To determine whether suprathreshold measures of auditory function, such as distortion-product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs), are correlated with noise exposure history in normal-hearing human ears. Recent data from animal studies have revealed significant deafferentation of auditory nerve fibers after full recovery from temporary noise-induced hearing loss. Furthermore, these data report smaller ABR wave I amplitudes in noise-exposed animal ears when compared with non–noise-exposed control animals or prenoise exposure amplitudes in the same animal. It is unknown whether a similar phenomenon exists in the normal-hearing, noise-exposed human ear.
Thirty normal-hearing human subjects with a range of noise exposure backgrounds (NEBs) participated in this study. NEB was quantified by the use of a noise exposure questionnaire that extensively queried loud sound exposure during the previous 12 months. DPOAEs were collected at three f2s (1, 2, and 4 kHz) over a range of L2s. DPOAE stimulus level began at 80 dB forward-pressure level and decreased in 10 dB steps. Two-channel ABRs were collected in response to click stimuli and 4 kHz tone bursts; one channel used an ipsilateral mastoid electrode and the other an ipsilateral tympanic membrane electrode. ABR stimulus level began at 90 dB nHL and was decreased in 10 dB steps. Amplitudes of waves I and V of the ABR were analyzed.
A statistically significant relationship between ABR wave I amplitude and NEB was found for clicked-evoked ABRs recorded at a stimulus level of 90 dB nHL using a mastoid recording electrode. For this condition, ABR wave I amplitudes decreased as a function of NEB. Similar systematic trends were present for ABRs collected in response to clicks and 4 kHz tone bursts at additional suprathreshold stimulation levels (≥70 dB nHL). The relationship weakened and disappeared with decreases in stimulation level (≤60 dB nHL). Similar patterns were present for ABRs collected using a tympanic membrane electrode. However, these relationships were not statistically significant and were weaker and more variable than those collected using a mastoid electrode. In contrast to the findings for ABR wave I, wave V amplitude was not significantly related to NEB. Furthermore, there was no evidence of a systematic relationship between suprathreshold DPOAEs and NEB.
A systematic trend of smaller ABR wave I amplitudes was found in normal-hearing human ears with greater amounts of voluntary NEB in response to suprathreshold clicks and 4 kHz tone bursts. These findings are consistent with the data from previous work completed in animals, where the reduction in suprathreshold responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest that a similar mechanism might be operating in human ears after exposure to high sound levels. However, evidence of this damage is only apparent when examining suprathreshold wave I amplitude of the ABR. In contrast, suprathreshold DPOAE level was not significantly related to NEB. This was expected, given noise-induced auditory damage findings in animal ears did not extend to the outer hair cells, the generator for the DPOAE response.
This study investigated auditory brainstem response (ABR) amplitude and distortion-product otoacoustic emission (DPOAE) level in normal-hearing adults with varying amounts of noise exposure background (NEB), as assessed via a detailed questionnaire. Supra-threshold wave I amplitude was systematically smaller in adults with greater amounts of NEB. In contrast, DPOAE level was not correlated with NEB. These findings are consistent with recent investigations in noise-exposed animals where smaller wave I amplitudes were a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. The data reported here suggest a similar mechanism might be operating in the human ear following exposure to loud sound.Supplemental Digital Content is available in the text.
Department of Hearing and Speech, University of Kansas Medical Center, Kansas City, Kansas, USA.
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This investigation was supported by a Student Investigator Research Grant from the American Academy of Audiology/American Academy of Audiology Foundation and by a grant from the National Institutes of Health (NIH) National Institute on Deafness and Other Communication Disorders (NIDCD) (R03 DC011367).
Portions of this work were presented at the 2014 MidWinter Meeting of the Association for Research in Otolaryngology.
The authors declare no other conflict of interest.
Address for correspondence: Tiffany A. Johnson, Department of Hearing and Speech, University of Kansas Medical Center, Mail Stop 3039, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA. E-mail: email@example.com
Received March 26, 2014; accepted August 15, 2014.