Although animal models show a clear link between noise exposure and damage to afferent cochlear synapses, the relationship between noise exposure and efferent function appears to be more complex. Animal studies indicate that high intensity noise exposure reduces efferent medial olivocochlear (MOC) reflex strength, whereas chronic moderate noise exposure is associated with a conditioning effect that enhances the MOC reflex. The MOC reflex is predicted to improve speech-in-noise perception and protects against noise-induced auditory damage by reducing cochlear gain. In humans, MOC reflex strength can be estimated by measuring contralateral inhibition of distortion product otoacoustic emissions (DPOAEs). The objective of this study was to determine the impact of military noise exposure on efferent auditory function by measuring DPOAE contralateral inhibition in young Veterans and non-Veterans with normal audiograms. Compared with non-Veteran controls, Veterans with high levels of reported noise exposure demonstrated a trend of reduced contralateral inhibition across a broad frequency range, suggesting efferent damage. Veterans with moderate noise exposure showed trends of reduced inhibition from 3 to 4 kHz but greater inhibition from 1 to 1.5 kHz, consistent with conditioning. These findings suggest that, in humans, the impact of noise exposure on the MOC reflex differs depending on the noise intensity and duration.

Although the relationship between noise exposure and outer hair cell (OHC) damage has been recognized for many years (e.g., Liberman and Dodds, 1984; Gao , 1992; Emmerich , 2000; Wang , 2002; Chen and Fechter, 2003), more recent animal studies have drawn attention to the effects of noise exposure on other components of the peripheral auditory system, such as the synapses between the inner hair cells (IHCs) and afferent auditory nerve fibers (e.g., Kujawa and Liberman, 2009). Cochlear synaptopathy has received a lot of attention as a potential explanation for auditory perceptual deficits such as difficulty understanding speech in background noise in the context of a normal audiogram (e.g., Kujawa and Liberman, 2015). However, animal studies indicate that the efferent system is also impacted by noise exposure (Spoendlin, 1971; Omata , 1992; Canlon , 1999; Boero , 2018) and damage to efferent function may have a negative impact on signal detection in noise (Winslow and Sachs 1988; Kawase , 1993; Kawase and Liberman, 1993). High levels of noise exposure are often encountered during military service and complaints of difficulty understanding speech in background noise are common among Veterans, even when hearing thresholds are normal (Theodoroff , 2015; Gordon , 2017). These complaints may be related not only to noise-related damage to cochlear synapses, as proposed by Kujawa and Liberman (2015), but also to noise-induced efferent damage.

The efferent auditory system includes two pathways, the lateral olivocochlear (LOC) reflex pathway, comprised of unmyelinated efferent fibers that terminate on the afferent auditory nerve fibers, and the medial olivocochlear (MOC) reflex pathway, consisting of myelinated efferent fibers that terminate on the OHCs (for a detailed review of auditory efferent physiology, see Guinan, 2006 and Lopez-Poveda, 2018). While the human LOC pathway is not clearly understood, the MOC reflex acts directly on the OHCs to modulate the gain of the cochlear amplifier and inhibit basilar membrane motion. MOC fibers originate in the medial part of the superior olivary complex and travel to the ipsilateral and contralateral OHCs. Because activation of the MOC reflex leads to a reduction in cochlear amplification, the reduction in otoacoustic emission (OAE) level associated with adding an ipsilateral, contralateral, or bilateral noise stimulus provides an estimate of the MOC reflex strength (i.e., a greater reduction indicates a stronger reflex). This MOC reflex-related reduction in OAE level is termed OAE inhibition. However, in humans, OAE inhibition effects can be small (1–2 dB; Lauer , 2022), which can make it difficult to distinguish them from measurement variability.

A number of studies in animal models have demonstrated that noise exposure can negatively impact efferent function. In a guinea pig model, Canlon (1999) observed a reduction in the number of efferent synapses on the OHCs following traumatic exposure to 1 and 6.3 kHz tones presented at 100–105 dB sound pressure level (SPL), exposures known to produce a permanent threshold shift. In a mouse model, Boero (2018) demonstrated that noise exposures producing only a temporary threshold shift (TTS) can result in loss of the MOC terminal connections with the OHCs. Other animal studies using exposure levels of 100–138 dB SPL have revealed similar relationships between high intensity noise exposure and efferent nerve terminal damage (Spoendlin, 1971; Omata , 1992). However, to date, few human studies have investigated the impact of noise exposure on efferent function. Sliwinska-Kowalska and Kotylo (2002) found approximately 1–1.25 dB reduction in contralateral inhibition of DPOAEs (using 4 kHz input/output functions) among metal factory workers routinely exposed to 85–92 dBA occupational noise when compared with control subjects. Megha (2021) found 0.8–1.09 dB reductions in contralateral inhibition of transient evoked OAEs (for 1–2 kHz stimuli) for a sample of young adults with occupational noise exposure compared with an unexposed control group, although no details about the type of occupational noise exposure were provided. Gunduz (2022) compared young violinists with clinically normal hearing with nonmusician controls and found the violinists had 1.8 dB less contralateral inhibition of DPOAEs at 1 and 2 kHz. Peng (2010) found a small (less than 1 dB) reduction in contralateral inhibition of DPOAEs at low frequencies (0.75–1 kHz) in frequent users of personal listening devices compared with controls, suggesting a noise exposure-related reduction in MOC reflex strength. Given the potentially important role of the efferent auditory system in speech perception and protection from noise damage, it is important to clarify the impact of noise exposure on efferent function in humans.

It has been proposed that the MOC reflex facilitates speech understanding in noise through a mechanism referred to as unmasking (reviewed in Guinan, 2006). Background noise raises the baseline firing rate of the afferent auditory nerve fibers, reducing their saturation rate and dynamic range (Costalupes , 1984). Inputs to the MOC efferent neurons from low and medium spontaneous rate afferent auditory nerve fibers may provide intensity level information to the MOC system, allowing for modulation of the cochlear amplifier in response to higher sound levels to optimize signal detection (Carney, 2018). Data from animal models show that MOC reflex-mediated reduction of OHC gain inhibits the response of auditory nerve fibers to background noise, improving signal detection in noise (Winslow and Sachs, 1988; Kawase , 1993; Kawase and Liberman, 1993), but results from human studies of the relationship between contralateral inhibition of OAEs and speech-in-noise perception have been mixed (Lauer , 2022).

