Effects Of Noise-induced Hearing Loss Research Articles

The effects of acute and chronic noise trauma on stimulus-evoked activity across primary auditory cortex layers.

Exposure to intense noise environments is a major cause of sensorineural hearing loss and auditory perception disorders, such as tinnitus and hyperacusis, which may have a central origin. The effects of noise-induced hearing loss on the auditory cortex have been documented in many studies. One limitation of these studies, however, is that the effects of noise trauma have been mostly studied at the granular layer (i.e, the main cortical recipient of thalamic input), while the cortex is a very complex structure, with six different layers each having its own pattern of connectivity and role in sensory processing. The present study aims to investigate the effects of acute and chronic noise trauma on the laminar pattern of stimulus-evoked activity in the primary auditory cortex of the anesthetized guinea pig. We show that acute and chronic noise trauma are both followed by an increase in stimulus-evoked cortical responses, mostly in the granular and supragranular layers. The cortical responses are more monotonic as a function of the intensity level after noise trauma. There was minimal change, if any, in local field potential (LFP) amplitude after acute noise trauma, while LFP amplitude was enhanced after chronic noise trauma. Finally, LFP and the current source density analysis suggest that acute but more specifically chronic noise trauma is associated with the emergence of a new sink in the supragranular layer. This result suggests that supragranular layers become a major input recipient. We discuss the possible mechanisms and functional implications of these changes.NEW & NOTEWORTHY Our study shows that cortical activity is enhanced after trauma and that the sequence of cortical column activation during stimulus-evoked response is altered, i.e. the supragranular layer becomes a major input recipient. We speculate that these large cortical changes may play a key role in the auditory hypersensitivity (hyperacusis) that can be triggered after noise trauma in human subjects.

Noise-induced hearing loss reduces inhibitory neurotransmitter synthesis in ventral hippocampus and contributes to the social memory deficits of mice

Despite affecting over 1.5 billion people globally, hearing loss (HL) has been referred to as an “invisible disability”, with noise exposure being a major causative factor. Accumulating evidence suggests that HL can induce cognitive impairment. However, relatively little is known about the effects of noise-induced hearing loss (NIHL) on social memory. This study aimed to further investigate the effect of NIHL on social behaviours in mice. We established a rodent model of NIHL using 4-week-old C57BL/6J mice who experienced narrow noise exposure at 116 dB for 3 h per day over two consecutive days. Hearing ability was subsequently evaluated through auditory brainstem response (ABR) testing, and potential changes in the morphology of cochlear hair cells were assessed using immunofluorescence. The sociability and social memory of the mice were evaluated using the three-chamber social interaction test. Noise exposure resulted in complete and persistent HL in C57BL/6J mice, accompanied by severe loss of cochlear hair cells. More importantly, social memory was impaired in adult NIHL mice, whereas their sociability remained intact, these changes were accompanied by a decrease in the protein levels of the inhibitory neuron marker glutamic acid decarboxylase 67 (GAD67) in the ventral hippocampus. This study is the first to confirm that long-term auditory deprivation from HL induced by noise exposure results in social memory deficits in mice without altering their sociability.

Investigation of the Relationship Between Noise-Induced Hearing Loss and Metabolic Syndrome in One of the Oil Industries in the South of Iran.

Investigating the non-auditory effects of noise on humans has been of interest from different aspects. In this study, the relationship between noise-induced hearing loss (NIHL) and metabolic syndrome. This cross-sectional study was performed on 1380 male workers of one of the oil and gas companies in the south of Iran. The data was obtained via clinical examination and hearing status assessment to evaluate the metabolic syndrome and its components, intravenous blood samples were taken and tested according to NCEPATPIII criteria. For statistical analysis, the data were analyzed using SPSS software version 25 at a significant level of 0.05. The results showed that the body mass index variable increased the chance of developing metabolic syndrome by 11.4%. NIHL increases the chance of developing metabolic syndrome (OR = 1.291). Also, the same results were observed in hypertriglyceridemia OR = 1.255, waist circumference (OR = 1.163), fasting blood sugar (OR = 1.159), blood pressure (OR = 1.068) and HDL (OR = 1.051). Considering the effect of NIHL on metabolic syndrome, it is possible to help reducing the incidence of metabolic syndrome and any of its components by controlling noise exposure and accordingly reducing non-auditory injuries to individuals.

High-Frequency Audiometry for Early Detection of Hearing Loss: A Narrative Review.

