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1.
Background: Few studies have investigated the independent health effects of different size fractions of particulate matter (PM) in multiple locations, especially in Europe.Objectives: We estimated the short-term effects of PM with aerodynamic diameter ≤ 10 μm (PM10), ≤ 2.5 μm (PM2.5), and between 2.5 and 10 μm (PM2.5–10) on all-cause, cardiovascular, and respiratory mortality in 10 European Mediterranean metropolitan areas within the MED-PARTICLES project.Methods: We analyzed data from each city using Poisson regression models, and combined city-specific estimates to derive overall effect estimates. We evaluated the sensitivity of our estimates to co-pollutant exposures and city-specific model choice, and investigated effect modification by age, sex, and season. We applied distributed lag and threshold models to investigate temporal patterns of associations.Results: A 10-μg/m3 increase in PM2.5 was associated with a 0.55% (95% CI: 0.27, 0.84%) increase in all-cause mortality (0–1 day cumulative lag), and a 1.91% increase (95% CI: 0.71, 3.12%) in respiratory mortality (0–5 day lag). In general, associations were stronger for cardiovascular and respiratory mortality than all-cause mortality, during warm versus cold months, and among those ≥ 75 versus < 75 years of age. Associations with PM2.5–10 were positive but not statistically significant in most analyses, whereas associations with PM10 seemed to be driven by PM2.5.Conclusions: We found evidence of adverse effects of PM2.5 on mortality outcomes in the European Mediterranean region. Associations with PM2.5–10 were positive but smaller in magnitude. Associations were stronger for respiratory mortality when cumulative exposures were lagged over 0–5 days, and were modified by season and age.  相似文献   

2.

Background

The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood.

Objective

We examined the effects and time course of exposure to fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania.

Methods

The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)-corrected QT measures: QT prolongation index (QTI), Bazett’s HR-corrected QT (QTcB), and Fridericia’s HR-corrected QT (QTcF). A personal PM2.5 monitor was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM2.5 exposures.

Results

The mean age of the participants was 56 ± 8 years, with 41% male and 74% white. The means ± SDs for QTI, QTcB, and QTcF were 111 ± 6.6, 438 ± 23 msec, and 422 ± 22 msec, respectively; and for PM2.5, the mean ± SD was 14 ± 22 μg/m3. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (β) between 30-min PM2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM2.5 exposure occurred within 3–4 hr. The multivariable adjusted β (SE, p-value) due to a 10-μg/m3 increase in lag 7 PM2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively.

Conclusions

Our results suggest a significant adverse effect of PM2.5 on ventricular repolarization. The time course of the effect is within 3–4 hr of elevated PM2.5.  相似文献   

3.
不同粒径大气颗粒物与死亡终点关系的流行病学研究回顾   总被引:1,自引:0,他引:1  
李林  周启星 《环境与职业医学》2015,32(2):168-174,180
越来越多的国内外流行病学调查与研究发现,大气颗粒物的暴露与居民不同疾病死亡率的上升存在着显著的相关关系。本文就不同粒径颗粒物与最严重的健康终点——死亡之间关系的流行病学研究,进行较为系统的回顾和评述。指出:大多数研究就可吸入颗粒物(PM10)对死亡终点的影响已进行了较为系统和深入的探讨,目前研究重点向细颗粒物(PM2.5)对健康终点的影响转移。而粗颗粒物(PM10~2.5)以及与PM2.5之间的比较性研究资料还较为有限。超细颗粒物(PM0.1)的暴露及健康影响数据也很有限。但由于其数量浓度的优势,可能会成为未来流行病学研究的重点。  相似文献   

