Herz. 2026 Jun 24. doi: 10.1007/s00059-026-05383-9. Online ahead of print.
ABSTRACT
Traffic-related environmental noise represents a widespread and relevant environmental factor in Europe that is associated with a substantial burden of disease. Current estimates indicate that a significant proportion of the population is exposed to noise levels linked to adverse health effects. Cardiovascular diseases are among the most extensively studied outcomes in this context. Epidemiological studies consistently demonstrate associations between long-term exposure to traffic noise and an increased risk of arterial hypertension, ischemic heart disease, myocardial infarction, heart failure and arrhythmias. These associations are often dose-dependent and also remain even after adjustment for air pollution. Experimental human studies provide complementary mechanistic evidence, showing that even short-term noise exposure can impair endothelial function, activate autonomic stress responses and disrupt sleep. Underlying mechanisms include activation of the sympathetic nervous system, dysregulation of the hypothalamic-pituitary-adrenal axis, oxidative stress and inflammatory processes. Overall, the available evidence supports a stronger consideration of traffic noise as a modifiable risk factor for cardiovascular disease. In addition to individual-level measures to reduce exposure, population-based strategies for noise reduction are essential.
PMID:42340388 | DOI:10.1007/s00059-026-05383-9