Home Email this page Print this page Bookmark this page Decrease font size Default font size Increase font size
Noise & Health  
 CURRENT ISSUE    PAST ISSUES    AHEAD OF PRINT    SEARCH   GET E-ALERTS    
 
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Email Alert *
Add to My List *
* Registration required (free)  
 


 
   Abstract
   Introduction
   Materials and Me...
   Results
   Discussion
   References
   Article Figures
   Article Tables
 

 Article Access Statistics
    Viewed4473    
    Printed219    
    Emailed14    
    PDF Downloaded95    
    Comments [Add]    
    Cited by others 7    

Recommend this journal

 


 
ARTICLE Table of Contents   
Year : 2009  |  Volume : 11  |  Issue : 43  |  Page : 103-110
Distortion product otoacoustic emissions in an industrial setting

1 Department of Otolaryngology, National University of Athens, Hippokration Hospital, Athens, Greece
2 Tzanion General Hospital, Piraeus, Greece

Click here for correspondence address and email
 
  Abstract 

Distortion product otoacoustic emissions (DPOAEs) is an objective sensitive test of cochlear function. The aim of this study was the evaluation of noise-induced hearing loss in a group of industrial workers, using this method in conjunction with standard puretone audiometry (PTA). One hundred and five subjects (210 ears) were included in the study. PTA, tympanometry, and DPOAEs were performed. Results were analyzed using a mixed analysis of variance model, and compared with the data of 34 normal persons of similar age and sex. We found statistically significant lower DPOAE levels in the noise-exposed group than in the control group. Additionally, the effect of frequency was significant, indicating that amplitude varied across frequency, with lower responses observed at 4 and 6 kHz, and maximum response found at 2 kHz. PTA showed a statistically significant effect of Group, owed to elevated puretone thresholds in the noise-exposed subjects, but a Frequency main effect was not found, although the interaction between Frequency and Group was statistically significant, as well as the interaction between Frequency and Ear. A main effect for Ear was found only in puretone thresholds, due to better thresholds in the left ears of the subjects, and not in DPOAE measurements. DPOAE levels were selectively affected at the higher frequencies, whereas puretone thresholds were affected at all frequencies. Direct comparison of the number of significantly affected ears between the two methods at 1, 2, and 4 kHz showed statistically significant differences at all comparisons, with more ears affected in PTA in comparison with DPOAEs at 4 kHz, whereas more ears were affected in DPOAEs at the lower frequencies (1 and 2 kHz). Therefore, it may be concluded that DPOAEs and PTA are both sensitive methods in detecting noise-induced hearing loss, with DPOAEs tending to be more sensitive at lower frequencies.

Keywords: Distortion product otoacoustic emission, hearing monitoring, noise exposure, occupational noise-induced hearing loss, permanent threshold shift

How to cite this article:
Korres GS, Balatsouras DG, Tzagaroulakis A, Kandiloros D, Ferekidou E, Korres S. Distortion product otoacoustic emissions in an industrial setting. Noise Health 2009;11:103-10

How to cite this URL:
Korres GS, Balatsouras DG, Tzagaroulakis A, Kandiloros D, Ferekidou E, Korres S. Distortion product otoacoustic emissions in an industrial setting. Noise Health [serial online] 2009 [cited 2020 Sep 24];11:103-10. Available from: http://www.noiseandhealth.org/text.asp?2009/11/43/103/50695

  Introduction Top


The vulnerability of the cochlea to long-term noise exposure has been well established by both behavioral and histological studies. [1],[2],[3] Most physiological changes after noise exposure may be seen in the hair cells of the cochlea. A greater susceptibility of the outer hair cells compared with the inner hair cells has been observed, probably due to their different location, structure, and function. [1],[4] The outer hair cells are known to participate in the cochlear amplifier, which appears to be responsible for the sensitivity and sharp tuning of the basilar membrane seen in tuning curves. [5] Noise-induced hearing loss (NIHL) is currently detected and monitored with behavioral audiometry and, whenever objective evidence is demanded, with time-consuming evoked potential techniques, including, recently, steady-state responses. [6],[7]

An alternative for cochlear assessment in NIHL is otoacoustic emissions (OAEs), which may be efficiently used as an accurate, objective, fast, noninvasive tool for assessing the function of outer hair cells in clinical practice. [8] In comparison with the vast literature on OAEs in neonatal hearing screening, there are limited data on screening in adults, particularly if hearing conservation programs are considered. It has been reported on several occasions that OAEs may be a more sensitive test of cochlear function than puretone audiometry (PTA) in indicating subclinical cochlear damage. [9],[10],[11],[12] Although both transiently evoked and distortion product OAEs (DPOAEs) have been used in studying the effect of noise on the cochlea, [13],[14] the latter are probably the most useful. It has been found that DPOAEs arise from localized sources along the cochlea, thus providing frequency specific information, and are quite stable in level. [15] Therefore, DPOAEs are very useful in monitoring cochlear status in specific frequency regions. Another useful feature of DPOAEs is that they perform very well in the high-frequency range. [16] This is a definite advantage of using DPOAEs, as the high frequencies are the most affected frequencies in NIHL. Although NIHL has been adequately studied by DPOAEs in basic research, [17],[18] only a few clinical studies in subjects exposed chronically to noise have been reported, [19],[20] and the issue of the noise effect on DPOAEs in comparison with puretone thresholds has not still been resolved.

