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The mammalian auditory system is susceptible to noise exposure injury resulting from damage to cells in the inner ear. Changes in function can be temporary or permanent (for review, see Ryan et al., 2016). The Occupational Safety and Health Administration (OSHA) federal noise regulations define an auditory “standard threshold shift” as a permanent change in hearing threshold, relative to one's baseline audiogram, of an average of 10-dB or more at 2, 3, and 4 kHz in either ear (OSHA, 1983). A temporary threshold shift (TTS), by definition, does not meet this regulatory standard for a workplace-induced noise injury. However, recent findings suggest that large TTS may result in permanent synaptic loss (Kujawa and Liberman, 2009), followed by slow, progressive neural degeneration (Kujawa and Liberman, 2006). Thus, exposures that result in TTS may be more harmful than previously believed (Kujawa and Liberman, 2015).

Noise exposures that result in a relatively robust TTS 24-h after the noise exposure have been accompanied by loss of the synaptic connections between inner hair cells (IHCs) and the afferent neurons in mice (Kujawa and Liberman, 2009; Wang and Ren, 2012; Fernandez et al., 2015) and guinea pigs (Lin et al., 2011; Furman et al., 2013). With this decrease in the neural output of the cochlea, the amplitude of Wave-I of the sound-evoked auditory brainstem response (ABR) is permanently reduced, even though the ABR Wave-I threshold remains unchanged (for reviews, see Kujawa and Liberman, 2015; Liberman and Kujawa, 2017). Because these noise exposures result in damage that cannot be detected by conventional audiometric threshold assessment, this synaptopathic injury has been referred to as “hidden hearing loss”, a term originally coined by Schaette and McAlpine (2011). Synaptopathic injury appears to be biased toward low spontaneous firing rate neurons, which have higher response thresholds and are responsible for coding higher intensity (suprathreshold) sounds (Furman et al., 2013). In contrast, synaptic contacts with the high-spontaneous rate neurons, which have lower response thresholds and are responsible for coding lower intensity sounds (i.e., audiometric thresholds), appear to be largely unaffected. This may explain why the threshold audiogram is not sensitive to loss of IHCs (Lobarinas et al., 2013) or afferent synapses (Kujawa and Liberman, 2009).

It has been suggested that noise-induced neuropathic damage may explain the disproportionate difficulties some individuals experience processing speech in noisy environments, despite clinically normal hearing thresholds (Kujawa and Liberman, 2009; Lin et al., 2011; Makary et al., 2011). More recently, there have been several suggestions that recreational noise could induce cochlear synaptopathy manifested as difficulty understanding speech in background noise with deficits “hidden” behind a standard audiogram. Liberman (2015) points to “the loud pop of Fourth of July fireworks or the roar of the crowds at a football game” as not only affecting hair cells, but also damaging the auditory neurons, and suggests that their research finding “raises questions about the risks of routine exposure to loud music at concerts and clubs and via personal listening devices.” Jensen et al. (2015) similarly point to the increasing sales of portable listening devices, and suggest that there has been a corresponding “shift of ‘at-risk’ users from adults to adolescents.” Suggestions such as these have led multiple groups to seek evidence that would suggest a potential synaptopathic injury in otherwise normal-hearing young adult cohorts (Stamper and Johnson, 2015a,b; Prendergast et al., 2017; Spankovich et al., 2017; Fulbright et al., in press).

