Associations between speech recognition at high levels, the middle ear muscle reflex and noise exposure in individuals with normal audiograms.

It has been hypothesized that noise-induced cochlear synaptopathy in humans may result in functional deficits such as a weakened middle ear muscle reflex (MEMR) and degraded speech perception in complex environments. Although relationships between noise-induced synaptic loss and the MEMR have been demonstrated in animals, effects of noise exposure on the MEMR have not been observed in humans. The hypothesized relationship between noise exposure and speech perception has also been difficult to demonstrate conclusively. Given that the MEMR is engaged at high sound levels, relationships between speech recognition in complex listening environments and noise exposure might be more evident at high speech presentation levels. In this exploratory study with 41 audiometrically normal listeners, a combination of behavioral and physiologic measures thought to be sensitive to synaptopathy were used to determine potential links with speech recognition at high presentation levels. We found decreasing speech recognition as a function of presentation level (from 74 to 104 dBA), which was associated with reduced MEMR magnitude. We also found that reduced MEMR magnitude was associated with higher estimated lifetime noise exposure. Together, these results suggest that the MEMR may be sensitive to noise-induced synaptopathy in humans, and this may underlie functional speech recognition deficits at high sound levels.

Effects of lifetime noise exposure on the middle-age human auditory brainstem response, tinnitus and speech-in-noise intelligibility.

Recent animal studies have shown that the synapses between inner hair cells and the dendrites of the spiral ganglion cells they innervate are the elements in the cochlea most vulnerable to excessive noise exposure. Particularly in rodents, several studies have concluded that exposure to high level octave-band noise for 2 h leads to an irreversible loss of around 50% of synaptic ribbons, leaving audiometric hearing thresholds unaltered. Cochlear synaptopathy following noise exposure is hypothesized to degrade the neural encoding of sounds at the subcortical level, which would help explain certain listening-in-noise difficulties reported by some subjects with otherwise 'normal' hearing. In response to this peripheral damage, increased gain of central stages of the auditory system has been observed across several species of mammals, particularly in association with tinnitus. The auditory brainstem response (ABR) wave I amplitude and waves I-V amplitude ratio have been suggested as non-invasive indicators of cochlear synaptopathy and central gain activation respectively, but the evidence for these hearing disorders in humans is inconclusive. In this study, we evaluated the influence of lifetime noise exposure (LNE) on the human ABR and on speech-in-noise intelligibility performance in a large cohort of adults aged 29 to 55. Despite large inter-subject variability, results showed a moderate, but statistically significant, negative correlation between the ABR wave I amplitude and LNE, consistent with cochlear synaptopathy. The results also showed (a) that central gain mechanisms observed in animal studies might also occur in humans, in which higher stages of the auditory pathway appear to compensate for reduced input from the cochlea; (b) that tinnitus was associated with activation of central gain mechanisms; (c) that relevant cognitive and subcortical factors influence speech-in-noise intelligibility, in particular, longer ABR waves I-V interpeak latencies were associated with poorer performance in understanding speech in noise when central gain mechanisms were active; and (d) absence of a significant relationship between LNE and tinnitus, central gain activation or speech-in-noise performance. Although this study supports the possible existence of cochlear synaptopathy in humans, the great degree of variability, the lack of uniformity in central gain activation and the significant involvement of attention in speech-in-noise performance suggests that noise-induced cochlear synaptopathy is, at most, one of several factors that play a role in humans' speech-in-noise performance.

Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure.

In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers ("cochlear synaptopathy") without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans. The present study is the first to test for evidence of cochlear synaptopathy in humans with significant SPiN impairment. Individuals were recruited on the basis of self-reported SPiN difficulties and normal pure tone audiometric thresholds. Performance on a listening task identified a subset with "verified" SPiN impairment. This group was matched with controls on the basis of age, sex, and audiometric thresholds up to 14 kHz. ABRs and envelope-following responses (EFRs) were recorded at high stimulus levels, yielding both raw amplitude measures and within-subject difference measures. Past exposure to high sound levels was assessed by detailed structured interview. Impaired SPiN was not associated with greater lifetime noise exposure, nor with any electrophysiological measure. It is conceivable that retrospective self-report cannot reliably capture noise exposure, and that ABRs and EFRs offer limited sensitivity to synaptopathy in humans. Nevertheless, the results do not support the notion that noise-induced synaptopathy is a significant etiology of SPiN impairment with normal audiometric thresholds. It may be that synaptopathy alone does not have significant perceptual consequences, or is not widespread in humans with normal audiograms.