The aim of this study was to evaluate NIHL in a group of industrial workers with both DPOAEs and PTA. DPOAEs might provide a useful alternative to PTA in monitoring cochlear changes in subjects exposed to occupational noise. Furthermore, this method might be a more sensitive test of cochlear function in the assessment of noise-induced hearing impairment.


  Materials and Methods Top


A total of 105 industry workers exposed to noise, were examined during a period of two years (2005-2006). The following inclusion criteria were used: (i) no previous history of head injury, taking aminoglycoside medications, or exposure to other sources of noise; (ii) absence of previous or active ear infections; (iii) no family history of hearing loss; and (iv) age not exceeding 55 years to avoid the phenomenon of presbycusis. Eighty six subjects were males and 53 females, with ages ranging between 24 and 54 years. The reference group included 34 healthy subjects (20 males and 14 females) measured at the same setting, using identical equipment and recording conditions. All controls were randomly selected from the same age group as the patients, ranging 25-53 years, and none of them had a history of a risk factor for hearing impairment.

The study was performed in the industrial setting of a pastry producing factory. All subjects worked at two locations, with similar noise levels. The 8-hour averaged A-weighted sound exposure equivalent measurements from these sites were 92 and 93 dB(A). All dB(A) values were measured with a sound level meter Larson Davis 820 (PCB Pieztronics, Buffalo NY, USA). Serial field measurements proved that the machinery noise could be considered a steady state noise, since variations did not exceed 6%. Sound peak pressure measurements were performed using the Bruel and Kjaer 4136 1/8-in, condenser microphone (Bruel and Kjaer, Nareum, Denmark). Data were digitally transferred to a computer as 'wav' files via an Asus Xonar D2/PM USB 24 bit audio card (AsusTek Computers Inc., Taipei, Taiwan) and Adobe Audition 2.0 software (Adobe Systems Inc., San Jose CA, USA). Spectral analysis was performed using MATLAB 6.5 software routines (The MathWorks, Natick, Massachusetts, USA). Octave band analysis of the noise waveform did not show any intense high- or low-frequency component.

Noise exposure of the subjects was determined according to the company records and according to information provided by the workers themselves. The factory administration had implemented a systematic hearing conservation program, informing the employees about the importance of bearing hearing protection during work time and providing hearing protectors. However, most of the subjects admitted that they avoided using hearing protectors most of the time, mainly because of feeling uncomfortable. Accurate data about exact time of using hearing protectors during work time were not available.

Otoscopy and a general otolaryngological examination were performed in every patient to rule out any middle ear pathology. Audiological examinations were conducted in a sound-treated room. Puretone audiometry was performed using a clinical audiometer (Amplaid A321 Twin-channel; Amplifon, Milan, Italy) and standard TDH-49 headphones. The audiometer was calibrated in decibels hearing level (dB HL), according to standards of the International Organization for Standardization [21] and the American National Standard Institute. [22]

Measurements were made with an ascending-descending technique, [23] in 5-dB steps and all thresholds were calculated in dB HL. The actual threshold was set after two out of three responses were consistent. A maximum threshold shift of 120 dB was recorded, and threshold shifts exceeding this value (no response to maximum sound signal) were treated as a 120 dB loss, according to standard practice. [24]

Standard single-frequency tympano­metry was also performed by an impedance audiometer (TM 262 Autotymp Tympanometer, Welch Allyn, New York), using an 85 dB sound pressure level tone set at 226 Hz. Normal results were found for each of our subjects.

DPOAEs were recorded using an ILO otodynamics analyzer (ILO292 DP Echoport) connected to a portable personal computer. The acoustic stimulation, the data recording, and the data analysis, were produced automatically with the aid of this system (software version 5; Otodynamics Ltd). Testing was performed using the serviceable general purpose ILO probe (type SGD) with disposable tips. Subjects were seated comfortably and were instructed to remain as relaxed and quiet as possible. Meatus response monitoring was used to check fitting conditions of the probe. Testing began only when by the check fit procedure a good fit was evident and the spectrum of the stimulus waveform was as flat as possible. The acoustic stimuli were two primary tones, f1 and f2 (f1 < f2), presented simultaneously to the ear. The frequency ratio f2:f1 was fixed at 1.2 and the primary tone levels were 60 and 45 dB SPL for f1 and f2, respectively. Basic work in humans and animals has established that the major contribution to the emitted distortion product at 2f1-f2 is generated in a cochlear site near the f2 location. [25] Consequently, the DPOAE findings are presented with respect to the f2-frequency.

