Showing papers in "Noise & Health in 2001"

Ear damage caused by leisure noise.

Abstract: Noise is a health risk. Recent findings suggest that leisure noise is a substantial danger especially to children, teenagers and young adults. Epidemiological studies of teenagers with no occupational noise exposure show an increasing number with a substantial and measurable irreversible inner ear damage. This is basically due to the wide spread exposition to very loud toys (pistols and squibs), crackers and exposure to electronically amplified music, e.g. from personal cassette players (PCP), at discos or concerts etc. Protection against irreversible ear damage by leisure noise has an important impact in preventive medical care. Therefore the general public must be informed that loud leisure activities may cause damage to the ear. In order to protect children, young people and adults, the legislature ought to set limits for sound levels in discos, concert halls and for music equipment and toys by establishing the necessary standards and regulations.

Low frequency noise "pollution" interferes with performance

Abstract: To study the possible interference of low frequency noise on performance and annoyance, subjects categorised as having a high- or low sensitivity to noise in general and low frequency noise in particular worked with different performance tasks in a noise environment with predominantly low frequency content or flat frequency content (reference noise), both at a level of 40 dBA. The effects were evaluated in terms of changes in performance and subjective reactions. The results showed that there was a larger improvement of response time over time, during work with a verbal grammatical reasoning task in the reference noise, as compared to the low frequency noise condition. The results further indicated that low frequency noise interfered with a proof-reading task by lowering the number of marks made per line read. The subjects reported a higher degree of annoyance and impaired working capacity when working under conditions of low frequency noise. The effects were more pronounced for subjects rated as high-sensitive to low frequency noise, while partly different results were obtained for subjects rated as high-sensitive to noise in general. The results suggest that the quality of work performance and perceived annoyance may be influenced by a continuous exposure to low frequency noise at commonly occurring noise levels. Subjects categorised as high-sensitive to low frequency noise may be at highest risk.

Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions

Abstract: The purpose of this study was to explore the application of the click-evoked and distortion products otoacoustic emissions (CEOAEs and DPOAEs, respectively) in the diagnosis and detection of noise-induced hearing loss (NIHL). The study group consisted of 283 noise-exposed subjects and 176 subjects with a history of noise exposure but with a normal audiogram. Findings were also compared with those in 310 young military recruits with no reported history of noise exposure and normal bilateral audiogram. In general, the features of noise-induced emissions loss (NIEL) closely resembled the behavioural NIHL parameters: both were bilateral and both affected primarily the high frequencies, with a "notch" at around 3 kHz in the DPOAEs. On average, CEOAEs were recorded up to 2 kHz, indicating that up to this frequency range (speech area), cochlear functioning is intact and the hearing threshold s better than 25 dBHL. A clear association between the OAEs and the severity of the NIHL was noted. As the severity of NIHL increased, the emissions range became narrower and the amplitude smaller. OAEs were found to be more sensitive to noise damage than behavioural audiometry. NIEL was found in subjects with normal audiograms but with a history of noise exposure. Owing to their objectivity and sensitivity, OAEs may sometimes provide indispensable information in medico-legal cases, in which the configuration of the audiometric threshold is needed to obtain an accurate diagnosis of NIHL and compensation is proportional to the severity of NIHL. Furthermore, OAE testing between ears with and without NIHL revealed a high sensitivity (79 - 95%) and specificity (84 - 87%). This study shows that OAEs provide objectivity and greater accuracy, complementing the behavioural audiogram in the diagnosis and monitoring of the cochlear status following noise exposure.

The impact of perceived tinnitus severity on health-related quality of life with aspects of gender.