Evidence of noise-induced subclinical hearing loss using auditory brainstem responses and objective measures of noise exposure in humans.

Exposure to loud sound places the auditory system at considerable risk, especially when the exposure is routine. The current study examined the impact of routine auditory overexposure in young human adults with clinically-normal audiometric thresholds by measuring the auditory brainstem response (ABR), an electrophysiological measure of peripheral and central auditory processing. Sound exposure was measured objectively with body-worn noise dosimeters over a week. Participants were divided into low-exposure and high-exposure groups, with the low-exposure group having an average daily noise exposure dose of ∼11% of the recommended exposure limit compared to the high-exposure group average of nearly 500%. Compared to the low-exposure group, the high-exposure group had delayed ABRs to suprathreshold click stimuli and this prolongation was evident at ABR waves I and III but strongest for V. When peripheral differences were corrected using the I-V interpeak latency, the high-exposure group showed greater taxation at faster stimulus presentation rates than the low-exposure group, suggestive of neural conduction inefficiencies within central auditory structures. Our findings are consistent with the hypothesis that auditory overexposure affects peripheral and central auditory structures even before changes are evident on standard audiometry. We discuss our findings within the context of the larger debate on the mechanisms and manifestations of subclinical hearing loss.

Effects of noise overexposure on tone detection in noise in nonhuman primates.

This report explores the consequences of acoustic overexposures on hearing in noisy environments for two macaque monkeys trained to perform a reaction time detection task using a Go/No-Go lever release paradigm. Behavioral and non-invasive physiological assessments were obtained before and after narrowband noise exposure. Physiological measurements showed elevated auditory brainstem response (ABR) thresholds and absent distortion product otoacoustic emissions (DPOAEs) post-exposure relative to pre-exposure. Audiograms revealed frequency specific increases in tone detection thresholds, with the greatest increases at the exposure band frequency and higher. Masked detection was affected in a similar frequency specific manner: threshold shift rates (change of masked threshold per dB increase in noise level) were lower than pre-exposure values at frequencies higher than the exposure band. Detection thresholds in sinusoidally amplitude modulated (SAM) noise post-exposure showed no difference from those in unmodulated noise, whereas pre-exposure masked detection thresholds were lower in the presence of SAM noise compared to unmodulated noise. These frequency-dependent results were correlated with cochlear histopathological changes in monkeys that underwent similar noise exposure. These results reveal that behavioral and physiological effects of noise exposure in macaques are similar to those seen in humans and provide preliminary information on the relationship between noise exposure, cochlear pathology and perceptual changes in hearing within individual subjects.

Subcortical amplitude modulation encoding deficits suggest evidence of cochlear synaptopathy in normal-hearing 18-19 year olds with higher lifetime noise exposure.

Noise exposure and aging can damage cochlear synapses required for suprathreshold listening, even when cochlear structures needed for hearing at threshold remain unaffected. To control for effects of aging, behavioral amplitude modulation (AM) detection and subcortical envelope following responses (EFRs) to AM tones in 25 age-restricted (18-19 years) participants with normal thresholds, but different self-reported noise exposure histories were studied. Participants with more noise exposure had smaller EFRs and tended to have poorer AM detection than less-exposed individuals. Simulations of the EFR using a well-established cochlear model were consistent with more synaptopathy in participants reporting greater noise exposure.

Effects of noise exposure on young adults with normal audiograms II: Behavioral measures.

