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Exposure to Diesel Exhaust and Plasma Cortisol Response: A Randomized Double-Blind Crossover Study

机译:暴露于柴油气排气和血浆皮质醇反应:随机双盲交叉研究

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Traffic-related air pollution (TRAP) is associated with a varietyof adverse health effects. Although a central role has been proposed for oxidative stress, elucidating underlying mechanismsremains an area of active investigation. Experimental work hasdemonstrated that glucocorticoid stress hormones are potentialmediators of pulmonary and systemic pollutant effects of bothparticulate and gaseous pollutants (Thomson 2019), but directevidence of TRAP-dependent stress axis activation is lacking.Moreover, although oxidative stress is a regulator of glucocorticoid signaling (Okamoto et al. 1999), involvement in pollutantinduced stress axis activation is unknown. In population studies,nitrogen dioxide was associated with a flattened salivary cortisolprofile in adolescents (Wing et al. 2018) and higher awakeningcortisol and flattened profile in 45 to 85-y-old adults (Hajat et al.2019), suggesting potential TRAP-related impacts. The presentstudy evaluated whether short-term exposure to diesel exhaustincreases plasma cortisol levels and considered effect modification by sex, asthma status, antioxidant gene variants, and antioxidant treatment.
机译:与交通相关的空气污染(陷阱)与各种不良健康影响有关。虽然已经提出了核酸胁迫的核心作用,但阐明了潜在的机制来激活调查区域。实验性工作具有糖皮质激素的肺皮质激素胁迫激素是肺癌和气态污染物(Thomson 2019)的肺部和全身污染物效应的潜在介质,但缺乏陷阱依赖应力轴激活的指导。然而,氧化应激是糖皮质激素信号调节器(Okamoto等等,1999),参与污染抑制的应力轴激活是未知的。在人口研究中,二氧化氮与青少年的扁平唾液皮质醇预防液(Wing等人2018)和更高的令人震惊的尖塔和455岁的成年人(Hajat等人),暗示潜在的陷阱相关影响。本文评估柴油易排出血浆皮质醇水平的短期暴露,并考虑了性,哮喘地位,抗氧化基因变体和抗氧化治疗的效果改性。

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