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   Abstract
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ARTICLES Table of Contents   
Year : 2001  |  Volume : 3  |  Issue : 12  |  Page : 19-31
Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions

1 Institute for Clinical Neurophysiology and Audiology, Schneider Children's Medical Center of Israel, Petah Tiqva, Israel
2 Institute for Noise Hazards Research, Israel Defence Forces, Israel
3 Middle East Association for Managing Hearing Loss (MEHA) in Jordan and Israel, Jabal Amman, Jordan
4 Department of Otorhinolaryngology, Rabin Medical Center, Beilinson Campus, Israel

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  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 noise­exposed 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 is 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.

Keywords: Noise-induced hearing loss; otoacoustic emissions; noise exposure; screening for NIHL; medico-legal.

How to cite this article:
Attias J, Horovitz G, El-Hatib N, Nageris B. Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions. Noise Health 2001;3:19-31

How to cite this URL:
Attias J, Horovitz G, El-Hatib N, Nageris B. Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions. Noise Health [serial online] 2001 [cited 2020 Jun 4];3:19-31. Available from: http://www.noiseandhealth.org/text.asp?2001/3/12/19/31799

  Introduction Top


Despite the efforts of medical and environmental authorities, noise-induced hearing loss (NIHL) continues to be a major occupational health hazard in military and industrial environments. Leisure noise may also be a significant cause of NIHL in adults and children. Already at the early stages, speech reception may be affected under conditions of background noise, though not under quiet conditions. Moreover, almost 30% of patients with NIHL have tinnitus, which may be even more detrimental to activities of daily life than the hearing loss itself. NIHL may be accompanied by social repercussions, considering that it affects such a wide range of people in all age groups, and it takes a high economic toll, including costs of compensation and hearing conservation programs. Yet NIHL is largely preventable, and when the noise exposure is terminated, the hearing loss remains constant.

NIHL is currently detected and monitored with pure-tone audiometry performed in a sound­attenuated room using a calibrated audiometer. The greatest loss usually occurs at around 4 kHz, and the earliest damage is in the highest frequencies (6 and/or 8 kHz). The average hearing loss is greater at the higher (4 - 8 kHz) than at the lower frequency ranges (0.25 - 2 kHz). Usually, and especially at the early stage of damage, the speech frequency area range (0.25 - 2 kHz) remains intact, with the loss starting at 3 kHz and above. Symmetry in hearing loss severity and configuration is essential for clinical diagnosis. Though some asymmetrical losses (up to 10 dB) may be observed in noise-exposed subjects, a significant asymmetric audiometric cochlear pattern should raise suspicions of other types of cochlear or retrocochlear lesions.

The main disadvantage of pure-tone behavioural audiometry is its insensitivity to subtle noise­induced cochlear changes. Furthermore, the audiogram reflects the entire auditory pathway, even though the only site affected in NIHL is the cochlea. The audiogram is also very subjective in that it requires full patient cooperation and is influenced by learning effects. Regrettably, in medico-legal situations, such cooperation is not always forthcoming; Luxon (1998) reported that an estimated 30% of claimants deliberately aggravate their true threshold of hearing. Thus, researchers continue to seek improved objective audiometric measures for routine use.

The outer hair cells situated in the organ of corti are the first to be affected by noise exposure, followed, depending on the degree of the acoustic trauma, by destruction of the inner hair cells and the nerve terminals. Thus, one of the main goals of conservative hearing programs is to detect this primary stage of damage. As such, an appropriate alternative or complementary approach to the behavioural pure-tone audiogram for detecting NIHL may be otoacoustic emissions (OAEs) testing. These low-level signals can be recorded by a sensitive microphone placed in the external ear canal. The emitted response is closely related to the integrity of the cochlear structures, mainly the outer hair cells. Furthermore, the test is short, need not be performed in a sound-attenuated room, and requires only minimum patient cooperation. Most importantly, the results are frequency-specific, objective, and relatively consistent and stable.

