Abstract
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.
| Original language | English |
|---|---|
| Journal | Hypertension |
| Volume | 80 |
| Issue number | 7 |
| Pages (from-to) | 1384-1392 |
| Number of pages | 9 |
| ISSN | 0194-911X |
| DOIs | |
| Publication status | Published - Jul 2023 |
Bibliographical note
This article was found as a 'Free version' at the Publisher on August 28, 2023. If the access closes, please contact [email protected]Funding
Funding Information: This study was supported by the Center for Translational Vascular Biology (CTVB) and funded by the Stiftung Mainzer Herz. S. Rajagopalan is supported by National Institutes of Health Grants 1R35ES031702 and R01ES017290.
Keywords
- air pollution
- cardiovascular diseases
- cytokines
- inflammation
- noise
- oxidative stress