深圳市大气PM2.5污染对早产急性影响的时间序列

目的研究深圳市大气细颗粒物(PM2.5)对早产的急性影响。方法从国家环境保护部获取2015年大气污染资料,深圳市气象局获得2015年气象资料,深圳市某妇幼保健院收集2015年逐日早产数资料。控制时间因素、气象因素等混杂因素的影响,采用广义可加模型(GAM)构建深圳市PM2.5与新生儿早产数模型。结果 2015年深圳市大气PM2.5日均浓度为29.9μg/m3。滞后效应和累积效应GAM时序分析结果显示,PM2.5单污染物模型的早产效应显著,滞后效应中早产效应维持在当天,当大气中PM2.5每升高10μg/m3,其相对危险度(RR)为1.031(95%CI=1.002-1.074),在累积效应中PM2.5的早产效应在滞后7d达到最大值,每升高10μg/m3,其RR为1.034(95%CI=1.002-1.088)。多污染物模型GAM时序分析结果显示,在PM2.5加入一氧化碳(CO)的双污染物模型中PM2.5滞后效应达最大,其RR为1.040(95%CI=1.001-1.075),而在PM2.5加入臭氧(O3)的双污染物模型中PM2.5累积效应达最大,其RR为1.037(95%CI=1.003-1.105)。结论深圳市大气中PM2.5、CO和O3污染对新生儿早产具有潜在的急性影响。     

宁波市6种大气污染物暴露与孕妇早产关系的时间序列分析

[目的]分析宁波市6种大气污染物[细颗粒物(PM_(2.5))、粗颗粒物(PM_(10))、二氧化硫(SO_2)、二氧化氮(NO_2)、一氧化碳(CO)、臭氧(O_3)]暴露对孕妇早产的影响。[方法]采用时间序列的广义线性分布滞后模型,将宁波市2014年1月—2015年12月每日早产人次的长期趋势、气象因素、星期几效应等混杂因素控制后,分析6种大气污染物质量浓度对早产人次的滞后效应和累积效应。[结果]PM_(2.5)、SO_2、NO_2每升高10μg/m~3,CO每升高0.1 mg/m~3,对增加早产人次存在滞后效应,RR及其95%CI分别为:PM_(2.5)滞后1 d,1.015(1.000~1.032);SO_2当日及滞后2、3、4 d,1.073(1.016~1.133)、1.053(1.000~1.109)、1.060(1.009~1.115)、1.062(1.010~1.116);NO_2当日及滞后1 d,1.031(1.005~1.058)、1.027(1.002~1.054);CO滞后3 d,1.350(1.079~1.688)。6种污染物中只有SO_2对早产人次增加存在1周和2周的累积效应,RR及其95%CI分别为1.099(1.019~1.186)、1.091(1.001~1.189)。[结论]大气污染物暴露能增加早产的发生,对增加早产人次存在滞后效应和累积效应。     

广州地区日均气温与早产关系的时间序列研究

目的量化评估广州地区日均气温与早产的关联性。方法采用时间序列方法,利用广州市白云与越秀2个区2005—2011年的早产、气象与空气污染物资料,应用分布滞后非线性模型研究日均气温与早产的关联性,并评估高低气温对早产的冷热效应及累积冷热效应。结果广州市白云与越秀2个区2005—2011年共活产分娩263 322名,早产儿22 903例,早产率为8.70%(95%CI:8.59%~8.81%);日均出生早产儿(9.01±5.61)例;日均气温为(23.35±6.51)℃;日均相对湿度为(66.98±13.98)%;日均SO2浓度为(43.48±28.88)μg/m3;日均NO2浓度为(50.60±50.14)μg/m3;日均PM10浓度为(80.46±61.61)μg/m3。日均气温在不同滞后日与早产的关联呈非线性,暴露—反应关系近似U形,根据累积相对危险度最小的值对应确定参照气温为25.9℃。在滞后期第0~21天内,日均气温的累积风险效应从31℃开始显现出统计学意义,RR值为1.280 3(95%CI:1.014 9~1.615 1),并在34℃时达到最大,RR值为1.689 9(95%CI:1.076 7~2.652 6)。对于冷效应及累积冷效应,在整个滞后期内均无统计学意义。对于热效应,高温(日均气温为32℃),滞后1 d时风险效应最大,RR值为1.052 8(95%CI:1.014 2~1.092 9);对于累积热效应,在滞后期为第0~14天内达到最大,RR值为1.511 7(95%CI:1.210 5~1.887 8)。结论在广州地区,高温是造成早产的重要影响因素,可增加早产的发生风险。     

