Toledo-Corral C M, Alderete T L, Herting M M, Habre R, Peterson A K, Lurmann F, Goran M I, Weigensberg M J, Gilliland F D
Department of Health Sciences, California State University Northridge, 18111 Nordhoff Street, Northridge, 91330, USA.
Department of Preventive Medicine, Environmental Health Division, University of Southern California, Keck School of Medicine, Los Angeles, USA.
Environ Health. 2021 Apr 8;20(1):39. doi: 10.1186/s12940-021-00713-2.
Hypothalamic-pituitary-adrenal (HPA)-axis dysfunction has been associated with a variety of mental health and cardio-metabolic disorders. While causal models of HPA-axis dysregulation have been largely focused on either pre-existing health conditions or psychosocial stress factors, recent evidence suggests a possible role for central nervous system activation via air pollutants, such as nitrogen dioxide (NO), ozone (O) and particulate matter (PM). Therefore, in an observational study of Latino youth, we investigated if monthly ambient NO, O, and PM with aerodynamic diameter ≤ 2.5 (PM) exposure were associated with morning serum cortisol levels.
In this cross-sectional study, morning serum cortisol level was assessed after a supervised overnight fast in 203 overweight and obese Latino children and adolescents (female/male: 88/115; mean age: 11.1 ± 1.7 years; pre-pubertal/pubertal/post-pubertal: 85/101/17; BMI z-score: 2.1 ± 0.4). Cumulative concentrations of NO O and PM were spatially interpolated at the residential addresses based on measurements from community monitors up to 12 months prior to testing. Single and multi-pollutant linear effects models were used to test the cumulative monthly lag effects of NO, O and PM on morning serum cortisol levels after adjusting for age, sex, seasonality, social position, pubertal status, and body fat percent by DEXA.
Single and multi-pollutant models showed that higher O exposure (derived from maximum 8-h exposure windows) in the prior 1-7 months was associated with higher serum morning cortisol (p < 0.05) and longer term PM exposure (4-10 months) was associated with lower serum morning cortisol levels (p < 0.05). Stratification by pubertal status showed associations in pre-pubertal children compared to pubertal and post-pubertal children. Single, but not multi-pollutant, models showed that higher NO over the 4-10 month exposure period associated with lower morning serum cortisol (p < 0.05).
Chronic ambient NO O and PM differentially associate with HPA-axis dysfunction, a mechanism that may serve as an explanatory pathway in the relationship between ambient air pollution and metabolic health of youth living in polluted urban environments. Further research that uncovers how ambient air pollutants may differentially contribute to HPA-axis dysfunction are warranted.
下丘脑 - 垂体 - 肾上腺(HPA)轴功能障碍与多种心理健康和心血管代谢紊乱有关。虽然HPA轴失调的因果模型主要集中在既有的健康状况或心理社会压力因素上,但最近的证据表明,通过空气污染物(如二氧化氮(NO)、臭氧(O₃)和颗粒物(PM))激活中枢神经系统可能起到一定作用。因此,在一项针对拉丁裔青少年的观察性研究中,我们调查了每月环境中NO、O₃和空气动力学直径≤2.5的颗粒物(PM₂.₅)暴露是否与早晨血清皮质醇水平相关。
在这项横断面研究中,对203名超重和肥胖的拉丁裔儿童及青少年(女性/男性:88/115;平均年龄:11.1±1.7岁;青春期前/青春期/青春期后:85/101/17;BMI z评分:2.1±0.4)在监督下进行过夜禁食后评估早晨血清皮质醇水平。根据测试前长达12个月社区监测器的测量数据,在居住地址对NO、O₃和PM₂.₅的累积浓度进行空间插值。在通过双能X线吸收法(DEXA)校正年龄、性别、季节性、社会地位、青春期状态和体脂百分比后,使用单污染物和多污染物线性效应模型来测试NO、O₃和PM₂.₅对早晨血清皮质醇水平的累积月度滞后效应。
单污染物和多污染物模型均显示,前1 - 7个月较高的O₃暴露(源自最长8小时暴露窗口)与较高的早晨血清皮质醇水平相关(p < 0.05),而长期的PM₂.₅暴露(4 - 10个月)与较低的早晨血清皮质醇水平相关(p < 0.05)。按青春期状态分层显示,与青春期和青春期后的儿童相比,青春期前儿童存在相关性。单污染物模型(而非多污染物模型)显示,在4 - 10个月的暴露期内较高的NO暴露与较低的早晨血清皮质醇水平相关(p < 0.05)。
慢性环境中的NO、O₃和PM₂.₅与HPA轴功能障碍存在差异关联,这一机制可能是污染城市环境中环境空气污染与青少年代谢健康之间关系的一种解释途径。有必要进一步开展研究以揭示环境空气污染物如何不同程度地导致HPA轴功能障碍。