An estimate of lifetime noise exposure was used as the primary predictor of performance on a range of behavioral tasks: frequency and intensity difference limens, amplitude modulation detection, interaural phase discrimination, the digit triplet speech test, the co-ordinate response speech measure, an auditory localization task, a musical consonance task and a subjective report of hearing ability. One hundred and thirty-eight participants (81 females) aged 18-36 years were tested, with a wide range of self-reported noise exposure. All had normal pure-tone audiograms up to 8 kHz. It was predicted that increased lifetime noise exposure, which we assume to be concordant with noise-induced cochlear synaptopathy, would elevate behavioral thresholds, in particular for stimuli with high levels in a high spectral region. However, the results showed little effect of noise exposure on performance. There were a number of weak relations with noise exposure across the test battery, although many of these were in the opposite direction to the predictions, and none were statistically significant after correction for multiple comparisons. There were also no strong correlations between electrophysiological measures of synaptopathy published previously and the behavioral measures reported here. Consistent with our previous electrophysiological results, the present results provide no evidence that noise exposure is related to significant perceptual deficits in young listeners with normal audiometric hearing. It is possible that the effects of noise-induced cochlear synaptopathy are only measurable in humans with extreme noise exposures, and that these effects always co-occur with a loss of audiometric sensitivity.

The effects of noise exposure and musical training on suprathreshold auditory processing and speech perception in noise.

Recent animal research has shown that exposure to single episodes of intense noise causes cochlear synaptopathy without affecting hearing thresholds. It has been suggested that the same may occur in humans. If so, it is hypothesized that this would result in impaired encoding of sound and lead to difficulties hearing at suprathreshold levels, particularly in challenging listening environments. The primary aim of this study was to investigate the effect of noise exposure on auditory processing, including the perception of speech in noise, in adult humans. A secondary aim was to explore whether musical training might improve some aspects of auditory processing and thus counteract or ameliorate any negative impacts of noise exposure. In a sample of 122 participants (63 female) aged 30-57 years with normal or near-normal hearing thresholds, we conducted audiometric tests, including tympanometry, audiometry, acoustic reflexes, otoacoustic emissions and medial olivocochlear responses. We also assessed temporal and spectral processing, by determining thresholds for detection of amplitude modulation and temporal fine structure. We assessed speech-in-noise perception, and conducted tests of attention, memory and sentence closure. We also calculated participants' accumulated lifetime noise exposure and administered questionnaires to assess self-reported listening difficulty and musical training. The results showed no clear link between participants' lifetime noise exposure and performance on any of the auditory processing or speech-in-noise tasks. Musical training was associated with better performance on the auditory processing tasks, but not the on the speech-in-noise perception tasks. The results indicate that sentence closure skills, working memory, attention, extended high frequency hearing thresholds and medial olivocochlear suppression strength are important factors that are related to the ability to process speech in noise.

Noise-induced hearing loss induces loudness intolerance in a rat Active Sound Avoidance Paradigm (ASAP).

Hyperacusis is a loudness hypersensitivity disorder in which moderate-intensity sounds are perceived as extremely loud, aversive and/or painful. To assess the aversive nature of sounds, we developed an Active Sound Avoidance Paradigm (ASAP) in which rats altered their place preference in a Light/Dark shuttle box in response to sound. When no sound (NS) was present, rats spent more than 95% of the time in the Dark Box versus the transparent Light Box. However, when a 60 or 90 dB SPL noise (2-20 kHz, 2-8 kHz, or 16-20 kHz bandwidth) was presented in the Dark Box, the rats'' preference for the Dark Box significantly decreased. Percent time in the dark decreased as sound intensity in the Dark Box increased from 60 dB to 90 dB SPL. Interestingly, the magnitude of the decrease was not a monotonic function of intensity for the 16-20 kHz noise and not related to the bandwidth of the 2-20 kHz and 2-8 kHz noise bands, suggesting that sound avoidance is not solely dependent on loudness but the aversive quality of the noise as well. Afterwards, we exposed the rats for 28 days to a 16-20 kHz noise at 102 dB SPL; this exposure produced a 30-40 dB permanent threshold shift at 16 and 32 kHz. Following the noise exposure, the rats were then retested on the ASAP paradigm. High-frequency hearing loss did not alter Dark Box preference in the no-sound condition. However, when the 2-20 kHz or 2-8 kHz noise was presented at 60 or 90 dB SPL, the rats avoided the Dark Box significantly more than they did before the exposure, indicating these two noise bands with energy below the region of hearing loss were perceived as more aversive. In contrast, when the 16-20 kHz noise was presented at 60 or 90 dB SPL, the rats remained in the Dark Box presumably because the high-frequency hearing loss made 16-20 kHz noise less audible and less aversive. These results indicate that when rats develop a high-frequency hearing loss, they become less tolerant of low frequency noise, i.e., high intensity sounds are perceived as more aversive and should be avoided.