广州市PM_(2.5)浓度与人群每日死亡风险的空间分布特征

目的了解广州市大气PM_(2.5)暴露对居民每日死亡的影响及其空间分布特征。方法收集2013年1月1日—2014年12月31日期间广州市十二个区(县级市)31个大气监测站点的PM_(2.5)每日数据、气象数据和居民每日死亡数据,采用克里格插值模型和分布滞后非线性模型的时间序列分析方法,分别从全市及12个行政区域的大气PM_(2.5)污染状况及其对居民每日死亡的影响进行评估分析。结果研究期间,全市PM_(2.5)的年平均暴露浓度为49.5±25.6μg/m3,呈西、南部区域PM_(2.5)污染重,东北区域相对较低的区域分布特征;全市范围PM_(2.5)暴露与每日总非意外死亡的滞后累积最大效应RR为1.017(1.001,1.034;95%CI);白云区、从化区、南沙区、越秀区和荔湾区PM_(2.5)暴露与每日总非意外死亡最佳滞后效应RR值范围1.010~1.014(此为各区RR值范围,而非95%CI),滞后累积最大效应RR值范围1.010~1.057(此为各区RR值范围,而非95%CI);从化区、南沙区、越秀区和荔湾区PM_(2.5)暴露与每日心血管系统疾病死亡的最佳滞后效应RR值范围1.006~1.021(此为各区RR值范围,而非95%CI),滞后累积最大效应RR值范围1.017~1.059(此为各区RR值范围,而非95%CI);南沙区和越秀区PM_(2.5)暴露与每日呼吸系统疾病死亡的最佳滞后效应RR值分别为1.004和1.034,滞后累积最大效应RR值分别为1.018和1.110。结论广州市不同区域大气PM_(2.5)暴露对当地居民每日死亡的影响各有不同;呈现南、北两端和西部部分人口密集,交通拥挤的区域风险较高,其他区域风险不明显的空间分布特征。     

妊娠窗口期大气颗粒物暴露对早产影响的meta分析

目的综合以往发表的相关文献,分析不同妊娠窗口期大气颗粒物(PM_(2.5)、PM_(10))暴露对早产的影响。方法检索国内外2000年1月1日—2015年10月1日公开发表的关于大气颗粒物暴露对早产影响的研究文献,根据纳入及排除标准筛选出符合要求的文献26篇,采用R 3.1.1软件的metafor统计包对入选文献进行异质性检验和相应的效应值合并,并对结果进行敏感性分析、发表偏倚检验和校正,评价妊娠窗口期颗粒物暴露对早产的影响。结果通过建立各妊娠窗口期大气颗粒物与早产的暴露-反应关系,发现大气PM_(2.5)浓度每升高10μg/m~3,妊娠早、中、晚期及整个妊娠期早产发生的合并OR(95%CI)分别为1.10(1.01~1.21),1.07(0.79~1.45),1.04(0.97~1.10),1.05(0.97~1.13);大气PM10浓度每升高10μg/m~3,妊娠早、中、晚期及整个妊娠期早产发生的合并OR(95%CI)分别为0.98(0.97~1.00),0.99(0.98~1.01),1.01(0.99~1.04)和1.00(1.00~1.00)。结论不同妊娠窗口期的大气颗粒物暴露所致早产发生风险存在差异,妊娠早期大气PM_(2.5)的暴露可明显增加早产风险。     