Although the mechanism is not fully understood, the MOC reflex protects the cochlea from noise exposure-related damage. For example, in a guinea pig model, Maison and Liberman (2000) showed an association between reduced efferent function and susceptibility to noise damage, where distortion product otoacoustic emission (DPOAE) inhibition was inversely correlated with the degree of noise-induced hearing loss as measured by compound action potential thresholds. Zheng (1997a) and Zheng (1997b) showed that, in chinchilla, surgical de-efferentation increases susceptibility to noise-induced cochlear damage, as measured by the amplitude of the cochlear microphonic and DPOAE input/output functions. The protection from cochlear damage extends beyond the OHCs. In mice, loss of efferent MOC neurons from surgical de-efferentation is associated with greater noise-induced (Maison , 2013) and age-related (Liberman , 2014) loss of afferent cochlear synapses. Conversely, mice with enhanced MOC feedback who are aged in a quiet environment experience less afferent synapse and OHC loss than control mice (Boero , 2020). In addition, in an earlier study, Boero (2018) showed that genetic enhancement of the MOC reflex in mice can provide future protection from noise damage as reflected in preserved MOC terminals and afferent synapses following acoustic trauma. These findings indicate that poor efferent function can lead to accelerated age- and noise exposure-related OHC and afferent cochlear synaptic loss. Results from several human studies are also consistent with the MOC reflex providing protection from noise damage. Lichtenhan (2016) showed that 65 dB SPL contralateral broadband noise designed to induce MOC activation reduced the overall output of the auditory nerve by 16% (equivalent to 1.98 dB attenuation), as measured by compound action potentials. Given that MOC activation is greater at higher sound levels (Guinan , 2003), a larger reduction in auditory nerve output would be expected for hazardous sound levels. Otsuka (2016) found that the strength of the MOC reflex, as measured by click-evoked OAE inhibition, is moderately predictive of the degree of TTS in violinists following a 1 h music practice session with greater TTS for violinists with weaker reflexes. In individuals with normal audiograms, Wolpert (2014) measured TTS after a 1 h exposure to a 94 dB SPL broadband noise and found a negative correlation between the amount of DPOAE contralateral inhibition and degree of TTS. Veuillet (2001) measured contralateral inhibition of evoked OAEs in young men with noise-induced pure tone threshold shifts related to firearm use. Greater contralateral inhibition was associated with better auditory threshold recovery at 3 days post exposure compared with an initial threshold measurement obtained <72 h after exposure. These findings suggest that the association between reduced efferent system function and increased susceptibility to noise-related cochlear damage may extend to humans.

The purpose of the current study was to use contralateral inhibition of DPOAEs to evaluate the impact of noise exposure on efferent function in a sample of young military Veterans and non-Veterans with clinically normal audiograms. The hypothesis was that high levels of self-reported noise exposure would be associated with reduced contralateral inhibition and moderate levels of self-reported noise exposure would be associated with more modest reductions in contralateral inhibition.

Seventy-seven young adults (49 military Veterans and 28 non-Veterans) aged 19–35 years old with clinically normal audiograms [thresholds ≤ 20 dB hearing level (HL) from 0.25 to 8 kHz] who participated in a hidden hearing loss study at the Veterans Affairs (VA) National Center for Rehabilitative Auditory Research (NCRAR) were included in this analysis. Study recruitment flyers were posted at multiple locations in the surrounding Portland area, including the VA Portland hospital, colleges, universities, and coffee shops. Potential participants were also recruited from a database of previously conducted studies at the NCRAR and a central VA database that included Veterans local to the Portland area. All of the participants reported a negative history of concussion or otologic disorders. Non-Veteran participants (the control group) were required to have minimal noise exposure history, including no firearm use, and no self-report of frequent or constant tinnitus or decreased sound tolerance because these could indicate the presence of auditory damage. Inclusion criteria also required all of the participants to have a normal 226-Hz tympanogram (compliance = 0.2–1.5 ml; peak pressure, ±50 daPa). Subjects were excluded for conductive hearing loss (no more than one air-bone gap of 15 dB) and any evidence of a noise notch from 3 to 6 kHz (thresholds that were 15 dB poorer than the adjacent frequencies within this range). In addition, to ensure that only individuals with robust OHC function were included in this study, a screening distortion product (DP)-gram was obtained from 1 to 8 kHz in 1/6 octave increments at a frequency ratio of f2/f1 = 1.2 and L1/L2 levels of 65/55 dB SPL. DPOAE amplitudes from 1.5 to 6 kHz were compared with data collected from a large study of individuals with abnormal pure tone thresholds (Table A1 from Gorga , 1997) and only participants with DPOAE amplitudes equal to or better than the 90th percentile were included. Specifically, the amplitude criteria were as follows: 0.43 dB SPL at 1.5 kHz, −3.5 dB SPL at 2 kHz, −5.55 dB SPL at 3 kHz, −4.42 dB SPL at 4 kHz, and −6.88 dB SPL at 6 kHz. There were no other DPOAE criteria for study inclusion.

TABLE I.

Participant characteristics by noise exposure group. For mean values, standard deviations are shown in parentheses. High MOS rating refers to a high probability of hazardous noise exposure associated with that MOS.

Non-Veteran control Veteran medium noise Veteran high noise
Mean age (years)  27.1 (4.8)  30.5 (3.7)  29.6 (3.3) 
Number of males  12  24 
Mean LENS-Q score  4.1 (0.8)  8.5 (1.0)  9.7 (0.6) 
Number with high MOS rating  N/A  23 
Total participants  28  17  32 
Non-Veteran control Veteran medium noise Veteran high noise
Mean age (years)  27.1 (4.8)  30.5 (3.7)  29.6 (3.3) 
Number of males  12  24 
Mean LENS-Q score  4.1 (0.8)  8.5 (1.0)  9.7 (0.6) 
Number with high MOS rating  N/A  23 
Total participants  28  17  32 

To qualify for the study, only one ear had to meet the study inclusion criteria because test measures were obtained in a single ear from each participant. The test ear was determined based on meeting the inclusion criteria; however, if both ears met the inclusion criteria and audiometric thresholds were similar, the ear judged to have better screening DPOAE responses (i.e., larger DPOAE levels) was selected as the test ear. Thirty-two participants had a non-test ear that did not meet the DPOAE, audiometric, or tympanogram criteria (10 non-Veteran control ears and 22 Veteran ears). Failure to meet the DPOAE criteria was the most common reason for the non-test ear not qualifying. Of the non-test ears that did not meet the audiometric criteria, all but two had audiometric thresholds ≤ 25 dB HL from 0.25 to 8 kHz. The remaining two non-test ears each had a single threshold from 0.25 to 8 kHz at 30–35 dB HL.