Abstract: The Nottingham Health Profile (NHP) has been used to investigate the health profiles in different medical conditions. It has, however, never been applied to tinnitus sufferers. The present study aimed at investigating relationships between the perceived severity of tinnitus, audiometric data, age, gender and non-disease specific health-related quality of life measured with the NHP divided into two sections; NHP I (topics related to health status) and NHP II (health induced problems in daily life). These parameters were statistically analysed to identify predictive factors to the perceived severity of tinnitus, described by the Tinnitus Severity Questionnaire (TSQ). A total of 186 consecutive tinnitus patients (57 females and 129 males) attending an audiological specialist clinic in Sweden were included in the study. The stepwise regression model used explained 37.8 per cent of the variance in the perceived severity of tinnitus, and the significant predictors were: "Emotions", "Sleep", and "Pain", three of the six dimensions of the NHP I. Differences between gender were found in NHP II and age-related differences emerged in NHP I when male and female patients were compared to normal controls.

The intrusiveness of sound: Laboratory findings and their implications for noise abatement.

Abstract: Environmental policy with regard to noise abatement has traditionally only considered whether the noise levels in a given setting are high enough to be deemed a source of annoyance, disturbance, or threat to well being. However, laboratory studies using both simple and more complex work-related tasks have shown that task-irrelevant sound, regardless of its intensity, intrudes upon cognitive processing and disrupts performance substantially; furthermore, its damaging effect does not diminish with repeated exposure to the sound over time. For tasks that require short-term memory processing (particularly the short-term maintenance of order information) sound assumes disruptive power if it is acoustically varying over its time course. However, other properties of sound (e.g., the semanticity of speech) can incur an additional cost if the primary task necessitates or tends to evoke the extraction of meaning. It will be argued that interference in each case is explained by reference to a conflict between two concurrent mental processes; that being demanded by the task and that being involuntarily applied to properties of the sound. Such harmful effects, as well as having direct consequences for the general well-being of those working in noisy environments, may have far reaching consequences for health insofar as extraneous sound is a feature of many safety-critical work settings. Implications for noise abatement policy are highlighted.

The Influence of Superoxide Dismutase and Glutathione Peroxidase Deficiencies on Noise-Induced Hearing Loss in Mice

Abstract: One consequence of noise exposure is increased production of reactive oxygen species (ROS), such as superoxide, hydrogen peroxide, and hydroxyl radicals, in the cochlea. ROS can cause oxidative damage to diverse cellular components, including membranes, proteins, and DNA, if they are not "neutralised" by antioxidant defences. Two important enzymes of the cochlear antioxidant defense system are cytosolic copper/zinc superoxide dismutase (SOD1) and selenium-dependent glutathione peroxidase (GPx1). These metalloenzymes work together to regulate ROS production in virtually every cell in the body, and they may be important for limiting cochlear damage associated with aging and acoustic overexposure. In this chapter, we describe a series of experiments using mice with targeted deletions of Sod1 or Gpx1, the mouse genes that code for SOD1 and GPx1, respectively, to study the cellular mechanisms underlying noise-induced hearing loss (NIHL). The results from Sod1 and Gpx1 knockout mice provide insights into the link between endogenous levels of antioxidant enzymes and susceptibility to NIHL.

Distortion-Product Otoacoustic Emissions as a Screening Tool for Noise-Induced Hearing Loss.

Abstract: Noise-induced hearing loss includes both temporary (TTS) and permanent (PTS) threshold shifts. Although TTS and PTS have many similarities, their underlying mechanisms are different. Both TTS and PTS are seen in hearing-conservation programs, making it important to consider both when making physiological measurements of inner-ear damage in applied settings. There are many ways that physiological mechanisms could be useful in screening for NIHL. Can normal-hearing and NIHL ears be differentiated from one another? Can the physiological measure be used in place of behavioural hearing-threshold measures of TTS and PTS? Can it be used to indicate sub-clinical damage (i.e., noise-induced permanent alterations to the inner ear without a corresponding hearing decrement)? Can it be used to indicate pre-clinical hearing loss (i.e., the sub-clinical damage eventually turns into hearing loss)? Finally, can the physiological measure be used to predict susceptibility to NIHL? Evoked otoacoustic emissions (EOAEs) depend on normal outer hair cells for their generation. Because this is the site in the inner ear in humans that is most susceptible to noise, there has been considerable interest in the application of EOAEs to NIHL screening. In this review, the application of distortion-product EOAEs (DPOAEs) is considered for this purpose, emphasizing work from our laboratory, but including that of others as well. Wherever possible, we compare the performance of DPOAEs as a screening tool to transient-evoked otoacoustic emissions (TEOAEs). We emphasize the importance of how well DPOAEs perform in screening for NIHL in individuals rather than for groups of people; the importance of using large numbers of subjects; and the importance of longitudinal studies.

