Abstract
Environmental exposures represent a significant health hazard, which cumulatively may be responsible for up to 2/3 of all chronic non-communicable disease and associated mortality (Global Burden of Disease Study and The Lancet Commission on Pollution and Health), which has given rise to a new concept of the exposome: the sum of environmental factors in every individual’s experience. Noise is part of the exposome and is increasingly being investigated as a health risk factor impacting neurological, cardiometabolic, endocrine, and immune health. Beyond the well-characterized effects of high-intensity noise on cochlear damage, noise is relatively well-studied in the cardiovascular field, where evidence is emerging from both human and translational experiments that noise from traffic-related sources could represent a risk factor for hypertension, ischemic heart disease, diabetes, and atherosclerosis. In the present review, we comprehensively discuss the current state of knowledge in the field of noise research. We give a brief survey of the literature documenting experiments in noise exposure in both humans and animals with a focus on cardiovascular disease. We also discuss the mechanisms that have been uncovered in recent years that describe how exposure to noise affects physiological homeostasis, leading to aberrant redox signaling resulting in metabolic and immune consequences, both of which have considerable impact on cardiovascular health. Additionally, we discuss the molecular pathways of redox involvement in the stress responses to noise and how they manifest in disruptions of the circadian rhythm, inflammatory signaling, gut microbiome composition, epigenetic landscape and vessel function.
Highlights
Around 50% of the world’s population currently resides in urban environments, following a trend of increasing worldwide urbanization which is expected to continue in the near future (The World Bank, 2020)
We have demonstrated additive effects of noise-induced oxidative stress with reactive oxygen species (ROS) formation originating from angiotensin-II triggered arterial hypertension, an animal model well-known for its pronounced activation of the NADPH oxidase 2 (Nox2) isoform of NADPH oxidases (Steven et al, 2020)
We find that oxidative stress in the aorta, heart, and brains of noise-exposed mice is significantly increased over those of unexposed controls, which is entirely mitigated in mice with a genetic deletion of Nox2 (Kroller-Schon et al, 2018)
Summary
Around 50% of the world’s population currently resides in urban environments, following a trend of increasing worldwide urbanization which is expected to continue in the near future (The World Bank, 2020). It may be speculated that noise-induced ROS formation promotes an inflammatory phenotype in the heart, vessels and the brain as central mediators of inflammatory reactions such as the NLR family pyrin domain containing 3 (NLRP3) inflammasome and high-mobility group box 1 protein (HMGB1) are activated under oxidative stress conditions via redox switches as well as redoxsensitive transcription factors such as nuclear factor kappa B (NFκB) (Wenzel et al, 2017; Steven et al, 2019) This is probably the reason, aside from stress hormone-dependent activation and infiltration of immune cells into the vasculature, for the observed noise-triggered inflammation in exposed mice (Munzel et al, 2017; Kroller-Schon et al, 2018; Steven et al, 2020; Eckrich et al, 2021; Frenis et al, 2021) and the shift to a proatherothrombotic phenotype of the plasma proteome of train noise-exposed healthy human subjects (Herzog et al, 2019), epigenetic changes that promote immune cell activation and expression of CRP (Cai et al, 2017; Eze et al, 2020) and amygdala activation driven coronary atherosclerosis (Osborne et al, 2020; Hahad et al, 2021a; Osborne et al, 2021).
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