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Ising H et al.  
Work noise as a risk factor in myocardial infarction

Journal of Clinical and Basic Cardiology 1999; 2 (1): 64-68

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Fig. 1: Lärmwahrnehmung - Lärmwirkung Fig. 2: Lärmwirkung Fig. 3: Lärmwirkung

Keywords: cortisolKalziumKatecholamineLärmstressmagnesiumMyokardinfarktcalciumcatecholaminescortisolmagnesiummyocardial infarctionnoise stress

Noise has the potential to cause stress reactions. Acute increases of catecholamines or cortisol were observed under noise exposure with maximal levels >= 90 dB (A) or >= 120 dB (A) respectively. However, if the noise disturbed activities such as conversation, concentration, recreation, sleep, acute increases of catecholamines and/or cortisol were observed even at environmental noise levels >= 50 dB (A). In sleeping persons, traffic noise with such levels caused significant increases of catecholamines and/or cortisol, which became chronic if the noise exposure was persistently repeated. An interaction process between endocrine reactions and intracellular Ca/Mg shifts was detected, which leads to pathological alterations in the myocardium and the vascular walls. These findings led to the hypothesis that chronic noise-induced stress increases the risk of myocardial infarction (MI). The hypothesis was tested in a case-control study with 395 MI patients (31-65 years) and 2148 controls. The relative risk of MI - adjusted for control variables (smoking, age, social status etc.) - was found to increase significantly and steadily with the loudness of work noise. Subjectively scaled work noise appeared to be the second greatest external risk factor in MI after smoking. Noise-induced chronic stress seems to be an important risk factor in myocardial infarction. Since in the reported study there was possibly bias due to overreporting of subjective noise exposure, additional studies on the relationship between cardiovascular diseases and work-related stressors including subjective and objective noise assessment are needed to quantify the risk of MI due to work noise. J Clin Basic Cardiol 1999; 2: 64-8.
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