孕期PM2.5暴露与子代认知-运动发育间关联性研究

目的 分析孕早期和孕中期PM2.5暴露与子代认知-运动发育间关联性,为孕期防护提供依据。方法 选取2014年6月-2015年4月期间来本院建卡并分娩的孕妇190例,于孕期建卡时进行问卷调查,获取孕妇的居住地址、房屋类型以及楼层分布等信息,通过渗透系数获得室外PM2.5进入室内部分的浓度,作为孕期PM2.5暴露水平。并于婴儿产后42 d体检时应用“年龄发育进程问卷-第三版”(ASQ-3)进行认知-运动发育水平评估。通过两独立样本t检验和多因素线性回归等方法分析孕期PM2.5暴露与子代认知-运动发育间的关联性。结果 孕早期正常暴露组孕妇所生婴儿粗大运动能区得分和精细运动能区得分均高于暴露超标组婴儿,且正常暴露组婴儿五个能区总分也高于暴露超标组婴儿,差异均有统计学意义(P<0.05)。孕早期孕妇暴露PM2.5水平每增高一个单位,ASQ-3各能区得分平均降低0.53~0.62分,ASQ-3总分平均降低2.0分,且以上差异有统计学意义(P<0.05)。与孕早期的PM2.5暴露效应不同,在孕中期虽然PM2.5暴露水平增高也呈现出ASQ-3多能区得分降低的趋势,但差异无统计学意义(P>0.05)。结论 相对于孕中期的PM2.5暴露,孕早期的暴露更容易对子代认知-运动发育水平产生影响,因此针对大气PM2.5的防护应从孕早期就开始并且应重点做好孕早期的暴露防护。     

兰州市沙尘颗粒物污染与儿童呼吸系统疾病日门诊人次的关联性研究

目的探讨兰州市沙尘天气颗粒物污染对儿童呼吸系统健康的影响。方法收集2015-2016年沙尘天气高发期(3~5月)兰州市儿童呼吸系统疾病门诊逐日资料和同期气象环境资料,采用分布滞后非线性模型(distributed lag non-linear model,DLNM)分析沙尘天气PM10和PM2.5浓度与儿童呼吸系统疾病日门诊人次的暴露-反应关系,并按年龄层建立模型。结果 2015-2016年3~5月,与非沙尘天气比较,沙尘天气日均相对湿度明显下降,PM10、PM2.5日均浓度显著上升(P0.05);SO_2和NO_2的日均浓度,日均气温,日均风速比较差异无统计学意义(P0.05)。沙尘天气PM10和PM2.5浓度上升与儿童呼吸系统疾病门诊人次的增加相关,呈滞后效应,滞后期2周,且PM2.5效应大于PM10效应。沙尘天气PM10累计效应在儿童全体、0~5岁、6~14岁儿童均以滞后0-14d最大,RR(95CI%)值分别是1.0055(1.001~1.0102)、1.0061(1.0012~1.0109)、1.0055(0.9967~1.0143)。PM2.5效应在儿童全体和0~5岁儿童均以滞后0-14d最大,RR(95CI%)值分别是1.0182(1.0037~1.033)、1.0210(1.0059~1.0364),6~14岁儿童滞后当天效应最大,RR(95CI%)值是1.0113(1.0007~1.0221)。结论兰州市沙尘天气颗粒物污染可增加儿童呼吸系统疾病门诊人次,呈滞后效应,0~5岁儿童是敏感人群。     

妊娠期PM_(2.5)暴露对早产影响

目的分析孕妇妊娠期空气中细颗粒物(PM_(2.5))的暴露水平与早产发生风险的关系。方法收集河北省22个危重孕产妇监测点在2015—2016年分娩的91 756名单胎产妇资料,利用其所在城市的每日空气质量数据测算不同妊娠阶段PM_(2.5)的暴露水平,并采用logistic回归模型分析妊娠期PM_(2.5)暴露水平对早产的影响。结果早产组孕期各时期PM_(2.5)暴露值均高于足月组,整个妊娠期、孕早期(孕13+6周以前)、孕晚期(孕28周以后)、妊娠开始第1个月、分娩前第1个月、第2个月PM_(2.5)平均暴露值每增加10μg/m~3,早产的发生风险分别增加9.9%、4.2%、7.4%、2.9%、3.4%、3.6%。高龄妊娠、多孕次、妊娠期高血压疾病、妊娠期糖尿病、低孕检次数、高文化程度、胎儿性别为男孩也是发生早产的危险因素。结论妊娠期PM_(2.5)高浓度暴露会显著增加早产发生的风险,尤其是孕早期和孕晚期,应注意做好孕期防护。     

