Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina USA.
Norwegian Institute of Public Health, Oslo, Norway.
Environ Health Perspect. 2018 May 10;126(5):057004. doi: 10.1289/EHP2358.
There is growing concern that phthalate exposures may have an impact on child neurodevelopment. Prenatal exposure to phthalates has been linked with externalizing behaviors and executive functioning defects suggestive of an attention-deficit hyperactivity disorder (ADHD) phenotype.
We undertook an investigation into whether prenatal exposure to phthalates was associated with clinically confirmed ADHD in a population-based nested case-control study of the Norwegian Mother and Child Cohort (MoBa) between the years 2003 and 2008.
Phthalate metabolites were measured in maternal urine collected at midpregnancy. Cases of ADHD (=297) were obtained through linkage between MoBa and the Norwegian National Patient Registry. A random sample of controls (=553) from the MoBa population was obtained.
In multivariable adjusted coexposure models, the sum of di-2-ethylhexyl phthalate metabolites (∑DEHP) was associated with a monotonically increasing risk of ADHD. Children of mothers in the highest quintile of ∑DEHP had almost three times the odds of an ADHD diagnosis as those in the lowest [OR=2.99 (95% CI: 1.47, 5.49)]. When ∑DEHP was modeled as a log-linear (natural log) term, for each log-unit increase in exposure, the odds of ADHD increased by 47% [OR=1.47 (95% CI: 1.09, 1.94)]. We detected no significant modification by sex or mediation by prenatal maternal thyroid function or by preterm delivery.
In this population-based case-control study of clinical ADHD, maternal urinary concentrations of DEHP were monotonically associated with increased risk of ADHD. Additional research is needed to evaluate potential mechanisms linking phthalates to ADHD. https://doi.org/10.1289/EHP2358.
越来越多的人担心邻苯二甲酸酯暴露可能对儿童神经发育产生影响。产前邻苯二甲酸酯暴露与外化行为和执行功能缺陷有关，这些缺陷提示存在注意力缺陷多动障碍（ADHD）表型。
我们在挪威母亲和儿童队列（MoBa）的一项基于人群的嵌套病例对照研究中，调查了 2003 年至 2008 年期间，产前邻苯二甲酸酯暴露是否与临床确诊的 ADHD 有关。
在妊娠中期采集母亲尿液，测量其中的邻苯二甲酸酯代谢物。通过 MoBa 与挪威国家患者登记处的链接，获得 ADHD（=297）病例。从 MoBa 人群中随机抽取 553 名对照。
在多变量调整的共同暴露模型中，邻苯二甲酸二（2-乙基己基）酯代谢物总和（∑DEHP）与 ADHD 的风险呈单调递增关系。母亲∑DEHP 含量最高五分位数的孩子患 ADHD 的几率几乎是最低五分位数的三倍[比值比（OR）=2.99（95%可信区间：1.47，5.49）]。当∑DEHP 作为对数线性（自然对数）项建模时，暴露每增加一个对数单位，ADHD 的几率就会增加 47%[OR=1.47（95%可信区间：1.09，1.94）]。我们没有发现性别存在显著的修饰作用，也没有发现产前母亲甲状腺功能或早产可以介导这种关系。
在这项基于人群的 ADHD 临床病例对照研究中，母亲尿液中 DEHP 的浓度与 ADHD 风险的增加呈单调相关。需要进一步研究评估潜在的将邻苯二甲酸酯与 ADHD 联系起来的机制。https://doi.org/10.1289/EHP2358.
