Wird die Häufigkeit von Bronchitis bei Kindern unter nächtlicher Belastung mit Straßen verkehrslärm erhöht? Welche Bedeutung haben dabei lärmbedingte Erhöhungen von Cortisol in der ersten Nachthälfte?

Long-term exposure to air pollution is generally accepted to be a health hazard. Additionally, exposure to noise facilitates diseases, which are caused by stress as a co-factor. Although traffic-related air pollution and noise are highly correlated, the combined health effects of these factors have not yet been studied. All 5–12-year-old children who visited two participating pediatric offices in the region of Osterode, near Harz Mountains, were registered (n = 401). Their annual rates of physician contacts during the last five years were evaluated retrospectively and their exposure to traffic-related air pollution and nighttime noise was objectively assessed. The association between exposure and physician contacts because of respiratory diseases was assessed by logistic regression analysis with adjustment for potential confounders. Of the total group, 371 children had contact with their physician for at least one year. Their total contacts because of asthma and bronchitis amounted to 612 and 2976, respectively. Compared to children with no or minimal exposure to traffic emissions, children with medium and high exposure had dose-dependent increases in asthma (OR 1.41 [95%, CI 0. 83−2.37] and 4.22 [95% CI 2.79−8.16], respectively) and frequent bronchitis (OR 1.95 [95% CI 1.11−3.42] and 13.8 [95% CI 7.19−26.4], respectively). Long-term exposure of children to the combination of traffic noise and air pollution may result in more adverse health effects than exposure to air pollution alone.Key Words: asthmabronchitischildrenair pollutiontraffic noisecombined exposure

BACKGROUND:The biologic plausibility for noise stress-related cardiovascular responses is well established. Epidemiologic studies on the relationship between transportation noise and ischemic heart disease suggest a higher risk of myocardial infarction in subjects exposed to high levels of traffic noise. METHODS:To determine the risk of road traffic noise for the incidence of myocardial infarction (MI), we carried out a hospital-based case-control study in the city of Berlin. We enrolled consecutive patients (n=1881), age 20-69 years, with confirmed diagnosis of MI from 1998 through 2001. Controls (n=2234) were matched according to sex, age, and hospital. Outdoor traffic noise level was determined for each study subject based on noise maps of the city. Standardized interviews were conducted to assess possible confounding factors and the annoyance from various noise sources. RESULTS:The adjusted odds ratio for men exposed to sound levels of more than 70 dB(A) during the day was 1.3 (95% confidence interval=0.88-1.8) compared with those where the sound level did not exceed 60 dBA. In the subsample of men who lived for at least 10 years at their present address, the odds ratio was 1.8 (1.0-3.2). Noise-exposed women were not at higher risk. CONCLUSIONS:The results support the hypothesis that chronic exposure to high levels of traffic noise increases the risk for cardiovascular diseases.

The relationship between subjective work noise exposure and the risk of myocardial infarction (MI) was assessed in a population based casecontrol study. 395 MI patients (31–65 years) were compared to 2148 controls from a random population sample with the same age/sex distribution. The relative risk (RR) for MI—adjusted for control variables (smoking, age, social status, etc.)—was found to increase significantly and steadily with noise category. Subjective work noise exposure was the second greatest risk factor for MI after smoking. Possible bias due to overreporting of subjective noise exposure is discussed. Interdisciplinary studies on the relationship between cardiovascular diseases and workrelated stressors including subjective and objective noise assessment are needed to quantify the risk of MI due to work noise.

Traffic noise is the most important source of environmental annoyance. According to the Environmental Expert Council of Germany, severe annoyance persistent over prolonged periods of time is to be regarded as causing distress. Previously, extraaural noise effects were mostly assessed using a paradigm in which the sound level played the major role. On the basis of this paradigm the relatively low sound level of environmental noise was not considered to be a potential danger to health. In contrast to this numerous empirical results have shown long-term noise-induced health risks. Therefore a radical change of attitude - a change of paradigm - is necessary. For an immediate triggering of protective reactions (fight/flight or defeat reactions) the information conveyed by noise is very often more relevant than the sound level. It was shown recently that the first and fastest signal detection is mediated by a subcortical area - the amygdala. For this reason even during sleep the noise from aeroplanes or heavy goods vehicles may be categorised as danger signals and induce the release of stress hormones. In accordance with the noise stress hypothesis chronic stress hormone dysregulations as well as increases of established endogenous risk factors of ischaemic heart diseases have been observed under long-term environmental noise exposure. Therefore, an increased risk of myocardial infarction is to be expected. The results of individual studies on this subject in most cases do not reach statistical significance. However, according to the Environmental Expert Council, these studies show a consistent trend towards an increased cardiovascular risk if the daytime immission level exceeds 65 dB(A). Most of the previous studies on the extraaural effects of occupational noise have been invalidated by exposure misclassifications. In future studies on health effects of noise a correct exposure assessment is one of the most important preconditions.

