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ARTICLES Table of Contents   
Year : 2001  |  Volume : 3  |  Issue : 10  |  Page : 29-37
Evaluation of transient and distortion product otoacoustic emissions before and after shooting practice

Military Medical University, Lodz, Poland

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

Keywords: otoacoustic emissions (TEOAE, DPOAE) firearms, shooting

How to cite this article:
Konopka W, Zalewski P, Pietkiewicz P. Evaluation of transient and distortion product otoacoustic emissions before and after shooting practice. Noise Health 2001;3:29-37

How to cite this URL:
Konopka W, Zalewski P, Pietkiewicz P. Evaluation of transient and distortion product otoacoustic emissions before and after shooting practice. Noise Health [serial online] 2001 [cited 2023 May 31];3:29-37. Available from: https://www.noiseandhealth.org/text.asp?2001/3/10/29/31760
The discovery of otoacoustic emission (OAE) has given a new possibility in early diagnosis of the auditory system. Since 1978 OAE has played an important role in clinical practice as a method of universal neonatal screening and monitoring of micromechanical function of the cochlea (Kemp et al.,1993). Transient evoked otoacoustic emission (TEOAE) and distortion product otoacoustic emission (DPOAE) are non­invasive, objective and frequency specific tests for evalua-ting hair cell damage caused by noise and other etiological factors (Franklin et al., 1991; Schmiedt et al., 1986).

Sounds of high intensity often cause damage to the organ of Corti. Many publications have described the pattern of cellular damage or their loss. It is well known that the outer hair cells often get damaged first (Zenner, 1997). There are data that OAEs in humans and in animals become weaker after short exposures to noise (Lonsbury-Martin et al., 1991; Sliwinska -Kowalska et al., 1993) and OAE measurements appear to be a sensitive method of monitoring the early cochlear changes after noise-induced trauma (Hotz et al., 1993).

The published results about hearing loss caused by industrial noise, show that TEOAE and DPOAE provide the possibility of monitoring the development of noise- induced trauma (CEliwiflska-Kowalska 1998). According to Oeken (1998) measuring the DPOAE upon acute acoustic trauma could be relevant to prognosis for therapy.

Noise induced hearing loss is usually measured as temporary threshold shifts (TTS) or permanent threshold shifts (PTS) by pure tone audiometry but very seldom by OAEs.

Firearms are a common source of impulse noise that may potentially damage the hearing organ. Especially in countries where military service is compulsory, a large portion of the population is exposed to such noise. It is very important for soldiers to identify their individual susceptibility to noise exposure. It is difficult to predict temporary or permanent damage to hearing sensitivity (Henderson et al., 1993).

The aims of this study were to evaluate transient evoked otoacoustic emissions and distortion­product otoacoustic emission before and after shooting and compare with conventional pure tone audiometry.

  Material and Methods Top

Our material comprises 10 male soldiers (20 ears) who were in obligatory military service, with an average age of 20 years. There were in military service for 3 months and it was their shooting training. Written consent was obtained from all subjects and the project was approved by the local University Ethics Committee. The soldiers were exposed to impulse noise from automatic gunfire. The shooting range included 15 single rounds ( 150-165 dB peak level measured at the ear ) of live ammunition. They did not use any hearing protectors.

Conventional pure tone audiometry, tympanometry, evoked transient and distortion product otoacoustic emissions, were recorded before and about 10-15 minutes after shooting practice.

All the testing was performed in a relatively quiet room in a building on the grounds of the military installation.

In the same group OAE and PTA were measured twice with a 10-minute pause without noise exposure.

Otoacoustic emissions were recorded using an ILO 292 Echoport version 5.0. TEOAE recordings of 260 sweeps were collected for every subject at a stimulus level of 80 + 2dB SPL using 80 s duration clicks. An artefact rejection level of 4.6 mPa (47.3 dB SPL) was used throughout the recording session. Each response was windowed from 2.5 to 20 ms post stimulus and bandpass filtered from 500 to 6000 Hz. DPOAE were recorded with the DP- Gram procedure. The 2f1-f2 DPOAE were recorded at a single level of 70 dB SPL. The f2 /f1 ratio was held constant at 1.22 while f1 and f2 varied from 0.8 to 5.2 kHz and from 1.0 to 6.3 kHz. Averaging was used until the "noise floor" did not change any more. Only responses with an amplitude at least two standard deviation above the noise were used in the results. The statistical analysis was done with the Wald-Wolfowitz test with a significance level set as p< 0.05.

