Cathey Amber L, Eaton Jarrod L, Watkins Deborah J, Ferguson Kelly K, Cantonwine David E, McElrath Thomas F, Meeker John D
Department of Environmental Health Sciences, University of Michigan School of Public Health, 1415 Washington Heights, Ann Arbor, MI, 48109, USA.
Epidemiology Branch, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA.
Environ Pollut. 2025 May 15;373:126134. doi: 10.1016/j.envpol.2025.126134. Epub 2025 Mar 26.
Environmental exposure to polycyclic aromatic hydrocarbons (PAH) is ubiquitous and may impact fetal development leading to adverse birth outcomes. PAHs result from incomplete combustion and exposure sources include inhalation of cigarette smoke and car exhaust, ingestion of charred meat, and many others. The purpose of this study was to determine associations between prenatal PAH biomarker concentrations and birth outcomes. Our nested case-control study included 123 preterm birth cases and 335 term controls from the LIFECODES cohort between 2006 and 2008 (n = 458). Eight urinary PAH metabolites were measured in urine samples collected at up to four study visits (median 12, 18, 24, 34 weeks gestation). Linear and logistic regression were used to model gestational geometric mean PAH biomarker concentrations in relation to preterm birth, birth weight z-score, and small or large for gestational age with adjustment for potential confounders. Effect modification by infant sex was also explored. Odds ratios for preterm birth were elevated for most PAH metabolites but confidence intervals included the null. For most PAH metabolites, a significant inverse association was observed for birth weight for gestational age z-score, and a corresponding increase in the odds of small for gestational age (SGA). For example, an interquartile range increase in 2-hydroxynapthalene (2-NAP) was associated with a significantly lower birth weight z-score (β: 0.22; 95 % CI: 0.36, -0.08) and 1.90 times the odds of SGA (95 %CI: 1.41, 2.55). Further study should aim to determine the extent and mechanisms by which PAH exposure impacts fetal growth.
环境中多环芳烃(PAH)的暴露无处不在,可能会影响胎儿发育,导致不良出生结局。多环芳烃源于不完全燃烧,暴露源包括吸入香烟烟雾和汽车尾气、摄入烧焦的肉类等等。本研究的目的是确定产前PAH生物标志物浓度与出生结局之间的关联。我们的巢式病例对照研究纳入了2006年至2008年间来自LIFECODES队列的123例早产病例和335例足月对照(n = 458)。在多达4次研究访视(妊娠12、18、24、34周的中位数)时采集的尿液样本中测量了8种尿PAH代谢物。采用线性回归和逻辑回归对妊娠几何平均PAH生物标志物浓度与早产、出生体重z评分以及小于或大于胎龄进行建模,并对潜在混杂因素进行调整。还探讨了婴儿性别对效应的修饰作用。大多数PAH代谢物早产的比值比升高,但置信区间包括无效值。对于大多数PAH代谢物,观察到出生体重与胎龄z评分之间存在显著的负相关,以及小于胎龄(SGA)几率相应增加。例如,2-羟基萘(2-NAP)四分位数间距增加与出生体重z评分显著降低(β:0.22;95%CI:0.36,-0.08)以及SGA几率增加1.90倍(95%CI:1.41,2.55)相关。进一步的研究应旨在确定PAH暴露影响胎儿生长的程度和机制。