Analysis of audiometric notch as a noise-induced hearing loss phenotype in US youth: data from the National Health And Nutrition Examination Survey, 2005-2010.

OBJECTIVE: Bilateral audiometric notch (BN) at 4000-6000 Hz was identified as a noise-induced hearing loss (NIHL) phenotype for genetic association analysis in college-aged musicians. This study analysed BN in a sample of US youth. DESIGN: Prevalence of the BN within the study sample was determined and logistic-regression analyses were performed to identify audiologic and other demographic factors associated with BN. Computer-simulated "flat" audiograms were used to estimate potential influence of false-positive rates in estimating the prevalence of the BN. STUDY SAMPLE: 2348 participants (12-19 years) following the inclusion criteria were selected from the National Health and Nutrition Examination Survey data (2005-2010). RESULTS: The prevalence of BN was 16.6%. Almost 55.6% of the participants showed notch in at least one ear. Noise exposure, gender, ethnicity and age showed significant relationship with the BN. Computer simulation revealed that 5.5% of simulated participants with "flat" audiograms showed BN. CONCLUSION: Association of noise exposure with BN suggests that it is a useful NIHL phenotype for genetic association analyses. However, further research is necessary to reduce false-positive rates in notch identification.

Big brown bats (Eptesicus fuscus) maintain hearing sensitivity after exposure to intense band-limited noise.

Thresholds to short-duration narrowband frequency-modulated (FM) sweeps were measured in six big brown bats (Eptesicus fuscus) in a two-alternative forced choice passive listening task before and after exposure to band-limited noise (lower and upper frequencies between 10 and 50 kHz, 1 h, 116-119 dB sound pressure level root mean square; sound exposure level 152 dB). At recovery time points of 2 and 5 min post-exposure, thresholds varied from -4 to +4 dB from pre-exposure threshold estimates. Thresholds after sham (control) exposures varied from -6 to +2 dB from pre-exposure estimates. The small differences in thresholds after noise and sham exposures support the hypothesis that big brown bats do not experience significant temporary threshold shifts under these experimental conditions. These results confirm earlier findings showing stability of thresholds to broadband FM sweeps at longer recovery times after exposure to broadband noise. Big brown bats may have evolved a lessened susceptibility to noise-induced hearing losses, related to the special demands of echolocation.

Development and validation of the Speech Reception in Noise (SPRINT) Test.

Since 1992, the Speech Recognition in Noise Test, or SPRINT, has been the standard speech-in-noise test for assessing auditory fitness-for-duty of US Army Soldiers with hearing loss. The original SPRINT test consisted of 200 monosyllabic words presented at a Signal-to-Noise Ratio (SNR) of +9 dB in the presence of a six-talker babble noise. Normative data for the test was collected on 319 hearing impaired Soldiers, and a procedure for making recommendations about the disposition of military personnel on the basis of their SPRINT score and their years of experience was developed and implemented as part of US Army policy. In 2013, a new 100-word version of the test was developed that eliminated words that were either too easy or too hard to make meaningful distinctions among hearing impaired listeners. This paper describes the development of the original 200-word SPRINT test, along with a description of the procedure used to reduce the 200-word test to 100 words and the results of a validation study conducted to evaluate how well the shortened 100-word test is able to capture the results from the full 200-word version of the SPRINT.

Crossmodal plasticity in auditory, visual and multisensory cortical areas following noise-induced hearing loss in adulthood.

