Aircraft Noise and Stress Hormone Release
We demonstrate cardiovascular effects of nighttime aircraft noise in young and healthy individuals with low cardiovascular risk. Nighttime aircraft noise increased plasma epinephrine levels, worsened sleep quality, and decreased pulse transit time, a parameter of arterial stiffness, which varies inversely to arterial blood pressure. A dose-dependent decrease in endothelial function after exposure to increasing levels of noise was also observed. Acute Vitamin C challenges improved endothelial function in a separate group of subjects exposed to Noise60. We found no effect of aircraft noise exposure on nocturnal motility, heart rate or blood cortisol, neutrophils, IL-6, or C-reactive protein.
Interestingly, a priming effect of aircraft noise on ED was observed, i.e. previous exposure to Noise30 caused Noise60 to have larger effects on endothelial function. These data demonstrate that aircraft noise can affect endothelial function, and that rather than habituation, prior exposure to noise seems to amplify the negative effect of noise on endothelial function. Although the mechanisms of these observations cannot be characterized at a molecular level in vivo in humans, it has been previously shown that other forms of mental stress lead to a decrease in endothelial function. With regards to the molecular mechanisms, previous studies indicate that noise leads to an up-regulation, rather than a downregulation, of the eNOS. Interestingly, such an increased eNOS activity does not necessarily result in improved endothelial responses. For instance, in animal models of diabetes and/or hypertension, increased expression of an uncoupled (superoxide-producing) eNOS is associated with impaired endothelial function (reviewed in). Since measurements of NO and/or superoxide production in the local vascular microenvironment are impossible to perform in humans, this question cannot be addressed at the present time. The improvement in FMD observed in our study 2 h after application of the antioxidant vitamin C in subjects exposed to Noise60 is compatible with this evidence, and it suggests that exposure to aircraft noise might lead to ED due to increased vascular oxidative stress.
We also demonstrate changes in PTT, a parameter that correlates inversely with changes in blood pressure. Briefly, PTT is measured as the time it takes a pulse wave to travel between two arterial sites. Rises in blood pressure cause vascular tone to increase, leading to increased arterial stiffness and a shorter PTT. As mentioned above, these data are compatible with those of the HYENA project, in which an increase prevalence of hypertension was reported in subjects exposed to nocturnal noise in the range of 50 dB (similar to our Noise60 condition; 46.3 dB). Similarly, acute noise events were associated in this study with increased systolic and diastolic blood pressure by 6.2 and 7.4 mmHg, a phenomenon which, interestingly, was not necessarily associated with awakenings.
With regard to the pathophysiological mechanism behind the changes in blood pressure and vascular function, we also report elevated epinephrine levels after exposure to noise. It has been demonstrated that intermittent release of adrenaline may be implicated in the development of hypertension. Epinephrine is released as a response to different stressors such as noise and increases the release and the effects of norepinephrine. Interestingly, increased epinephrine levels have been found in patients with borderline hypertension, suggesting a role in the early history of hypertension.
Importantly, increased plasma catecholamines have also been shown to correlate negatively with endothelial function as measured by FMD. A recent study has linked autonomic sympathetic activation to the development of hypertension in elderly patients independent of the cause of activation of the autonomic nervous system.
Our results are congruent with the growing amount of data linking short sleep duration or sleep disturbances of various kinds to the development of cardiovascular disease. For example, shift work has been shown to cause impaired endothelial function, sympathetic activation, and metabolic changes. Extensive evidence exists for the relation between obstructive sleep apnoea, hypertension, ED, and subsequently cardiovascular disease. Recently, the restless legs syndrome has been identified as another cause for sleep disruption, and it has been shown to increase the risk for myocardial infarction in women. There is ample evidence that nocturnal aircraft noise exposure disturbs and fragments sleep, leads to changes in sleep structure, increases sleepiness during the following day, and leads to impairments of cognitive performance. The results of our study suggest that these changes in sleep structure negatively affect the cardiovascular system, and that these changes, in the case of long-term exposure, may predispose to the development of hypertension and cardiovascular disease.
The study by design eliminated noise adaptation processes, which can often mask effects of environmental influences. Therefore, it is unclear whether the negative cardiovascular effects observed in this study persist after weeks or months with continued noise exposure. However, biologic adaptation is often incomplete and requires physiologic resources therefore also putting strain on the system as a whole. Effects of aircraft noise in population-based studies are likely to be mitigated by partial physiologic adaptation and avoidance of residential areas with high levels of noise exposure by highly sensitive individuals. Other environmental factors like air pollution, which has also been shown to influence endothelial function, may interfere with noise effects in epidemiological studies. Therefore, data from interventional studies may be helpful in judging the effect of nocturnal noise on cardiovascular health and disease.
