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Year : 2010  |  Volume : 12  |  Issue : 47  |  Page : 129--136

Experimental studies on the effects of nocturnal noise on cortisol awakening response

Barbara Griefahn, Sibylle Robens 
 Leibniz Research Centre for Working Environment and Human Factors at TU Dortmund University, Ardeystr. 67, D-44139 Dortmund, Fed. Rep., Germany

Correspondence Address:
Barbara Griefahn
Leibniz Research Centre for Working Environment and Human Factors at TU Dortmund University, Ardeystr. 67, D-44139 Dortmund, Fed. Rep


Cortisol awakening response (CAR), a considerable increase in cortisol concentrations post-awakening, is considered a reliable indicator of the reactivity of the hypothalamus-pituitary-adrenal axis (HPA). As noise has been shown to activate the HPA-axis, this analysis focuses on CAR as a possible indicator of noise-induced sleep disturbances. This analysis focuses on CAR using two studies. In Study 1, six women and six men (18-26 years) slept for 13 nights each in the laboratory. They were exposed to the noises of three different trains, each with 20, 40 or 80 pass-bys, with equivalent noise levels varying between 44 and 58 dBA, on nine nights. In Study 2, 23 persons slept first for four nights and then four days, in the laboratory; finally 23 persons slept in the reverse order. During six sleep periods, they were randomly exposed to road or rail traffic noises with L Aeq varying between 42 and 56 dBA. To determine the CAR, salivary cortisol concentrations were ascertained in both studies after night sleep immediately after awakening, and 15 and 45 minutes later; in Study 2 also after 30 and 60 minutes later. The time of awakening was determined using the polysomnogram and the participants rated their subjective sleep quality every morning. Subjective sleep quality was rated worse after noisy when compared to quiet nights. CAR was, however, attenuated only after the noisiest nights in a subgroup of Study 2. These persons had just performed a sequence of four consecutive night shifts. They were obviously still in the process of re-adjustment to their usual day-oriented schedule and probably in a state of elevated vulnerability. The study concludes that nocturnal noise exposure affects the CAR only if a person is in a state of at least temporarily elevated vulnerability.

How to cite this article:
Griefahn B, Robens S. Experimental studies on the effects of nocturnal noise on cortisol awakening response.Noise Health 2010;12:129-136

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Griefahn B, Robens S. Experimental studies on the effects of nocturnal noise on cortisol awakening response. Noise Health [serial online] 2010 [cited 2022 Sep 28 ];12:129-136
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Cortisol is the major mediator of the neuroendocrine response to stress. Its diurnal profile represents the secretory activity of the hypothalamus-pituitary-adrenal axis (HPA). Cortisol levels are lowest around midnight and increase steadily during late sleep. A characteristic feature is the cortisol awakening response (CAR), i.e. an enhanced increase within the first hour post-awakening followed by a gradual decline during the day. [1],[2],[3] The CAR that indicates the reactivity of the HPA-axis [1] is highly stable across days and even weeks in one and the same individual; however, it varies remarkably between individuals, thus, possibly reflecting a personal trait. [1],[3],[4],[5],[6] Its extent is not determined by age, smoking habits, sleep duration and sleep quality, mode of awakening (spontaneous vs. alarm), body posture, normal ambulatory activity or the environment (home, laboratory). [1],[4],[5],[7],[8],[9],[10] The CAR is, however, modified by gender, stress, possibly by light intensity and by the temporal location of sleep that changes repeatedly in shift workers. [1],[6],[11],[12],[13]

In most studies on CAR, participants are advised to collect saliva samples immediately after awakening and then after predefined periods. It has been shown, however, that up to a fourth of the participants do not adhere to the prescribed protocol and delay the sampling times. As the first sample is then taken at a higher point of the cortisol profile, the consecutive increase to the maximum is reduced, thus, pretending a blunted response to awakening. [13],[14],[15],[16]

