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Year : 2010  |  Volume : 12  |  Issue : 47  |  Page : 95--109

Aircraft noise effects on sleep: Mechanisms, mitigation and research needs

Mathias Basner1, Barbara Griefahn2, Martin van den Berg3,  
1 Unit for Experimental Psychiatry, Division of Sleep and Chronobiology, University of Pennsylvania School of Medicine, Philadelphia, USA, German Aerospace Center (DLR), Institute of Aerospace Medicine, Cologne, Germany
2 Institute for Occupational Physiology, Dortmund University, Germany
3 Ministry of Environment, The Netherlands

Correspondence Address:
Mathias Basner
Unit for Experimental Psychiatry, Division of Sleep and Chronobiology, Department of Psychiatry, University of Pennsylvania School of Medicine, 1013 Blockley Hall, 423 Guardian Drive, Philadelphia, PA,19104-6021


There is an ample number of laboratory and field studies which provide sufficient evidence that aircraft noise disturbs sleep and, depending on traffic volume and noise levels, may impair behavior and well-being during the day. Although clinical sleep disorders have been shown to be associated with increased risk of cardiovascular diseases, only little is known about the long-term effects of aircraft noise disturbed sleep on health. National and international laws and guidelines try to limit aircraft noise exposure facilitating active and passive noise control to prevent relevant sleep disturbances and its consequences. Adopting the harmonized indicator of the European Union Directive 2002/49/EC, the WHO Night Noise Guideline for Europe (NNG) defines four Lnight , outside ranges associated with different risk levels of sleep disturbance and other health effects (<30, 30-40, 40-55, and >55 dBA). Although traffic patterns differing in number and noise levels of events that lead to varying degrees of sleep disturbance may result in the same Lnight , simulations of nights with up to 200 aircraft noise events per night nicely corroborate expert opinion guidelines formulated in WHO's NNG. In the future, large scale field studies on the effects of nocturnal (aircraft) noise on sleep are needed. They should involve representative samples of the population including vulnerable groups like children and chronically ill subjects. Optimally, these studies are prospective in nature and examine the long-term consequences of noise-induced sleep disturbances. Furthermore, epidemiological case-control studies on the association of nocturnal (aircraft) noise exposure and cardiovascular disease are needed. Despite the existing gaps in knowledge on long-term health effects, sufficient data are available for defining limit values, guidelines and protection concepts, which should be updated with the availability of new data.

How to cite this article:
Basner M, Griefahn B, Berg M. Aircraft noise effects on sleep: Mechanisms, mitigation and research needs.Noise Health 2010;12:95-109

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Basner M, Griefahn B, Berg M. Aircraft noise effects on sleep: Mechanisms, mitigation and research needs. Noise Health [serial online] 2010 [cited 2021 Dec 3 ];12:95-109
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The demand for mobility in general and air traffic in particular has been strongly increasing over the past few years. As a minimum interval between two starting or two landing planes is necessary for safety reasons, evasion of air traffic to shoulder hours and even the night-time has been observed in the past and will even increase in the future. Therefore, the strain of residents living in the vicinity of airports is likely to increase due to noise emitted from nocturnal air traffic. Most of the complaints about traffic noise concern the night, [1],[2] i.e. the time of the day when people try to sleep and regenerate mental and physical powers depleted during the day. In a representative German survey, when asked for reasons of existing sleep problems, external noise sources were mentioned in third position, outnumbered only by somatic disorders and problems of getting away from the strains of the day. [3] Another study reported that noise-induced sleep disturbances were stated in fourth position, by 12% of the observed sample. [4] Intensive night operations at airports caused fierce reactions in the population, often leading to a cessation of activities (e.g., Maastricht, Liege, and Oostende). According to Anotec, [5] 400,000 people are exposed to levels of Lnight > 45 dB (350,000 > 55 dB) around 53 major airports in the European Union and this is likely to increase to 550,000 in 2015, notwithstanding the continuous efforts to reduce the noise produced by individual airplanes.

Sleep experts around the world usually state that we still do not have sufficient knowledge on why we sleep. On the other hand, the fact that we sleep every night, and most animals do likewise, caused Rechtschaffen to remark: "If sleep doesn't serve an absolutely vital function, it is the biggest mistake evolution ever made". The best we can say is that sleep serves many functions, some of which could be demonstrated in humans, others in animals. Undisturbed sleep is a prerequisite for recuperation. The human organism recognizes, evaluates and reacts to environmental sounds even while asleep. [6] These reactions are part of an integral activation process of the organism and express themselves e.g. as changes in sleep structure or increases in heart rate. Environmental noise may decrease the restorative power of sleep by means of repeatedly occurring activations, where the extent of the reduction depends on the magnitude as well as on the frequency of these activations. [7] Probability and magnitude of the activation are predominantly influenced by the type and sound pressure level of the noise event, besides many other moderating factors. [8]

The World Health Organization (WHO) recently published the Night Noise Guideline for Europe (NNG) according to the WHO guidelines for epidemiological review. [9] The NNG extensively covers how noise may disturb sleep and how clinical sleep disorders may impair health. The document is current and most of the relevant studies on noise effects on sleep are covered. In order to avoid duplications, we will focus on aircraft noise, its mitigation and future research needs, which were not or less extensively covered in the NNG.