The protocol was designed as a field study with minimal sleep disruption due to environment and equipment, thus creating ecologically valid conditions. We avoided on purpose a pure laboratory environment where ambient conditions, sound levels, and external stimuli can be controlled at the expense of creating artificial rather than familiar conditions. Sleep quality is very sensitive to changes in surroundings and study subjects usually show more pronounced alterations of sleep in the laboratory than in the field. There were no adaptation nights prior to study nights due to logistic constraints and because, since subjects were not required to sleep in non-familiar environments, our study design did not demand such adaptation. Reinforcing this, the analysis did not show a significant first-night effect for our primary outcome, which supports the validity of our study design and results. Study subjects were healthy, young, and with a female majority and are therefore not representative of the whole population. In general, younger adults usually show less sleep problems and disturbance than older persons when exposed to noise, and the fact that noise had an impact also on such a low-risk population rather emphasizes the potential clinical relevance of the present findings. Finally, endothelium-independent vasodilation was not systematically measured and the data are not presented: nitroglycerin responses were measured initially, but these measures were discontinued due to refusal by many study participants related to the side effects of the drug.
In a group of young and healthy volunteers, we found evidence for significant impairment of endothelial function after only one night of aircraft noise exposure with 60 noise events. Pointing to a significant contribution of oxidative stress in this phenomenon, these adverse changes of the vasculature were markedly improved by acute Vitamin C challenges. Endothelial dysfunction was paralleled by significant increases in circulating adrenaline levels and a substantial, dose-dependent decrease in sleep quality and an increase in systolic blood pressure. These findings indicate that hypertension observed in response to nighttime exposure to noise might be explained by increased sympathetic activation but also by the occurrence of vascular dysfunction. Accumulating data increasingly confirms that sleep disturbance of different causes might represent a novel, important health risk. An undisturbed night's sleep is important for health and well-being and should be protected as far as possible, and reducing nocturnal aircraft noise can therefore be regarded as a preventive measure for cardiovascular disease. Since the present studies demonstrate adverse effects of endothelial function and stress hormones in healthy adults, the implications for patients with known cardiovascular disease will need to be tested in further studies.
Discussion
We demonstrate cardiovascular effects of nighttime aircraft noise in young and healthy individuals with low cardiovascular risk. Nighttime aircraft noise increased plasma epinephrine levels, worsened sleep quality, and decreased pulse transit time, a parameter of arterial stiffness, which varies inversely to arterial blood pressure. A dose-dependent decrease in endothelial function after exposure to increasing levels of noise was also observed. Acute Vitamin C challenges improved endothelial function in a separate group of subjects exposed to Noise60. We found no effect of aircraft noise exposure on nocturnal motility, heart rate or blood cortisol, neutrophils, IL-6, or C-reactive protein.
Interestingly, a priming effect of aircraft noise on ED was observed, i.e. previous exposure to Noise30 caused Noise60 to have larger effects on endothelial function. These data demonstrate that aircraft noise can affect endothelial function, and that rather than habituation, prior exposure to noise seems to amplify the negative effect of noise on endothelial function. Although the mechanisms of these observations cannot be characterized at a molecular level in vivo in humans, it has been previously shown that other forms of mental stress lead to a decrease in endothelial function. With regards to the molecular mechanisms, previous studies indicate that noise leads to an up-regulation, rather than a downregulation, of the eNOS. Interestingly, such an increased eNOS activity does not necessarily result in improved endothelial responses. For instance, in animal models of diabetes and/or hypertension, increased expression of an uncoupled (superoxide-producing) eNOS is associated with impaired endothelial function (reviewed in). Since measurements of NO and/or superoxide production in the local vascular microenvironment are impossible to perform in humans, this question cannot be addressed at the present time. The improvement in FMD observed in our study 2 h after application of the antioxidant vitamin C in subjects exposed to Noise60 is compatible with this evidence, and it suggests that exposure to aircraft noise might lead to ED due to increased vascular oxidative stress.
We also demonstrate changes in PTT, a parameter that correlates inversely with changes in blood pressure. Briefly, PTT is measured as the time it takes a pulse wave to travel between two arterial sites. Rises in blood pressure cause vascular tone to increase, leading to increased arterial stiffness and a shorter PTT. As mentioned above, these data are compatible with those of the HYENA project, in which an increase prevalence of hypertension was reported in subjects exposed to nocturnal noise in the range of 50 dB (similar to our Noise60 condition; 46.3 dB). Similarly, acute noise events were associated in this study with increased systolic and diastolic blood pressure by 6.2 and 7.4 mmHg, a phenomenon which, interestingly, was not necessarily associated with awakenings.