A few studies focus on the hypothesis that noise stimulates the HPA-axis and thereby an elevated cortisol release even while asleep. Ehrenstein and Mόller-Limmroth [17] exposed six young men, during eight laboratory nights, to the noise of a vivid road traffic (L Aeq = 76 dB) but found the same urinary cortisol output as on quiet nights. Maschke et al. [18] delivered 16 or 64 overflights with maximum levels of 55 or 65 dBA via loudspeakers into the bedrooms of 28 residents (35-65 years) near an airport. They observed a higher cortisol excretion than on the previous quiet nights. Using the same method, Harder et al. [19] exposed 16 residents (35-65 years), during 40 nights each, to 32 overflights (L Amax = 65 dB). The initially increased cortisol excretion returned to normal after two nights. A field study performed by Evans et al. [20] revealed no alterations of cortisol output in children after the opening of a new airport. Nocturnal cortisol output of children in a noisier area was, however, higher than of those in a quieter area. [21] The largest laboratory and field studies ever done with 128 and 64 participants (18-65 years) respectively did not show any association between nocturnal aircraft noise and cortisol excretion. [22],[23]

The CAR as a possible indicator of the effects of nocturnal noise was investigated in three studies. In a pilot study with 12 men, Persson Waye et al. [24] found a lesser cortisol increase after nocturnal exposure to low frequency noise but could not replicate this in a consecutive study with 26 men. [25] Michaud et al. [10] exposed 12 persons (seven women, five men, 19-25 years) to multiple trains of 1.000-Hz tones with 80 or 60 dB observed, accordingly, there was no alteration of the CAR as compared to quiet nights.

This paper focuses on the analysis of CAR and of subjective sleep quality ascertained in two unpublished experiments where healthy young persons were exposed to noise during sleep. Adherence to the sampling protocol was enforced by the experimenter and the time of awakening was determined from the polysomnogram. (Further results will be published later).

This explorative analysis aims to ascertain whether sleep under noisy conditions causes CAR alterations. It is assumed that CAR varies with the overall noise load as indicated by the equivalent noise level, but not with the type of noise (road, rail, type of brake).

 Materials and Methods

Methods and material were, to a large extent, the same in the two studies analyzed. This section, therefore, starts with the common aspects that concern selection of participants, experimental procedure, technical equipment and treatment of the recorded noise.

Selection of participants: Applicants completed questionnaires on habitual sleep behavior patterns, personality traits (Freiburg personality inventory; [26] state-trait anxiety inventory, [27] morningness [28] ) and health status including consumption of alcohol and drugs. Hearing acuity was determined by audiometry. Exclusion criteria were: reduced hearing acuity (age-related hearing loss of at least 10 dB on average or of 20 dB for a single frequency (ISO 1999) [29] ), chronic diseases, suspected abuse of alcohol or drugs, more than five cigarettes a day, extreme values of neuroticism (exceeding a score of 9 for women and of 8 for men on a 14-point scale) or anxiety (exceeding a score of 44 for women and 41 for men of a maximum score of 80), habitual bedtimes before 22 or after 24 hours, or sleep durations less than six hours or more than 10 hours. None of the applicants had to be excluded, certainly due to a self-selection as the design and the purpose of the studies were already given in the announcement.

The participants gave their written informed consent - that they were informed about the goals and of the fact that they would be exposed to noise during several nights. The schedules of noise presentation were of course not disclosed. Both studies were approved by the local Ethics Committee.

Experimental procedure: After the electrodes for the registration of the polysomnogram (PSG: two electroencephalograms, two electrooculograms, one electromyogram) were fixed, the participants went to bed. Lights were according to the protocol extinguished at 2300 or at 1400 hours. The PSG was registered and the noise was applied throughout the following eight hours until the wake-up call by the experimenter at 0700 hours or 2200 hours when the first saliva sample (C 0 ) was taken. During the following hour where further saliva samples were taken (see Study 1, 2) the participants were not allowed to brush their teeth, eat, drink or smoke. Saliva was collected with cotton wool swabs (Salivetteδ) that were moved within the mouth until soaked. The swabs were then centrifuged and saliva was stored at -20΀ C until assayed. Analysis was performed with a luminescence immunoassay (LIA, IBL) where the detection limit was 0.16 ng/ml saliva.

Technical equipment and noise load: The participants slept in separate sound shielded rooms that were equipped with two loudspeakers each (Genelec 1031A 48 Hz to 22 kHz, free field frequency response ± 2 dB). The background noise produced by the air conditioning was 28 dBA. The presentation of traffic noise was controlled by NUENDO TM -software (Steinberg Media Technologies) using a Soundcard DMX Wave. All noises were outdoor recordings that were filtered and attenuated depending on the frequencies by at least 15 dB to up to almost 25 dB to simulate a tilted window and the room absorption. This paper refers to indoor levels at the ear of the sleeper.