Factors influencing subjective noise sensitivity in an urban population

Abstract: This study was designed to define the individual variables influencing subjective noise sensitivity in an urban population and to investigate the distribution of subjective noise sensitivity with regard to noise exposure. A general questionnaire, a ten-graded noise annoyance scale, the Weinstein's Noise Sensitivity Scale, and the Eysenck Personality Questionnaire were applied to a sample of 413 inhabitants of Belgrade. Distribution of noise sensitivity scores was normal and independent of noise exposure. No significant differences in average noise sensitivity scores were observed concerning gender and exposure to low (Leq 65 dBA). Multiple regression analysis revealed that neuroticism was the best individual predictor for SNS, for both sexes in the noisy area and for women only, in the quiet area (P < 0.001). Age, education level and introversion were not significantly related to noise sensitivity. Positive relation between reported noise annoyance and noise sensitivity was highly significant (P < 0.0001).

Factors affecting the use of hearing protectors in a population of printing workers.

Abstract: This study examined the reasons offered by rotogravure printing workers from Sao Paulo, Brazil, for not consistently using hearing protectors. The study group was comprised of 124 workers exposed to various levels of noise. Data on work history, psychosocial aspects of their job, medical history, present health, stress, occupational and non-occupational exposures to noise or chemicals and lifestyle factors were collected through an interview. The participants underwent pure-tone audiometry and had their noise exposures assessed. Seventy-nine workers of a total of 124 noise-exposed (64%) indicated that they wore hearing protectors, but only 16 (20%) of that subgroup stated that they wore the device all the time when noise­exposed. The variables significantly associated with the decision for not consistently wearing hearing protectors included interference with communication, interference with job performance, comfort issues, and self-perception of hearing condition.

Evaluation of Transient and Distortion Product Otoacoustic Emissions before and after shooting practice.

Abstract: Firearms are a common source of impulse noise that may potentially damage a hearing organ. It is not easy to predict soldiers' personal susceptibility to noise exposure. The purpose of this study was to evaluate of the transient evoked otoacoustic emission (TEOAE) and distortion-product otoacoustic emission (DPOAE) before and after shooting and compare it with conventional pure tone audiometry. Standard pure tone audiometry, tympanometry, TEOAE and DPOAE measurements were recorded before and 10-15 minutes after shooting. Ten male soldiers (20 ears) were exposed to impulse noise from automatic gunfire (15 single rounds of live ammunition). They did not use any earplugs. The reduction in amplitude of the TEOAE after shooting was 3.1 and 5.1 as SPL for 3 and 4 kHz respectively for the right ear and 4.3 dB SPL for 1 kHz and 0.6 dB SPL at 2 kHz for the left ear. The greatest reduction in DPOAE occurred at frequencies of 1.0 kHz (3.8dB SPL) and 3.0 kHz (2.9 dB SPL) for the left ear. There were no differences in the audiometric thresholds before and after shooting. Emissions appear to be more sensitive for monitoring early cochlear changes after shooting, than pure tone audiometry.

