期刊
HYPERTENSION
卷 80, 期 7, 页码 1384-1392出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.123.20617
关键词
air pollution; cardiovascular diseases; cytokines; inflammation; noise; oxidative stress
Traffic noise and air pollution are significant risk factors for cardiovascular events, with various mediating pathways involved. Existing evidence suggests that interventions targeting these environmental stressors can alleviate the adverse effects on blood pressure and intermediate pathways, providing support for a causal link. However, there are still gaps in our understanding of the underlying mechanisms, highlighting the need for further research.
Traffic noise and air pollution are environmental stressors found to increase risk for cardiovascular events. The burden of disease attributable to environmental stressors and cardiovascular disease globally is substantial, with a need to better understand the contribution of specific risk factors that may underlie these effects. Epidemiological observations and experimental evidence from animal models and human controlled exposure studies suggest an essential role for common mediating pathways. These include sympathovagal imbalance, endothelial dysfunction, vascular inflammation, increased circulating cytokines, activation of central stress responses, including hypothalamic and limbic pathways, and circadian disruption. Evidence also suggests that cessation of air pollution or noise through directed interventions alleviates increases in blood pressure and intermediate surrogate pathways, supporting a causal link. In the second part of this review, we discuss the current understanding of mechanisms underlying and current gaps in knowledge and opportunities for new research.
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