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      The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk

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          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.

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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            Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies.

            Aims To assess the relationship between duration of sleep and morbidity and mortality from coronary heart disease (CHD), stroke, and total cardiovascular disease (CVD). Methods and results We performed a systematic search of publications using MEDLINE (1966-2009), EMBASE (from 1980), the Cochrane Library, and manual searches without language restrictions. Studies were included if they were prospective, follow-up >3 years, had duration of sleep at baseline, and incident cases of CHD, stroke, or CVD. Relative risks (RR) and 95% confidence interval (CI) were pooled using a random-effect model. Overall, 15 studies (24 cohort samples) included 474 684 male and female participants (follow-up 6.9-25 years), and 16 067 events (4169 for CHD, 3478 for stroke, and 8420 for total CVD). Sleep duration was assessed by questionnaire and incident cases through certification and event registers. Short duration of sleep was associated with a greater risk of developing or dying of CHD (RR 1.48, 95% CI 1.22-1.80, P < 0.0001), stroke (1.15, 1.00-1.31, P = 0.047), but not total CVD (1.03, 0.93-1.15, P = 0.52) with no evidence of publication bias (P = 0.95, P = 0.30, and P = 0.46, respectively). Long duration of sleep was also associated with a greater risk of CHD (1.38, 1.15-1.66, P = 0.0005), stroke (1.65, 1.45-1.87, P < 0.0001), and total CVD (1.41, 1.19-1.68, P < 0.0001) with no evidence of publication bias (P = 0.92, P = 0.96, and P = 0.79, respectively). Conclusion Both short and long duration of sleep are predictors, or markers, of cardiovascular outcomes.
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              Quantity and Quality of Sleep and Incidence of Type 2 Diabetes

              OBJECTIVE To assess the relationship between habitual sleep disturbances and the incidence of type 2 diabetes and to obtain an estimate of the risk. RESEARCH DESIGN AND METHODS We conducted a systematic search of publications using MEDLINE (1955–April 2009), EMBASE, and the Cochrane Library and manual searches without language restrictions. We included studies if they were prospective with follow-up >3 years and had an assessment of sleep disturbances at baseline and incidence of type 2 diabetes. We recorded several characteristics for each study. We extracted quantity and quality of sleep, how they were assessed, and incident cases defined with different validated methods. We extracted relative risks (RRs) and 95% CI and pooled them using random-effects models. We performed sensitivity analysis and assessed heterogeneity and publication bias. RESULTS We included 10 studies (13 independent cohort samples; 107,756 male and female participants, follow-up range 4.2–32 years, and 3,586 incident cases of type 2 diabetes). In pooled analyses, quantity and quality of sleep predicted the risk of development of type 2 diabetes. For short duration of sleep (≤5–6 h/night), the RR was 1.28 (95% CI 1.03–1.60, P = 0.024, heterogeneity P = 0.015); for long duration of sleep (>8–9 h/night), the RR was 1.48 (1.13–1.96, P = 0.005); for difficulty in initiating sleep, the RR was 1.57 (1.25–1.97, P < 0.0001); and for difficulty in maintaining sleep, the RR was 1.84 (1.39–2.43, P < 0.0001). CONCLUSIONS Quantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers.
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                Author and article information

                Journal
                Antioxid Redox Signal
                Antioxid. Redox Signal
                ars
                Antioxidants & Redox Signaling
                Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
                1523-0864
                1557-7716
                20 March 2018
                20 March 2018
                20 March 2018
                : 28
                : 9
                : 873-908
                Affiliations
                [ 1 ]The Center for Cardiology, Cardiology 1, Johannes Gutenberg University Medical Center , Mainz, Germany.
                [ 2 ]Danish Cancer Society Research Center , Copenhagen, Denmark.
                [ 3 ]Institute for Molecular Genetics, Johannes Gutenberg University , Mainz, Germany.
                Author notes

                Reviewing Editors: Ann Baldwin, Mara Benfato, Eric C. Bielefeld, Pascal Goldschmidt-Clermont, John Keaney, and Vickram Ramkumar

                Address correspondence to: Prof. Dr. Thomas Münzel, Zentrum für Kardiologie, Kardiologie 1, Universitätsmedizin der Johannes Gutenberg-Universität Mainz Gebäude 605, Langenbeckstr. 1, 55131 Mainz, Germany

                E-mail: tmuenzel@ 123456uni-mainz.de
                Article
                10.1089/ars.2017.7118
                10.1089/ars.2017.7118
                5898791
                29350061
                87aad040-e926-425c-9e3b-7fec60b7ff74
                © Thomas Münzel, et al., 2018; Published by Mary Ann Liebert, Inc.

                This Open Access article is distributed under the terms of the Creative Commons License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 11 April 2017
                : 11 November 2017
                : 14 November 2017
                Page count
                Figures: 19, Tables: 2, References: 284, Pages: 36
                Categories
                Comprehensive Invited Review

                environmental risk factors,traffic noise exposure,aircraft noise exposure,stress hormones,endothelial dysfunction,oxidative stress

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