With regard to the pathophysiological mechanism behind the changes in blood pressure and vascular function, we also report elevated epinephrine levels after exposure to noise. It has been demonstrated that intermittent release of adrenaline may be implicated in the development of hypertension. Epinephrine is released as a response to different stressors such as noise and increases the release and the effects of norepinephrine. Interestingly, increased epinephrine levels have been found in patients with borderline hypertension, suggesting a role in the early history of hypertension.
Importantly, increased plasma catecholamines have also been shown to correlate negatively with endothelial function as measured by FMD. A recent study has linked autonomic sympathetic activation to the development of hypertension in elderly patients independent of the cause of activation of the autonomic nervous system.
Our results are congruent with the growing amount of data linking short sleep duration or sleep disturbances of various kinds to the development of cardiovascular disease. For example, shift work has been shown to cause impaired endothelial function, sympathetic activation, and metabolic changes. Extensive evidence exists for the relation between obstructive sleep apnoea, hypertension, ED, and subsequently cardiovascular disease. Recently, the restless legs syndrome has been identified as another cause for sleep disruption, and it has been shown to increase the risk for myocardial infarction in women. There is ample evidence that nocturnal aircraft noise exposure disturbs and fragments sleep, leads to changes in sleep structure, increases sleepiness during the following day, and leads to impairments of cognitive performance. The results of our study suggest that these changes in sleep structure negatively affect the cardiovascular system, and that these changes, in the case of long-term exposure, may predispose to the development of hypertension and cardiovascular disease.
The study by design eliminated noise adaptation processes, which can often mask effects of environmental influences. Therefore, it is unclear whether the negative cardiovascular effects observed in this study persist after weeks or months with continued noise exposure. However, biologic adaptation is often incomplete and requires physiologic resources therefore also putting strain on the system as a whole. Effects of aircraft noise in population-based studies are likely to be mitigated by partial physiologic adaptation and avoidance of residential areas with high levels of noise exposure by highly sensitive individuals. Other environmental factors like air pollution, which has also been shown to influence endothelial function, may interfere with noise effects in epidemiological studies. Therefore, data from interventional studies may be helpful in judging the effect of nocturnal noise on cardiovascular health and disease.
Limitations of the Study
The protocol was designed as a field study with minimal sleep disruption due to environment and equipment, thus creating ecologically valid conditions. We avoided on purpose a pure laboratory environment where ambient conditions, sound levels, and external stimuli can be controlled at the expense of creating artificial rather than familiar conditions. Sleep quality is very sensitive to changes in surroundings and study subjects usually show more pronounced alterations of sleep in the laboratory than in the field. There were no adaptation nights prior to study nights due to logistic constraints and because, since subjects were not required to sleep in non-familiar environments, our study design did not demand such adaptation. Reinforcing this, the analysis did not show a significant first-night effect for our primary outcome, which supports the validity of our study design and results. Study subjects were healthy, young, and with a female majority and are therefore not representative of the whole population. In general, younger adults usually show less sleep problems and disturbance than older persons when exposed to noise, and the fact that noise had an impact also on such a low-risk population rather emphasizes the potential clinical relevance of the present findings. Finally, endothelium-independent vasodilation was not systematically measured and the data are not presented: nitroglycerin responses were measured initially, but these measures were discontinued due to refusal by many study participants related to the side effects of the drug.
Summary and Conclusions
In a group of young and healthy volunteers, we found evidence for significant impairment of endothelial function after only one night of aircraft noise exposure with 60 noise events. Pointing to a significant contribution of oxidative stress in this phenomenon, these adverse changes of the vasculature were markedly improved by acute Vitamin C challenges. Endothelial dysfunction was paralleled by significant increases in circulating adrenaline levels and a substantial, dose-dependent decrease in sleep quality and an increase in systolic blood pressure. These findings indicate that hypertension observed in response to nighttime exposure to noise might be explained by increased sympathetic activation but also by the occurrence of vascular dysfunction. Accumulating data increasingly confirms that sleep disturbance of different causes might represent a novel, important health risk. An undisturbed night's sleep is important for health and well-being and should be protected as far as possible, and reducing nocturnal aircraft noise can therefore be regarded as a preventive measure for cardiovascular disease. Since the present studies demonstrate adverse effects of endothelial function and stress hormones in healthy adults, the implications for patients with known cardiovascular disease will need to be tested in further studies.
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