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There is an announcement for the International Conference on Neonatal Screening, thic coming November : The invitation text goes like this :
In Europe, approximately 5 million newborns are screened yearly based on the drawing of a drop of blood from an infant's heel or from a dorsal hand vein. European policies around newborn screening are challenges by various policy controversies, including questions to what degree newborn screening panels should be expanded, to what degree informed consent of parents should be obtained, how carrier status results should managed, and how storage and research use should be dealt with.

   Continuing on the experiences of various projects, the University of Leuven (Belgium) and the VU University Medical Centre Amsterdam (The Netherlands) are organizing on 19 November 2012 the international conference 'Newborn Screening: Challenges for Europe' in Brussels.
A flyer on the conference is available on following website:
The conference has received the kind support of the Flemish Agency for Care and Health (Flanders, Belgium) and the Centre for Genomics and the Life Sciences (the Netherlands).
Participation is free, but registration is required before 12 November through following website:
We are looking forward to meet you in Brussels in November.
Kind regards,

Prof. Pascal Borry (University of Leuven)
Prof. Martina Cornel (VU University Medical Center Amsterdam)

July - September 2003: OAEs in early detection and monitoring of Noise-Induced Hearing Loss (NIHL)

1.  Introduction

       This editorial attempts to provide some answers and insights to the question of whether the otoacoustic emissions (OAEs) can serve as a clinical tool in the early diagnosis and monitoring of noise-induced hearing loss (NIHL).

        OAEs are sounds originating mainly from the micromechanical properties of the normal functioning OHCs (1). These sounds could be recorded in the external ear canal either spontaneously or after sound stimulation. OAEs elicited by sound stimulation are known as Evoked OAEs, and depending on the stimulus, they called Transiently Evoked OAEs and Distortion Product OAEs. The stimulus for TEOAEs consists of broad band non-linear clicks. This type of emissions reflect the OHCs' activity throughout the length of the basilar membrane at threshold level. DPOAEs are elicited by two simultaneously presented pure-tone stimuli and reflect the OHCs' activity at specific places on the basilar membrane at supra-threshold level. OAEs are used as an objective, sensitive and non-invasive test for screening the functional status of the cochlear amplifier.
        In general, TEOAEs can be recorded from all normal hearing ears (2) and DPOAEs from ears with pure-tone hearing thresholds up to 50-55 dB HL (3), provided that the tympanic membrane and middle ear are functioning normally. TEOAEs recorded from normal hearing adults have an overall amplitude of at least 6 to 7 dB SPL and a frequency range greater than 3 kHz 2. Mean overall DPOAEs amplitude of normal hearing ears is greater than 6 dB SPL, showing greater peaks at 1.2 kHz and 5.3 kHz. DPOAEs can be recorded across a frequency range from 0.8 to 8 kHz (3).
        It is well established that OHCs are extremely vulnerable to sound over-stimulation and are the first to be affected amongst the inner ear cells (4). Noise results in either temporary or permanent changes of the stereocilia bundle of the OHCs(5). Since otoacoustic emissions mirror OHCs activity, it has been proposed that they have the necessary features to serve as an objective, sensitive and quick tool for the diagnosis of NIHL.
        NIHL is currently detected and monitored with Pure Tone Audiogram (PTA). NIHL is largely preventable but when the noise exposure is terminated the hearing loss remains constant. One of the main goals of hearing conservation programs is to detect noise-induced OHCs functional alterations at primary and still reversible stages. PTA is insensitive to such subtle cochlear changes and cannot serve as a method for early detection and prevention of NIHL. On the contrary, OAEs might be the ideal non-invasive method for that purpose. Another disadvantage of the PTA is that this sort of hearing assessment is not an objective hearing test. Many authors have reported that an estimated 30% of claimants aggravate their true hearing threshold for compensation reasons (6). In this context, the need for an objective and reliable audiometric test for routine clinical use becomes evident. Due to their objectivity and sensitivity, OAEs might provide indispensable information in medico-legal cases.

       So, is there sufficient scientific evidence suggesting that OAEs could serve for screening AND early diagnosis and monitoring of NIHL? It is rather difficult to give a straight answer to that. In order to do so, one has to answer the following questions:

1. Can OAEs detect Temporary Threshold Shift (TTS)?

2. Can OAEs detect Permanent Threshold Shift (PTS)? Both TTS and PTS are seen in hearing conservation programs. It is, thus, really important to consider both, when making physiological measurements of cochlear damage in applied settings.

3. How well can OAEs differentiate ears with NIHL from those with normal hearing? 4. Can OAEs detect noise-induced cochlear changes before they become evident as threshold shift in PTA (sub-clinical changes)?