4.
Background: Few European studies have investigated the effects of long-term exposure to both fine particulate matter (≤ 2.5 µm; PM2.5) and nitrogen dioxide (NO2) on mortality.Objectives: We studied the association of exposure to NO2, PM2.5, and traffic indicators on cause-specific mortality to evaluate the form of the concentration–response relationship.Methods: We analyzed a population-based cohort enrolled at the 2001 Italian census with 9 years of follow-up. We selected all 1,265,058 subjects ≥ 30 years of age who had been living in Rome for at least 5 years at baseline. Residential exposures included annual NO2 (from a land use regression model) and annual PM2.5 (from a Eulerian dispersion model), as well as distance to roads with > 10,000 vehicles/day and traffic intensity. We used Cox regression models to estimate associations with cause-specific mortality adjusted for individual (sex, age, place of birth, residential history, marital status, education, occupation) and area (socioeconomic status, clustering) characteristics.Results: Long-term exposures to both NO2 and PM2.5 were associated with an increase in nonaccidental mortality [hazard ratio (HR) = 1.03 (95% CI: 1.02, 1.03) per 10-µg/m3 NO2; HR = 1.04 (95% CI: 1.03, 1.05) per 10-µg/m3 PM2.5]. The strongest association was found for ischemic heart diseases (IHD) [HR = 1.10 (95% CI: 1.06, 1.13) per 10-µg/m3 PM2.5], followed by cardiovascular diseases and lung cancer. The only association showing some deviation from linearity was that between NO2 and IHD. In a bi-pollutant model, the estimated effect of NO2 on mortality was independent of PM2.5.Conclusions: This large study strongly supports an effect of long-term exposure to NO2 and PM2.5 on mortality, especially from cardiovascular causes. The results are relevant for the next European policy decisions regarding air quality.  相似文献   

5.
Background: In air pollution time-series studies, the temporal pattern of the association of fine particulate matter (PM2.5; particulate matter ≤ 2.5 μm in aerodynamic diameter) and health end points has been observed to vary by disease category. The lag pattern of PM2.5 chemical constituents has not been well investigated, largely because daily data have not been available.Objectives: We explored the lag structure for hospital admissions using daily PM2.5 chemical constituent data for 5 years in the Denver Aerosol Sources and Health (DASH) study.Methods: We measured PM2.5 constituents, including elemental carbon, organic carbon, sulfate, and nitrate, at a central residential site from 2003 through 2007 and linked these daily pollution data to daily hospital admission counts in the five-county Denver metropolitan area. Total hospital admissions and subcategories of respiratory and cardiovascular admissions were examined. We assessed the lag structure of relative risks (RRs) of hospital admissions for PM2.5 and four constituents on the same day and from 1 to 14 previous days from a constrained distributed lag model; we adjusted for temperature, humidity, longer-term temporal trends, and day of week using a generalized additive model.Results: RRs were generally larger at shorter lags for total cardiovascular admissions but at longer lags for total respiratory admissions. The delayed lag pattern was particularly prominent for asthma. Elemental and organic carbon generally showed more immediate patterns, whereas sulfate and nitrate showed delayed patterns.Conclusion: In general, PM2.5 chemical constituents were found to have more immediate estimated effects on cardiovascular diseases and more delayed estimated effects on respiratory diseases, depending somewhat on the constituent.  相似文献   

6.
A time-series study was conducted to ascertain the short-term effects of different-sized airborne particulate matter (PM) on daily respiratory and cardiovascular cause-specific mortality in winter and summer, among subjects aged over 75 years in Madrid. Poisson regression was used to analyse the time-series, in which the dependent variable was daily mortality due to different specific respiratory and circulatory causes, and the principal independent variables were daily mean PM10, PM2.5 and PM10-2.5 concentrations; other variables: other air pollutants (chemicals, biotic and acoustic), influenza, trend, seasonality and autocorrelation of the series. The results indicated an association between coarser PM fractions (PM10 and PM10-2.5) and respiratory-specific mortality on the one hand, and between PM2.5 and cardiovascular-specific mortality on the other. While the risk of mortality due to exposure to particulate matter was greater in summer than in winter, this difference was statistically significant solely for total organic-cause mortality.  相似文献   