Data collection and evaluation: Cortisol awakening response (CAR): As the CAR is considerably reduced after day sleep, [12],[13] this analysis focuses only on night sleep scheduled from 2300 to 0700 hours in both studies. The first night was discarded [30] as well as any CAR if awakening occurred 10 minutes or more prior to the wake-up call by the experimenter or if technical problems with the PSG prevented the determination of the exact wake-up time.

Subjective sleep quality (SSQ): Using six 10-point scales, the participants estimated the difficulty to fall asleep (very easy - very difficult), sleep depth (very sound - very shallow), sleep length (very long - very short), calmness of sleep (very calm - very restless), restoration (very high - very low), body movements (very little - very much). The scales were summed up and subtracted from the maximum achievable number (60). [31]

Study 1

The primary goal of Study 1 was to test the assumption that the noise of trains equipped with carbon composite brakes causes less sleep disturbances than the noise of trains that are equipped with conventional iron cast brakes or a mixture of both brakes. (Remark: when braking iron cast brakes roughen the treads of the wheels. This roughness then causes higher noise levels than smooth wheels).

Participants: Twelve healthy persons (six men, six women, 18-26 years).

Experimental design: After a habituation night (Sunday night) the participants slept for three consecutive weeks, four consecutive nights each week (Monday to Thursday night) in the laboratory. The four nights of each week included a permuted sequence of a quiet and three noisy nights with 20, 40 or 80 pass-by train noises. The noises of trains with one of the three brake systems were applied with weekly permuted changes. During the day the participants followed their usual daily schedule. They were asked to abstain from caffeine. During the week prior to the experiments, the participant answered a short questionnaire every morning where they stated their sleep duration.

Noise load: The acoustic features of the three trains, equipped with iron cast brakes, with carbon composite brakes or a mixture of both are given in [Table 1].

CAR: Saliva samples were taken 0, 15 and 45 minutes post-awakening (C 0 , C 15 , C 45 ). The CAR was defined as the cortisol increase within the 45 minutes post-awakening (CAR1 = C 45 - C 0 ). 15 CARs were discarded (nine due to technical problems, six due to premature awakening).

Evaluation and statistics: Differences in gender and pair-wise comparisons between Study 1 and 2 were calculated with t-tests. Repeated measurements ANOVAs with Greenhouse-Geisser adjusted P-values were calculated to test differences in CAR1 and SSQ due to the type of brakes, the number of pass-bys and the equivalent noise level.

Study 2

Study 2 was done to test the validity of the rail bonus for sleep. This bonus allows, in several countries, a 5 dBA higher equivalent noise level for railway than for road traffic noise.

Participants: ND-group consisted of 11 women and 12 men (19-29 years). The DN-group consisted of 13 women and 10 men (19-30 years).

Experimental design: The ND-group slept first four consecutive nights (Monday to Thursday night, 2300-0700 hours) and then (after a one-day break) four consecutive days (Sunday to Wednesday, 1400-2200 hours) in the laboratory. The DN-group slept first during the day and then during the night. Each sleep period was one hour later followed by an eight-hour experimental work shift. During that time the participants did performance tests every hour (25 minutes) and were allowed to read or write between the tests. During the following leisure time they followed their usual schedule. The first sleep period in the laboratory was noise-free. Another randomly chosen sleep period was spent in quiet. The remaining six sleep periods were spent under noise exposure. The order of noise conditions was randomized with the restriction that each person was exposed once to the condition Rail4 and Road4 (see below). Caffeine consumption was not allowed. During the week prior to the experiments the participants answered a short questionnaire every morning where they stated their time of going to bed and getting up.

Noise load: The noise scenarios were recorded along three railway tracks and three roads that are characterized by different numbers of pass-bys (rail: 20, 40, 57; road: 1300, 4300, 8600). Recordings were made at three distances for rail noises (25 meters, 50 meters, 100 meters). This systematic variation was not available for road traffic noises. Recordings were made at two distances each (1300 pass-bys at 15 meters and 20 meters, 4300 pass-bys at 20 meters and 32 meters, 8300 pass-bys at 24 meters and 26 meters). The number of pass-bys, the recording distances and the corresponding A-weighted equivalent noise levels are listed in [Table 2].

CAR: Saliva samples were taken 0, 15, 30, 45 and 60 minutes post-awakening (C 0 , C 15 , C 30 , C 45 , C 60) . Further to CAR1 (see Study 1), the CAR was also indicated by CAR2. For this the five cortisol levels were integrated to a single value, the area under curve with respect to increase (AUCI [32] ). 12 CARs were discarded due to premature awakening.