5. Is it possible to have any information about the individual susceptibility to NIHL?

An overview of the current literature may give some answers. All the following data are derived from human studies. The characteristic changes of OAEs in both TTS and PTS are presented separately.


2. TEOAEs in detecting TTS


        Changes of TEOAEs after brief overexposure to noise have been studied in both laboratory settings, where experimental control of the exposure is possible, and in field settings, which have the advantage of higher noise level than those allowed in the lab. All studies showed that TTS is accompanied by:

1. A reduction of the overall TEOAEs amplitude (7,8-10)

2. Amplitude reduction of TEOAEs at high frequencies. If the subjects have been exposed to narrow band noise, the maximum affected OAEs are those at ½ or 1 octave above the center frequency of the exposure noise (8,9,11).

3. Some studies showed that, in a number of subjects, noise-induced emission changes were recorded even in the absence of TTS, as estimated by PTA (8-10).

4. There are contradicting evidence regarding the existence of any correlation between TTS and noise-induced temporary emission changes. It is noteworthy that in a study conducted by Sliwinska-Kowalska et al (1999), a strong positive correlation was found between the pre- and post- exposure amplitude of TEOAEs. Furthermore, Vinck et al. have reported that TEOAE and TTS recovery time patterns were not the same; while TTS was fully recovered 4h after exposure, the TEOAE shift in 4kHz was only partially recovered. This might suggest that OAEs are more sensitive than the behavioral audiogram in detecting subtle cochlear changes.

3. DPOAEs in detecting TTS

        The possibility of detecting TTS with DPOAEs has been assessed in a number of studies. Most of them confirm that TTS is usually accompanied by DP-gram changes, which are characterized by:

1. A significant amplitude reduction at the cubic distortion product frequency in the high frequencies, if subjects were exposed to broad band noise, and a maximum amplitude reduction of ½ -1 octave above the center frequency of the noise, when the subjects were exposed to narrow band noise (8,12,13).

2. A strong positive relationship between TTS and the amplitude reduction of DPOAEs (13). Earlier studies (14,15) do not report such a correlation. This might be due to the methodology used (for example: time of post-exposure measurements and level of the primary tones).

3. The recovery patterns of DPOAEs Temporary Shift and TTS are the same (12,13).

4. TEOAEs in detecting PTS

         Regarding the use of TEOAEs for the detection of PTS, there is a great body of evidence that PTS is accompanied by characteristic emission noise-induced changes, which more or less resemble those of TTS cases.

1. TEOAEs are greatly reduced in amplitude, throughout their frequency range (16-19). Furthermore, emissions at lower frequencies are less affected than those at higher frequencies. Two possible explanations are available : (a) that the OHCs at the medial and upper turn of the cochlea are already affected by noise, despite normal hearing at low and medium audiogram frequencies; or (b) that the functional integrity of the OHCs at the first turn of the cochlea significantly contributes to the TEOAEs generation.

2. TEOAEs are recorded in a narrow frequency range (16,19-22). In fact, the last peak of TEOAEs spectrum in adult subjects is at or just below the frequency at which NIHL begins. A study conducted by Attias et al in a large sample of young adults suffering NIHL, showed that the highest frequency at which TEOAEs could be reliably recorded was 2 kHz, while in normal hearing adults this limit is approximately at 3.8 kHz. The above results suggest that TEOAEs might serve as a frequency specific monitor of the cochlear status.

3. Finally, as the hearing loss increases the overall response and frequency range of TEOAEs becomes smaller (19,23).


5. DPOAEs in detecting PTS

         DPOAEs are sensitive in detecting PTS, showing some characteristic changes as well.

1. There is a reduced overall amplitude and/or absence of the emissions in the geometric mean frequency range between 2 and 4 kHz. The frequency at 3 kHz is usually the most affected (17,19,24).

2. Presumably due to DPOAEs frequency specificity, the DP-gram follows the pattern of PTA (24,25).

        Many researchers suggest that the sensitivity of DPOAEs in detecting NIHL, even at early stages, depends on the stimuli characteristics. Greatest sensitivity has been established when the intensity of the primary tones is below 60 dB SPL and when L2 is less than L1. It is thought that under such a condition, the primary site for distortion product 2f2-f1 generation is near or at the place on the basilar membrane which is tuned to f2, thus increasing the frequency selectivity of the method. Furthermore, when the primary tones are of low intensity, the main source of the emissions is related linearly with the cochlear amplifier. On the contrary, DPOAEs generated by higher level primaries are probably reflect an indirect relationship with the micromechanics of the basilar membrane (12, 13,26,27) . Another way to increase the DPOAE sensitivity in establishing TTS and PTS, is to perform the sampling and analysis of data at the maxima of DPOAE microstructure (12).