7.
Background: The association of all-cause mortality and cardiovascular outcomes with air pollution exposures has been well established in the literature. The number of studies examining chronic exposures in cohorts is growing, with more recent studies conducted among women finding risk estimates of greater magnitude. Questions remain regarding sex differences in the relationship of chronic particulate matter (PM) exposures with mortality and cardiovascular outcomes.Objectives: In this study we explored these associations in the all-male Health Professionals Follow-Up Study prospective cohort.Methods: The same spatiotemporal exposure estimation models, similar outcomes, and biennially updated covariates were used as those previously applied in the female Nurses’ Health Study cohort.Results: Among 17,545 men residing in the northeastern and midwestern United States, there were 2,813 deaths, including 746 cases of fatal coronary heart disease (CHD). An interquartile range change (4 µg/m3) in average exposure to PM ≤ 2.5 µm in diameter in the 12 previous months was not associated with all-cause mortality [hazard ratio (HR) = 0.94; 95% confidence interval (CI), 0.87–1.00] or fatal CHD (HR = 0.99; 95% CI, 0.87–1.13) in fully adjusted models. Findings were similar for separate models of exposure to PM ≤ 10 µm in diameter and PM between 2.5 and 10 µm in diameter and for copollutant models.Conclusions: Among this cohort of men with high socioeconomic status living in the midwestern and northeastern United States, the results did not support an association of chronic PM exposures with all-cause mortality and cardiovascular outcomes in models with time-varying covariates. Whether these findings suggest sex differences in susceptibility or the protective impact of healthier lifestyles and higher socioeconomic status requires additional investigation.  相似文献   

8.
目的了解成都市公共场所集_中空调通风系统送风中可吸入颗粒物(PM10)污染现状,分析主要影响因素,探讨改善集中空调通风系统PM10污染状况的办法。方法对40家使用集中空调场所进行现场调查,检测通风系统送风中的PM10浓度。结果40家场所中有9家合格,合格率为22%,集中空调经过清洗的场所PM10浓度比未经过清洗的场所低(t=4.528,P=0.001),但集中空调清洗和未清洗场所的合格率比较没有统计学意义(x2=2.634,P=0.105)。结论集中空调管道内的清洁状况仅是送风中PM10的一项影响因素;集中空调通风系统送风中PM10浓度受外部环境影响很大,要改善集中空调通风系统PM10污染状况,集中空调使用单位应在新风口位置和集中空调设施做一些改进。  相似文献   

9.
Between 1990 and 1995, 9 French cities provided data on daily air pollution, total mortality, cardiovascular mortality, and respiratory mortality. Personnel in individual cities performed Poisson regressions, controlling for trends in seasons, calendar effects, influenza epidemics, temperature, and humidity, to assess the short-term effects of air pollution. The authors describe results obtained from the quantitative pooling of these local analyses. When no heterogeneity could be detected, a fixed-effect model was used; otherwise, a random-effect model was used. Significant and positive associations were found between total daily deaths in these cities and the 4 air pollution indicators studied: (1) Black Smoke, (2) sulfur dioxide, (3) nitrogen dioxide, and (4) ozone. A 50-μg/m3 increase in Black Smoke (24 hr), sulfur dioxide (24 hr), nitrogen dioxide (24 hr), or ozone (8 hr) was associated with increases in total mortality of 2.9% (95% confidence interval [Cl]) = 1.3, 4.4), 3.6% (95% Cl = 2.1, 5.2), 3.8% (95% Cl = 2.0, 5.5), and 2.7% (95% Cl = 1.3,4.1), respectively. Similar results were obtained for cardiovascular mortality. Except for sulfur dioxide, positive—but not significant—associations were found with respiratory mortality. The internal consistency among the cities studied, as well as consistency with previously published results, favors a causal interpretation of these associations.  相似文献   

10.

Background

Population-based studies have estimated health risks of short-term exposure to fine particles using mass of PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter) as the indicator. Evidence regarding the toxicity of the chemical components of the PM2.5 mixture is limited.

Objective

In this study we investigated the association between hospital admission for cardiovascular disease (CVD) and respiratory disease and the chemical components of PM2.5 in the United States.