Two types of stimuli are used in OAEs testing. Click-evoked OAEs (CEOAEs) reflect the outer hair cell activity at the threshold level, two simultaneous pure-tone stimuli (distortion product OAEs, or DPOAEs) reflect the outer hair cell activity at the supra-threshold level. Studies of the effects of short or chronic noise exposure on OAEs showed that, in general, changes in CEOAEs corresponded to the behavioural audiometric changes, though some cochlear changes were noted that were overlooked by the audiogram (Attias & Bresloff, 1996; Attias et al., 1996; Attias et al., 1998; Franklin et al., 1991; Probst et al., 1987; Reshef et al., 1993). DPOAEs showed a reduced amplitude primarily at the half-octave frequency, that is, beyond the central frequency of noise (Attias & Bresloff, 1996; Engdahl, 1996; Sutton et al., 1994).

The purpose of the present study was to test the application of OAEs testing for the diagnosis and screening of NIHL and to compare its characteristics with behavioural audiometry.


  Method Top


Three groups of subjects were tested. The first was composed of 283 personnel (548 ears) undergoing either a periodic health examination or referred to our audiological institute for hearing evaluation. All had audiometrically confirmed NIHL (defined as a hearing threshold more than 25 dBHL at the high-frequency range) owing to repeated exposure to high levels of impulsive or continuous noise. Ages ranged between 18 and 61 years, with a mean of 35 years (SD = 10). The second group was composed of 176 subjects (336 ears) with normal audiograms but with a documented history of exposure to hazardous industrial or military noise. Mean age was 37 years. The third group consisted of 310 randomly selected new military recruits (613 ears). None had a formal history of noise exposure and all had bilateral hearing thresholds equal to or better than 20 dBHL (0.25 - 8 kHz). Mean age of this group was 17.5 years.

Audiometry

All subjects underwent hearing threshold testing with a GSI 16 audiometer in a standard sound­attenuated room. Air and bone conduction hearing thresholds were measured for audiometric frequencies of 0.25 to 8 kHz and 0.25 to 4 kHz, respectively. For each subject, the lowest audiometric frequency at which the threshold was equal to or more than 25 dBHL was defined as the beginning-of- hearing-loss frequency (BHLF).

OAEs testing

CEOAEs were elicited with the ILO 88 Otodynamic Analyzer (version 3.94D, Otodynamic, London, UK) in the nonlinear or quick default modes. Recordings were made in a sound-attenuated room. Clicks were presented in 260 blocks of four clicks each in a nonlinear paradigm at 80 dBSPL (peak). The clicks were elicited by pulses of 80 µsec duration presented at a rate of 20/sec. The responses at each frequency band between 0.8 and 4 kHz as well as the global CEOAE response were recorded from the ILO analyser. Emissions were considered present when the CEOAE level was greater than 0 dB. In cases of a negative value, the CEOAE level was assigned a value of 0 and emissions were considered absent. For each subject's CEOAE trace, the highest recordable emission frequency (HEF) was measured.

DPOAEs were recorded according to the DP­Gram procedure. Recordings were done with the adult probe after calibrating with the 1-cc calibrating cavity. Prior to testing, a checkfit procedure was conducted to obtain a reasonably flat spectral frequency response between 0.5 and 6.0 kHz. The f1-f2 DPOAEs obtained at a single level of 70 dBHL and the primary tones were presented simultaneously at f2 frequencies to correspond to the audiometric frequencies 1, 2, 3, 4 and 6 kHz. Low-tone DPOAEs were not considered to be of particular relevance to NIHL, which is characterized by high-frequency hearing loss. The f1/f2 ratio was held at 1.22, while f1 and f2 varied from 0.8 to 5.2 kHz and from 1 to 6.3 kHz, respectively, with recordings at three points per octave. DPOAEs were considered to be present only if values (in dBSPL) were greater than at least 2 standard deviations above the upper noise floor at the corresponding frequency.

Statistics

The statistical analysis was performed with the BMDP statistical software (1992). We used mainly analysis of variance and covariance with repeated measures, stepwise logistic regression analysis, and two-way and multiway frequency tables.


  Results Top


[Figure - 1] shows the CEOAEs, DPOAEs and audiogram of a typical subject with NIHL. The audiogram is characterized by a "notch" at 4 kHz, and remains intact at the low frequencies. Both types of emissions are absent at the high frequencies where the audiometric thresholds were impaired. CEOAEs were not recorded above 2 kHz, and DPOAEs were absent in the "notch" range between 2 and 4 kHz. It is noteworthy that both types of emissions, and primarily the DPOAEs, reflected the slight differences in the audiogram between the left and right ear.

