Abstract
Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke. Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signaling. According to the noise reaction model introduced by Babisch and colleagues, chronic low levels of noise can cause so-called nonauditory effects, such as disturbances of activity, sleep, and communication, which can trigger a number of emotional responses, including annoyance and subsequent stress. Chronic stress in turn is associated with cardiovascular risk factors, comprising increased blood pressure and dyslipidemia, increased blood viscosity and blood glucose, and activation of blood clotting factors, in animal models and humans. Persistent chronic noise exposure increases the risk of cardiometabolic diseases, including arterial hypertension, coronary artery disease, diabetes mellitus type 2, and stroke. Recently, we demonstrated that aircraft noise exposure during nighttime can induce endothelial dysfunction in healthy subjects and is even more pronounced in coronary artery disease patients. Importantly, impaired endothelial function was ameliorated by acute oral treatment with the antioxidant vitamin C, suggesting that excessive production of reactive oxygen species contributes to this phenomenon. More recently, we introduced a novel animal model of aircraft noise exposure characterizing the underlying molecular mechanisms leading to noise-dependent adverse oxidative stress-related effects on the vasculature. With the present review, we want to provide an overview of epidemiological, translational clinical, and preclinical noise research addressing the nonauditory, adverse effects of noise exposure with focus on oxidative stress. Antioxid. Redox Signal. 28, 873–908.
Highlights
Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke
Whereas most research was directed toward classical risk factors such as diabetes, smoking, or arterial hypertension, more recent evidence suggests that environmental factors contribute to the development of chronic noncommunicable disease [143]
Environmental stressors such as noise and air pollution are becoming more and more important in our industrialized world and especially traffic noise from road, aircraft, and railway transportation represents a potential novel cardiovascular risk factor [162, 166], and numerous studies demonstrate that noise plays a role for the development of cardiovascular as well as metabolic disease [167]
Summary
There was a shift of the global burden of disease from communicable (e.g., of perinatal, nutritional nature) to noncommunicable causes (e.g., atherosclerosis) [143]. Whereas most research was directed toward classical risk factors such as diabetes, smoking, or arterial hypertension, more recent evidence suggests that environmental factors contribute to the development of chronic noncommunicable disease [143]. Environmental stressors such as noise and air pollution are becoming more and more important in our industrialized world and especially traffic noise from road, aircraft, and railway transportation represents a potential novel cardiovascular risk factor [162, 166], and numerous studies demonstrate that noise plays a role for the development of cardiovascular as well as metabolic disease [167]. Noise-induced cardiovascular damage is a multifactorial process and the different pathomechanisms may be active at differing time points of noise exposure [167]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