Participants were split into three groups [non-Veteran control (n = 28), Veteran medium noise (n = 17), and Veteran high noise (n = 32)] based on their Veteran status, self-reported lifetime noise exposure, and military occupational specialty (MOS, the job performed during military service). Auditory brainstem response (ABR), envelope following response (EFR), and middle ear muscle reflex (MEMR) measurements for the same grouping of this cohort have been reported previously (Bramhall , 2021; Bramhall , 2022). All of the participants provided written informed consent prior to any study-related activities and were compensated for the study visits. All of the study procedures were approved by the VA Portland Health Care System Institutional Review Board.

1. DPOAEs

DPOAE responses were obtained using a custom system comprised of an Etymotic ER-10B+ probe microphone (Etymotic Research, Elk Grove Village, IL) and EMAV software developed at Boys Town National Research Hospital (Neely and Liu, 1993). The primary frequencies were digitized separately, converted to analog voltages, passed through an amplifier to separate Etymotic Research (ER-2) transducers and then transferred to the ear canal through separate ports in the probe. Digital-to-analog and analog-to-digital conversions were performed using 24-bit resolution with a sampling rate of 48 kHz and the preamplifier gain was set to +20 dB. The voltage sent to the transducers was adjusted using in-ear calibration to set L1 and L2 to the desired levels. The distortion of this system is estimated to be below –20 dB SPL based on coupler measurements. Stopping rules were implemented such that 30 s of artifact free data (<2 mPa) were collected at each test frequency, or until the noise floor measured below −15 dB SPL. This allowed measurements to stop more quickly for quiet participants, allowing for more sweeps to be collected during the test session, while ensuring the noise floor was as consistent as possible across participants.

Contralateral inhibition of DPOAEs was measured from DP-grams consisting of two primary tones at discrete frequencies (24 points per octave from 1–6 kHz – 63 frequencies) with a fixed primary frequency ratio of f2/f1 = 1.2 and stimulus levels of L1/L2 = 55/40 dB SPL. Low stimulus levels were used to limit activation of ipsilateral efferent activity (Guinan , 2003). Note that this was a separate DP-gram from the screening DP-gram described in Sec. II A that was used to determine study inclusion. Because interference between distortion and reflection DPOAE components can lead to underestimates or overestimates of measured inhibition depending on the proximity to peaks or dips in the DPOAE microstructure (Guinan, 2006), fine frequency DPOAE measurements were obtained to provide a large number of inhibition measurements across the frequency range. During testing, participants were seated in a comfortable chair in a double-walled sound-treated booth and watched a silent movie with closed captions. In the inhibited condition, a continuous 60 dB SPL broadband noise stimulus bandpass filtered from 0.1–4 kHz was presented on an Apple iPod to the contralateral (non-test) ear over an Etymotic ER-3A insert earphone routed through a GSI-61 audiometer (Grason-Stadler, Eden Prairie, MN). The noise was turned on at least 2 s before taking the inhibited DPOAE measurement to allow time for activation of the MOC reflex, and there was a minimum of 2 s of silence between each run to allow for return to baseline. Uninhibited and inhibited DPOAE frequency sweeps were alternated (i.e., all of the 63 frequencies were tested without inhibition and then all of the frequencies were tested with inhibition) until the 2-h time limit for the test session was reached. In-ear calibration was completed before starting each individual sweep. Across participants, the number of pairs of uninhibited and inhibited sweeps varied based on the time it took to complete a sweep (range, 1–10 pairs of sweeps; mean, 3.2 pairs of sweeps). For each participant, all uninhibited sweeps were averaged together and all of the inhibited sweeps were averaged together. Some participants had high levels of physiological noise and/or difficulty keeping still, which made it time consuming to meet the stopping conditions. Two participants (a non-Veteran and a Veteran with high noise exposure) had only a single pair of sweeps, therefore, their sweeps could not be averaged. For these two participants, a single sweep took approximately 30 min to complete. Statistical modeling was completed with and without the data from these two participants, and the impact on the model results was minimal, thus, their data were retained.

Inhibition was calculated as the difference in DPOAE amplitude at each frequency between the uninhibited and inhibited conditions (i.e., the DPOAE amplitude in dB SPL of the inhibited condition was subtracted from the DPOAE amplitude of the uninhibited condition). To be considered a valid DPOAE response, DPOAE amplitude had to exceed −20 dB SPL, a conservative estimate of the system distortion, and the DPOAE amplitude had to be at least 10 dB greater than the measured noise level [i.e., signal-to-noise ratio (SNR)]. The noise floor used to calculate the SNR was specific to each participant, sweep, and frequency. Absent DPOAEs (DPOAE amplitudes <−20 dB SPL, regardless of the SNR) were set to the level of the system distortion (−20 dB SPL) and DPOAEs with high noise (SNR < 10 dB) that were above the estimated system distortion level were set to missing. These criteria were applied to uninhibited and inhibited DPOAE responses. Only MEMR and DPOAE inhibition data were collected at this test session.

2. MEMR

Contralateral MEMR thresholds were measured using a wideband acoustic immittance system (i.e., using a wideband probe) to ensure that the MEMR was not activated by the contralateral broadband noise stimulus, which could alter the immittance properties of the middle ear and impact DPOAE amplitude. The MEMR activator was broadband noise, low pass filtered at 8 kHz, presented at levels ranging from 55 to 100 dB SPL in 5 dB steps. A recent paper by Schairer (2022) indicates that, on average, contralateral MEMR thresholds for a broadband noise activator measured with a wideband acoustic immittance system at ambient pressure are 16.6 dB lower than MEMR thresholds measured using a clinical system. As with measurement of DPOAE contralateral inhibition, the contralateral activator was presented to the non-test ear. MEMR thresholds were measured using a wideband research system, consisting of an Interacoustics AT235 tympanometer (Eden Prairie, MN) with modified firmware as described in Bramhall (2022), except that the MEMR was measured at ambient pressure rather than at tympanometric peak pressure because the ear was not pressurized during DPOAE testing. MEMR threshold was calculated as described by Keefe (2017). Individuals with contralateral wideband MEMR thresholds < 65 dB SPL (with the activator in the non-test ear) were excluded from the analysis to avoid potential MEMR contamination of the contralateral inhibition measurement. Note that the bandwidth of broadband noise MEMR activator was broader than the broadband contralateral noise used to measure DPOAE inhibition. Given that broader bandwidths are associated with lower MEMR thresholds by about 4 dB/octave (Margolis , 1980), the broader activator bandwidth provided a slightly more conservative estimate of MEMR threshold and increased the probability that an ear would be excluded because of a low MEMR threshold.

