太原市空气污染对早产的急性影响

目的探讨太原市空气污染对早产的急性影响。方法通过太原市出生监测系统收集2005年11月1日—2007年1月7日期间太原市早产儿资料,从山西省气象局获得气象资料(平均温度、相对湿度),大气污染资料(PM10、SO2、NO2)来源于太原市环境保护监测站。应用病例交叉设计和SAS 9.0中的条件Logistic回归模型对太原市空气污染与早产发生之间的联系进行分析,并调整气象因素的混杂影响。结果PM10较强效应期滞后5 d及滞后6 d,SO2较强效应期为滞后7 d及累积8 d。当PM10、SO2浓度每升高50μg/m3时,PM10滞后5 d、滞后6 d的OR值分别为1.169(95%CI:1.058～1.292),1.235(95%CI:1.115～1.367)。SO2滞后7 d、累积8 d的OR值分别为1.346(95%CI:1.122～1.616),2.203(95%CI:1.517～3.201)。敏感性分析表明,PM10对早产的滞后效应稳健,SO2对早产的累积效应较稳健。结论太原市空气污染物对早产发生有急性效应。     

太原市大气污染对妊娠结局的影响

目的探讨大气污染对妊娠结局的影响。方法收集太原市1997—2004年6个国控监测点大气PM10和SO2浓度资料以及同期妊娠结局的资料,对妊娠结局的相关危险因素及不同妊娠时期大气中PM10和SO2浓度对妊娠结局的影响进行分析。结果空气中PM10和SO2浓度每增加100μg/m3与妊娠结局的Logistic回归结果表明,PM10空气污染对早产、出生缺陷和死胎死产有显著影响,早产的OR值为1.17～1.76,最高OR值为1.76(95%CI:1.64～1.90),出现在怀孕前3个月;出生缺陷的OR值为1.37～1.67,最高OR值为1.67(95%CI:1.28～2.17),出现于第3个孕月。关于SO2空气污染,只观察到对早产的显著影响,且发生于第1、2个孕月,相应的OR值分别为1.27(95%CI:1.21～1.34)和1.07(95%CI:1.01～1.14)。结论太原市空气污染已对妊娠结局造成一定影响,应采取严格的空气污染控制措施,降低不良妊娠结局发生率。     

北京市大气污染对不良妊娠结局影响的病例对照研究

目的 定量分析和评价北京市大气污染对新生儿早产、低出生体重及出生缺陷等不良妊娠结局的影响.方法 收集北京市海淀区妇幼保健院2007年7月-2009年7月分娩个案资料、同期北京市大气污染物二氧化硫(SO2)、二氧化氮(NO2)、可吸入颗粒物(PM10)及气象因素资料.采用多因素Logistic回归模型调整气象因素和妊娠期妇女个体信息的基础上,研究北京市大气污染物对不良妊娠结局的影响.结果 控制气象因素、孕妇分娩次数、年龄、胎儿性别、不良接触史等因素后,妊娠后第1个月SO2浓度每升高100μg/m3,对低出生体重的影响的OR值为1.50(95％CI:1.09～2.05);妊娠后前3个月、分娩前第1个月SO2浓度每升高100 μg/m3,对早产影响的OR值分别为1.50 (95％CI:1.04～2.18)和1.79(95％CI:1.30～2.46);分娩前第2个月PM10浓度每升高100 μg/m3,对早产的影响的OR值为1.45(95％CI:1.15～1.84);妊娠后3～8周内,NO2浓度每升高100 μg/m3,对出生缺陷的影响的OR值为2.85(95％CI:1.08～7.50).结论 本次调查的北京市妊娠期妇女在妊娠后期的大气PM10暴露浓度、妊娠早期的大气SO2暴露浓度与早产的发生存在统计学关联;妊娠3～8周时NO2暴露浓度与出生缺陷的发生存在统计学关联.     

