Abstract
Transportation noise is recognized as an important cardiovascular risk factor. Key mechanisms are noise-triggered vascular inflammation and oxidative stress with subsequent endothelial dysfunction. Here, we test for adaptation or tolerance mechanisms in mice in response to chronic noise exposure. 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). Chronic aircraft noise exposure up to 28d caused persistent endothelial dysfunction and elevation of blood pressure. Likewise, 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 exposure. Increased superoxide formation in the brain was mirrored by a downregulation of neuronal nitric oxide synthase (Nos3) and transcription factor Foxo3 genes, whereas Vcam1 mRNA, a marker for inflammation was upregulated in all noise exposure groups. Induction of a pronounced hearing loss in the mice was excluded by auditory brainstem response audiometry. Endothelial dysfunction and inflammation were present during the entire 28d of aircraft noise exposure. ROS formation gradually increases with ongoing exposure without significant adaptation or tolerance in mice in response to chronic noise stress at moderate levels. These data further illustrate health side effects of long-term noise exposure and further strengthen a consequent implementation of the WHO noise guidelines in order to prevent the development of noise-related future cardiovascular disease.
Highlights
Transportation noise is increasingly recognized as an important cardiovascular risk factor (Munzel et al, 2020; Munzel et al, 2021)
NO signaling disruption was highlighted in a gradual reduction in nitrite levels in the plasma, a surrogate parameter for NO bioavailability, indicating that an oxidative phenotype was present, though the progressive decline reached a plateau by 14-28d (Figure 2C)
Our present studies demonstrate distinct changes of the cardiovascular/cerebral system in response to a 4-weeks aircraft noise exposure period
Summary
Transportation noise is increasingly recognized as an important cardiovascular risk factor (Munzel et al, 2020; Munzel et al, 2021). Short-term nighttime aircraft or railway noise exposure in healthy subjects and patients with established coronary artery disease causes endothelial dysfunction, hypertension and increased stress hormone release (Schmidt et al, 2013; Schmidt et al, 2015; Herzog et al, 2019). Noise has a negative impact on the cognitive development of children (Stansfeld et al, 2005) such as learning and memory and may cause mental disease including in particular Alzheimer’s disease (Cantuaria et al, 2021), depression and anxiety disorders (Beutel et al, 2016). Previous studies have demonstrated that annoyance and mental stress in response to noise is strongly connected to an adaptation/habituation processes (Stansfeld, 1992). We recently demonstrated that the experience of a previous nighttime noise sensitized rather than desensitized the vasculature to develop endothelial dysfunction (Schmidt et al, 2013). Other groups established that cardiac arousal responses caused by noise do not display habituation (Griefahn et al, 2008; Basner et al, 2011)
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