The WHO considers hearing loss to be a major global problem. A literature search was conducted to see whether high-frequency audiometry (HFA) could be used for the early detection of hearing loss. A further aim was to see whether any differences exist in the hearing threshold using conventional audiometry (CA) and HFA in workers of different age groups exposed to workplace noise. Our search of electronic databases yielded a total of 5938 scientific papers. The inclusion criteria were the keywords “high frequency” and “audiometry” appearing anywhere in the article and the participation of unexposed people or a group exposed to workplace noise. Fifteen studies met these conditions; the sample size varied (51–645 people), and the age range of the people studied was 5–90 years. Commercial high-frequency audiometers and high-frequency headphones were used. In populations unexposed to workplace noise, significantly higher thresholds of 14–16 kHz were found. In populations with exposure to workplace noise, significantly higher statistical thresholds were found for the exposed group (EG) compared with the control group (CG) at frequencies of 9–18 kHz, especially at 16 kHz. The studies also showed higher hearing thresholds of 10–16 kHz in respondents aged under 31 years following the use of personal listening devices (PLDs) for longer than 5 years. The effect of noise-induced hearing loss (NIHL) first became apparent for HFA rather than CA. However, normative data have not yet been collected. Therefore, it is necessary to establish a uniform evaluation protocol accounting for age, sex, comorbidities and exposures, as well as for younger respondents using PLDs.

Effectiveness of Hearing Loss Prevention Education for Active Duty Military Personnel: A Preliminary Study

Purpose The combination of effective hearing health education and hearing protection establishes a strong foundation of hearing loss prevention efforts in the military; however, it is not clear which elements of the educational materials used in hearing loss prevention programs are the most effective in preventing noise-induced hearing loss. To explore this question, a cohort of Excellence in Government Fellowship participants and the Army Hearing Program conducted a preliminary study examining two hearing health education materials. Method A convenience sample of active duty personnel reviewed a hearing health education Technical Guide and video, developed by the military for hearing conservation programs. A “pre- and posteducation” questionnaire was administered to assess the participants' knowledge regarding hearing protection, causes of noise-induced hearing loss, effects of noise on hearing, noise exposure both on and off duty, and satisfaction with educational materials provided during the session. Results Short-term learning effects from the educational materials was achieved for some knowledge-based items (> 10% change from pre-education to posteducation), particularly for questions related to the effect of noise-induced hearing loss on ability to hear speech or hear at a distance. Thirty five percent of study participants reported using hearing protection in hazardous noise 75%–100% of the time. Primary reason for not using hearing protection was comfort. Conclusions Despite hearing loss prevention efforts in the military, hearing loss and tinnitus (ringing in the ears) continue to be prevalent service-connected disabilities among veterans. This study offers some insights regarding current hearing loss prevention understanding and practices for a group of active duty U.S. military personnel. Results from this study can inform future improvements in military hearing loss prevention education.

Paired measurements of cochlear function and hair cell count in Dutch-belted rabbits with noise-induced hearing loss

The effects of noise-induced hearing loss have yet to be studied for the Dutch-belted strain of rabbits, which is the only strain that has been used in studies of the central auditory system. We measured auditory brainstem responses (ABRs), 2f1−f2 distortion product otoacoustic emissions (DPOAEs), and counts of cochlear inner and outer hair cells (IHCs and OHCs, respectively) from confocal images of Myo7a-stained cochlear whole-mounts in unexposed and noise-overexposed, Dutch-belted, male and female rabbits in order to characterize cochlear function and structure under normal-hearing and hearing-loss conditions. Using an octave-band noise exposure centered at 750 Hz presented under isoflurane anesthesia, we found that a sound level of 133 dB SPL for 60 min was minimally sufficient to produce permanent ABR threshold shifts. Overexposure durations of 60 and 90 min caused median click-evoked ABR threshold shifts of 10 and 50 dB, respectively. Susceptibility to overexposure was highly variable across ears, but less variable across test frequencies within the same ear. ABR and DPOAE threshold shifts were smaller, on average, and more variable in male than female ears. Similarly, post-exposure survival of OHCs was higher, on average, and more variable in male than female ears. We paired post-exposure ABR and DPOAE threshold shift data with hair cell count data measured in the same ear at the same frequency and cochlear frequency location. ABR and DPOAE threshold shifts exhibited critical values of 46 and 18 dB, respectively, below which the majority of OHCs and IHCs survived and above which OHCs were wiped out while IHC survival was variable. Our data may be of use to researchers who wish to use Dutch-belted rabbits as a model for the effects of noise-induced hearing loss on the central auditory system.