Although Stamper and Johnson (2015a) presented evidence that was interpreted as consistent with a synaptopathic noise injury (reduction in ABR Wave-I amplitude) secondary to recreational noise history in normal-hearing young adults, the investigation did not account for differences in ABR Wave-I amplitude as a function of sex. After controlling for sex, the observed effects were limited to females (Stamper and Johnson, 2015b). More recently, Prendergast et al. (2017), Fulbright et al. (in press), and Spankovich et al. (2017) were unable to provide evidence consistent with noise-induced synaptopathic injury in other young adult populations with varying recreational noise histories. However, failure to detect deficits in ABR Wave-I amplitude in young adults with recreational noise exposure histories is perhaps not that surprising. In animal models, shorter or less intense noise exposures that result in smaller TTS changes do not result in synaptopathic injury, functional deficits, or progressive neuronal loss (Hickox and Liberman, 2014; Fernandez et al., 2015; Jensen et al., 2015; Lobarinas et al., 2017). In studies with rodents, 20–30 dB TTS 24 h post noise generally has not been associated with synaptopathic change, whereas 40–50 dB TTS 24 h post noise clearly has been associated with synaptopathic damage. Thus, typical recreational noise exposures commonly experienced by young adults likely are not sufficient to result in an acute neural pathology. The lack of deficits observed in studies assessing young adults with a history of recreational noise exposure (Prendergast et al., 2017; Spankovich et al., 2017; Fulbright et al., in press) does not preclude the possibility that damage emerges with louder, longer, or more frequently repeated noise exposures, such as firearm exposure (Bramhall et al., 2017), explosions (Remenschneider et al., 2014), and blast exposure in the course of military service (Helfer et al., 2011; Gallun et al., 2012a,b; Saunders et al., 2015). The data from Bramhall et al. (2017) are compelling in showing reduced ABR Wave-I amplitude in civilians and military personnel with high noise exposure, and the data from Liberman et al. (2016) raise important questions about the potential for hazard for musicians. The issue of unknown damage-risk criteria for synaptopathic injury and hidden hearing loss is a challenge not only for public health hearing loss prevention efforts targeting adolescents, but also for the protection of noise-exposed workers (for discussion, see Dobie and Humes, 2017; Murphy and Le Prell, 2017).

The current investigation is the first to describe prospective monitoring of young adults attending loud recreational venues for potential changes in both auditory evoked potentials and functional performance (tone detection and speech-in-noise testing) as a consequence of acute recreational noise exposure. The unique features of this study were (1) collection of data pre- and post-noise exposure, (2) the use of a sound-pressure-level meter smartphone app to document exposure during loud events attended by participants, and (3) the integration of functional word-in-noise tests with evoked potential measures in assessing effects of recreational noise. These data were collected with the specific goal of generating evidence that will provide insight into the potential hazards of individual recreational events, as a function of the accrued noise dose, so that future investigations can more precisely target at-risk populations. In addition to the use of prospective test design, the current investigation adds data on the relationship between hearing-in-noise and noise exposure history. Distortion product otoacoustic emission (DPOAE) amplitude was assessed in order to differentiate potential damage to the outer hair cell (OHC) and IHC populations.

This study was approved by the Institutional Review Board at the University of Texas at Dallas. Signed consent forms were obtained from participants prior to study enrollment. Participants were recruited from the University of Texas at Dallas campus in Richardson, Texas and the Callier Center for Communication Disorders in Dallas, Texas. All study procedures were performed using dedicated clinical research equipment located at the Callier Center for Communication Disorders in Dallas, TX. All study procedures were conducted by students in their third or fourth year of training in the Doctor of Audiology program. Participants were allowed to withdraw at any time; they were compensated for each laboratory visit.

Participants included 32 young adults (13 male, 19 female; mean age 23.5 years, range 21–27 years). Participants were asked to self-identify sex; we are not aware of any participants for whom gender identity was different from biological sex. All participants met the study enrollment criteria, including normal otoscopic examination bilaterally (visualization of the tympanic membranes with no apparent abnormalities), normal tympanometric examination bilaterally (Type A with 226 Hz probe tone), and normal hearing (defined as thresholds of 25 dB HL or better from 0.25 to 8 kHz bilaterally).

