The present data demonstrate for the first time that nighttime aircraft noise markedly attenuates endothelium-dependent vasodilation in patients with established and/or at high risk for CAD. The magnitude of this effect was such that the study was terminated early as the predefined stopping criteria were fulfilled at 60 % of the initially planned recruitment. An increase in blood pressure and a marked decrease in sleep quality were also observed in response to aircraft noise. Collectively, this evidence may concur to explain the reported association between nighttime aircraft noise and arterial hypertension, myocardial infarction and stroke.
Aircraft noise and cardiovascular disease: evidence from epidemiological studies
A growing body of evidence documents that, beyond causing annoyance, aircraft noise should be considered a true cardiovascular risk factor (for review [
5]).
In particular, recently published studies clearly substantiate the cardiovascular side effects of aircraft noise. In a multi-airport retrospective study in more than 6 Million people aged >65 years residing near airports, Correia et al. [
11] reported a 3.5 % higher admission rate for cardiovascular disease such as ischemic coronary artery disease, cerebrovascular disease and heart failure for each 10 dB(A) increase in noise.
Another study in 3.6 million residents living close to Heathrow airport revealed that aircraft noise increased hospital admissions in a significant linear trend with increased risk with higher levels of both daytime and nighttime aircraft noise [
12]. When areas experiencing the highest levels of daytime aircraft noise were compared with those experiencing the lowest levels (>63 dB vs. ≤51 dB), the relative risk of hospital admissions for stroke was 1.24 for coronary heart disease, 1.21 for cardiovascular disease and it remained 1.14 after adjustment for age, sex, ethnicity, deprivation, and a smoking proxy (lung cancer mortality). The authors concluded that high levels of aircraft noise were associated with increased risks of stroke, coronary heart disease and cardiovascular disease for both hospital admissions and mortality in areas near Heathrow airport in London.
Likewise, Floud et al. [
13] reported a significant association between nighttime average aircraft noise and the endpoint ‘heart disease and stroke’ in the Hypertension and Environmental Noise near Airports (HYENA) study in 4,712 participants (276 cases) who lived near airports in six European countries (UK, Germany, Netherlands, Sweden, Greece, Italy). The result was not changed after adjustment for socio-demographic confounders for participants who had lived in the same place for ≥20 years. The authors concluded that exposure to aircraft noise over many years may increase risks of heart disease and stroke.
Effects of simulated noise on vascular function
More recently, we provided some insight into potential mechanisms leading to vascular dysfunction and subsequently cardiovascular disease in response to nighttime aircraft noise. In a field study, we showed that nighttime aircraft noise simulation caused endothelial dysfunction and tended to increase blood pressure [
6]. This pathophysiological study demonstrated the existence of a dose–response relationship between noise and endothelial function impairment, and the mechanism of noise-induced endothelial dysfunction was demonstrated to be linked with increased oxidative stress within the vasculature, because endothelial dysfunction was partly corrected by the antioxidant vitamin C. We also observed a priming effect, i.e. the impact of noise was larger when subjects had already been exposed to noise, suggesting that the vasculature is rather sensitized than preconditioned. The changes were paralleled and/or caused by increases in circulating adrenaline levels and were strongly associated with impaired sleep quality.
The present studies provide several important new information concerning cardiovascular risk and nighttime aircraft noise.
1. For the first time we demonstrate that nighttime noise substantially reduces FMD in patients with -or at risk for- coronary artery disease despite optimal, guideline conform concomitant cardiovascular medication including ACE-Inhibitors, AT-1 receptor blocker, statins and antiplatelet agents.
Importantly, endothelial dysfunction of forearm vessels has been shown to correlate well with endothelial dysfunction (and with the presence of atherosclerosis) in coronary vessels [
14] and it has been shown to be associated with future cardiovascular events in patients with coronary and peripheral artery disease, heart failure, arterial hypertension and stroke (for review [
15]).
2. In addition, there was evidence that nighttime aircraft noise simulation increased systolic blood pressure during the night by approximately 4 mmHg in patients with CAD. The observed 4 mmHg increase in systolic blood pressure is considered clinically relevant if sustained in the long-term, since recent studies have demonstrated that every 1 mmHg increase in systolic blood pressure in elderly with isolated systolic hypertension is associated with a 1 % increase new onset heart failure [
16].
In the present studies, the increase in blood pressure was not associated with a change in plasma adrenaline concentration, possibly due to the background therapy with beta receptor-blocker or ACE/inhibitors and AT1 receptor blockers, substances that are known to have substantial inhibitory actions on the activity of the adrenergic and the renin angiotensin system [
17,
18].
3. These data also demonstrate for the first time that detrimental vascular consequences in response to nighttime aircraft noise occur independently of the conscious perception of noise and the subject´s cognitive awareness (Fig.
2).
4. With regard to influence of noise on coagulation we detected a notable reduction in the level of Coagulation Factor XII (Hageman-Factor). While the role of factor XII in vivo remains controversial, associations of mildly reduced levels with increased coronary risk have been reported [
19,
20].
The FMD measured in our patient group with cardiovascular disease was just slightly reduced compared to the FMD measured in healthy subjects [
6], which may reflect optimal medical therapy.
It is important to note that our previous study clearly demonstrated that vessels are getting sensitized to noise-induced vascular damage rather than getting habituated since the blunting in FMD was in particular evident, when subjects were exposed first to 30 and then to 60 night noise events [
6]. With the present studies we can already demonstrate a highly significant reduction in FMD in patients with CAD or being at high risk for CAD being exposed to 60 night noise events alone. Since patients living close to airports experience numerous noise events it seems likely that the degree of deterioration of endothelial function measured in the present study underestimates strongly the vascular damage induced by nighttime aircraft noise in the real world.
As in the previous study, noise exposure had a negative influence on subjective sleep quality of study participants. This finding may be regarded as clinically important, since self reported sleep quality is closely related to vascular calcification [
21] and endothelial function [
22]. Reduced sleep quality likely increases annoyance, which itself is associated with a higher probability of developing hypertension due to noise [
23]. Recent evidence suggests a strong link between sleep duration and cardiovascular risk factors [
24], which may explain increased extent of coronary artery disease lesions in persons with daytime sleepiness [
25] due to insufficient sleep quality. The blunting in endothelial function and the increase in blood pressure were in our study not associated with impaired sleep quality on a patient level. These two adverse effects were also not prevented by guideline conform cardiovascular therapy.
In the current study, we could not detect changes in measures of immune function like cortisol levels, CRP, IL-6 or neutrophil count.