  Results Top

All subjects had bilateral audiometric thresholds from 10 to 20 dB HL for the audiometric frequencies to 3 kHz, and 25-30 dB HL for 4 to 8 kHz. [Table - 1],[Table - 2] before and after shooting. We did not notice any significant differences.

The tympanograms were normal (type A, with middle-ear pressure between -80 and +50 daPa) and the presence of acoustic reflex at normal levels.

The results were separately analysed for each ear immediately after noise exposure. The mean change in TEOAE level was calculated separately for each frequency band. Significant reduction in amplitude of the TEOAE after shooting was found for the frequencies 1, 1.5, 2, 3 and 4, kHz for the right ear with a mean change of 2.6 dB SPL and for 3 kHz, 3.1 dB SPL (p<0.02 ) and for 4 kHz, 5.1 dB SPL (p<0.03).

The decrease in amplitude of the TEOAE was significant for the left ear for only 1 kHz (4.3 dB SPL, p<0.01) and 2 kHz (0.6 dB SPL, p<0.05) after noise exposure.

DPOAE alteration as a amplitude reduction was seen in 19 of the 20 tested ears. The mean amplitude of the DPOAE was decreased over the whole range. The mean change for the right ear was 0.8 dB SPL, and for the left ear 2.0 dB SPL for the frequencies 1, 2, 2.5, 3, 4, 5 and 6 kHz. The greatest reduction occurred for 1.0 kHz -(3.8 dB SPL, p<0.01) and 3.0 kHz - ( 2.9 dB SPL, p<0.04 ) for the left ear .

  Discussion Top

Exposure to impulse noise during compulsory military service depends on the number of shots, or explosion impulses, distance of injured ear from causal firearm as well as on hearing protectors usage.

Changes induced by moderate or severe noise exposure that give rise to TTS, have been shown to alter the amplitude or frequency composition of transient evoked otoacoustic emissions (Kemp, 1982), distortion product otoacoustic emissions (Schmiedt, 1986; Martin et al. 1987; Sutton et al 1994) and spontaneous otoacoustic emissions, (Norton et al. 1989; Furst et al. 1992). Hotz et al. (1993) used OAEs to monitor changes in cochlear function resulting from exposure to firearms, among military personnel after a 17­week training period. Significant bilateral changes in click evoked OAE amplitudes were observed in the frequency range 2-4 kHz. No preponderance of the left ears was noted.

Attias et al. (1996) found reduced click evoked OAE levels for the frequencies 1, 2, 3 and 4 kHz in patients with normal audiograms, after noise exposure (10 minutes exposure to white noise at 90 dB SL).

In our group, reduction of the TEOAE amplitude was found especially for 3 and 4 kHz for the right ear and for 1 and 2 kHz for the left ear. The amplitude reduction of the TEOAE was actually greater in the right ear than in the left one for most frequencies.

The greatest effect of noise exposure on the DPOAE amplitude concerned left ear for 1.0 and 3.0 kHz.

All our shooters were right-handed and probably the asymmetrical effect resulted from the shooting posture depending on the shadow effect of the body.

We did not notice any differences between audiometric threshold before and after shooting.

Reduced TEOAE and DPOAE levels in noise exposed soldiers may be the first early indication of potential hearing loss. Clinical experience with otoacoustic emissions indicates that OAE may play a role as a screening method for the soldiers exposed to noise and as a tool for monitoring early changes in the cochlea. TTS measurement is still the most widely used method for investigating reversible cochlear effects in the human. In our opinion small changes in the function of the cochlea can be monitored by measuring TEOAE and DPOAE especially in cases where classical audiometry is less sensitive.