Participants were invited to attend three test sessions. In order to avoid enticing participants to attend a loud recreational event, the second session was specified as being either (A) the day after attending a loud recreational event of their choice, or (B) a second baseline session during which the participant would be retested to establish retest reliability in the absence of attending a loud event. The third session was completed 1-week later. Although having plans to attend a loud event was not an enrollment criterion, all participants already had plans to attend common “loud” recreational events at the time of study enrollment (concert, n = 16; multi-day music festival, n = 2; bar with live music, n = 3; bar with digital music, n = 4; dance event, n = 3; movie, n = 1). The participants self-identified events as “loud,” and there was no duration requirement; as such, the recreational events varied with respect to type, level, and duration.

Noise levels were estimated using the smartphone app “SPL Graph,” installed on each participant's phone prior to event attendance. Data presented by Grinn et al. (2017) showed this app to be accurate within 2-dB of a class 1 sound level meter (SLM) across 25 used (not-new) iPhones (models 5, 5S, 6, 6S, 6S Plus, and 7) for test signals including steady-state broadband noise (90–110 dBA) and five pop songs (85–105 dBA). To assure that individual participants in this study were able to accurately measure sound levels using this app, the app was installed on participant iPhones and accuracy was verified against a class 1 SLM (Brüel and Kjær, type 2250; calibration verified using a Brüel and Kjær Type 4231 calibrator prior to use). At the baseline test session, participants were taught how to use the app and demonstrated the ability to point their phone microphone at a sound source to capture a measurement. Ten instantaneous sound level measurements (dBA) were captured by each participant at various moments throughout their loud event; the average event sound level was estimated using these 10 instantaneous sound level measurements. Event duration was recorded and reported by the participant. Estimated noise dose per individual participant was calculated using 29 CFR 1910.95 Appendix A (OSHA, 1983) based on the measured levels and the reported duration of attendance.

Taken together, the overall design included 3 test sessions completed as follows: (1) baseline test prior to attending a loud event, (2) retest within 24 h after the loud event, (3) retest 1-week after the loud event. Of the 32 participants enrolled in the study, 26 completed all 3 test sessions and their data are included in both the retrospective and prospective analyses. Two additional participants completed the first two test sessions, but not the final 1-week post noise session. Data from these participants was included in the analyses. Three additional participants completed only the baseline test session and their data are included only in the retrospective analysis, as there were no post-noise data to include for these two participants. One additional participant completed the online surveys but did not complete any test sessions; their survey data were excluded as there were no audiologic data for this participant.

In the first part of this investigation, a retrospective analysis in which noise survey responses were used to compare previous noise exposure history to current auditory function, there was no evidence that a history of self-reported common recreational exposures resulted in audiometric, functional, or electrophysiological deficits. These data parallel Prendergast et al. (2017), Fulbright et al. (in press), and Spankovich et al. (2017), who evaluated three different normal-hearing young adult cohorts with varying amounts of recreational noise exposure history. In contrast to these four studies, ABR Wave-I amplitude was reported to be reduced in young adults (or, at least in young adult females) as a function of recreational noise exposure by Stamper and Johnson (2015a,b). Of note, none of these populations had significant occupational noise exposure histories or systematic exposure to loud music as rehearsing or performing musicians.

In contrast to the negative results from the above studies, Liberman et al. (2016) described statistically significant differences in extended high frequency (EHF) threshold sensitivity, word recognition performance in difficult listening conditions, SP amplitude, and the SP/AP ratio when high risk participants (15M, 7F; largely, college students enrolled in a music conservatory) were compared to low risk participants (4M, 8F; largely, college students enrolled in a communication sciences program). Bramhall et al. (2017) has also described deficits in ABR Wave-I amplitude as a function of noise exposure; they compared the amplitude of ABR Wave-I in civilians and military personnel without significant noise exposure to civilians who use firearms and military personnel with significant noise exposure (including firearm use). Taken together, the majority of data across retrospective studies now appear to be generally consistent in revealing no statistically significant relationships between common recreational noise exposure histories and ABR Wave-I (or AP) amplitude, whereas statistically significant relationships between firearm, blast, and other significant noise exposure and ABR Wave-I amplitude have emerged (Bramhall et al., 2017).

