Mathias Basner

Auditory and non-auditory effects of noise on health

Noise is pervasive in everyday life and can cause both auditory and non-auditory health effects. Noise-induced hearing loss remains highly prevalent in occupational settings, and is increasingly caused by social noise exposure (eg, through personal music players). Our understanding of molecular mechanisms involved in noise-induced hair-cell and nerve damage has substantially increased, and preventive and therapeutic drugs will probably become available within 10 years. Evidence of the non-auditory effects of environmental noise exposure on public health is growing. Observational and experimental studies have shown that noise exposure leads to annoyance, disturbs sleep and causes daytime sleepiness, affects patient outcomes and staff performance in hospitals, increases the occurrence of hypertension and cardiovascular disease, and impairs cognitive performance in schoolchildren. In this Review, we stress the importance of adequate noise prevention and mitigation strategies for public health.

Cardiovascular effects of environmental noise exposure

The role of noise as an environmental pollutant and its impact on health are being increasingly recognized. Beyond its effects on the auditory system, noise causes annoyance and disturbs sleep, and it impairs cognitive performance. Furthermore, evidence from epidemiologic studies demonstrates that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, and stroke. Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. This review focuses on the cardiovascular consequences of environmental noise exposure and stresses the importance of noise mitigation strategies for public health.

Aircraft noise effects on sleep: Application of the results of a large polysomnographic field study

The Institute of Aerospace Medicine at the German Aerospace Center (DLR) investigated the influence of nocturnal aircraft noise on sleep in polysomnographic laboratory and field studies between 1999 and 2004. The results of the field studies were used by the Regional Council of Leipzig (Germany) for the establishment of a noise protection plan in the official approval process for the expansion of Leipzig/Halle airport. Methods and results of the DLR field study are described in detail. Special attention is given to the dose-response relationship between the maximum sound pressure level of an aircraft noise event and the probability to wake up, which was used to establish noise protection zones directly related to the effects of noise on sleep. These protection zones differ qualitatively and quantitatively from zones that are solely based on acoustical criteria. The noise protection plan for Leipzig/Halle airport is presented and substantiated: (1) on average, there should be less than one additional awakening induced by aircraft noise, (2) awakenings recalled in the morning should be avoided as much as possible, and (3) aircraft noise should interfere as little as possible with the process of falling asleep again. Issues concerned with the representativeness of the study sample are discussed.

Sleep deprivation and neurobehavioral dynamics

Lifestyles involving sleep deprivation are common, despite mounting evidence that both acute total sleep deprivation and chronically restricted sleep degrade neurobehavioral functions associated with arousal, attention, memory and state stability. Current research suggests dynamic differences in the way the central nervous system responds to acute versus chronic sleep restriction, which is reflected in new models of sleep-wake regulation. Chronic sleep restriction likely induces long-term neuromodulatory changes in brain physiology that could explain why recovery from it may require more time than from acute sleep loss. High intraclass correlations in neurobehavioral responses to sleep loss suggest that these trait-like differences are phenotypic and may include genetic components. Sleep deprivation induces changes in brain metabolism and neural activation that involve distributed networks and connectivity.

Agreement Between 24-Hour Salt Ingestion and Sodium Excretion in a Controlled Environment

Accurately collected 24-hour urine collections are presumed to be valid for estimating salt intake in individuals. We performed 2 independent ultralong-term salt balance studies lasting 105 (4 men) and 205 (6 men) days in 10 men simulating a flight to Mars. We controlled dietary intake of all constituents for months at salt intakes of 12, 9, and 6 g/d and collected all urine. The subjects’ daily menus consisted of 27 279 individual servings, of which 83.0% were completely consumed, 16.5% completely rejected, and 0.5% incompletely consumed. Urinary recovery of dietary salt was 92% of recorded intake, indicating long-term steady-state sodium balance in both studies. Even at fixed salt intake, 24-hour urine collection for sodium excretion (UNaV) showed infradian rhythmicity. We defined a ±25 mmol deviation from the average difference between recorded sodium intake and UNaV as the prediction interval to accurately classify a 3-g difference in salt intake. Because of the biological variability in UNaV, only every other daily urine sample correctly classified a 3-g difference in salt intake (49%). By increasing the observations to 3 consecutive 24-hour collections and sodium intakes, classification accuracy improved to 75%. Collecting seven 24-hour urines and sodium intake samples improved classification accuracy to 92%. We conclude that single 24-hour urine collections at intakes ranging from 6 to 12 g salt per day were not suitable to detect a 3-g difference in individual salt intake. Repeated measurements of 24-hour UNaV improve precision. This knowledge could be relevant to patient care and the conduct of intervention trials.

