Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America; Department of Research & Evaluation, Kaiser Permanente Southern California, Pasadena, CA, United States of America.
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States of America.
Environ Int. 2019 Dec;133(Pt A):105110. doi: 10.1016/j.envint.2019.105110. Epub 2019 Oct 11.
Ambient air pollution and maternal diabetes may affect common biological pathways underlying adverse neurodevelopmental effects. However, joint effects of maternal diabetes and air pollution on autism spectrum disorder (ASD) have not been studied.
We evaluated whether prenatal and early-life air pollution exposure interacts with maternal diabetes status to affect ASD risk.
This retrospective cohort study included 246,420 singleton children born in Kaiser Permanente Southern California hospitals in 1999-2009. Children were followed from birth until age 5, during which 2471 ASD cases were diagnosed. Ozone (O), particulate matter < 2.5 μm (PM) and <10 μm in aerodynamic diameter, and nitrogen dioxide measured at regulatory air monitoring stations were interpolated to estimate exposures during preconception and each pregnancy trimester, and first year of life at each child's birth address. Hazard ratios (HRs) for ASD were estimated adjusting for birth year, KPSC service areas, and relevant maternal and child characteristics. For each exposure window, interactions were tested between pollutants and a 4-category maternal diabetes variable (none, GDM ≥ 24 and <24 weeks' gestation, and pre-existing type 2 diabetes). For an exposure window with statistically significant global interaction between pollutant and diabetes (p < 0.05), pollutant-associated HRs were estimated separately for each category of maternal diabetes.
There were associations of ASD with preconception, first and third trimesters, and first year of life PM, but not with other pollutants. There were, however, interactions of maternal diabetes with first trimester and first year of life O. Increased ASD risk was associated with first trimester O among mothers with GDM < 24 weeks' gestation [adjusted HR 1.50 per 15.7 ppb O (95% CI: 1.08-2.09)]. No O associations with ASD were observed in other categories of maternal diabetes.
GDM onset early in pregnancy may increase children's susceptibility to prenatal O-associated ASD risk. These novel findings merit further investigation.
环境空气污染和母体糖尿病可能影响到导致不良神经发育影响的共同生物学途径。然而,母体糖尿病和空气污染对自闭症谱系障碍(ASD)的联合影响尚未得到研究。
我们评估了产前和生命早期的空气污染暴露是否与母体糖尿病状态相互作用,从而影响 ASD 风险。
这项回顾性队列研究纳入了 1999 年至 2009 年期间在凯撒永久南加州医院出生的 246420 名单胎儿童。儿童从出生开始随访至 5 岁,在此期间诊断出 2471 例 ASD 病例。臭氧(O)、小于 2.5μm(PM)和小于 10μm 空气动力学直径的颗粒物以及氮氧化物在监管空气质量监测站进行测量,以估算在受孕前和每个妊娠期间以及每个儿童出生地址的第一年的暴露情况。使用出生年份、KPSC 服务区域以及相关的母婴特征对 ASD 的危害比(HR)进行调整。对于每个暴露窗口,测试污染物与母体糖尿病的 4 个类别变量(无、妊娠 24 周及以上的 GDM 和先前存在的 2 型糖尿病)之间的交互作用。对于在污染物和糖尿病之间存在统计学上显著的全局交互作用的暴露窗口(p<0.05),根据母体糖尿病的每个类别单独估计污染物相关的 HR。
ASD 与受孕前、第一和第三个妊娠期间以及第一年的 PM 有关,但与其他污染物无关。然而,母体糖尿病与第一和第三个妊娠期间和第一年的 O 存在交互作用。在妊娠 24 周前 GDM 的母亲中,与 O 相关的 ASD 风险增加[调整后的 HR 为 15.7ppb O 每增加 15.7ppb (95% CI:1.08-2.09)]。在其他类别的母体糖尿病中,未观察到 O 与 ASD 的关联。
妊娠早期 GDM 的发病可能会增加儿童对产前 O 相关 ASD 风险的易感性。这些新发现值得进一步研究。