Methods

We used a national database comprising daily data for 2000–2006 on emergency hospital admissions for cardiovascular and respiratory outcomes, ambient levels of major PM2.5 chemical components [sulfate, nitrate, silicon, elemental carbon (EC), organic carbon matter (OCM), and sodium and ammonium ions], and weather. Using Bayesian hierarchical statistical models, we estimated the associations between daily levels of PM2.5 components and risk of hospital admissions in 119 U.S. urban communities for 12 million Medicare enrollees (≥ 65 years of age).

Results

In multiple-pollutant models that adjust for the levels of other pollutants, an interquartile range (IQR) increase in EC was associated with a 0.80% [95% posterior interval (PI), 0.34–1.27%] increase in risk of same-day cardiovascular admissions, and an IQR increase in OCM was associated with a 1.01% (95% PI, 0.04–1.98%) increase in risk of respiratory admissions on the same day. Other components were not associated with cardiovascular or respiratory hospital admissions in multiple-pollutant models.

Conclusions

Ambient levels of EC and OCM, which are generated primarily from vehicle emissions, diesel, and wood burning, were associated with the largest risks of emergency hospitalization across the major chemical constituents of PM2.5.  相似文献   

11.
Background: Many epidemiological studies have linked daily counts of hospital admissions to particulate matter (PM) with an aerodynamic diameter ≤ 10 μm (PM10) and ≤ 2.5 μm (PM2.5), but relatively few have investigated the relationship of hospital admissions with coarse PM (PMc; 2.5–10 μm aerodynamic diameter).Objectives: We conducted this study to estimate the health effects of PMc on emergency hospital admissions for respiratory diseases in Hong Kong after controlling for PM2.5 and gaseous pollutants.Methods: We conducted a time-series analysis of associations between daily emergency hospital admissions for respiratory diseases in Hong Kong from January 2000 to December 2005 and daily PM2.5 and PMc concentrations. We estimated PMc concentrations by subtracting PM2.5 from PM10 measurements. We used generalized additive models to examine the relationship between PMc (single- and multiday lagged exposures) and hospital admissions adjusted for time trends, weather conditions, influenza outbreaks, PM2.5, and gaseous pollutants (nitrogen dioxide, sulfur dioxide, and ozone).Results: A 10.9-μg/m3 (interquartile range) increase in the 4-day moving average concentration of PMc was associated with a 1.94% (95% confidence interval: 1.24%, 2.64%) increase in emergency hospital admissions for respiratory diseases that was attenuated but still significant after controlling for PM2.5. Adjusting for gaseous pollutants and altering models assumptions had little influence on PMc effect estimates.Conclusion: PMc was associated with emergency hospital admissions for respiratory diseases in Hong Kong independent of PM2.5 and gaseous pollutants. Further research is needed to evaluate health effects of different components of PMc.  相似文献   

12.
[目的]分析大气污染对居民每日死亡的急性效应。[方法]采用时间序列的广义相加模型(GAM),在控制了时间的长期趋势、季节趋势、周效应、气象因素等混杂因素的基础上,研究上海市闵行区2001年1月1日~2004年12月31日大气污染与居民日死亡的关系。[结果]大气中可吸入颗粒物(PM10)、二氧化硫(SO2)以及二氧化氮(NO2)的日均浓度每增加10μg/m3,对应居民死亡相对危险度分别为1.0030(95%CI:1.0005~1.0055)、1.0123(95%CI:1.0051~1.0195)和1.0126(95%CI:1.0059~1.0194)。[结论]上海市闵行区大气污染物PM10、NO2、SO2的浓度变化对居民日死亡人数有影响。  相似文献   