Effects of noise-induced hearing loss on speech-in-noise envelope coding: Inferences from single-unit and non-invasive measures in animals

Speech-intelligibility models (SIM) can be used for systematic fitting of hearing-aids and cochlear-implants, potentially improving clinical outcomes in noisy environments. Existing SIMs are suitable for predicting performance of normal-hearing subjects, but not for hearing-impaired subjects due to our limited understanding of the effects of cochlear hearing impairment on speech-in-noise coding. In this work, we collected auditory-nerve (AN) single-unit responses and envelope following responses (EFR) in normal- and hearing-impaired chinchillas to speech, spectrally-matched stationary-noise, and noisy-speech. Our data show increased correlation between AN-fiber response envelopes of noisy-speech and noise-alone for hearing-impaired fibers in speech-relevant modulation-frequency bands, suggesting a greater degree of distraction from inherent envelope fluctuations following cochlear hearing loss. This novel finding is significant given the emphasis recent SIMs [e.g., Jørgensen and Dau, JASA (2011)] have placed on the importance of inherent noise-envelope fluctuations in addition to speech-coding fidelity in predicting noisy-speech perception. Preliminary data also show enhanced fundamental-periodicity coding at the expense of place-specific formant coding, and a degradation of burst envelopes of high-frequency fricatives for the hearing-impaired group. EFRs show evidence for degraded tonotopic coding, as observed in single-unit responses [e.g., Henry et al., J. Neurosci. (2016)]. [Work supported by Action on Hearing Loss (UK).]

Knowledge, attitude, and practice of printing press workers towards noise-induced hearing loss.

Context:Noise-induced hearing loss (NIHL) is considered as a common occupational hazard among the industrial workers. The printing press is one of the common industrial set up where noise levels are often high. The awareness of people working in such a setup is generally less towards the hazards that is caused by noise exposure.Aim:The current study was designed to identify the knowledge, attitude, and practice (KAP) of printing press workers towards NIHL.Settings and Design:Cross-sectional study was carried using an adapted and validated KAP questionnaire. It was administered on 57 workers in Thiruvananthapuram, Kerala.Methods and Material:The study was carried out in two phases: phase I included the adaptation and validation of KAP questionnaire to printing press workers. Phase II comprised of the administration of the questionnaire among the study population. Statistical analysis used: Descriptive statistics was used to compile the results. To measure the internal consistency Cronbach’s alpha scale was used.Results:The responses obtained from workers showed inadequate knowledge, negative attitudes in certain subdomains and poor practice.Conclusions:The findings from the present study sheds light on the dearth of awareness in printing press workers on hearing conservation and need of training programs to educate the printing press workers towards the effects of NIHL.

Effects of noise-induced hearing loss on parvalbumin and perineuronal net expression in the mouse primary auditory cortex

Noise induced hearing loss is associated with increased excitability in the central auditory system but the cellular correlates of such changes remain to be characterized. Here we tested the hypothesis that noise-induced hearing loss causes deterioration of perineuronal nets (PNNs) in the auditory cortex of mice. PNNs are specialized extracellular matrix components that commonly enwrap cortical parvalbumin (PV) containing GABAergic interneurons. Compared to somatosensory and visual cortex, relatively less is known about PV/PNN expression patterns in the primary auditory cortex (A1). Whether changes to cortical PNNs follow acoustic trauma remains unclear. The first aim of this study was to characterize PV/PNN expression in A1 of adult mice. PNNs increase excitability of PV+ inhibitory neurons and confer protection to these neurons against oxidative stress. Decreased PV/PNN expression may therefore lead to a reduction in cortical inhibition. The second aim of this study was to examine PV/PNN expression in superficial (I-IV) and deep cortical layers (V-VI) following noise trauma. Exposing mice to loud noise caused an increase in hearing threshold that lasted at least 30 days. PV and PNN expression in A1 was analyzed at 1, 10 and 30 days following the exposure. No significant changes were observed in the density of PV+, PNN+, or PV/PNN co-localized cells following hearing loss. However, a significant layer- and cell type-specific decrease in PNN intensity was seen following hearing loss. Some changes were present even at 1 day following noise exposure. Attenuation of PNN may contribute to changes in excitability in cortex following noise trauma. The regulation of PNN may open up a temporal window for altered excitability in the adult brain that is then stabilized at a new and potentially pathological level such as in tinnitus.

