胞表达CD25,从而可能参与类似于过敏性哮喘的变态反应过程。方法BEAS-2B暴露于3.75、7.5、15μg/mlPM2.5有机提取物,双抗夹心ELISA法检测培养上清液中IL-8I、L-1β、SICAM-1的变化;将BEAS-2B细胞损伤后释放的炎症因子作用于人外周血淋巴细胞,流式细胞仪检测淋巴细胞CD25阳性表达率。结果阴性对照组有少量IL-8I、L-1β、SICAM-1表达,且随着时间延长略有增加;与阴性对照组相比,随着PM2.5有机提取物染毒剂量的增加和作用时间的延长,IL-8I、L-1β、SICAM-1的表达也增高,差异具有统计学意义(P<0.01)。结论BEAS-2B细胞暴露于PM2.5有机提取物后,释放与气道炎症反应及气道高变应性相关的IL-8I、L-1β、SICAM-1等炎性因子;BEAS-2B细胞损伤后释放的IL-1β等炎性因子能够促进T淋巴细胞表达CD25分子,从而可能参与类似于过敏性哮喘的变态反应过程。     

2017年北京市怀柔区大气PM_(2.5)中重金属污染特征及健康风险评价

目的研究怀柔区大气中PM_(2.5)浓度和PM_(2.5)中重金属污染特征及对人体的危害。方法 2017年1月—12月采集怀柔地区环境大气PM_(2.5)样品,共84份样品,用SPSS 23.0对PM_(2.5)及镉(Cd)、六价铬(Cr)、镍(Ni)、锰(Mn)、铅(Pb)等5种重金属元素的浓度特征进行分析,用美国环境保护署健康风险评价模型对重金属元素进行呼吸暴露的非致癌风险值和致癌风险值进行计算,并评价其健康风险。结果怀柔区大气PM_(2.5)年均浓度为46.39μg/m~3,低于我国环境空气质量二级标准(75μg/m~3);重金属浓度高低依次为Pb>Mn>Cr>Ni>Cd,5种重金属的非致癌风险值HQ儿童>成年男性>成年女性,3种重金属的致癌风险值由高到底依次为Ni>Cd>Cr,成年男性的致癌风险最大,其次是成年女性,对儿童的致癌风险相对最小。结论 5种重金属的非致癌风险值HQ均小于1,表明对人体健康影响较小。     

PM_(2.5)亚慢性染毒对小鼠肺部炎症及Th17/Treg的影响

目的研究大气细颗粒物(PM2.5)亚慢性染毒对小鼠肺部炎症的影响,以及Th17/Treg细胞及其相关细胞因子的改变。方法将32只C57BL/6雄性小鼠随机分为4组,每组8只。PM2.5染毒低、中、高剂量组分别为1.5、7.5和15 mg/kg BW,对照组给予相同体积的生理盐水。采用气管滴注的方式进行染毒,每周2次,连续染毒3个月。末次暴露24 h后,麻醉动物,经气管肺泡灌洗收集肺泡灌洗液(BALF),ELISA法测定BALF中细胞因子IL-6、IL-17、IL-10和TGF-β的含量。Real-time PCR法测定肺组织中Th17细胞特异性转录因子ROR-γt及Treg细胞特异性转录因子Foxp3+mRNA的相对表达量。未经灌洗的左肺用4%多聚甲醛固定,进行病理学观察。结果中、高剂量PM2.5暴露引起小鼠BALF中IL-17显著升高,IL-10显著降低(P"0.05)。肺组织中ROR-γt mRNA表达量随染毒剂量的增加而升高,而Foxp3+mRNA表达量则随染毒剂量的增加呈降低趋势。结论大气细颗粒物亚慢性染毒可引起小鼠肺部持续的炎症、免疫损伤,导致Th17/Treg细胞失衡及其相关细胞因子分泌的改变。     

大气PM2.5及其成分对人群健康影响的研究进展

随着城市人口的快速增长、城市和工业的盲目扩展,以及交通工具数量的显著增加,使得城市大气污染尤其是颗粒物污染成为目前全世界面临的主要环境问题。大气细颗粒物PM_2.5是指大气中空气动力学当量直径小于或等于2.5μm的颗粒物,也称为可吸入颗粒物,来源广泛、成分复杂。     

可吸入颗粒物与血管内皮细胞功能紊乱的关系

研究表明,人群长期暴露可吸入颗粒物后,其心率变异性、血压、血黏度发生改变,心血管疾病的发病率和死亡率升高.可吸入颗粒物诱导血管内皮细胞氧化应激,激活细胞外调节蛋白激酶(ERK)、核转录因子-κB(NF-κB)、促分裂素原活化蛋白激酶(MAPK)、c-jun氨基末端激酶(JNK)等信号通路,促进炎症因子、组织因子、黏附因子等释放,导致心血管内皮细胞功能发生紊乱,进而诱发心血管疾病.该文综述了可吸入颗粒物对内皮细胞功能的影响及其对细胞信号通路的分子作用机制.     

