抚顺城区大气悬浮颗粒物污染与心脑血管疾病死亡率的定量分析

目的 定量分析抚顺城区大气总悬浮颗粒物(TSP)对心脑血管疾病死亡率的影响.方法 采用生态学方法,分析1999-2003年抚顺市大气中TSP浓度与心脑血管疾病死亡率的相关关系.结果 在控制了时间、气象等因素后,当日TSP浓度每增加50μg/m3,男性组、老年男性组心脑血管疾病死亡率增加的OR值分别为1.015 42和1.02240;滞后4日TSP浓度每增加50μg/m3,总人群、男性组和老年男性组心脑血管疾病死亡率增加的OR值分别为1.008 26、1.016 27和1.016 65.结论 抚顺市区大气TSP污染可能与当地居民心脑血管疾病死亡率增加有关.     

成都市大气颗粒物对居民心脑血管疾病死亡的急性影响研究

目的 探讨成都市大气颗粒物的急性暴露与居民每日心脑血管疾病死亡的关系。方法 收集2013-2015年成都市大气PM2.5、PM10、SO2和NO2的日平均浓度、气象因素(包括日平均气温和相对湿度)及心脑血管疾病日死亡数。采用广义相加模型(Generalized Additive Models,GAM)建立单污染物、多污染物模型,分析大气PM2.5、PM10浓度对居民心脑血管疾病日死亡数的影响。结果 大气污染物PM2.5、PM10浓度分别为75.9、119.7μg/m3,PM2.5高于GB3095-2012《环境空气质量标准》 二级标准。单污染物模型中,大气PM2.5(lag1)和PM10(lag01)浓度每增加10μg/m3,心脑血管疾病日死亡数分别增加0.29%(95%CI:0.01%~0.56%)和0.27%(95%CI:0.09%~0.45%)。PM2.5和PM10浓度与心脑血管疾病死亡的暴露反应关系基本呈线性。多污染物模型中,PM2.5和PM10单独或同时引入SO2、NO2时,对心脑血管疾病日死亡数的影响消失(P>0.05)。结论 成都市大气PM2.5和PM10浓度升高可能导致居民心脑血管疾病日死亡数增加。     

大气颗粒物与心脑血管疾病之间关系的研究进展

高血压、冠心病和脑卒中心脑血管疾病(CVD)已成为重要的公共卫生问题.2006年浙江省人群因冠心病、高血压、慢性风湿性心脏病、先天性心脏病和脑血管病5种CVD而损失的期望寿命为2.05岁[1].     

我国空气污染物与人群呼吸系统疾病死亡急性效应的Meta分析

目的 回顾我国空气污染与呼吸系统疾病健康效应的研究, 定量分析空气污染物[空气动力学直径<2.5 μm的细颗粒物(PM_2.5)和<10 μm的可吸入颗粒物(PM₁₀)、二氧化硫(SO₂)、二氧化氮(NO₂)和臭氧(O₃)]与人群呼吸系统疾病急性死亡的关系。方法 系统收集1989-2014年在PubMed、SpringerLink、Embase、Medline、中国期刊全文数据库、中国生物医学文献数据库和维普中文科技期刊全文数据库公开发表的有关我国空气污染与呼吸系统疾病健康效应的研究文献, 总结该类研究在我国各省份的覆盖情况;并依据Meta分析法分别对PM₁₀、PM_2.5、NO₂、SO₂和O₃与人群呼吸系统疾病急性死亡关系的定量研究进行分析, 采用Stata 12.0软件进行异质性分析后利用固定或随机效应模型合并效应值, 并检验发表偏倚。结果 共收集到有关空气污染与人群呼吸系统疾病健康效应的研究文献157篇, 覆盖我国79.4%的省份。Meta分析结果显示, PM₁₀、PM_2.5、NO₂、SO₂和O₃浓度每上升10 μg/m³, 人群呼吸系统疾病死亡率分别增加0.50%(95%CI: 0~0.90%)、0.50%(95%CI: 0.30%~0.70%)、1.39%(95%CI: 0.90%~1.78%)、1.00%(95%CI: 0.40%~1.59%)和0.10%(95%CI: -1.21%~1.39%), 各研究均未发现明显发表偏倚。结论 我国PM₁₀、PM_2.5、NO₂、SO₂浓度的上升均会导致人群呼吸系统疾病急性死亡的增加。     