Armed and Exposed

Armed and Exposed

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

The effects of intense noise exposure on the classical auditory pathway have been extensively investigated; however, little is known about the effects of noise-induced hearing loss on non-classical auditory areas in the brain such as the lateral amygdala (LA) and striatum (Str). To address this issue, we compared the noise-induced changes in spontaneous and tone-evoked responses from multiunit clusters (MUC) in the LA and Str with those seen in auditory cortex (AC) in rats. High-frequency octave band noise (10–20kHz) and narrow band noise (16–20kHz) induced permanent threshold shifts at high-frequencies within and above the noise band but not at low frequencies. While the noise trauma significantly elevated spontaneous discharge rate (SR) in the AC, SRs in the LA and Str were only slightly increased across all frequencies. The high-frequency noise trauma affected tone-evoked firing rates in frequency and time-dependent manner and the changes appeared to be related to the severity of noise trauma. In the LA, tone-evoked firing rates were reduced at the high-frequencies (trauma area) whereas firing rates were enhanced at the low-frequencies or at the edge-frequency dependent on severity of hearing loss at the high frequencies. The firing rate temporal profile changed from a broad plateau to one sharp, delayed peak. In the AC, tone-evoked firing rates were depressed at high frequencies and enhanced at the low frequencies while the firing rate temporal profiles became substantially broader. In contrast, firing rates in the Str were generally decreased and firing rate temporal profiles become more phasic and less prolonged. The altered firing rate and pattern at low frequencies induced by high-frequency hearing loss could have perceptual consequences. The tone-evoked hyperactivity in low-frequency MUC could manifest as hyperacusis whereas the discharge pattern changes could affect temporal resolution and integration.

Neurophysiological effects of noise-induced hearing loss

Noise over-exposure is known to cause sensorineural hearing loss (SNHL) through damage to sensory hair cells and subsequent cochlear neuronal loss. These same histopathological changes can result from other etiological factors (e.g., aging, ototoxic drugs). Audiologically, each is currently classified as SNHL, despite differences in etiology. Functionally, noise-induced hearing loss can differ significantly from other SNHL etiologies; however, these differences remain hidden from current audiological diagnostic tests. For example, noise-induced mechanical damage to stereocilia on inner- and outer-hair cells results in neurophysiological responses that complicate the common view of loudness recruitment. Also, mechanical effects of noise overexposure appear to affect the tip-to-tail ratio of impaired auditory-nerve-fiber tuning curves in ways that create a much more significant degradation of the cochlear tonotopic representation than does a metabolic form of age-related hearing loss. Even temporary threshold shifts due to moderate noise exposure can cause permanent synaptic loss at inner-hair-cell/auditory-nerve-fiber synapses, which reduces neural-coding redundancy for complex sounds and likely degrades listening in background noise. These pathophysiological results suggest that novel diagnostic measures are now required to dissect the single audiological category of SNHL to allow for better individual fitting of hearing aids to restore speech intelligibility in real-world environments. [Work supported by NIH.]

Prestin Regulation and Function in Residual Outer Hair Cells after Noise-Induced Hearing Loss

The outer hair cell (OHC) motor protein prestin is necessary for electromotility, which drives cochlear amplification and produces exquisitely sharp frequency tuning. TectaC1509G transgenic mice have hearing loss, and surprisingly have increased OHC prestin levels. We hypothesized, therefore, that prestin up-regulation may represent a generalized response to compensate for a state of hearing loss. In the present study, we sought to determine the effects of noise-induced hearing loss on prestin expression. After noise exposure, we performed cytocochleograms and observed OHC loss only in the basal region of the cochlea. Next, we patch clamped OHCs from the apical turn (9–12 kHz region), where no OHCs were lost, in noise-exposed and age-matched control mice. The non-linear capacitance was significantly higher in noise-exposed mice, consistent with higher functional prestin levels. We then measured prestin protein and mRNA levels in whole-cochlea specimens. Both Western blot and qPCR studies demonstrated increased prestin expression after noise exposure. Finally, we examined the effect of the prestin increase in vivo following noise damage. Immediately after noise exposure, ABR and DPOAE thresholds were elevated by 30–40 dB. While most of the temporary threshold shifts recovered within 3 days, there were additional improvements over the next month. However, DPOAE magnitudes, basilar membrane vibration, and CAP tuning curve measurements from the 9–12 kHz cochlear region demonstrated no differences between noise-exposed mice and control mice. Taken together, these data indicate that prestin is up-regulated by 32–58% in residual OHCs after noise exposure and that the prestin is functional. These findings are consistent with the notion that prestin increases in an attempt to partially compensate for reduced force production because of missing OHCs. However, in regions where there is no OHC loss, the cochlea is able to compensate for the excess prestin in order to maintain stable auditory thresholds and frequency discrimination.