广州地区气象因素对早产影响的时间序列研究

目的研究广州地区气象因素与早产的关系。方法采用时间序列方法,利用广州市白云、越秀、番禺三区2004—2010年早产、气象与空气污染物资料,应用分布滞后非线性模型研究气象因素与早产的关联。结果广州市白云、越秀、番禺三区2004—2010年共活产分娩438 021例,早产儿29973例,早产率为6.84%(95%CI:6.77%~6.92%);日均出生早产儿(11.72±5.63)例,气温均值为(23.41±6.38)℃,相对湿度均值为(67.34±13.84)%,气压均值为(1012.94±6.88)h Pa;风速均值为(6.99±3.70)m/s。气象因素在不同滞后日与早产的关联呈非线性,总体上各气象因素与早产的风险效应呈正向关联。气温、相对湿度、气压和风速分别达到最大值(34℃、100%、1 032.2 h Pa、26 m/s)时,在滞后期(0~26、0~1、0~25、0~24 d)内总体风险效应达到最高,RR值分别为2.01(95%CI:1.28~3.16),1.25(95%CI:1.08~1.45),1.67(95%CI:1.03~2.71)和4.91(95%CI:0.63~38.11)。累积热效应在滞后期0~26 d内最高,RR值为1.47(95%CI:1.16~1.86);累积潮湿风险效应在滞后0 d时最高,RR值为1.12(95%CI:1.05~1.19);累积高气压效应在滞后期0~25 d内最高,RR值为1.34(95%CI:1.01~1.78)。首次怀孕、首次分娩、男婴及孕33~36周的早产亚组对气象因素较为易感,特别是对高温因素。结论广州地区的气温、相对湿度、风速和气压等气象因素可能是早产的重要影响因素。     

某市空气污染对早产急性影响的Poisson广义可加模型分析

目的研究广东某市大气污染物对早产的急性影响。方法根据2007年广东某市的出生监测系统、围产保健数据和住院分娩病历获得妊娠结局资料,从广东某市气象局获得2007年气象资料,2007年大气污染资料来源于广东某市环境监测站。采用广义可加模型(general additive model,GAM)进行广东某市大气污染与新生儿早产发生率的Poisson回归分析,控制气象因素、时间趋势、工作日效应混杂因素的影响。结果 2007年广东某市空气中NO2、PM10、SO2的日均浓度分别为61.04、82.51、51.67μg/m3;2007年广东某市新生儿平均出生早产数为21.47例/日。Pearson相关分析结果表明,NO2、PM10、SO2浓度与温度及相对湿度均呈负相关。滞后效应和累积效应GAM时序分析结果均显示,单污染物的健康效应显著。在滞后效应中3种污染物的健康效应均仅维持在当天,当大气中NO2、PM10、SO2浓度每升高100μg/m3,其RR值分别为1.0425(95%CI:1.0068～1.0781)、1.0512(95%CI:1.0087～1.0938)、1.1118(95%CI:1.0479～1.1757)。在累积效应中NO2、SO2的健康效应均在滞后3d达到最大值,每升高100μg/m3,其RR值分别为1.0542(95%CI:1.0080～1.1003)、1.1298(95%CI:1.0480～1.2116);PM10的健康效应在滞后4d达到最大值,每升高100μg/m3,其RR值为1.0688(95%CI:1.0074～1.1301)。多污染物模型GAM时序分析结果显示,在SO2加入NO2的双污染物模型中SO2滞后效应达最大值,而NO2和PM10的滞后效应和累积效应均有下降,且在模型中未呈现统计学意义。结论广东某市大气NO2、PM10、SO2污染对新生儿早产发生率具有潜在的急性影响。     

Time-to-event analysis of fine particle air pollution and preterm birth: results from North Carolina, 2001-2005

