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青少年慢性吸入交通相关二氧化氮与皮质醇反应迟钝。

Chronic exposure to inhaled, traffic-related nitrogen dioxide and a blunted cortisol response in adolescents.

机构信息

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, 650 Charles E Young Dr S, Los Angeles, CA 90095, USA.

Department of Pediatrics, University of California, San Diego, 9500 Gilman Drive #0828 La Jolla, CA 92093, USA.

出版信息

Environ Res. 2018 May;163:201-207. doi: 10.1016/j.envres.2018.01.011. Epub 2018 Feb 22.

Abstract

BACKGROUND

Chronic health effects of traffic-related air pollution, like nitrogen dioxide (NO), are well-documented. Animal models suggested that NO exposures dysregulate cortisol function.

OBJECTIVES

We evaluated the association between traffic-related NO exposure and adolescent human cortisol concentrations, utilizing measures of the cortisol diurnal slope.

METHODS

140 adolescents provided repeated salivary cortisol samples throughout one day. We built a land use regression model to estimate chronic NO exposures based on home and school addresses. We then generated model-based estimates of the association between cortisol and NO exposure one year prior to cortisol sampling, examining changes in cortisol diurnal slope. The final model was adjusted other criteria pollutants, measures of psychosocial stress, anthropometry, and other demographic and covariates.

RESULTS

We observed a decrease in diurnal slope in cortisol for adolescents exposed to the estimated 75th percentile of ambient NO (high exposure) relative to those exposed at the 25th percentile (low exposure). For a highly exposed adolescent, the log cortisol was lower by 0.06 µg/dl at waking (95% CI: -0.15, 0.02), 0.07 µg/dl at 30 min post waking (95% CI: -0.15, 0.02), and higher by 0.05 µg/dl at bedtime (95% CI: 0.05, 0.15), compared to a low exposed adolescent. For an additional interquartile range of exposure, the model-based predicted diurnal slope significantly decreased by 0.12 (95% CI: -0.23, -0.01).

CONCLUSIONS

In adolescents, we found that increased, chronic exposure to NO and the mixture of pollutants from traffic sources was associated with a flattened diurnal slope of cortisol, a marker of an abnormal cortisol response which we hypothesize may be a mechanism through which air pollution may affect respiratory function and asthma in adolescents.

摘要

背景

交通相关空气污染(如二氧化氮[NO])对慢性健康的影响已有充分记录。动物模型表明,NO 暴露会使皮质醇功能失调。

目的

我们评估了交通相关 NO 暴露与青少年人体皮质醇浓度之间的关系,利用皮质醇昼夜节律斜率的测量值。

方法

140 名青少年在一天内多次提供唾液皮质醇样本。我们构建了一个基于土地利用的回归模型,根据家庭和学校地址来估计慢性 NO 暴露。然后,我们生成了基于模型的一年前皮质醇采样时 NO 暴露与皮质醇之间的关联估计值,同时检查了皮质醇昼夜节律斜率的变化。最终模型还调整了其他标准污染物、心理社会应激措施、人体测量学以及其他人口统计学和协变量。

结果

与暴露在第 25 百分位(低暴露)的青少年相比,暴露在估计的第 75 百分位(高暴露)环境 NO 下的青少年皮质醇昼夜斜率下降。对于一个高暴露的青少年,在醒来时(95%置信区间:-0.15,0.02),皮质醇的对数低了 0.06μg/dl;在醒来后 30 分钟(95%置信区间:-0.15,0.02),皮质醇的对数低了 0.07μg/dl;在睡前(95%置信区间:0.05,0.15),皮质醇的对数高了 0.05μg/dl。与低暴露的青少年相比,暴露增加一个四分位距,模型预测的昼夜斜率显著降低 0.12(95%置信区间:-0.23,-0.01)。

结论

在青少年中,我们发现,慢性、高浓度的 NO 暴露以及交通源污染物混合物与皮质醇昼夜斜率的平坦化有关,这是皮质醇反应异常的一个标志,我们假设这可能是空气污染影响青少年呼吸功能和哮喘的机制之一。

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