Complete or partial hearing loss results in an increased responsiveness of neurons in the core auditory cortex of numerous species to visual and/or tactile stimuli (i.e., crossmodal plasticity). At present, however, it remains uncertain how adult-onset partial hearing loss affects higher-order cortical areas that normally integrate audiovisual information. To that end, extracellular electrophysiological recordings were performed under anesthesia in noise-exposed rats two weeks post-exposure (0.8-20 kHz at 120 dB SPL for 2 h) and age-matched controls to characterize the nature and extent of crossmodal plasticity in the dorsal auditory cortex (AuD), an area outside of the auditory core, as well as in the neighboring lateral extrastriate visual cortex (V2L), an area known to contribute to audiovisual processing. Computer-generated auditory (noise burst), visual (light flash) and combined audiovisual stimuli were delivered, and the associated spiking activity was used to determine the response profile of each neuron sampled (i.e., unisensory, subthreshold multisensory or bimodal). In both the AuD cortex and the multisensory zone of the V2L cortex, the maximum firing rates were unchanged following noise exposure, and there was a relative increase in the proportion of neurons responsive to visual stimuli, with a concomitant decrease in the number of neurons that were solely responsive to auditory stimuli despite adjusting the sound intensity to account for each rat's hearing threshold. These neighboring cortical areas differed, however, in how noise-induced hearing loss affected audiovisual processing; the total proportion of multisensory neurons significantly decreased in the V2L cortex (control 38.8 ± 3.3% vs. noise-exposed 27.1 ± 3.4%), and dramatically increased in the AuD cortex (control 23.9 ± 3.3% vs. noise-exposed 49.8 ± 6.1%). Thus, following noise exposure, the cortical area showing the greatest relative degree of multisensory convergence transitioned ventrally, away from the audiovisual area, V2L, toward the predominantly auditory area, AuD. Overall, the collective findings of the present study support the suggestion that crossmodal plasticity induced by adult-onset hearing impairment manifests in higher-order cortical areas as a transition in the functional border of the audiovisual cortex.

Tinnitus with a normal audiogram: Relation to noise exposure but no evidence for cochlear synaptopathy.

In rodents, exposure to high-level noise can destroy synapses between inner hair cells and auditory nerve fibers, without causing hair cell loss or permanent threshold elevation. Such "cochlear synaptopathy" is associated with amplitude reductions in wave I of the auditory brainstem response (ABR) at moderate-to-high sound levels. Similar ABR results have been reported in humans with tinnitus and normal audiometric thresholds, leading to the suggestion that tinnitus in these cases might be a consequence of synaptopathy. However, the ABR is an indirect measure of synaptopathy and it is unclear whether the results in humans reflect the same mechanisms demonstrated in rodents. Measures of noise exposure were not obtained in the human studies, and high frequency audiometric loss may have impacted ABR amplitudes. To clarify the role of cochlear synaptopathy in tinnitus with a normal audiogram, we recorded ABRs, envelope following responses (EFRs), and noise exposure histories in young adults with tinnitus and matched controls. Tinnitus was associated with significantly greater lifetime noise exposure, despite close matching for age, sex, and audiometric thresholds up to 14 kHz. However, tinnitus was not associated with reduced ABR wave I amplitude, nor with significant effects on EFR measures of synaptopathy. These electrophysiological measures were also uncorrelated with lifetime noise exposure, providing no evidence of noise-induced synaptopathy in this cohort, despite a wide range of exposures. In young adults with normal audiograms, tinnitus may be related not to cochlear synaptopathy but to other effects of noise exposure.

Lifetime leisure music exposure associated with increased frequency of tinnitus.

Tinnitus has been linked to noise exposure, a common form of which is listening to music as a leisure activity. The relationship between tinnitus and type and duration of music exposure is not well understood. We conducted an internet-based population study that asked participants questions about lifetime music exposure and hearing, and included a hearing test involving speech intelligibility in noise, the High Frequency Digit Triplets Test. 4950 people aged 17-75 years completed all questions and the hearing test. Results were analyzed using multinomial regression models. High exposure to leisure music, hearing difficulty, increasing age and workplace noise exposure were independently associated with increased tinnitus. Three forms of music exposure (pubs/clubs, concerts, personal music players) did not differ in their relationship to tinnitus. More males than females reported tinnitus. The objective measure of speech reception threshold had only a minimal relationship with tinnitus. Self-reported hearing difficulty was more strongly associated with tinnitus, but 76% of people reporting usual or constant tinnitus also reported little or no hearing difficulty. Overall, around 40% of participants of all ages reported never experiencing tinnitus, while 29% reported sometimes, usually or constantly experiencing tinnitus that lasted more than 5 min. Together, the results suggest that tinnitus is much more common than hearing loss, but that there is little association between the two, especially among the younger adults disproportionately sampled in this study.

