Personal ozone exposure and stress hormones in the hypothalamus-pituitary-adrenal and sympathetic-adrenal-medullary axes.

Abstract

The effect of ozone exposure on neuroendocrine responses in humans has not been fully studied. 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 3days (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. At lag 0-8h, personal ozone exposure ranged from 4.5ppb to 104.3ppb with an average of 21.0±14.7ppb, which was approximately half of the ambient ozone concentration. Per 10-ppb increase in personal ozone exposure (lag 0-8h) 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. Short-term exposure to low levels of ozone may lead to activation of the HPA and SAM axes.