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。     

长沙市大气污染物与脑卒中急诊关系的病例交叉研究

目的探讨长沙市大气污染物日均浓度与脑卒中急诊的相关性。方法收集2008—2009年中南大学湘雅三医院每日脑出血和脑梗死急诊数据,及长沙市同期大气二氧化硫(SO2)、二氧化氮(NO2)、可吸入颗粒物(PM10)和相关气象数据,采用季节分层的单向回顾性1∶4配对病例交叉设计建立单污染物和多污染物模型并进行分析。结果在调整气象因素(气温和相对湿度)的单污染物滞后模型中,秋季SO2、NO2、PM10日均浓度每增加10μg/m3,滞后0~3 d的脑出血与脑梗死OR值均大于1,且关联有统计学意义(P0.05)。多污染物模型中,控制PM10+NO2后秋季SO2浓度每增加10μg/m3时,脑梗死急诊的OR值(95%CI)为1.446(1.130~1.850);控制PM10+SO2后秋季NO2浓度每增加10μg/m3时,脑出血急诊的OR值(95%CI)为1.615(1.131~2.305);控制其他污染物后冬季NO2、PM10浓度每增加10μg/m3,脑出血急诊的OR值(95%CI)分别为1.325(1.019~1.724)和1.117(1.024~1.218),关联均有统计学意义(P0.05)。结论长沙市秋季SO2、NO2、PM10浓度与脑出血和脑梗死急诊均呈正向关联,其中SO2对脑梗死急诊影响更明显,NO2对脑出血急诊影响更明显;冬季NO2、PM10浓度与脑出血急诊亦呈正向关联。     

围孕期空气污染暴露与子代先天性甲状腺功能减退的关系:基于中国30个省份的研究

目的探讨围孕期母体空气污染暴露水平对子代先天性甲状腺功能减退症(CH)发病风险的影响。方法回顾性收集中国2014年10月1日至2015年9月31日30个省份CH的发病率。遵循空气污染对妊娠期效应的滞后性和累积性原则,回顾性收集中国30个省份2014年1月1日至2015年9月31日PM2.5、PM10、NO2、SO2、CO和O3的平均暴露水平。构建二项Logistic回归模型,并纳入各省份人均国民生产总值、废水中铅、汞和砷的暴露量作为混杂因素,分析围孕期空气污染暴露对子代CH发病风险的影响。结果我国2015年CH的年发病率约为4.31/万人,其中浙江省(7.42/万人)和福建省(7.34/万人)的发病率最高,发病率最低的省份为新疆(1.88/万人)。围孕期母体PM2.5高暴露会显著增加CH的发病风险,围孕期PM2.5的暴露水平每上升1μg/m3,该地区CH高发的风险将会增加0.102倍(OR=1.102, 95%CI:1.001~1.213,P <0.05)。此外,围孕期NO2平均暴露水平的升高也会显著增加CH的发病风险(OR=1.211, 95%CI:1.033~1.419, P <0.05)。在双污染物模型中,围孕期母体PM2.5和NO2的高暴露仍会显著增加CH的发病风险,当对PM10的暴露水平进行调整后,PM2.5和NO2暴露对CH发病率的影响均最为显著(OR=1.585、1.580,均P <0.05)。但PM10、SO2、CO和O3对CH的发病风险没有显著的影响(OR=1.007、0.987、0.925、0.061,均P>0.05)。结论本研究通过大数据分析发现,围孕期母体PM2.5和NO2高暴露会显著增加子代CH的发病风险。围孕期空气污染暴露可能影响子代腺体功能的发育。     

