Lupo Philip J, Symanski Elaine, Langlois Peter H, Lawson Christina C, Malik Sadia, Gilboa Suzanne M, Lee Laura J, Agopian A J, Desrosiers Tania A, Waters Martha A, Romitti Paul A, Correa Adolfo, Shaw Gary M, Mitchell Laura E
Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas School of Public Health, Houston, TX 77030, USA.
Birth Defects Res A Clin Mol Teratol. 2012 Nov;94(11):875-81. doi: 10.1002/bdra.23071. Epub 2012 Sep 3.
There is evidence in experimental model systems that exposure to polycyclic aromatic hydrocarbons (PAHs) results in congenital heart defects (CHDs); however, to our knowledge, this relationship has not been examined in humans. Therefore, we conducted a case-control study assessing the association between estimated maternal occupational exposure to PAHs and CHDs in offspring.
Data on CHD cases and control infants were obtained from the National Birth Defects Prevention Study for the period of 1997 to 2002. Exposure to PAHs was assigned by industrial hygienist consensus, based on self-reported maternal occupational histories from 1 month before conception through the third month of pregnancy. Logistic regression was used to evaluate the association between maternal occupational PAH exposure and specific CHD phenotypic subtypes among offspring.
The prevalence of occupational PAH exposure was 4.0% in CHD case mothers (76/1907) and 3.6% in control mothers (104/2853). After adjusting for maternal age, race or ethnicity, education, smoking, folic acid supplementation, and study center, exposure was not associated with conotruncal defects (adjusted odds ratio [AOR], 0.98; 95% confidence interval [CI], 0.58-1.67), septal defects (AOR, 1.28; 95% CI, 0.86-1.90), or with any isolated CHD subtype.
Our findings do not support an association between potential maternal occupational exposure to PAHs and various CHDs in a large, population-based study. For CHD phenotypic subtypes in which modest nonsignificant associations were observed, future investigations could be improved by studying populations with a higher prevalence of PAH exposure and by incorporating information on maternal and fetal genotypes related to PAH metabolism. Birth Defects Research (Part A), 2012.
在实验模型系统中有证据表明,接触多环芳烃(PAHs)会导致先天性心脏病(CHDs);然而,据我们所知,这种关系尚未在人类中进行研究。因此,我们开展了一项病例对照研究,评估估计的母亲职业性接触PAHs与后代CHDs之间的关联。
1997年至2002年期间的先天性心脏病病例和对照婴儿的数据来自国家出生缺陷预防研究。PAHs暴露由工业卫生学家根据自受孕前1个月至怀孕第三个月的母亲职业史自我报告,通过共识进行分配。使用逻辑回归来评估母亲职业性PAH暴露与后代中特定CHD表型亚型之间的关联。
先天性心脏病病例母亲中职业性PAH暴露的患病率为4.0%(76/1907),对照母亲中为3.6%(104/2853)。在调整了母亲年龄、种族或族裔、教育程度、吸烟、叶酸补充和研究中心后,暴露与圆锥动脉干缺陷(调整后的优势比[AOR],0.98;95%置信区间[CI],0.58 - 1.67)、间隔缺损(AOR,1.28;95% CI,0.86 - 1.90)或任何孤立的CHD亚型均无关联。
在一项基于人群的大型研究中,我们的研究结果不支持母亲职业性潜在接触PAHs与各种CHDs之间存在关联。对于观察到适度非显著关联的CHD表型亚型,未来的研究可以通过研究PAH暴露患病率较高的人群以及纳入与PAH代谢相关的母亲和胎儿基因型信息来改进。《出生缺陷研究(A部分)》,2012年。