Stress effects of noise in a field experiment in comparison to reactions to short term noise exposure in the laboratory.

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.

Low frequency noise and stress: bronchitis and cortisol in children exposed chronically to traffic noise and exhaust fumes.

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.

Health effects caused by noise: evidence in the literature from the past 25 years.

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.

Respiratory and dermatological diseases in children with long-term exposure to road traffic immissions.

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.