Exposure to air pollution during pregnancy has been suggested to be a risk factor for preterm birth; however, epidemiologic evidence remains mixed and limited. The authors examined the association between ambient levels of particulate matter <2.5 μm in aerodynamic diameter (PM(2.5)) and the risk of preterm birth in North Carolina during the period 2001-2005. They estimated the risks of cumulative and lagged average exposures to PM(2.5) during pregnancy via a 2-stage discrete-time survival model. The authors also considered exposure metrics derived from 1) ambient concentrations measured by the Air Quality System (AQS) monitoring network and 2) concentrations predicted by statistically fusing AQS data with process-based numerical model output (the Statistically Fused Air and Deposition Surfaces (FSD) database). Using the AQS measurements, an interquartile-range (1.73 μg/m(3)) increase in cumulative PM(2.5) exposure was associated with a 6.8% (95% posterior interval: 0.5, 13.6) increase in the risk of preterm birth. Using the FSD-predicted levels and accounting for prediction error, the authors also found significant adverse associations between trimester 1, trimester 2, and cumulative PM(2.5) exposure and preterm birth. These findings suggest that exposure to ambient PM(2.5) during pregnancy is associated with increased risk of preterm birth, even in a region characterized by relatively good air quality.     

A time-series analysis of air pollution and preterm birth in Pennsylvania, 1997-2001

Preterm delivery can lead to serious infant health outcomes, including death and lifelong disability. Small increases in preterm delivery risk in relation to spatial gradients of air pollution have been reported, but previous studies may have controlled inadequately for individual factors. Using a time-series analysis, which eliminates potential confounding by individual risk factors that do not change over short periods of time, we investigated the effect of ambient outdoor particulate matter with diameter < or = 10 microm (PM10) and sulfur dioxide on risk for preterm delivery. Daily counts of preterm births were obtained from birth records in four Pennsylvania counties from 1997 through 2001. We observed increased risk for preterm delivery with exposure to average PM10 and SO2 in the 6 weeks before birth [respectively, relative risk (RR) = 1.07; 95% confidence interval (CI), 0.98-1.18 per 50 microg/m3 increase; RR = 1.15; 95% CI, 1.00-1. 32 per 15 ppb increase], adjusting for long-term preterm delivery trends, co-pollutants, and offsetting by the number of gestations at risk. We also examined lags up to 7 days before the birth and found an acute effect of exposure to PM10 2 days and 5 days before birth (respectively, RR = 1.10; 95% CI, 1.00-1.21; RR = 1.07; 95% CI, 0.98-1.18) and SO2 3 days before birth (RR = 1.07; 95% CI, 0.99-1.15), adjusting for covariates, including temperature, dew point temperature, and day of the week. The results from this time-series analysis, which provides evidence of an increase in preterm birth risk with exposure to PM10 and SO2, are consistent with prior investigations of spatial contrasts.     

Relationships between air pollution and preterm birth in California

Air pollution from vehicular emissions and other combustion sources is related to cardiovascular and respiratory outcomes. However, few studies have investigated the relationship between air pollution and preterm birth, a primary cause of infant mortality and morbidity. This analysis examined the effect of fine particulate matter (PM(2.5)) and carbon monoxide (CO) on preterm birth in a matched case-control study. PM(2.5) and CO monitoring data from the California Air Resources Board were linked to California birth certificate data for singletons born in 1999-2000. Each birth was mapped to the closest PM monitor within 5 miles of the home address. County-level CO measures were utilised to increase sample size and maintain a representative population. After exclusion of implausible birthweight-gestation combinations, preterm birth was defined as birth occurring between 24 and 36 weeks' gestation. Each of the 10 673 preterm cases was matched to three controls of term (39-44 weeks) gestation with a similar date of last menstrual period. Based on the case's gestational age, CO and PM(2.5) exposures were calculated for total pregnancy, first month of pregnancy, and last 2 weeks of pregnancy. Exposures were divided into quartiles; the lowest quartile was the reference. Because of the matched design, conditional logistic regression was used to adjust for maternal race/ethnicity, age, parity, marital status and education. High total pregnancy PM(2.5) exposure was associated with a small effect on preterm birth, after adjustment for maternal factors (adjusted odds ratio [AOR] = 1.15, [95% CI 1.07, 1.24]). The odds ratio did not change after adjustment for CO. Results were similar for PM(2.5) exposure during the first month of pregnancy (AOR = 1.21, 95% CI [1.12, 1.30]) and the last 2 weeks of pregnancy (AOR = 1.17, 95% CI [1.09, 1.27]). Conversely, CO exposure at any time during pregnancy was not associated with preterm birth (AORs from 0.95 to 1.00). Maternal exposure to PM(2.5), but not CO, is associated with preterm birth. This analysis did not show differences by timing of exposure, although more detailed examination may be needed.     

