Department of Nutritional Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA.
Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA.
Environ Res. 2022 Mar;204(Pt A):111977. doi: 10.1016/j.envres.2021.111977. Epub 2021 Aug 29.
The neurobiological processes involved in establishing sleep regulation are vulnerable to environmental exposures as early as seven weeks of gestation. Studies have linked in utero pesticide exposure to childhood sleep-disordered breathing. However, the impact of in utero pesticide exposure on the sleep health of adolescents remains unexplored.
Data from 137 mother-adolescent pairs from a Mexico City cohort were analyzed. We used maternal urinary 3-phenoxybenzoic acid (3-PBA, pyrethroid metabolite) and 3, 5, 6-trichloro-2-pyridinol (TCPy, chlorpyrifos metabolite) from trimester three to estimate in utero pesticide exposure. Among adolescents, we obtained repeated measures of objectively assessed sleep duration, midpoint, and fragmentation using wrist-actigraphy devices for 7 consecutive days in 2015 and 2017. Unstratified and sex-stratified associations between maternal urinary 3-PBA and TCPy and adolescent sleep measures were examined using generalized linear mixed models (GLMMs). We also examined the interactive effects of maternal pesticide exposure and offspring sex on sleep outcomes.
3-PBA and TCPy were detected in 44.4% and 93% of urine samples, respectively. Adjusted findings demonstrated that higher exposure to maternal TCPy was associated with longer sleep duration and later sleep timing. Findings from interaction tests between maternal pesticide exposure and offspring sex were not statistically significant, although adjusted sex-stratified findings showed that the association between TCPy with duration and midpoint was evident only among female offspring. To illustrate, those in the highest tertile of exposure had a 59 minute (95% CI: 12.2, 104.8) (p, trend = 0.004) longer sleep duration and a 0.6 hour (95% CI: 0.01, 1.3) (p, trend = 0.01) later sleep midpoint. We found no significant associations between 3-PBA and sleep outcomes.
Within a cohort of mother-adolescent pairs, we found associations between maternal prenatal pesticide exposure and longer sleep duration and later sleep timing among adolescent offspring. Further, this association may be female-specific.
早在妊娠 7 周时，参与建立睡眠调节的神经生物学过程就容易受到环境暴露的影响。研究已经将子宫内接触杀虫剂与儿童睡眠呼吸障碍联系起来。然而，子宫内接触杀虫剂对青少年睡眠健康的影响仍未得到探索。
分析了来自墨西哥城队列的 137 对母子的数据。我们使用母亲在妊娠第三阶段的尿液中 3-苯氧基苯甲酸（3-PBA，拟除虫菊酯代谢物）和 3,5,6-三氯-2-吡啶醇（TCPy，毒死蜱代谢物）来估计子宫内接触杀虫剂的情况。在青少年中，我们使用手腕活动记录仪在 2015 年和 2017 年连续 7 天获得了反复的客观评估的睡眠时间、中点和碎片化测量值。使用广义线性混合模型（GLMM）检查了母亲尿液中的 3-PBA 和 TCPy 与青少年睡眠测量值之间的无分层和性别分层关联。我们还检查了母体农药暴露和后代性别对睡眠结果的交互影响。
3-PBA 和 TCPy 分别在 44.4%和 93%的尿液样本中被检测到。调整后的发现表明，母体 TCPy 暴露水平越高，睡眠时间越长，睡眠开始时间越晚。母体农药暴露与后代性别之间的交互作用测试结果没有统计学意义，尽管调整后的性别分层发现表明，TCPy 与持续时间和中点之间的关联仅在女性后代中明显。例如，暴露量最高的三分位组的睡眠时间长 59 分钟（95%置信区间：12.2，104.8）（p，趋势=0.004），睡眠中点晚 0.6 小时（95%置信区间：0.01，1.3）（p，趋势=0.01）。我们没有发现 3-PBA 与睡眠结果之间存在显著关联。
在母子队列中，我们发现母体产前接触杀虫剂与青少年后代睡眠时间延长和睡眠开始时间晚之间存在关联。此外，这种关联可能是女性特有的。
