Portuguese Version

Year:  2002  Vol. 68   Ed. 1 - (3º)

Artigo Original

Pages: 15 to 20

PDF PT  

Distortion-product otoacoustic emissions and pure tone audiometry: a study of temporary threshold shifts

Author(s): Silvana Frota 1,
Maria Cecília Martinelli Iório 2

Keywords: hearing, otoacoustic emissions, noise, acoustic stimulation.

Abstract:
Introduction: Noise-induced hearing loss is one of the most common causes for sensorineural hearing impairment. Objective: The purpose of this study was to evaluate pure tone and distortion product otoacoustic emissions (DPOAE) pre and post white noise exposition at high levels (100 dB SPL for 10 minutes), considering gender and ear variables, aiming at investigating pure tone audiometry and DPOAE efficiency in detecting subtle temporary threshold shifts (TTS). Study design: prospectivo clinical randomized. Material and method: Forty subjects, 20 male and 20 female ranging from 18 to 36 years old with no otological complaints were evaluated. Pure tone audiometry and DPOAE were carried out pre and post white noise exposure. Results: Pure tone audiometry was sensitive in detecting temporary threshold shifts after white noise exposition in 2, 3 and 4 kHz, with no significant differences concerning gender and ear, whereas DPOAE revealed temporary shifts in audibility evidenced by amplitude reduction, in 2588 and 3614 in female subjects and in 932, 1304, 2588 and 5128 Hz in male subjects. Conclusion: We could conclude that either pure tone audiometry or DPOAE were sensitive in determining significant temporary shifts in hearing thresholds and amplitude, respectively, after white noise exposition, according to the involved frequency range.

1 Audiologist, Master in Human Communication Disorders, Federal University of São Paulo - Escola Paulista de Medicina (UNIFESP-EPM), Assistant Professor of Audiology, UFRJ.
2 Audiologist, Ph.D. in Human Communication Disorders, Federal University of São Paulo - Escola Paulista de Medicina.

Joint Professor, Discipline of Hearing Disorders, Department of Otorhinolaryngology and Human Communication Disorders, UNIFESP - EPM.

Master Dissertation presented to Federal University of São Paulo - Escola Paulista de Medicina, Master degree in Human Communication Disorders: Audiology and Speech Disorders.

Paper presented at XVI Encontro Internacional de Audiologia - April 2001 - Rio de Janeiro - RJ

Address correspondence to: Silvana Frota: Av. Niemeyer 925,Bl.2 aptº 1102 - São Conrado - Rio de Janeiro - RJ - 22450-221 - E-mail: frota@antares.com.br

Article submitted on September 10, 2001. Article accepted on November 20, 2001.

---

Introduction

Technology advancement has brought, in addition to a modern and easy life, a substantial increment in harmful and foreign stimuli to the human body. Noise is one of the physical agents resultant from these environmental changes that occur within work, transport, leisure and human social interactions.

Hearing loss induced by high levels of sound pressure is currently one of the main causes of sensorineural hearing losses. A number of factors influence the onset of such losses, especially sound pressure levels, duration of noise exposure, intensity and frequency of noise and individual susceptibility.

Noise-induced hearing losses occur primarily as reversible situations, as a result of temporary threshold shifts in the frequency range of 2000 to 6000Hz3. Temporary threshold shifts have been widely studied because the extent of their presence shows a susceptibility prognosis for permanent losses.

Pathology studies have shown that in hearing loss induced by high levels of sound pressure there are mechanical and metabolic changes affecting mainly the outer hair cells of Corti's organ, especially those located in the basal portion of the basilar membrane, since they are the most sensitive ones1, 11, 14, 20, 23.

No one questions the importance otoacoustic emissions have gained in the past decades in the otological field. David Kemp12, in his first publication about the topic in 1978, described the existence of cochlear echo that could be measured in the external auditory canal. After the study, a number of other papers were conducted to improve the knowledge about the existence of the active cochlear mechanism, originated from the biomechanics of outer hair cells (OHC) of Corti's organ.

Slow and fast contractions of the cochlea determine its biomechanical properties. Thus, the electromotility of OHC generates mechanical energy, released during the fast contraction, which follows cycle after cycle the stimulation frequency up to tenths of kHz, working as a cochlear amplifier capable of having precise frequency selectivity.

