Transportation noise pollution and cardiovascular disease

Nature Reviews Cardiology, Journal Year: 2021, Volume and Issue: 18(9), P. 619 - 636

Published: March 31, 2021

Language: Английский

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Effects of gaseous and solid constituents of air pollution on endothelial function

European Heart Journal, Journal Year: 2018, Volume and Issue: 39(38), P. 3543 - 3550

Published: July 25, 2018

Ambient air pollution is a leading cause of non-communicable disease globally. The largest proportion deaths and morbidity due to now known be cardiovascular disorders. Several particulate gaseous pollutants can trigger acute events (e.g. myocardial infarction, stroke, heart failure). While the mechanisms by which undergoing continual refinement, preponderant evidence support rapid effects diversity including all course, fine, ultrafine particles) such as ozone, on vascular function. Indeed alterations in endothelial function seem critically important transducing signals eventually promoting disorders hypertension, diabetes, atherosclerosis. Here, we provide an updated overview impact from human animal studies. for causal mechanistic pathways both studies that various hypothesized general their individual collective highlighted. We also discuss current gaps knowledge trials evaluating personal-level strategies reduce exposure fine matter (PM2.5) function, given lack definitive randomized using hard endpoints. conclude exhortation formal inclusion major risk factor societal guidelines provision recommendations prevent adverse attributable pollution.

Language: Английский

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

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 13

Published: Nov. 11, 2019

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

Language: Английский

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Targeting dysregulation of redox homeostasis in noise-induced hearing loss: Oxidative stress and ROS signaling

Free Radical Biology and Medicine, Journal Year: 2019, Volume and Issue: 135, P. 46 - 59

Published: Feb. 22, 2019

Language: Английский

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The contribution of the exposome to the burden of cardiovascular disease

Nature Reviews Cardiology, Journal Year: 2023, Volume and Issue: 20(10), P. 651 - 669

Published: May 10, 2023

Large epidemiological and health impact assessment studies at the global scale, such as Global Burden of Disease project, indicate that chronic non-communicable diseases, atherosclerosis diabetes mellitus, caused almost two-thirds annual deaths in 2020. By 2030, 77% all are expected to be by diseases. Although this increase is mainly due ageing general population Western societies, other reasons include increasing effects soil, water, air noise pollution on health, together with environmental risk factors climate change, unhealthy city designs (including lack green spaces), lifestyle habits psychosocial stress. The exposome concept was established 2005 a new strategy study effect environment health. describes harmful biochemical metabolic changes occur our body owing totality different exposures throughout life course, which ultimately lead adverse premature deaths. In Review, we describe focus physical chemical their burden cardiovascular disease. We discuss selected highlight relevance for future research well preventive medicine. also challenges limitations studies. Münzel colleagues Additionally, they

Language: Английский

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Health position paper and redox perspectives - Disease burden by transportation noise

Redox Biology, Journal Year: 2023, Volume and Issue: 69, P. 102995 - 102995

Published: Dec. 19, 2023

Transportation noise is a ubiquitous urban exposure. In 2018, the World Health Organization concluded that chronic exposure to road traffic risk factor for ischemic heart disease. contrast, they quality of evidence link other diseases was very low moderate. Since then, several studies on impact various have been published. Also, investigating mechanistic pathways underlying noise-induced health effects are emerging. We review current regarding and related disease-mechanisms. Several high-quality cohort consistently found be associated with higher disease, failure, diabetes, all-cause mortality. Furthermore, recent indicated railway may increase not commonly investigated in an environmental context, including breast cancer, dementia, tinnitus. The harmful activation physiological stress response nighttime sleep disturbance. Oxidative inflammation downstream hormone signaling dysregulated circadian rhythms identified as major disease-relevant pathomechanistic drivers. discuss role reactive oxygen species present results from antioxidant interventions. Lastly, we provide overview oxidative markers adverse redox processes reported noise-exposed animals humans. This position paper summarizes all available epidemiological, clinical, preclinical transportation important public discusses its implications population level.

Language: Английский

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Exposome in ischaemic heart disease: beyond traditional risk factors

European Heart Journal, Journal Year: 2024, Volume and Issue: 45(6), P. 419 - 438

Published: Jan. 18, 2024

Abstract Ischaemic heart disease represents the leading cause of morbidity and mortality, typically induced by detrimental effects risk factors on cardiovascular system. Although preventive interventions tackling conventional have helped to reduce incidence ischaemic disease, it remains a major death worldwide. Thus, attention is now shifting non-traditional in built, natural, social environments that collectively contribute substantially burden perpetuate residual risk. Of importance, these complex interact non-linearly unpredictable ways often enhance attributable single or collection factors. For this reason, new paradigm called ‘exposome’ has recently been introduced epidemiologists order define totality exposure The purpose review outline how emerging may occurrence with particular impact long-term different environmental pollutants, socioeconomic psychological factors, along infectious diseases such as influenza COVID-19. Moreover, potential mitigation strategies for both individuals communities will be discussed.