3. Assessment of lifetime noise exposure history

All of the participants completed the Lifetime Exposure to Noise and Solvents Questionnaire (LENS-Q; Griest-Hines , 2021), a detailed survey about noise exposure history and use of hearing protection. Participants reported the frequency and duration of their lifetime exposure to various types of noise sources, including military, non-military occupational, and recreational. The LENS-Q was scored as described in Griest-Hines (2021), except that MOS was not included in the LENS-Q score. Each MOS is rated by the Veterans Benefits Administration based on the probability of experiencing hazardous noise exposure while performing job duties (low, medium, or high; Veterans Benefits Administration, 2010). Following Bramhall (2021) and Bramhall (2022), Veteran participants were divided into two groups (Veteran high noise and Veteran medium noise) based on overall LENS-Q score and reported MOS. Any Veteran with a LENS-Q score in the top 25th percentile for all of the Veterans in the sample or a MOS rated as having a high probability of hazardous noise exposure was placed in the Veteran high noise group (see Table I). Veterans did not need to meet both the LENS-Q and MOS criteria to be placed in the Veteran high noise group. The remaining Veterans were assigned to the Veteran medium noise group.

4. Statistical analysis

The primary goal of the statistical analysis was to estimate the population mean DPOAE inhibition by noise exposure group. DPOAE inhibition at each frequency was nested within participants, therefore, we used a liner mixed-effects model with a compound symmetry covariance matrix (Singer and Willett, 2003) to analyze the relationship between noise exposure population and DPOAE inhibition. This analytic approach has the advantage of being robust to unequal group size and missing observations. The mixed-effects model allows for the estimation of the average intercept by noise exposure population and frequency via fixed effects and individual deviation from the average via estimation of random effects. A multilevel model of the population mean DPOAE inhibition was used as shown in
μ i = β 0 + β 1 Veteran medium noise i + β 2 Veteran high noise i + β 3 frequency i + β 4 Veteran medium noise i frequency i + β 5 Veteran high noise i frequency i + θ s [ i ] intercept .
Each observation in the dataset is indexed by i. For example, Veteran high noise i is an indicator variable that takes a value of one if the noise group attached to the ith observation is equal to “Veteran high noise” and zero otherwise. Similarly, Veteran medium noise i is an indicator variable taking on a value of one if the noise group attached to the ith observation is equal to “Veteran medium noise” and zero otherwise. Frequency i is the f2 frequency (Hz) producing the ith DPOAE amplitude. Note that the model includes a noise group by frequency interaction term. β is a fixed effect parameter, and θ s is a vector of participant-specific random effects for the intercept. Knowing a priori that military noise exposure varies by sex, we considered sex as a potential confounder of the association between noise exposure and DPOAE inhibition. To address potential confounding by sex, we reran the model defined above with sex included, but the results did not appreciably change (data not shown). To confirm that variation in uninhibited DPOAE level across participants was not impacting estimated DPOAE inhibition, we also reran the model with an adjustment for uninhibited DPOAE level. This adjustment had little effect on the overall results and was, therefore, not included in the final model (see Fig. 2 in the supplementary material for a plot of modeled noise exposure population inhibition contrasts with the adjustment for uninhibited DPOAE level1).

The model defined above was also used to assess population mean uninhibited DPOAE differences between noise groups by frequency. Model quality was assessed through graphical examination of model residuals. The resulting residual plots showed points generally distributed around zero with no strong deviations, suggesting that the residuals are normally distributed and the linear regression model is appropriate for the research question.

Here, we report modeled point estimates of mean contralateral inhibition for each noise exposure population at each measured f2 frequency and averaged across 1/3 octave frequency intervals, along with 95% confidence intervals (CIs) instead of p-values. This is similar to our approach in Bramhall (2022). This information provides a better description of the data's support for the hypothesis than a binary classification of “significant” or “not significant” based on a p-value (Greenland , 2016). Average population differences in DPOAE inhibition were calculated as the contrast between the model-based population mean DPOAE inhibition for the two populations of interest.

Characteristics of the participants in the three noise exposure groups (non-Veteran control, Veteran medium noise, and Veteran high noise) are summarized in Table I. Mean age is similar across the groups. While the non-Veteran control and Veteran medium noise groups have roughly equal numbers of males and females, the Veteran high noise group is predominantly male. Mean LENS-Q scores are lowest (indicating less noise exposure) for the non-Veteran control group and highest for the Veteran high noise group. Note that because the LENS-Q is scored on a log scale, a one point increase in score represents a tenfold increase in noise exposure. This suggests that, on average, the noise exposure history of the Veteran high noise group is more than ten times the exposure of the Veteran medium noise group. In addition, 23 individuals in the Veteran high noise group reported a MOS that is rated as having a high probability of hazardous noise exposure—examples from this sample include combat engineer, heavy equipment operator, flight deck crew, infantry, fire direction officer, aviation supply specialist, master at arms, and radar technician. Examples of reported military jobs in this sample that are rated as having a low or medium probability of hazardous noise exposure include security forces, weather forecaster, motor pool, cargo specialist, supply specialist, and cryptologic linguist. All of the Veterans reported use of firearms (either during their military service, recreationally, or both). None of the non-Veterans reported any history of firearm use because this was one of the inclusion criteria for non-Veterans.

This dataset consists of a total of 4851 DPOAE amplitude observations (i.e., the average DPOAE amplitude at 63 discrete frequencies for each participant). Of these observations, 19 uninhibited DPOAE observations (0.39% of total) and 31 inhibited DPOAE level observations (0.64% of total) did not meet the 10 dB SNR criterion and were set to missing. Missing data were most common for the Veteran high noise group (1% of the group total) and least common for the Veteran medium noise group (0.09% of the group total). All further descriptions of the DPOAE data refer to data that met the 10 dB SNR criterion.

Measured DPOAE amplitudes from 1 to 6 kHz are plotted for each noise exposure group in Fig. 1 and modeled mean amplitudes for each group are plotted in Fig. 2. Although the DPOAE screening criteria ensure that all of the participants have robust DPOAEs, there are some differences in mean DPOAE levels across groups. Modeled contrasts between groups are plotted in Fig. 3. In the lower frequencies (1–1.5 kHz), mean DPOAE response levels are lowest for the Veteran medium noise group and highest for the non-Veteran control group. In addition, from 5 to 6 kHz, mean DPOAE amplitudes are lowest for the Veteran high noise group and highest for the Veteran medium noise group.