It is possible that statistically significant associations between AP (or, ABR Wave-I amplitude) and recreational noise history would emerge if larger cohorts were studied, which would increase power to detect subtle relationships. However, based on the observed Pearson R and Spearman Rho values of 0.15 or less across stimulus conditions (see Figure 2), new, prospective power analysis indicates that a sample size of 400 participants would be necessary to achieve 85% power to detect relationships of the size (i.e., R = 0.15) obtained in this retrospective analysis. Even if a large study with the power to detect small associations was conducted, it is not clear that the weak relationships indicated by R values of 0.15 would be clinically significant. As an alternative, study power presumably would be increased if additional higher-risk participants were included, assuming that the hypothesis that the strength of the observed relationships will increase as participants with increasing exposure are added is true. It is not yet clear if risk will increase relatively linearly along some graded continuum as noise exposure increases, or if there is some critical boundary at which risk of injury suddenly increases in an “all or nothing” fashion; a better understanding of this relationship is critically important with respect to the design of future studies and the eventual development of evidence-based risk criteria. Systematic manipulation of noise exposure using rodent models may provide some insight into these relationships and inform the design of human translational studies. Data from non-human primates are also likely to be necessary in order to understand risk across species, and would support additional inference related to human risk.

Most investigations assessing the potential for hidden hearing loss in humans have used NEQ-based approaches. These studies rely on an assumption that reports of noise exposure within the past 12-months provide information that is relevant and accurate. These studies further assume that exposure over the past 12-months is representative of previous lifetime noise history. If there was significantly more or less noise exposure within the past 12-months than in earlier years, the previous 12-month L_Aeq8760 metric would provide limited utility for comparisons with current functional status. Fulbright (2016) used a variety of surveys to assess both L_Aeq8760 and lifetime noise. No notable differences in outcomes were observed when current audiometric function was assessed as a function of L_Aeq8760 or lifetime noise; however, in this young adult population, lifetime noise estimates tended to be reduced relative to previous year estimates. In other words, noise exposure as a young adult was increased relative to noise exposure in earlier childhood years. Thus, it cannot be assumed that every participant in every study has a 12-month noise history (and L_Aeq8760) that is representative of their lifetime noise exposure history; careful interview is necessary to assure that there was no significant noise exposure in earlier years that would suggest a participant is at higher risk than their current L_Aeq8760 might suggest.

We did not survey self-reported difficulties in noise. It is tempting to assume that self-reported difficulty listening in noise may be a useful measure, as this approach is now being used in large epidemiological studies that rely on survey data to assess hearing problems (see for example Curhan et al., 2012). The use of surveys may also resolve challenges related to the ceiling effects observed for some speech-in-quiet and speech-in-noise tests. Certainly, there is a lack of consensus regarding an accepted “gold standard” for speech-in-noise testing (for discussion, see Le Prell and Lobarinas, 2015; Le Prell and Brungart, 2016; Le Prell and Clavier, 2017). The data collected here used the WIN test, while Bramhall et al. (2015) collected data using the QuickSin, and Liberman et al. (2016) used the widely available NU6 words within a custom hearing-in-noise test which included the addition of time compression and reverberation to NU6 words to increase the difficulty of the standardized test. There is a need for standardized, quantitative speech-in-noise performance data; as background noise levels increase, every participant (and patient) will have relatively increased difficulty understanding speech in background noise at some point. Some people may qualitatively rate their difficulties as more significant than others, even if their quantitative speech-in-noise test scores (and actual performance in real-world noise backgrounds) are equivalent. In other words, someone who self-reports difficulty understanding speech in noise, but has normal hearing thresholds and normal speech-in-noise test scores, may be functionally equivalent to others who do not report as much difficulty. Thus, a normal hearing person who self-reports difficulty understanding speech in noisy backgrounds may not necessarily have an abnormality or pathology (i.e., they may have normal hearing and speech-in-noise test scores), but could instead have different expectations regarding their performance across listening environments of varying difficulty (e.g., a one on one conversation in a co-worker's office vs. happy hour drinks with half the office staff at a busy restaurant). Such cases may potentially result in an opportunity for counseling of realistic speech-in-noise expectations and listening strategies, rather than a diagnosis of auditory dysfunction. The challenges of rehabilitation of deficits when patients do not meet the criteria for amplification were recently discussed by Kraus and White-Schwoch (2016), in their discussion of “Not-So-Hidden” Hearing Loss. This challenge of self-assessed perceptual difficulty directly parallels challenges related to the issue of tinnitus, as the self-assessed “bothersomeness” of tinnitus varies significantly from patient to patient, with no clear relationship to psychophysical parameters determined during pitch or level matching (for additional discussion, see Le Prell and Lobarinas, 2016).