低浓度空气污染与妊娠结局

立陶宛学者最近研究了空气污染与低出生体重和早产的关系。调查了１９９８年Kaunas市出生的３９９８名新生儿生出情况和他们的母亲孕期暴露于空气污染的情况。研究发现在控制混杂因素后，低出生体重调整的OR值随空气甲醛浓度的上升而上升；孕妇暴露于NO２的浓度每增加１０mg／m３其早产的危险就增加２５％（调整的OR＝１．２５，９５％CI：１．０７～１．４６）。妊娠前３个月孕妇暴露于空气污染物的情况对妊娠结局最有影响，而其他妊娠阶段暴露于空气污染物（如NO２和甲醛）与妊娠结局的低出生体重和早产关系不显著。说明新生儿低出生…     

大气污染对低出生体重和早产影响的Meta分析

目的 研究各主要大气污染物对低出生体重(LSW)和早产的影响.方法 通过计算机检索收集国内外1999-2009年公开发表的有关大气污染对不良妊娠结局影响的相关文献14篇,按照制定的纳入排除标准对文献进行筛选,利用Stata9.0的Meta模块对人选文献进行异质性检验和相应的效应值合并.采用Meta分析获得的合并OR值作为最终的合并效应值.结果 建立各主要污染物与低出生体重和早产的暴露.反应关系,其中PM10浓度每升高50μg/m3,所对应的低出生体重及早产发生的合并OR值分别为1.07(95%CI:1.024～1.119,P＜0.01)、1.217(95%CI:1.045～1.415,P＜0.05);SO2浓度每升高43λg/m3(15 ppb),所对应的低出生体重或早产发生的合并OR值分别为1.137(95%CI:1.047～1.235,P＜0.05)、1.163(95%CI:1.082～1.250,P＜0.01);NO2每升高21μg/m3(10 ppb),所对应的低出生体重发生的合并OR值为1.03(95%CI:1.008～1.054,P＜0.01);CO每升高1.25 mg/m3(1 ppm),所对应的低出生体重发生的合并OR值为1.066(95%C1:1.016～1.117,P＜0.01);NO2以及CO对早产影响的合并效应值无统计学意义(P＞0.05).结论 本研究综合定量分析的结果 表明,大气污染能够增加低出生体重和早产发生的危险,妊娠期妇女有必要采取有效的措施减少大气污染的暴露.     

空气污染物对出生体重影响的研究

目的研究空气污染物可吸入颗粒物（PM10）、二氧化硫（SO2）、二氧化氮（NO2）对新生儿出生体重的影响。方法收集了广东某地2003—2005年分娩时孕满37周的围产数据。调查的因素包括产妇的年龄、职业、文化、出生地、是否有准生证、孕周、是否有高危因素、末次月经时间、分娩日期、孕次、产次；产妇丈夫的职业、文化；新生儿的性别、出生身高、体重。用2002—2005年的空气污染数据估计暴露水平。结果性别、母亲年龄、母亲职业、母亲原地址、孕期高危情况、孕次、是否有准生证分组，出生体重组间差异有统计学意义；不同孕期PM10、SO2、NO2暴露分组之间出生体重差异有统计学意义。多元线性回归分析显示可吸入颗粒物PM10、SO2、NO2浓度每增加10μg/m^3，出生体重分别减少1．90～3．94g、1．65～2．73g、2．70～3．76g。结论空气污染物与低出生体重有关，空气污染对妊娠结局的影响值得关注。     

空气污染对早产和低出生体重影响的流行病学研究现况

空气污染对不良妊娠结局的影响研究日益被国内外的专家所关注,空气污染物与早产和低出生体重的研究有待进一步开展。该文就近年来有关空气污染物(可吸入颗粒物、细颗粒物、CO、NO2、SO2等)对早产和低出生体重影响的流行病学研究进行了综述,为控制空气污染和减少不良妊娠结局的发生以及进一步探索其可能的机制提供有益的参考。     