6. OAEs for NIHL screening

         To use OAEs as a screening method for NIHL, it is of great importance to know how well can OAEs differentiate ears with NIHL from normal hearing ears. This means that we need a method with high sensitivity and specificity. Attias et al (1993), have conducted a study on large samples of subjects, so that the results could be of statistical significance. They studied the noise-induced emission changes in a group of 283 adults, with NIHL according to PTA, due to chronic exposure to industrial or military noise, and in a group of 176 age-matched subjects with documented exposure to hazardous noise but with normal hearing thresholds. Results were compared to those of 310 adults with normal hearing and no history of exposure to intense noise (19).
         The analysis was performed using as criteria for distinguishing ears with NIHL the presence of TEOAEs at 2 and 3 kHz. The results showed a correct discrimination rate of NIHL of 92.1% (sensitivity) and correct discrimination rate of NH of 79% (specificity) with an overall correct prediction rate of 84.4%. The fact that TEOAEs at high frequencies could be affected in noise-exposed subjects, despite normal PTA thresholds, may serve as a possible explanation for the relatively low specificity in this sample.
        A similar analysis performed for DPOAEs at 2,3 and 4 kHz showed an 89% sensitivity, 92.5% specificity with an overall correct prediction rate of 87%. When the same criteria were applied only to the normal hearing - no noise exposed group, a specificity of 95.2% was found.


7. OAEs in detecting sub-clinical noise-induced cochlear changes

         The most challenging field in the use of OAEs in hearing conservation programs is about the evidence than OAEs could possibly provide for sub-clinical cochlear noise-induced changes, which have not become evident as PTA threshold shifts.
          Studies performed on large samples of normal hearing adults but documented exposure to noise, showed that a noise-induced emission loss or reduced amplitude at high frequencies was noted for both types of Evoked Emissions (8,9,18,23,28). Thus, it seems that noise-induced emission loss provides the first and silent sign of cochlear damage.
          Another finding which supports that TEOAEs are very sensitive in detecting sub-clinical noise-induced cochlear changes is that, after exposure to noise, TTS recovers more quickly than TEOAEs noise-induced loss does (9).
          Comparing the two types of evoked OAEs for their sensitivity in detecting sub-clinical cochlear changes, some authors report greater sensitivity of TEOAEs (24) , but others support the idea that DPOAEs could be of equal sensitivity with TEOAEs if recordings are performed with low intensity primaries and at the highest frequency resolution (12,19,29).


8. OAEs in detecting susceptibility to NIHL.

         It would be advantageous to be able to determine a priori who is most at risk for noise-induced TTS and PTS. A number of ways about how OAEs might be used have been proposed, but they all need further investigation. For the moment, there are only a few and contradictory data and we surely need more longitudinal studies for establishing whether OAEs can be used for this purpose and how.
          According to the results of the study conducted by Marshall et al, (2000)., a low overall TEOAEs amplitude is associated for greater risk for developing PTS. It is under investigation whether the development of noise-induced sub-clinical emission changes and abnormal contralateral suppression is predictive of higher risk for NIHL. No data have been published yet.
           The more the role of the efferent auditory system is being understood the more it is believed that it plays an important protective role against high level auditory stimuli. Thus, it has been proposed that the efferent strength, as measured with OAEs suppression, could serve as a tool for prediction of susceptibility to NIHL. It has been found that greater DPOAEs suppression is associated with greater TTS but less PTS (14,31). Also, a significant positive correlation between the magnitude of TEOAEs suppression and the TTS recovery has been established in another recent study (32). Results from the great majority of experimental studies in guinea pigs show that destruction of olivo-cochlear bundle is significantly associated with greater TTS, PTS and OHC loss (33-36). Only one study conducted by Liberman in cats failed to prove the same (37).


9. Conclusions

1. Spectral analysis of TEOAEs and DPOAEs is an efficient tool that could objectively identify normal hearing ears from those with NIHL.

2. Both TEOAEs and DPOAEs may be used for early diagnosis of subclinical noise-induced cochlear damage and for monitoring the cochlear status in noise-exposed subjects.

3. Expectation exists that OAEs could provide information about individual susceptibility to NIHL.

4. It is unlikely that OAEs could replace PTA in hearing conservation programs or legal cases, but could be used complementary to identify malingerers.