Reactions to noise-induced communication disturbance of 42 men during a seminar were investigated. Stress reactions with or without road traffic noise (Lm = 60 dBA) were compared. Traffic noise was played back via loudspeakers during one day in the seminar room. The following parameters were measured: Fatigue and mental tension by questionnaire; blood pressure and heart rate; excretion of adrenaline, noradrenaline and cAMP from the collected urine. The same subjects participated in a laboratory test where the blood pressure was measured during 5 minutes of rest and after 5 minutes of exposure to intermittent white noise (Lm=97 dBA). It was found that the noise in the field experiment caused psychological and physiological stress effects in half of the subjects. Increased mental tension was correlated to increases as well as decreases of the blood pressure. Systolic blood pressure reactions were stronger than the reactions of diastolic blood pressure. Noise sensitive subjects reacted stronger than the others. In the short-term laboratory test, systolic blood pressure increases were smaller than the diastolic increases. At the end of the 5 minutes noise exposure only the diastolic blood pressure increases were significant. There was no correlation between the blood pressure reactions in the two different noise exposure experiments. There existed a positive correlation between noise sensitivity and the systolic blood pressure increases during the seminar, whilst the correlation, between noise sensitivity and systolic blood pressure increases in the laboratory exposure, was negative. From these results we conclude that short-term noise exposure experiments do not provide information about the effects of long-term real life exposure to environmental noise. Potential health effects of chronic noise-induced disturbances of activities are discussed.

A correlation of respiratory diseases to traffic related air pollution and noise was observed in an interview study. Since in that study the exposure was subjectively assessed, in the present field study nitrogen dioxide as indicator for vehicle exhausts and the mean night-time noise level were measured outside the children's windows in representative locations. Based on these measurements each child was placed in one of the following categories: low, medium or high traffic immission (ambient emissions). The physician contacts due to bronchitis of 68 children were assessed retrospectively from the files of the participating paediatricians. Saliva samples were collected from all children and the cortisol concentration was estimated. Children under high noise exposure (L(night, 8h) = 54-70dB(A)) had in comparison to all other children significantly increased morning saliva cortisol concentrations, indicating an activation of the hypothalamus-pituitary-adrenal (HPA) axis. Analysing a subgroup of children without high noise exposure showed, that children with frequent physician contacts due to bronchitis did not have increased morning saliva cortisol. However, multiple regression analysis with stepwise exclusion of variables showed that bronchitis was correlated more closely to morning salvia cortisol than to traffic immissions. On the other hand, the rate of physician contacts due to bronchitis increased in a dose dependent manner and significantly with increasing traffic immissions. From these results it can be concluded that high exposure to traffic noise, especially at nighttime, activates the HPA axis and this leads in the long term to an aggravation of bronchitis in children. This seems to be more important than the effect of exhaust fumes on bronchitis symptoms. The results of the present study should be subjected to further investigation using specially designed studies.

Annoyance and sleep disturbance are generally accepted effects of environmental noise. Traffic noise is the most important source of noise induced annoyance. Long-term derogation of the recovery function of sleep by traffic noise has the potential to increase the sensitivity to daytime noise annoyance as well as the risk of cardiovascular and several other diseases. Noise induced arousal and secretion of cortisol especially in the first half of the night seem to be more sensitive indicators for noise induced detriment of sleep than remembered awakening reactions. The evidence of cardiovascular risk due to traffic noise is assessed as “limited or sufficient”. In most studies the daytime traffic noise level was related to the increase of cardiovascular risk. Nevertheless there is evidence that traffic noise exposure at night plays a more important role in the pathogenesis of noise stress induced increase of the cardiovascular risk than traffic noise exposure during the day. This was confirmed by the Spandau Health Survey, where a clear distinction was made between day time and night time traffic noise exposure. Among other diseases also chronic bronchitis and bronchial asthma were found to be related to traffic noise. These findings are in agreement with the results of study in children under combined exposure to traffic related noise and air pollution. The relative risks of chronic bronchitis, asthma and neurodermitis of the exposed children cannot be explained by air pollution alone. Therefore long-term traffic noise induced derogation of sleep must have had an adjuvant effect in the pathogenesis of these diseases. Finally noise induced hearing impairment due to military low altitude flight noise, impulsive noise from toy pistols etc., and long-term overexposure by loud music are summarised. Acoustic limiting values are proposed to avoid inner ear damage. To avoid traffic noise related health defects maximal indoor levels should be Lmax < 40 dB(A) or in the case of predominant low frequency noise Lmax < 60 dB(C).