Air pollution and low birth weight in the city of Rio de Janeiro, Brazil, 2002

The objective of this study was to evaluate the effect of air pollution on low birth weight in full term singleton newborns in the city of Rio de Janeiro, Brazil. The study adopted a cross-sectional design based on the year 2002. Data on live births were obtained from the Live Birth Information System of the Brazilian Ministry of Health. Low birth weight was defined as less than 2,500 g. Maternal exposure to air pollution was defined as the mean for a given pollutant over each trimester of pregnancy and was assessed taking birth date into account. Adjusted odds ratios (OR) were estimated for each potential risk factor. For PM(10), CO, and NO(2), no significant increases were detected. For SO(2), the OR of the fourth interquartile range of exposure in the third trimester of pregnancy was 1.149 (95%CI: 1.016-1.301). For O(3), the estimated OR was 0.830 (95%CI: 0.750-0.987). When exposure variable was regarded as a continuous measure, the OR for PM(10), CO, and SO2 in the third trimester were not statistically significant and were 1.089, 2.223, and 1.259, respectively.     

Exposures to air pollutants during pregnancy and preterm delivery

The association between preterm delivery (PTD) and exposure to air pollutants has recently become a major concern. We investigated this relationship in Incheon, Republic of Korea, using spatial and temporal modeling to better infer individual exposures. The birth cohort consisted of 52,113 singleton births in 2001-2002, and data included residential address, gestational age, sex, birth date and order, and parental age and education. We used a geographic information system and kriging methods to construct spatial and temporal exposure models. Associations between exposure and PTD were evaluated using univariate and multivariate log-binomial regressions. Given the gestational age, birth date, and the mother's residential address, we estimated each mother's potential exposure to air pollutants during critical periods of the pregnancy. The adjusted risk ratios for PTD in the highest quartiles of the first trimester exposure were 1.26 [95% confidence interval (CI), 1.11-1.44] for carbon monoxide, 1.27 (95% CI, 1.04-1.56) for particulate matter with aerodynamic diameter < or = 10 microm, 1.24 (95% CI, 1.09-1.41) for nitrogen dioxide, and 1.21 (95% CI, 1.04-1.42) for sulfur dioxide. The relationships between PTD and exposures to CO, NO2, and SO2 were dose dependent (p < 0.001, p < 0.02, p < 0.02, respectively) . In addition, the results of our study indicated a significant association between air pollution and PTD during the third trimester of pregnancy. In conclusion, our study showed that relatively low concentrations of air pollution under current air quality standards during pregnancy may contribute to an increased risk of PTD. A biologic mechanism through increased prostaglandin levels that are triggered by inflammatory mediators during exposure periods is discussed.     

Association between maternal exposure to elevated ambient sulfur dioxide during pregnancy and term low birth weight

This retrospective cohort study investigated whether the risk of delivering full term (37-44 completed weeks of gestation) low birth weight (LBW) infants is associated with differences in exposure to air pollutants in different trimesters. Full-term infants (37 completed weeks of gestation) with a birth weight below 2500 g were classified as term LBW infants. The study infants comprised 92,288 full-term live singletons identified from the Taiwan birth registry and born in the city of Taipei or Kaoshiung in Taiwan between 1995 and 1997. Maternal exposures to various air pollutants including CO, SO2, O3, NO2, and PM10 in each trimester of pregnancy was estimated as the arithmetic means of all daily measurements taken by the air quality monitoring station nearest to the district of residence of the mother at birth. The multivariable logistic regression model with adjustment for potential confounders was used to assess the independent effect of specific air pollutants on the risk of term LBW. This study suggested a 26% increase in term LBW risk given maternal ambient exposure to SO2 concentration exceeding 11.4 ppb during pregnancy compared to low exposure (<7.1 ppb) (OR=1.26, 95% CI=1.04-1.53). Since the relative risk of term LBW was reassessed according to exposure level in each trimester, mothers exposed to >12.4 ppb of SO2 in the last trimester showed 20% higher risk (OR=1.20, 95% CI=1.01-1.41) of term LBW delivery than mothers with lower exposure (<6.8 ppb). No significant elevation ORs was observed for other air pollutants.     