大气颗粒物污染对慢性呼吸道疾病的影响

本文报道了对不同大气颗粒物污染地区3021名居民慢性呼吸道疾病的流行病学研究结果。运用分层和logistic回归分析探讨了大气颗粒物污染、吸烟等因素与常见慢性呼吸道疾病和症状的关系。结果表明,大气颗粒物污染、吸烟、年龄为慢性咳嗽、咳痰、气急、慢性支气管炎和肺气肿的危险因素。年龄越大、吸烟越多、颗粒物污染越严重,居民患病的危险性越大。TSP浓度增加100ug/m~3时,咳嗽、咳痰、气急、慢支和肺气肿发生者患病的优势比(OR)为1.20、1.23、1.13、1.29和1.59。     

太原市大气CO污染对65岁及以上人群心脑血管疾病死亡率的急性影响

目的研究太原市大气一氧化碳(CO)污染对长期高暴露环境下65岁及以上城市居民每日心脑血管疾病死亡率的急性影响。方法根据太原市大气污染物的变化趋势,将研究期分为4个阶段:上升期(10—11月)、高峰期(12—3月)、下降期(4—5月)、低谷期(6—9月)。采用病例交叉设计方法和 SAS 9.0中的条件 Logistic 回归模型分析太原市2003至2004年不同空气污染特征下 CO 与太原市65岁及以上城市居民心脑血管疾病每日死亡率的关系。结果 CO 48 h 累积影响最大,平均浓度每增加100μg/m~3,对心脑血管疾病总死亡影响的 OR 值为1.006,心脏病 OR 值为1.010,缺血性心脏病 OR 值为1.007,心肌梗死 OR 值为1.005,心衰 OR 值为1.005,心律失常 OR 值为1.006,中风 OR 值为1.012。不同空气污染特征下,CO 对心脑血管疾病死亡的影响不同,污染的低谷期呈现出较高的危险度,其次为上升期和下降期,污染高峰期未发现 CO 浓度与各病种有关联。结论太原市的 CO 空气污染已对65岁以上居民心脑血管疾病死亡产生一定影响,应采取严格的空气污染措施以降低 CO 污染水平,降低太原市居民心脑血管疾病死亡率。     

大气细颗粒物污染与居民每日死亡关系的Meta分析

目的综合分析国内外大气细颗粒物(PM2.5)短期暴露与人群死亡关系的流行病学资料,以获取大气PM2．5-居民死亡的暴露-反应关系。方法在联机检索文献的基础上,对多篇文献的综合评价采用Meta分析的方法进行,定量确定PM2.5居民每日死亡的暴露-反应关系。结果建立了居民短期接触大气PM2.5污染的暴露-反应关系,即大气PM2.5浓度每升高100μg／m^3,居民死亡发生增加的百分比为12．07％(95％可信区间：8．31％-15．82％)。结论本研究建立的暴露-反应关系,可用于我国及各城市大气细颗粒物污染的健康危险度评价工作。     

银川市大气颗粒物对人群循环系统疾病死亡影响的时间序列分析

目的探讨银川市大气颗粒物污染水平及其对居民循环系统疾病死亡的暴露-反应关系。方法通过收集银川市2013—2015年空气质量监测数据、气象监测数据和居民死亡监测资料,采用广义相加模型,分析银川市大气颗粒物物对与居民循环系统疾病死亡的暴露-反应关系。结果大气PM_(10)和PM_(2.5)年均浓度均超过GB 3095—2012《环境空气质量标准》二级标准。大气PM_(10)和PM_(2.5)浓度每升高10μg/m~3对人群循环系统疾病死亡的超额危险度分别为0.56%(95%CI:0.15%~0.97%),1.33%(95%CI:0.46%~2.21%);大气PM_(10)和PM_(2.5)浓度对小于65岁组的循环系统疾病死亡的影响无统计学意义(P0.05),对65岁以上年龄组人群循环系统疾病死亡的超额危险度分别在滞后7、5 d时达到最大效应,分别为1.24%(95%CI:0.21%~2.28%)和0.57%(95%CI:0.08%~1.06%);大气PM_(10)、PM_(2.5)浓度对女性循环系统疾病死亡的超额危险度高于男性。结论研究期间银川市大气颗粒物浓度较高,且对人群循环系统疾病死亡存在一定的暴露-反应关系。     

