Objectives To determine if supra-threshold 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 following full recovery from temporary noise-induced hearing loss (NIHL). Furthermore, these data report smaller ABR wave I amplitudes in noise-exposed animal ears when compared to non-noise exposed control animals or pre-noise exposure amplitudes in the same animal. It is unknown if a similar phenomenon exists in the normal-hearing, noise-exposed human ear. Design 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 over the previous 12 months. DPOAEs were collected at three f2’s (1, 2, and 4 kHz) over a range of L2’s. DPOAE stimulus level began at 80 dB FPL (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 utilized an ipsilateral mastoid electrode and the other an ipsilateral tympanic membrane (TM) 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. Results 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 supra-threshold 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 TM 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 supra-threshold DPOAEs and NEB. Conclusions 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 supra-threshold clicks and 4 kHz tone bursts. These findings are consistent with data from previous work completed in animals, where the reduction in supra-threshold responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest a similar mechanism might be operating in human ears following exposure to high sound levels. However, evidence of this damage is only apparent when examining supra-threshold wave I amplitude of the ...

These results suggest that ABR thresholds can be used to predict pure-tone behavioral thresholds for a wide range of frequencies. Although controversial, the data reviewed in this paper suggest that click-evoked ABR thresholds result in reasonable predictions of the average behavioral thresholds at 2 and 4 kHz. However, there were cases for which click-evoked ABR thresholds underestimated hearing loss at these frequencies. There are several other reasons why click-evoked ABR measurements were made, including that they (1) generally result in well-formed responses, (2) assist in determining whether auditory neuropathy exists, and (3) can be obtained in a relatively brief amount of time. Low-frequency thresholds were predicted well by ABR thresholds to a single-cycle, 250-Hz tone burst. In combination, click-evoked and low-frequency tone burst-evoked ABR threshold measurements might be used to quickly provide important clinical information for both ends of the audiogram. These measurements could be supplemented by ABR threshold measurements at other frequencies, if time permits. However, it may be possible to plan initial intervention strategies based on data for these two stimuli.

Background Exposure to both occupational and non-occupational noise is recognized as a risk factor for noise-induced hearing loss (NIHL). Although audiologists routinely inquire regarding history of noise exposure, there are limited tools available for quantifying this history or for identifying those individuals who are at highest risk for NIHL. Identifying those at highest risk would allow hearing conservation activities to be focused on those individuals. Purpose To develop a detailed, task-based questionnaire for quantifying an individual’s annual noise exposure arising from both occupational and non-occupational sources (aim 1) and to develop a short screening tool that could be used to identify individuals at high risk of NIHL (aim 2). Research Design Review of relevant literature for questionnaire development followed by a cross-sectional descriptive and correlational investigation of the newly developed questionnaire and screening tool. Study Sample One hundred fourteen college freshmen completed the detailed questionnaire for estimating annual noise exposure (aim 1) and answered the potential screening questions (aim 2). An additional 59 adults participated in data collection where the accuracy of the screening tool was evaluated (aim 2). Data Collection and Analysis In study aim 1, all subjects completed the detailed questionnaire and the potential screening questions. Descriptive statistics were used to quantify subject participation in various noisy activities and their associated annual noise exposure estimates. In study aim 2, linear regression techniques were used to identify screening questions that could be used to predict a subject’s estimated annual noise exposure. Clinical decision theory was then used to assess the accuracy with which the screening tool predicted high and low risk of NIHL in a new group of subjects. Results Responses on the detailed questionnaire indicated that our sample of college freshmen reported high rates of participation in a variety of occupational and non-occupational activities associated with high sound levels. Although participation rates were high, annual noise exposure estimates were below highest-risk levels for many subjects because the frequency of participation in these activities was low in many cases. These data illustrate how the Noise Exposure Questionnaire (NEQ) could be used to provide detailed and specific information regarding an individual’s exposure to noise. The results of aim 2 suggest that the screening tool, the 1-Minute Noise Screen, can be used to identify those subjects with high- and low-risk noise exposure, allowing more in-depth assessment of noise exposure history to be targeted at those most at risk. Conclusions The NEQ can be used to estimate an individual’s annual noise exposure and the 1-Minute Noise Screen can be used to identify those subjects at highest risk of NIHL. These tools allow audiologists to focus hearing conservation efforts on those individuals who are most in need of those services.