The development of noise-induced hearing loss in the Swedish County of Östergötland in the 1980s and the 1990s

Abstract: This retrospective cross-sectional study of median hearing threshold levels of males employed in two specific occupations shows that the trend with decreasing noise-induced hearing loss in Sweden during the 1970s and 1980s continues into the 1990s. In the occupational categories mechanical work and wood processing men in age groups 30-39, 40-49 and 50-59 years old examined during the time period 1971-76, 1981-86 and 1991-96 were compared. Possible explanations to the improvement might be a wider use of hearing protectors at work and less exposure to noise during military service. The results show that the awareness of noise-induced occupational hearing loss has improved but the hearing conservation programs are still necessary as hearing threshold levels in these occupational groups continue to be poorer than expected in relation to age.

The influence of psychological factors on self-reported physiological effects of noise.

Abstract: We examine the possibility that physiological effects of noise may result not only from noise exposure per se, but also from people's beliefs about the noise. Due to widely publicised changes to the runway configuration at Sydney Airport, aircraft noise levels in nearby areas were expected to either increase, decrease or remain the same. As part of the Sydney Airport Health Study, residents in each of these 3 expected-change areas (N=1015) completed a structured interview which included indices of noise reaction (including annoyance) and physical and mental health, prior to the anticipated changes. Concurrent (pre-change) measures of aircraft noise levels were taken. Self-reported physiological/health effects differed across areas with the same aircraft noise level consistently with differences in psychological reaction across these areas. Expected change in noise level added to the level of self-reported physiological symptoms predicted by noise level in regression analyses. Dose-response functions differed across the expected-change areas. These results are consistent with the hypothesis that noise exposure produces physiological symptoms, but that expectations regarding future noise levels also contribute to the physiological impact of noise, which may be reduced by addressing psychosocial factors related to noise reaction.

Otoacoustic emissions in industrial hearing loss assessment.

Abstract: Otoacoustic emissions (OAEs) are a sensitive and frequency-specific tool for assessing cochlear damage. Parameters of an OAE signal decrease at the frequency that approximately corresponds with the injured region. However, damage in the basal turn of the cochlea is important for signal processing and OAE generation in the higher cochlear partition. In workers exposed to noise, the amplitude of OAEs decreases at the frequencies characteristic for acoustic trauma. These changes may occur prior to the audiometric threshold shift, which supports the superiority of OAEs in early detection of noise-induced damage. Therefore, OAEs may be applied as a quantitative test for individual assessment and monitoring of industrial hearing loss. Otoacoustic emissions are an established screening tool in the examination of newborn and infant hearing. In addition, studies on adult patients demonstrate high sensitivity and specificity if applied in screening sensorineural hearing loss, especially with multivariate analyses engaged. OAEs may be used as a screening test in subjects with an increased risk of exposure to noise and in epidemiological studies on industrial and environmental noise effects. Although otoacoustic emissions have a remarkable advantage in the evaluation of industrial hearing loss, there are some doubts about their utility in hearing conservation programs. The legislation and financial compensation associated with the diagnosis of occupational illness are based on the quantitative gold standard, pure-tone audiometry. In addition, as it is not possible to reproduce the audiogram precisely, the OAEs may not be currently applied as a reliable test of hearing loss in malingerers. However, in some countries where tinnitus is eligible for compensation, OAEs may indeed appear helpful in the reliable diagnosis of cochlear damage within the respective frequency range.

Gene Expression Changes in Chinchilla Cochlea from Noise-Induced Temporary Threshold Shift.

Abstract: Acoustic overstimulation produces many anatomical, biochemical and physiological changes in the inner ear. However, the changes in gene expression that underlie these biological changes are poorly understood. Our approach to investigating this problem is to use gene microarrays to measure the changes in gene expression in the chinchilla inner ear following a 3 h or 6 h noise exposure (95 dB SPL, 707-1414 Hz). This noise exposure causes a temporary threshold shift (~40 dB) and a temporary reduction in distortion product otoacoustic emissions (DPOAE), but no permanent hearing loss or hair cell loss. Here, we present data showing (1) the suitability of mouse and human complementary DNA (cDNA) clones for detecting chinchilla cochlear gene transcripts, and (2) the change in cochlear gene transcripts in noise exposed chinchillas. Chinchilla cochlear transcript probes exhibited strong and discrete signals on both mouse and human cDNA filter arrays. Since the strongest hybridization occurred with mouse clones, mouse cDNA microarrays were used to study noise-induced changes in gene expression. Chinchilla cDNA probes were differentially labelled with Cy3 (control) or Cy5 (noise exposed) by random primed synthesis, hybridized to 8750 mouse cDNAs arrayed on microscope slides and analysed by laser fluorescent microscopy. Several classes of genes exhibited time-dependent up regulation of transcription, including those involved in protein synthesis, metabolism, cytoskeletal proteins, and calcium binding proteins. The results are discussed in relationship to previous studies showing noise-induced changes in structural proteins, calcium binding proteins, metabolic enzymes and membrane bound vesicles.