On the basis of fast Fourier transformation, a signal analyzer divided the ear-canal signal into its discrete frequency components so that DPOAEs at the 2f1-f2 frequency were extracted as level (amplitude) spectra. Time-averaging was used with 16 samples of the ear-canal signal, before a spectrum was computed. Spectral averaging was based on eight discrete spectra. Simultaneously, an evaluation of the background noise was performed. The 2f1-f2 level was statistically compared with the mean noise floor level for each DPOAE measure. If the 2f1-f2 level was included within the 95% confidence interval of the noise floor, the DPOAEs were considered as insignificant. If the 2f1-f2 level exceeded the upper limit of the 95% confidence interval of the noise floor, the DPOAEs were considered as present.

DPOAEs were collected as DP-grams in the stimulus frequency domain, obtained from every ear examined. The DP-grams were recorded in half-octave steps, spanning an f2 frequency range from 1001-6006 Hz. In this manner, six discrete DPOAEs frequencies were tested (f2 = 1001, 1501, 2002, 3003, 4004, and 6006 Hz). The two primary tones were presented at a stimulus level of 50 dB SPL. The DP-grams were not extended below 1.001 kHz (f2), because subject noise makes low-frequency DPOAEs difficult to measure. For the plotting of DP-grams, the six recorded f2-frequencies were used (f2 = 1.001, 1.501, 2.002, 3.003, 4.004, 5.005, and 6.006 kHz) close to the audiometric frequencies 1.0, 1.5, 2.0, 3.0, 4.0, 5.0, and 6.0 kHz.

Data were imported in a statistical computer program (SPSS 15.0) for further evaluation and analysis. DPOAE data were analyzed using a mixed-model analysis of variance (ANOVA). In this model DPOAE level and noise level were measured in the group of the noise-exposed subjects and in the control group, in separate analyses. Group (noise-exposed group and controls) was the between-groups factor and Frequency separated by Ears was the within-groups factors. Frequency was the dependent variable measured across half-octave frequency bands centered at 1000, 1501, 2002, 3003, 4004, and 6006 Hz (repeated measures factor Frequency with six levels). The resulting design was 2 × 6 × 2 mixed-model ANOVA design, where the first factor (Group) was between-groups factor, and the last two factors (Frequency and Ear) were within-groups factors. Two separate mixed-models ANOVA were conducted, one for DPOAE level across the six frequencies and one for noise level at the same frequency. To compensate for the violations of sphericity and compound symmetry for within-groups factors, the Greenhouse and Geisser approach was used. Hearing thresholds across six octave band frequencies (250, 500, 1000, 2000, 4000, and 8000 Hz) were examined using a similar mixed-model ANOVA. The design was a three-factorial mixed 2 × 6 × 2 model, where the first factor was Group (a between-groups factor with two levels: noise-exposed group and control group), and the other two factors were within-group factors: Frequency (six levels) and Ear (two levels, left and right). Bonferroni t -tests for multiple comparisons were used for post-hoc analyses. Percentages of ears with significant changes in puretone thresholds and DPOAE levels were compared by the χ2 test. Finally, Pearson's correlation test was used to compare the changes in puretone thresholds and DPOAE levels. The adopted level of statistical significance was 0.05.


  Results Top


The mean age of the exposed to noise subjects was 42.1 (± 8.4) years (range 22-55). The mean time of noise exposure was 11.2 (± 6.7) years (range 1-30). The mean age of the controls was 38.9 (± 9.2) years (range 21-51).

DPOAE measurements

In [Table 1] descriptive statistics of the two groups are presented (mean DPOAE level, mean noise level, and standard deviation of the noise-exposed group and of the control group) separately for the right and left ears. Increased standard deviations in the mean DPOAE levels were found, denoting increased variability, whereas standard deviations of noise levels were lower. [Figure 1] and [Figure 2] show a plot of DPOAE mean levels as a function of frequency in one-half octave bands between the noise-exposed group and the control group, illustrated separately for the right and the left ears. In these figures it is evident that DPOAE levels are lower in the noise-exposed group than in the control group. This finding is consistent with the mixed ANOVA outcome. The ANOVA summary table [Table 2] indicates that the main effect of Group was statistically significant (Group: F = 4.8, P < 0.05). The effect of the Ear was not statistically significant (Ear: F = 0.01, P = 0.91). The within-groups factor of DPOAE levels across six frequencies was significant (Frequency: F = 4.5, P < 0.001), indicating that amplitude also varies across frequency with maximum response observed at 2 kHz. All interactions (Frequency × Group, Ear × Group, Frequency × Ear, and Frequency × Ear × Group) remained insignificant. Tukey's post-hoc analyses did not show any significant interactions of Group or Ear at any of the frequencies.