13.
太原市空气污染与医院日死亡构成的相关性   总被引:2,自引:0,他引:2  
[目的]探讨空气污染对人体健康的影响。[方法]对大原市100所医院1994-1998年的死亡病例资料、同期大原市的wH0全球大气监测点的空气监测资料及同期山西省气象资料,应用时间序列分析法中的wHo模型,结合线性回归分析方法,进行空气污染与医院日死亡构成比的相关性研究。[结果]研究期内太原市TSP和SO2浓度均值高于WHO推荐标准,空气污染在采暖期与非采暖期有显著性差异;其他死因每日死亡均数两期有显著性差异;TSP对于呼吸系统疾病的日死亡构成比具有较强的独立性,SO2在非采暖期与恶性肿瘤日死亡构成比呈显著相关,在采暖期TSP和SO2的协同作用对慢性阻塞性肺部疾病和恶性肿瘤日死亡构成比呈显著相关。[结论]太原市的空气污染已引起人群死亡量的增加,TSP是影响人群健康最危险的污染物。SO2的影响表现在非采暖期及与TSP的协同作用上。  相似文献   

14.
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 (PM2.5)]. 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 PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults.Methods: We assigned estimates of exposure to ambient PM2.5 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 PM2.5. 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 PM2.5 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 PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 μg/m3; interquartile range, 6.2 μg/m3) than those reported previously.  相似文献   

15.
空气污染与2型糖尿病发病密切相关,其中以细颗粒物(particulate matter 2.5,PM2.5)的影响最受关注.此文首先阐述PM2.5对2型糖尿病和胰岛素敏感性的影响;其次就胰岛素作用的靶组织,对参与调控糖尿病发病生物学机制的国内外研究成果展开综述,包括炎症反应、氧化应激、内质网应激和线粒体功能失调等多种机制相互作用,出现脂肪组织蓄积、产热减少、肝脏脂肪沉积,骨骼肌葡萄糖摄取障碍等多器官糖代谢、脂代谢异常,从而促进糖尿病的发生.  相似文献   

16.
大气颗粒物污染对慢性呼吸道疾病的影响   总被引:19,自引:0,他引:19  
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。  相似文献   

17.

Background

During the last week of June 2008, central and northern California experienced thousands of forest and brush fires, giving rise to a week of severe fire-related particulate air pollution throughout the region. California experienced PM10–2.5 (particulate matter with mass median aerodynamic diameter > 2.5 μm to < 10 μm; coarse ) and PM2.5 (particulate matter with mass median aerodynamic diameter < 2.5 μm; fine) concentrations greatly in excess of the air quality standards and among the highest values reported at these stations since data have been collected.

Objectives

These observations prompt a number of questions about the health impact of exposure to elevated levels of PM10–2.5 and PM2.5 and about the specific toxicity of PM arising from wildfires in this region.

Methods

Toxicity of PM10–2.5 and PM2.5 obtained during the time of peak concentrations of smoke in the air was determined with a mouse bioassay and compared with PM samples collected under normal conditions from the region during the month of June 2007.

Results

Concentrations of PM were not only higher during the wildfire episodes, but the PM was much more toxic to the lung on an equal weight basis than was PM collected from normal ambient air in the region. Toxicity was manifested as increased neutrophils and protein in lung lavage and by histologic indicators of increased cell influx and edema in the lung.

Conclusions

We conclude that the wildfire PM contains chemical components toxic to the lung, especially to alveolar macrophages, and they are more toxic to the lung than equal doses of PM collected from ambient air from the same region during a comparable season.  相似文献   

18.
[目的]探讨灰霾天气细颗粒物(PM2.5)对人支气管上皮细胞(human bronchial epithelial cells,16-HBE)凋亡的影响。[方法]分别以8、16、32、64、128μg/mL浓度的PM2.5作用于16-HBE 24、48、72h,检测PM2.5对16-HBE细胞存活率及凋亡率的影响。[结果]染毒24、48、72h后,64、128μg/mL组细胞存活率均明显低于对照组(P〈0.05),细胞凋亡率均明显高于对照组(P〈0.05);72h各浓度组细胞存活率均低于24h相应处理组(P〈0.05),当染毒浓度大于8μg/mL时,72h各浓度组细胞总凋亡率与24h相比均明显增加(P〈0.05)。[结论]灰霾天气细颗粒物PM2.5对16-HBE具有细胞毒性,能诱导其凋亡,且具有剂量和时间反应关系。  相似文献   

19.