Effects of noise exposure on young adults with normal audiograms I: Electrophysiology.

Noise-induced cochlear synaptopathy has been demonstrated in numerous rodent studies. In these animal models, the disorder is characterized by a reduction in amplitude of wave I of the auditory brainstem response (ABR) to high-level stimuli, whereas the response at threshold is unaffected. The aim of the present study was to determine if this disorder is prevalent in young adult humans with normal audiometric hearing. One hundred and twenty six participants (75 females) aged 18-36 were tested. Participants had a wide range of lifetime noise exposures as estimated by a structured interview. Audiometric thresholds did not differ across noise exposures up to 8 kHz, although 16-kHz audiometric thresholds were elevated with increasing noise exposure for females but not for males. ABRs were measured in response to high-pass (1.5 kHz) filtered clicks of 80 and 100 dB peSPL. Frequency-following responses (FFRs) were measured to 80 dB SPL pure tones from 240 to 285 Hz, and to 80 dB SPL 4 kHz pure tones amplitude modulated at frequencies from 240 to 285 Hz (transposed tones). The bandwidth of the ABR stimuli and the carrier frequency of the transposed tones were chosen to target the 3-6 kHz characteristic frequency region which is usually associated with noise damage in humans. The results indicate no relation between noise exposure and the amplitude of the ABR. In particular, wave I of the ABR did not decrease with increasing noise exposure as predicted. ABR wave V latency increased with increasing noise exposure for the 80 dB peSPL click. High carrier-frequency (envelope) FFR signal-to-noise ratios decreased as a function of noise exposure in males but not females. However, these correlations were not significant after the effects of age were controlled. The results suggest either that noise-induced cochlear synaptopathy is not a significant problem in young, audiometrically normal adults, or that the ABR and FFR are relatively insensitive to this disorder in young humans, although it is possible that the effects become more pronounced with age.

Sensory coding and cognitive processing of sound in Veterans with blast exposure.

Recent anecdotal reports from VA audiology clinics as well as a few published studies have identified a sub-population of Service Members seeking treatment for problems communicating in everyday, noisy listening environments despite having normal to near-normal hearing thresholds. Because of their increased risk of exposure to dangerous levels of prolonged noise and transient explosive blast events, communication problems in these soldiers could be due to either hearing loss (traditional or "hidden") in the auditory sensory periphery or from blast-induced injury to cortical networks associated with attention. We found that out of the 14 blast-exposed Service Members recruited for this study, 12 had hearing thresholds in the normal to near-normal range. A majority of these participants reported having problems specifically related to failures with selective attention. Envelope following responses (EFRs) measuring neural coding fidelity of the auditory brainstem to suprathreshold sounds were similar between blast-exposed and non-blast controls. Blast-exposed subjects performed substantially worse than non-blast controls in an auditory selective attention task in which listeners classified the melodic contour (rising, falling, or "zig-zagging") of one of three simultaneous, competing tone sequences. Salient pitch and spatial differences made for easy segregation of the three concurrent melodies. Poor performance in the blast-exposed subjects was associated with weaker evoked response potentials (ERPs) in frontal EEG channels, as well as a failure of attention to enhance the neural responses evoked by a sequence when it was the target compared to when it was a distractor. These results suggest that communication problems in these listeners cannot be explained by compromised sensory representations in the auditory periphery, but rather point to lingering blast-induced damage to cortical networks implicated in the control of attention. Because all study participants also suffered from post-traumatic disorder (PTSD), follow-up studies are required to tease apart the contributions of PTSD and blast-induced injury on cognitive performance.

