Personal ozone exposure and stress hormones in the hypothalamus–pituitary–adrenal and sympathetic-adrenal-medullary axes. (15th January 2022)

• Record Type: Journal Article
• Authors: Xia, Yongjie; Niu, Yue; Cai, Jing; Liu, Cong; Meng, Xia; Chen, Renjie; Kan, Haidong
• Is Part Of: Environment international. Volume 159(2022)
• Publication Date: 2022-01-15
• Subjects: Ozone -- Stress hormone -- Hypothalamus–pituitary–adrenal axis -- Sympathetic-adrenal-medullary axis -- Panel study; Environmental protection -- Periodicals; Environmental health -- Periodicals; Environmental monitoring -- Periodicals; Environmental Monitoring -- Periodicals; Environnement -- Protection -- Périodiques; Hygiène du milieu -- Périodiques; Environnement -- Surveillance -- Périodiques; Environmental health; Environmental monitoring; Environmental protection; Periodicals; 333.705
• DOI: 10.1016/j.envint.2021.107050
• Languages: English
• ISSNs: 0160-4120

Abstract

Graphical abstract: Highlights: A longitudinal panel study with four rounds of visits among 43 college students. Accurate exposure assessments by conducting personal ozone monitoring. Activation of the hypothalamus–pituitaryadrenal axis in relation to ozone exposure. Activation of the sympathetic-adrenal-medullary axis in relation to ozone exposure. Abstract: Background: The effect of ozone exposure on neuroendocrine responses in humans has not been fully studied. Methods: We conducted a longitudinal panel study with four rounds of visits among 43 college students in Shanghai, China, from May to October 2016. For each visit, we monitored personal real-time ozone exposure for consecutive 3 days (from 8:00 a.m. to 6:00p.m. each day), followed by blood sample collection. We measured serum levels of three hormones in the hypothalamus–pituitaryadrenal (HPA) axis, including corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol, and three catacholamines indicating sympathetic-adrenal-medullary (SAM) axis activation, including adrenaline, noradrenaline, and dopamine. We applied linear mixed-effect models to evaluate the associations between ozone exposure and these neurohormones and further compared models using personal and fixed-site ozone measurements. Main Results: At lag 0–8 h, personal ozone exposure ranged from 4.5 ppb to 104.3 ppb with an average of 21.0 ± 14.7 ppb, which was approximately half of the ambient ozone concentration. Per 10-ppb increase in personal ozone exposure (lag 0–8 h) was associated with increases of 5.60% [95% confidence interval (CI): 2.30%, 9.01%] in CRH, 5.91% (95% CI: 0.55%, 11.56%) in cortisol, and 10.13% (95% CI: 2.75%, 18.05%) in noradrenaline, whereas associated with a 12.15% (95% CI: 1.23%, 21.87%) decrease in dopamine. Overall, models using personal ozone measurements yielded larger effect estimates and better model fits than models using fixed-site measurements. Conclusions: Short-term exposure to low levels of ozone may lead to activation of the HPA and SAM axes.