 Measurement of Sleep and Sleep Related Events

Polysomnography, i.e. the simultaneous recording of the electroencephalogram (EEG), the electrooculogram (EOG), and the electromyogram (EMG) remains the gold standard to measure sleep. According to specific conventions, [10],[11] the night sleep is usually divided into 30-second epochs. Depending on EEG frequency and amplitude, specific patterns in the EEG, muscle tone in the EMG, and the occurrence of slow or rapid eye movements in the EOG, different stages of sleep are assigned to each epoch. Wake is differentiated from sleep. Sleep is divided into rapid eye movement sleep (REM sleep) and non-REM sleep, which is again classified into light (stages S1 and S2) or deep sleep (stages S3 and S4, also called slow wave sleep - SWS). SWS and REM sleep seem to be very important for restoration and memory consolidation during sleep (see below). [12] Wake and S1 are typical indicators of disturbed or fragmented sleep, and they do not (or only very little) contribute to the recuperative value of sleep. [13]

Even shorter activations (≥3 seconds) in the EEG and EMG, so-called arousals that would not qualify to be scored as an awakening, can be detected with the polysomnogram. [11],[14] These arousals are usually accompanied by cardiac activations (see below) that may be responsible for long-term adverse health effects of noise on the cardiovascular system. [15],[16],[17] Sleep researchers recognized quite a while ago that only some of the symptoms of sleep disorders could be explained by changes in sleep macrostructure defined by Rechtschaffen and Kales (R&K). [10] It is assumed that sleep may be fragmented by many short arousals, leading to decreased sleep recuperation without relevant changes in sleep macrostructure, [18-20] however, the independence of changes in sleep macro- and microstructure are still controversial. [13],[21] In the meantime, EEG arousals are routinely scored in clinical sleep laboratories.

However, polysomnography also has some disadvantages. EEG, EOG, and EMG electrodes and wires are somewhat invasive and may influence sleep. The instrumentation of subjects is cumbersome and cannot be done by the subjects themselves. Finally, sleep stage classification requires trained personnel and is known to have high inter- and intra-observer variabilities. [22],[23] Hence, only a few polysomnographic noise effects studies have been conducted with relatively small sample sizes in the past. [24]

Several other methods can be used to measure sleep and the influence of noise on sleep. The easiest way to gather information on sleep is via questionnaires. However, the validity of this method is at least questionable as during most of the night the sleeper is unconscious and not aware of the surroundings. Only the process of falling asleep and longer wake periods during the night contribute to subjective estimates of sleep quality and quantity, which may therefore differ substantially from objective measures. [25] Nevertheless, subjective measures of noise-induced sleep disturbance are still important, as both objective and subjective criteria should be addressed or improved by noise mitigation measures.

Several studies investigated the influence of traffic noise on signaled awakening (also called behavioral awakening).[26],[27] Here, the subject has to give a prescribed signal (e.g. pressing a button) to indicate the awakening. However, the method has a low sensitivity and reliability. Consciousness is only regained during prolonged wake periods, and relevant activations of the central nervous system (CNS) may be missed. By demanding an active cooperation of the subject, the importance of the signal, reaction probability, and sleep itself may be altered. [28],[29] On the other hand, subjects may forget to give the signal or they may be too tired or languid to give the signal.

Actigraphy[30],[31] and seismosomnography[32] have been used to measure body movements during sleep. Although the number of EEG awakenings and the number of body movements are correlated, prolonged periods of wakefulness without body movements and awakenings not accompanied by body movements may be wrongly classified as sleep, whereas body movements without relevant activations of the central nervous system (CNS) may be wrongly classified as wake or a sleep disturbance, limiting the validity of actigraphy and seismosomnography.

Noise induces activations of the autonomic nervous system, like increases in blood pressure and heart rate, which can be measured easily with electrocardiography (ECG) or plethysmography. [33],[34] Repeated noise-induced autonomic activations may play a key role in the genesis of hypertension and associated cardiovascular diseases. However, as of today, there is no generally accepted convention on what exactly constitutes a cardiac arousal, e.g., how strong a heart rate increase must be in order to be classified as a relevant cardiac activation. Although Martin et al. [35] suggest that daytime functioning may be impaired by increases in the number of sub cortical arousals alone, this has been questioned by Wesensten et al. [13] because the procedure used by Martin et al. inevitably induced cortical arousals and changes in sleep structure besides autonomic activations. Recent findings of a carefully designed experiment by Guilleminault et al. [36] support the thesis that EEG arousals are a prerequisite for the detrimental effects of sleep fragmentation on daytime functioning. It is absolutely legitimate to use methods other than polysomnography in order to gather information on the effects of noise on sleep. However, one has to be aware that these alternative methods never cover all aspects of sleep. For example, relevant changes in sleep structure may be overlooked, or changes may be indicated without relevant activations of the CNS.