[Figure - 2] shows the grand average audiogram for NIHL and normal hearing with the corresponding DPOAEs. The audiogram shows a bilateral, symmetric high-tone hearing loss (NIHL), and the DPOAEs likewise show a bilateral, almost symmetric loss in the high­frequency tones (noise-induced emission loss). The maximal emission loss (3 kHz) precedes the notch on the audiogram (around 6 kHz). Thus, the behavioural audiogram closely resembles the emission configuration.

Regarding CEOAEs, on average, the highest frequency for which emissions could be reliably recorded (HEF) in subjects with NIHL was 1.8 kHz (SD = 0.84), and in subjects with normal hearing, 3.2 kHz (SD = 0.8). The mean BHLF in subjects with NIHL was 2 kHz.

[Table - 1] details the standard deviations of the DPOAE amplitudes and the hearing thresholds. In relation to their means, the standard deviations of the emissions did not differ significantly among the hearing thresholds.

Differences between right and left ears

Analysis of variance and covariance with repeated measures of the DPOAEs in the subjects with NIHL or normal hearing revealed a significant main effect for each side (p <0.01) with a significant interaction (p <0.04). In the NIHL group, for each frequency, the response of the left ear was reduced compared to the right ear, at a rate ranging from 12% for 2 kHz to 2% for 6 kHz. Similarly, the HEF for the CEOAEs was significantly narrower (p <0.01) and reduced in amplitude (p <0.03) on the left side compared to the right. Analysis of variance of the audiograms showed the same main effect for side (p <0.01).

Thus, according to both measures, the sensitivity of the left ear to noise damage was inferior to that of the right ear.

Sensitivity of otoacoustic emissions to noise damage

[Figure - 3] depicts the incidence of nonrecordable DPOAEs and CEOAEs at distinct frequencies at which the hearing threshold was intact (less than 25 dBHL) for the noise-exposed and non­exposed groups. Emission loss was evident in both groups for both kinds of emissions, although for each frequency, CEOAEs were more marked in the noise-exposed group. The loss of DPOAEs rose gradually from 9% at 2 kHz to 52% at 6 kHz. Similarly, CEOAE loss increased from 17% at 2 kHz to 62% at 4 kHz (p <0.001). This trend was also evident in the non­exposed group, but was less marked (p <0.001). Another indication of the better sensitivity of the emissions testing over the audiogram is demonstrated in [Figure - 4]. The figure shows the audiogram of a 40-year-old man who had been exposed during army service to intensive impulsive noise. He later suffered right head trauma from a heavy iron ball, with right ear tinnitus, transient facialis, and minor subdural haemorrhage. The audiogram, done two years after the injury, showed only a slight difference between the right and left ears in the 6 - 8 kHz range, except where the right ear had a poorer hearing threshold by 10 - 15 dBHL. By contrast, DPOAEs were absent in the right ear above 2 kHz, while in the left ear only in the 3 - 4 kHz range. Similarly, no CEOAEs were obtained in the right ear, though CEOAEs up to 1.9 kHz were obtained in the left ear.

Diagnosis of NIHL with emissions testing

[Figure - 5] depicts the relationship between the HEF and the BHLF. The CEOAE frequency range became narrower as the NIHL involved lower frequencies. The HEF was always lower than the BHLF. At the same time, the power spectrum of the emissions decreased as the BHLF decreased [Figure - 6]. Pearson correlation analysis between the hearing threshold and the DPOAEs at the corresponding frequencies revealed significant negative coefficients (p <0.01) in the order of -0.22 at 6 kHz to a maximum of -0.38 at 4 kHz. [Table - 2] summarizes the incidence of the presence and absence of CEOAEs and DPOAEs at each frequency in subjects with a normal or abnormal hearing threshold (equal to or more than 25 dBHL). In those with a normal threshold, emissions at 3 or 4 kHz could be recorded in only 65% and 47%, respectively. By contrast, abnormal hearing thresholds were associated with no emissions at these frequencies in 85.7 - 98.8% of cases. DPOAEs were present at 6 kHz in 63.7% of those with normal threshold and at 2 kHz, in 97%. The rates for those with abnormal thresholds were 85.7% at 3 kHz and 61% at 4 kHz.