大气PM10污染与心脑血管疾病死亡的病例交叉研究

目的探讨南京市大气颗粒物(PM10)污染对心脑血管疾病死亡的影响。方法收集2011年1月1日—2012年12月31日南京市死因资料、大气污染物数据及相关气象资料,应用时间分层的病例交叉设计研究对数据进行分析。结果在控制当日气温、相对湿度的影响后,PM10日均浓度每增加10μg/m3,滞后2 d的总心脑血管疾病死亡发生的OR值为1.013(95%CI:1.005~1.021);模型中加入SO2后,PM10日均浓度每增加10μg/m3,滞后2 d的总心脑血管疾病死亡的OR值为1.004(95%CI:1.001~1.007),关联均有统计学意义(P0.05)。结论本研究区域内PM10浓度升高可能导致心脑血管疾病死亡危险增加。     

宁波市大气颗粒物与人群因心脑血管疾病死亡的时间序列研究

目的 探讨宁波市空气中粒径≤2.5μm的颗粒物(PM_2.5)和≤10μm的颗粒物(PM₁₀)对人群因心脑血管疾病死亡的影响。方法 采用时间序列的广义相加模型,控制时间的长期趋势、季节效应、气象因素及"星期几效应"等混杂因素后,分析2011-2014年宁波市大气颗粒物日均浓度对人群心脑血管疾病死亡的短期效应。结果 单污染物模型分析显示,宁波市大气颗粒物浓度在滞后2 d对心脑血管疾病死亡的效应最强。PM_2.5和PM₁₀的移动平均浓度(滞后2~3 d和滞后2~4 d)每升高10μg/m³分别造成心脑血管疾病死亡增加0.55%(0.23%~0.87%)和0.53%(0.28%~0.78%)。多污染物模型分析显示,调整了其他污染物后,PM₁₀与人群心脑血管疾病死亡增加相关,纳入PM_2.5后,心脑血管疾病死亡增加0.58%(0.09%~1.07%);PM_2.5与人群心脑血管疾病死亡增加无关。结论 大气颗粒物浓度升高与宁波市人群因心脑血管疾病死亡增加相关。     

Wildfire air pollution and daily mortality in a large urban area

Unusual air pollution episodes, such as when smoke from wildfires covers a large urban area, can be used to attempt to detect associations between short-term increases in particulate matter (PM) concentrations and subsequent mortality without relying on the sophisticated statistical models that are typically required in the absence of such episodes. The objective of this study was to explore whether acute increases in PM concentrations from wildfire smoke cause acute increases in daily mortality. The temporal patterns of daily nonaccidental deaths and daily cardiorespiratory deaths for June of 2002 in the Denver metropolitan area were examined and compared to those in two nearby counties in Colorado that were not affected by the wildfire smoke and to daily deaths in Denver in June of 2001. Abrupt increases in PM concentrations in Denver occurred on 2 days in June of 2002 as a result of wildfire smoke drifting over the Denver area. Small peaks in mortality corresponded to both of the PM peaks, but the first mortality peak also corresponded to a peak of mortality in the control counties, and cardiorespiratory deaths began to increase on the day before the second peak. Further, there was no detectable increase in cardiorespiratory deaths in the hours immediately following the PM peaks. Although the findings from this study do not rule out the possibility of small increases in mortality due to abrupt and dramatic increases in PM concentrations from wildfire smoke, in a population of over 2 million people no perceptible increases in daily mortality could be attributed to such events.     

