Cai Anran, Portengen Lützen, Govarts Eva, Martin Laura Rodriguez, Schoeters Greet, Legler Juliette, Vermeulen Roel, Lenters Virissa, Remy Sylvie
Institute for Risk Assessment Sciences, Department of Population Health Sciences, Utrecht University, Utrecht, the Netherlands; VITO Health, Flemish Institute for Technological Research (VITO), Mol, Belgium.
Institute for Risk Assessment Sciences, Department of Population Health Sciences, Utrecht University, Utrecht, the Netherlands.
Chemosphere. 2023 Feb;314:137695. doi: 10.1016/j.chemosphere.2022.137695. Epub 2022 Dec 29.
Children are born with a burden of persistent organic pollutants (POPs) which may have endocrine disrupting properties and have been postulated to contribute to the rise in childhood obesity. The current evidence is equivocal, which may partly because many studies investigate the effects at one time point during childhood. We assessed associations between prenatal exposure to POPs and growth during infancy and childhood.
We used data from two Belgian cohorts with cord blood measurements of five organochlorines [(dichlorodiphenyldichloroethylene (p,p'-DDE), hexachlorobenzene (HCB), polychlorinated biphenyls (PCB-138, -150, -180)] (N = 1418) and two perfluoroalkyl substances [perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS)] (N = 346). We assessed infant growth, defined as body mass index (BMI) z-score change between birth and 2 years, and childhood growth, characterized as BMI trajectory from birth to 8 years. To evaluate associations between POP exposures and infant growth, we applied a multi-pollutant approach, using penalized elastic net regression with stability selection, controlling for covariates. To evaluate associations with childhood growth, we used single-pollutant linear mixed models with random effects for child individual, parametrized using a natural cubic spline formulation.
PCB-153 was associated with increased and p,p'-DDE with decreased infant growth, although these results were imprecise. No clear association between any of the exposures and longer-term childhood growth trajectories was observed. We did not find evidence of effect modification by child sex.
Our results suggest that prenatal exposure to PCB-153 and p,p'-DDE may affect infant growth in the first two years, with no evidence of more persistent effects.
儿童出生时即携带持久性有机污染物(POPs),这些污染物可能具有内分泌干扰特性,并被推测与儿童肥胖率上升有关。目前的证据并不明确,部分原因可能是许多研究仅在儿童期的一个时间点调查其影响。我们评估了产前暴露于持久性有机污染物与婴儿期和儿童期生长之间的关联。
我们使用了来自两个比利时队列的数据,其中一个队列测量了1418名儿童脐带血中的五种有机氯化合物[二氯二苯二氯乙烯(p,p'-DDE)、六氯苯(HCB)、多氯联苯(PCB-138、-150、-180)],另一个队列测量了346名儿童脐带血中的两种全氟烷基物质[全氟辛酸(PFOA)和全氟辛烷磺酸(PFOS)]。我们评估了婴儿期生长(定义为出生至2岁期间体重指数(BMI)z评分的变化)和儿童期生长(以出生至8岁期间的BMI轨迹为特征)。为了评估持久性有机污染物暴露与婴儿期生长之间的关联,我们采用了多污染物方法,使用带稳定性选择的惩罚弹性网络回归,并对协变量进行控制。为了评估与儿童期生长的关联,我们使用了单污染物线性混合模型,并对儿童个体进行随机效应分析,采用自然三次样条公式进行参数化。
PCB-153与婴儿期生长增加有关,p,p'-DDE与婴儿期生长减少有关,尽管这些结果并不精确。未观察到任何一种暴露与儿童期长期生长轨迹之间存在明确关联。我们没有发现儿童性别对效应产生修饰作用的证据。
我们的结果表明,产前暴露于PCB-153和p,p'-DDE可能会影响婴儿头两年的生长,没有证据表明存在更持久的影响。