Sensorineural hearing loss amplifies neural coding of envelope information in the central auditory system of chinchillas

People with sensorineural hearing loss often have substantial difficulty understanding speech under challenging listening conditions. Behavioral studies suggest that reduced sensitivity to the temporal structure of sound may be responsible, but underlying neurophysiological pathologies are incompletely understood. Here, we investigate the effects of noise-induced hearing loss on coding of envelope (ENV) structure in the central auditory system of anesthetized chinchillas. ENV coding was evaluated noninvasively using auditory evoked potentials recorded from the scalp surface in response to sinusoidally amplitude modulated tones with carrier frequencies of 1, 2, 4, and 8 kHz and a modulation frequency of 140 Hz. Stimuli were presented in quiet and in three levels of white background noise. The latency of scalp-recorded ENV responses was consistent with generation in the auditory midbrain. Hearing loss amplified neural coding of ENV at carrier frequencies of 2 kHz and above. This result may reflect enhanced ENV coding from the periphery and/or an increase in the gain of central auditory neurons. In contrast to expectations, hearing loss was not associated with a stronger adverse effect of increasing masker intensity on ENV coding. The exaggerated neural representation of ENV information shown here at the level of the auditory midbrain helps to explain previous findings of enhanced sensitivity to amplitude modulation in people with hearing loss under some conditions. Furthermore, amplified ENV coding may potentially contribute to speech perception problems in people with cochlear hearing loss by acting as a distraction from more salient acoustic cues, particularly in fluctuating backgrounds.

The Effects of Noise-Induced Hearing Loss on Children and Young Adults

The Effects of Noise-Induced Hearing Loss on Children and Young Adults

Investigating the effects of noise-induced hearing loss on serotonin transporters in rat brain using 4-[18F]-ADAM/small animal PET

The serotonin transporter (SERT) is an important marker of the status of serotonergic neurons. The main function of SERT is to regulate the serotonin concentration in the synapse. Recent studies have shown that SERT is expressed in the central auditory pathway and may play a role in the auditory process. However, little is known about the effects of noise on the cerebral serotonin system. In this study, we explored the status of brain SERT in a rat model of noise-induced hearing loss using 4-[(18)F]-ADAM (a SERT imaging agent) and small animal positron emission tomography (PET) imaging. Male Sprague Dawley rats were exposed to an 8 kHz noise at 118 dB sound pressure level for 3.5h. An auditory brainstem response test and 4-[(18)F]-ADAM/small animal PET were performed at different time points after noise exposure. The specific uptake ratios (SURs) for 4-[(18)F]-ADAM were calculated from the PET imaging data in six brain regions. Immunohistochemistry and surface preparation of the cochleae were performed 30 days after noise exposure. Our data clearly showed that the hearing and cochlear outer hair cells of the rats were lost after noise exposure. In the PET study, the SURs of SERT were markedly reduced by 35%-58% in various brain regions one day after noise exposure. The decrement remained on days 8 and 15 and was approximately 26%-48% on day 29. The distribution and intensity of SERT immunostaining in the brain paralleled the PET imaging data. These results suggest that noise-induced hearing loss involves a reduction in SERT expression in various regions of the rat brain and that changes in SERT are detectable by 4-[(18)F]-ADAM/small animal PET in vivo.

Noise-induced hearing loss alters the temporal dynamics of auditory-nerve responses

Auditory-nerve fibers demonstrate dynamic response properties in that they adapt to rapid changes in sound level, both at the onset and offset of a sound. These dynamic response properties affect temporal coding of stimulus modulations that are perceptually relevant for many sounds such as speech and music. Temporal dynamics have been well characterized in auditory-nerve fibers from normal-hearing animals, but little is known about the effects of sensorineural hearing loss on these dynamics. This study examined the effects of noise-induced hearing loss on the temporal dynamics in auditory-nerve fiber responses from anesthetized chinchillas. Post-stimulus-time histograms were computed from responses to 50-ms tones presented at characteristic frequency and 30 dB above fiber threshold. Several response metrics related to temporal dynamics were computed from post-stimulus-time histograms and were compared between normal-hearing and noise-exposed animals. Results indicate that noise-exposed auditory-nerve fibers show significantly reduced response latency, increased onset response and percent adaptation, faster adaptation after onset, and slower recovery after offset. The decrease in response latency only occurred in noise-exposed fibers with significantly reduced frequency selectivity. These changes in temporal dynamics have important implications for temporal envelope coding in hearing-impaired ears, as well as for the design of dynamic compression algorithms for hearing aids.