Described in 1979 by David Kemp13, distortion product otoacoustic emissions (DPOAE) are evoked as the intermodulation response of two simultaneous pure tones of close frequencies (F1 and F2), called primary tones, that have a capacity determined by frequency. DPOAE is normally a quick, objective, non-invasive, non-painful and easy to perform test.

Therefore, cochlear impairments resultant from exposure to high levels of sound pressure should cause early changes of amplitude of DPOAE, which originate in Corti's organ by the OHCs.

The purpose of the present study was to study audibility thresholds and distortion production otoacoustic emissions before and after exposure to high levels of white noise, trying to define efficacy of both tests to detect small temporary threshold shifts.

Material and Method

The present study was carried out in the Ambulatory of Clinical Audiology, Department of Otorhinolaryngology, Federal University of Rio de Janeiro, UFRJ. Forty normal hearing subjects were enrolled in the study, 20 male and 20 female subjects, ranging in age from 18 to 36 years. We assessed 80 ears in total.

Figure 1. Schematic representation of distortion product otoacoustic emissions (DP) (indicated by the arrows), and background noise level (NF), for each tested frequency.

Pure tone audiometry and distortion product otoacoustic emissions were performed in a soundproof booth.

We used an audiometer brand Interacoustics, model CE 10 standard ANSI-69 and phones TDH - 39 MX 41. To record distortion product otoacoustic emissions we used the device AuDX, brand BIO-LOGIC SYSTEMS CORP, coupled to a 486 PC.

Subjects were submitted to the tests according to the following sequence:

·Distortion product evoked otoacoustic emissions and pure tone audiometry before noise exposure;
·Exposure to white noise (100 dB SPL) for a 10-minute period;
·Distortion product evoked otoacoustic emissions and pure tone audiometry after noise exposure.

The stimulus used to evoke the otoacoustic emissions consisted of two pure tones of different frequencies (F1 and F2), presented simultaneously. The numeric relation between the two stimuli F2/F1 was approximately 1.22. Intensities of F1 and F2 were respectively 65 dB SPL (L1) and 55dB SPL (L2).

We analyzed the amplitude of distortion product in relation to sound frequency, whose characteristics are demonstrated in Table 1, with values of primary frequencies F1 and F2, geometrical mean of F1 and F2, F2/F1 proportion and value of 2F2 - F1 (Table 1).

We analyzed geometrical means (GM) of frequencies 932, 1304, 1818, 2599, 3614 and 5128 Hz.

Distortion product otoacoustic emissions (PD) were considered present when recorded above the background noise (NF) recorded from the noise of the subjects and the recording system (Figure 1).

The difference resulting from amplitude of distortion product and background noise level (PD - NF) was the parameter chosen to compare and analyze pre and post-acoustic stimulation amplitudes.

We selected a statistical study for pure tone audiometry responses and otoacoustic emissions, considering variables gender and ear, using the non-parametric Wilcoxon and Mann-Whitney tests.

Results

Upon comparing pre and post-exposure pure tone audiometry, we observed that audibility levels of subjects of both genders presented significant differences, varying within the studied frequencies (Tables 2, 3, 4, 5 and 6). The main changes in audibility thresholds (worsening) were noticed in frequencies of 3000 (5.75 dBHL) and 4000 Hz (6.0 dBHL) in both genders.

As to DPOAE amplitudes, we observed that few remained unaltered after stimulation with white noise.

Since we did not detect statistically significant differences between amplitudes of DPOAE of right and left ears in both genders, values were grouped. When observing the individual values of DPOAE amplitude we found amplitude changes (worsening) in all frequencies, but in different frequencies according to gender. The main amplitude changes, considering mean values, were observed in frequencies 3614 Hz (2.41 dB SPL), in female subjects and in 1304 Hz (2.5 dB SPL) in male subjects (Table 7).

For female subjects, we found statistically significant differences in frequencies 2588 and 3614 Hz and for male subjects, there were statistically significant differences in amplitude of otoacoustic emissions in frequencies 932, 1304, 2588 and 5128 Hz (Table 8).

