Impulse noise causes evidently more severe hearing loss than steady state noise. The additional effect of occupational impulse noise on hearing has been shown to be from 5 to 12 dB at 4 kHz audiometric frequency. Reported cases for compensated for hearing loss are prevalent in occupations where noise is impulsive. For impulse noise two measurement methods have been proposed: the peak level method and energy evaluation method. The applicability of the peak level method is difficult as even the recurrent impulses have different time and frequency characteristics. Various national risk criteria differ from international risk criteria. In France the maximum A-weighted peak level is 135 dB, and in the United Kingdom the C-weighted peak sound pressure is limited to 200 Pa (140 dB). This criterion of unweighted 200 Pa (140 dB) is used in European Union (EU) directive 86/188 and ISO 1999-1990 regardless of the number of impulses. The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended that no exposure in excess of a C-weighted peak sound pressure level of 140 dB should be permitted. At work places these norms do not cause any practical consequences since the impulses seldom exceed 140 dB peak level. In several occupations the impulses are so rapid that they contribute only a minimal amount to the energy content of noise. These impulses can damage the inner ear even though they cause reduced awareness of the hazard of noise. Based to the present knowledge it is evident that there is the inadequacy of the equal energy principle in modelling the risk for hearing loss. The hearing protectors attenuate industrial impulse noise effectively due to the high frequency contents of impulses. Directive regarding the exposure of workers to the risks arising from noise requires that in risk assessment attention should be paid also to impulsive noise. So far there is no valid method to combine steady state and impulse noise. A statistical method for the measurements of industrial impulse noise is needed to get a preferably single number for risk assessment. There is an urgent task to develop risk assessment method and risk criteria for impulsive noise to meet the requirements of the upcoming European Union noise directive.

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Stress is an unavoidable every-day phenomenon. Physiological coping with stress depends on the appropriate release of stress hormones as well as their alleviation at the termination of the stress. Despite quite a body of research indicating that stress affects inner ear function, this concept has found little application in otolaryngology. Today's evidence clearly indicates that the inner ear is equipped to detect stress hormones and some of these hormones have been shown to affect the inner ear function. Major stress control pathways shown to affect the inner ear include several third order axes, the hypothalamus-pituitary-adrenal axis, the hypothalamus-pituitary-thyroid axis and the hypothalamus-pituitary-gonadal axis whose functioning are interactive and inter-dependent. Less well-studied are the second order hypothalamus-pituitary control axis and its interaction with other hormones. To explore these we carried out a retrospective study on a series of Meniere's patients who had undergone a neurotomy of the vestibular nerve in the dept of ORL at the Hopital Nord, Marseille. Meniere's patients were particularly appropriate for this study since stress has long been recognised as a factor associated with the triggering of the symptoms of this pathology. Patients with acoustic neuroma and facial spasm were taken as a control population. We investigated the level of a battery of stress hormones including prolactin (3-endorphin and growth hormone. The blood sample was taken on the morning before surgery. The most striking observation was the presence of hyperprolactinemia in 30% of the Meniere patients (more than 20 µµg/l) with confirmation of prolactinoma in 6 patients. The level of O-endorphin could also be elevated. Horner, K.C., Guieu, R., Magnan, J., Chays, A. and Cazal, Y. Neuropysychopharmacology, (2001) 26:135-138. These observations suggest that neuroendocrinological feedback pathways controlling stress can be disturbed in Meniere's patients and depression of hypothalamic dopaminergic inhibition of prolactin secretion might be implicated. A further study on non-operated Meniere's patients presenting hyperprolactinemia and on dopamine agonist treatment, is needed in order to assess the role of stress in Meniere's patients. Progress in this domain could open the door towards integration of the stress concept into clinical management of various inner ear disorders.

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A lifetime of exposure to noise is likely to have negative effects on the hearing, but the interaction between noise-induced hearing loss (NIHL) and age-related hearing loss is difficult to determine. The most commonly accepted assumption is a simple accumulating effects of noise and ageing on the hearing. However, both a less than additive effect as well as a supra­additive effect has been proposed. Recently an interesting interaction between NIHL and age­related hearing loss has been reported (Gates et al., 2000). NIHL before old age reduces the effects of ageing at noise-associated frequencies, but accelerates the deterioration of hearing in adjacent frequencies. Findings from the longitudinal and cross-sectional gerontological and geriatric population study of 70-year-olds in Gothenburg, Sweden supports these observations. The incidence of tinnitus increases in old age, but not at the same high rate as presbyacusis. According to the gerontological and geriatric population study in Gothenburg tinnitus in old age is related more to hearing loss than to ageing. There are no simple correlations between exposure to noise during the active years and tinnitus in old age.

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There is increasing evidence that at least one function of both the medial and the lateral olivocochlear efferent systems is to provide adjustment of the set point of activity in their post­synaptic target, the outer hair cells and afferent processes, respectively. New results, summarized in this review, suggest that both efferent systems can provide protection from noise through this mechanism. There are also intracellular pathways that can provide protection from noise-induced cellular damage in the cochlea. This review also summarizes new results on the pathways that regulate and react to levels of reactive oxygen species in the cochlea as well as the role of stress pathways for the heat shock proteins and for neurotrophic factors in protection, recovery and repair.