 Indicators of Noise-Induced Sleep Disturbance

The restorative power of sleep is not only influenced by sleep duration but also by sleep structure. Present scientific knowledge assumes that sleep stages differ in their recuperative value, although the functions of the different sleep stages and the mechanisms of these functions are still not exactly known. SWS is considered to be particularly important for the restorative power of sleep because of its proximity to sleep onset, its immediate rebound after sleep deprivation, and its association with high sensory thresholds and the excretion of growth hormones. [37] Results of the recent past indicate that both SWS and REM sleep are important for memory consolidation processes. [38],[39] Wake and Stage 1 do not contribute to the recuperative value of sleep or only very little, respectively, [13] whereas sleep stage S2 takes an intermediate position.

Arousals, sleep-stage changes, and awakenings are immediate effects of noise on sleep that can be detected in the polysomnogram indicating gradually increasing cortical excitations rather than qualitatively different responses. These alterations may either replace the respective spontaneous alterations (three to seven awakenings / hour and three to four times more arousals [40] ) that would have taken place at the same time or slightly later, anyway, or lead to an increase of their total number overnight (i.e., result in additional responses). The increasing frequency of these activations causes a general elevation of the arousal level, thus, reducing the time for slow-wave-sleep (SWS, deep sleep) and/or REM-sleep. Where the causal relations between noise events and immediate effects are obvious, the reduction of SWS and of REM sleep may be influenced by further environmental factors. There are, however, numerous studies supporting a causal relation between noise exposure and the reduction of SWS (see Annex).

Some of the event related effects, in particular awakenings, are subject to habituation. This explains for instance the discrepancies found in laboratory and field studies. [13] In contrast to awakenings, autonomic arousals do not seem to habituate, neither during the course of a night nor across successive nights. [41] There are two ways to investigate noise-induced sleep disturbances. An event-related analysis concentrates on the reactions (such as awakenings or body movements) of the sleeper to a single aircraft noise event (ANE). The other kind of analysis concentrates on structural changes in sleep based on the whole sleep period (e.g. sleep efficiency, wake after sleep onset, amounts of the different sleep stages, number of events per h sleep). Of course, both outcomes (event-related and whole night) are interrelated.

 Event-related Analysis

An event-related analysis establishes a direct temporal association between the occurrence of an ANE and the reaction of the investigated subject. [24,31,42] The reactions of sleeping subjects to aircraft noise are non-specific because they are also observed spontaneously in undisturbed nights or between noise events (spontaneously here meaning "of reasons other than noise"). Two important implications follow.

First, if the sleeper reacts while exposed to aircraft noise, it is unclear whether this reaction was induced by noise or spontaneous, because there is currently no method to identify the underlying cause of the reaction for a given single event. Three situations can be differentiated: [43],[44] (a) The reaction was caused by noise, (b) the reaction occurred spontaneously, (c) the reaction was caused by noise but would also have occurred spontaneously or the reaction occurred spontaneously but would also have been caused by noise. Situations (a) and (b) are non-ambiguous. In situation (c), the reaction can either be attributed to noise or classified as spontaneous. If the reaction is classified as spontaneous, the probability of reactions additionally caused by noise is calculated as:


Here, P noise is the reaction probability observed under the influence of noise, and P spontaneous is the reaction probability observed in undisturbed nights. If the reaction is attributed to noise, the probability of noise-induced reactions is calculated as:


As P spontaneous > 0, P induced is always greater than P additional , and the difference between both probabilities increases with increasing P spontaneous . However, the differences between P additional and P induced are usually small, as situation (c) is relatively rare compared to situations (a) and (b). The biologic plausibility of P additional is higher, [43],[44] and only reactions additionally caused by noise can be prevented with protection concepts, anyway.

From the above follows that noise induced events (awakenings, body movements, etc.) anticipate spontaneous alterations, i.e. these events would have also occurred without the noise event, only later. Hence, it may be possible that the overall number of adverse effects does not differ between nights with and without noise exposure. [45],[46] The recuperative value of the noise exposure night may nevertheless be reduced as the noise-induced effects are, in contrast to at least some of the spontaneous alterations, unplanned and not part of the physiological sleep process (especially in case (a) above). Furthermore, it is possible that sleep during noise-free intervals between noise events may be altered by noise exposure.