[Figure 1] and [Figure 2] show also a plot of noise mean levels as a function of frequency in one-half octave bands between the noise-exposed group and the control group, presented separately for the right and the left ears, respectively. As can be seen in these figures, the noise level across one-half octave bands is comparable between the noise-exposed group and the control group. This observation is consistent with the mixed ANOVA outcome, in which the effect of Group was not significant (Group: F = 2.0, P = 0.15). The effect of Ear was not significant as well (Ear: F = 1.2, P = 0.26), but the interaction between Group and Ear was statistically significant (Ear × Group: F = 8.2, P < 0.005). The within-groups factor of noise across six frequencies was significant (Frequency: F = 7.6, P < 0.001), indicating that the noise varies across frequency with lower noise levels obtained at 3, 4, and 6 kHz. Additionally, the interaction between Frequency and Group was significant (Frequency × Group: F = 2.5, P < 0.05). The interaction between Frequency and Ear, and the interaction between Frequency, Ear, and Group were insignificant.

Hearing sensitivity

In [Table 3] descriptive statistics of the two groups are presented (mean hearing thresholds and standard deviation of the noise-exposed group and of the control group) separately for the right and left ears.

The ANOVA summary table [Table 4] indicates that the main effect of Ear and the effect of Group were statistically significant (Ear: F = 4.7, P < 0.05; Group: F = 25.5, P < 0.001). Better thresholds were obtained in the control group and in the left ears of the subjects. The within-groups factor of hearing thresholds across the six measured frequencies was not significant (Frequency: F = 1.7, P = 0.16), indicating that thresholds did not vary significantly across frequency. However, the interaction between Frequency and Group was statistically significant (Frequency × Group: F = 9.5, P < 0.001), as well as the interaction between Frequency and Ear (Frequency × Ear: F = 2.7, P < 0.05). All other interactions (Ear × Group and Frequency × Ear × Group) remained insignificant.

Significant puretone and DPOAE shifts for individual ears

Although there were significant group changes in puretone thresholds and DPOAE levels between the noise-exposed subjects and the controls, measuring changes in individual ears rather than in groups is quite interesting. Therefore, the percentage of ears, which had experienced significant puretone threshold shifts were compared with the percentage of ears with significant changes in DPOAE levels, using the χ2 test [Table 5]. The widely accepted significant changes in puretone thresholds of >10 dB HL (NIOSH, 1998) and in DPOAE levels of ≥6 dB SPL [26],[27] were adopted, as compared to mean control values. Parallel changes were observed on both tests, in most affected ears. However, in some ears changes were found in only one test performed, indicating different sensitivity among ears.

In standard audiometry performed in the noise-exposed group, 60% of the ears had threshold shift >10 dB HL at 4 kHz, whereas lower percentages were found with significant threshold shifts at 2 (23.3%) and at 8 kHz (45.2%). In the lower frequency range 0.25-1 kHz, elevated thresholds were observed in a smaller proportion of ears. It appears, thus, that puretone thresholds were mostly affected at 4 kHz. In DPOAEs, also, a high percentage of tested ears had significantly reduced levels in the frequency range 3-6 kHz. Most ears were affected at the frequencies of 4 (48.1%) and 6 kHz (52.8%).

Direct comparison of the number of significantly affected ears between the two methods was possible at 1, 2, and 4 kHz. Statistically significant differences were found at all comparisons (all P < 0.001), with more ears affected in PTA in comparison with DPOAEs at 4 kHz, whereas more ears were affected in DPOAEs at the lower frequencies (1 and 2 kHz). Comparison between the elevation of thresholds in behavioral audiometry and the reduction of levels in DPOAEs showed significant correlation across all frequencies (1, 2, and 4 kHz).


  Discussion Top


Noise-induced hearing loss is commonly measured as a temporary or permanent threshold shift by PTA. Although PTA is considered the gold standard test in this issue, the method is subjective, time consuming, and not quite sensitive to small changes in puretone thresholds. [6] Whenever a permanent threshold shift is recorded in a hearing conservation program, there is already significant damage to the inner ear. [28] Furthermore, although the only site affected by noise exposure is the cochlea, the audiometry examines the entire auditory pathway. Another major disadvantage of PTA is that it requires full patient cooperation, and thus, it may be unsuitable for medicolegal cases, where claimants tend to exaggerate their hearing loss. [29] Accordingly, more sensitive tests of hearing are needed, providing objective information as well, because aggravation of true-hearing thresholds in subjects exposed to noise is commonly encountered when compensations or other issues are involved. For these reasons, evoked potential techniques [30] and recently steady state responses [7] have been used, but these tests have increased technical demands regarding the various recording parameters and are quite time consuming. OAEs is another examination which has been proposed as an alternative method for monitoring cochlear function in cases with noise exposure. This test might provide a more direct and reliable measurement of early changes and damage to the inner ear than audiometry, and could probably play an important role in increasing the effectiveness of hearing conservation programs.