Discussion

In our study with audiologically normal adult subjects, regardless of ear or gender, all of them presented statistically significant differences when comparing audibility thresholds pre and post-exposure to white noise in frequencies 2000, 3000 and 4000Hz.

Other authors3, 4, 18, 21, 22 studied audibility threshold shifts after exposure to noise and found the same results concerning high frequencies.

As to otoacoustic emissions, a number of other studies9, 10, 15, 16, 17, 24 referred shifts in otoacoustic emissions amplitude (worsening) after noise exposure. The studies diverged regarding affected frequencies and the methodology adopted.

Another study15 showed significant differences of 20dB in one or more amplitudes of distortion product otoacoustic emissions of right and left ears only in 4000Hz. Analysis of curve amplitude demonstrated that women present lower thresholds, close to 10 dB.

In our study, there were statistically significant differences between amplitudes of DPOAE in the right and left ears, allowing the analysis by group. However, when we conducted the study according to the variable gender, we found statistically significant differences in the frequency of 3614 Hz.

Using the protocol with L1 different from L224, sensitivity to detect amplitude differences pre and post-exposure to noise (105 dB SPL centered in the frequency 2800Hz) was greater, amounting to a 5 to 6 dB difference. In another study, it was reported that the amplitude reduction of DPOAE was related, but not linearly, to the reduction of audibility thresholds. For each 1dB SPL decreased in amplitude of DPOAE, the author found 2dB in pure tone thresholds. The authors concluded that this difference L1/L2 was important because it showed more sensitivity to detect OHC abnormalities.

A study with a group of guinea pigs5 exposed to 80dB SPL noise at half an octave band of 6000Hz, for four hours, whose parameters for evoked DPOAE stimuli were F2/F1 and L2=L1-10, found attenuation of emissions, which was maximum in the frequency of half octave band of exposure. Using the same parameters, the experience was repeated at 90dB SPL and resulted in deficit of emissions, especially of high frequencies, which were recovered after 8 days of exposure, whereas the first recovery took place two days after exposure.

Another author also studied guinea pigs6, submitted to noise exposure for 10 consecutive days, two different groups of guinea pigs: those used and those not used to sound stimuli. Distortion product otoacoustic emissions were used to monitor noise-induced hearing loss. As a result, the authors observed that the group used to sound was significantly less affected by the over stimulation during the first days of noise exposure, when compared to the group not used to sounds. The guinea pigs used to sound became gradually more affected by the over stimulation in the subsequent daily sessions.

Another experiment7 used, among other tests, DPOAE to investigate the temporary alteration of the cochlear function. They used a 102dB SPL noise centered in the frequency of 2000Hz. The magnitude of the noise exposure effect was seen by the amplitude of distortion product otoacoustic emissions between 2000 and 4000Hz. As a result, after the exposure to noise, the reduction in the mean amplitude of DPOAE in frequencies 2000 to 4000Hz (being 3000Hz as the most affected one) was more significant, measured at the first minute (14.7 dB), compared to reduction of amplitude after two minutes that was 6.8 dB and twenty minutes that was 4.1 dB. The authors concluded that temporary thresholds shift (TTS) was greater in the first minute and that there was no correlation between TTS and amplitude of DPOAE after 22 minutes of exposure.

Another study8 observed greater reduction of DPOAE amplitude in approximately half an octave of the noise frequency. The degree of amplitude reduction was greater when low frequency stimuli were used.

In recording amplitude shifts of DPOAE after exposure to 90 dB SPL2, it was noticed a reduction of 5dB in the same amplitude after exposure.

Recent studies19 measuring DPOAE thresholds in 102 ears of otologically normal subjects, before and after noise exposure, recorded temporary threshold shift immediately after noise, especially in 4000Hz. These reductions in amplitude varied from 2000 to 5000Hz. The authors observed recovery of amplitude as time went by.

A comparative study9 of pure tone audiometry and distortion product otoacoustic emissions in 450 workers of a steel company production line, exposed to different levels of noise, showed that otoacoustic emissions in subjects exposed to noise are characterized by impairment mainly in high frequencies. The shift progresses leading to reduction of intensity and amplitude of distortion product and increase of affected frequency range, towards middle and low frequencies. It was also found by the authors that there is inversely proportional relation between audiometry and otoacoustic emissions, that is, the more the auditory thresholds increases, the more distortion product decreases. According to the authors, distortion product otoacoustic emissions should not replace pure tone audiometry.