Stepwise logistic regression analysis was used to explore the relationship between an absence or DPOAEs and the threshold at specific frequencies. The findings are shown in [Table - 3]. A threshold more than 25 dBHL was associated with the absence of CEOAEs in 72 - 84% of cases, and thresholds less than 25 dBHL were associated with the presence of recordable CEOAEs in 75 - 83% of cases. Similar results were obtained for DPOAEs, but with thresholds ranging between 25 and 45 dBHL. For both measures, the correct prediction ranged between 66% and 84%.

Screening ears with or without NIHL

On binary index, ears with NIHL could be distinguished by the presence of CEOAEs at 2 and 3 kHz. The results showed a 92.1% sensitivity (correct discrimination of NIHL) and 79% specificity (correct discrimination of normal audiogram), with an overall correct prediction of 84.4%. A similar analysis performed for DPOAEs at 2, 3 and 4 kHz yielded an 82% sensitivity, 92.5% specificity, and overall correct prediction of 87%.

Applying the same criteria to the new recruits with no history of noise exposure (and a normal audiogram) resulted in a 95.2% specificity.


  Discussion Top


To evaluate the audiological relevance of otoacoustic emissions (OAEs) to the clinical evaluation of noise-induced hearing loss (NIHL), a large sample of subjects with and without a history of noise exposure was tested. The association between the presence and absence of OAEs to hearing loss, the characteristics of OAEs in NIHL, the sensitivity of emissions compared to the traditional behavioural pure-tone audiogram in detecting NIHL, and the efficiency of OAEs as a screening tool for NIHL were analysed.

Potentially, OAEs testing has the necessary features to serve as an objective, sensitive, and quick tool for the diagnosis of NIHL. The emissions are believed to be evoked by the outer hair cells situated within the cochlea, the first site affected by noise. OAEs are also highly vulnerable to cochlear trauma, such as exposure to ototoxins or loud noises, which are also known to affect hearing thresholds (Furst et al., 1992).

On average, noise-induced emissions loss (NIEL) is bilateral, affecting primarily the high frequencies. In both types of emissions, the response level is reduced in noise-exposed subjects and the range of emissions is narrower. When two pure-tone stimuli are presented (DPOAEs), a "notch" is found at around 3 kHz, closely resembling the hearing configuration usually seen after chronic noise exposure (notch at 4 - 6 kHz). Clicks induce a response, on average, at up to 2 kHz, leaving the area at lower frequencies intact, and like for NIHL, the left ear is inferior to the right, showing a narrower emission frequency range and lower emission amplitude. The difference may be related to inherent high-level cortical sites and to an inherited priority of the right over the left side. This issue is, however, beyond the scope of the present study.

We noted a clear association between the OAEs and the severity of the NIHL. For the CEOAEs, as the audiometric beginning of hearing loss frequency (BHLF) decreased, the emission range also decreased, owing to the loss of emission energy above this frequency. The highest emission frequency (HEF) was nearly always lower than or equal to the audiometric BHLF. Regardless of the frequency, the presence of CEOAEs was associated with hearing thresholds better than about 25 dBHL, but the absence of CEOAEs frequently corresponded to a NIHL worse than 25 dBHL (Attias & Bresloff, 1996). Moreover, the hearing thresholds at frequencies lower than the HEF were roughly better than 25 dBHL. In contrast to CEOAEs, the absence of DPOAEs was highly correlated with hearing thresholds between 25 dBHL at 2 kHz to 30 - 45 dBHL at 3, 4 and 6 kHz. Thus, CEOAEs and DPOAEs may complement each other in the objective determination of hearing threshold at specific frequencies. While CEOAEs provide cochlear information at threshold levels, DPOAEs indicate the gross motility of the outer hair cells.

One of the most interesting findings of this study is the greater sensitivity of OAEs to noise damage compared to the audiogram. This was reflected in a variety of ways. NIEL was found in subjects with normal audiograms with a proven history of noise exposure. For both types of emissions, NIEL was noted primarily in the high frequencies and was more pronounced in the noise-exposed than the non-exposed subjects. The reduction in motile activity of the outer hair cells at high frequencies is well known and is probably associated with their generation in close proximity to the cochlear base, the increased stiffness of all elements at this site, and the smaller number of hair cells corresponding to high frequencies than to low frequencies. NIEL without hearing loss provides the first and sometimes the silent sign of cochlear damage induced by noise (Attias et al., 1996; Anjali et al., 1999). Therefore, NIEL may serve as an important and objective monitoring tool to prevent deterioration of hearing by further exposures to hazardous noises. However, the precise association between NIEL at a specific frequency and its sensitivity to further noise exposures at that frequency is not yet fully understood. Another indication of the sensitivity of OAEs over the audiogram was demonstrated in cases of head trauma. Our clinical experience shows that the emission loss frequently exists on the side of the head that experienced the trauma and may sometimes be the only overt audiological measure. Similarly, in some cases, NIEL is the only audiological feature associated with persistent tinnitus. CEOAEs seem to be more sensitive than DPOAEs [Figure - 3]. Apparently, the soft motility functions at threshold levels (in response to CEOAEs) are more susceptible to noise trauma than DPOAEs, reflecting the grosser activity of the outer hair cells at higher levels of stimulation.