Background

Chronic epidemiologic studies of particulate matter (PM) are limited by the lack of monitoring data, relying instead on citywide ambient concentrations to estimate exposures. This method ignores within-city spatial gradients and restricts studies to areas with nearby monitoring data. This lack of data is particularly restrictive for fine particles (PM with aerodynamic diameter < 2.5 μm; PM2.5) and coarse particles (PM with aerodynamic diameter 2.5–10 μm; PM10–2.5), for which monitoring is limited before 1999. To address these limitations, we developed spatiotemporal models to predict monthly outdoor PM2.5 and PM10–2.5 concentrations for the northeastern and midwestern United States.

Methods

For PM2.5, we developed models for two periods: 1988–1998 and 1999–2002. Both models included smooth spatial and regression terms of geographic information system-based and meteorologic predictors. To compensate for sparse monitoring data, the pre-1999 model also included predicted PM10 (PM with aerodynamic diameter < 10 μm) and extinction coefficients (km−1). PM10–2.5 levels were estimated as the difference in monthly predicted PM10 and PM2.5, with predicted PM10 from our previously developed PM10 model.

Results

Predictive performance for PM2.5 was strong (cross-validation R2 = 0.77 and 0.69 for post-1999 and pre-1999 PM2.5 models, respectively) with high precision (2.2 and 2.7 μg/m3, respectively). Models performed well irrespective of population density and season. Predictive performance for PM10–2.5 was weaker (cross-validation R2 = 0.39) with lower precision (5.5 μg/m3). PM10–2.5 levels exhibited greater local spatial variability than PM10 or PM2.5, suggesting that PM2.5 measurements at ambient monitoring sites are more representative for surrounding populations than for PM10 and especially PM10–2.5.

Conclusions

We provide semiempirical models to predict spatially and temporally resolved long-term average outdoor concentrations of PM2.5 and PM10–2.5 for estimating exposures of populations living in the northeastern and midwestern United States.  相似文献   

20.
Background: A growing body of evidence has associated maternal exposure to air pollution with adverse effects on fetal growth; however, the existing literature is inconsistent.Objectives: We aimed to quantify the association between maternal exposure to particulate air pollution and term birth weight and low birth weight (LBW) across 14 centers from 9 countries, and to explore the influence of site characteristics and exposure assessment methods on between-center heterogeneity in this association.Methods: Using a common analytical protocol, International Collaboration on Air Pollution and Pregnancy Outcomes (ICAPPO) centers generated effect estimates for term LBW and continuous birth weight associated with PM10 and PM2.5 (particulate matter ≤ 10 and 2.5 µm). We used meta-analysis to combine the estimates of effect across centers (~ 3 million births) and used meta-regression to evaluate the influence of center characteristics and exposure assessment methods on between-center heterogeneity in reported effect estimates.Results: In random-effects meta-analyses, term LBW was positively associated with a 10-μg/m3 increase in PM10 [odds ratio (OR) = 1.03; 95% CI: 1.01, 1.05] and PM2.5 (OR = 1.10; 95% CI: 1.03, 1.18) exposure during the entire pregnancy, adjusted for maternal socioeconomic status. A 10-μg/m3 increase in PM10 exposure was also negatively associated with term birth weight as a continuous outcome in the fully adjusted random-effects meta-analyses (–8.9 g; 95% CI: –13.2, –4.6 g). Meta-regressions revealed that centers with higher median PM2.5 levels and PM2.5:PM10 ratios, and centers that used a temporal exposure assessment (compared with spatiotemporal), tended to report stronger associations.Conclusion: Maternal exposure to particulate pollution was associated with LBW at term across study populations. We detected three site characteristics and aspects of exposure assessment methodology that appeared to contribute to the variation in associations reported by centers.  相似文献   

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