Audiologic characteristics in a sample of recently-separated military Veterans: The Noise Outcomes in Servicemembers Epidemiology Study (NOISE Study).

Military Service Members are often exposed to high levels of occupational noise, solvents, and other exposures that can be damaging to the auditory system. Little is known about hearing loss and how it progresses in Veterans following military service. This epidemiology study is designed to evaluate and monitor a cohort of Veterans for 20 years or more to determine how hearing loss changes over time and how those changes are related to noise exposure and other ototoxic exposures encountered during military service. Data reported here are from baseline assessments of the first 100 study participants (84 males; 16 females; mean age 33.5 years; SD 8.8; range 21-58). Each participant was asked to complete a comprehensive audiologic examination and self-report questionnaires regarding sociodemographic characteristics, noise and solvent exposures, health conditions common among post-deployment Veterans, and the social and emotional consequences of hearing loss. For this relatively young cohort, 29% exhibited hearing loss, defined as average hearing threshold >20 dB HL in the conventional audiometric range. Forty-two percent exhibited hearing loss in the extended-high-frequency audiometric range using the same criterion (average hearing threshold >20 dB HL). Certain factors were found to be associated with poorer hearing in both conventional and extended-high-frequency ranges, including age, type of military branch, years of military service, number of military deployments, noise exposure, tinnitus, and a positive screen for post-traumatic stress disorder. Although the majority of participants had hearing within normal limits, 27% reported a self-perceived mild/moderate hearing handicap and 14% reported a significant handicap. Further research is needed to identify a cause for this discrepancy in audiologic results versus self-report. The information obtained from this longitudinal study could be used in future resource planning with the goal of preventing, as much as possible, the development of hearing loss during military service, and the exacerbation of prevalent hearing loss after military service and over Veterans' lifetimes.

Going wireless and booth-less for hearing testing in industry.

OBJECTIVE: To assess the test-retest variability of hearing thresholds obtained with an innovative, mobile wireless automated hearing-test system (WAHTS) with enhanced sound attenuation to test industrial workers at a worksite as compared to standardised automated hearing thresholds obtained in a mobile trailer sound booth. DESIGN: A within-subject repeated-measures design was used to compare air-conducted threshold tests (500-8000 Hz) measured with the WAHTS in six workplace locations, and a third test using computer-controlled audiometry obtained in a mobile trailer sound booth. Ambient noise levels were measured in all test environments. STUDY SAMPLE: Twenty workers served as listeners and 20 workers served as operators. RESULTS: On average, the WAHTS resulted in equivalent thresholds as the mobile trailer audiometry at 1000, 2000, 3000 and 8000 Hz and thresholds were within ±5 dB at 500, 4000 and 6000 Hz. CONCLUSIONS: Comparable performance may be obtained with the WAHTS in occupational audiometry and valid thresholds may be obtained in diverse test locations without the use of sound-attenuating enclosures.

Evidence of "hidden hearing loss" following noise exposures that produce robust TTS and ABR wave-I amplitude reductions.

In animals, noise exposures that produce robust temporary threshold shifts (TTS) can produce immediate damage to afferent synapses and long-term degeneration of low spontaneous rate auditory nerve fibers. This synaptopathic damage has been shown to correlate with reduced auditory brainstem response (ABR) wave-I amplitudes at suprathreshold levels. The perceptual consequences of this "synaptopathy" remain unknown but have been suggested to include compromised hearing performance in competing background noise. Here, we used a modified startle inhibition paradigm to evaluate whether noise exposures that produce robust TTS and ABR wave-I reduction but not permanent threshold shift (PTS) reduced hearing-in-noise performance. Animals exposed to 109 dB SPL octave band noise showed TTS >30 dB 24-h post noise and modest but persistent ABR wave-I reduction 2 weeks post noise despite full recovery of ABR thresholds. Hearing-in-noise performance was negatively affected by the noise exposure. However, the effect was observed only at the poorest signal to noise ratio and was frequency specific. Although TTS >30 dB 24-h post noise was a predictor of functional deficits, there was no relationship between the degree of ABR wave-I reduction and degree of functional impairment.