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      MiRNA-92a-3p mediated the association between occupational noise exposure and blood pressure among Chinese adults

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      Science of The Total Environment
      Elsevier BV

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          Abstract

          <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto" id="d532768e125">Evidence on the association between occupational noise exposure and blood pressure is inconsistent, and the underlying mechanism remains unknown. This study aimed to evaluate the association between occupational noise exposure and blood pressure, and explore the potential role of miRNAs in the association. A total of 894 subjects from two companies in Wuhan, China were included. Occupational noise exposure was assessed using cumulative noise exposure (CNE), and six candidate plasma miRNAs (miR-92a-3p, miR-21-5p, miR-200a-3p, miR-200b-3p, miR-200c-3p, and miR-1-3p) which were not only associated with blood pressure/hypertension but also related to oxidative stress were selected according to previous studies and tested. A linear dose-response relationship was found between occupational noise exposure and blood pressure, including systolic blood pressure (SBP) and diastolic blood pressure (DBP). Each 1-unit increase in CNE levels was significantly associated with a 0.130 (95 % confidence interval [CI] = 0.026, 0.234) unit increase in SBP and a 0.141 (95 % CI = 0.063, 0.219) unit increase in DBP. However, the association between occupational noise and hypertension is not statistically significant (P &gt; 0.05). In the meanwhile, occupational noise exposure was negatively associated with miRNA-92a-3p (β = -0.019, 95 % CI = -0.032, -0.006) and miRNA-21-5p (β = -0.031, 95 % CI = -0.052, -0.010), and miRNA-92a-3p mediated 24.66 % of the association between occupational noise exposure and DBP. In addition, bilateral high-frequency hearing loss was not only positively associated with occupational noise exposure (OR = 1.974, 95 % CI = 1.084, 3.702) but also DBP (β = 2.546, 95 % CI = 0.160, 4.932). Our study suggests that occupational noise exposure is positively associated with SBP and DBP, and miRNA-92a-3p partially mediate the association between occupational noise exposure and DBP. </p>

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          Auditory and non-auditory effects of noise on health

          Noise is pervasive in everyday life and can cause both auditory and non-auditory health effects. Noise-induced hearing loss remains highly prevalent in occupational settings, and is increasingly caused by social noise exposure (eg, through personal music players). Our understanding of molecular mechanisms involved in noise-induced hair-cell and nerve damage has substantially increased, and preventive and therapeutic drugs will probably become available within 10 years. Evidence of the non-auditory effects of environmental noise exposure on public health is growing. Observational and experimental studies have shown that noise exposure leads to annoyance, disturbs sleep and causes daytime sleepiness, affects patient outcomes and staff performance in hospitals, increases the occurrence of hypertension and cardiovascular disease, and impairs cognitive performance in schoolchildren. In this Review, we stress the importance of adequate noise prevention and mitigation strategies for public health. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Oxidative Stress, Inflammation, and Vascular Aging in Hypertension.

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              Effects of noise on vascular function, oxidative stress, and inflammation: mechanistic insight from studies in mice

              Abstract Aims Epidemiological studies indicate that traffic noise increases the incidence of coronary artery disease, hypertension and stroke. The underlying mechanisms remain largely unknown. Field studies with nighttime noise exposure demonstrate that aircraft noise leads to vascular dysfunction, which is markedly improved by vitamin C, suggesting a key role of oxidative stress in causing this phenomenon. Methods and results We developed a novel animal model to study the vascular consequences of aircraft noise exposure. Peak sound levels of 85 and mean sound level of 72 dBA applied by loudspeakers for 4 days caused an increase in systolic blood pressure, plasma noradrenaline and angiotensin II levels and induced endothelial dysfunction. Noise increased eNOS expression but reduced vascular NO levels because of eNOS uncoupling. Noise increased circulating levels of nitrotyrosine, interleukine-6 and vascular expression of the NADPH oxidase subunit Nox2, nitrotyrosine-positive proteins and of endothelin-1. FACS analysis demonstrated an increase in infiltrated natural killer-cells and neutrophils into the vasculature. Equal mean sound pressure levels of white noise for 4 days did not induce these changes. Comparative Illumina sequencing of transcriptomes of aortic tissues from aircraft noise-treated animals displayed significant changes of genes in part responsible for the regulation of vascular function, vascular remodelling, and cell death. Conclusion We established a novel and unique aircraft noise stress model with increased blood pressure and vascular dysfunction associated with oxidative stress. This animal model enables future studies of molecular mechanisms, mitigation strategies, and pharmacological interventions to protect from noise-induced vascular damage.
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                Author and article information

                Journal
                Science of The Total Environment
                Science of The Total Environment
                Elsevier BV
                00489697
                January 2024
                January 2024
                : 907
                : 168148
                Article
                10.1016/j.scitotenv.2023.168148
                37898218
                a6e55de0-ce2b-4af5-b9a0-a9381545ae24
                © 2024

                https://www.elsevier.com/tdm/userlicense/1.0/

                https://doi.org/10.15223/policy-017

                https://doi.org/10.15223/policy-037

                https://doi.org/10.15223/policy-012

                https://doi.org/10.15223/policy-029

                https://doi.org/10.15223/policy-004

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