Language: Английский

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Higher Aircraft Noise Exposure Is Linked to Worse Heart Structure and Function by Cardiovascular MRI

Journal of the American College of Cardiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Aircraft noise is a growing concern for communities living near airports. This study aimed to explore the impact of aircraft on heart structure and function. Nighttime levels (Lnight) weighted 24-hour day-evening-night (Lden) were provided by UK Civil Aviation Authority 2011. Health data came from Biobank (UKB) participants 4 major airports (London Heathrow, London Gatwick, Manchester, Birmingham) who had cardiovascular magnetic resonance (CMR) imaging starting 2014 self-reported no hearing difficulties. Generalized linear models investigated associations between exposure CMR metrics (derived using validated convolutional neural network ensure consistent image segmentations), after adjustment demographic, socioeconomic, lifestyle, environmental confounders. Mediation risk factors was also explored. Downstream adverse cardiac events (MACE) tested in separate prospective UKB subcohort (n = 21,360), understand potential clinical any noise-associated remodeling. Of 3,635 included, 3% experienced higher Lnight (≥45 dB) 8% Lden (≥50 dB). Participants exposed 7% (95% CI: 4%-10%) greater left ventricular (LV) mass 4% 2%-5%) thicker LV walls with normal septal-to-lateral wall thickness ratio. concentric remodeling relevant because associates 32% MACE. They worse myocardial dynamics (eg, an [95% 4%-12%] lower global circumferential strain which 27% MACE). Overall, hypothetical individual experiencing typical abnormalities associated may have times Findings clearest but broadly similar analyses Lden. Body index hypertension appeared mediate 10% 50% observed associations. did not move home during follow-up continuously worst phenotype. Higher remodeling, potentially due increasing obesity hypertension. are existing literature disease, need be considered policymakers aviation industry.

Language: Английский

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Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction—Signatures of the internal exposome

BioFactors, Journal Year: 2019, Volume and Issue: 45(4), P. 495 - 506

Published: April 2, 2019

Environmental noise is a well-recognized health risk and part of the external exposome-the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise-related complications, including increased incidence hypertension, heart failure, myocardial infarction, stroke. Previous data suggest works through two paired pathways proposed reaction model for exposure. As nonspecific stressor, chronic low-level exposure can cause disruption sleep communication leading annoyance subsequent sympathetic endocrine stress responses blood pressure, rate, hormone levels, particular more oxidative stress, being responsible vascular dysfunction representing changes internal exposome. Chronic generates cardiovascular factors on its own such as viscosity, glucose, activation coagulation. To this end, persistent increases cardiometabolic diseases, arterial coronary artery disease, arrhythmia, diabetes mellitus type 2, The present review discusses mechanisms nonauditory noise-induced metabolic consequences, focusing mental signaling pathways, hypothalamic-pituitary-adrenocortical axis nervous system, association these activations with inflammation, onset dysfunction. © 2019 BioFactors, 45 (4):495-506, 2019.

Language: Английский

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HMGB1/RAGE axis mediates stress-induced RVLM neuroinflammation in mice via impairing mitophagy flux in microglia

Journal of Neuroinflammation, Journal Year: 2020, Volume and Issue: 17(1)

Published: Jan. 10, 2020

Abstract Background Microglial mediated neuroinflammation in the rostral ventrolateral medulla (RVLM) plays roles etiology of stress-induced hypertension (SIH). It was reported that autophagy influenced inflammation via immunophenotypic switching microglia. High-mobility group box 1 (HMGB1) acts as a regulator and initiates production proinflammatory cytokines (PICs), but underlying mechanisms remain unclear. Methods The stressed mice were subjected to intermittent electric foot shocks plus noises administered for 2 h twice daily 15 consecutive days. In mice, blood pressure (BP) renal sympathetic nerve activity (RSNA) monitored by noninvasive tail-cuff method platinum-iridium electrodes placed respectively. Microinjection siRNA-HMGB1 (siHMGB1) into RVLM study effect HMGB1 on microglia M1 activation done. mRFP-GFP-tandem fluorescent LC3 (tf-LC3) vectors transfected evaluate process autolysosome formation/autophagy flux. expression RAB7, lysosomal-associated membrane protein (LAMP1), lysosomal pH change used function Mitophagy identified transmission electron microscopic observation or checking MitoTracker colocalization under confocal microscope. Results We showed chronic stress increased cytoplasmic translocations upregulation its receptor RAGE mitochondria injury, oxidative stress, polarization attenuated Cre-CX3CR1/RAGE fl/fl mice. HMGB1/RAGE axis at early stage mitophagy flux while impairing late stages microglia, revealed decreased GFP fluorescence quenching GFP-RFP-LC3-II puncta lysosomes with mitochondria. expressions RAB7 LAMP1 knockout reversed these effects caused an increase acidity lysosomes. siHMGB1 resulted BP lowering RSNA decreasing SIH When inducer, rapamycin, is facilitate flux, this treatment results NF-κB reduced PIC release exogenous disulfide (ds-HMGB1)-stimulated Conclusions Collectively, we demonstrated inhibition led hence reducing microglia-mediated consequently vasoconstriction drive RVLM.

Language: Английский

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