FIG. 1.

(Color online) Measured DP-grams by noise exposure group. Symbols show DPOAE amplitudes for individual participants in response to a stimulus where L1/L2 = 55/40 dB SPL with a separate panel for each group. Solid lines show average DPOAE amplitude across f2 frequency for each noise exposure group. The black dotted line shows the average noise floor.

FIG. 1.

(Color online) Measured DP-grams by noise exposure group. Symbols show DPOAE amplitudes for individual participants in response to a stimulus where L1/L2 = 55/40 dB SPL with a separate panel for each group. Solid lines show average DPOAE amplitude across f2 frequency for each noise exposure group. The black dotted line shows the average noise floor.

Close modal
FIG. 2.

(Color online) Modeled DP-grams by noise exposure population. Each panel shows modeled DPOAE amplitude across frequency for a different noise exposure population. Symbols indicate point estimates while the gray lines show the 95% CIs. The solid lines are LOESS smooth lines.

FIG. 2.

(Color online) Modeled DP-grams by noise exposure population. Each panel shows modeled DPOAE amplitude across frequency for a different noise exposure population. Symbols indicate point estimates while the gray lines show the 95% CIs. The solid lines are LOESS smooth lines.

Close modal
FIG. 3.

(Color online) Modeled noise exposure population DP-gram contrasts. Each panel shows the contrast in modeled DPOAE amplitudes across frequency between two noise exposure populations. Symbols indicate point estimates while gray lines show the 95% CIs. The solid lines are LOESS smooth lines. Values above zero indicate that the first population has a greater estimated mean DPOAE amplitude than the second population (e.g., in the first panel, the control population has higher modeled mean DPOAE amplitudes than the Veteran medium noise population in the low frequencies).

FIG. 3.

(Color online) Modeled noise exposure population DP-gram contrasts. Each panel shows the contrast in modeled DPOAE amplitudes across frequency between two noise exposure populations. Symbols indicate point estimates while gray lines show the 95% CIs. The solid lines are LOESS smooth lines. Values above zero indicate that the first population has a greater estimated mean DPOAE amplitude than the second population (e.g., in the first panel, the control population has higher modeled mean DPOAE amplitudes than the Veteran medium noise population in the low frequencies).

Close modal

Measured DPOAE contralateral inhibition (uninhibited DPOAE amplitude–inhibited DPOAE amplitude) is plotted for each noise exposure group in Fig. 4, with locally estimated scatterplot smoothing (LOESS) smooth lines for each group plotted in Fig. 5. Across groups, inhibition is greatest in the low frequencies and decreases for f2 frequencies that are above 2 kHz. Compared with controls, mean inhibition is lower for the Veteran high noise group at frequencies above 1 kHz, with the greatest decreases in inhibition observed from 3 to 6 kHz. In the Veteran medium noise group, inhibition is lower than for controls from 3 to 4 kHz and slightly greater than controls in the low frequencies (1–2 kHz). Several examples of negative inhibition/enhancement (i.e., greater DPOAE amplitude in the inhibited condition than in the uninhibited condition) are apparent in Fig. 4. Enhancement is unexpected given that we would expect activation of the MOC reflex to result in decreased DPOAE amplitude rather than increased amplitude. Enhancements occurred in all three of the noise groups and in most cases, enhancements occurred at dips in the DPOAE fine structure (see Fig. 1, example A in the supplementary material1), suggesting that these enhancements were due to interactions between DPOAE distortion and reflection components (Guinan 2006) rather than a MOC-mediated increase in DPOAE amplitude. However, in two participants from the Veteran high noise group, there was a systematic enhancement across a broad frequency range (see Fig. 1, examples B and C in the supplementary material1). The source of this enhancement is unclear. It is interesting to note that both of these participants reported bilateral tinnitus, which could indicate that the enhancement is secondary to tinnitus-related central changes in the balance between inhibitory and excitatory pathways. However, there were other participants in the sample who reported bilateral tinnitus but did not show similar enhancements.

FIG. 4.

(Color online) Measured contralateral inhibition by noise exposure group. Symbols show contralateral inhibition (uninhibited DPOAE amplitude - inhibited DPOAE amplitude) across f2 frequency for each participant. Each panel shows the data for a different noise exposure group. Positive values indicate inhibition while negative values indicate enhancement (i.e., DPOAE amplitudes were larger when the contralateral stimulus was presented), as indicated by the blue arrows. LOESS smooth lines show the contralateral DPOAE inhibition by frequency relationship.

FIG. 4.

(Color online) Measured contralateral inhibition by noise exposure group. Symbols show contralateral inhibition (uninhibited DPOAE amplitude - inhibited DPOAE amplitude) across f2 frequency for each participant. Each panel shows the data for a different noise exposure group. Positive values indicate inhibition while negative values indicate enhancement (i.e., DPOAE amplitudes were larger when the contralateral stimulus was presented), as indicated by the blue arrows. LOESS smooth lines show the contralateral DPOAE inhibition by frequency relationship.

Close modal
FIG. 5.

(Color online) Trends in contralateral inhibition by noise exposure group. LOESS smooth lines show the contralateral DPOAE inhibition by frequency relationship for each group.

FIG. 5.

(Color online) Trends in contralateral inhibition by noise exposure group. LOESS smooth lines show the contralateral DPOAE inhibition by frequency relationship for each group.

Close modal

Model estimates of mean DPOAE contralateral inhibition for each noise exposure population are plotted by frequency in Fig. 6. Estimated mean inhibition varies considerably from one frequency to the next, which is expected based on the proximity to peaks or dips in the DPOAE microstructure (Guinan 2006). Modeling average contralateral inhibition across the entire frequency range or across 1/3 octave frequency intervals (Fig. 7) provides a better picture of the overall trends in the data. When averaged across frequency from 1 to 6 kHz, modeled mean inhibition is 0.89 dB (95% CI = 0.69–1.09 dB) for controls, 0.85 dB (CI = 0.60–1.11 dB) for Veterans with medium noise exposure, and 0.66 dB (CI = 0.47–0.85 dB) for Veterans with high noise exposure. When modeled across 1/3 octave frequency intervals, estimated mean inhibition in the low frequencies (1.25–1.5 kHz) is slightly greater for Veterans with medium noise exposure (1.26 dB, CI = 0.93–1.58 dB) than for controls (1.07 dB, CI = 0.81–1.32 dB), whereas estimated mean inhibition from 3 to 4 kHz is greater for controls (0.86 dB, CI = 0.60–1.11 dB) than for Veterans with medium noise exposure (0.48 dB, CI = 0.16–0.80 dB). Mean modeled inhibition is greater for controls than for Veterans with high noise exposure at all of the 1/3 octave frequency intervals with the greatest differences at 1.5–2 kHz (1.18 dB, CI = 0.92–1.44 dB for controls vs 0.88 dB, CI = 0.63–1.12 dB for the Veteran high noise population), 2.5–3 kHz (0.67 dB, CI = 0.42–0.93 dB for controls vs 0.37 dB, CI = 0.14–0.61 dB for the Veteran high noise population), 3–4kHz (0.86 dB, CI = 0.60–1.11 dB for controls vs 0.52 dB, CI = 0.29–0.76 dB for the Veteran high noise population), and 5–6 kHz (0.51 dB, CI = 0.25–0.76 dB for controls vs 0.18 dB, CI = −0.05–0.42 dB for the Veteran high noise population). Modeled inhibition values by frequency interval and noise exposure population are shown in Table II.