Gene-based therapy for inner ear disease.

Abstract: Environmental inner ear insults often lead to hair cell injury and loss. Therapeutic measures for the prevention of hair cell loss are currently limited. Several reports have demonstrated the applicability of growth factors for hair cell protection. The goal of the experiments presented here was to assess the protective capability of the human GDNF transgene against noise trauma in the guinea pig cochlea. The left ears of guinea pigs were inoculated with a recombinant adenovirus with a human GDNF insert (Ad.GDNF). Four days later, animals were exposed to noise trauma. One week later, animals were sacrificed and hair cells counted in the left (inoculated) and right (non-inoculated) ears. Auditory brainstem thresholds were measured before the inoculation and just prior to sacrifice. Control groups included inoculation with a reporter gene vector (Ad.lacZ) and Ad.GDNF in normal ears with no noise exposure. The results show that intracochlear inoculation with adenovirus into normal ears does not compromise hair cell counts and ABR thresholds. Both Ad.GDNF and Ad.lacZ vectors can protect the cochlear hair cells and hearing from the noise insult. The difference between the protection afforded by Ad.GDNF and that of the Ad.lacZ vector is not statistically significant. The mechanism of Ad.lacZ protection needs to be elucidated. The data demonstrate the general feasibility of gene therapy for over-expression of neurotrophic factors against noise trauma, and emphasize the complexity of the technique and the problems of variability between subjects.

Therapeutic effect of magnesium on noise-induced hearing loss

Abstract: This study examined the therapeutic effect of magnesium (Mg) on noise trauma in anesthetized guinea pigs exposed to an impulse noise series (1/s) of Lpeak 167 dB (Leq,1s 127 dB) for 38 min. The permanent hearing threshold shift (PTS) was measured 1 week post-exposure, using auditory brain stem response audiometry (frequency range, 0.5-32 kHz). The total Mg concentrations of perilymph, cerebrospinal fluid and plasma were analyzed by atomic absorption spectrometry. In a first series, animals maintained on physiologically low Mg received subcutaneous injections of either different Mg doses (0.11-0.33 mmol MgSO4/100 g per day) for 3 days and drinking water with an additive of 39 mmol MgCl2/l for 1 week or saline as a placebo and tap water alone. The treatment began immediately after the impulse noise exposure. The dose of 0.29 mmol Mg/100 g per day was found to be most effective and reduced the hearing loss by 13-20 dB compared to placebo. The PTS and the perilymph Mg level showed a close negative correlation, suggesting that the intracochlear Mg level plays an important role in bringing about these protective effects. In a second series, we tested the therapeutic efficacy as a function of the post-exposure time of onset of the optimal Mg treatment (1 min, 2 and 4 hours), using normal Mg animals. The therapeutic effect decreased with the length of time elapsed between the end of exposure and the beginning of treatment. In a parallel scanning electron microscopic test, we also found a Mg-related difference in the susceptibility of hair cell stereocilia to impulse noise exposure.