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction

Previous research demonstrated consistent associations between ambient air pollution and emergency room visits, hospitalizations, and mortality. Effect of air pollution on perinatal outcomes has recently drawn more attention. We examined the association between intrauterine growth restriction (IUGR) among singleton term live births and sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and fine particles (PM2.5) present in ambient air in the Canadian cities of Calgary, Edmonton, and Montreal for the period 1985-2000. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for IUGR, based on average daily levels of individual pollutants over each month and trimester of pregnancy after adjustment for maternal age, parity, infant gender, season, and city of residence. A 1 ppm increase in CO was associated with an increased risk of IUGR in the first (OR=1.18; 95% CI 1.14-1.23), second (OR=1.15; 95% CI 1.10-1.19) and third (OR=1.19; 95% CI 1.14-1.24) trimesters of pregnancy, respectively. A 20 ppb increase in NO2 (OR=1.16; 95% CI 1.09-1.24; OR=1.14; 95% CI 1.06--1.21; and OR=1.16; 95% CI 1.09-1.24 in the first, second, and third trimesters) and a 10 mug/m3 increase in PM2.5 (OR=1.07; 95% CI 1.03-1.10; OR=1.06; 95% CI 1.03-1.10; and OR=1.06; 95% CI 1.03-1.10) were also associated with an increased risk of IUGR. Consistent results were found when ORs were calculated by month rather than trimester of pregnancy. Our findings add to the emerging body of evidence that exposure to relatively low levels of ambient air pollutants in urban areas during pregnancy is associated with adverse effects on fetal growth.     

Ambient air pollution and low birth weight in Connecticut and Massachusetts

BACKGROUND: Several studies have examined whether air pollution affects birth weight; however results vary and many studies were focused on Southern California or were conducted outside of the United States. OBJECTIVES: We investigated maternal exposure to particulate matter with aerodynamic diameter < 10, < 2.5 microm (PM(10), PM(2.5)), sulfur dioxide, nitrogen dioxide, and carbon monoxide and birth weight for 358,504 births in Massachusetts and Connecticut from 1999 to 2002. METHODS: Analysis included logistic models for low birth weight (< 2,500 g) and linear models with birth weight as a continuous variable. Exposure was assigned as the average county-level concentration over gestation and each trimester based on mother's residence. We adjusted for gestational length, prenatal care, type of delivery, child's sex, birth order, weather, year, and mother's race, education, marital status, age, and tobacco use. RESULTS: An interquartile increase in gestational exposure to NO(2), CO, PM(10), and PM(2.5) lowered birth weight by 8.9 g [95% confidence interval (CI), 7.0-10.8], 16.2 g (95% CI, 12.6-19.7), 8.2 g (95% CI, 5.3-11.1), and 14.7 g (95% CI, 12.3-17.1), respectively. Lower birth weight was associated with exposure in the third trimester for PM(10), the first and third trimesters for CO, the first trimester for NO(2) and SO(2), and the second and third trimesters for PM(2.5). Effect estimates for PM(2.5) were higher for infants of black mothers than those of white mothers. CONCLUSIONS: Results indicate that exposure to air pollution, even at low levels, may increase risk of low birth weight, particularly for some segments of the population.     

Relationship between low birthweight and air pollution in the city of Sao Paulo, Brazil

OBJECTIVE: Air pollution has been investigated as a potential determinant for low birthweight. The aim of the present study was to study the effect of air pollution on birthweight. METHODS: We analyzed all deliveries by mothers living in the municipality of Sao Paulo, Southeastern Brazil, between 1998 and 2000. We estimated the prevalence of low birthweight according to newborn, mother, and delivery characteristics. Only births occurring in the most central districts of the city were analyzed, totaling 311.735 events. For the evaluation of the effects of air pollution, we excluded preterm and multiple deliveries. Pollutants analyzed were ozone (O3), sulfur dioxide (SO2), nitrogen dioxide (NO2), suspended particles (PM10), and carbon monoxide (CO). The effect of maternal exposure to air pollution on birthweight was evaluated using linear and logistic regression. RESULTS: A total of 4.6% of newborns weighed less than 2,500 g at birth. Maternal exposure to CO, PM10, and NO2 during the first trimester of pregnancy was significantly associated with decreased birthweight. CONCLUSIONS: Our results reinforce the notion that maternal exposure to air pollution during the first trimester of pregnancy may contribute to lesser weight gain in the fetus.     