FIG. 6.

(Color online) Modeled contralateral inhibition by noise exposure population. The first three panels each show modeled contralateral inhibition (uninhibited DPOAE amplitude–inhibited DPOAE amplitude) across frequency for a different noise exposure population. Symbols indicate point estimates while the gray lines show the 95% CIs. LOESS smooth lines show the modeled contralateral DPOAE inhibition by frequency relationship. The fourth panel shows modeled inhibition for each population when averaged across frequency from 1 to 6 kHz.

FIG. 6.

(Color online) Modeled contralateral inhibition by noise exposure population. The first three panels each show modeled contralateral inhibition (uninhibited DPOAE amplitude–inhibited DPOAE amplitude) across frequency for a different noise exposure population. Symbols indicate point estimates while the gray lines show the 95% CIs. LOESS smooth lines show the modeled contralateral DPOAE inhibition by frequency relationship. The fourth panel shows modeled inhibition for each population when averaged across frequency from 1 to 6 kHz.

Close modal
FIG. 7.

(Color online) Modeled contralateral inhibition by noise exposure population. Each panel shows modeled contralateral inhibition (uninhibited DPOAE amplitude–inhibited DPOAE amplitude) for a different noise exposure population across 1/3 octave frequency intervals. Symbols indicate point estimates while the gray lines show the 95% CIs. LOESS smooth lines show the modeled contralateral DPOAE inhibition by frequency relationship.

FIG. 7.

(Color online) Modeled contralateral inhibition by noise exposure population. Each panel shows modeled contralateral inhibition (uninhibited DPOAE amplitude–inhibited DPOAE amplitude) for a different noise exposure population across 1/3 octave frequency intervals. Symbols indicate point estimates while the gray lines show the 95% CIs. LOESS smooth lines show the modeled contralateral DPOAE inhibition by frequency relationship.

Close modal
TABLE II.

Modeled mean contralateral inhibition by frequency range and noise exposure population. Inhibition values are in dB with 95% CIs in parentheses.

Frequency range Non-Veteran control Veteran medium noise Veteran high noise
1–1.25 kHz  1.24 (0.99–1.49)  1.32 (1.00–1.64)  1.22 (0.98–1.46) 
1.25–1.5 kHz  1.07 (0.82–1.32)  1.26 (0.93–1.58)  0.96 (0.72–1.20) 
1.5–2 kHz  1.18 (0.92–1.44)  1.20 (0.86–1.53)  0.88 (0.63–1.12) 
2–2.5 kHz  0.94 (0.69–1.19)  0.84 (0.52–1.16)  0.72 (0.48–0.95) 
2.5–3 kHz  0.67 (0.42–0.92)  0.69 (0.37–1.02)  0.37 (0.14–0.61) 
3–4 kHz  0.86 (0.60–1.11)  0.48 (0.16–0.80)  0.52 (0.29–0.76) 
4–5 kHz  0.69 (0.44–0.95)  0.56 (0.24–0.88)  0.45 (0.22–0.69) 
5–6 kHz  0.51 (0.25–0.76)  0.51 (0.19–0.84)  0.18 (−0.05–0.42) 
1–6 kHz  0.89 (0.69–1.09)  0.85 (0.60–1.11)  0.66 (0.47–0.85) 
Frequency range Non-Veteran control Veteran medium noise Veteran high noise
1–1.25 kHz  1.24 (0.99–1.49)  1.32 (1.00–1.64)  1.22 (0.98–1.46) 
1.25–1.5 kHz  1.07 (0.82–1.32)  1.26 (0.93–1.58)  0.96 (0.72–1.20) 
1.5–2 kHz  1.18 (0.92–1.44)  1.20 (0.86–1.53)  0.88 (0.63–1.12) 
2–2.5 kHz  0.94 (0.69–1.19)  0.84 (0.52–1.16)  0.72 (0.48–0.95) 
2.5–3 kHz  0.67 (0.42–0.92)  0.69 (0.37–1.02)  0.37 (0.14–0.61) 
3–4 kHz  0.86 (0.60–1.11)  0.48 (0.16–0.80)  0.52 (0.29–0.76) 
4–5 kHz  0.69 (0.44–0.95)  0.56 (0.24–0.88)  0.45 (0.22–0.69) 
5–6 kHz  0.51 (0.25–0.76)  0.51 (0.19–0.84)  0.18 (−0.05–0.42) 
1–6 kHz  0.89 (0.69–1.09)  0.85 (0.60–1.11)  0.66 (0.47–0.85) 

Modeled population inhibition contrasts across 1/3 octave frequency intervals are plotted in Fig. 8. The plotted point estimates show the most probable true inhibition contrasts between noise exposure populations, whereas the 95% CIs indicate the range of true population inhibition contrasts that are consistent with the data. Estimated inhibition is greater for controls than for Veterans with high noise exposure at frequencies above 1.5 kHz by up to 0.33 dB (for 3–4 kHz, CI = −0.01–0.58 dB). The CIs indicate that even larger decreases in inhibition for Veterans with high noise exposure compared with controls or very small increases are also plausible given the data. Estimated inhibition is slightly smaller in controls compared with Veterans with medium noise exposure in the low frequencies (by 0.19 dB from 1.5 to 2 kHz, CI= −0.44–0.40 dB) and greater in controls from 3 to 4 kHz (by 0.38 dB, CI = −0.03–0.79 dB). For this contrast, the CIs indicate that larger decreases in inhibition or very small increases for Veterans with medium noise exposure compared with controls are plausible from 3 to 4 kHz and either increases or decreases are plausible from 1.5 to 2 kHz.

