University of Washington, Department of Epidemiology, Box 357236, Seattle, WA 98195, USA.
Johns Hopkins University, Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, 1830 E. Monument Street, Room 9052, Baltimore, MD 21287, USA.
Environ Int. 2019 Oct;131:105062. doi: 10.1016/j.envint.2019.105062. Epub 2019 Aug 15.
Cortisol, a stress hormone released by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, is critical to the body's adaptive response to physiological and psychological stress. Cortisol has also been implicated in the health effects of air pollution through the activation of the sympathetic nervous system. This study evaluates the cross-sectional and longitudinal association between several air pollutants and salivary cortisol.
We used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort of 45-85 years old participants from six US cities. Salivary cortisol was evaluated at two time points between 2004 and 2006 and then again from 2010 to 2012. Cortisol samples were taken several times per day on two or three consecutive days. Particulate matter <2.5 μm in diameter (PM), nitrogen dioxide (NO) and nitrogen oxides (NO) in the year prior to cortisol sampling were examined. We used piecewise linear mixed models that were adjusted for demographics, socioeconomic status and cardiovascular risk factors to examine both cross-sectional and longitudinal associations. Longitudinal models evaluated change in cortisol over time.
The pooled cross-sectional results revealed largely null results with the exception of a 9.7% higher wake-up cortisol associated with a 10 ppb higher NO (95% CI, -0.2%, 20.5%). Among all participants, the features of the cortisol curve became flatter over 5 years. The wake-to-bed slope showed a more pronounced flattening over time (0.014, 95% CI, 0.0, 0.03) with a 10 ppb higher NO level. Other air pollutants were not associated with change in cortisol over time.
Our results suggest only a moderate association between traffic related air pollution and cortisol. Very few epidemiologic studies have examined the long-term impact of air pollution on the stress response systems, thus warranting further exploration of these findings.
皮质醇是下丘脑-垂体-肾上腺(HPA)轴激活时释放的一种应激激素,对身体对生理和心理压力的适应反应至关重要。皮质醇也通过激活交感神经系统与空气污染对健康的影响有关。本研究评估了几种空气污染物与唾液皮质醇之间的横断面和纵向关联。
我们使用了来自美国六个城市的多民族动脉粥样硬化研究(MESA)队列中 45-85 岁参与者的数据。唾液皮质醇在 2004 年至 2006 年之间的两个时间点进行了评估,然后在 2010 年至 2012 年再次进行了评估。皮质醇样本在连续两天的几天内每天采集几次。在皮质醇采样前一年检查了直径<2.5μm 的颗粒物(PM)、二氧化氮(NO)和氮氧化物(NO)。我们使用分段线性混合模型,根据人口统计学、社会经济地位和心血管危险因素进行调整,以检查横断面和纵向关联。纵向模型评估了皮质醇随时间的变化。
总体上,横断面结果基本为零,除了与 10ppb 更高的 NO 相关的醒来皮质醇升高 9.7%(95%CI,-0.2%,20.5%)外。在所有参与者中,皮质醇曲线的特征在 5 年内变得更加平坦。随着时间的推移,醒来至入睡斜率变得更加平坦(0.014,95%CI,0.0,0.03),NO 水平升高 10ppb。其他空气污染物与皮质醇随时间的变化无关。
我们的结果表明,交通相关空气污染与皮质醇之间只有中度关联。很少有流行病学研究检查空气污染对压力反应系统的长期影响,因此需要进一步探讨这些发现。