Transportation noise pollution as a cardiovascular risk factor: from epidemiological evidence to mechanistic insights.

📖 Top 20% JournalJan 19, 2026EXCLI journal

Transportation noise pollution linked to heart health risks: evidence and possible causes

AI simplified

Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

More than 113 million people in Europe are chronically exposed to transportation noise levels above 55 dB(A).

Transportation noise is linked to a loss of approximately 1.3 million healthy life-years annually due to its impact on cardiovascular health.
Epidemiological studies show associations between transportation noise and various cardiovascular conditions, including ischemic heart disease, heart failure, and stroke.
Activation of the sympathetic nervous system and stress hormone release may contribute to health issues related to noise exposure.
Chronic noise exposure is associated with endothelial dysfunction, vascular inflammation, and oxidative stress.
Neuroimaging studies indicate that chronic noise activates the amygdala, connecting stress perception with cardiovascular inflammation.
Adverse cardiovascular effects of noise exposure are more severe at night, potentially disrupting sleep and exacerbating health risks.

AI simplified

Transportation noise from road, rail, and aircraft traffic is now recognized as a major cardiovascular risk factor. In Europe, more than 113 million people are chronically exposed to levels above 55 dB(A), resulting in an estimated 1.3 million healthy life-years lost annually from traffic-related noise. Large epidemiological studies consistently demonstrate associations with ischemic heart disease, heart failure, stroke, and type 2 diabetes, with additional links to hypertension, atrial fibrillation, and obesity. Translational and experimental research has clarified the biological plausibility of these findings. The central "noise reaction model" involves activation of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, with subsequent release of catecholamines and cortisol. These stress responses provoke endothelial dysfunction, vascular inflammation, and oxidative stress, largely through NADPH oxidase 2 activation and nitric oxide synthase uncoupling. At the molecular level, noise alters gene expression networks, disrupts circadian clock regulation, downregulates FOXO3, and induces pro-inflammatory epigenetic modifications. Neuroimaging studies reveal chronic noise activates the amygdala, linking stress perception to vascular inflammation and major adverse cardiovascular events. Adverse effects are most pronounced at night, when noise fragments restorative sleep and amplifies neurohormonal imbalance. Importantly, these pathways overlap with mechanisms of traditional cardiovascular risk factors - diabetes, hypertension, smoking, and hyperlipidemia - suggesting that noise accelerates vascular aging through convergent mechanisms. Combined exposure to noise and air pollution further exerts additive or synergistic effects, underscoring the value of the exposome concept in identifying vulnerable populations. Transportation noise should therefore be considered an established cardiovascular risk factor, requiring equal priority in prevention guidelines and public health policy. See also the graphical abstract(Fig. 1).

Full Text

We can’t show the full text here under this license. Use the link below to read it at the source.

View on DOI ↗View on PubMed ↗