DPOAEs have been occasionally used in such studies as a sensitive test of cochlear function. According to various reports, the outer hair cells are the dominant source of DPOAEs. It was found that DPOAEs are completely unaffected in chinchillas with massive inner hair-cell loss, indicating little or no contribution of this cell population to DPOAE amplitude. [31] However, in chinchillas with outer hair cells destroyed by carboplatin, DP amplitude decreases at a rate of 4.1 dB for every 10% increase in outer hair cell loss. [32] It has been established that chronic exposure to industrial noise at moderately high levels, commonly encountered in industrial settings, brings about damage to the cochlear sensory elements, with outer hair cells being the most susceptible to this kind of damage. [33] Therefore, OAEs seem to be an entirely appropriate test for NIHL, supported from the findings of several studies, in which DPOAE amplitudes were depressed following noise exposure. Another reason why we used DPOAEs in the present study is their frequency specificity and broader range of test frequencies. [34]

In our study, we found statistically significant lower DPOAE levels in the noise-exposed group than in the control group. Additionally, the effect of frequency was significant, indicating that amplitude also varied across frequency with lower responses observed at 4 and 6 kHz, and maximum response found at 2 kHz. In comparison, analysis of audiometric results showed a statistically significant effect of Group, owed to elevated puretone thresholds in the noise-exposed subjects. However, a frequency main effect was not found, implying that thresholds did not vary significantly across Frequency, although the interaction between Frequency and Group was statistically significant, as well as the interaction between Frequency and Ear. A main effect for Ear was found only in puretone thresholds, due to better thresholds in the left ears of the subjects, and not in DPOAE measurements. This finding contradicts the present notion that hearing sensitivity is increased in the right ear, resulting from fundamental differences in the bilateral organization of the human auditory system. [35] However, these differences were small and probably of minor clinical importance and may be owed to sample variation or even may reflect the differential effect of the noise sources upon the left or the right ear according to location.

Our results are consistent with previous reports. [36],[37] However, an issue not fully elucidated yet is whether DPOAEs is a more sensitive method in estimating NIHL compared with audiometry. Sutton et al. [38] evaluated the sensitivity of DPOAEs in a group of industrial workers exposed to acoustic overstimulation. The authors found that the time course of the recovery of DPOAE amplitudes was very similar to behaviorally measured temporary threshold shift, suggesting that DPOAEs can be as sensitive as routine audiometry. In another study of overexposure to high levels of music, Liebel et al. [39] compared PTA, transiently evoked OAEs, and DPOAEs in the detection of temporary threshold shift. They concluded that both OAE tests are not ideal instruments in the detection of temporary threshold shift after noise exposure. Furthermore, in several other studies DPOAEs have been found to be a more sensitive method than PTA. In a discotheque experiment, Vinck et al. [40] found significant changes in both transiently evoked and DPOAEs during noise exposure. After studying the recovery pattern of temporary threshold shift between the applied methods, the authors found that both types of emissions at the 4 kHz frequency region did not recover completely to the pre-exposure reference level. This finding indicated that OAEs are more sensitive than the behavioral audiogram in detecting subtle changes in outer hair cell function.

In a more recent report, Attias et al. [37] concluded that both transiently evoked OAEs and DPOAEs had greater sensitivity to noise damage compared to audiogram. This was supported by several findings: (1) Loss of OAEs in subjects with a proven exposure to noise with otherwise normal audiograms; (2) loss of OAEs was the only audiological feature associated with persistent tinnitus; and (3) in cases with head trauma, the emission loss existed on the involved side of the head, and sometimes was the only overt audiological measure. The authors concluded that OAEs may reveal subtle cochlear changes that may be overlooked by the audiogram and thereby complement the behavioral tests for NIIHL diagnosis. Lapsley Miller et al. [36] reported the longitudinal changes in evoked OAEs and puretone thresholds measured in a noise-exposed group and found that hearing threshold increased by 1.2 dB and DPOAEs amplitude decreased by 1.3 dB, when analyzed between 2 and 4 kHz. The authors remarked, however, that due to a wide age range and variation in noise-exposure history it is difficult to put an absolute number on the expected rate of hearing or emission deterioration. They finally concluded, that although OAEs show promise in detecting NIHL, large-scale, long-term longitudinal studies will be required to achieve a full understanding of the relationship between OAEs and NIHL.

In the present study, we found that DPOAE levels were selectively affected at the higher frequencies and remained robust at 2 kHz, whereas puretone thresholds were affected at all frequencies and only the interaction of Frequency with either the Ear (right/left) measured or the Group (noise exposed or control) was statistically significant. Direct comparison of the number of significantly affected ears between the two methods at 1, 2, and 4 kHz showed statistically significant differences at all comparisons, with more ears affected in PTA in comparison with DPOAEs at 4 kHz, whereas more ears were affected in DPOAEs at the lower frequencies (1 and 2 kHz). Comparison between the elevation of thresholds in behavioral audiometry and the reduction of levels in DPOAEs showed significant correlation across all frequencies. From these results, we may conclude that DPOAEs and PTA are both sensitive methods in detecting NIHL, with DPOAEs tending to be more sensitive at lower frequencies. Probably DPOAEs may be better for detecting noise-induced inner ear changes than the audiogram, because they represent a more direct measurement of cochlear processes.

