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20 SLEEP AND HEALTH vegetative, motor and sensory functions independently of each other. One of the possible factors indicating disturbed sleep is a vegetative arousal index. A vegetative arousal index of more than 30 per hour is certainly considered as serious, more than 20 per hour as intermediate and more than 10 as a light form of sleep disorder. With respect to insomnia (section 2.1.2), there is the possibility of misclassification if the general practitioner (GP) overlooks excessive noise as the possible cause of the complaint. There is also the possibility that the insomnia is aggravated by noise. 2.1.3 CONCLUSIONS Published information on normal sleep can serve as an outline for normal values in PSG. However, these values are only informative, because each sleep laboratory must study control subjects to identify any significant effects on sleep that result from differences in technique or environment. Excessive daytime sleepiness is a consequence of disturbed night sleep and can be objectively assessed by MSLT, which provides an objective quantification of “sleepiness”. 2.2 LONG-TERM HEALTH RISK MEDIATED BY SLEEP DISTURBANCES 2.2.1 STRESSORS, NEUROBEHAVIOURAL DATA AND FUNCTIONAL NEUROIMAGING It is generally accepted that insufficient sleep and particularly sleep loss has a great influence on metabolic and endocrine functions (Spiegel, Leproult and van Cauter, 1999), as well as on inflammatory markers, and contributes to cardiovascular risk. C-reactive protein (CRP) as a major marker of the acute phase response to inflammatory reaction promotes secretion of inflammatory mediators by vascular endothelium and may be therefore directly involved in the development of atherosclerotic lesions. CRP as a risk predictor of strokes and heart attacks linearly increases with total and/or partial sleep loss (Meier-Ewert et al., 2004). An additional factor, closely linked to cardiovascular health, glucose regulation and weight control, is leptin. Leptin is one of the major regulators of energy homeostasis and its circadian profile interacts closely with sleep. Secretion of leptin increases at night and decreases during the day. A decreased leptin level, that is connected with sleep loss, increases appetite and predisposes to weight gain, impaired glucose tolerance and impaired host response. Other studies have focused on how sleep loss affects neurobehavioural functions, especially neurocognitive performance. Functional brain imaging and EEG brain mapping studies show that the patterns of functional connectivity between brain regions, evident in the performance of specific cognitive tasks, are altered by sleep loss (NCSDR, 2003). According to this finding, the maintenance of sustained performance during sleep loss may depend upon regional functional plasticity. NIGHT NOISE GUIDELINES FOR EUROPE
SLEEP AND HEALTH 21 Cumulative waking, neurocognitive deficits and instability of state that develop from chronic sleep loss have a basis in a neurobiological process that can integrate homoeostatic pressure for sleep across days. Increased efforts have helped to determine the roles of REM and non-REM sleep in memory. Functional brain imaging techniques, such as positron emission tomography (PET), functional magnetic resonance imaging (fMRI), magnetic resonance spectroscopy (MRS), single photon emission computed tomography (SPECT) and magneto-electroencephalography (MEG), have recently been analysed in a study of sleep and waking (NCSDR, 2003). These techniques allow the measurement of metabolic and neurochemical activity throughout the brain, and can reveal dynamic patterns of regional cerebral activity during various brain states, including stages of sleep and levels of alertness during wakefulness or during functional challenge. These techniques can also help identify both normal and abnormal sleep/wake processes. In the last five years, functional neuroimaging techniques (particularly PET) have revealed that non-REM sleep is associated with the deactivation of central encephalic regions (brainstem, thalamus, basal ganglia) and multimodal association cortices (for instance, prefrontal and superior temporal/inferior parietal regions). REM sleep is characterized by reactivation of all central encephalic regions deactivated during non-REM sleep except the multimodal association areas. PET studies during sleepdeprived wakefulness have revealed regional cerebral deactivations that are especially prominent in prefrontal and inferior parietal/superior temporal cortices, and in the thalamus. This pattern is consistent and helpful in explaining the nature of cognitive performance deficits that occur during sleep loss. As revealed by means of fMRI techniques during cognitive task performance, the maintenance of performance following sleep loss may be a function of the extent to which other cortical brain regions can be recruited for task performance in the sleep-deprived state. PET, SPECT and fMRI studies have revealed, in depressed patients, initially elevated activation in anterior cingulate and medial orbital cortices (NCSDR, 2003). In these patients, sleep deprivation reduces this regional hyperactivation, and improvements in mood are a function of the extent to which this activity is reduced. These studies point to possible mechanisms by which antidepressant drugs may exert their effects. Further research should be oriented towards neuroimaging and measurements of changes in the brain’s metabolic activity at the neurotransmitter level. 2.2.2 SIGNALS MEDIATED BY A SUBCORTICAL AREA (THE AMYGDALA), THE ROLE OF STRESS HORMONES IN SLEEP DISTURBANCE AND THEIR HEALTH CONSEQUENCES Experimental as well as clinical studies (Waye et al., 2003; Ising and Kruppa, 2004) showed that the first and fastest signal of stressors introduced by noise is detected and mediated by a subcortical area represented by the amygdala while the stress response to noise is mediated primarily by the hypothalamus-pituitary-adrenal (HPA) axis. A major intrinsic marker of the circadian rhythm is in the level of circulating corticosteroids derived from activity within the HPA axis. A protracted stress response with activation of the HPA axis is a major physiological response to environmental stressors. The cortisol response to awakening is an index of adrenocortical activity, and long-term nocturnal noise exposures may lead, in persons liable to be stressed by noise, to permanently increased cortisol concentration above the nor- NIGHT NOISE GUIDELINES FOR EUROPE
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Page 4 and 5: Keywords NOISE - ADVERSE EFFECTS -
Page 6 and 7: IV CONTENTS CHAPTER 3 EFFECTS OF NI
Page 8 and 9: VI ABSTRACT The WHO Regional Office
Page 10 and 11: VIII LIST OF CONTRIBUTORS Torbjörn
Page 12 and 13: X EXECUTIVE SUMMARY PROCESS OF DEVE
Page 14 and 15: XII EXECUTIVE SUMMARY An example of
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Page 30 and 31: 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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70 EFFECTS ON HEALTH Regarding airc
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72 EFFECTS ON HEALTH 4.5.10 DOSE-RE
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74 EFFECTS ON HEALTH larger increas
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76 EFFECTS ON HEALTH 4.5.14 RISK EV
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78 EFFECTS ON HEALTH No particular
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80 EFFECTS ON HEALTH Research into
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82 EFFECTS ON HEALTH tle direct res
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84 EFFECTS ON HEALTH level of expos
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86 EFFECTS ON HEALTH lage newly exp
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88 EFFECTS ON HEALTH ting the stres
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90 EFFECTS ON HEALTH In a United Ki
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92 EFFECTS ON HEALTH 4.8.14 ASSOCIA
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94 EFFECTS ON HEALTH noise-related
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96 EFFECTS ON HEALTH have had exper
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98 EFFECTS ON HEALTH • number of
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100 EFFECTS ON HEALTH Furthermore,
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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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