A cohort study of traffic-related air pollution impacts on birth outcomes

BACKGROUND: Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts. OBJECTIVES: We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics. METHODS: With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) microm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth. RESULTS: Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07-1.49] and an 11% (95% CI, 1.01-1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00-1.04; IDW: OR = 1.05; 95% CI, 1.03-1.08 per 10-microg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance. CONCLUSION: Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.     

Effect of air pollution on preterm birth among children born in Southern California between 1989 and 1993

We evaluated the effect of air pollution exposure during pregnancy on the occurrence of preterm birth in a cohort of 97,518 neonates born in Southern California. We used measurements of carbon monoxide (CO), nitrogen dioxide, ozone, and particulate matter less than 10 microm (PM10) collected at 17 air-quality-monitoring stations to create average exposure estimates for periods of pregnancy. We calculated crude and adjusted risk ratios (RRs) for premature birth by period-specific ambient pollution levels. We observed a 20% increase in preterm birth per 50-microg increase in ambient PM10 levels averaged over 6 weeks before birth [RRcrude = 1.20; 95% confidence interval (CI) = 1.09-1.33] and a 16% increase when averaging over the first month of pregnancy (RRcrude = 1.16; 95% CI = 1.06-1.26). PM10 effects showed no regional pattern. CO exposure 6 weeks before birth consistently exhibited an effect only for the inland regions (RRcrude = 1.13; 95% CI = 1.08-1.18 per 3 parts per million), and during the first month of pregnancy, the effect was weak for all stations (RRcrude = 1.04; 95% CI = 1.01-1.09 per 3 parts per million). Exposure to increased levels of ambient PM10 and possibly CO during pregnancy may contribute to the occurrence of preterm births in Southern California.     

Preterm delivery and exposure to active and passive smoking during pregnancy: a case-control study from Italy

The aim of this study was to assess the relationship between preterm/early preterm delivery and active smoking as well as environmental tobacco smoke (ETS) exposure in a sample of pregnant Italian women. A case-control study was conducted in nine cities in Italy between October 1999 and September 2000. Cases of preterm birth were singleton babies born before the 37th gestational week; babies born before the 35th gestational week were considered early preterm births. Controls were babies with gestational ages >or= 37th week. A total of 299 preterm cases (including 105 early preterm) and 855 controls were analysed. A self-administered questionnaire was used to assess active smoking and ETS exposure, as well as potential confounders. Multivariable logistic regression analysis showed a relationship between active smoking during pregnancy and preterm/early preterm delivery [adjusted ORs: 1.53; 95% CI 1.05, 2.21 and 2.00; 95% CI 1.16, 3.45, respectively]. A dose-response relationship was found for the number of cigarettes smoked daily. The adjusted ORs were 1.54 and 1.69 for preterm babies and 1.90 and 2.46 for early preterm babies for 1-10 and >10 cigarettes/day respectively. ETS exposure was associated with early preterm delivery [adjusted OR 1.56; 95% CI 0.99, 2.46] with a dose-response relationship with the number of smokers in the home. Smoking during pregnancy was strongly associated with preterm delivery with a dose-response effect. ETS exposure in non-smoking women was associated only with early preterm delivery.     