Another important finding which has been also reported in previous studies, [41] is that although parallel changes were observed on both PTA (elevation of thresholds) and DPOAEs (reduction of amplitude) in most affected ears, in some ears changes were found in only one test performed, indicating different sensitivity among ears. Reduced DPOAEs in the presence of normal audiogram may be explained along several lines. Firstly, the theory of outer hair cell redundancy has been proposed, according to which only some of them are required for normal hearing. [28] Consequently, extensive loss of outer hair cells may occur, without change in puretone thresholds, and OAEs, which accurately reflect outer hair cell activity may be diminished, exhibiting noise-induced subclinical changes. Secondly, test-retest variability is lower in OAEs than audiometry, resulting in detection of smaller noise-induced changes. [36] Thirdly, it is possible that high-frequency hearing loss may affect lower frequency OAEs, due to intermodulation distortion of the OAE components. [41] And, fourthly, a differential effect of age on OAEs and hearing has been reported in several studies, which have shown that OAEs decrease with age, even when audiometric thresholds are controlled. [42] Additionally, noise exposure further accelerates the loss of outer hair cells throughout life. [43]

However, in a number of ears, the opposite finding is evident, intact DPOAEs despite noise-induced cochlear hearing loss evidenced by abnormal audiogram. A plausible explanation could be that noise affected inner hair cells, synapses, or dendrites of auditory neurons in those ears, sparing the outer hair cells. [14] Direct evidence of this has been provided by Borg and Engstrom, [44] who proved that in some laboratory animals with noise-induced cochlear lesions, scanning electron microscopy revealed considerable permanent damage to the inner hair cells despite intact outer hair cells. It appears thus that if these ears with inner hair cell involvement could be detected, the sensitivity of DPOAEs in the remaining majority of ears would greatly increase. The method of mapping dead cochlear regions with absent inner hair cells, introduced by Moore, [45] represents an interesting possibility for evaluating the respective contributions of outer and inner hair cell damage, documenting thus NIHL loss at a much finer level than that usually achieved in standard audiometry.