AIMS:Traffic noise is a psychosocial stressor. Epidemiological studies suggest chronic noise stress to be a risk factor for cardiovascular disorders.METHODS:In a prospective cohort study, the association between annoyance and disturbances due to road traffic noise and the incidence of ischaemic heart disease (IHD) was studied in 3950 middle aged men.RESULTS:Depending on the questionnaire item, non-significant odds ratios for IHD incidence ranging from 0.9 to 1.4 were found for the highly noise annoyed/disturbed subjects when compared with the less annoyed/disturbed subjects, over the six year follow up period. However, this relation was strongly modified by the prevalence of pre-existing chronic diseases. In subjects free of any chronic disease at the beginning of the follow up, significant odds ratios between 1.7 and 3.0 were seen. In the subgroup with chronic diseases no such noise effects were seen. This surprising result of no effect in the group of people with a potential risk, due to pre-existing health problems, may be because of the dilution of the true effect due to recall bias.CONCLUSIONS:Annoyance and disturbance due to road traffic noise is associated with a higher incidence of IHD. Prevalence of disease can be an important effect modifier of the relation between noise annoyance and health outcomes.

The pathogenesis of allergies can be stimulated by adjuvant effects--i.e. air pollutants such as NOx and particles from diesel engines as well as noise--the latter especially during night-time. During sleep, noise signals which are associated with danger (i.e. lorry noise) have the potential to trigger stress reactions even if the noise level is low. Increases of cortisol in the first half of the night seem to play an important role.--In a blind interview study, the combined effects of chronic exposure to traffic related air pollution and noise, upon the risk of skin and respiratory diseases in children were studied. All children between 5-12 years, who had consulted one of two participating pediatricians were included in the study. The pediatricians' diagnoses of 400 children were analysed together with their parents answers on the density of road traffic on their street and several confounding factors. Multiple regression analyses resulted in relative risks of asthma, chronic bronchitis and neurodermitis, which increased significantly with increasing traffic load. A comparison with the literature on such effects caused by air pollution alone, showed that traffic noise during the night might have an adjuvant effect on the pathogenesis of the mentioned diseases.

The pathogenesis of allergies can be stimulated by adjuvant effects--i.e. air pollutants such as NO(2) and particles from diesel exhausts as well as noise--the latter especially during night-time. During sleep, noise signals which are associated with danger (i.e. lorry noise) have the potential to trigger stress reactions even if the noise level is low. Increases of cortisol in the first half of the night seem to play an important role. In a blind interview study, the combined effects of chronic exposure to traffic related air pollution and noise, upon the risk of skin and respiratory diseases in children were studied. All children between 5-12 years, who had consulted one of two participating paediatricians were included in the study. The paediatricians diagnoses of 400 children were analysed together with their parents answers regarding the density of road traffic on their street and several confounding factors. Multiple regression analyses resulted in relative risks of asthma, chronic bronchitis and neurodermitis, which increased significantly with increasing traffic load. A comparison with the literature on such effects caused by air pollution alone, showed that traffic noise during the night might have an adjuvant effect on the pathogenesis of the mentioned diseases.

Zusammenfassung Die Entstehung von Allergien kann durch adjuvante Effekte – z. B. Immissionen aus dem Verkehrsbereich – gefördert werden. Zu solchen Immissionen zählen gas- und partikelförmige Schadstoffe wie Stickoxide und Dieselruß sowie Lärm, insbesondere in der Nacht. Während des Schlafs können Geräusche, die mit Gefahren assoziiert sind (z. B. Lkw-Geräusche) auch bei niedrigen Pegeln Stressreaktionen auslösen. Kortisolerhöhungen in der ersten Hälfte der Nacht scheinen dabei eine wichtige Rolle zu spielen. In einer “einfach-blind” durchgeführten Befragungsstudie wurden langzeitige Auswirkungen einer Kombinationsbelastung aus verkehrsbedingten Luftverschmutzungen und Lärm auf das Risiko für allergische Haut- und Atemwegserkrankungen bei Kindern untersucht. Die ärztlichen Diagnosen von 400 Kindern im Alter von 5–12 Jahren, die innerhalb eines Monats einen der beiden teilnehmenden Kinderärzte aufsuchten, wurden zusammen mit Angaben der Eltern über die Verkehrsbelastung ihrer Wohnungen und über andere mögliche Einflussfaktoren ausgewertet. Multiple Regressionsanalysen ergaben für Asthma, chronische Bronchitis und Neurodermitis relative Risiken, die mit der Belastung signifikant anstiegen. Ein Vergleich mit der Literatur über entsprechende Wirkungen von Luftverschmutzung ergab, dass nächtlicher Verkehrslärm wahrscheinlich eine verstärkende (adjuvante) Wirkung bei der Entstehung der genannten Krankheiten hat.