FIG. 8.

(Color online) Modeled noise exposure population inhibition contrasts. Each panel shows the contrast in modeled DPOAE contralateral inhibition between two noise exposure populations for each 1/3 octave frequency interval. Symbols indicate point estimates while gray lines show the 95% CIs. Values above zero indicate that the first population has greater estimated mean inhibition than the second population (e.g., in the second panel, the control population tends to have greater mean modeled inhibition than the Veteran high noise population). LOESS smooth lines show the population contrast by frequency relationship.

FIG. 8.

(Color online) Modeled noise exposure population inhibition contrasts. Each panel shows the contrast in modeled DPOAE contralateral inhibition between two noise exposure populations for each 1/3 octave frequency interval. Symbols indicate point estimates while gray lines show the 95% CIs. Values above zero indicate that the first population has greater estimated mean inhibition than the second population (e.g., in the second panel, the control population tends to have greater mean modeled inhibition than the Veteran high noise population). LOESS smooth lines show the population contrast by frequency relationship.

Close modal

As hypothesized, model results showed a trend of reduced DPOAE contralateral inhibition for high noise Veterans compared with non-Veteran controls. This suggests that high levels of noise exposure experienced during military service may lead to weakening of the MOC reflex. This is consistent with previous animal (Spoendlin, 1971; Omata , 1992; Canlon , 1999; Boero , 2018) and human (Sliwinska-Kowalska and Kotylo, 2002; Peng , 2010; Gunduz , 2022; Megha , 2021) studies showing reduced MOC reflex strength following noise exposure. In the current study, the modeled mean reduction in contralateral inhibition from 1 to 2 kHz for the Veteran high noise population compared with the control population was 0.14 dB. Previous studies of DPOAE contralateral inhibition in humans found noise exposure-related reductions in inhibition from 1 to 2 kHz of 0.32–0.89 dB (Peng , 2010; Gunduz , 2022; Megha , 2021). In contrast with these previous studies, reductions in contralateral inhibition for Veterans with high noise exposure in the current study were greater in the high frequencies (0.33 dB from 3 to 4 kHz) than in the low frequencies. Although the noise exposure effect sizes reported here may seem small, it is important to remember that the effects of contralateral inhibition themselves are small with a modeled estimate of a mean reduction in DPOAE amplitude from 3 to 4 kHz due to contralateral inhibition of 0.86 dB in the control population. Therefore, the estimated mean reduction in DPOAE contralateral inhibition from 3 to 4 kHz for the Veteran high noise population of 0.33 dB represents a 30% reduction relative to inhibition in the control population.

The model results show trends that suggest that the effect of moderate noise exposure on contralateral inhibition differs depending on the frequency of the measurement. From 3 to 4 kHz, model estimates indicate a 0.38 dB mean decrease in inhibition for Veterans with medium noise exposure compared with controls. In the low frequencies (1–1.5 kHz), although the CIs for the modeled contrasts between the control and Veteran medium noise population overlap zero, the modeled mean contrasts, which represent our best estimate of the true contrast given the data, suggest a trend toward an increase in low frequency contralateral inhibition for Veterans with medium noise exposure compared with controls. This is surprising given their history of military noise exposure and firearm use. However, mean LENS-Q scores suggest lifetime noise exposure that is more than ten times lower for the Veteran medium noise group than for the Veteran high noise group. In addition, reported exposure to high intensity impulse/impact noise sources such as artillery, small arms fire, and explosions differed between groups. Of the Veteran medium noise participants, 47%, 71%, and 18% reported exposure to artillery, small arms fire, and explosions, respectively, during their military service. Of these participants, 75%–100% reported using hearing protection “most of the time” or “always” when exposed to these noise sources. In contrast, 56%, 97%, and 56% of the Veteran high noise participants reported exposure to artillery, small arms fire, and explosions, respectively, and during these exposures, they reported using hearing protection most of the time or always only 14%–61% of the time. While both Veteran groups experienced military noise exposure, this suggests considerably more exposure to high intensity impulse/impact noise for the Veteran high noise group compared to the Veteran medium noise group. Several animal studies have demonstrated that chronic exposure to moderate levels of noise (78–95 dB SPL) can protect against future noise-induced cochlear damage (e.g., Campo , 1991; Henselman , 1994; Kujawa and Liberman, 1997; Canlon , 1999), a phenomenon referred to as sound conditioning. In a chinchilla model, Campo (1991) measured evoked potential threshold shift (using an electrode implanted in the inferior colliculus) after a traumatic exposure to a 106 dB SPL octave band noise centered at 0.5 kHz in animals sound conditioned 6 h a day for 10 days to the same octave band noise at 95 dB SPL. They found that the conditioned animals showed less threshold shift than a control group of unconditioned animals. Henselman (1994) sound conditioned chinchillas by exposing them to intermittent 95 dB SPL octave band noise centered at 0.5 kHz for 10 days. Following conditioning, the animals were exposed to a 150 dB SPL impulse noise and showed less permanent threshold shift than the controls. Some studies have also shown conditioning-related MOC impacts. Canlon (1999) found that guinea pigs who received conditioning with a chronic low level tone (78–81 dB SPL) prior to exposure to an intense noise (100–105 dB SPL) experienced less noise-related loss of the MOC efferent nerve terminals than animals that were exposed only to the intense noise. However, they did not observe an increase in MOC efferent terminals after sound conditioning alone. Brown (1998) found that guinea pigs conditioned with intermittent exposure to an 85 dB SPL 2–4 kHz noise for 10 days showed increased MOC reflex activity compared to control animals, with the largest increases from 3 to 8 kHz. Kujawa and Liberman (1997) showed that the same conditioned animals from the study by Brown (1998) experienced considerably less permanent threshold shift (for the compound action potential) when exposed to the same noise at a higher intensity (109 dB SPL). In the study by Brown (1998), the frequency range of the increased MOC reflex activity was shifted upward slightly compared to the conditioning stimulus. Given that military noise exposure (e.g., from tracked vehicles, helicopters, airplanes, firearms, explosions, and aircraft carriers) tends to consist of broadband noise with peak intensities in the low frequencies (approximately 0.1–2 kHz; Versfeld and Vos, 1997; Khardi, 2009; Pater , 2009; Schaal , 2019), the observed trend toward an increase in inhibition from 1 to 1.5 kHz (i.e., the upper end of the frequency range of expected peak noise exposure) for the Veteran medium noise population compared to non-Veteran controls is not inconsistent with the results of the study by Brown (1998). Although the underlying mechanisms of sound conditioning are not well understood, Kujawa and Liberman (1999) proposed that conditioning may be mediated by physiological changes to the OHCs, MOC reflex, and/or MEMR.