The finding of emission loss in young subjects without a history of noise exposure may confirm earlier reports that even the noise of everyday life may damage cochlear function (Glorig & Nixon, 1962). Thus, emissions can indicate cochlear damage that is not always associated with corresponding changes in the audiogram.

The association noted here between the existence of emissions and the hearing threshold further supports the use of OAEs for the audiologic diagnosis of NIHL. The existence of CEOAEs at a certain range of frequencies indicates a hearing threshold within normal limits (up to 25 dBHL) at the frequencies up to the edge of this range. In patients with NIHL, CEOAEs were obtained up to approximately 2 kHz. This knowledge provides audiologists a means to obtain more precisely and more quickly the true hearing threshold at frequencies before the HEF and particularly, at the speech frequency area. This is important for decisions regarding the exclusion of workers from noisy areas and when hearing rehabilitation is required. Furthermore, a finding of an absence of CEOAEs with a presence of DPOAEs at certain frequencies can predict the range of the hearing threshold (25 - 45 dBHL), thereby enabling the audiologist to estimate the audiometric pure-tone configuration. Our results showed that the variation in OAEs across subjects with or without NIHL is not higher than the behavioural hearing threshold on the audiogram. Furthermore, a recording of emissions is nearly always indicative of an intact conductive system. In cases where emissions are recorded in the presence of conductive hearing loss, especially in the high-tone frequencies, ear canal collapse should be suspected.

Owing to their objectivity and sensitivity, OAEs may sometimes provide indispensable information in medico-legal cases, in which the configuration of the audiometric thresholds is needed to obtain an accurate diagnosis of NIHL and compensation depends on the severity of the hearing impairment, primarily if the speech area is involved. This is doubly important in light of studies showing that claimants in such cases often conceal their true threshold of hearing. When emissions are absent, auditory brain stem response to specific frequencies or cortical evoked potentials (Prasher et al., 1993) should be applied.

Another aspect of the OAEs is their efficacy in detecting NIHL in subjects before or after occupational noise exposure. Our study showed that when the presence or absence of CEOAEs at 2 and 3 kHz was adopted as the pass-fail criterion for NIHL, the rate of correct prediction was 84% in noise-exposed subjects, with a 21% false-negative rate. Close inspection of the false- negatives revealed that most of these individuals had intact hearing and absence of CEOAEs. The 7.9% false-positive rate was due mainly to incorrect auditory threshold determination or mild losses (30 - 35 dBHL) at or around 2 or 3 kHz. When the non-exposed subjects underwent CEOAEs testing, 75.6% were correctly diagnosed as having a normal audiogram. This low rate of correct prediction is surprising, especially in light of the 98% reported rate of emissions in ears with normal audiograms (Rubinitte, 1992). However, in the present study, we found emissions in more than two frequencies in 92% of the normal ears. Indeed, only in 2.6% were no emissions recorded at all frequencies. The latter may have been caused by a subclinical middle-ear dysfunction, technical reasons, or anatomical malformations.

Using the DPOAEs pass-fail criterion, we found an 87% correct prediction rate of having normal audiogram in the noise-exposed subjects and an almost 95% rate in the non-exposed subjects. We assume that combining CEOAEs and DPOAEs in screening for NIHL will most probably result in higher sensitivity and specificity. Overall, these data demonstrate the efficacy of OAEs in screening subjects both before and after occupational noise exposure, making OAEs a valuable tool in hearing conservation programs.