石家庄市大气颗粒物与儿童急性下呼吸道感染门诊量的时间序列分析

目的探讨石家庄市大气颗粒物(PM2.5和PM10)对儿童急性下呼吸道感染日门诊量的影响,为大气环境治理和儿童呼吸道感染的预防控制提供理论依据。方法应用Poison分布广义可加模型分析PM2.5和PM10对儿童急性下呼吸道感染日门诊量的影响进行(0-5)d的滞后分析及多污染物模型分析;计算颗粒物每增加10μg/m3,日门诊量增加的比值比。结果PM2.5在lag0 d、lag1 d和累积lag01 d^lag03 d对儿童急性下呼吸道感染日门诊量的影响具有统计学意义PM10在lag0 d^lag2 d和累积滞后lag01 d^lag05 d对儿童急性下呼吸道感染日门诊量的影响具有统计学意义;PM2.5在暴露当天、累积滞后1 d以及PM10在累积滞后1 d、2 d对日门诊量的影响最大PM2.5或PM10浓度每增加10μg/m3,儿童急性下呼吸道感染的日门诊量均增加0.35%。多污染物模型的分析结果显示PM2.5只有在引入SO2后模型才具有统计学意义,PM10在引入其他污染物后均具有统计学意义,但引入SO2后效应最大。结论石家庄市PM2.5和PM10度的增加会导致儿童急性下呼吸道感染的门诊量增加,且PM10的滞后效应较PM2.5强。     

湖北省HIV感染孕产妇早产现状与影响因素分析

目的 了解湖北省HIV感染孕产妇早产的流行情况,探讨其相关影响因素,为制定预防HIV感染孕产妇早产的策略和措施提供参考依据。方法 收集2004—2020年全国预防艾滋病母婴传播管理信息系统中湖北地区报告的已分娩的HIV感染孕产妇相关流行病学调查资料,采用单因素χ2检验和Poisson回归模型,分析HIV感染孕产妇早产情况及其影响因素。结果 湖北省HIV感染孕产妇早产率为10.70%（66/617）,呈逐年上升趋势（χ2趋势 = 4.942,P = 0.026）,不同地区间HIV感染孕产妇早产率的差异无统计学意义。Poisson回归模型分析结果显示,年龄（35～49）岁（RR = 2.080,95%CI:1.177～3.678）、注射毒品感染HIV（RR = 2.899,95%CI:1.540～5.456）、孕期末次病毒载量≥1 000拷贝/mm3（RR = 4.567,95%CI:1.984～10.516）、胎膜早破（RR = 2.395,95%CI:1.063～5.393）、妊娠合并肝病（RR = 2.268,95%CI:1.154～4.455）和妊娠期高血压（RR = 3.540,95%CI:2.063～6.075）是影响HIV感染孕产妇早产的危险因素（P＜0.05）,不含蛋白酶抑制剂（PI）的三联用药方式（RR = 0.461,95%CI:0.231～0.917）是影响HIV感染孕产妇早产的保护性因素（P＜0.05）。结论 对于HIV感染孕产妇而言,加强围产期保健,采用不含PI的三联抗病毒治疗方案,控制孕期病毒载量水平、妊娠高血压疾病、妊娠合并肝病、胎膜早破等风险因素是降低其早产发生率的重要措施。     

Local variations in CO and particulate air pollution and adverse birth outcomes in Los Angeles County, California, USA

We extended our previous analyses of term low birth weight (LBW) and preterm birth to 1994-2000, a period of declining air pollution levels in the South Coast Air Basin. We speculated that the effects we observed previously for carbon monoxide, particulate matter < 10 microm in aerodynamic diameter (PM10), and traffic density were attributable to toxins sorbed to primary exhaust particles. Focusing on CO, PM10, and particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), we examined whether varying residential distances from monitoring stations affected risk estimates, because effect attenuation may result from local pollutant heterogeneity inadequately captured by ambient stations. We geocoded home locations, calculated the distance to the nearest air monitors, estimated exposure levels by pregnancy period, and performed logistic regression analyses for subjects living within 1-4 mi of a station. For women residing within a 1-mi distance, we observed a 27% increase in risk for high (> or = 75th percentile) first-trimester CO exposures and preterm birth and a 36% increase for high third-trimester pregnancy CO exposures and term LBW. For particles, we observed similar size effects during early and late pregnancy for both term LBW and preterm birth. In contrast, smaller or no effects were observed beyond a 1-mi distance of a residence from a station. Associations between CO and PM10 averaged over the whole pregnancy and term LBW were generally smaller than effects for early and late pregnancy. These new results for 1994-2000 generally confirm our previous observations for the period 1989-1993, again linking CO and particle exposures to term LBW and preterm birth. In addition, they confirm our suspicions about having to address local heterogeneity for these pollutants in Los Angeles.