Long-term effects of aircraft noise exposure on vascular oxidative stress, endothelial function and blood pressure

Introduction 

Air craft noise is recognized as an important cardiovascular risk factor. Key mechanisms are noise-triggered vascular inflammation and oxidative stress with subsequent endothelial dysfunction.

Objective 

Adaptation or tolerance mechanisms in mice in response to chronic noise exposure were evaluated.

Material & methods 

C57BL/6J mice were exposed to aircraft noise for 0, 4, 7, 14 and 28 d at a mean sound pressure level of 72 dB(A) and peak levels of 85 dB(A) comparing with unexposed controls. Auditory brainstem response (ABR) audiometry was used for determination of hearing thresholds. Non-invasive blood pressure measurements (NIBP) were performed. Concentration-relaxation curves were derived from the aortic ring assay. Reactive oxygen species (ROS) formation as determined by dihydroethidium (DHE) staining and superoxide formation was assayed by HPLC.

Results 

Chronic aircraft noise exposure up to 28d caused persistent endothelial dysfunction and elevation of blood pressure. Likewise, ROS and superoxide formation in the aorta, heart and brain were time-dependently increased. Induction of a pronounced hearing loss in the mice was excluded by ABR. ROS formation gradually increased with ongoing exposure without significant adaptation or tolerance in mice in response to chronic noise stress at moderate levels.

Conclusion 

These data further illustrate the development of cardiovascular disease as side effect of long-term aircraft noise exposure.

Boehringer Ingelheim Stiftung

Conflict of Interest

The author declares that there is no conflict of interest.

Publication History

Article published online:
24 May 2022