Noise has been found associated with annoyance, stress, sleep disturbance, and impaired cognitive performance. Furthermore, epidemiological studies have found that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, heart failure, and stroke. Observational and translational studies indicate that especially nighttime noise increases levels of stress hormones and vascular oxidative stress, which may lead to endothelial dysfunction and arterial hypertension. Novel experimental studies found aircraft noise to be associated with oxidative stress-induced vascular damage, mediated by activation of the NADPH oxidase, uncoupling of endothelial nitric oxide synthase, and vascular infiltration with inflammatory cells. Transcriptome analysis of aortic tissues from animals exposed to aircraft noise revealed changes in the expression of genes responsible for the regulation of vascular function, vascular remodeling, and cell death. This review focuses on the mechanisms and the epidemiology of noise-induced cardiovascular diseases and provides novel insight into the mechanisms underlying noise-induced vascular damage.

Nocturnal train noise exposure has been associated with hypertension and myocardial infarction. It remains unclear whether acute nighttime train exposure may induce subclinical atherosclerosis, such as endothelial dysfunction and other functional and/or biochemical changes. Thus, we aimed to expose healthy subjects to nocturnal train noise and to assess endothelial function, changes in plasma protein levels and clinical parameters. In a randomized crossover study, we exposed 70 healthy volunteers to either background or two different simulated train noise scenarios in their homes during three nights. After each night, participants visited the study center for measurement of vascular function and assessment of other biomedical and biochemical parameters. The three nighttime noise scenarios were exposure to either background noise (control), 30 or 60 train noise events (Noise30 or Noise60), with average sound pressure levels of 33, 52 and 54 dB(A), respectively. Flow-mediated dilation (FMD) of the brachial artery was 11.23 ± 4.68% for control, compared to 8.71 ± 3.83% for Noise30 and 8.47 ± 3.73% for Noise60 (p < 0.001 vs. control). Sleep quality was impaired after both Noise30 and Noise60 nights (p < 0.001 vs. control). Targeted proteomic analysis showed substantial changes of plasma proteins after the Noise60 night, mainly centered on redox, pro-thrombotic and proinflammatory pathways. Exposure to simulated nocturnal train noise impaired endothelial function. The proteomic changes point toward a proinflammatory and pro-thrombotic phenotype in response to nocturnal train noise and provide a molecular basis to explain the increased cardiovascular risk observed in epidemiological noise studies.Electronic supplementary materialThe online version of this article (10.1007/s00395-019-0753-y) contains supplementary material, which is available to authorized users.

Abstract Aims Nighttime aircraft noise exposure has been associated with increased risk of hypertension and myocardial infarction, mechanistically linked to sleep disturbance, stress and endothelial dysfunction. It is unclear, whether the most widely used metric to determine noise exposure, equivalent continuous sound level (Leq), is an adequate indicator of the cardiovascular impact induced by different noise patterns. Methods and results In a randomized crossover study, we exposed 70 individuals with established cardiovascular disease or increased cardiovascular risk to two aircraft noise scenarios and one control scenario. Polygraphic recordings, echocardiography and flow-mediated dilation was determined for 3 study nights. The noise patterns consisted of 60 (Noise60) and 120 (Noise120) noise events, respectively, but with comparable Leq, corresponding to a mean value of 45 dB. Mean value of noise during control nights was 37 dB. During the control night, flow-mediated vasodilation (FMD) was 10.02±3.75%, compared to 7.27±3.21% for Noise60 nights and 7.21±3.58% for Noise120 nights (p&lt;0.001). Sleep quality was impaired after noise exposure in both noise scenario nights (p&lt;0.001). Serial echocardiographic assessment demonstrated an increase in the E/E’ ratio, a measure of diastolic function, within the three exposure nights, with a ratio of 6.83±2.26 for the control night, 7.21±2.33 for Noise60 and 7.83±3.07 for Noise120 (p=0.043). Conclusions Nighttime exposure to aircraft noise with similar Leq, but different number of noise events, results in a comparable worsening of vascular function. Adverse effects of nighttime aircraft noise exposure on cardiac function (diastolic dysfunction) seemed stronger the higher number of noise events. Translational perspective With the present field study, we tested whether 60 versus 120 simulated aircraft noise events with an equal average sound pressure level (Leq) have comparable adverse effects on endothelial and diastolic function of the heart of subjects with established cardiovascular disease or at increased cardiovascular risk. The results demonstrated that two different nighttime noise patterns with similar Leq, despite different number of noise events, results in a comparable worsening of vascular and cardiac diastolic function. These results may explain at least in part the increased incidence of coronary heart disease and heart failure being observed in response to nighttime aircraft noise.

A series of human field studies demonstrated that simulated nocturnal traffic noise exposure impaired sleep quality and endothelial function, which could be significantly improved after intake of vitamin C in case of endothelial function. However, it remains unclear whether these changes follow a sex-specific pattern. Thus, we aimed to analyze the effect of simulated nocturnal train noise exposure on sleep quality, endothelial function and its associated changes after vitamin C intake, and other hemodynamic and biochemical parameters in young healthy men and women. We used data from a randomized crossover study, wherein 70 healthy volunteers (50% women) were each exposed to one control pattern (regular background noise) and two different train noise scenarios (30 or 60 train noise events per night, with average sound pressure levels of 52 and 54 dB(A), respectively, and peak sound level of 73–75 dB(A)) in their homes for three nights. After each night, participants visited the study center for the measurement of endothelial function as well as other hemodynamic and biochemical parameters. Sleep quality measured via self-report was significantly impaired after noise 30 and noise 60 nights in both men and women (p < 0.001 vs. control). Likewise, endothelial function measured by flow-mediated dilation (FMD) was significantly impaired after noise 30 and noise 60 nights in both men and women (p < 0.001 vs. control). While in women, vitamin C intake significantly improved FMD after both noise 30 and noise 60 study nights compared to control nights, no significant changes were observed in men. Exposure to simulated nocturnal train noise impairs sleep quality and endothelial function in both men and women, whereas a significant improvement of endothelial function after noise exposure and vitamin C intake could only be observed in women. These findings suggest for the first time that in men other mechanisms such as oxidative stress causing endothelial dysfunction may come into play.