 
  References Top

1.Lim DJ. Functional structure of the organ of Corti: A review. Hear Res 1986;22:117-46.  Back to cited text no. 1  [PUBMED]  
2.Quaranta A, Portalatini P, Henderson D. Temporary and permanent threshold shift: An overview. Scand Audiol Suppl 1998;48:75-86.  Back to cited text no. 2  [PUBMED]  
3.Clark WW, Bohne BA. Effects of noise on hearing. JAMA 1999;281:1658-9.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Nadol JB Jr. Comparative anatomy of the cochlea and auditory nerve in mammals. Hear Res 1988;34:253-66.  Back to cited text no. 4  [PUBMED]  
5.Dallos P, Evans BN. High-frequency motility of outer hair cells and the cochlear amplifier. Science 1995;267:2006-9.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Hone SW, Norman G, Keogh I, Kelly V. The use of cortical evoked response audiometry in the assessment of noise-induced hearing loss. Otolaryngol Head Neck Surg 2003;128:257-62.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Hsu WC, Wu HP, Liu TC. Objective assessment of auditory thresholds in noise-induced hearing loss using steady-state evoked potentials. Clin Otolaryngol 2003;28:195-8.  Back to cited text no. 7  [PUBMED]  
8.Probst R, Harris FP. Otoacoustic emissions. Adv Otorhinolaryngol 1997;53:182-204.  Back to cited text no. 8  [PUBMED]  
9.Attias J, Furst M, Furman V, Reshef I, Horowitz G, Bresloff I. Noise induced otoacoustic emission loss with or without hearing loss. Ear Hear 1995;16:612-8.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Prasher D, Sulkowski W. The role of otoacoustic emissions in screening and evaluation of noise damage. Int J Occup Med Envir Health 1999;12:183-92.  Back to cited text no. 10    
11.Korres S, Balatsouras D, Manta P, Yiotakis I, Economou C, Adamopoulos G. Cochlear dysfunction in patients with mitochondrial myopathy. ORL J Otorhinolaryngol Relat Spec 2002;64:315-20.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Balatsouras D, Korres S, Simaskos N, Kandiloros D, Ferekidis E, Economou C. Otoacoustic emissions in patients with hypotension. J Laryngol Otol 2003;117:265-9.  Back to cited text no. 12    
13.Jedrzejczak WW, Blinowska KJ, Konopka W. Time-frequency analysis of transiently evoked otoacoustic emissions of subjects exposed to noise. Hear Res 2005;205:249-55.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Avan P, Bonfils P. Distortion-product otoacoustic emission spectra and high-resolution audiometry in noise-induced hearing loss. Hear Res 2005;209:68-75.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Probst R, Lonsbury-Martin BL, Martin GK. A review of otoacoustic emissions. J Acoust Soc Am 1991;89:2027-67.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]
16.Gorga MP, Neely ST, Bergman BM, Beauchaine KL, Kaminski JR, Peters J, et al . A comparison of transient-evoked and distortion product emissions in normal-hearing and hearing-impaired subjects. J Acoust Soc Am 1993;94:2639-48.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Davis B, Qiu W, Hamernik RP. Sensitivity of distortion product otoacoustic emissions in noise-exposed chinchillas. J Am Acad Audiol 2005;16:69-78.  Back to cited text no. 17  [PUBMED]  
18.Linss V, Emmerich E, Richter F, Linss W. Is there a close relationship between changes in amplitudes of distortion product otoacoustic emissions and hair cell damage after exposure to realistic industrial noise in guinea pigs? Eur Arch Otorhinolaryngol 2005;262:488-95.  Back to cited text no. 18  [PUBMED]  [FULLTEXT]
19.Sisto R, Chelotti S, Moriconi L, Pellegrini S, Citroni A, Monechi V, et al . Otoacoustic emission sensitivity to low levels of noise-induced hearing loss. J Acoust Soc Am 2007;122:387-401.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Marshall L, Lapsley Miller JA, Heller LM. Distortion-product otoacoustic emissions as a screening tool for noise-induced hearing loss. Noise Health 2001;3:43-60.  Back to cited text no. 20  [PUBMED]  Medknow Journal
21.International Organization for Standardization. Technical report. Acoustics - Reference zero for the calibration of audiometric equipment - Part 5: Reference equivalent threshold sound pressure levels for pure tones in the frequency range 8 kHz to 16 kHz. ISO/TR 389-5. ISO, Geneva: 2006.   Back to cited text no. 21    
22.American National Standard Institute. Specification for audiometers. NSI S3.6-2004. 2204. ANSI, New York: 2004.  Back to cited text no. 22    
23.International Organization for Standardization. Acoustics. Pure tone audiometric test methods. Part 1: Basic pure tone air and bone conduction threshold audiometry. ISO 8253-1. ISO, Geneva: 1989.  Back to cited text no. 23    
24.Tambs K, Hoffman HJ, Borchgrevink HM, Holmen J, Engdahl B. Hearing loss induced by occupational and impulse noise: Results on threshold shifts by frequencies, age and gender from the Nord-Trøndelag Hearing Loss Study. Int J Audiol 2006;45:309-17.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Kummer P, Janssen T, Arnold W. The level and growth behaviour of the 2f1-f2 distortion product otoacoustic emission and its relationship to auditory sensitivity in normal hearing and cochlear hearing loss. J Acoust Soc Am 1998;103:3431-4.  Back to cited text no. 25  [PUBMED]  [FULLTEXT]
26.Plinkert PK, Hemmert W, Wagner W, Just K, Zenner HP. Monitoring noise susceptibility: sensitivity of otoacoustic emissions and subjective audiometry. Br J Audiol 1999;33:367-82.  Back to cited text no. 26  [PUBMED]  
27.Balatsouras DG, Tsimpiris N, Korres S, Karapantzos I, Papadimitriou N, Danielidis V. The effect of impulse noise on distortion product otoacoustic emissions. Int Audiol 2005;44:540-9.  Back to cited text no. 27    
28.LePage EL, Murray NM. Click-evoked otoacoustic emissions: Comparing emissions strengths with pure tone audiometric thresholds. Aust J Audiol 1993;15:9-22.  Back to cited text no. 28    
29.Balatsouras DG, Kaberos A, Korres S, Kandiloros D, Ferekidis E, Economou C. Detection of pseudohypacusis: A prospective, randomized study of the use of otoacoustic emissions. Ear Hear 2003;24:518-27.  Back to cited text no. 29  [PUBMED]  [FULLTEXT]
30.Fraenkel R, Freeman S, Sohmer H. Use of ABR threshold and OAEs in detection of noise induced hearing loss. J Basic Clin Physiol Pharmacol 2003;14:95-118.  Back to cited text no. 30  [PUBMED]  
31.Trautwein P, Hofstetter P, Wang J, Salvi R, Nostrant A. Selective inner hair cell loss does not alter distortion product otoacoustic emissions. Hear Res 1996;96:71-82.  Back to cited text no. 31  [PUBMED]  
32.Hofstetter P, Ding D, Powers N, Salvi RJ. Quantitative relationship of carboplatin dose to magnitude of inner ear and outer hair cell loss and the reduction in distortion product otoacoustic emission amplitude in chinchillas. Hear Res 1997;112:199-215.  Back to cited text no. 32  [PUBMED]  
33.Sliwinska-Kowalska M, Kotylo P. Otoacoustic emissions in industrial hearing loss assessment. Noise Health 2001;3:75-84.  Back to cited text no. 33  [PUBMED]  Medknow Journal
34.Lonsbury-Martin BL, Martin GK, Probst R, Coats AC. Acoustic distortion products in the rabbit ear canal. I. Basic features and physiological vulnerability. Hear Res 1987;28:173-89.  Back to cited text no. 34    
35.McFadden D. A speculation about the parallel ear asymmetries and sex differences in hearing sensitivity and otoacoustic emissions. Hear Res 1993;68:143-51.  Back to cited text no. 35  [PUBMED]  
36.Lapsley Miller JA, Marshall L, Heller LM. A longitudinal study of changes in evoked otoacoustic emissions and pure-tone thresholds as measured in a hearing conservation program. Int J Audiol 2004;43:307-22.  Back to cited text no. 36  [PUBMED]  
37.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.  Back to cited text no. 37  [PUBMED]  Medknow Journal
38.Sutton LA, Lonsbury-Martin BL, Martin GK, Whitehead ML. Sensitivity of distortion product otoacoustic emissions in humans to tonal overexposure: Time course of recovery and effects of lowering L2. Hear Res 1994;75:161-74.  Back to cited text no. 38  [PUBMED]  
39.Liebel J, Delb W, Andes C, Koch A. Measurement of noise effects in a discotheque by means of otoacoustic emissions. Laryngol Rhinol Otol 1996;75:259-64.  Back to cited text no. 39    
40.Vinck BM, Van Cauwenberge PB, Leroy L, Corthals P. Sensitivity of transient evoked and distortion product otoacoustic emissions to the direct effects of noise on the human cochlea. Audiology 1999;38:44-52.  Back to cited text no. 40  [PUBMED]  
41.Lapsley Miller JA, Marshall L, Heller LM, Hughes LM. Low-level otoacoustic emissions may predict susceptibility to noise-induced hearing loss. J Acoust Soc Am 2006;120:280-96.  Back to cited text no. 41  [PUBMED]  [FULLTEXT]
42.Dorn PA, Piskorski P, Keefe DH, Neely ST, Gorga MP. On the existence of an age/threshold/frequency interaction in distortion product otoacoustic emissions. J Acoust Soc Am 1998;104:964-71.  Back to cited text no. 42  [PUBMED]  [FULLTEXT]
43.Murray NM, LePage EL. Age dependence of otoacoustic emissions and apparent rates of ageing of the inner ear in an Australian population. Aust J Audiol 1993;15:59-70.  Back to cited text no. 43    
44.Borg E, Engstrom B. Noise level, inner hair cell damage, audiometric features, and equal-energy hypthesis. J Acoust Soc Am 1989;86:1776-82.  Back to cited text no. 44    
45.Moore BCJ. Dead regions in the cochlea: conceptual foundations, diagnosis, and clinical applications. Ear Hear 2004;25:98-116.  Back to cited text no. 45    

