The health impacts of environmental noise are a growing concern. At least one million healthy life years are lost every year from traffic-related noise in the western part of Europe. This publication summarises the evidence on the relationship between environmental noise and health effects, including cardiovascular disease, cognitive impairment, sleep disturbance, tinnitus, and annoyance. For each one, the environmental burden of disease methodology, based on exposure-response relationship, exposure distribution, background prevalence of disease and disability weights of the outcome, is applied to calculate the burden of disease in terms of disability-adjusted life-years. Data are still lacking for the rest of the WHO European Region. This publication provides policy-makers and their advisers with technical support in their quantitative risk assessment of environmental noise. International, national and local authorities can use the procedure for estimating burdens presented here to prioritize and plan environmental and public health policies.

Burden of Disease from Environmental Noise: Quantification of Healthy Life Years Lost in Europe

The role of sleep hygiene in promoting public health: A review of empirical evidence.

Research suggests that visual impressions of natural compared with urban environments facilitate recovery after psychological stress. To test whether auditory stimulation has similar effects, 40 subjects were exposed to sounds from nature or noisy environments after a stressful mental arithmetic task. Skin conductance level (SCL) was used to index sympathetic activation, and high frequency heart rate variability (HF HRV) was used to index parasympathetic activation. Although HF HRV showed no effects, SCL recovery tended to be faster during natural sound than noisy environments. These results suggest that nature sounds facilitate recovery from sympathetic activation after a psychological stressor.

/pdf/stress-recovery-during-exposure-to-nature-sound-and-4lrp9xs1yd.pdf

Stress recovery during exposure to nature sound and environmental noise.

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.

https://www.klein-winternheim.de/lokale-agenda/d43d5e550c96630fc05d6c66ec88f0f4_Elsner-eurheartj.ehu030.full.pdf

Cardiovascular effects of environmental noise exposure

Methodology of frontal and executive function

Noise emitted from road, rail and air traffic and their effects on sleep

TRANSIENT EXCITATIONS OF THE CENTRAL AND OF THE AUTONOMIC NERVOUS SYSTEM WITH A COMMON ORIGIN IN THE BRAINSTEM OCCUR FREQUENTLY and spontaneously (with no obvious reason) during normal sleep. Cortical arousals, which might lead to sleep stage changes or awakenings, are usually accompanied by autonomic arousals. As the reverse is not true, the latter may occur alone.1,2 Autonomic arousals are transient elevations of the sympathetic tone. They encompass increases of ventilation, of systolic and diastolic blood pressure, and of peripheral resistance; but they but are most often indicated by alterations of heart rate (HR). These cardiac arousals start to increase well before the visually detectable onset of cortical arousals.1–3 Their extent and patterns vary with the duration of the cortical arousals. With cortical arousals lasting up to 10 s, cardiac arousals are typically biphasic: an initial acceleration is followed by a deceleration below the baseline. The baseline is then regained after a gradual increase 15–30 s after stimulus onset.1,3–5 With longer lasting arousals the deceleration becomes gradually flatter, thus leading to a monophasic elevation of heart rate.1,4–5

Similar alterations are evoked by various external stimuli, in particular by acoustic stimuli.6–8 Research in this area was usually performed with artificial sounds, mostly with tones of up to 4 kHz and durations up to 5 s.6–12 The extents and the patterns of these responses were analyzed in detail and were shown to depend at least on stimulus intensity and on the sleep stage at the time of stimulation.

Traffic noises are a major cause of extrinsic sleep disturbances with after effects on mood, performance, and health.13 Despite this, cardiac responses to traffic noise have only occasionally been studied.14–17 A detailed analysis of these responses was performed only for sonic booms, which evoked the typical biphasic cardiac arousals described above.18

This paper deals with the cardiac responses of 24 persons to noises from aircraft, rail, and road vehicles during sleep in the laboratory. It investigates possible influences of acoustical parameters, time of night and momentary sleep stage. Such an analysis is highly relevant as numerous residents living in the vicinity of airports, along busy streets, and along railway tracks are permanently exposed to these noises while sleeping. Long-term exposure to these noises is assumed to contribute to the genesis of cardiovascular diseases.19

/pdf/autonomic-arousals-related-to-traffic-noise-during-sleep-1aher2oc8g.pdf

Autonomic arousals related to traffic noise during sleep.

The existing questionnaires for determining the noise sensitivity of individuals provide information only about global noise sensitivity, although empirical data suggest that measuring noise sensitivity for different situations in daily life might be more logical. Therefore, the "Noise-Sensitivity-Questionnaire" (NoiSeQ) was developed to measure global noise sensitivity as well as the sensitivity of five domains of daily life, namely, leisure, work, habitation, communication, and sleep. The assessment of the measurement characteristics was based on the Generalizability (G) theory. The results of the G-study (N=66) proved that a single application of the questionnaire is sufficient for determining an individual's noise sensitivity. Furthermore, the ratings are age and gender independent. The subsequently conducted Decision (D)-study (N=288) provides information on the reliability of NoiSeQ. If the questionnaire is used for measuring global noise sensitivity, the reliability (relative and absolute G-coefficient) reaches a value above 0.90. According to ISO 10075-3, the questionnaire satisfies the precision level 1 "accurate measurement" in this case. The G-coefficients for all the subscales exceed the lower limit 0.70, with the exception of subscale leisure, which did not prove satisfactory. However, this subscale can reach a reliability of more than 0.70 if additional items are included. The validity of the instrument was proven for the subscales habitation (N=72) and work (N=72). In both the studies, the participants were asked to rate the annoyance in the presence of several rail and traffic noise scenarios. The subjects were characterized as low and high noise sensitive according to their sensitivity values obtained from NoiSeQ. In conclusion, a significant difference in annoyance rates was observed between the low and high noise sensitive groups for both the subscales habitation and work. This data support the validity of NoiSeQ.

The development of the noise sensitivity questionnaire.

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.

Event-related awakenings caused by nocturnal transportation noise.

The after-effects of nocturnal traffic noise on cognitive performance and inhibitory brain activity were investigated. Twenty participants (18-30 years) performed an easy and a difficult visual Go/Nogo task with simultaneous EEG recording after a quiet night and then during three nights when aircraft noise was presented with equivalent noise levels of 39, 44, and 50 dBA, respectively, between 11 p.m. to 7 a.m. Based on subjective sleep quality rating, participants were separated into "good" versus "bad" sleepers. The performance and inhibition-related components (N2, P3) of event-related potentials were analysed. The N2 and P3 amplitudes were smaller and latencies were prolonged in the difficult than in the easy task. This effect was more pronounced for Nogo than for Go trials. The Nogo-P3 amplitude was smaller in Noise than in "Quiet" conditions in the difficult task only. In the difficult task, the Nogo-P3 latency was prolonged in bad sleepers than in good sleepers. The Nogo-P3 amplitude was reduced in Noise as compared to "Quiet" conditions in bad sleepers only. Sleep quality in bad sleepers worsened steadily with increasing noise levels. No effects of noise or subjective sleep quality on performance were found. Inhibitory processes appear to be selectively impaired after nocturnal noise exposure. The task difficulty and perceived sleep quality are important factors modulating noise effects. The results suggest that nocturnal traffic noise increase physiological costs for inhibitory functioning on the day even if no overt performance decrement is observed.

Anke Marks

Papers

Noise emitted from road, rail and air traffic and their effects on sleep

Autonomic arousals related to traffic noise during sleep.

The development of the noise sensitivity questionnaire.

Event-related awakenings caused by nocturnal transportation noise.

Executive brain functions after exposure to nocturnal traffic noise: effects of task difficulty and sleep quality