Home Email this page Print this page Bookmark this page Decrease font size Default font size Increase font size
Noise & Health  
 CURRENT ISSUE    PAST ISSUES    AHEAD OF PRINT    SEARCH   GET E-ALERTS    
 
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Email Alert *
Add to My List *
* Registration required (free)  
 


 
 

 Article Access Statistics
    Viewed4713    
    Printed177    
    Emailed2    
    PDF Downloaded197    
    Comments [Add]    

Recommend this journal

 


 
EDITORIAL Table of Contents   
Year : 2000  |  Volume : 2  |  Issue : 7  |  Page : 5-6
Noise as a stressor and its impact on health

1 Institute for Water, Soil and Air Hygiene, Federal Environmental Agency Berlin, Corrensplatz 1, 14195 Berlin, Germany
2 Institute of Laryngology and Otology, University College London, 330 Gray's Inn Road, London WC1X 8EE, United Kingdom

Click here for correspondence address and email
 
How to cite this article:
Ising H, Prasher D. Noise as a stressor and its impact on health. Noise Health 2000;2:5-6

How to cite this URL:
Ising H, Prasher D. Noise as a stressor and its impact on health. Noise Health [serial online] 2000 [cited 2019 Oct 18];2:5-6. Available from: http://www.noiseandhealth.org/text.asp?2000/2/7/5/31746
In this special issue of Noise & Health we consider health effects of chronic stress induced by noise or other stressors. A number of studies have employed other stressors but the results may also be relevant to noise as a stressor.

The papers in this issue were presented at the international symposium on "Environmental Noise, Stress and Cardiovascular Risk" held in Berlin. A conference report on this symposium was published in Vol. 2 (Jan.-March 1999) in Noise & Health. Three papers (Lundberg, Kirschbaum and Melamed) from this conference have already been published and one is accepted for publication (A review by Babisch: Epidemiological studies on cardiovascular risk) and some are in preparation.

The basic idea of this issue is to give the reader an overview of the psychophysiology of stress reactions during sleep (Born & Fehm) and its consequences on the hypothalamic-pituitary­adrenal (HPA) system. The hypo- and hypercortisolism as well as diagnostic and therapeutic aspects are also presented for a better understanding of the system (Oelkers).

The connection between environmental noise and stress reactions during sleep is explained by Spreng in terms of an effect on a specialised brainstem region for acoustic signal detection, the amygdala. This closes a gap in our previous understanding of stress reactions. They try to explain that even low level noise signals have the potential to trigger stress reactions with increased release of cortisol.

The learning capacity of the amygdala enables it to identify noise signals by its acoustical properties which carry the information of an impending danger. This newly achieved knowledge is most important for the theoretical understanding of noise induced stress reactions. In particular it explains that even in people sleeping, stress reactions are influenced more by the information carried by a noise signal than by its level. In humans, as in animals the auditory system is used for fast coping reactions. Mostly in dangerous situations the fight / flight reaction will be adequate for persons who are awake but useless for those who are sleeping. In this case a reaction which optimises the chances for survival during defeat seems to be adequate. It would be detrimental to health, however, if this reaction which includes an activation of the HPA axis and an increase of cortisol, would be triggered by all kinds of noises i.e. wind, rain or even snoring of the partner. Therefore, the ability of the amygdala to learn to distinguish danger indicating noise stimuli from neutral ones, is essential for health.

The problem of traffic noise is illustrated by the following example. The amygdala of modern man has learned that it is necessary for survival to trigger the flight reaction when he hears the noise of an approaching lorry while crossing the road. However, if he watches the traffic from a balcony the same noise will not trigger a flight reaction because the amygdala is overruled by the cortex. In contrast to this, an unexpected and sudden very loud noise will quite probably cause a shock reaction and a prickling sensation right down to the toes. This is caused by adrenaline release in the flight reaction. In this case reasoning is too slow to prevent the flight reaction. If on the other hand, modern man is sleeping near a busy road, his amygdala has no other option than to react to the lorry noise with the defeat reaction. Since nearly 20% of the European population is exposed to high levels of traffic noise during the night, chronically repeated reactions with cortisol increase will be a widespread problem. Born & Fehm show that cortisol increase during early sleep is detrimental to health, at least when this occurs repeatedly over years.

A review of the empirical studies on noise induced stress hormone increase demonstrates the present state of knowledge. The most important result is the indication that chronic traffic noise exposure at night time may lead to chronic increase of cortisol and that is increase may even exceed the normal range of cortisol (Ising & Braun). Support for the credibility of these results of human studies is supplied by animal experiments. This may appear rather strange for the noise effect expert, since normally the influence of the cortex is predominant in reactions to noise, and in all situations where reasoning plays a major role in noise effects, animal experiments are useless.

On the other hand, for the stress expert, animal experiments are the basis for knowledge and the applicability to humans is generally accepted. Therefore, it is necessary to consider the pre­conditions under which stress effects of noise are similar in animals and humans. From the above arguments it follows as an important pre­condition that reasoning must not influence the effects of noise. Obviously this condition is met in sleeping person/animals. More generally speaking, the condition is that the noise effects should not be influenced substantially by cortical processes. An influence of the brainstem, however, will not invalidate an animal experiment as a model of human stress responses to noise.

In addition to the animal experiments, the possible long term health consequences of chronic cortisol increase are discussed by Spreng. On this basis it is not surprising that Babisch could demonstrate from the literature consistent evidence for an increase of cardiovascular risk in people exposed to traffic noise. His review will be published in a later volume of Noise & Health while in this special issue the paper of Neus and Boikat gives an evaluation of the traffic noise related cardiovascular risk in comparison to the cancer risk induced by air pollution. This risk evaluation is a first step towards a comprehensive risk assessment as demanded at the Third Ministerial Conference on Environment and Health (London, June 1999).

Top
Correspondence Address:
Deepak Prasher
Institute of Laryngology and Otology, University College London, 330 Gray's Inn Road, London WC1X 8EE
United Kingdom
Login to access the Email id

Source of Support: None, Conflict of Interest: None


PMID: 12689467

Rights and PermissionsRights and Permissions




 

Top