Interactions between particulate air pollution and temperature in air pollution mortality time series studies

In many community time series studies on the effect of particulate air pollution on mortality, particulate air pollution is modeled additively. In this study, we investigated the interaction between daily particulate air pollution and daily mean temperature in Cook County, Illinois and Allegheny County, Pennsylvania, using data for the period 1987-1994. This was done through the use of joint particulate air pollution-temperature response surfaces and by stratifying the effect of particulate air pollution on mortality by temperature. Evidence that the effect of particulate air pollution on mortality may depend on temperature is found. However, the results were sensitive to the number of degrees of freedom used in the confounder adjustments, the particulate air pollution exposure measure, and how the effects of temperature on mortality are modeled. The results were less sensitive to the estimation method used--generalized linear models and natural cubic splines or generalized additive models and smoothing splines. The results of this study suggest that in community particulate air pollution mortality time series studies the possibility of an interaction between daily particulate air pollution and daily mean temperature should be considered.     

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.     

Association of daily cause-specific mortality with ambient particle air pollution in Wuhan, China

In Asia, limited literature has been published on the association between daily mortality and ambient air pollution. We examined the associations of daily cause-specific mortality with daily mean concentrations of particulate matter (PM) with a mass median aerodynamic diameter less than 10 microm (PM(10)) in Wuhan, China using 4 years of data (2001-2004). There are approximately 4.5 million residents in Wuhan who live in the city core area of 201 km(2) where air pollution levels are higher and pollution ranges are wider than the majority of cities in the published literature. We use quasi-likelihood estimation within the context of the generalized additive models (GAMs) (natural spline (NS) models in R) to model the natural logarithm of the expected daily death counts as a function of the predictor variables. We found consistent PM(10) effects on mortality with the strongest effects on lag 0 day. Every 10 microg/m(3) increase in PM(10) daily concentration at lag 0 day was significantly associated with an increase in non-accidental (0.36%; 95% CI 0.19-0.53%), cardiovascular (0.51%; 95% CI 0.28-0.75%), stroke (0.44%; 95% CI 0.16-0.72%), cardiac (0.49%; 95% CI 0.08-0.89%), respiratory (0.71%; 95% CI 0.20-1.23%), and cardiopulmonary (0.46%; 95% CI 0.23-0.69%). In general, these effects were stronger among the elderly (65 years > or = 45 years) than among the young. The exploration of exposure-response relationships between PM(10) and cause-specific mortality suggests the appropriateness of assuming linear relationships, where the PM(10) concentration in Wuhan ranged from 24.8 to 477.8 microg/m(3). We conclude that there is consistent evidence of acute effects of PM(10) on cardiopulmonary mortality. A linear no threshold exposure-response relationship is suggested between PM(10) and the studied cause-specific mortality.     

室内颗粒物污染对儿童哮喘影响的病例对照研究

目的探讨室内大气颗粒物对儿童哮喘的影响。方法于2012—2013年采用病例-对照研究方法,对武汉市82名儿童居室内环境污染情况等进行问卷调查,对室内颗粒物浓度进行检测。结果病例组儿童室内PM_(10)平均浓度高于对照组(P0.05)。将两种颗粒物质量浓度划分为0μg/m~3~、100μg/m~3~、150μg/m~3~、200μg/m~3~不同等级,以0μg/m~3~为参照组,随着污染物浓度的升高,儿童哮喘发生的OR值逐渐升高;在调整混杂因素后,其OR值仍呈增加趋势,尤其是PM_(10)浓度在200μg/m~3以上时,调整后OR值为27.05(95%CI:1.52~482.94)。结论室内PM_(2.5)和PM_(10)对儿童哮喘有影响,且存在剂量-反应关系。     

大气污染对血压影响研究进展

高血压是威胁人类健康的心血管疾病之一,遗传因素和环境因素均是诱发高血压的危险因素,近年来日益严重的大气污染对血压的影响已成为国际上的研究热点,但结论并不一致.该文对大气污染物对血压影响的研究进展进行综述,并提出未来研究方向,旨在为今后的研究提供相关资料.     

