Auditory and non-auditory effects of noise on health

Noise is pervasive in everyday life and can cause both auditory and non-auditory health eff ects. Noise-induced hearing loss remains highly prevalent in occupational settings, and is increasingly caused by social noise exposure (eg, through personal music players). Our understanding of molecular mechanisms involved in noise-induced haircell and nerve damage has substantially increased, and preventive and therapeutic drugs will probably become available within 10 years. Evidence of the non-auditory eff ects of environmental noise exposure on public health is growing. Observational and experimental studies have shown that noise exposure leads to annoyance, disturbs sleep and causes daytime sleepiness, aff ects patient outcomes and staff performance in hospitals, increases the occurrence of hypertension and cardiovascular disease, and impairs cognitive performance in schoolchildren. In this Review, we stress the importance of adequate noise prevention and mitigation strategies for public health.

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Auditory and non-auditory eff ects of noise on health

The interest in the systematic study of the circadian typology (CT) is relatively recent and has developed rapidly in the two last decades. All the existing data suggest that this individual difference affects our biological and psychological functioning, not only in health, but also in disease. In the present study, we review the current literature concerning the psychometric properties and validity of CT measures as well as individual, environmental and genetic factors that influence the CT. We present a brief overview of the biological markers that are used to define differences between CT groups (sleep-wake cycle, body temperature, cortisol and melatonin), and we assess the implications for CT and adjustment to shiftwork and jet lag. We also review the differences between CT in terms of cognitive abilities, personality traits and the incidence of psychiatric disorders. When necessary, we have emphasized the methodological limitations that exist today and suggested some future avenues of work in order to overcome these. This is a new field of interest to professionals in many different areas (research, labor, academic and clinical), and this review provides a state of the art discussion to allow professionals to integrate chronobiological aspects of human behavior into their daily practice.

Circadian typology: a comprehensive review.

Sleep and circadian rhythm disruption are frequently observed in patients with psychiatric disorders and neurodegenerative disease. The abnormal sleep that is experienced by these patients is largely assumed to be the product of medication or some other influence that is not well defined. However, normal brain function and the generation of sleep are linked by common neurotransmitter systems and regulatory pathways. Disruption of sleep alters sleep-wake timing, destabilizes physiology and promotes a range of pathologies (from cognitive to metabolic defects) that are rarely considered to be associated with abnormal sleep. We propose that brain disorders and abnormal sleep have a common mechanistic origin and that many co-morbid pathologies that are found in brain disease arise from a destabilization of sleep mechanisms. The stabilization of sleep may be a means by which to reduce the symptoms of--and permit early intervention of--psychiatric and neurodegenerative disease.

Sleep and circadian rhythm disruption in psychiatric and neurodegenerative disease

Melatonin is a ubiquitous molecule and widely distributed in nature, with functional activity occurring in unicellular organisms, plants, fungi and animals. In most vertebrates, including humans, melatonin is synthesized primarily in the pineal gland and is regulated by the environmental light/dark cycle via the suprachiasmatic nucleus. Pinealocytes function as 'neuroendocrine transducers' to secrete melatonin during the dark phase of the light/dark cycle and, consequently, melatonin is often called the 'hormone of darkness'. Melatonin is principally secreted at night and is centrally involved in sleep regulation, as well as in a number of other cyclical bodily activities. Melatonin is exclusively involved in signaling the 'time of day' and 'time of year' (hence considered to help both clock and calendar functions) to all tissues and is thus considered to be the body's chronological pacemaker or 'Zeitgeber'. Synthesis of melatonin also occurs in other areas of the body, including the retina, the gastrointestinal tract, skin, bone marrow and in lymphocytes, from which it may influence other physiological functions through paracrine signaling. Melatonin has also been extracted from the seeds and leaves of a number of plants and its concentration in some of this material is several orders of magnitude higher than its night-time plasma value in humans. Melatonin participates in diverse physiological functions. In addition to its timekeeping functions, melatonin is an effective antioxidant which scavenges free radicals and up-regulates several antioxidant enzymes. It also has a strong antiapoptotic signaling function, an effect which it exerts even during ischemia. Melatonin's cytoprotective properties have practical implications in the treatment of neurodegenerative diseases. Melatonin also has immune-enhancing and oncostatic properties. Its 'chronobiotic' properties have been shown to have value in treating various circadian rhythm sleep disorders, such as jet lag or shift-work sleep disorder. Melatonin acting as an 'internal sleep facilitator' promotes sleep, and melatonin's sleep-facilitating properties have been found to be useful for treating insomnia symptoms in elderly and depressive patients. A recently introduced melatonin analog, agomelatine, is also efficient for the treatment of major depressive disorder and bipolar affective disorder. Melatonin's role as a 'photoperiodic molecule' in seasonal reproduction has been established in photoperiodic species, although its regulatory influence in humans remains under investigation. Taken together, this evidence implicates melatonin in a broad range of effects with a significant regulatory influence over many of the body's physiological functions.