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The condition in which individuals with normal pure tone audiograms complain of hearing difficulties, especially in the presence of background noise, (normal pure tone audiograms), has had a number of different names. The present term King-Kopetzky Syndrome was coined by Hinchcliffe in 1992. This is a common condition reported in 5 - 10% of those attending clinics complaining of hearing problems. A dominant genetic aetiology has been found in a proportion of cases. It may be associated with minor peripheral or central auditory dysfunction, and frequently the individuals exhibit anxious or depressive personalities. We found no relationship with noise exposure in a series of patients compared with matched controls. Here we review the evidence for and against such an influence and present fresh data in an attempt to define the role of noise, if any, in the causation of this condition. Our final conclusion is that there is no clear association between KKS and noise exposure

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In order to improve the living conditions for respondents highly exposed to traffic noise, it has been recommended that one side of the building should face a "quiet side". Quiet may, however, be spoilt by noise from installations such as ventilation and air-conditioning systems. The noises generated by installations of this kind often have a dominant portion of low frequencies (20-200 Hz) and may be a source of great annoyance and sleep disturbance. This paper describes the cross-sectional part of an intended intervention study among residents exposed to traffic noise on one side of the building and to low frequency noise from installations on the other side of the building. A questionnaire masked as a general living environment study was delivered to a randomly selected person in each household. In total 41 respondents answered the questionnaire (71% response rate). Noise from installations was measured indoors in a bedroom facing the courtyard in a selection of apartments and outdoors in the yard. 24h traffic noise outdoor and indoor levels were calculated. The noise levels from installations were slightly above or at the Swedish recommendations for low frequency noise indoors with the window closed and exceeded the recommendations by about 10 dB SPL when the window was slightly opened. The proportion of persons who reported that they were very or extremely annoyed indoors from noise from installations was more than twice as high as for traffic noise. Installation noise also affected respondents' willingness to have their windows open and to sleep with an open window. The high disturbance of installation noises found in this study indicates the importance of also regulating the noise exposure on the "quiet side" of buildings. Further studies will give a better base for the extent of annoyance and acceptable levels of installation noises.

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Individual animals and humans show differing susceptibility to noise damage even under very carefully controlled exposure conditions. This difference in susceptibility may be related to unknown genetic components. Common experimental animals (rats, guinea pigs, chinchillas, cats) are outbred-their genomes contain an admixture of many genes. Many mouse strains have been inbred over many generations raeducing individual variability, making them ideal candidates for studying the genetic modulation of individual susceptibility. Erway et al. (1993) demonstrated a recessive gene associated with early presbycusis in the C57BL/6J inbred mouse. A series of studies have shown that mice homozygous for Ahlallele are more sensitive to the damaging effects of noise. Recent work has shown that mice homozygous for Ahl are not only more sensitive to noise, but also are probably damaged in a different manner by noise than mice containing the wild-type gene (Davis et al., 2001). Recent work in Noben-Trauth's lab (Di Palma et al., 2001) has shown that the wild-type Ahl gene codes for a hair cell specific cadherin. Cadherins are calcium dependent proteins that hold cells together at adherins junctions to form tissues and organs. The cadherin of interest named otocadherin or CDH23, is localized to the stereocillia of the outer hair cells. Our working hypothesis, suggests that otocadherin may form the lateral links between stereocilia described by Pickles et al (1989). Reduction of, or missing otocadherin weakens the cell and may allow stereocilia to be more easily physically damaged by loud sounds and by aging.

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In order to investigate whether the energy-equivalence principle is at least acceptable for exposures with a duration in the range of hours and in order to disclose the actual physiological responses to exposures which varied with respect to the time structure and the semantic quality of sounds, a series of tests was carried out where physiological costs associated with varying exposures were measured audiometrically. In a cross-over test design, 10 Subjects (Ss) participated in test series with 3 energetically equal sound exposures on different days. The exposures corresponded with a tolerable rating level of 85 dB / 8 h. In a first test series (TS I), the Ss were exposed to a prototype of industrial noise with a sound pressure level of 94 dB(A) / 1 h. In a second test series (TS II), the same type of noise was applied, but the exposure time of a reduced level of 91 dB(A) was increased to 2 hours. In a third test series (TS III), classical music was provided also for 2 h at a mean level of 91 dB(A). The physiological responses to the 3 exposures were recorded audiometrically via the temporary threshold shift TTS ₂ , the restitution time t(0 dB), and the IRTTS-value. IRTTS is the integrated restitution temporary threshold shift which is calculated by the sum of all threshold shifts. It represents the total physiological costs the hearing must "pay" for the sound exposure. Physiological responses of the hearing to the industrial noise exposures in TS I and TS II, all in all, were identical in the 3 parameters. Maximum threshold shifts of approximately 25 dB occurred which did not dissipate completely until 2½ h after the end of the exposure and IRTTS-values of about 800 dBmin were calculated. Therefore, at least for exposure times in the range of hours, the equilibration of intensity and duration of sound exposures according to the energy-equivalence principle seems to have no influence on the hearing. Classical music was associated with the least severe TTS of less than 10 dB which disappeared much more quickly. IRTTS added up to just about 100 dBmin and, in comparison with 800 dBmin as specific responses to industrial noise, amounted to only about 12%. The substantially lower physiological costs of classical music apparently indicate a decisive influence of the type of sound exposures. Making inferences from the results of the study, the conventional approach of rating sound exposures exclusively by the principle of energy­equivalence can lead to gravely misleading assessments of their actual physiological costs.

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