Fig. 16.

Noise triggers a neuronal stress response, leading to oxidative stress, inflammation, and vasoconstriction. Traffic noise results in mental stress that causes activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis with subsequent release of catecholamines (e.g., adrenaline, noradrenaline) and cortisol, a glucocorticoid. This process is accompanied by neuronal activation via inflammation and oxidative stress (exacerbated ROS formation, mostly O₂^•− and H₂O₂), which promotes neuropsychiatric and sleep disorders. Sympathetic and HPA axis activation leads to adverse signaling via catecholamines, angiotensin II (AT-II), endothelin-1 (ET-1), and glucocorticoids, leading to an inflammatory phenotype, oxidative stress, downregulation of eNOS and diminished nitric oxide (^•NO) bioavailability, and vasoconstriction. These adverse signaling events contribute to increased blood pressure, atherosclerosis, and higher cardiovascular risk. Redrawn and modified from Refs. [29,43] with permission.