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加利福尼亚州圣华金谷的环境空气污染和交通暴露与先天性心脏病。

Ambient air pollution and traffic exposures and congenital heart defects in the San Joaquin Valley of California.

机构信息

Stanford University, Stanford 94305, USA.

出版信息

Paediatr Perinat Epidemiol. 2013 Jul;27(4):329-39. doi: 10.1111/ppe.12055. Epub 2013 Apr 21.

DOI:10.1111/ppe.12055
PMID:23772934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3694598/
Abstract

BACKGROUND

Congenital anomalies are a leading cause of infant morbidity and mortality. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited.

METHODS

We used data from the California Center of the National Birth Defects Prevention Study and the Children's Health and Air Pollution Study to estimate the odds of 27 congenital heart defects with respect to quartiles of seven ambient air pollutant and traffic exposures in California during the first 2 months of pregnancy, 1997-2006 (n = 822 cases and n = 849 controls).

RESULTS

Particulate matter < 10 microns (PM10 ) was associated with pulmonary valve stenosis [adjusted odds ratio (aOR)Fourth Quartile  = 2.6] [95% confidence intervals (CI) 1.2, 5.7] and perimembranous ventricular septal defects (aORThird Quartile  = 2.1) [95% CI 1.1, 3.9] after adjusting for maternal race/ethnicity, education and multivitamin use. PM2.5 was associated with transposition of the great arteries (aORThird Quartile  = 2.6) [95% CI 1.1, 6.5] and inversely associated with perimembranous ventricular septal defects (aORFourth Quartile  = 0.5) [95% CI 0.2, 0.9]. Secundum atrial septal defects were inversely associated with carbon monoxide (aORFourth Quartile  = 0.4) [95% CI 0.2, 0.8] and PM2.5 (aORFourth Quartile  = 0.5) [95% CI 0.3, 0.8]. Traffic density was associated with muscular ventricular septal defects (aORFourth Quartile  = 3.0) [95% CI 1.2, 7.8] and perimembranous ventricular septal defects (aORThird Quartile  = 2.4) [95% CI 1.3, 4.6], and inversely associated with transposition of the great arteries (aORFourth Quartile  = 0.3) [95% CI 0.1, 0.8].

CONCLUSIONS

PM10 and traffic density may contribute to the occurrence of pulmonary valve stenosis and ventricular septal defects, respectively. The results were mixed for other pollutants and had little consistency with previous studies.

摘要

背景

先天性畸形是婴儿发病率和死亡率的主要原因。研究表明,环境污染物与某些畸形之间存在关联,尽管证据有限。

方法

我们使用了加利福尼亚国家出生缺陷预防研究中心和儿童健康与空气污染研究的数据,来估计在妊娠前 2 个月(1997-2006 年),加利福尼亚州 7 种环境空气污染物和交通暴露的四分位数与 27 种先天性心脏病之间的关联,共有 822 例病例和 849 例对照。

结果

与其他三分位相比,细颗粒物<10 微米(PM10 )与肺动脉瓣狭窄相关(调整后的优势比[第四四分位数]为 2.6 [95%置信区间(CI)1.2, 5.7])和膜周室间隔缺损(调整后的优势比[第三四分位数]为 2.1 [95%CI 1.1, 3.9]),调整了母亲的种族/民族、教育和多种维生素的使用。PM2.5 与大动脉转位相关(调整后的优势比[第三四分位数]为 2.6 [95%CI 1.1, 6.5]),与膜周室间隔缺损呈负相关(调整后的优势比[第四四分位数]为 0.5 [95%CI 0.2, 0.9])。继发孔房间隔缺损与一氧化碳(调整后的优势比[第四四分位数]为 0.4 [95%CI 0.2, 0.8])和 PM2.5(调整后的优势比[第四四分位数]为 0.5 [95%CI 0.3, 0.8])呈负相关。交通密度与肌部室间隔缺损(调整后的优势比[第四四分位数]为 3.0 [95%CI 1.2, 7.8])和膜周室间隔缺损(调整后的优势比[第三四分位数]为 2.4 [95%CI 1.3, 4.6])相关,与大动脉转位呈负相关(调整后的优势比[第四四分位数]为 0.3 [95%CI 0.1, 0.8])。

结论

PM10 和交通密度可能分别导致肺动脉瓣狭窄和室间隔缺损的发生。其他污染物的结果参差不齐,与以前的研究几乎没有一致性。

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