Background: Transportation noise is recognized as an important cardiovascular risk factor. Key mechanisms seem to include noise-triggered inflammation and oxidative stress with subsequent endothelial dysfunction. Here, we test for adaptation or tolerance mechanisms in mice in response to chronic noise exposure. 

Methods and Results: C57BL/6J mice were exposed  to aircraft noise for 0, 4, 7, 14 and 28d at a mean sound pressure level of 72 dB(A) and peak levels of 85 dB(A). Induction of hearing loss in the mice was excluded by auditory brainstem response audiometry. Endothelial dysfunction and elevation of blood pressure was present for 4-28d of noise. Reactive oxygen species (ROS) formation as determined by dihydroethidium (DHE) staining and HPLC-based measurement of superoxide formation in the aorta/heart/brain was time-dependently increased by noise. Oxidative burst in the whole blood showed a maximum at 4d or 7d of noise. Superoxide formation in the brain was mirrored by downregulation of Nos3 and Foxo3 genes, whereas Vcam1 mRNA was upregulated in all noise exposure groups. Other markers showed more complex kinetic profiles.

Conclusion: Endothelial dysfunction and inflammation is present upon short-term noise exposure, whereas ROS formation gradually increases with longer exposure times without induction of hearing loss. We were not able to identify adaptation or tolerance mechanisms in noise-exposed mice that would effectively counteract the inflicted damage were not identified but clusters of mice for some of the parameters that may indicate (non-)responders.