Aircraft Noise and Stress Hormone Release
Aircraft Noise and Stress Hormone Release
Aims Aircraft noise disturbs sleep, and long-term exposure has been shown to be associated with increases in the prevalence of hypertension and an overall increased risk for myocardial infarction. The exact mechanisms responsible for these cardiovascular effects remain unclear.
Methods and results We performed a blinded field study in 75 healthy volunteers (mean age 26 years), who were exposed at home, in random order, to one control pattern (no noise) and two different noise scenarios [30 or 60 aircraft noise events per night with an average maximum sound pressure level (SPL) of 60 dB(A)] for one night each. We performed polygraphy during each study night. Noise caused a worsening in sleep quality (P < 0.0001). Noise60, corresponding to equivalent continuous SPLs of 46.3 dB (Leq) and representing environmental noise levels associated with increased cardiovascular events, caused a blunting in FMD (P = 0.016). As well, although a direct comparison among the FMD values in the noise groups (control: 10.4 ± 3.8%; Noise30: 9.7 ± 4.1%; Noise60: 9.5 ± 4.3%, P = 0.052) did not reach significance, a monotone dose-dependent effect of noise level on FMD was shown (P = 0.020). Finally, there was a priming effect of noise, i.e. the blunting in FMD was particularly evident when subjects were exposed first to 30 and then to 60 noise events (P = 0.006). Noise-induced endothelial dysfunction (ED) was reversed by the administration of Vitamin C (P = 0.0171). Morning adrenaline concentration increased from 28.3 ± 10.9 to 33.2 ± 16.6 and 34.1 ± 19.3 ng/L (P = 0.0099). Pulse transit time, reflecting arterial stiffness, was also shorter after exposure to noise (P = 0.003).
Conclusion In healthy adults, acute nighttime aircraft noise exposure dose-dependently impairs endothelial function and stimulates adrenaline release. Noise-induced ED may be in part due to increased production in reactive oxygen species and may thus be one mechanism contributing to the observed association of chronic noise exposure with cardiovascular disease.
The WHO estimates that in high-income Western European countries (population ~340 million) at least 1 million healthy life years are lost every year due to environmental noise. The negative health outcomes of noise include annoyance, sleep disturbance, cardiovascular disease, and impairment of cognitive performance in children.
Aircraft noise has been shown to be more annoying than road- and railway noise at the same equivalent noise level. Epidemiologic studies have demonstrated associations between long-term exposure to aircraft noise and an increased incidence of arterial hypertension and therefore cardiovascular disease. The mechanisms underlying these adverse cardiovascular effects of aircraft noise are not fully understood. Nocturnal noise exposure seems to be more relevant for the genesis of cardiovascular disease than daytime noise exposure, probably due to repeated autonomic arousals that have been shown to habituate to a lesser degree to noise than, e.g. cortical arousals. In general, the risk increases with exposure duration, and is higher in those who decide to sleep with open windows.
Undisturbed sleep of sufficient length is obligatory for the maintenance of daytime performance and health. The human organism recognizes, evaluates, and reacts to environmental sounds even while asleep. These reactions are part of an integral activation process of the organism that expresses itself, e.g. as changes in sleep structure or increases in blood pressure and heart rate. Environmental noise may decrease the restorative power of sleep by means of repeatedly occurring activations (so-called sleep fragmentation) that are associated with more awakenings/arousals, less deep sleep and rapid eye movement sleep, and early awakenings in the morning. Although healthy subjects have been shown to habituate to aircraft noise exposure to a certain degree, the habituation is not complete, and noise-induced awakenings and, especially, activations of the autonomic nervous system can still be observed in subjects that have been exposed to aircraft noise for several years. Sleep disturbance and especially sleep restriction in turn have been shown to cause hormonal and metabolic changes, which could predispose to a future development of cardiovascular disease.
Circadian changes related to altered sleep may also adversely affect the immune system and may increase the responsiveness of the heart to hypertrophic stimuli. Although plausible, the link between polysomnographic evidence of sleep disturbance during aircraft noise exposure and cardiovascular outcomes is not well established. It is largely unknown which changes or indices predict long-term risk.
Furthermore, polysomnography (i.e. the simultaneous measurement of the electroencephalogram, electrooculogram, and electromyogram) is a complex and cumbersome method, which is not very well suited for larger studies in the general population. Therefore, other methods, like actigraphy (a non-invasive technique to monitor human rest/activity cycles) and behaviourally confirmed awakenings, have been used in this context.
In the case of aircraft noise, hypertension may be a consequence of the noise-induced release of stress hormones such as epi- and norepinephrine and/or the development of vascular (endothelial) dysfunction. Endothelial dysfunction (ED) is considered an early step in the development of atherosclerotic changes of the vasculature (for review see ) and can be assessed non-invasively. Recent studies indicate that in patients with coronary artery disease and hypertension, ED assessment in the forearm may have prognostic implications.
Based on these considerations, the primary aim of the present study was to test whether nocturnal exposure to aircraft noise may induce ED. The morning plasma level of adrenaline was a secondary endpoint. In a subgroup of noise 60 subjects, we also tested whether acute vitamin C challenges may improve ED.