There is an urgent need for validated, clinical tests that can be used to quantify patient self-report of difficulty understanding speech in noisy backgrounds. The ideal test will be sensitive to differences in performance within normal hearing listeners. For the WIN, a change of 3.5 dB-S/B (corresponding to a difference of approximately 4 words out of the 35 words presented) has been described as clinically meaningful (Wilson and McArdle, 2007). Many individual participants had changes of at least 4 words the day after noise exposure (Figure 5A), but not 1-week later (Figure 5E). The WIN should be considered for use in future studies not only based on the availability of the validated test as part of the NIH Toolbox (Zecker et al., 2013), but also based on the sensitivity of the test to acute, noise-induced changes in study participants. It may be the case that even greater sensitivity could be achieved in tests completed with higher background noise levels, or perhaps modifications (such as those of Liberman et al., 2016) that more appropriately reflect and reproduce the difficult listening environments found in real-world noisy and reverberative environments, such as restaurants, gymnasiums, bars, clubs, and other common venues with significant background noise.

The second part of this investigation was a prospective study measuring changes in audiologic function after new, acute recreational noise exposure. Audiometric, electrophysiological, and functional measures were monitored subsequent to noise exposure. There was no evidence that common recreational exposures resulted in permanent audiometric, functional, or electrophysiological deficits. Selective cochlear synaptopathy, resulting in an accompanying reduction in ABR Wave-I amplitude, has been clearly demonstrated in animals in association with noise exposures that induce a robust TTS the day after the noise exposure (for reviews, see Kujawa and Liberman, 2015; Liberman and Kujawa, 2017). The common, real-world recreational noise exposures that our participants experienced at concerts, multi-day music festivals, loud bars, etc. (see Figure 3), did not result in robust TTS the day after the exposure (most TTS < 15 dB, see Figure 8), nor did they result in decreases in AP amplitude (see Figure 7). Thus, they did not produce any evidence that would be interpreted as consistent with new, noise-induced cochlear synaptopathy following common, recreational noise exposure.

TTS was highly variable across individuals, which is a major challenge for studies such as these. The variability in TTS was consistent with that reported by others, as individual variability is significant after free-field exposures (Mills et al., 2001; Strasser et al., 2003) as well as controlled exposures delivered via personal music player devices (Le Prell et al., 2012, 2016; Kil et al., 2017). Across music player studies, a 100% noise dose (based on 29 CFR 1910.95) has resulted in highly variable TTS across participants, ranging from 0 dB to approximately 20 dB at 4 kHz, but with largely complete recovery the following day. Most, if not all, assessments of the effects of recreational noise have been completed immediately post exposure, with changes frequently being on the order of 8–10 dB as participants exit concerts (Opperman et al., 2006; Derebery et al., 2012; Ramakers et al., 2016) or clubs (Kramer et al., 2006); thus, the current data contribute further insight to the potential for changes in audiologic function the day after recreational exposure.

