Traffic-Related Air Pollution and a Rise in Cortisol Levels
Prior research has shown that traffic-related air pollution (TRAP) plays a key role in oxidative stress, but its effect on underlying mechanisms, such as glucocorticoid signaling, is still being determined. It is known that glucocorticoids mediate the effects of particulate and gaseous pollutants, but before now, there was no direct evidence of this concerning TRAP.
In a recent study, Thomson et. al set out to determine if short-term diesel exposure increases plasma cortisol levels. Considering variables such as participants’ sex, asthma diagnosis, antioxidant gene variants, and antioxidant treatment, participants were exposed to 2 hours of either filtered air or diesel exhaust. Using Arbor Assays’ Cortisol ELISA Kit (K003-H), the authors measured plasma cortisol post-exposure.
The authors found that the short-term exposure to diesel exhaust “rapidly and transiently” raised plasma cortisol levels, solidifying cortisol’s role as a potential mediator of TRAP-dependent health effects. Across participants’ age, sex, asthma diagnosis, etc., the variation in cortisol response due to diesel exhaust exposure matched the known variation in response that occurs due to acute stressors. Additionally, despite a correlation between asthma and increased cortisol response, airway hyper-responsiveness was not significantly impacted in those with asthma diagnoses. The variability in cortisol responses across individual characteristics illustrated in this study may be useful for assessing health risks of air pollutants.
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