Maternal occupational exposure to polycyclic aromatic hydrocarbons and congenital heart defects among offspring in the national birth defects prevention study.
Maternal occupational exposure to polycyclic aromatic hydrocarbons and congenital heart defects among offspring in the national birth defects prevention study.
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在国家出生缺陷的预防研究中，母体职业暴露于多环芳族烃和先天性心脏缺陷。
DOI：
10.1002/bdra.23071
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发表时间：
2012-11
期刊：
影响因子：
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通讯作者：
National Birth Defects Prevention Study
中科院分区：
文献类型：
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作者：
Lupo PJ;Symanski E;Langlois PH;Lawson CC;Malik S;Gilboa SM;Lee LJ;Agopian AJ;Desrosiers TA;Waters MA;Romitti PA;Correa A;Shaw GM;Mitchell LE;National Birth Defects Prevention Study
在实验模型系统中有证据表明，暴露于多环芳烃（PAH）会导致先天性心脏病（CHD）;然而，据我们所知，这种关系尚未在人类中进行过研究。因此，我们进行了一项病例对照研究，评估估计母亲职业暴露于多环芳烃和心脏病在后代之间的关联。CHD病例和对照婴儿的数据来自1997年至2002年期间的国家出生缺陷预防研究。根据怀孕前1个月至怀孕第3个月的母亲自我报告的职业史，通过工业卫生学家共识分配了多环芳烃暴露。采用Logistic回归分析评价母亲职业性PAH暴露与子代中特定CHD表型亚型之间的关系。CHD病例组母亲PAH职业暴露率为4.0%（76/1907），对照组母亲PAH职业暴露率为3.6%（104/2853）。在校正了母亲年龄、种族、教育、吸烟、叶酸补充和研究中心后，暴露与圆锥动脉干缺陷（校正比值比[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亚型无关。我们的研究结果不支持在一项大型的、以人群为基础的研究中，母亲潜在的职业暴露于多环芳烃与各种冠心病之间存在关联。对于CHD表型亚型，其中观察到适度的非显着性关联，未来的研究可以通过研究PAH暴露的患病率较高的人群，并通过纳入母亲和胎儿基因型PAH代谢相关的信息进行改进。
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.