In a field study on aircraft noise effects, Passchier-Vermeer et al. [31] found that average motility was substantially higher than would be expected on the basis of the instantaneous extra motility at the times of the noise events, suggesting persistent arousal during sleep related to aircraft noise. In contrast to that in two independent laboratory studies on traffic noise effects on sleep, Basner et al. [45],[47] found no relevant difference in awakening frequency between ANEs compared to spontaneous awakening frequency in noise-free baseline nights in two laboratory studies on the effects of noise on sleep. It is not clear why the persistent arousal was observed in the field study but not in the laboratory studies, especially as higher degrees of sleep disturbance are usually observed in laboratory studies compared to field studies.

Second, a certain interval after the beginning of the noise event is usually screened for a reaction of the sleeper. On the one hand, this interval should be long enough to detect all noise-related reactions. On the other hand, if the interval is too long, too many spontaneous reactions are picked up, and repeated activations within the same subject are possible. [43],[44] On the single event level, several indicators for noise-induced sleep disturbance have been used: EEG awakenings (changes to stage wake from any other sleep stage), changes to stage wake or S1 from any other sleep stage, [24],[48] changes to lighter sleep stages (e.g. from S4 to S2), EEG arousals 11, signaled awakenings, [26],[27] or body movements [31] (see below).

However, it is currently unclear which indicator predicts long-term health effects of noise-disturbed sleep more reliably. [43] If polysomnography was performed, EEG awakenings have been used most often as indicators of noise-induced sleep disturbances for the following reasons:

Awakenings are the strongest form of activation of the sleeping organism. The consequences for the restorative functions of sleep are accordingly severe.Awakenings are relatively specific, i.e. the frequency of spontaneous awakenings is relatively low compared to other indicators. According to a normative study by Bonnet and Arand, [40] 2.9 to 7.3 spontaneous awakenings per hour total sleep time (TST) and 10.6 to 21.9 spontaneous EEG arousals per hour TST, i.e. three to four times more, can be found in healthy subjects depending on age.In contrast to EEG arousals, awakenings are usually accompanied by prolonged and unimodal increases in heart rate [33],[49] [Figure 1]. These cardiac activations seem to play an important role in the development of high blood pressure and associated diseases of the cardiovascular system (e.g., myocardial infarction, stroke). [48]The majority of awakenings lasts for exactly one sleep epoch (15 to 45 seconds) and, therefore, these awakenings are too short to be remembered on the next day. On the other hand, an awakening may last longer and, therefore, be associated with the occurrence of waking consciousness. Basner and Siebert [50] showed that the probability to recall an awakening the next morning increases steadily with awakening duration. Only noise-events perceived during periods with waking consciousness can result in annoyance because these longer awakenings may be recalled in the morning. In this case, they will also dominate the subjective assessment of sleep quality and quantity.Within the Ollerhead study, [42] a group of experts was asked to specify a suitable indicator for noise-induced sleep disturbances. Although different opinions existed, there was consensus that R&K EEG awakenings definitely indicated a relevant change in sleep structure.

A recent study [52] systematically compared polysomnographic indicators of noise-induced sleep disturbance and concluded that most information on sleep disturbances can be achieved by investigating robust classic parameters like awakenings or sleep stage changes to wake and S1, although American Sleep Disorders Association (ASDA) EEG arousals might add relevant information in situations with low maximum sound pressure levels (SPLs), chronic sleep deprivation or chronic exposure. On the whole night level, the different indicators for noise-induced sleep disturbance are correlated, e.g. the number of body movements usually increases with a simultaneously increasing number of EEG awakenings. However, these correlations are not 1, and reactions may occur independently of each other (e.g. awakenings without body movements and vice versa).

Event-related analyses on noise-induced awakenings only apply to subjects momentarily asleep. However, aircraft noise may not only induce awakenings from sleep, but it may interfere with the process of falling asleep again in subjects awake due to spontaneous or noise-induced awakenings. This may be especially problematic in early morning hours, where sleep pressure is usually low, the sleeper is easily aroused form sleep and it is harder to fall asleep again. [53] However, there are more complex models which are irrespective of the momentary sleep stage, capable of predicting total sleep structure based on the number and timing of aircraft noise events. [54],[55]

Dose-response relationships based on event-related analyses are presented below.

 Whole Night Sleep Parameters

Depending on their frequency, immediate noise effects on sleep (arousals, awakenings) cause a general elevation of the organism's arousal level that consequently leads to a redistribution of time spent in the different sleep stages with an increase of the amounts of wake and stage S1, and a decrease of SWS and REM-sleep. [51],[52],[56],[57] The alterations are, however, small. SWS was reduced by nine minutes in a study that focused on aircraft [57] and by 2.5 minutes in another study where aircraft, road and rail traffic noise was applied with the same equivalent and the same maximum levels. Road and rail traffic noise in the latter study caused a 4.6 and a 8.7 minutes decrease, respectively. [51] Compared to the impact of other sleep disorders like obstructive sleep apnea, where sleep may be heavily fragmented with a total loss of slow wave sleep, the noise induced changes in sleep structure are subtle. Nevertheless, in sensitive populations and in chronic exposure situations, they could well reach clinical relevance in terms of short-term (e.g. daytime sleepiness) or long-term (e.g. incidence of hypertension) health consequences.