Melatonin: Nature's most versatile biological signal?

Effects of infrared radiation on the diurnal rhythms of melatonin, rectal temperature and heart rate

In two experimental series (19 resp. 53 nights, 2 different persons in each series, test-time 10.30 p.m. to 3.00 a.m.) pulse rate after sonic booms had been recorded during sleep. In the first 3 nights the subjects slept undisturbed by noise. In the following 11 resp. 30 nights sonic booms were applied alternately 2 or 4 times. In the main series after 10 more nights without any noise 4 nights with 8 and 16 sonic booms alternately followed. The last 6 undisturbed nights in both series were used as comparison phase. The interval between two sonic booms was 40 min in nights with 2 booms, 20 min in nights with 4 sonic booms and in the nights with 8 and 16 sonic booms 8.6 resp. 4.6 min. Sound level of the sonic booms ranged from 0.48 mbar to 1.45 mbar, 1 mbar 83.5 dB (A) in the average. The first sonic boom was applied if one of the two subjects had entered the deepest stage of sleep. Sonic booms induced a biphasic reaction in pulse rate. After an initial increase in frequency with a maximum in the 4th sec pulse rate decreased below the value before sonic boom; it was followed by a slow increase towards the baseline value. This reaction was analysed with special regard to the following factors: 1. Intensity. Due to very fast increase of noise intensity there was no significant correlation between the intensity of sonic boom and the pulse reaction. 2. Exogenic variables. There is no significant connection between postboom pulse rate and noiseless time before the sonic boom, the duration of the test series and the ambient temperature. 3. Endogenic variables. No correlation could be found between the stage of sleep and the reaction. On the contrary a very significant correlation was found between the maximum of postboom increase of pulse rate and the pulse rate before boom. With increasing pulse rate the extent of reaction becomes smaller. Language: de

Changes of pulse rate caused by sonic bomms during sleep

Night-time noise annoyance

It was hypothesized that acclimation is similar for any climate with the same value of a given thermal index. Therefore, 8 subjects each were exposed during 15 consecutive days to either a warm-humid, a hot-dry, or a climate with radiant load with ever the same wet bulb globe temperature (WBGT). As expected, heart rates and core temperatures decreased gradually, and sweat rates increased. Heart rates level off first, followed by core temperatures, and finally by sweat loss. The courses of acclimation are similar for the 3 climates, but this process is most rapid during the warm-humid condition and it needs the longest time for radiant load.. The hot-dry condition is the most strainous.

Acclimation to 3 Different Climates with the Same Wet Bulb Globe Temperature

In zwei Versuchsserien mit einer Dauer von 19 bzw. 53 Nachten (Versuchszeit ca. 22.30 Uhr bis 3 Uhr) wurde (bei je 2 Versuchspersonen) die Veranderung der Pulsfrequenz durch Uberschallknalle wahrend des naturlichen Nachtschlafes gepruft. Nach 3 Ruhenachten wurden 11 bzw. 30 Nachte lang 2 bzw. 4 Uberschallknalle im Wechsel appliziert. In der Hauptversuchsserie wurden den Probanden nach weiteren 10 Ruhenachten 4 Nachte lang abwechselnd 8 bzw. 16 Knalle dargeboten. Beide Versuchsserien wurden mit 6 abschliesenden Ruhenachten beendet. Die Pausendauer zwischen je 2 Knallen betrug in den Nachten mit 2 Knallen 40 min, mit 4 Knallen 20 min, mit 8 bzw. 16 Knallen 8,6 bzw. 4,6 min. Die Intensitat der Knalle erreichte im Schlafraum durchschnittlich etwa 1 mbar (0,48–1,45 mbar). Der erste Knall wurde ausgelost, sobald eine der beiden Versuchspersonen die Tiefschlafphase erreicht hatte. Die Uberschallknalle losten in aller Regel einen biphasischen Frequenzverlauf aus, wobei eine anfangliche Pulsfrequenzsteigerung, deren Maximum in der 4. sec liegt, in eine rasche, unter das Ausgangsniveau fallende Frequenzabnahme ubergeht, die von einem langsamen Wiederanstieg zum Ausgangswert gefolgt ist. Die Prufung der Zusammenhange zwischen dem poststimulatorischen Frequenzverlauf bzw. den einzelnen Frequenzparametern und den Moderatorvariablen ergab folgendes Bild: Wahrend die Schlaftiefe keine Reaktionsanderung bewirkt, besteht zwischen dem Maximum der poststimulatorischen Frequenzsteigerung und der Ruhepulsfrequenz ein signifikantes indirekt proportionales Verhaltnis.

Barbara Griefahn

Papers

Effects of infrared radiation on the diurnal rhythms of melatonin, rectal temperature and heart rate

Changes of pulse rate caused by sonic bomms during sleep

Night-time noise annoyance

Acclimation to 3 Different Climates with the Same Wet Bulb Globe Temperature

Pulsfrequenzänderung durch Überschallknalle während des Schlafes