空气细颗粒物与呼吸系统的健康损害

空气细颗粒物(PM 2.5)是重要的环境空气污染物,主要来源于工业生产、汽车尾气和城市建设等人为活动.随着我国经济的高速发展,越来越严重的空气颗粒物污染可引起一系列健康危害,汇总国内外相关研究内容显示,长期接触高浓度的空气细颗粒可引起成人和儿童肺功能下降,增加慢性阻塞性肺病的发作,表现为慢阻肺的人院率和死亡率升高.人群流行病学研究提示空气细颗粒物可能增加儿童哮喘的发病和发作,并与成人哮喘急性发作有关.空气细颗粒导致慢阻肺和哮喘的机制仍不十分清楚,可能与颗粒物及组分造成的呼吸道氧化损伤、炎性反应、粘液大量分泌,以及直接对小气道壁的损伤有关,详细机制有待深入研究.     

Long-term effects of exposure to particulate air pollution

Considerable work has been done to elucidate the effects of polluted air, most of which has studied acute effects of particles. Studies suggest that the effects of longer term exposures are more than just the daily sum of the acute effects. Because most of the studies of acute effects have examined changes in health status occurring within days of the exposure, this article takes a broad definition of long-term exposure to include averaging times of months to years. It concludes that health effects increase as length of exposure increases, but much of that increase occurs within the first year.     

Acute effects of fine particulate air pollution on cardiac arrhythmia: the APACR study

Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood.Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania.Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM_2.5 nephelometer was used to measure individual-level real-time PM_2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM_2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m³ increases in average PM_2.5 over 30-min intervals and ectopy counts.Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM_2.5 exposure was 13 ± 22 μg/m³, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m³ in average PM_2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM_2.5 was not significantly associated with PAC count.Conclusion: PM_2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.     

Cumulative exposure to particulate matter air pollution and long-term post-myocardial infarction outcomes

Introduction

Chronic environmental exposure to particulate matter < 2.5 μm in diameter (PM_2.5) has been associated with cardiovascular disease; however, the effect of air pollution on myocardial infarction (MI) survivors is not clear. We studied the association of chronic exposure to PM_2.5 with death and recurrent cardiovascular events in MI survivors.

Methods

Consecutive patients aged ≤ 65 years admitted to all medical centers in central Israel after first-MI in 1992–1993 were followed through 2005 for cardiovascular events and 2011 for survival. Data on sociodemographic and prognostic factors were collected at baseline and during follow-up. Residential exposure to PM_2.5 was estimated for each patient based on data recorded at air quality monitoring stations. Cox and Andersen–Gill proportional hazards models were used to study the pollution-outcome association.

Results

Among the 1120 patients, 469 (41.9%) died and 541 (48.3%) experienced one or more recurrent cardiovascular event. The adjusted hazard ratios associated with a 10 μg/m³ increase in PM_2.5 exposure were 1.3 (95% CI 0.8–2.1) for death and 1.5 (95% CI 1.1–1.9) for multiple recurrences of cardiovascular events (MI, heart failure and stroke).

Conclusion

When adjustment for socio-demographic factors is performed, cumulative chronic exposure to PM_2.5 is positively associated with recurrence of cardiovascular events in patients after a first MI.     

Risk of nonaccidental and cardiovascular mortality in relation to long-term exposure to low concentrations of fine particulate matter: a Canadian national-level cohort study

Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM_2.5)]. This is the first national-level cohort study to investigate these risks in Canada.Objective: We investigated the association between long-term exposure to ambient PM_2.5 and cardiovascular mortality in nonimmigrant Canadian adults.Methods: We assigned estimates of exposure to ambient PM_2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models.Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-μg/m³ increase in concentrations of PM_2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM_2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities.Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM_2.5. Associations were observed with exposures to PM_2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m³; interquartile range, 6.2 μg/m³) than those reported previously.     

Intrauterine exposure to fine particulate matter as a risk factor for increased susceptibility to acute broncho-pulmonary infections in early childhood

Over the last decades many epidemiologic studies considered the morbidity patterns for respiratory diseases and lung function of children in the context of ambient air pollution usually measured in the postnatal period. The main purpose of this study is to assess the impact of prenatal exposure to fine particulate matter (PM_2.5) on the recurrent broncho-pulmonary infections in early childhood.     