Differential gene expression following noise trauma in birds and mammals

Abstract: Acoustic overstimulation has very different outcomes in birds and mammals. When noise exposure kills hair cells in birds, these cells can regenerate and hearing will recover. In mammals, however, the hair cell loss, and resulting hearing loss, is permanent. Changes in gene expression form the basis for important biological processes, including repair, regeneration, and plasticity. We are therefore using a battery of molecular approaches to identify and compare changes in gene expression following noise trauma in birds and mammals. Both differential display and subtractive hybridisation were used to identify genes whose expression increased in the chick basilar papilla immediately following exposure to an octave band noise (118 dB, centre frequency 1.5 kHz) for 4-6 hr. Among those upregulated genes were two involved in actin signalling: the CDC42 gene encoding a Rho GTPase, and WDR1, which encodes a protein involved in actin dynamics. A third gene, UBE3B, encodes an E3 ubiquitin ligase involved in protein turnover. A fourth gene encodes a cystein-rich secreted protein that may interact with calcium channels. To examine the mammalian response, gene microarrays on nylon membranes (Clontech Atlas Gene Arrays) were used to examine global changes in gene expression 30 minutes after TTS (110 dB broadband noise 50% duty cycle) or PTS (125 dB, 100% duty cycle) noise overstimulation (each for 90 minutes) in the rat cochlea. Several genes, including classic immediate early response genes such as c-fos, EGR1/NGFI-A, and NGFI-B, were upregulated at this early time point following the PTS exposure, but were not upregulated following the TTS exposure.

Absence of hair cell protection by exogenous FGF-1 and FGF-2 delivered to guinea pig cochlea in vivo.

Abstract: Recent findings that glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT­3), and transforming growth factor α can protect the auditory hair cells from acoustic trauma or aminoglycoside ototoxicity in vivo raise the question of whether other neurotrophic factors can also protect the hair cells in vivo. Fibroblast growth factor-2 (FGF-2) can protect hair cells from neomycin ototoxicity in vitro, and in vivo study has shown upregulation of FGF receptor­3 in the cochlea following noise exposure, suggesting that some FGF family members might play a role in protection or repair of the cochlea from damage. We therefore examined if FGF­1 and FGF-2 chronically delivered to the cochlea prior to noise overstimulation can attenuate noise-induced hair cell damage in vivo under conditions in which GDNF and NT-3 were effective. Pigmented female guinea pigs underwent left scala tympani implantation of a microcannula attached to an osmotic pump filled with artificial perilymph only or containing FGFs (10 or 1 µµg/ml FGF-1 or 10 µµg/ml FGF-2). They were exposed to noise (4 kHz octave band, 115 dB SPL, 5 hr) 4 days after surgery. Threshold shifts 10 days postexposure were essentially equivalent at all frequencies tested across different treatment groups. No significant difference in threshold shifts was observed between the treated and untreated ears in any of the groups. The extent of hair cell damage was also comparable among the different treatment groups. These findings indicate that exogenous FGF-1 or FGF-2 does not influence noise­induced hair cell damage under the experimental conditions used in this study, suggesting that these FGFs are not good candidates as auditory hair cell protectors in vivo.

Effect of long-term, low-level noise exposure on hearing thresholds, DPOAE and suppression of DPOAE in rats.

Abstract: Loss of adaptability rather than loss of sensitivity may be one of the initial signs of auditory impairment following exposure to noise. One way to examine the adaptability of hearing in experimental investigation is to measure the magnitude of the suppression, exerted by the medial olivocochlear efferent system, on the ipsilateral otoacoustic emissions in response to contralateral sound stimulation. Thus, in order to test the hypothesis it was decided to measure hearing thresholds (HT), the cubic DPOAE and suppression of cubic DPOAE by contralateral wide band noise in rats exposed to long-term, low level noise (90 days of 90 dBlin 4-20 kHz wide band noise 4 hours/day, 5 days/week). Measurements of HT were performed by assessment of the ABR, elicited by tone-pips from the same probe assembly used in the measurements of DPOAE. The suppression of the cubic distortion product (CDP) was determined in ketamine/xylazine anaesthesia, allowing a stable response for a minimum of 20 min. Of the frequencies tested, the rats exposed to noise had an increase in HT at 12.8 kHz only (6.8 dB, P<0.05), while a reduction on the CDP was evident with f2 going from 9.2 kHz to the upper limit at 17.4 kHz. Further, the rats exposed to noise had little suppression of the CDP at low levels of contralateral noise (CN), but no difference from the control animals was seen as the CN noise level was increased. The measurement of DPOAE suppression did not reveal any effects of the low level noise exposure that was not paralleled also by shifts in hearing thresholds. The most sensitive assessment of the auditory changes in the study was the measurements of DPOAE, and further elaboration on the bandwidth and frequency distribution of the CN is necessary, before auditory changes in the high frequency range can be probably assessed.