56 children age 7 - 10 had a medical check-up and they and their mothers completed questionnaires. Additionally the children's excretion of free cortisol was measured by HPLC in two urine samples collected at 1 p.m. and in the morning. The children lived either at a busy road with 24 h lorry traffic or in quiet areas. At the side of the road the noise level was registered during five nights. In the bedrooms representative measurements of the short-term maximal sound level (L(Amax) and L(Cmax)) and of the frequency spectrum were taken. During the night on average every 2 minutes a lorry with L(max) > 80 dB(A) passed by the houses. The indoor levels of the higher exposed half of the children were L(max) = 33-52 dB(A) resp. 55-78dB(C)). The frequency spectrum had its maximum below 100 Hz. 74% of the higher exposed never opened their windows as compared to 25% in the lower exposed half group. The excretion of free cortisol and its metabolites in the first half of the night was significantly correlated to L(Cmax) (co-variables: age, sex, and the day of the week) as well as to impaired sleep, memory and ability to concentrate. The cortisol excretion in the second half of the night was not correlated to the noise level. Disturbances of the normal circadian rhythm of cortisol can be quantified by the quotient of the cortisol excretion in the first half of the night in relation to that in the second half. Children under long-term road traffic noise exposure during the night had an increased risk of chronic stress hormone regulation disturbances. These disturbances were significantly correlated to L(Cmax) and findings of allergy and/or asthma bronchial. Long-term low frequency noise exposure with Lmax < 55 dB(A) during the night resulted in chronic increases of children's excretion of free cortisol in the first half of the night and in serious disturbances of the circadian rhythm of cortisol. Indications of increased risks of asthma bronchial and allergies in noise exposed children with stress hormone regulation disturbances need further clarification

Noise is a health risk. Recent findings suggest that leisure noise is a substantial danger especially to children, teenagers and young adults. Epidemiological studies of teenagers with no occupational noise exposure show an increasing number with a substantial and measurable irreversible inner ear damage. This is basically due to the wide spread exposition to very loud toys (pistols and squibs), crackers and exposure to electronically amplified music, e.g. from personal cassette players (PCP), at discos or concerts etc. Protection against irreversible ear damage by leisure noise has an important impact in preventive medical care. Therefore the general public must be informed that loud leisure activities may cause damage to the ear. In order to protect children, young people and adults, the legislature ought to set limits for sound levels in discos, concert halls and for music equipment and toys by establishing the necessary standards and regulations.

Although accumulating evidence over the past two decades points towards noise as an ambient stressor for children, all of the data emanate from studies in high-intensity, noise impact zones around airports or major roads. Extremely little is known about the nonauditory consequences of typical, day-to-day noise exposure among young children. The present study examined multimethodological indices of stress among children living under 50 dB or above 60 dB (A-weighted, day-night average sound levels) in small towns and villages in Austria. The major noise sources were local road and rail traffic. The two samples were comparable in parental education, housing characteristics, family size, marital status, and body mass index, and index of body fat. All of the children were prescreened for normal hearing acuity. Children in the noisier areas had elevated resting systolic blood pressure and 8-h, overnight urinary cortisol. The children from noisier neighborhoods also evidenced elevated heart rate reactivity to a discrete stressor (reading test) in the laboratory and rated themselves higher in perceived stress symptoms on a standardized index. Furthermore girls, but not boys, evidenced diminished motivation in a standardized behavioral protocol. All data except for the overnight urinary neuroendocrine indices were collected in the laboratory. The results are discussed in the context of prior airport noise and nonauditory health studies. More behavioral and health research is needed on children with typical, day-to-day noise exposure.

The authors tested the hypothesis that prolonged exposure to road traffic noise causes ischemic heart disease in a 10-y follow-up cohort study of middle-aged men. in the Caerphilly and Speedwell studies, 2 512 and 2 348 men, respectively, who were 45-59 y of age were seen in the initial cross-sectional phase and at follow-up intervals of 10 y. Adjusted odds ratios of 1.1 (95% confidence interval = 0.6, 1.9) and 0.9 (95% confidence interval = 0.6, 1.4) were found in the total cohorts. However, the relative risk was 1.3 (95% confidence interval = 0.8, 2.2) in the pooled reconstructed cohort of men who were followed for 6 y (i.e., from phase 2 to phase 3) and for whom room orientation and window-opening habits could be considered. Furthermore, the relative risk increased to 1.6 (95% confidence interval = 0.9, 3.0) in the subsample of men who had lived at least 15 y in their present homes at the time of recruitment. Living adjacent to streets with high traffic noise levels was associated with an adjusted (for covariates) increase in relative risk of 1.01-1.02/y in residence-a result that was only borderline significant (p <.10).