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62 EFFECTS ON HEALTH Noise Exposure (Sound Level) Direct pathway Indirect pathway Hearing loss Disturbance of activities, sleep, communication Cognitive and emotional response Annoyance Stress Indicators Fig. 4.3 Noise effects reaction scheme Physiological stress reactions (unspecific) – Autonomic nervous system (sympathetic nerve) – Endocrine system (pituitary gland, adrenal gland) Risk Factors Source: Babisch, 2002. Blood pressure Cardiac output Blood lipids Blood glucose Blood viscosity Blood clotting factors Manifest Disorders Cardiovascular Diseases Hypertension Arteriosclerosis Ischaemic heart disease noise are known to be classical cardiovascular risk factors, the hypothesis has emerged that chronic noise exposure increases the risk of hypertension, arteriosclerosis and IHD. Its relevance for public health comes from the high prevalence of cardiovascular diseases in developed and industrialized countries. It is unclear as to what extent chronically repeated noise-induced sleep disturbance contributes to the development of somatic health disorders. Only a few epidemiological studies address this particular issue. Epidemiological noise research has seldom distinguished between day and night exposures, or between the exposure of the living room and the bedroom. However, some deduction can be made from daytime to night-time exposure. 4.5.2 NOISE AND STRESS–REACTION MODEL The auditory system is continuously analysing acoustic information, which is filtered and interpreted by different cortical and subcortical brain structures. The limbic system, including the hippocampus and the amygdala, plays an important role in the emotional processing pathways (Spreng, 2000). It has a close connection to the hypothalamus that controls the autonomic nervous system and the hormonal balance of the body. Laboratory studies found changes in blood flow, BP and heart rate in reaction to noise stimuli as well as increases in the release of stress hormones including the catecholamines adrenaline and noradrenaline, and the corticosteroid NIGHT NOISE GUIDELINES FOR EUROPE
EFFECTS ON HEALTH 63 cortisol (Berglund and Lindvall, 1995; Maschke, Rupp and Hecht, 2000; Babisch, 2003). Such changes also occur during sleep without the involvement of cortical structures. The amygdala has the capacity to learn due to its plasticity, particularly with respect to the meaning of sound stimuli (for example, danger of an approaching lorry) (Spreng, 2000, 2004). Acoustic stimulation may act as an unspecific stressor that arouses the autonomous nervous system and the endocrine system. The generalized psychophysiological concept given by Henry and Stephens can be applied directly to noise-induced stress reaction (Henry, 1992). The stress mechanism as such is genetically determined but it may be modified by experience and environmental factors. Its biological function is to prepare the organism to cope with a demanding stressor. The arousal of the sympathetic and endocrine system is associated with changes in physiological functions and the metabolism of the organism, including BP, cardiac output, blood lipids (cholesterol, triglycerides, free fatty acids, phosphatides), carbohydrates (glucose), electrolytes (magnesium, calcium), blood clotting factors (thrombocyte aggregation, blood viscosity, leukocyte count) and others (Friedman and Rosenman, 1975; Cohen, Kessler and Underwood Gordon, 1995; Lundberg, 1999). In the long term, functional changes and dysregulation may occur, thus increasing the risk of manifest diseases. Fig. 4.3 shows the principal reaction schema used in epidemiological noise research for hypothesis testing (Babisch, 2002). It simplifies the cause–effect chain, that is: sound – annoyance (noise) – physiological arousal (stress indicators) – (biological) risk factors – disease – and mortality (the latter is not explicitly considered in the graph). The mechanism works “directly” through synaptic nervous interactions and “indirectly” through the emotional and the cognitive perception of the sound. It should be noted that the “direct” pathway is relevant even at low sound levels particularly during sleep, when the organism is at its nadir of arousal. The objective noise exposure (sound level) and the subjective noise “exposure” (annoyance) may serve independently as exposure variables in the statistical analyses of the relationship between noise and health end points. Principally, the effects of environmental noise cannot directly be extrapolated from results of occupational noise studies. The two noise environments cannot simply be merged into one sound energy-related dose–response model (for example, a simple 24-hour average noise level measured with a dose-meter). Noise effects are not only dependent on the sound intensity but also on the frequency spectrum, the time pattern of the sound and the individuals’ activities which are disturbed. Therefore, epidemiological studies carried out under real-life conditions can provide the basis for a quantitative risk assessment provided that there is adequate control over confounding and exposure variables. Other noise sources might act as confounders and/or effect modifiers on the association of interest. The effects of road traffic noise (at home) were shown to be stronger in subjects who were also exposed to high noise levels at work (Babisch et al., 1990). 4.5.3 PREVIOUS REVIEWS ON ENVIRONMENTAL NOISE AND CARDIOVASCULAR RISK Causality in epidemiology can never be completely proven (Schlesselman, 1987; Christoffel and Teret, 1991; Weed, 2000). It is a gradual term for which evidence is increasing with the increasing number of facts. However, the magnitude of effect, the presence of a dose–response relationship and consistency with other studies in different populations and with different methodology and biological plausibility are NIGHT NOISE GUIDELINES FOR EUROPE
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NIGHT NOISE GUIDELINES FOR EUROPE
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Keywords NOISE - ADVERSE EFFECTS -
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IV CONTENTS CHAPTER 3 EFFECTS OF NI
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VI ABSTRACT The WHO Regional Office
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VIII LIST OF CONTRIBUTORS Torbjörn
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X EXECUTIVE SUMMARY PROCESS OF DEVE
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XII EXECUTIVE SUMMARY An example of
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XIV EXECUTIVE SUMMARY Effect Indica
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XVI EXECUTIVE SUMMARY 50 100 Fig. 4
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XVIII EXECUTIVE SUMMARY For the pri
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2 METHODS AND CRITERIA impact on th
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4 METHODS AND CRITERIA ITALY: NETHE
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6 METHODS AND CRITERIA There are im
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8 METHODS AND CRITERIA use and heal
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10 METHODS AND CRITERIA L night = L
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Page 36 and 37: 16 SLEEP AND HEALTH • Stage 2 req
Page 38 and 39: 18 SLEEP AND HEALTH Table 2.3 Mean
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Page 66 and 67: 46 EFFECTS ON SLEEP ing sleep stage
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Page 122 and 123: 102 GUIDELINES AND RECOMMENDATIONS
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112 Ancoli-Israel S, Roth T (1999).
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114 Bistrup ML (2003). Prevention o
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116 Cartwright J, Flindell I (2000)
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118 der Streßforschung (Bonner Ver
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120 Goto K, Kaneko T (2002). Distri
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122 Ishihara K (1999). The effect o
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124 Kogi K, Ohta T (1975). Incidenc
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126 Marth E et al. (1988). Fluglär
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128 Nieminen P et al. (2002). Growt
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130 Reyner et al. (1995). Patterns
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132 Suter AH (1992). Noise sources
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134 Weed DL (2000). Interpreting ep
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136 APPENDICES Term/acronym Definit
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138 APPENDICES APPENDIX 3. ANIMAL S
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140 APPENDICES cause a certain habi
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142 APPENDICES • Acute exposure t
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144 APPENDICES dence indicate that
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146 APPENDICES Fig.1 Effects of 12
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) 148 APPENDICES 50 40 Young rats O
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150 APPENDICES neuronal degeneratio
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152 Gesi M et al. (2002a). Morpholo
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154 APPENDIX 4. NOISE AND SLEEP IN
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156 APPENDICES during quiet sleep (
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158 APPENDICES (American Academy of
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160 APPENDICES cents, 12.2% of adol
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162 REFERENCES Abel SM (1990). The
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The WHO Regional Office for Europe
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