Evaluation and statistics: The influences of subgroups, types of noise, equivalent noise levels and gender were analyzed with an ANOVA including interactions. Pair-wise comparisons between the two subgroups were calculated with t-tests. Statistical analyses were done with SAS, version 9.1 and P-values ͳ .05 were considered significant.


Comparison of studies: According to the questionnaire filled in for the selection of the participants, the usual bed time was the same for Study 1 participants, or those who belonged to the ND- or to the DN-group of Study 2, namely: 23.4 ± 0.4 hours, 23.4 ± 0.9 hours, 23.4 ± 0.9 hours. The respective sleep durations were 7.7 ± 1.4 hours, 7.8 ± 0.8 hours, 8.0 ± 0.8 hours with no significant differences between the three groups (P=.52). The sleep durations reported every morning in the week before the experiment were, however, somewhat shorter with 7.4 ± 1.0 hours, 7.5 ± 1.1 hours, 7.6 ± 0.8 hours, again with no statistical difference between the groups (P=.82). The cortisol concentration upon awakening (C 0 ), CAR1 and SSQ were calculated for the quiet nights of the participants of Study 1 and the ND-group of Study 2. The t-test revealed no significant differences with P-values being .19, .07, and .51.

Study 1

There were no gender-related differences either for CAR1 (male vs. female: 5.3 ± 1.2 vs. 6.6 ± 2.0 ng/ml) or SSQ (male vs. female: 33.7 ± 5.5 vs. 34.5 ± 6.3). CAR1 and SSQ were submitted to ANOVAs that included noise load either expressed as the type of brakes (carbon composite brakes, iron cast brakes, mixture of both brakes), the number of pass-bys (20, 40, 80) or the equivalent noise level (L Aeq : 54 dB). The results shown in [Figure 1] revealed that the CAR was not associated with either of these noise parameters. SSQ, however, was rated worse after noisy than after quiet nights with worst ratings after the nights with the highest noise load either expressed by the type of noise (iron cast brakes), the number of pass-bys (80 pass-bys) or the equivalent noise level (> 54 dBA). Pair-wise comparisons performed between each of the conditions defined by the type of brake, the number of pass-bys and the equivalent noise levels revealed significant differences only for SSQ. This was 'quiet vs. iron cast brakes' (P=.02), 'quiet vs. 80 pass-bys' (P 54 dBA' (P=.03).

Study 2

Comparison between subgroups: [Table 3] shows CAR1, CAR2 and SSQ averaged over the quiet nights, separately for both subgroups. Due to the t-test, the difference was significant. The cortisol levels upon awakening (C 0 ) were lower and CAR2 was smaller in the DN- than in the ND-group.

CAR1, CAR2 and SSQ were submitted to an ANOVA that included the subgroup (ND, DN), type of noise (road, rail), equivalent noise level (quiet, L Aeq Aeq >48) and gender. According to [Table 4], neither CAR1 nor CAR2 nor SSQ were influenced by the type of noise or by gender whereas the equivalent noise level and the subgroup had a significant main effect on all three variables. CAR1 and CAR2 were, as shown in [Figure 2], greater and sleep quality was rated worse in the ND- than in the DN-group. The effect of the equivalent noise level was restricted to the DN-group. CAR1 was similar after quiet nights and after nights with equivalent noise levels of less than 48 dBA but significantly reduced after nocturnal exposure to noise levels above 48 dBA. CAR2 shows a similar feature but failed to become significant. Concerning SSQ, there was a rather gradual decrease from quiet (42.4 ± 4.5) over the low (38.8 ± 5.6) to the highest (31.8 ± 9.1) noise level (ND-group: 35.5 ± 8.1, 32.4 ± 8.8, 30.5 ± 10.2). Pair-wise comparison revealed significant differences (P Methodological aspects: Most studies on the CAR include cortisol levels 30 minutes after awakening. In Study 1 the third saliva sample was taken after 45 minutes instead. This is justified by a meta-analysis of several publications [1],[5],[8],[9],[12],[24],[25],[33],[34],[35],[36],[37],[38],[39],[40] where cortisol levels were ascertained 30 and 45 minutes post-awakening of overall 1,456 participants. Means and standard deviations of these samples differed, not significantly, from each other (C 30 : 22.6 ± 5.6; C 45 : 22.3 ± 5.5 nmol / l, P=.17).

