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22 SLEEP AND HEALTH mal range. The hypothesis that an increased risk of cardiovascular diseases is connected with stress concepts is generally accepted (Ekstedt, Åkerstedt and Soderstrom, 2004; Ising and Kruppa, 2004). Stress reactions may lead to derangement of normal neurovegetative and hormonal processes and influence vital body functions. Cardiovascular parameters such as BP, cardiac function, serum cholesterol, triglycerides, free fatty acids and haemostatic factors (fibrinogen) impede the blood flow through increased viscosity and presumably blood sugar concentration as well. Insulin resistance and diabetes mellitus, stress ulcers and immune system deficiency are also frequent consequences of stress reaction. Disturbed sleep may lead to immunosuppression and diminished protein synthesis (Horne, 1988). As well as nonspecific effects of the stress response on the functioning of the immune system, there is considerable evidence for a relation between sleep, especially SWS, and the immune system (Brown, 1992). This evidence includes surges of certain immune parameters and growth hormones at onset of SWS, correlation of non-REM sleep, total sleep time and sleep efficiency with natural killer cell activity, and correlation of SWS with recovery from infections. These data, taken together with information on the effect of intermittent transportation noise on SWS during the first sleep cycles and overnight, suggest that the immune response could also be impacted directly by environmental noise during sleep (Carter, 1996). 2.2.3 SLEEP RESTRICTION, ENVIRONMENTAL STRESSORS (NOISE) AND BEHAVIOURAL, MEDICAL AND SOCIAL HEALTH CONSEQUENCES OF INSUFFICIENT SLEEP: RISK OF MORBIDITY AND MORTALITY Sleep restriction due to environmental stressors leads to primary sleep disorders, but health is also influenced by the consequence of stress response to noise mediated by the HPA axis and/or by restriction of specific sleep stages (see above). Sleep restriction leads, in approximately 40% of affected subjects, to daytime sleepiness that interferes with work and social functioning. Excessive daytime sleepiness is thus a major public health problem, as it interferes with daily activities, with consequences including cognitive problems, motor vehicle accidents (especially at night), poor job performance and reduced productivity (Lavie, Pillar and Malhotra, 2002). In the last decade, experimentally based data have been collected on chronic restriction of sleep (by 1–4 hours a night), accumulating daytime sleepiness and cognitive impairment. Most individuals develop cognitive deficits from chronic sleep debt after only a few nights of reduced sleep quality or quantity. New evidence suggests additional important healthrelated consequences of sleep debt related to common viral illnesses, diabetes, obesity, heart disease, depression and other age-related chronic disorders. The effects and consequences of sleep deprivation are summarized in Table 2.4 (Lavie, Pillar and Malhotra, 2002). The relationship between sleep quantity and quality and estimates of morbidity and mortality remains controversial. Epidemiological data (NCSDR, 2003) suggest that habitually short sleep (less than 6 hours sleep per night) is associated with increased mortality. Epidemiological studies in recent years elucidated, however, that too much sleep is a problem as well. Kripke et al. (2002) evaluated a questionnaire study of 1.1 million men and women aged 30–102 years and found the lowest mortality risk between respondents sleeping 7 hours per night. NIGHT NOISE GUIDELINES FOR EUROPE
SLEEP AND HEALTH 23 Type Short-term Long-term Behavioural Sleepiness Depression/mania Mood changes Violence Irritability and nervousness Cognitive Impairment of function Difficulty in learning new skills Short-term memory problems Difficulty with complex tasks Slow reaction time Neurological Mild and quickly Cerebellar ataxia, reversible effects nystagmus, tremor, ptosis, slurred speech, increased reflexes, increased sensitivity to pain Biochemical Increased metabolic Decreased weight rate despite increased Increased thyroid caloric intake activity (in animals) Insulin resistance Diabetes, obesity (in humans) Others Hypothermia Susceptibility to Immune function viral illness impairment Table 2.4 Consequences of sleep deprivation Mortality risk significantly increased when sleep duration was less than 6 or higher than 8 hours per night. Other authors have also published similar results (Patel et al., 2004; Tamakoshi and Ohno, 2004). Patel et al. (2004) in a prospective study of sleep duration and mortality risk in 5409 women confirmed previous findings that mortality risk is lowest among those sleeping 6–7 hours per night. The mortality risk for death from other causes significantly increased in women sleeping less than 5 and more than 9 hours per night. It is not clear how the length of sleep can increase this risk, although animal evidence points to a direct link between sleep time and lifespan (see section 2.5 in this chapter). Up to now, no epidemiological prospective study has been published that examines the relationship between sleep and health outcomes (morbidity and mortality) with subjective and objective estimates. Recent studies, however, show that sleep duration of least 8 hours is necessary for optimal performance and for prevention of daytime sleepiness and accumulation of sleep debt. Environmental stressors, including noise, mostly cause insomnia. Insomnia also involves daytime consequences, such as tiredness, lack of energy, difficulty concentrating and irritability. A reasonable prevalence estimate for chronic insomnia in the general population is about 10%; for insomnia of any duration or severity this rises to between 30% and 50%, and incidence increases with ageing. In the course of perimenopausal time, women are particularly vulnerable to developing this complaint. The major consequences and co-morbidity of chronic insomnia (see Table 2.5) consist of behavioural, psychiatric and medical problems. Several studies also report a higher mortality risk (Zorick and Walsh, 2000). 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 22 and 23: 2 METHODS AND CRITERIA impact on th
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Page 26 and 27: 6 METHODS AND CRITERIA There are im
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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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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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