Although these global noise-induced alterations may be influenced by other environmental influences (e.g. room temperature, other acoustic stimuli) there is sufficient evidence that these alterations are causally related to the intruding noise (see Annex.). A noise-induced prolongation of sleep onset latency is plausible and reported by some authors, but this alteration has not been studied sufficiently, and noise exposure was started after sleep onset in many studies.

These alterations of whole night changes in sleep structure depend crucially on the number of noise events, the acoustical properties (like LAmax ) of noise events, the placement of noise events within the night and on noise-free intervals between noise events. [54],[55]

 Dose-response Relationships

Several studies derived dose-response relationships between acoustical properties of a single ANE (e.g. Lmax , LAE) and the respective reactions of the sleeper (e.g. EEG awakenings, body movements, signaled awakenings). Five dose-response relationships based on field study data are shown in [Figure 2].

The "FICAN 1997" curve was published by the Federal Interagency Committee on Aviation Noise in 1997. [58] It combines several field studies on the effects of aircraft noise on signaled (or behavioral) awakening. [58] According to FICAN, the "curve represents the upper limit of observed field data, and should be interpreted as predicting the 'maximum percent of the exposed population expected to be behaviorally awakened".

p (behavioral awakening, FICAN) =

8.7*10 -3 *(LAE - 30) 1.79 (1)

Passchier-Vermeer [59] used 110 aggregated data points derived from eight field studies on commercial aviation noise and behavioral awakening to derive the following dose-response relationship based on 175,000 ANEs:

p(additional behavioral awakening, P-V) =

-0.564*1.909*10 -4 *LAE 2 (2)

The TNO curve is based on actigraphy data of 418 subjects who were investigated for 10 consecutive nights in the vicinity of Amsterdam airport. [31] Here, the probability of (the onset of) body movements additionally induced by aircraft noise is shown on the ordinate depending on LAmax

p(additional onset of motility, TNO) =

3.14*10 -5 *(Lmax - 32) 2 + 6.33*10 -4 *(Lmax - 32) (3)

The DLR curve is based on 576 subject nights of 61 subjects investigated in a polysomnographic field study in the vicinity of Cologne/Bonn airport. [24] Here, the probability of EEG awakenings additionally induced by aircraft noise (see chapter 3.1 for definition of additional awakenings) are shown on the ordinate depending on LAmax

p(additional EEG awakening, DLR) =

1.894*10 -3 *Lmax 2 + 4.008*10 -4 * Lmax - 3.3243*10 -2 (4)

The "Elias and Finegold" [60] curve is based on a meta-analysis of eight field studies on behavioral awakening due to aircraft noise.

p(behavioral awakening, Elias & Finegold) =

0.58 + 4.3*10 -8 *LAE4.11 (5)

All five dose-response curves show monotonously increasing reaction probabilities with simultaneously increasing LAmax . The dose-response curve for behavioral additional awakening derived by Passchier-Vermeer predicts considerably fewer behavioral awakenings at the same LAmax compared to the FICAN and Elias and Finegold curve, most likely for two reasons. First, the FICAN curve predicts the maximum, not the average, percent of the exposed population expected to be behaviorally awakened. Second, the FICAN and the Elias and Finegold curves seem to include spontaneous behavioral awakenings, whereas the Passchier-Vermeer curve concerns behavioral awakenings additional to spontaneous awakenings. Compared to FICAN (behavioral awakening) and TNO (motility), the steepness of the DLR curve is a little higher. Interestingly, both TNO and DLR dose-response relationships emerge from the background reaction probability at very low maximum sound pressure levels (32 and 33 dBA, respectively). This is physiologically plausible; noise-induced reactions should be observed once the human auditory system is able to differentiate the ANE from background noise (which was assumed at 27.1 dBA in the DLR regression model). However, it must be pointed out that reaction probabilities just above the threshold are very low, i.e. only a minority of affected people will actually react to ANEs with LAmax near the threshold.

It has been repeatedly observed that at the same LAmax , reaction probabilities derived from laboratory studies exceed those derived from field studies, [53],[61] which may be at least in part explained by the familiar environment, the familiar sound exposure, and partly habituated subjects in field studies compared to the laboratory. [62] However, this habituation is not complete, and it does not (or to a lesser extent) seem to involve autonomic responses like increases in blood pressure and heart rate. [63] Because of the higher ecologic validity, dose response relationships from field studies should be preferably used for aircraft noise protection concepts (see below). However, laboratory studies remain an important instrument for the investigation of basic noise effect mechanisms.