Abstract and Introduction
Abstract
Aims Aircraft noise disturbs sleep, and long-term exposure has been shown to be associated with increases in the prevalence of hypertension and an overall increased risk for myocardial infarction. The exact mechanisms responsible for these cardiovascular effects remain unclear.
Methods and results We performed a blinded field study in 75 healthy volunteers (mean age 26 years), who were exposed at home, in random order, to one control pattern (no noise) and two different noise scenarios [30 or 60 aircraft noise events per night with an average maximum sound pressure level (SPL) of 60 dB(A)] for one night each. We performed polygraphy during each study night. Noise caused a worsening in sleep quality (P < 0.0001). Noise60, corresponding to equivalent continuous SPLs of 46.3 dB (Leq) and representing environmental noise levels associated with increased cardiovascular events, caused a blunting in FMD (P = 0.016). As well, although a direct comparison among the FMD values in the noise groups (control: 10.4 ± 3.8%; Noise30: 9.7 ± 4.1%; Noise60: 9.5 ± 4.3%, P = 0.052) did not reach significance, a monotone dose-dependent effect of noise level on FMD was shown (P = 0.020). Finally, there was a priming effect of noise, i.e. the blunting in FMD was particularly evident when subjects were exposed first to 30 and then to 60 noise events (P = 0.006). Noise-induced endothelial dysfunction (ED) was reversed by the administration of Vitamin C (P = 0.0171). Morning adrenaline concentration increased from 28.3 ± 10.9 to 33.2 ± 16.6 and 34.1 ± 19.3 ng/L (P = 0.0099). Pulse transit time, reflecting arterial stiffness, was also shorter after exposure to noise (P = 0.003).
Conclusion In healthy adults, acute nighttime aircraft noise exposure dose-dependently impairs endothelial function and stimulates adrenaline release. Noise-induced ED may be in part due to increased production in reactive oxygen species and may thus be one mechanism contributing to the observed association of chronic noise exposure with cardiovascular disease.
Introduction
The WHO estimates that in high-income Western European countries (population ~340 million) at least 1 million healthy life years are lost every year due to environmental noise. The negative health outcomes of noise include annoyance, sleep disturbance, cardiovascular disease, and impairment of cognitive performance in children.
Aircraft noise has been shown to be more annoying than road- and railway noise at the same equivalent noise level. Epidemiologic studies have demonstrated associations between long-term exposure to aircraft noise and an increased incidence of arterial hypertension and therefore cardiovascular disease. The mechanisms underlying these adverse cardiovascular effects of aircraft noise are not fully understood. Nocturnal noise exposure seems to be more relevant for the genesis of cardiovascular disease than daytime noise exposure, probably due to repeated autonomic arousals that have been shown to habituate to a lesser degree to noise than, e.g. cortical arousals. In general, the risk increases with exposure duration, and is higher in those who decide to sleep with open windows.
Undisturbed sleep of sufficient length is obligatory for the maintenance of daytime performance and health. The human organism recognizes, evaluates, and reacts to environmental sounds even while asleep. These reactions are part of an integral activation process of the organism that expresses itself, e.g. as changes in sleep structure or increases in blood pressure and heart rate. Environmental noise may decrease the restorative power of sleep by means of repeatedly occurring activations (so-called sleep fragmentation) that are associated with more awakenings/arousals, less deep sleep and rapid eye movement sleep, and early awakenings in the morning. Although healthy subjects have been shown to habituate to aircraft noise exposure to a certain degree, the habituation is not complete, and noise-induced awakenings and, especially, activations of the autonomic nervous system can still be observed in subjects that have been exposed to aircraft noise for several years. Sleep disturbance and especially sleep restriction in turn have been shown to cause hormonal and metabolic changes, which could predispose to a future development of cardiovascular disease.
Circadian changes related to altered sleep may also adversely affect the immune system and may increase the responsiveness of the heart to hypertrophic stimuli. Although plausible, the link between polysomnographic evidence of sleep disturbance during aircraft noise exposure and cardiovascular outcomes is not well established. It is largely unknown which changes or indices predict long-term risk.
Furthermore, polysomnography (i.e. the simultaneous measurement of the electroencephalogram, electrooculogram, and electromyogram) is a complex and cumbersome method, which is not very well suited for larger studies in the general population. Therefore, other methods, like actigraphy (a non-invasive technique to monitor human rest/activity cycles) and behaviourally confirmed awakenings, have been used in this context.
In the case of aircraft noise, hypertension may be a consequence of the noise-induced release of stress hormones such as epi- and norepinephrine and/or the development of vascular (endothelial) dysfunction. Endothelial dysfunction (ED) is considered an early step in the development of atherosclerotic changes of the vasculature (for review see ) and can be assessed non-invasively. Recent studies indicate that in patients with coronary artery disease and hypertension, ED assessment in the forearm may have prognostic implications.
Based on these considerations, the primary aim of the present study was to test whether nocturnal exposure to aircraft noise may induce ED. The morning plasma level of adrenaline was a secondary endpoint. In a subgroup of noise 60 subjects, we also tested whether acute vitamin C challenges may improve ED.