In conclusion, this study shows that OAEs provide objectivity and greater accuracy than audiograms in the diagnosis and monitoring of the cochlear status following noise exposure. Both CEOAEs and DPOAEs demonstrated high efficacy in detecting and screening subjects with and without NIHL. NIEL has very similar features to the behavioural NIHL; it is almost always bilateral and affects the high frequency range first. OAEs may reveal subtle cochlear alterations that may be overlooked by the audiogram and thereby complement the behavioural tests for NIHL diagnosis.


  Acknowledegment Top


Mrs Pnina Lilos is gratefully acknowledged for her statistical assistance, as is Mr. Bresloff for his helpful comments and ideas. The authors also wish to thank Gloria Ginzach and Marian Propp for their editorial and secretarial assistance.

This study was supported by the Middle East Association for Managing Hearing Loss (MEHA) and the Canada International Scientific Exchange Program (CISEPO) based at Mount Sinai Hospital and the University of Toronto, Canada.[14]

 
  References Top

1.Attias J., Bresloff I. (1996) Noise induced temporary otoacoustic emissions shifts. J. Basic Clin. Physiol. Pharmacol. 7: 221-223  Back to cited text no. 1    
2.Attias J., Bresloff I., Reshef I., Horowitz G., Furman V. (1998) Evaluating noise induced hearing loss with distortion product otoacoustic emissions. Br. J. Audiol. 32: 39-46  Back to cited text no. 2    
3.Attias J., Furst M., Furman V., Reshef I., Horowitz G., Bresloff I. (1996) Noise induced emissions loss with or without hearing loss. Ear Hear. 16: 612-618  Back to cited text no. 3    
4.Desai A., Reed D., Cheyne A., Richards S., Prasher D. (1999) Absence of otoacoustic emissions in subjects with normal audiometric thresholds implies exposure to noise. Noise Health 2: 50-58  Back to cited text no. 4    
5.Engdahl B. (1996) Effects of noise and exercises on distortion product otoacoustic emissions. Hear. Res. 93: 72-82  Back to cited text no. 5    
6.Franklin D.J., Lonsbury-Martin B.L., Stanger B.B., Martin G.K. (1991) Altered susceptibility of 2fl-f2 acoustic­distortion products to the effects of repeated noise exposure in rabbits. Ear Hear. 53: 185-208  Back to cited text no. 6    
7.Furst M., Reshef (Haran) I., Attias J. (1992) Manifestations of intense noise stimulation on spontaneous otoacoustic emissions and threshold microstructure: Experimental model. Acoust. Soc. Am. 91: 1003-1014  Back to cited text no. 7    
8.Glorig A., Nixon J. (1962) Hearing loss as a function of age. Laryngoscope 72: 1560-1610  Back to cited text no. 8    
9.Luxon L.M. (1998) The clinical diagnosis of noise­induced hearing loss. In Advances in Noise Research. Prasher D., Luxon L.M., eds. Whurr Publishers, London, pp 83-114  Back to cited text no. 9    
10.Prasher D.K., Mula M., Luxon L.M. (1993) Cortical evoked potential criteria in the objective assessment of auditory threshold: a comparison of noise induced hearing loss with Meniere's disease. J. Laryngol. Otol. 107: 780­786  Back to cited text no. 10    
11.Probst R., Lonsbury-Martin B.L., Martin G.K., Coats A.C. (1987) Otoacoustic emissions in ears with hearing loss. Am. J. Otolaryngol. 8: 73-81  Back to cited text no. 11    
12.Reshef, I., Attias, J., Furst, M. (1993) The characteristics of click-evoked otoacoustic emissions in ears with normal hearing and with noise-induced hearing loss. Br. J. Audiol. 27: 387-395  Back to cited text no. 12    
13.Rubinitte M.S. (1992) Clinical observations with transient evoked otoacoustic emissions with adults. Semin. Hear. 13: 23-36  Back to cited text no. 13    
14.Sutton L.A., Lonsbury-Martin B.L., Martin G.K., Whitehead M.L. (1994). Sensitivity of distortion products otoacoustic emissions in human(s?) to tonal over­exposure: Time course of recovery and effects of lowering L2. Hear. Res. 75: 161-174  Back to cited text no. 14    

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Correspondence Address:
Joseph Attias
Institute for Clinical Neurophysiology and Audiology, Schneider Children's Medical Center of Israel, Petah Tiqva
Israel
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Source of Support: None, Conflict of Interest: None


PMID: 12678938

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    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6]
 
 
    Tables

  [Table - 1], [Table - 2], [Table - 3]



 

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