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Review
. 2019 Nov 11:2019:4623109.
doi: 10.1155/2019/4623109. eCollection 2019.

Environmental Noise-Induced Effects on Stress Hormones, Oxidative Stress, and Vascular Dysfunction: Key Factors in the Relationship between Cerebrocardiovascular and Psychological Disorders

Omar Hahad  1 , Jürgen H Prochaska  1   2 , Andreas Daiber  1   3 , Thomas Muenzel  1   3
Affiliations
Review

Environmental Noise-Induced Effects on Stress Hormones, Oxidative Stress, and Vascular Dysfunction: Key Factors in the Relationship between Cerebrocardiovascular and Psychological Disorders

Omar Hahad et al. Oxid Med Cell Longev. .

Abstract

The role of noise as an environmental pollutant and its adverse effects on health are being increasingly recognized. Beyond its direct effects on the auditory system (e.g., hearing loss and tinnitus induced by exposure to high levels of noise), chronic low-level noise exposure causes mental stress associated with known cardiovascular complications. According to recent estimates of the World Health Organization, exposure to traffic noise is responsible for a loss of more than 1.5 million healthy life years per year in Western Europe alone, a major part being related to annoyance, cognitive impairment, and sleep disturbance. Underlying mechanisms of noise-induced mental stress are centered on increased stress hormone levels, blood pressure, and heart rate, which in turn favor the development of cerebrocardiovascular disease such as stroke, arterial hypertension, ischemic heart disease, and myocardial infarction. Furthermore, traffic noise exposure is also associated with mental health symptoms and psychological disorders such as depression and anxiety, which further increase maladaptive coping mechanisms (e.g., alcohol and tobacco use). From a molecular point of view, experimental studies suggest that traffic noise exposure can increase stress hormone levels, thereby triggering inflammatory and oxidative stress pathways by activation of the nicotinamide adenine dinucleotide phosphate oxidase, uncoupling of endothelial/neuronal nitric oxide synthase inducing endothelial and neuronal dysfunction. This review elucidates the mechanisms underlying the relationship between noise exposure and cerebrocardiovascular and psychological disorders, focusing on mental stress signaling pathways including activation of the autonomous nervous system and endocrine signaling and its association with inflammation, oxidative stress, and vascular dysfunction.

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Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

Figures

Figure 1
Figure 1
Proposed expanded noise reaction model characterizing the adverse health effects of environmental noise exposure. The direct pathway refers to effects on the auditory system by exposure to high levels of noise (e.g., hearing loss and tinnitus). The indirect pathway is associated with cognitive and emotional stress responses, leading to sympathetic and endocrine activation triggering alterations in cerebrocardiovascular risk factors. Additionally, chronic noise stress is associated with increased risk for psychological symptoms and disorders, which in turn impairs cerebrocardiovascular function. As a consequence, noise exposure may promote maladaptive coping mechanisms and decrease stress resistance, further negatively affecting cerebrocardiovascular function. Adapted from Babisch [7, 8] and Münzel et al. [5] with permission.
Figure 2
Figure 2
(a) Degrees of overall annoyance according to different sources of noise. (b) Sources of extreme annoyance. Adapted from Beutel et al. [19] with permission.
Figure 3
Figure 3
Associations between total noise annoyance, (a) atrial fibrillation, (b) depression, and generalized anxiety in the Gutenberg Health Study. AF: atrial fibrillation; adj. PR: adjusted prevalence ratio for sex, age, and socioeconomic status; CI: confidence interval. Adapted from (a) Hahad et al. [15] and (b) Beutel et al. [19] with permission.
Figure 4
Figure 4
Noise causes annoyance and stress responses characterized by activation of the hypothalamic-pituitary-adrenal axis, oxidative stress-induced endothelial dysfunction, inflammation, thrombosis, and altered gene expression. Adapted from Münzel et al. [6]. Ang II: angiotensin II; AT1: angiotensin receptor type 1; ATM: ataxia telangiectasia mutated; eNOS: endothelial nitric oxide synthase; Fas: cell death signaling molecule (CD95); FOXO: forkhead-box-protein O3; HPA: hypothalamic-pituitary-adrenal; iNOS: inducible nitric oxide synthase; NADPH: nicotinamide adenine dinucleotide phosphate; Nox: NADPH oxidase; NO: nitric oxide; O2: oxygen; TGF: transforming growth factor. Adapted from Münzel et al. [6] with permission.
Figure 5
Figure 5
Environmental noise exposure and subsequent mental stress cause a stress reaction through activation of either the hypothalamus-pituitary-adrenal (HPA) axis with subsequent cortisol release or by the activation of the sympathetic nervous system (SNS) with subsequent catecholamine formation. As a consequence, cerebral and vascular inflammatory and oxidative stress pathways as well as altered gene expression become active, leading to endothelial dysfunction. Taken together, these consequences contribute and interact with traditional risk factors, leading to neuronal, cerebrocardiovascular, and psychological disorders. Modified from Münzel et al. [100] and adapted from Daiber et al. [71] with permission.
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