Of course, LAmax or LAE explain only parts of the variance in reaction behavior. The latter is also influenced by individual (e.g. noise sensitivity, age, gender), situational (e.g. current sleep stage, elapsed sleep time), and acoustic factors other than LAmax or LAE, which can be incorporated in regression models that predict reaction probability. For example, the DLR dose-response curve includes background noise level, prior sleep stage, and elapsed sleep time as well as LAmax . [24]

 Mitigation of Aircraft Noise Effects

Obviously, the best way to minimize the effects of noise is to reduce noise emitted from the aircraft, which can be achieved both technologically (reduction of engine noise, aerodynamic noise) and operationally (noise reduced starting and landing procedures). These measures should be promoted but are not discussed in this paper.

Noise protection of sleeping residents can be achieved either by restricting the number of permissible flights (including curfews, active noise control) or by sound insulation (passive noise control). Night-time traffic curfews will be discussed separately from concepts that concede sound insulation to airport residents once a certain limit value is exceeded.

Traffic curfews

Besides the number of affected subjects living in the vicinity of an airport, the magnitude of noise effects on sleep is mainly determined by the time of going to bed, wake-up time and sleep duration, which vary considerably between individuals. Regarding noise protection, a curfew should cover those time periods when most of the people are "in bed" with the intention to sleep. The proportion of time in bed covered by a curfew is determined by the position and duration of the curfew; each curfew duration has an optimal position maximizing the proportion of covered time in bed [Figure 3]. Information on sleep habits of the population is needed to determine the optimal position. This information can be extracted from time use and other surveys. For the analysis presented below, data extracted from a representative survey of 2,312 subjects, aged 17-97 years, living in the vicinity of Frankfurt Airport were used. [64] Obviously, conclusions will differ based on the sleep habits of the population of interest, i.e. they will most likely differ between different countries.

[Figure 3]a shows the proportion of the 17-97 year old population in bed depending on time of day. The leaps in the relative frequency distribution are caused by preferences of the respondents to specify "round" times like 22:00 or 22:30. More than 90% of the adult population was in bed between 0:00 and 6:00; before 22:00 not more than 3.4% and after 8:00 not more than 5.5% were in bed. [65]

[Figure 3]b shows the proportion of time in bed covered by five, six, seven and eight-hour curfews depending on curfew start time. The optimal start time, defined as the time where the curfew covers most of the time in bed, shifts to earlier start times with increasing curfew duration. Optimal curfew times depending on curfew duration were: 0:30-5:30 (five-hour curfew, 63.2% of time in bed covered), 0:00-6:00 (six-hour curfew, 75.1% covered), 23:30-6:30 (seven-hour curfew, 84.8% covered), and 23:00-7:00 (eight-hour curfew, 92.7% covered).

Obviously, night-time traffic curfews oppose the existing demand for freight and passenger traffic during the night. A potentially problematic side-effect of night-time traffic curfews is that part of the traffic which would have otherwise taken place during the night may be rescheduled to hours before and after the curfew, thus increasing traffic during shoulder hours of the day. Therefore, aircraft noise is likely to increase for individuals who go to bed or have to go to bed very early or very late (children, shift-workers). Additionally, traffic during shoulder hours, and therefore outside the defined night period from 22:00 to 6:00, is usually not part of night-time noise regulations or protection concepts. Generally air traffic during shoulder hours should be part of protection concepts, at least at airports with substantial amount of air traffic during shoulder hours. [54],[55],[65]

Passive noise control

Passive noise control is equivalent to sound insulation of the bedroom. It usually involves the installation of ventilators that allow affected people to close the windows during the night. In areas with high levels of noise exposure, more extensive sound insulation measures like the installation of special windows and the insulation of the building faηade are taken. However, although passive noise control is effective in the sense that it reduces SPLs in the bedroom and therefore reduces the degree of sleep disturbance, it also has disadvantages: Ventilators make noise, and the resulting air quality within the bedroom may be lower compared to open or tilted windows, especially during warm summer nights. The choice of the sleeping site is restricted to the (sound insulated) bedroom. These disadvantages may be the reason for comparatively low acceptance rates of sound insulation measures. On the one hand, not all residents eligible for sound insulation measures have them installed and, on the other hand, the usage rates of sound insulation measures by those who have them installed are astonishingly low. In a field study on the effects of aircraft noise on sleep, [66] of the subjects who had sound insulation measures installed, only 31% slept with closed windows, while 61% slept with tilted and seven per cent with fully opened windows.

