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      Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

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          Abstract

          Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.

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          Highlights

          • Noise exposure causes non-auditory cardiovascular/cerebral adverse health effects by oxidative stress and inflammation.

          • Aircraft noise causes exacerbated adverse effects on blood pressure and endothelial dysfunction in hypertensive mice.

          • Aircraft noise and hypertension potentiate inflammation, ROS formation and oxidative damage in the brain, vessels and heart.

          • Aircraft noise and hypertension seem to have enhanced adverse effects on stress responses in different organs.

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          Most cited references41

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          Systolic Blood Pressure Reduction and Risk of Cardiovascular Disease and Mortality

          Clinical trials have documented that lowering blood pressure reduces cardiovascular disease and premature deaths. However, the optimal target for reduction of systolic blood pressure (SBP) is uncertain.
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            Aircraft and road traffic noise and children's cognition and health: a cross-national study.

            Exposure to environmental stressors can impair children's health and their cognitive development. The effects of air pollution, lead, and chemicals have been studied, but there has been less emphasis on the effects of noise. Our aim, therefore, was to assess the effect of exposure to aircraft and road traffic noise on cognitive performance and health in children. We did a cross-national, cross-sectional study in which we assessed 2844 of 3207 children aged 9-10 years who were attending 89 schools of 77 approached in the Netherlands, 27 in Spain, and 30 in the UK located in local authority areas around three major airports. We selected children by extent of exposure to external aircraft and road traffic noise at school as predicted from noise contour maps, modelling, and on-site measurements, and matched schools within countries for socioeconomic status. We measured cognitive and health outcomes with standardised tests and questionnaires administered in the classroom. We also used a questionnaire to obtain information from parents about socioeconomic status, their education, and ethnic origin. We identified linear exposure-effect associations between exposure to chronic aircraft noise and impairment of reading comprehension (p=0.0097) and recognition memory (p=0.0141), and a non-linear association with annoyance (p<0.0001) maintained after adjustment for mother's education, socioeconomic status, longstanding illness, and extent of classroom insulation against noise. Exposure to road traffic noise was linearly associated with increases in episodic memory (conceptual recall: p=0.0066; information recall: p=0.0489), but also with annoyance (p=0.0047). Neither aircraft noise nor traffic noise affected sustained attention, self-reported health, or overall mental health. Our findings indicate that a chronic environmental stressor-aircraft noise-could impair cognitive development in children, specifically reading comprehension. Schools exposed to high levels of aircraft noise are not healthy educational environments.
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              Is oxidative stress a therapeutic target in cardiovascular disease?

              An abnormal production of reactive oxygen species (ROS) and the subsequent decrease in vascular bioavailability of nitric oxide (NO) have long been proposed to be the common pathogenetic mechanism of the endothelial dysfunction, resulting from diverse cardiovascular risk factors such as hypercholesterolaemia, diabetes mellitus, chronic smoking, metabolic syndrome, and hypertension. Superoxide produced by the nicotinamide dinucleotide phosphate (NADPH) oxidase, mitochondrial sources, or the xanthine oxidase may react with NO, thereby resulting in excessive formation of peroxynitrite, a reactive nitrogen species that has been demonstrated to accelerate the atherosclerotic process by causing direct structural damage and by causing further ROS production. Despite this sound biological rationale and a number of pre-clinical and clinical lines of evidence, studies testing the effects of classical antioxidants such as vitamin C, vitamin E, or folic acid in combination with vitamin E have been disappointing. Rather, substances such as statins, angiotensin-converting enzyme inhibitors, or AT1-receptor blockers, which possess indirect antioxidant properties mediated by the stimulation of NO production and simultaneous inhibition of superoxide production (e.g. from the NADPH oxidase), have been shown to improve vascular function in pre-clinical and clinical studies and to reduce the incidence of cardiovascular events in patients with cardiovascular disease. Today, oxidative stress remains an attractive target for cardiovascular prevention and therapy. However, a deeper understanding of its source, and of its role in vascular pathology, is necessary before new trials are attempted.
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                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                18 April 2020
                July 2020
                18 April 2020
                : 34
                : 101515
                Affiliations
                [a ]Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany
                [b ]Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany
                [c ]Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland
                [d ]Institute of Neuropathology, University Hospital, Zurich, Switzerland
                [e ]Department of Physiology, Justus-Liebig University Gießen, Germany
                [f ]Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland
                [g ]Danish Cancer Society, Copenhagen, Denmark
                [h ]Department of Natural Science and Environment, Roskilde University, Roskilde, Denmark
                [i ]German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany
                Author notes
                []Corresponding authors. Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany. daiber@ 123456uni-mainz.de tmuenzel@ 123456uni-mainz.de
                [1]

                S.S., K.F. and S.K.-S., T.M. contributed equally and should be considered joint first or senior authors.

                Article
                S2213-2317(20)30280-9 101515
                10.1016/j.redox.2020.101515
                7327989
                32345536
                c37b3ea0-5f15-4696-84ca-68e85ddaceae
                © 2020 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 19 February 2020
                : 18 March 2020
                : 19 March 2020
                Categories
                Articles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber

                environmental noise exposure,arterial hypertension,vascular oxidative stress,inflammation,endothelial function

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