As to otoacoustic emissions, it was much more difficult to compare the results of the present study with that of other authors because we selected parameters for the study of DPOAE that were L1 and L2, and F1 and F2 that could be randomly selected.

Another issue to be considered, which has also hindered the comparison of results, concerned noise exposure and type and spectrum of noise, as well as duration of exposure.

As a common point in all studies, we noticed that regardless of the criteria adopted, they all detected some kind of shift (reduction) in the amplitude of otoacoustic emissions, varying according to the studied frequency.

Conclusion

Based on the critical analysis of the results, we concluded that:

I - Pure tone audiometry was sensitive to temporary threshold shifts after exposure to white noise in frequencies of 2000, 3000 and 4000Hz, regardless of ear or gender.

II - Pure tone audiometry also showed temporary threshold shifts that were statistically significant after exposure to white noise, in frequencies 1000Hz (except for male subjects on the right ear) and 6000Hz for female subjects on the right, and male subjects on the left.

III - Distortion product otoacoustic emissions showed temporary auditory sensitivity shifts evidenced by statistically significant reduction in amplitudes, after exposure to white noise, in frequencies 2588 to 3614 Hz for female subjects and in frequencies 932, 1304, 2588 and 5128 Hz for male subjects.

Both tests performed in the study - pure tone audiometry and distortion product otoacoustic emissions proved to be sensitive to detect statistically significant temporary shifts in audibility and amplitude, respectively, after exposure to white noise.

