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The auditory system is permanently open - even during sleep. Its quick and overshooting excitations caused by noise signals are subcortically connected via the amygdala to the hypothalamic-pituitary-adrenal-axis (HPA-axis). Thus noise causes the release of different stress hormones (e.g. corticotropin releasing hormone: CRH; adrenocorticotropic hormone: ACTH) especially in sleeping persons during the vagotropic night/early morning phase. These effects occur below the waking threshold of noise and are mainly without mental control.
Animal experiments show noise-induced changes in sensitivity of cellular cortisol receptors by increase of heat-shock proteins, and ultrastructural changes in the tissue of the heart and the adrenal gland. Increased cortisol levels have been found in humans when exposed to aircraft noise or road traffic noise during sleep.
The effects of longer-lasting activation of the HPA-axis, especially long term increase of cortisol, are manifold: immuno suppression (e.g. eosinopenia), insulin resistance (e.g. diabetes), cardiovascular diseases (e.g. hypertension and arteriosclerosis), catabolism (e.g. ostoeporosis), intestinal problems ( e.g. stress ulcer) etc.
Even worse may be the widespread extrahypothalamical effects of CRH/and/or ACTH which have the potential to influence nearly all regulatory systems, causing for example stressdysmenorrhea etc. as signs of disturbed hormonal balance. Keywords: Noise, stress, cortisol receptors, health effects.
How to cite this article:
Spreng M. Possible health effects of noise induced cortisol increase. Noise Health 2000;2:59-63 |
| Introduction | |  |
The auditory system usually reacts to both amplitude and frequency modulations of changing environmental sounds with considerable overshooting excitations reaching the brainstem regions within 5 to 10 ms and the cortical areas within 20 to 100 ms from the beginning of the stimulus onset. This was demonstrated both in animals and in awake humans using recordings of the brainstem and the cortical responses to the sounds being modulated with 10 to 100 dB/s or 2 to 14 kHz/s respectively (Spreng, 1980; 1985; 1997).
The lateral amygdala is an important subcortical part of the auditory system (Masterton, 1996). Its close connection to the hypothalamus and therefore to the main control system of the autonomic nervous system (Feldmann, 1998) is important for the immediate influence of noise upon the organisms. In addition the plasticity of amygdala and supporting neurons is the basis for increasing sensitisation to adverse sounds (Spreng, 2000).
Thus it is easy to understand why via the continuously open auditory system noise as the main environmental stressor produces remarkable release of hypothalamic hormones such as the corticotropin releasing hormone (CRH) and the adrenocorticotropic hormone (ACTH). Besides other extrahypothalamic impacts within the brain, these substances increase the activity of the hypothalamopituitary-adrenal-axis (HPA-axis) and the release of corticosterone (e.g. cortisol) from the adrenal cortex. This happens mainly without the possibility to use mentally controlled coping strategies, often during sleep and without waking-up those exposed persons (Maschke et al. 1995). Therefore these noise effects are not accompanied with a feeling of annoyance.
Noise and stress hormone reactions in animals
There exist a considerable number of newer animal experiments emphasising the effects of noise stress upon the corticosterone related systems and therefore upon different levels in living beings.
In this connection it is very important, that the cytoplasmatic steroid (cortisol) receptors, acting with so called heat-shock proteins (HSP), in most functional parts of the organism (e.g. heart, kidney, gonads) seem to change their behaviour. Those HSPs, which have been shown to provide information on the biological impact of environmental stress to organisms, are increased by different stressors. In the myocardial tissue of birds exposed to loud noise an increase of HPS70 has been found recently (Hoekstra et al., 1998).
For this reason, findings are not surprising which show for instance changes of the myocardial ultrastructure (subcellular alterations of cardiomyocytes, mitochondria, vesiculated sarcoplasmatic reticulum) ) combined with an increase of corticosterone levels in rats after exposure to noise for 7 days (6 hours). Remarkable are also the ultrastructural changes in the adrenal gland of rats after noise exposure (1 to 12 hours, Pellegrini et al., 1997). This gland, producing cortisol (controlled by ACTH) and androgens, showed clearly after noise exposure affected cells (diluted cytoplasm, disarranged endoplasmic reticulum, some altered mitochondria) in its reticular zone.
