TY - JOUR
AU - Kuntic, Marin
AU - Kuntic, Ivana
AU - Krishnankutty, Roopesh
AU - Gericke, Adrian
AU - Oelze, Matthias
AU - Junglas, Tristan
AU - Bayo Jimenez, Maria Teresa
AU - Stamm, Paul
AU - Nandudu, Margaret
AU - Hahad, Omar
AU - Keppeler, Karin
AU - Daub, Steffen
AU - Vujacic-mirski, Ksenija
AU - Rajlic, Sanela
AU - Strohm, Lea
AU - Ubbens, Henning
AU - Tang, Qi
AU - Jiang, Subao
AU - Ruan, Yue
AU - Macleod, Kenneth G.
AU - Steven, Sebastian
AU - Berkemeier, Thomas
AU - Pöschl, Ulrich
AU - Lelieveld, Jos
AU - Kleinert, Hartmut
AU - Von Kriegsheim, Alex
AU - Daiber, Andreas
AU - Münzel, Thomas
PY - 2022
DA - December
TI - Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice
JO - Redox Biology
VL - 59
DO - https://doi.org/10.1016/j.redox.2022.102580
AB - Worldwide, up to 8.8 million excess deaths/year have been attributed to air pollution, mainly due to the exposure to fine particulate matter (PM). Traffic-related noise is an additional contributor to global mortality and morbidity. Both health risk factors substantially contribute to cardiovascular, metabolic and neuropsychiatric sequelae. Studies on the combined exposure are rare and urgently needed because of frequent co-occurrence of both risk factors in urban and industrial settings. To study the synergistic effects of PM and noise, we used an exposure system equipped with aerosol generator and loud-speakers, where C57BL/6 mice were acutely exposed for 3d to either ambient PM (NIST particles) and/or noise (aircraft landing and take-off events). The combination of both stressors caused endothelial dysfunction, increased blood pressure, oxidative stress and inflammation. An additive impairment of endothelial function was observed in isolated aortic rings and even more pronounced in cerebral and retinal arterioles. The increase in oxidative stress and inflammation markers together with RNA sequencing data indicate that noise particularly affects the brain and PM the lungs. The combination of both stressors has additive adverse effects on the cardiovascular system that are based on PM-induced systemic inflammation and noise-triggered stress hormone signaling. We demonstrate an additive upregulation of ACE-2 in the lung, suggesting that there may be an increased vulnerability to COVID-19 infection. The data warrant further mechanistic studies to characterize the propagation of primary target tissue damage (lung, brain) to remote organs such as aorta and heart by combined noise and PM exposure
PB - Elsevier
UR - https://www.research.ed.ac.uk/en/publications/cc03f67f-ded8-42e9-bf6f-428c6366d77a
KW - Coronavirus (COVID-19)
KW - Environment, community and place
ER