Understanding the link between exposure to fine particulate matter and internalizing problem behaviors among children in South Korea: Indirect effects through maternal depression and child abuse

Exposure to air pollution is known to have detrimental effects on health. Previous studies have also found that exposure to fine particulate matter can cause adverse mental health outcomes. However, the link between exposure to fine particulate matter and children's mental health outcomes remains largely unknown. Thus, this study aimed to understand the mechanisms of the effects of exposure to fine particulate matter on children's mental health outcomes, particularly focusing on internalizing problem behaviors. Using fine particulate data from the Ministry of Environment's Air Korea initiative and data from the Panel Study on Korean Children in 2018, this study employed structural equation models to examine the associations between exposure to fine particulate matter, maternal depressive symptoms, child abuse, and children's internalizing problems. Findings suggest that living in neighborhoods with higher exposure to fine particulate matter is positively associated with maternal depressive symptoms, increasing emotional abuse and neglect, which in turn is positively associated with children's internalizing problem behavior. However, physical abuse was not a significant mediator of children's internalizing problem behaviors. It may be necessary for policies that provide interventions for primary caregivers to reduce depression and child abuse to promote mental health outcomes for children, even in the presence of severe fine particulates.     

Infant exposure to fine particulate matter and traffic and risk of hospitalization for RSV bronchiolitis in a region with lower ambient air pollution

Few studies investigate the impact of air pollution on the leading cause of infant morbidity, acute bronchiolitis. We investigated the influence of PM_2.5 and other metrics of traffic-derived air pollution exposure using a matched case-control dataset derived from 1997 to 2003 birth and infant hospitalization records from the Puget Sound Region, Washington State. Mean daily PM_2.5 exposure for 7, 30, 60 and lifetime days before case bronchiolitis hospitalization date were derived from community monitors. A regional land use regression model of NO₂ was applied to characterize subject's exposure in the month prior to case hospitalization and lifetime average before hospitalization. Subject's residential proximity within 150 m of highways, major roadways, and truck routes was also assigned. We evaluated 2604 (83%) cases and 23,354 (85%) controls with information allowing adjustment for mother's education, mother's smoking during pregnancy, and infant race/ethnicity. Effect estimates derived from conditional logistic regression revealed very modest increased risk and were not statistically significant for any of the exposure metrics in fully adjusted models. Overall, risk estimates were stronger when restricted to bronchiolitis cases attributed to respiratory syncytial virus (RSV) versus unspecified and for longer exposure windows. The adjusted odds ratio (OR_adj) and 95% confidence interval per 10 mcg/m³ increase in lifetime PM_2.5 was 1.14, 0.88-1.46 for RSV bronchiolitis hospitalization. This risk was also elevated for infants who resided within 150 m of a highway (OR_adj 1.17, 0.95-1.44). This study supports a developing hypothesis that there may be a modest increased risk of bronchiolitis attributable to chronic traffic-derived particulate matter exposure particularly for infants born just before or during peak RSV season. Future studies are needed that can investigate threshold effects and capture larger variability in spatial contrasts among populations of infants.     

大气PM2.5持续高暴露对中老年人群心血管代谢风险的影响

目的  探索京津冀及周边地区大气中细颗粒物(fine particulate matters, PM_2.5)持续高暴露对中老年人群心血管代谢风险的影响。方法  于2017年4月9日―2019年3月31日在京津冀及周边共6个省、市开展横断面调查,选择40~＜90岁社区中老年人作为研究对象,共计2 415名。通过问卷调查获取居民个人基本情况、社会经济状况和生活方式等信息,通过体格检查以获得腰围、血压、FPG、TG和HDL-C水平,根据2005年国际糖尿病联盟发布的共识声明定义代谢风险因素聚集。以PM_2.5日均浓度≥75 μg/m³、≥各县、区参与调查当天PM_2.5日均浓度的P₉₀及不同持续时间(≥2 d和≥3 d)定义PM_2.5高暴露情景和持续状态。采用Logistic回归分析模型分析大气PM_2.5持续高暴露对人群心血管代谢风险聚集的影响。结果  大气PM_2.5持续高暴露与人群代谢风险聚集风险存在关联,尤其是PM_2.5浓度≥P₉₀且持续2 d、3 d以上时可观察到具有统计学意义的结果,人群代谢风险因素聚集影响的OR(95% CI)值分别为1.58(1.00~2.50)和2.57(1.27~5.22)。其中FPG上升、TG水平上升是较为敏感的代谢风险因素。亚组分析结果显示,PM_2.5持续高暴露对男性和＜65岁人群代谢风险的影响更强。结论  京津冀及周边地区大气PM_2.5持续高浓度暴露可增加中老年人群心血管代谢风险。