References

1. ALBERNAZ, P.L.M.; COVELL, W.P. - Acoustic trauma lesions by fluorescence microscopy. Laryngoscope, 72:1278-96, 1962.
2. ATTIAS, J.; BRESLOFF, I. - Noise induced temporary otoacoustic emission shifts. J. Basic Clin. Physiol., 7(3):221-33,1996.
3. AZEVEDO, A.P.; OKAMOTO, V.A.; BERNARDI, R.C. - Considerações sobre Ruído. In: COSTA, D.F.; CARMO, J.C.; SETTIMI, M.M.; SANTOS, U.P. Programa de Saúde dos Trabalhadores. São Paulo, Hucitec, 1989.
4. BUNCH, C.C. - The diagnosis of occupational or traumatic deafness. A historical and audiometry study. Laryngoscope, 47:615-91, 1937.
5. CHANG, K.W.; NORTON, S.J. - The Effects of Continuous Versus Interrupted Noise Exposures on Distortion Product Otoacoustic Emission in Guinea Pigs. Hear. Res., 96 (1-2):1-12, 1996.
6. DAGLI, S.; CANLON, B. - The Effect of Repeated Daily Noise Exposure on Sound - Conditioned and Unconditioned Guinea Pigs. Hear. Res, 104 (1-2):39-46, 1997.
7. ENGDAHL, B. - Effects of Noise and exercise on Distortion Product Otoacoustic Emissions. Hearing Research, 93:72-82, 1996.
8. ENGDAHL, B.; KEMP, D.T. - The Effect of Noise Exposure on the Details of Distortion Product Otoacoustic Emissions in Humans. J. Soc. Am., 99:1573-87, 1996.
9. FUKUDA, C.; MUNHOZ, M.S.L.; TOLEDO, F.B.; HASSAN, E.S. - Emissões otoacústicas por produto de distorção em trabalhadores expostos a ruído. Acta Awho, 17 (4):176-85,1998.
10. GORGA,M.P.; NEELY, S.T.; BERGMAN, B.; BEAUCHAINE, K.L.; KAMINSKI, J.R.; PETERS, J.; JESTEADT, W. - Otoacoustic emissions from normal-hearing and hearing-impaired subjects: distortion product responses. J. Acoust. Soc. Am., 93(2):2050-60,1993.
11. INGRASIAS M.; SCHUKNECHT, H.F.; MYERS, E.N. - Cochlear pathology in humans with stimulation deafness. The Journal of Laryngology and Otology, 78:115-23, 1964.
12. KEMP, D.T. - Stimulated acoustic emission from within the human auditory System. J. Acoustic. Soc. Am., 64(5):1386-91,1978.
13. 13. KEMP, D.T. - Evidence of mechanical non-linearity and frequency selective wave amplification in the cochlea. Arch. Oto- Rhino-Laryngol., 224:37-45,1979.
14. LIM, D.J.; MEINICK. - Acoustic damage of the cochlea; A scanning and transmission electron microscopic observation. Arch. Otolaryng., 94:294, 1971.
15. LONSBURY-MARTIN, B.L.; HARRIS, F.P.; STAGNER, B.B.; HAWKINS, M. D.; MARTIN, G.K. - Distortion product emissions in humans. Basic properties in normally hearing subjects. Ann. Otol. Rhinol. Laryngol., 147:3-14, 1990. Suppl. 99.
16. LOPES, O.; CARLOS, R. - Produto de Distorção das Emissões Otoacústicas. Rev. Bras. Med. Otorrinolaringol.,3(5):224-37, 1996.
17. LOPES, O.; CARLOS, R. - Emissões Otoacústicas. In: LOPES FILHO, O. Tratado de Fonoaudiologia. São Paulo, Roca. p.221-237, 1997
18. MIRANDA, C.R., DIAS, C.R. - Perda Auditiva Induzida pelo Ruído em Trabalhadores em Bandas e Trios Elétricos de Salvador, Bahia. Rev. Bras. Otorrinolaringol, 64(5), 1999.
19. OEKEN, J.; MENZ, D. - Amplitude changes in distortion products of otoacoustic emission after acute noise exposure. Laryngorhinootologie, 75(5):265-9, 1996.
20. OLIVEIRA, J. - Fisiologia clínica da Audição. In: NUDELMANN, A. A.; COSTA, E. A.; SELIGMAN, J.; IBAÑEZ, R.N. Perda Auditiva Induzida por Ruído. Porto Alegre, Bagagem. p.101-42, 1997.
21. SANTOS, U.P.; COSTA, D. F.; CARMO, J.C. - Programa de Conservação Auditiva em Trabalhadores Expostos à Ruído. In: COSTA, D.F.; CARMO, J.C.; SETTIMI, M.M.; SANTOS, U.P. Programa de Saúde de Saúde dos Trabalhadores. São Paulo, Hucitec. p.125-55, 1989.
22. RUSSO, I.C.P.; SANTOS, T.M.M.; BUSGAIB, B.B.; OSTERNE, F.J.V. - Um Estudo Comparativo Sobre os Efeitos da Exposição à Música de Trio Elétrico. Rev. Bras. Otorrinolaringol, 61(6):477-84, 1995.
23. SULKOWSKI, W.J. - Industrial Noise Pollution and Hearing Impairment Springfield, US Department of Commerce. 1980. National Technical Information Service.
24. SUTTON, L.A.; LONSBURY-MARTIN, B.L.; MARTIN, G.K; WHITEHEAD, M.L. - Sensitivity of distortion-product otoacoustic emissions in humans to tonal over-exposure: Time course of recovery and effects of lowering L2. Hearing Research, 75:161-74, 1994.

Table 1. Values of primary frequencies of distortion product stimuli.

Table 2. Audibility thresholds and central tendency measures - mean, standard deviation and median in dBHL, pre and post-exposure to noise, female subjects, right ear.

Table 3. Audibility thresholds and central tendency measures - mean, standard deviation and median in dBHL, pre and post-exposure to noise, female subjects, left ear.

Table 4. Audibility thresholds and central tendency measures - mean, standard deviation and median in dBHL, pre and post-exposure to noise, male subjects, right ear.

Table 5. Audibility thresholds and central tendency measures - mean, standard deviation and median in dBHL, pre and post-exposure to noise, female subjects, left ear.

Table 6. p values calculated based on Wilcoxon test of audibility thresholds pre and post-exposure to noise, according to variables ear and gender.

Table 7. Results of DPOAE and central tendency measures side - mean, standard deviation and median in dB SPL, pre and post-exposure, male and female subjects.

Table 8. Results of Wilcoxon test for pre and post-exposure DPOAE for both genders.

Print: