ABSTRACT

Acute reactions to noise can be divided into direct and indirect reactions. Direct reactions are mediated by nervous and/or endocrine transduction without cortical intermediation.

Indirect noise effects are mediated by noise-induced disturbances to various activities followed by cortical responses, including psychological stress reactions, and lead to physiological stress reactions. Occupational noise exposure causes acute increases of noradrenaline and/or adrenaline and blood pressure. Traffic noise exposure during several hours of lectures, which reduced the intelligibility of syllables but not of sentences, had similar effects. Other indirect noise effects are increases of total cholesterol and decreases of magnesium, a recently detected risk factor for angina pectoris and sudden cardiac death. The mechanism of elevated magnesium excretion involves a temporary increase of Mg in blood serum and results in a long lasting decrease of intracellular Mg, e.g. in erythrocytes, which was correlated to increases of blood pressure. Pysiological effects of environmental noise exposure are usually accompanied by increases of noradrenaline or adrenaline. Nocturnal noise exposure, which alters the time pattern of sleep phases, causes stronger adrenaline increases than during the active phase. The combination of occupational noise exposure with traffic noise exposure at home causes increases of blood pressure and total cholesterol. Long-term extra-aural health effects of noise cannot be discussed on the basis of 24h –L_eq since the noise level, at which disturbance occurs, differs greatly from one activity to another. Noise-induced health effects correlate more closely to noise-induced disturbances of activities than to noise levels.

Our present knowledge about long-term extra aural health effects is sufficient to substantiate the need for protection against noise exposure causing severe disturbances, in order to prevent health risks.