Sound insulation measures are usually, at least partially, financed by the airport once certain limit values are exceeded. These limit values are usually based on national law, although special rules may apply at specific airports. The integrated noise measure LAeq is most often used for the definition of limit values and protection zones. Here, all ANEs occurring within a reference period (e.g., 22:00 to 6:00) are averaged. It is implicitly assumed that if the maximal permissible LAeq is not exceeded, no relevant adverse noise effects will be observed in the population that is to be protected. However, the acoustic prognosis usually refers to long time periods (e.g., the busiest six months of the year). Depending on weather conditions, actual noise exposure within a given night may exceed average values. Limit values should be chosen accordingly; i.e. associated noise effects in single nights with higher than average noise exposure should be tolerable for a few nights.

More recently, concepts explicitly limiting the degree of sleep fragmentation have been developed. [24],[67],[68] Aircraft noise is intermittent, i.e. each ANE is perceived as a single entity by the organism and hence the above mentioned concepts are based on reaction probabilities to single noise events [see exposure-response functions shown in [Figure 2]]. They also try to take into account that the probability of physiologic reactions to noise events depends, among others, on maximum SPL or sound exposure level (LAE ), on the number of noise events, and on the placement of noise events within the night. This information is lost in the process of energetically averaging all noise events within a given period to derive LAeq , and different traffic scenarios may calculate to the same LAeq but nevertheless lead to different degrees of sleep fragmentation, which is illustrated in [Figure 4].

However, the calculations put forward in the alternative concepts assume that reactions to consecutive noise events are independent of each other, which is unlikely. [43],[69] Awakening probabilities were shown to depend on the number of preceding noise events, the noise-free interval between events, and time of night. [53],[70] Non-independence of noise events may, depending on the noise pattern, lead to increases or decreases of whole night sleep disturbance levels. More complex models taking these interactions into account already exist, [50],[54],[55] but their validity still has to be established. Also, dose-response curves are usually based on the average response in the investigated population. If protection concepts are based on this average response, the protection will necessarily be too high for some and too low for other parts of the population. In order to prevent that considerable parts of the population are not well enough protected, preventive measures such as artificially elevating the dose-response curve or setting lower limit values than necessary can be taken (based on the average reaction in the population). [71]

 WHO's Night Noise Guideline for Europe

According to the Environmental Noise Directive (END, European Union Directive 2002/49/EC), European Union Member States have to produce maps indicating noise exposure to traffic noise. Based on these noise maps, action plans have to be generated. END proposes Lnight as the night-time noise indicator for sleep disturbances. Lnight is defined as "A-weighted long-term average sound level as defined in ISO 1996-2: 1987, determined over all night periods of a year measured four meters high outside the faηade." Noise events in the period between 23:00 and 7:00 contribute to the calculation of Lnight . Following the harmonized indicator of END, WHO's Night Noise Guideline for Europe (NNG) [9] defines ranges of the continuous sound level Lnight,outside [Table 1]. The category boundaries (55 dB, 40 dB, and 30 dB) are defined as interim and final targets by NNG.

Data from the DLR field study on the effects of aircraft noise on sleep were used to simulate single nights with 1 to 200 ANEs per night. Both Lnight,outside and the number of additional EEG awakenings induced by aircraft noise according to the DLR 2006 exposure-response function [24] shown in [Figure 2] were calculated and used to predict the degree of sleep fragmentation based on Lnight,outside . The results are shown in [Figure 5]a.

The exposure-response relationship, as shown in [Figure 5]a, supports the expert consensus of the NNG nicely. The expected number of awakenings additionally induced by aircraft noise per year according to [Figure 5]a is given for each Lnight,outside range in [Table 1].

The relevance of the number of noise events for sleep disturbance is shown in [Figure 5]b, demonstrating that at the same Lnight , the degree of sleep fragmentation may differ substantially depending on the number of noise events contributing to this Lnight . At Lnight 55 dB, the number of additional EEG awakenings induced by aircraft noise per year increases from 106 (N = 20 noise events), to 192 (N = 40), to 262 (N = 60), to 323 (N = 80), and to 375 (N = 100). [Figure 5]b, therefore, illustrates that additional information on the number of noise events contributing to Lnight would substantially increase the precision of the prediction of the degree of sleep disturbance. The END explicitly states that it may be advantageous to use maximum SPL (LAmax ) or sound exposure levels (LAE ) as supplementary noise indicators for night period protection. In reality, it may be more practical to gather information on the average number of noise events contributing to Lnight .

 Vulnerable Groups

Children have higher awakening thresholds than adults and therefore are often seen to be less sensitive to night noise. [72] However, children are developmentally in a very sensitive phase and relatively minor sleep disturbances may have detrimental effects for the development of the child. Additionally, children also spend more time in bed and usually go to bed and get up during busy shoulder hours. For these reasons children are considered a risk group. Since with age sleep structure becomes more fragmented, elderly people are more vulnerable to noise induced sleep disturbance. This also happens in pregnant women and people with ill health, so they too are a group at risk.