Premature awakening: The determination of the CAR requires a strict sampling schedule. In field studies where the participants keep to their preferred sleep-activity schedule compliance is a major problem. Up to a fourth of the participants do not adhere to the prescribed protocol. [6],[14],[15],[16] Poor compliance causes a delay in saliva sampling and results in a smaller post-awakening cortisol increase. In the present studies adherence to the temporal schedule was enforced by the experimenters. Errors corresponding to delayed-sampling occurred, however, with premature awakenings. Thus, all CARs were discarded if awakening occurred 10 minutes or more before the first saliva sample. [6],[16]

Gender: In the ND-group, the CAR was significantly greater in the female than in the male participants. Similar differences were e.g. reported by several authors. [1],[4],[6],[33] However, there are also studies where gender-related differences did not occur as it is true for the participants of Study 1 and for the DN-group in Study 2. [41] These incongruent reports are certainly the consequence of the huge variance of cortisol levels upon awakening and of the post-awakening cortisol increases.

Effects of noise: In Study 1, subjective sleep quality [SSQ, [Figure 1]] was rated significantly worse after noisy than after quiet nights, where the strongest decrease concerned the nights with the highest noise load either indicated by the number of pass-bys (80), the equivalent noise level (> 54 dBA) or the type of brake (iron cast). The strong reaction to the iron cast brakes is most likely related to the fact that [Table 1] the maximum levels (and thereby the equivalent noise levels) are highest for this type of noise. An indication for this conclusion is a previous study, where SSQ was significantly determined by the equivalent level, however, not by the type of noise (aircraft, rail or road traffic noise). [31] In Study 2, SSQ decreased gradually from quiet nights over nights with low to nights with high noise levels, which was only significant in the DN-group. This decrease of SSQ with the noise was expected and frequently reported in the literature and it proved that the noise applied had at least for subjective evaluation the expected effect. [23],[24],[25],[31]

In contrast, the CAR was neither in Study 1 nor in the ND-group of Study 2 associated with nocturnal noise exposure. This is supported by Persson Waye et al. [25] who observed 26 young men whom they exposed during one night to low frequency noise and by Michaud et al. [10] who exposed 12 young persons to trains of tones of 80 or 60 dB. Again, no alteration of the CAR was found in a study where 13 women were woken up thrice during the night by phone calls. [42] The CAR indicates the reactivity of the hypothalamus-pituitary adrenal axis and is expected to vary with the sympathetic tone. The variation of the latter was apparently too small in Study 1 and in the ND-group of study 2. This conclusion bases on several recent reports according to which the overall sleep structure is usually rather little affected even in nights with high noise load. [22],[31]

The DN-group of study 2 revealed, however, a significantly attenuated CAR after the nights with the highest noise load (> 48 dBA). Reduced CARs are characteristic for several health disorders. They were observed in persons with health problems in general, [9],[43] with chronic fatigue syndrome, [44],[45] with post-traumatic stress disorder, [46] with early loss experience, [47] in depressive persons [48,49] and alcoholics. [50] Temporarily reduced CARs are characteristic in persons who sleep after night shifts during the day. [12],[13],[51] The participants of the DN-group had, in contrast to those of Study 1 and of the ND-group, just changed after four consecutive night shifts back to their usual day-oriented schedule. Night work has, as shown by 'phase-assessment-procedures' performed before and after the night shifts advanced their cortisol profiles by 5 hours [Figure 3]. Their low cortisol concentrations upon awakening [C 0 , see [Table 3]] suggest that they were, when saliva samples were taken for this analysis, not yet fully re-adjusted. In this situation, the attenuation of the CAR results from the fact that awakening occurred not as usual before but after the acrophase of the cortisol profile [13] where the responsiveness of the HPA-axis is reduced. [52] The symptoms of 'shift-lag', i.e. fatigue, dizziness and general wariness, may contribute to this effect.

It is, therefore, conceivable to assume that the attenuated CAR after high nocturnal noise exposure results in the DN-group from an elevated vulnerability during the process of re-adjustment to the normal sleep-activity cycle. A hint to the particular vulnerability in this group is certainly the strong decrease of subjective sleep quality after the noisiest as compared to the quiet nights. This difference was 11 as compared to five scale points in the ND-group.

In conclusion, the present results suggest consideration of the literature that nocturnal noise exposure causes alterations of the CAR predominantly in persons with at least-temporarily-elevated vulnerability.


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