Top
Correspondence Address:
Dimitrios G Balatsouras
23 Achaion Str. – Agia Paraskevi, 15343 – Athens
Greece
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1463-1741.50695

Rights and Permissions


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

This article has been cited by
1 Conventional Audiometry, Extended High-Frequency Audiometry, and DPOAE for Early Diagnosis of NIHL
Amir Houshang Mehrparvar,Seyyed Jalil Mirmohammadi,Mohammad Hossein Davari,Mehrdad Mostaghaci,Abolfazl Mollasadeghi,Maryam Bahaloo,Seyyed Hesam Hashemi
Iranian Red Crescent Medical Journal. 2014; 16(1)
[Pubmed] | [DOI]
2 Distortion Product Otoacoustic Emission (DPOAE) as an Appropriate Tool in Assessment of Otoprotective Effects of Antioxidants in Noise-Induced Hearing Loss (NIHL)
Afsaneh Doosti,Yones Lotfi,Abdollah Moosavi,Enayatollah Bakhshi,Azita Hajhossein Talasaz
Indian Journal of Otolaryngology and Head & Neck Surgery. 2014;
[Pubmed] | [DOI]
3 Oto-toxic effect of gastric reflux
Develioglu, O.N. and Yilmaz, M. and Caglar, E. and Topak, M. and Kulekci, M.
Journal of Craniofacial Surgery. 2013; 24(2): 640-644
[Pubmed]
4 Evoked otoacoustic emissions in workers exposed to noise: A review
De Souza Alcarás, P.A. and Lüders, D. and Franča, D.M.V.R. and Klas, R.M. and De Lacerda, A.B.M. and De Oliveira Gončalves, C.G.
International Archives of Otorhinolaryngology. 2012; 16(4): 515-522
[Pubmed]
5 Football match spectator sound exposure and effect on hearing: A pretest-post-test study
Swanepoel, D.W., Hall III, J.W.
South African Medical Journal. 2010; 100(4): 239-242
[Pubmed]
6 Temporary reduction of distortion product otoacoustic emissions (DPOAEs) immediately following auditory brainstem response (ABR)
Anand N. Mhatre,Bobby Tajudeen,Elena M. Welt,Christopher Wartmann,Glenis R. Long,Anil K. Lalwani
Hearing Research. 2010; 269(1-2): 180
[Pubmed] | [DOI]
7 Temporary reduction of distortion product otoacoustic emissions (DPOAEs) immediately following auditory brainstem response (ABR)
Mhatre, A.N., Tajudeen, B., Welt, E.M., Wartmann, C., Long, G.R., Lalwani, A.K.
Hearing Research. 2010; 269(1-2): 180-185
[Pubmed]



 

Top