Correlations among Distortion Product Otoacoustic Emissions, Thresholds and Sensory Cell Impairments.

Abstract: Distortion product otoacoustic emissions (DPOAE) are increasingly used as an objective test for noninvasive hearing screening When two pure tones with frequencies f1 and f2 are sent to the cochlea, the most prominent DPOAE is the cubic one produced at 2f1-f2, and this presentation will mainly emphasize its properties DPOAEs are undoubtedly generated by cochlear nonlinearities It is widely held that they arise from certain stages of sound processing by the outer hair cells (OHC) and that OHCs ensure normal cochlear sensitivity and tuning Thus, DPOAEs should provide a privileged tool for monitoring the harmful effects of loud sound because OHCs are known to be one of the main targets of NIHL Although DPOAEs provide the clinicians with a reliable screening limit of about 30 dB HL around f2, no reliable relationship has been found thus far between possible residual DPOAEs and either hearing loss or amount of impaired sensory cells Furthermore, puzzling contradictory findings have been reported as to the presence of DPOAEs despite a large hearing loss (ie >30-40 dB) notably with high-level stimuli These observations raise the following issues What is the generation site of DPOAEs in a normal or pathological cochlea (OHCs, basilar membrane, place tuned to f2, 2f1-f2, places basal to f2)? Is it necessary to account for interferences between several discrete sources, arising from different locations or different mechanisms and possibly exhibiting differential susceptibility to sensory cell damage? Do DPOAE changes depend on the nature of OHC pathology (NIHL, anoxia, ototoxic drugs, genetics)? Once a source of DPOAE is characterized, is there any means of modelling the physiological process of its generation and deriving what might quantitatively relate DPOAE amount to sensory cell activity and thresholds? The goal of this presentation is to examine these issues, review the available data and propose a comparatively simple model

Objective evidence for tinnitus from spontaneous emission variability

Abstract: Noise exposure is the most common cause for the generation of tinnitus. This study evaluated the variability of spontaneous emissions in industrial workers exposed to noise and reporting the presence of tinnitus in comparison with those exposed to noise but without tinnitus. The assumption being that exposure to noise leads to some instability within the cochlea, which alters the spontaneous emission activity. Thus those experiencing tinnitus may show greater variability than those without tinnitus. 198 mill workers in Poland exposed to noise levels between 85-95dBA for a mean of 12+/-6.6 years, 104 of whom had reported the presence tinnitus and 94 without tinnitus were evaluated for otoscopy, audiometry and otoacoustic emissions. The tests were repeated between 5-10 days in most subjects to check for variability. There were significant differences in the mean age, pure tone average, transient emissions amplitude and variability between groups with and without tinnitus. There were no significant differences between sessions for these measures in either group. Those with tinnitus had poorer thresholds by an average of around 15dB, and reduced TOAE of around 2.6dB compared with those without tinnitus. There are a number of factors such as age, pure tone thresholds and tinntius, which may be responsible for the reduction in emissions. For the purposes of examining SOAE stability, all SOAE peaks were classed as stable if SOAE frequency in the two sessions remained unchanged and variable if SOAE peaks were present in both sessions but shifted in frequency or present in one sessions and absent in the other. SOAE were present in 73.1% of tinnitus group and in 50% of non-tinnitus group. Of these 92% of the tinnitus group had present and variable SOAE whereas 48.9% of the non-tinnitus group did. Thus the positive predictive value was calculated at 65% for those with variable SOAE having tinnitus and significantly higher at 86% negative predictive value for those with stable SOAE having no tinntus. The likelihood ratio of tinnitus being present given that SOAE are present and variable is 1.87 and is significantly reduced for no tinnitus given that SOAE are present and stable at 0.156. This study has clearly demonstrated that the incidence of spontaneous emissions is higher in noise-exposed workers than previously observed and the stability from week to week is significantly lower in those with subjective tinnitus.