A distributed lag approach to fitting non-linear dose-response models in particulate matter air pollution time series investigations

The majority of studies that have investigated the relationship between particulate matter (PM) air pollution and mortality have assumed a linear dose-response relationship and have used either a single-day's PM or a 2- or 3-day moving average of PM as the measure of PM exposure. Both of these modeling choices have come under scrutiny in the literature, the linear assumption because it does not allow for non-linearities in the dose-response relationship, and the use of the single- or multi-day moving average PM measure because it does not allow for differential PM-mortality effects spread over time. These two problems have been dealt with on a piecemeal basis with non-linear dose-response models used in some studies and distributed lag models (DLMs) used in others. In this paper, we propose a method for investigating the shape of the PM-mortality dose-response relationship that combines a non-linear dose-response model with a DLM. This combined model will be shown to produce satisfactory estimates of the PM-mortality dose-response relationship in situations where non-linear dose response models and DLMs alone do not; that is, the combined model did not systemically underestimate or overestimate the effect of PM on mortality. The combined model is applied to ten cities in the US and a pooled dose-response model formed. When fitted with a change-point value of 60 microg/m(3), the pooled model provides evidence for a positive association between PM and mortality. The combined model produced larger estimates for the effect of PM on mortality than when using a non-linear dose-response model or a DLM in isolation. For the combined model, the estimated percentage increase in mortality for PM concentrations of 25 and 75 microg/m(3) were 3.3% and 5.4%, respectively. In contrast, the corresponding values from a DLM used in isolation were 1.2% and 3.5%, respectively.     

我国大气可吸入颗粒物污染对人群死亡率的影响

目的 综合相关文献并以暴露-反应关系的形式探讨中国可吸入颗粒物( PM10)污染对人群死亡率的影响.方法 收集符合纳入标准的中国大气颗粒物污染与居民总死亡率、心脑血管疾病死亡率、呼吸系统疾病死亡率关系的文献,共纳入21篇文献.采用Stata9.0软件进行统计分析,提取PM10与人群死亡率的暴露-反应系数,利用固定或随机效应模型合并效应值,并对结果进行敏感性分析、发表偏倚检验与校正.结果 我国大气PM10每上升10 μg/m3,人群每日总死亡率、心脑血管疾病和呼吸系统疾病死亡率的相对危险度(RR)分别为1.0033(95％ CI:1.0022～1.0044)、1.0045(95％ CI:1.0029 ～1.0062)和1.0056(95％CI:1.0033～1.0079);校正发表偏倚后,人群每日总死亡率、心脑血管疾病和呼吸系统疾病死亡率的RR值降为1.0012(95％CI:1.0002～1.0022)、1.0011(95％ CI:0.9996～1.0026)和1.0023(95％ CI:1.0001～1.0045).结论 大气中PM10浓度的上升会导致我国人群每日总死亡率、心脑血管疾病死亡率和呼吸系统疾病死亡率的增加.     

大气颗粒物与居民脑卒中发作 或死亡之间关系的Meta分析

目的 研究大气颗粒物污染(PM10、PM25)与居民脑卒中发作或死亡之间的关系.方法 检索文献数据库,应用Meta分析法对符合文献纳入标准的16个有关大气颗粒物与居民脑卒中每日发作或死亡关系的定量研究进行综合分析.根据异质性检验结果选用固定效应模型或随机效应模型,采用大气颗粒物每上升10 μg/m3,居民脑卒中死亡的危险度(OR)为效应值进行效应值合并,做敏感性分析.结果 PM10浓度每上升10 μg/m3,居民脑卒中发作的OR=1.011(95%CI:1.001～1.021),即发作增加1.09%(95%CI:0.10%～2.08%),死亡的OR=1.007(95%CI:1.006～1.008),即死亡增加0.70%(95%CI:0.60%～0.80%),说明PM10浓度上升与居民脑卒中发作或死亡均有统计学相关,敏感性分析结果均稳定;PM25浓度每上升10 μg/m3,居民脑卒中发作的OR=1.001(95%CI:0.992～1.010),死亡的OR=1.052(95%CI:0.958～1.154).结论 研究结果表明PM10的空气污染对居民脑卒中发作率和死亡率的增加有统计学相关,PM25浓度增高与脑卒中发作或死亡无统计学相关.