TY - JOUR
T1 - Noise and Air Pollution as Risk Factors for Hypertension
T2 - Part II - Pathophysiologic Insight
AU - Hahad, Omar
AU - Rajagopalan, Sanjay
AU - Lelieveld, Jos
AU - Sørensen, Mette
AU - Kuntic, Marin
AU - Daiber, Andreas
AU - Basner, Mathias
AU - Nieuwenhuijsen, Mark
AU - Brook, Robert D.
AU - Münzel, Thomas
N1 - This article was found as a 'Free version' at the Publisher on August 28, 2023. If the access closes, please contact [email protected]
PY - 2023/7
Y1 - 2023/7
N2 - 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.
AB - 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.
KW - air pollution
KW - cardiovascular diseases
KW - cytokines
KW - inflammation
KW - noise
KW - oxidative stress
KW - air pollution
KW - cardiovascular diseases
KW - cytokines
KW - inflammation
KW - noise
KW - oxidative stress
UR - https://www.ahajournals.org/doi/epub/10.1161/HYPERTENSIONAHA.123.20617
U2 - 10.1161/HYPERTENSIONAHA.123.20617
DO - 10.1161/HYPERTENSIONAHA.123.20617
M3 - Review
C2 - 37073733
AN - SCOPUS:85162739161
SN - 0194-911X
VL - 80
SP - 1384
EP - 1392
JO - Hypertension
JF - Hypertension
IS - 7
ER -