5. More data sets are needed, so as to establish well defined criteria for successful use of OAEs in clinical settings.


10. Bibliography

  1. Kemp DT. (1978) Stimulated acoustic emissions from within the human auditory system. J Acoust Soc Am 64:1386-1391.
  2. Glattke Th, Robinette MS. (1997). Transient evoked otoacoustic emissions. In Otoacoustic Emissions: Clinical Applications. Glattke Th, Robinette MS (eds). Thieme, New York-Stuttgart, pp 63-82.
  3. Lonsbury-Martin BL, Martin G, Whitehead ML. (1997). Distortion product otoacoustic emissions. In Otoacoustic Emissions: Clinical Applications. Glattke Th, Robinette MS (eds). Thieme, New York-Stuttgart, pp 83-109.
  4. Hamernick RP, Patterson JH, Turrentine GA, Ahroon WA (1989). The quantitative relation between sensorycell loss and hearing thresholds. Hear Res 38: 199-212.
  5. Patuzzi RB (1998). A four state kinetic model of the temporary threshold shift after loud sound based on inactivation of hair cell transduction channels. Hear Res 125: 39-70.
  6. Luxon LM. (1998). Clinical diagnosis of noise-induced hearing loss. In Advances in Noise Research. Prasher D, Luxon LM (eds). Whurr Publishers, London, pp 83-114.
  7. Kvaerner KJ, Engdahl B, Arnesen AR, Mair IWS. (1995). Temporary threshold shift and otoacoustic emissions after industrial noise exposure. Scand Audiol 24: 137-41.
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  10. Sliwinska-Kowalska M, Kotylo P, Hendler B. (1999). Comparing changes in transient-evoked otoacoustic emission and pure-tone audiometry following short exposure to industrial noise. Noise Health 2: 50-57.
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  19. Attias J, Horowitz G, El-Hatib N, Nageris B. (2001). Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions. Noise Health 3: 19-31.
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  21. Avan P, Bonfils P, Loth D, Wit HP. (1993). Temporal patterns of transient-evoked otoacoustic emissions in normal and impaired cochleae. Hear Res 70: 109-20.
  22. Xu ZM, Van Cauwenberge PB, Vinck B, De Vel E. (1998). Sensitive detection of noise-induced damage in human subjects using transiently evoked otoacoustic emissions. Acta Otorhinolaryngol Belg 52: 19-24.
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  24. Attias J, Bresloff I, Reshef I, Horowitz G, Furman V. (1998). Evaluating noise-induced hearing loss with distorion product otoacoustic emissions. Br J Audiol 32: 39-46.
  25. Marshall L, Lapsey Miller JA, Heller LM. (2001). Distortion-product otoacoustic emisions as a screening tool for noise-induced hearing loss. Noise Health 3: 43-60.
  26. Engdahl B, Kemp D. (1996). The effect of noise exposure on the details of distortion product otoacoustic emissions in humans. J Acoust Soc Am 99: 1573-87.
  27. Delb W, Hoppe U, Liebel J, Iro H. (1999). Determination of acute noise effects using distortion product otoacoustic emissions. Scand Audiol 28: 67-76.
  28. Kowalska S, Sulkowski W. (1997). Measurments of click-evoked otoacoustic emission in industrial workers with noise-induced hearing loss. Int J Occup Med Environ Health 10: 441-59.
  29. Knight RD, Kemp DT. (2000). Indications of different distortion product otoacoustic emission mechanisms from a detailed f1,f2 area study. J Acoust Soc Am 107: 457-73.
  30. Marshall L, Heller LM, Westhusin LJ, Lapsey Miller JA. (2000). TEOAE/DPOAE changes associated with developing NIHL. Assoc Res Otolaryngol Abs pp 66.
  31. Maison SF, Liberman MC. (2000). Predicting vulnerability to acoustic injury with a noninvasive assay of olivocochlear reflex strength. J Neurosci 20: 4701-7.
  32. Veuillet E, Martin V, Suc B, Vesson JF, Morgon A, Collet L. (2001). Otoacoustic emissions and medial olivocochlear suppression during auditory recovery from acoustic trauma in humans. Acta Otolaryngol 121: 278-83.
  33. Hildesheimer M, Makai E, Muchnik C, Rubinstein M. (1990). The influence of the efferent system on acoustic overstimulation. Hear Res 43: 263-67.
  34. Patuzzi RB, Thompson ML. (1991). Cochlear efferent neurones and protection against acoustic trauma: protection of outer hair cell receptor current and interanimal variability. Hear Res 54: 45-58.
  35. Liberman MC, Gao WY. (1995). Chronic cochlear de-efferentation and susceptibility to permanent acoustic injury. Hear Res 90: 158-68.
  36. Zheng XY, Henderson D, McFadden SL, Hu BH. (1997). The role of the cochlear efferent system in acquired resistance to noise-induced hearing loss. Hear Res 104: 191-203.
  37. Liberman MC. (1991). The olivocochlear efferent bundle and susceptibility of the inner ear to acoustic injury. J Neurophysiol 65: 123-132.

            Supplemental material for this editorial can be found in a powepoint on-line lecture, authored by Dr. Lalaki, in the clinical OAE applications section.