Time‐dependent induction of vascular oxidative stress, inflammation, endothelial dysfunction and high blood pressure by aircraft noise exposure in mice
Authors: Kalinovic Sanela , Frenis Katie , Al Zuabi Ahmad , Oelze Matthias , Steven Sebastian , Kvandova Miroslava , Ernst Benjamin , Strieth Sebastian , Daiber Andreas , Kröller-Schön Swenja , Münzel Thomas 
Published: April 2020

Background

Transportation noise is recognized as an important cardiovascular risk factor. It was shown that traffic noise exposure is associated with cerebro/cardiovascular diseases such as hypertension, myocardial infarction, and stroke. Aircraft noise causes endothelial dysfunction, inflammation and increases cerebral/cardiovascular oxidative stress in mice and traffic noise in general increased stroke mortality in large population studies. Chronic aircraft noise also causes learning and memory impairment in children. We recently studied the effects of different time exposure protocols (sleep versus awake phase) of aircraft noise exposure on C57Bl/6JRj mice and demonstrated that sleep phase noise exposure impairs the circadian clock and causes oxidative stress, endothelial dysfunction and high blood pressure.

Methods and Results

Before the main study, we ensured that the longest noise exposure did not cause hearing loss in the mice by using audiometry. C57Bl/6JRj mice were exposed to aircraft noise for 4, 7, 14 and 28 days at a maximum sound level of 85 dB(A) and a mean sound pressure level of 72 dB(A) and compared with unexposed control mice. The induction of endothelial dysfunction and elevation of blood pressure was comparable in all exposure groups. Oxidative burst in the whole blood, stimulated with phorbol 12,13‐dibutyrate (PDBu) or zymosan A, was increased in all exposed groups with a maximum at 4 or 7 days. Vascular ROS formation as envisaged by dihydroethidium (DHE) staining was increased in noise‐exposed mice without a significant time response. Noise‐induced aortic, cardiac and cerebral superoxide formation as measured by DHE HPLC analysis increased in dependence of noise exposure duration. Similarly, levels of interleukin‐6 (IL‐6) were time dependently increased by trend in plasma and brain tissue in all noise exposed mice. We also established increased NOX‐2 expression in aortic tissue of noise exposed mice, while levels of P‐VASP were decreased after exposure.

Conclusion

We here present novel data on the effects of different aircraft noise exposure protocols (4–28 days) indicating that most adverse vascular effects are established already after 4 days. Importantly, our present data prove that the applied moderate noise levels do not cause induction of hearing loss, even not after long‐term exposures. Thus our present data provide important technical insights in noise exposure protocols for future translational studies in mice with relevance for the human situation.

Support or Funding Information

Our experimental studies on noise effects in mice were supported by vascular biology research grants from the Boehringer Ingelheim Foundation for the collaborative research group „Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications” and Foundation Heart of Mainz