Considerations on assessing the risk of work-related hearing loss.

Abstract: The large intersubject variability observed in demographic studies of noise-induced hearing loss illustrates how difficult it can be to estimate with precision the risk posed by exposure to noise. One possible source of the variability is the result of evaluating a diverse set of acoustic conditions with a simple metric A-weighted energy. In this paper the limitations of the energy­based criteria are reviewed. The benefits of evaluating a noise exposure in terms of energy and the metrics of frequency and time-domain kurtosis are discussed. A second source of variability in industrial noise studies may be related to non-acoustic factors such as chemical exposures that contribute to hearing loss acquired on the job

Health profiles for patients with Ménière's disease.

Abstract: The Nottingham Health Profile (NHP) has been used to investigate the health profiles for many medical conditions, such as herpes zoster infection, migraine, cancer and epilepsy. However, so far, it has not been used to investigate the health profile for patients suffering from Meniere's disease, but only for patients with dizziness, severe hearing loss and tinnitus. Each of these three symptoms have shown to have a significant impact on the quality of life. In the present study, 116 consecutive patients with Meniere's disease, diagnosed according to the AAO-HNS guidelines, visiting at the department of Audiology were included in the study. The NHP was used to measure the health related quality of life and includes the following subscales: "Sleep", "Energy", "Emotional reaction", "Pain", "Physical mobility", "Social isolation" and items concerning daily activity. The Tinnitus Severity Questionnaire (TSQ) was used to measure symptoms specific to tinnitus. The results showed that the perceived severity of tinnitus in patients with Meniere's disease had a significant negative influence on their health related quality of life. The patients with Meniere's disease suffered from more sleep disturbances and social isolation than patients referred to our clinic due to tinnitus. The quality of life was, on the whole, worse for patients of working age compared to retired pensioners. Emotional disturbances could explain 40.3 % of the variance of the tinnitus severity in patients with Meniere's disease. This can be compared with 20.6% in patients with tinnitus. This underscores the importance of providing psychological and psychiatric interventions and support to patients with Meniere's disease.

Tinnitus, attendance at night-clubs and social drug taking in students.

Abstract: A questionnaire was used to collect data from 545 students of the Manchester Metropolitan University. The aim of the study was to investigate associations between the attendance of university students at night-clubs (NCs) that play loud music and the incidence and duration of post exposure tinnitus (PET) and spontaneous tinnitus (ST). The possible effects of taking social drugs in NCs on tinnitus was also investigated. Descriptive analyses and Chi squared association analyses were carried out. The study showed that 87% of students attended noisy NCs and there was a significant association between the attendance at NCs and the duration of PET. There was no significant association between frequency of attendance and the incidence of tinnitus, however non attendees were significantly less likely to get ST. The amount of social drug-taking was not as high as expected, only 19% taking drugs more than rarely, although the incidence may be under-reported. Taking drugs while at night-clubs would appear to exacerbate the effects of noise exposure on tinnitus. Non drug taking males were less susceptible to PET lasting longer than 2 hours and ST than non drug taking females, whereas drug taking males were more susceptible than drug taking females. Whereas PET has yet to be proved to be related to auditory damage, this study would suggest the effect of night­club noise exposure impedes tinnitus recovery and could prove to be an early sign of permanent damage.