Our study found no statistically significant reduction in AP amplitude the day after exposure to common, loud, recreational events (see Figure 7). Although some participants had TTS exceeding typical test-retest of ±5 dB, there were no statistically significant relationships between changes in audiometric threshold sensitivity and noise dose (see Figure 4). There was a temporary statistically significant decrease in performance on the WIN test as a function of noise exposure in the overall analysis the day after the noise exposure (see Figure 5A), and for a small number of participants, the temporary deficits met the definition of clinically significant decrease in performance. However, due to a lack of a statistically significant decrease in either DPOAE amplitude (see Figure 6) or AP amplitude (see Figure 7) as a function of increasing noise exposure, it is not possible to directly attribute changes in performance on the WIN to specific OHC or synaptic injuries. It is possible to speculate that OHC injuries are more likely to underlie changes in performance on the WIN, based on the decreasing DPOAE amplitude at 6 kHz that was observed with increasing TTS (see Figure 8I), but these changes were limited to one frequency and it is not clear why 3 and 4 kHz failed to show similar noise-induced changes.

All of the evidence from animal models to date indicates that if noise-induced synaptopathy develops, it is immediate, and it is permanent. Thus, data from this prospective study showing temporary noise-related changes in performance on the WIN, in the absence of relationships between noise-exposure and changes in DPOAE and AP amplitude the day after noise exposure, cannot be interpreted as consistent with or otherwise suggesting synaptopathic damage in these human participants. In live human participants, cochlear synaptopathy cannot be directly measured, as synapse counts require ex vivo extraction of the temporal bone. The only direct evidence of synaptopathy in human cochlear tissues comes from Viana et al. (2015), who provided preliminary evidence of an age-related synaptopathy based on differences across five temporal bones. Those data are supplemented by Makary et al. (2011), who documented an age-related decrease in spiral ganglion survival which could be secondary to an age-related loss of their synaptic targets. Temporal bones may be a resource for new tissues, but unfortunately, noise history data are not always available for these tissues.

Human studies to date have generally relied on the amplitude of ABR Wave-I or the AP as an indirect proxy for potential synaptopathy (Stamper and Johnson, 2015a,b; Liberman et al., 2016; Bramhall et al., 2017; Prendergast et al., 2017; Spankovich et al., 2017; Fulbright et al., in press). ABR Wave-I amplitude has been highly correlated with synaptopathy in the animal studies thus far (Liberman and Kujawa, 2017); however, ABR measurements in anesthetized animals are much “cleaner” than ABR measurements in awake, resting humans.

At this time, there are no functional consequences that have been reliably associated with decreases in ABR Wave-I amplitude in normal hearing listeners. Bramhall et al. (2015) showed a statistically significant relationship between ABR Wave-I amplitude and performance on the QuickSin, but only in the presence of overt hearing loss; no statistically significant relationship was demonstrated between ABR Wave-I amplitude and performance on the QuickSin in participants with normal hearing. Data from rats showed that the functional deficits associated with decreases in ABR Wave-I amplitude were limited to the frequencies at which ABR Wave-I amplitude was decreased, and functional deficits were observed only in the most difficult listening condition (poorest signal to noise ratio) tested (Lobarinas et al., 2017). Although it is not clear how directly these results will translate to humans, it remains reasonable to hypothesize that speech-in-noise tests have the potential to reveal noise-induced deficits prior to the development of overt hearing loss in humans.

There are a variety of suggestions for other electrophysiological and psychophysical tools that might be considered for detection of hidden hearing loss in humans; various proposed metrics include the envelope following response (EFR) (Shaheen et al., 2015; Paul et al., 2017), middle ear muscle reflex (Valero et al., 2016), psychophysical manipulation of amplitude modulation in detection tasks (Paul et al., 2017), ABR Wave-V latency changes during forward masking (Mehraei et al., 2017), and binaural detection (Bernstein and Trahiotis, 2016). There are also suggestions to consider normalizing the amplitude of ABR Wave-I relative to the amplitude of ABR Wave-V (a measure of central response that does not appear to be affected by synaptopathy) (Verhulst et al., 2016), or relative to the amplitude of the summating potential (i.e., SP/AP ratio) (Liberman et al., 2016).