Finally, shift workers are under a particular risk. [73],[74] They must sleep during the day at an adverse phase of their circadian rhythm, which already causes a partial sleep deprivation by two to four hours. In addition, daytime equivalent noise levels are 8 to 15 dBA higher compared to the night. However, little is known about the contribution of noise to the sleep disturbances of shift workers.

 Relationship Between Noise, Sleep Disturbance, and Health

Although the odds ratios are usually low, there is sufficient evidence that traffic noise exceeding equivalent continuous noise levels LAeq of 60 dB outside during the day are associated with higher risks of cardiovascular events, and therefore impair health. [16] Recent epidemiological research suggests that long-term aircraft noise exposure increases the risk for cardiovascular disease, especially if people are exposed during the night. The HYENA study involved 4,861 persons, 45-70 years of age, who had lived at least for five years near any of six major European airports. [75] For night-time aircraft noise, a 10-dB increase in exposure was associated with an odds ratio of 1.14 (95% confidence interval (CI), 1.01-1.29). The exposure-response relationships were similar for road traffic noise and stronger for men with an OR of 1.54 (95% CI, 0.99-2.40) in the highest exposure category (> 65 dB; ptrend = 0.008).

As the night is almost exclusively used for sleeping, nocturnal noise effects research assumes that not only short term effects [pathway "a" in [Figure 6]] but also long-term effects of noise [pathway "b" in [Figure 6]] are determined or at least mediated by effects of noise on sleep. There is an ample amount of studies that have investigated the effects of nocturnal noise on sleep and immediate consequences with polysomnography, actigraphy, seismosomnography, signaled awakening, and questionnaires, and there is no doubt that noise affects sleep relevantly [pathway "a" in [Figure 6]]. [76] However, all these studies were restricted in sample size and age range, usually involved healthy subjects only and did not include risk-groups.

Therefore, the representativeness of these studies and their results (e.g. derived exposure response curves) is restricted. One way to handle the lack of representativeness is to adopt limit values that are lower than would be needed to protect the observed samples. But this is unsatisfactory, as it remains uncertain whether the chosen protection level is too high or too low. Although prospective studies are extremely scarce, [77] there is evidence that clinical sleep disorders leading to chronically disturbed sleep increase the incidence of cardiovascular disease [78],[79] and therefore impair health (equivalent to pathway "b" in [Figure 6]).

Although these sleep disorders disturb sleep in similar ways, as noise (increased sleep fragmentation), the mechanisms are not identical. For instance, sleep disordered breathing not only leads to sleep fragmentation, but also to periodic decreases in hemoglobin oxygen saturation and periodic increases in intra-thoracic pressure; the latter may at least in part be responsible for the associated higher risk of cardiovascular disease. It is therefore unclear whether noise-induced sleep fragmentation will lead to similar consequences comparable to clinical sleep disorders.

 Research Needs

First, large scale field studies on the effects of nocturnal (aircraft) noise on sleep are needed. These should involve representative samples of the population and also include risk groups like children and chronically ill subjects. Methodologically relevant physiological variables should be assessed and the SPLs should be recorded inside and outside the dwelling. If the study was prospective and involved relevant health outcomes (e.g. incidence of hypertension), it would be possible not only to gain relevant knowledge on pathway "a" in [Figure 6], but also on pathway "b". However, these studies can be costly and are difficult to conduct.

Second, well-designed epidemiological case-control studies of adequate size on the association of nocturnal (aircraft) noise exposure and cardiovascular disease are needed. Because of long induction periods, it is extremely important that the assessment of noise exposure (past and present) is as accurate as possible in order to avoid random misclassification of exposure leading to bias towards the null.

Third, research on noise mitigation measures is needed to establish whether they are effective in reducing noise induced sleep disturbances and to improve the protection of affected residents in the long run.

Future legislation and protection concepts against adverse effects of nocturnal (aircraft) noise should be based on experimental studies on acute effects of noise on sleep as well as epidemiological studies on long-term health effects of nocturnal noise exposure, for the following reasons: If legislation is solely based on studies on acute effects of noise on sleep, although a sound sleep may be guaranteed, it remains unclear whether long-term health effects will also be obviated. On the other hand, protection concepts based on epidemiological studies may guarantee that long-term health is not adversely affected by noise exposure; however, it remains unclear whether this also assures a sound sleep. In practice, protection zones based on studies on the acute effects of noise on sleep and on epidemiological studies will most likely overlap to a large extent.


Parts of this manuscript are based on our input to a WHO workshop "Aircraft Noise and Health: Evidence Review Meeting" held on October 11-12, 2007 in Bonn, Germany. We would like to thank Rokho Kim for his valuable input to this manuscript. Dr. Basner has received compensation for consulting from Purdue University for the FAA PARTNER Center of Excellence Project 25B. Dr. Basner has made a paid presentation to the American Academy of Sleep Medicine (AASM). Both Dr. Basner and Dr. Griefahn have made paid presentations to the World Health Organization (WHO, German office).


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