Maritime offshore operations—occupational noise monitoring, assessment and control

With increasing emphasis on occupational health as a component of maritime safety case requirements for Australia, the National Offshore Petroleum Safety Authority (NOPSA), in keeping with their goal of improving health and safety outcomes across the industry, has ramped up their expectations on noise management plans (NMP). Now the expectation includes noise risk assessments and evaluation and implementation of feasible engineering noise controls, and NOPSA have added scrutiny of ototoxic substances as well, all of which parallel international trends. NOPSA surveys have found rather poor industry compliance with noise management requirements overall, and have stated that they will continue to promote the issues and will not hesitate to take enforcement action to improve compliance. Occupational noise induced hearing loss (NIHL) is 100% permanent and 100% preventable. Failing to prevent NIHL has significant human, economic, legal and operational impacts. NIHL results in diminished quality of life including isolation and communication problems that affect social interactions. The economic effects of NIHL include lost time and decreased productivity, loss of otherwise qualified and experienced workers through medical disqualification, workers’ compensation costs and disability settlements, retraining costs and expenses related to medical intervention and treatment. Noise-impaired communications affect workplace operational and health and safety performance, and noisy ship and maritime platform accommodations and common areas adversely affect staff comfort, fatigue, morale and general well-being.

Noise-Induced Hearing Loss in School-Age Children: What Do We Know?

An increasing number of children are exposed to louder sounds at younger ages, which may increase their risk for developing earlier and more severe noise-induced hearing losses. Factors that may be mediators or confounders of this noise exposure-hearing loss relationship include noise intensity and type, noise exposure incidences and duration, and individual susceptibility. The status of descriptive epidemiology in this area and the public health effects of noise-induced hearing loss are summarized. Results are analyzed using Hill's epidemiologic causal criteria. Longitudinal epidemiologic research is needed that will measure children's sound exposures and hearing outcomes within the same study to determine the extent of the problem and to improve understanding of possible causal pathways. In addition, hearing conservation programs need to be implemented more widely, and the programs' outcomes in increasing both knowledge and preventive behaviors need to be demonstrated in diverse locations. Some public policy health issues concerning prevention of noise-induced hearing loss in children are discussed.

Effects of Noise-Induced Hearing Loss at Young Age on Voice Onset Time and Gap-in-Noise Representations in Adult Cat Primary Auditory Cortex

Here we show that mild hearing loss induced by noise exposure in early age causes a decrease in neural temporal resolution when measured in adulthood. We investigated the effect of this chronic hearing loss on the representation of a voice onset time (VOT) and a gap-duration continuum in primary auditory cortex (AI) in cats, which were exposed at the age of 6 weeks to a 120-dB SPL, 5-kHz 1/3 octave noise band for 2 h. The resulting hearing loss measured using auditory brainstem responses and cortical multiunit thresholds at 4-6 months of age was 20-40 dB between 1 and 32 kHz. Multiple single-unit activity was recorded in seven noise-exposed cats and nine control cats related to the presentation of a/ba/-/pa/ continuum in which VOT was varied in 5-ms step from 0 to 70 ms. We also obtained data for noise bursts with gaps, of duration equal to the VOT, embedded in noise 5 ms after the onset. Both stimuli were presented at 65 dB SPL. Minimum VOT and early-gap duration were defined as the lowest value in which an on-response, significantly above the spontaneous activity, to both the leading and trailing noise bursts or vowel was obtained. The mild chronic noise-induced hearing loss increased the minimum detectable VOT and gap duration by 10 ms. We also analyzed the maximum firing rate (FRmax) and the latency of the responses as a function of VOT and gap duration and found a significant reduction in the FRmax to the trailing noise burst for gap durations above 50 ms. This suggests that mild hearing loss acquired in early age may affect cortical temporal processing in adulthood.