The argument that the SP/AP ratio is useful in revealing selective neural damage is based on the premise that SP is dominated by the OHC receptor potential (which is not expected to be affected by damage to the IHC/AN synapses), whereas AP is generated by the cochlear nerve. Early work by Durrant et al. (1998) attempted to resolve controversy over the relative contributions of the IHC and OHC populations to the SP; they concluded that while the OHCs made a significant contribution, the IHCs had a relatively greater contribution to the SP. Additional arguments that SP is appropriate for use normalizing AP are based on the observation that SP is more stable than AP after a variety of insults (for discussion see Liberman et al., 2016). However, the stability of SP may, in part, rely on the use of stimuli that are matched with respect to sensation level (i.e., the dB amount above individual threshold), as SP amplitude was constant across mice only when signal levels were equal sensation level (Sergeyenko et al., 2013). Furthermore, we point to data from Nam and Won (2004), who measured SP and AP after inducing TTS in human participants. They found that SP amplitude increased, but AP amplitude was unchanged, resulting in an increase in the SP/AP ratio. This finding parallels the increase in SP reported by Liberman et al. (2016) and, like Liberman et al. (2016), evidenced noise-induced changes in the SP/AP ratio to be driven by increased SP amplitude. If the SP is the measure relatively more affected by noise exposure, then the AP is essentially being normalized against a moving target, which seems counter-intuitive to the identification of selective neural deficits. Taken together, the noise-induced changes in SP and corresponding changes in SP/AP ratio (given that AP was unchanged) in those studies may be more appropriately interpreted as consistent with OHC based dysfunction, rather than synaptic neural dysfunction. Increasing OHC dysfunction as a function of increasing TTS was detected here (at least at 6 kHz), and noise-induced OHC dysfunction would be consistent with new work from Hoben et al. (2017) which importantly suggests that OHC loss or dysfunction may drive speech-in-noise deficits. Of note, the SP waveform is generally more difficult to resolve (Roland and Roth, 1997), and is highly variable across normal hearing listeners (Ferraro et al., 1994). In the current study, SP data were collected, as per the methods section, to permit calculation of SP/AP ratios following Liberman et al. (2016). Approximately 45% of the right and left ears had scorable SPs across the stimulus conditions. We initially included this ratio in the retrospective regression models, and found no statistically significant relationships detected for the subset of participants with reliable SPs. However, based on the above general concerns regarding the use of SP/AP ratios to identify selective neural damage, we did not assess potential changes in this ratio as a function of acute recreational noise exposure. Regardless, there was no relationship between AP amplitude and retrospective noise history (Figure 2), AP amplitude and acute recreational noise exposure (Figure 7), or change in AP amplitude and maximum observed TTS (Figure 8).

Other approaches that have been presented at recent scientific meetings include the normalization of ABR Wave-I amplitude for 4 kHz signals relative to ABR Wave-I amplitude for 1 kHz signals (Earl et al., 2017), and ABR Wave-I latency based comparisons instead of amplitude based comparisons (Skoe et al., 2017). As these different metrics and measures make their way through the peer-review process, it will hopefully become possible to begin to define the most informative strategies for those seeking evidence of hidden hearing loss in humans. If metrics selected for use in future studies include high level tone pips, some caution may be warranted with respect to interpretation of the frequency-specific effects; it is possible that high level tone bursts will activate relatively broader regions of the cochlea, perhaps even resembling the response to a click stimulus. The lack of agreed on metrics is clearly a major issue for translational human studies on hidden hearing loss (Le Prell and Lobarinas, 2016; Hickox et al., 2017; Kobel et al., 2017; Liberman and Kujawa, 2017).

The current investigation provided no evidence of noise-induced decreases in human AP amplitude in the retrospective analyses of noise exposure history, nor in the prospective analyses following common recreational noise exposure. The current data indicate that intra-participant changes in AP (ABR Wave-I) amplitude can be reliably monitored longitudinally; response waveforms were reliable and repeatable within individual participants, within and across sessions.