The observed trend of a reduction in low frequency but not high frequency uninhibited DPOAE amplitudes for the Veteran medium noise population compared to the other two populations may also be an indicator of stronger low frequency MOC reflex activity in this population. Guinan (2003) observed contralateral inhibition of human stimulus frequency OAEs by DPOAE primary tones at L1/L2 = 50/40 dB SPL, which are similar to the L1/L2 = 55/40 dB SPL primary tones used in the current study. Although Guinan (2003) specifically evaluated contralateral inhibition, it is not implausible that the DPOAE primaries can also activate ipsilateral inhibition. In the low frequencies, given the observed increase in contralateral inhibition for the Veterans with medium noise exposure compared to controls, they may also have increased ipsilateral inhibition. If this is the case, it could result in lower uninhibited low frequency DPOAE levels for the Veteran medium noise population compared to the other populations. This could explain why low frequency but not high frequency uninhibited DPOAE levels were weaker for the Veterans with medium noise exposure than for controls or Veterans with high noise exposure. Supporting this interpretation of a conditioning effect on the ipsilateral and contralateral MOC reflexes in the Veteran medium noise group, Yin (2020) observed not only increased contralateral inhibition of DPOAEs after chronic moderate noise exposure in mice (6 h a day of 11.2–22.4 kHz noise at 80 dB SPL for 4 weeks) but also increased ipsilateral DPOAE inhibition. Note, however, that ipsilateral DPOAE inhibition resulting from the DPOAE primaries was not specifically evaluated in the current study.

Some human studies have also found a noise exposure-related increase in MOC reflex strength, indicative of a conditioning effect. For example, using a detailed occupational and recreational noise exposure questionnaire, Bhatt (2017) found a positive association between self-reported noise exposure and MOC reflex strength as measured with contralateral inhibition of click-evoked OAEs in a sample of young undergraduate university students with clinically normal hearing. Bidelman (2017) found increased MOC reflex strength as measured by contralateral and ipsilateral inhibition of DPOAEs in musicians with normal hearing when compared with age-matched nonmusicians. In addition, MOC reflex strength was positively correlated with self-reported years of musical training. Sound conditioning could potentially explain conflicting findings across previous human studies of the impacts of noise trauma on MOC reflex strength with high intensity exposures resulting in a weakened reflex and more moderate exposures leading to an unaltered or strengthened MOC reflex.

We previously evaluated physiological indicators of cochlear synaptopathy (ABR wave I amplitude, EFR magnitude, and wideband MEMR magnitude) in the same sample of Veterans and non-Veterans, grouped based on noise exposure (Bramhall , 2021; Bramhall , 2022). Reductions in these physiological indicators for the Veteran high noise population compared with the non-Veteran control population suggest that high levels of military noise exposure are associated with cochlear synaptopathy (or other forms of cochlear deafferentation). In contrast, there were not clear differences in ABR, EFR, or MEMR magnitudes between the non-Veteran control and Veteran medium noise populations. The results of the current study indicate that high levels of military noise exposure may also be associated with impaired efferent function. Taken together, these findings suggest that noise-induced afferent and efferent cochlear damage may co-occur, even among individuals with clinically normal audiograms.

Given that previous animal and human studies have suggested that the MOC reflex aids in signal-in-noise detection (reviewed in Lopez-Poveda, 2018) and protects against future cochlear damage (reviewed in Fuente, 2015), the finding that military noise exposure may impact contralateral inhibition of DPOAEs has important implications. The results of the current study suggest that moderate noise exposures may strengthen the MOC reflex in the low frequencies, whereas high intensity noise exposures appear to weaken the MOC reflex across a broad frequency range. This could result in protection from future noise- and age-related cochlear damage for individuals exposed to moderate levels of noise and poorer speech-in-noise perception and increased vulnerability to cochlear damage for individuals with greater noise exposure histories. Future studies that investigate afferent function, efferent function, and speech-in-noise perception in individuals with moderate vs high noise exposure histories will be necessary to clarify these relationships.

To limit the impacts of OHC dysfunction on our measurements, participation in this study was restricted to individuals with robust DPOAEs. However, this could result in the selection of a population of Veterans who are resistant to noise-related auditory damage because military noise exposure is associated with reductions in OAE amplitudes (e.g., Lapsley Miller , 2006). Given that the cell types involved in OHC damage likely differ from those involved in damage to the MOC reflex, susceptibility to these two types of auditory damage may not be linked (i.e., Veterans with good OHC function after military noise exposure may still have efferent damage). However, if the population of Veterans sampled for this study is more resistant to noise-induced damage to the MOC reflex, the results of this study would underestimate the damage experienced by a less restricted population of young Veterans.

The results of this study suggest a complex relationship between noise exposure and the MOC reflex in humans. Compared with non-Veteran controls, estimated reflex strength (as indicated by DPOAE contralateral inhibition) showed a trend across a broad frequency range of a reduction for Veterans with a history of high intensity noise exposure. In contrast, for Veterans with a more moderate noise exposure history, model estimates indicated trends toward reduced inhibition compared with controls from 3 to 4 kHz but increased inhibition from 1 to 1.5 kHz. This highlights the importance of specifying the degree of exposure when studying the effects of noise exposure on the cochlea. Expanding our understanding of how noise exposure damages the auditory system beyond hair cell and cochlear synapse loss could improve clinical diagnostics, leading to more effective treatment, monitoring, and prevention of noise-induced hearing loss.

This work was supported by the Department of Veterans Affairs, Veterans Health Administration, Rehabilitation Research and Development Service, Award No. C2104-W/I01 RX003804 (to N.F.B.) and resources and facilities at the VA National Center for Rehabilitative Auditory Research (NCRAR) Center Award No. C2361C/I50 RX002361 at the VA Portland Health Care System in Portland, OR. Research audiologist support was also provided by the Department of Defense Hearing Center of Excellence and zCore Business Solutions, Inc. The opinions and assertions presented are private views of the authors and are not to be construed as official or as necessarily reflecting the views of the VA or the Department of Defense.

1

See supplementary material at https://www.scitation.org/doi/suppl/10.1121/10.0016590 for a plot showing examples of DPOAE enhancement and a plot of modeled noise exposure population inhibition contrasts with a statistical adjustment for uninhibited DPOAE level.

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