  Conclusions Top

  1. The effect of noise exposure on TEOAE was seen especially for 3 and 4 kHz and on DPOAE for 1.0 and 3 kHz.
  2. The amplitude reduction of the TEOAE was often greater in the right ear while DPOAE showed changes in the left ear. 3. Emissions seem to be more sensitive for monitoring cochlear changes than pure tone audiometry.[16]

  References Top

1.Attias J., Bresloff I. (1996) Noise Induced Temporary Otoacoustic Emission Shifts. Journal of Basic Clinical Physiology Pharmacology, 7(3): 221-233.  Back to cited text no. 1    
2.Franklin DJ., Lonsbury-Martin B. L., Stagner B. B., Martin G.K. (1991) Altered susceptibility of 2 f1-f2 acoustic-distortion products to the effects of repeated noise exposure in rabbits. Hear. Res. 53: 185-208.  Back to cited text no. 2    
3.Furst M., Reshef I., Attias J. (1992) Manifestations of intense noise stimulation on spontaneous otoacoustic emission and threshold microstructure: experiment and model. J. Acoust. Soc. Am. 91: 1003-1014.  Back to cited text no. 3    
4.Henderson D, Subramaniam M, Boettcher FA. (1993) Individual susceptibility to noise-induced hearing loss: an old topic revisited. Ear Hear, 14: 152-168.  Back to cited text no. 4    
5.Hotz M. A., Probst F. P., Harris, Hauser R.(1993) Monitoring the effects of noise exposure using transiently evoked otoacoustic emissions. Acta Otolaryngol. /Stockh/. 113: 478-482  Back to cited text no. 5    
6.Kemp D.T. (1982) Cochlear echoes: implications for noise-induced hearing loss. In New Perspectives on Noise­induced Hearing Loss. Hamernik R.P., Henderson D., Salvi R.J., eds., Raven Press, New York, pp. 189-206.  Back to cited text no. 6    
7.Kemp D. T., Ryan S. (1993) The use of transient evoked otoacoustic emissions in neonatal hearing screening programs. Seminars in Hearing. 14: 30-44.  Back to cited text no. 7    
8.Lonsbury-Martin B.L., Whitehead M.L., Martin G.K. (1991) Clinical application of otoacoustic emissions. J. Speech Hear. Res. 34: 964-81.  Back to cited text no. 8    
9.Norton S. J., Mott J. B. Champlin C.A. (1989) Behaviour of spontaneous otoacoustic emissions following intense ipsilateral acoustic stimulation. Hear. Res. 38: 243-258.  Back to cited text no. 9    
10.Oeken J. (1998) Distortion Product Otoacoustic Emissions in acute acoustic trauma. Noise Health 1: 56-66  Back to cited text no. 10    
11.Schmied R. A. (1986) Acoustic distortion product in ear canal. I. Cubic difference tones: effects of acute noise injury. J. Acoust. Soc. Am. 79: 1481-1490.  Back to cited text no. 11    
12.Subramaniam M., Henderson D., Spongr V. (1994) The relationship among distortion-product otoacoustic emissions, evoked potential thresholds and outer hair cells following interrupted noise exposures. Ear Hear. 15: 299­309.  Back to cited text no. 12    
13.Sutton L.A., Lonsbury-Martin B.L., Martin G.K., Whitehead M. L. (1994) Sensitivity of distortion-product otoacoustic emissions in humans to tonal over-exposure: time course of recovery, and effects of lowering L2. Hear. Res. 75: 161-174.  Back to cited text no. 13    
14.Sliwifiska-Kowalska M., Sulkowski W., Jedlifiska J., Rydzynski K.(1993) Relationships between functional and morphological changes in the cochlea of guinea pigs after exposure to industrial noise. Proc 6 th International Congress Noise Man. 93, 2: 127-130  Back to cited text no. 14    
15.Sliwifiska-Kowalska M. (1998) The role of evoked and distortion-product otoacoustic emissions in diagnosis of occupational noise-induced hearing loss. Journal of Audiological Medicine 7(1): 29-45.  Back to cited text no. 15    
16.Zenner H.P. (1997) The role of outer hair cell damage in the loss of hearing. Ear Nose Throat J. 76 (3), 140: 143­144  Back to cited text no. 16    

Correspondence Address:
Wieslaw Konopka
Department of Otolaryngology Military Medical University, Zeromskiego 113, 90-549 Lodz
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Source of Support: None, Conflict of Interest: None

PMID: 12689453

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

  [Table - 1], [Table - 2]