Low levels of ambient air pollution during pregnancy and fetal growth among term neonates in Brisbane, Australia

There is mounting evidence that maternal exposure to ambient air pollution during pregnancy is associated with adverse birth outcomes. We examined birth weight and small for gestational age (SGA <10th percentile for age and gender) among 26,617 singleton full-term births in Brisbane, Australia (July 2000-June 2003), in relation to ambient pollution during pregnancy. We also examined head circumference (HC) and crown-heel length (CHL) among a sub-sample (n=21,432) of the term neonates. Maternal exposure to PM(10), visibility reducing particles (bsp), O(3) and NO(2) was assessed by calculating average exposure estimates over months and trimesters of pregnancy based on a citywide average of the pollutants. Linear and logistic regression models were employed to examine the effect of these pollutants on the birth outcomes after adjusting for potential confounders and season of birth. The regression coefficients were based on an inter-quartile range (IQR) increase in exposure as well as quartiles of exposure with the lowest used as a reference category. Trimester- and monthly specific exposures to all pollutants were not significantly associated with a reduction in either birth weight or HC, or an increased risk of SGA. An IQR increase in NO(2) during the third trimester was associated with a reduction in CHL (beta=-0.15cm, 95% CI -0.25 to -0.05cm) and this was concentrated around exposure during month nine. No other pollutants were associated with a reduction in CHL. In conclusion, there was no strong evidence suggesting that ambient air pollution during pregnancy is associated with sub-optimal fetal growth in Brisbane.     

妊娠期大气二氧化氮暴露与孕妇维生素D缺乏症的关联

目的 孕妇维生素D缺乏症与妊娠期糖尿病、妊娠期高血压、孕妇贫血以及胎儿生长受限和早产等不良妊娠结局密切相关。本研究旨在探讨妊娠期大气二氧化氮（nitrogen dioxide,NO2）暴露与孕妇维生素D缺乏症的关联。方法 选取2013年5月-至2014年５月,在某市妇幼保健院建卡的孕妇作为初始研究对象。按照入选和排除标准最终纳入3244名孕妇进入本研究。通过问卷调查收集孕妇的一般人口学信息;利用环境监测站点的数据模拟孕妇在妊娠期间大气NO2的暴露水平;采用酶联免疫吸附法检测孕晚期孕妇血清中25（OH）D的浓度。结果 孕妇在孕早期、中期、晚期以及整个孕期NO2暴露水平的中位数分别为:39.52、36.84、28.09以及31.90μg/m3。孕晚期血清中25(OH)D浓度的平均值为42.09nmol/L。多元线性回归分析的结果显示,孕中期、孕晚期以及整个孕期NO2的暴露水平每增加10μg / m3,孕妇血清中25（OH）D的水平分别降低2.224nmol/L（95%CI:-2.777,-1.671）,2.240nmol/L（95%CI:-2.665,-1.816）以及5.299 nmol/L（95%CI:-6.481,-4.177）。多元logistic回归分析的结果显示,随着孕中期、孕晚期以及整个孕期NO2的暴露水平的增加,孕妇VD缺乏症发生的风险增加,其OR值分别为1.338（95%CI:1.225,1.461）,1.347（95%CI:1.259,1.442）以及2.049（95%CI:1.709～2.456）。结论 孕期NO2暴露是孕妇维生素D缺乏症发生的一个危险因素。在制订维生素D缺乏症的防控措施时需要考虑孕期NO2的暴露。