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噪声的急慢性内分泌影响:水、土壤与空气卫生研究所开展的研究综述

Acute and chronic endocrine effects of noise: Review of the research conducted at the Institute for Water, Soil and Air Hygiene.

作者信息

Ising H., Braun C.

机构信息

Institute for Water, Soil and Air Hygiene, Federal Environmental Agency Berlin, Corrensplatz 1, 14195 Berlin, Germany.

出版信息

Noise Health. 2000;2(7):7-24.

Abstract

This is a review of the research into endocrine effects of noise since the early 1980s at the Institute for Water, Soil and Air Hygiene. According to our knowledge, no other group has studied systematically the endocrine effects of acute and chronic noise exposure. Mechanisms of acute noise-induced stress reactions as well as long-term increase of stress hormones in animal and persons under chronic noise exposure were studied. Our theoretical background was Henry's psychophysiological stress model with the two reaction alternatives : (i) The fight-flight reaction, characterised by an increase in adrenalin and noradrenaline (ii) The defeat reaction with increased cortisol. Extremely intense acute noise exposure near the threshold of pain caused an increased release of cortisol from the suprarenal cortex but acute noise exposure with levels between 90 and 100 dB(A) caused an increase of catecholamines. Non-habituated noise increased primarily the release of adrenalin from the suprarenal medulla, whereas habituated noise caused a chronic increase of noradrenaline from the sympathetic synapses under longterm noise exposure at work. Environmental noise exposure (Leq >/= 60 dB(A)) caused catecholamine increase if activities such as conversation, concentration, recreation etc were disturbed through noise. In sleeping persons, traffic noise with only Leq >/= 30 dB (A) and Lmax >/= 55 dB(A) caused significant acute increase of cortisol, which developed into chronic increase if the noise exposure was repeated consistently. Parallel to cortisol, chronic noradrenaline increase was also observed. Based upon the empirical results, a noise stress model was developed which is a first step forward in the theoretical understanding of endocrine noise effects.

摘要

这是一篇对自20世纪80年代初以来,水、土壤与空气卫生研究所关于噪声对内分泌影响的研究综述。据我们所知,没有其他研究团队系统地研究过急性和慢性噪声暴露对内分泌的影响。我们研究了急性噪声诱发应激反应的机制,以及慢性噪声暴露下动物和人类体内应激激素的长期增加情况。我们的理论基础是亨利的心理生理应激模型,该模型有两种反应模式:(i)战斗-逃跑反应,其特征是肾上腺素和去甲肾上腺素增加;(ii)失败反应,伴随皮质醇增加。接近疼痛阈值的极强急性噪声暴露会导致肾上腺皮质释放的皮质醇增加,但90至100分贝(A)的急性噪声暴露会导致儿茶酚胺增加。未适应的噪声主要增加肾上腺髓质中肾上腺素的释放,而适应的噪声在长期工作噪声暴露下会导致交感神经突触中去甲肾上腺素的慢性增加。如果交谈、集中注意力、娱乐等活动因噪声受到干扰,环境噪声暴露(等效连续A声级≥60分贝(A))会导致儿茶酚胺增加。在睡眠者中,等效连续A声级仅≥30分贝(A)且最大声级≥55分贝(A)的交通噪声会导致皮质醇显著急性增加,如果持续重复噪声暴露,这种增加会发展为慢性增加。与皮质醇增加同时,还观察到了去甲肾上腺素的慢性增加。基于实证结果,我们开发了一个噪声应激模型,这是在从理论上理解噪声对内分泌影响方面向前迈出的第一步。

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