Mars 520-d mission simulation reveals protracted crew hypokinesis and alterations of sleep duration and timing

The success of interplanetary human spaceflight will depend on many factors, including the behavioral activity levels, sleep, and circadian timing of crews exposed to prolonged microgravity and confinement. To address the effects of the latter, we used a high-fidelity ground simulation of a Mars mission to objectively track sleep–wake dynamics in a multinational crew of six during 520 d of confined isolation. Measurements included continuous recordings of wrist actigraphy and light exposure (4.396 million min) and weekly computer-based neurobehavioral assessments (n = 888) to identify changes in the crews activity levels, sleep quantity and quality, sleep–wake periodicity, vigilance performance, and workload throughout the record-long 17 mo of mission confinement. Actigraphy revealed that crew sedentariness increased across the mission as evident in decreased waking movement (i.e., hypokinesis) and increased sleep and rest times. Light exposure decreased during the mission. The majority of crewmembers also experienced one or more disturbances of sleep quality, vigilance deficits, or altered sleep–wake periodicity and timing, suggesting inadequate circadian entrainment. The results point to the need to identify markers of differential vulnerability to hypokinesis and sleep–wake changes during the prolonged isolation of exploration spaceflight and the need to ensure maintenance of circadian entrainment, sleep quantity and quality, and optimal activity levels during exploration missions. Therefore, successful adaptation to such missions will require crew to transit in spacecraft and live in surface habitats that instantiate aspects of Earths geophysical signals (appropriately timed light exposure, food intake, exercise) required for temporal organization and maintenance of human behavior.

Effect of nighttime aircraft noise exposure on endothelial function and stress hormone release in healthy adults

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.

Sleep deprivation potentiates HPA axis stress reactivity in healthy adults.

OBJECTIVE This article describes an experiment that was designed to investigate the effects of sleep deprivation on physiological stress responses in healthy adults. METHOD Twenty-six participants, ages 22-49, completed a 3-night laboratory experiment with randomization to one night of sleep-deprivation or a normal-sleep control condition. After a night of baseline sleep, 12 participants were sleep deprived and 14 were not. After the sleep manipulation, each participant completed the Trier Social Stress Test, a task that requires delivering a speech and performing difficult arithmetic in front of a stern, three-person panel. The stressor was administered from 5:00 p.m.-5:30 p.m. and saliva samples were collected 20 and 5 min before (baseline) and 5, 20, and 40 min after the stressor. Samples were assayed for cortisol (a biomarker for the HPA axis) and alpha-amylase (a putative biomarker for the sympatho-adrenal medullar system). RESULTS Sleep deprivation was associated with higher cortisol levels at baseline (p < .0001) and an amplified cortisol response to the stressor relative to control participants (pinteraction = 0.0039). Alpha-amylase showed a significant main effect of the stressor (p = .0026), but there was no effect of sleep loss at baseline or in response to the stressor. CONCLUSIONS Sleep deprivation is associated with both elevated resting cortisol release and with an exaggerated cortisol response to a stressor indicative of elevated HPA axis responses in healthy adults. Individual differences in the magnitude of this response may represent a risk factor for psychological and physical health consequences associated with heightened cortisol exposure.

How acute total sleep loss affects the attending brain: a meta-analysis of neuroimaging studies.

STUDY OBJECTIVES Attention is a cognitive domain that can be severely affected by sleep deprivation. Previous neuroimaging studies have used different attention paradigms and reported both increased and reduced brain activation after sleep deprivation. However, due to large variability in sleep deprivation protocols, task paradigms, experimental designs, characteristics of subject populations, and imaging techniques, there is no consensus regarding the effects of sleep loss on the attending brain. The aim of this meta-analysis was to identify brain activations that are commonly altered by acute total sleep deprivation across different attention tasks. DESIGN Coordinate-based meta-analysis of neuroimaging studies of performance on attention tasks during experimental sleep deprivation. METHODS The current version of the activation likelihood estimation (ALE) approach was used for meta-analysis. The authors searched published articles and identified 11 sleep deprivation neuroimaging studies using different attention tasks with a total of 185 participants, equaling 81 foci for ALE analysis. RESULTS The meta-analysis revealed significantly reduced brain activation in multiple regions following sleep deprivation compared to rested wakefulness, including bilateral intraparietal sulcus, bilateral insula, right prefrontal cortex, medial frontal cortex, and right parahippocampal gyrus. Increased activation was found only in bilateral thalamus after sleep deprivation compared to rested wakefulness. CONCLUSION Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity.

Event-related awakenings caused by nocturnal transportation noise.

The present study focussed on awakenings caused by nocturnal noises emitted from aircraft, road and rail vehicles with maximum levels ranging from 40 to 76 dBA. A laboratory study with 24 participants (12 male, 12 female, 19-28 years) was performed with polysomnographic recordings during 13 nights (including a preceding habituation night). Multivariable random subject effect logistic regression models containing acoustical, situational and individual parameters were used to determine the probability of event-related awakenings for each traffic mode. Awakening probability increased significantly with maximum sound pressure level (SPL), slope of rise (dB/s), noise duration and the noise-free interval between noise events. Gender, noise sensitivity and age did not influence awakening probability significantly (the latter only in a combined model). Awakening probability increased with elapsed time after sleep onset, and was significantly lower during slow wave sleep compared to S2 sleep, but not during REM sleep. After adjusting for differences in study design (acoustical macrostructure), awakening probability decreased in the order rail, road and air traffic noise, but only rail and air traffic noise differed significantly (p= 0.002). After further adjusting for slope of rise and noise duration (acoustical microstructure), differences between traffic modes decreased, but rail and air traffic noise still differed significantly (p=0.044). Acoustical properties other than slope of rise and noise duration may account for the residual difference. The results of this study suggest that the reduction of maximum SPLs, rise slopes, and traffic volume during the second part of the night might reduce the number of noise-induced awakenings.