In animal models, the gold standard for identification of cochlear synaptopathy is the post-mortem counting of synaptic ribbons. Reductions in synapse count are highly correlated with the amplitude of Wave-I of the ABR (Sergeyenko et al., 2013). Liberman and Kujawa (2017) have therefore suggested that when DPOAE amplitude has returned to baseline (after noise exposure), or has not yet deteriorated (in the case of aging), the amplitude of ABR Wave-I is highly predictive of cochlear synaptopathy. In humans, there is a search for supra-threshold evoked potential metrics that will be sensitive to and specific for cochlear synaptopathy. The clinical (i.e., functional, “real-world”) relevance of reduced ABR Wave-I amplitude (AP amplitude) remains to be determined, despite much speculation. Even if a permanent noise-induced reduction of human ABR Wave-I amplitude is found following noise exposure in human participants, a meaningful, real-world functional effect must be identified in order for the ABR Wave-I amplitude reduction to serve as a clinically relevant finding in audiology. Here, the correlation analyses revealed a statistically significant relationship between noise dose/TWA and change in performance on the WIN, with statistically significant growth in deficits as TWA increased. For the majority of the participants, the individual noise-induced changes in WIN performance were small (1–3 word deficits at the test session the day after recreational noise exposure) but there were some participants with deficits of 4–6 words, which meets the criteria set by Wilson and McArdle (2007) for clinically significant change.

To be successful in the identification of noise-induced synaptopathic deficits in humans, it may ultimately be the case that future studies will need to include human populations exposed to noise insults that result in the magnitude of TTS minimally necessary to observe synaptopathic injury in animals. Such TTS changes appear to be unlikely to be produced from common recreational noise exposure, but are perhaps likely to be observed within military cohorts or safety officers, based on the data of Bramhall et al. (2017). Weapons training may provide more controlled access to noise-exposed participants, but enrollment in hearing conservation studies can influence the use of hearing protection devices (HPDs) that prevent the deficits of interest (see for example Le Prell et al., 2011). Regardless of the boundary at which risk begins, or the specific relationship between TTS and “hidden hearing loss,” it may ultimately prove difficult to identify a human cohort exposed to noise that is loud enough and long enough to cause neural damage, but leaves OHC function unaltered. This specific challenge was recently discussed in detail by Hickox et al. (2017), who point to the prevalence of mixed pathologies in human populations. A major remaining unknown is the extent to which repetition of noise exposure has the potential to result in a synaptopathic injury over time if smaller TTS changes are induced at each exposure (for additional discussion see Dobie and Humes, 2017; Murphy and Le Prell, 2017).

It is possible to imagine changes in conventional test batteries and/or metrics used for monitoring the effects of noise exposure if there were both compelling evidence of ABR Wave-I amplitude changes and accompanying functional deficits following noise exposure. Further research will be needed to more carefully assess the effects of noise exposures that have the potential to result in more severe TTS. Ethical practices for educating participants about the potential for auditory injury will need to be carefully considered, as per the recent commentary on TTS studies by Maison and Rauch (2017). Participants should be provided with HPDs if the investigator has reason to believe that the participant may be at risk for acoustic trauma resulting in permanent functional changes on threshold or suprathreshold measures of function. Such studies will also need to carefully assess OHC function and threshold sensitivity (including EHF threshold assessment) in order to systematically differentiate between OHC damage and potential neural synaptic damage, and document both overt and relatively more hidden supra-threshold hearing deficits.

This study was carried out in accordance with the recommendations of the Institutional Review Board at the University of Texas at Dallas with written informed consent from all subjects. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocol was approved by the Institutional Review Board at the University of Texas at Dallas.

SG: contributed to study design, data collection, data interpretation, and writing the manuscript. KW: contributed to study design, data collection, statistical analysis, data interpretation, and writing the manuscript. JB: contributed to study design, data collection, data interpretation, and reviewed the manuscript. CL: contributed to study design, statistical analysis, data interpretation, and writing the manuscript.