Comparing the dynamic pattern of basal and noise stimulated HPA activity in rats, revealed the existence of a clear relationship between basal and stimulated activities (Windle et al., 1998). A significant increase by a factor two was seen, when noise stress coincided with the rising (secretory active) phase of a basal (circadian) rhythm. In contrast, when noise stress coincided with a falling phase a significantly smaller response was evoked. Thus, the alternate periods of secretion and inhibition which generate the basal hypothalamo-pituitaryadrenal activity, are important determinants of responses to acute stress.
Noise induced increase of cortisol in men
Some newer publications report significantly increased cortisol levels when noise influenced mental effort (arithmetic calculation, Tafalla and Evans, 1997; Miki et al., 1998). In addition increased levels of cortisol were reported in persons, who were experimentally exposed to aircraft noise with maximal levels of 55-65 dB(A) (Maschke et al., 1995) during sleep at home. In several cases the excretion exceeded the normal range (Spreng, 1996 and 1997).
In a study with experimental nighttime noise exposure for five weeks, Harder et al. (1999) found different types of cortisol reactions: Long term habituation, hyperreaction and hyporeaction. The latter two can be interpreted as an indication of long term dysregulation of the HPA axis. The results of Ising and Braun (2000) show that long term road traffic noise may lead to chronic increase of cortisol - in some cases above the normal range.
Health effects of increased cortisol
The following health effects of chronically high cortisol levels are long known:
- Catabolic effects
Protein degradation is accelerated in muscles, skin and lymphatic tissue. Promotion of osteoporosis. Transformation of amino acids to glucose.
- Anti-anabolic effects
Reduced synthesis of muscle proteins because of inhibited transport of amino acids into the cells.
- Diabetogenic effect
Inhibition of transport and utilisation of glucose with increasing levels of glucose in blood.
- Hypertonic effects
Enhanced sensibility of the adreno receptors of the vasomotors. Increased renal retention of sodium.
- Immuno suppression
Reduction of thymus and lymphatic tissue. Decrease of circulating eosinophilic (eosinopenia) and basophilic granulocytes and of leucocytes. Lowering of the effect of most of the lymphokines.
Inhibition or prolongation of wound healing.
- Stress ulcer
Increased secretion of gastric juice. Inhibition of healing.
- Adipose tissue metabolism
Lipolysis of triglycerides increase the level of fatty acids in blood and the risk of arteriosclerosis.
Besides these well known negative health effects recent publications additionally emphasise manifold effects of a longer-lasting activation of the HPA- axis and thus elevated levels of cortisol.
Overactivation of the HPA axis leads to the genesis of disease precursors (Bjorntorp, 1997) such as abdominal obesity and decreased secretions of sex steroids as well as of growth hormone. Furthermore, these hormonal abnormalities seem to contribute to the development of insulin resistance. Activation of the HPA axis results in metabolic abnormalities including early signs of diabetes. Raised plasma cortisol concentrations are inversely related to measures of glucose intolerance (Clark, 1998).
Chronically increased cortisol promotes a net central fat deposition, since the intracellular lipolysis is decreased, reflecting decreased hormone-sensitive lipase action in this region. It also increase systemic glycerol and nonesterified fatty acids in the blood, thus raising the risk of arteriosclerosis and myocardial infarction (Samra et al., 1998).
The widespread extrahypothalamically distributions of CRH and/or ACTH are able to influence nearly all the regulatory systems. This includes alterations of the cardiovascular, gonadal (Fabbri, 1990), digestive and metabolic functions (Yasuda and Nakamura, 1997). For instance the hypothalamic-pituitary-ovarian axis may play a role in the pathogenesis of stress-dysmenorrhea. Hyperandrogenicity in woman is probably another consequence. Reproductive functions are suppressed during high levels of CRH induced by stress (Rivier and Vale, 1984). In addition digestive functions and endocrine activities of the pancreatic islets are altered when CRH release is enhanced (Moltz et al., 1984; Williams et al. 1987).
These facts indicate that endocrine noise effects may play a role in widespread functional disorders or even diseases. Especially the results of epidemiological studies on traffic noise and the cardiovascular risk can be explained theoretically by noise-induced chronic increase of cortisol.[25]
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Correspondence Address:
M Spreng
Dept. Physiology and Experimental Pathophysiology, University of Erlangen, Universitaetsstrasse 17, D-91054 Erlangen
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 12689472 
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