Impulse Noise Exposure Research Articles

Intratympanic administration of methylprednisolone reduces impact of experimental intensive impulse noise trauma on hearing

Conclusion. The present findings demonstrated that intratympanic methylprednisolone (MP) reduces the impact of impulse noise trauma on hearing and in part preserves the hair cells from death 1 h after exposure to intensive impulse noise. Objective. To examine the treatment efficiency of intratympanic MP (IT-MP) with different methods of administration on cochlear injury induced by exposure to intensive impulse noise. Materials and methods. Fifty-five guinea pigs were assigned into six groups and exposed to intensive impulse noise, i.e. 60 impulses at 165 dB SPL peak pressure with 0.5 ms duration and 2 s intervals. The auditory brainstem response (ABR) was used to examine the hearing thresholds. Cochlear morphology was examined to estimate the inner and outer hair cell loss induced by impulse noise exposure. MP was applied as a rescue agent via different modalities of administration. Results. The ABR threshold value of IT-MP1 or IT-MP4 groups significantly decreased at 4 weeks as compared with the IT-NS (IT 0.9% physiological saline) group. The ABR threshold value of the group that received intramuscular administration of MP (IM-MP) also decreased at 4 weeks as compared with the IT-NS group. Significant hair cell loss was observed at the region 40–50% from the apex in the present model. Within this region, the residual hair cell number in the IT-MP1 or IT-MP4 groups was significantly greater than that in the IT-NS group.

Ten-year longitudinal study of the effect of impulse noise exposure from gunshot on inner ear function

This longitudinal study investigated how chronic gunshot noise exposure affects cochlear and saccular function in police officers who engaged in regular target shooting practice using dual protection (ear plugs plus earmuffs) for >10 years. In 1997, 20 male police officers underwent audiometry before and two weeks after shooting. Twelve of the original subjects were re-examined by audiometry coupled with vestibular evoked myogenic potential (VEMP) test in 2007. Significant deterioration of mean hearing thresholds at frequencies of 500 Hz through 4000 Hz was noted ten years later, affecting both ears. However, only the frequencies of 4000 and 6000 Hz on the left ear revealed significant difference in mean hearing thresholds compared with healthy controls. Abnormal VEMP responses were evident in nine police officers (75%), including absent VEMPs 7 and delayed VEMPs 2. In conclusion, deterioration to hearing may occur after long term exposure to gunshots, even when double hearing protection is used. Further study is in progress regarding how to preserve both cochlear and saccular function during long term gunshot exposure.

Estimates of the auditory risk from outdoor impulse noise I: Firecrackers

Firecrackers are common impulse noise exposures in the United States. In this study, impulses produced outdoors by consumer firecrackers were recorded, described, and analyzed with respect to the amount of the auditory risk they pose to the unprotected listener under various listening conditions. Risk estimates were obtained using three contemporary damage risk criteria (DRC), including a waveform parameter-based approach (peak SPL and B duration), an energy-based criterion (A-weighted sound exposure level and equivalent continuous level), and a physiological model (the AHAAH model developed by Price and Kalb). Results from these DRC were converted into numbers of maximum permissible unprotected exposures to facilitate comparison. Acoustic characteristics of firecracker impulses varied with the distance, but only subtle differences were observed across firecrackers. Typical peak levels ranged between 171 dB SPL at 0.5 m and 142 dB SPL at 8 m. Estimates of the auditory risk did not differ significantly across firecrackers, but varied with the distance. Vast differences in maximum permissible exposures were observed, and the directions of the differences varied with the level of the impulse. Typical estimates of maximum permissible exposures ranged between 0 and 2 at 0.5 m and between 31 and 227,000 at 8 m. Unprotected exposures to firecracker impulses should be limited or avoided entirely if the firecrackers are ignited in batches within 8 m of the listener. Differences across DRC are inconsequential at 0.5 m, but have substantial implications at distances of 1 m and more.

Comparison of impulse noise damage risk criteria using the Albuquerque blast overpressure walkup study data

The 1968 CHABA recommendations to limit impulsive noise exposure to levels below 140 dB SPL form the basis of current United States occupational and military standards. The U.S. military standard, MIL‐STD‐1474D, estimates the number of allowable shots to which a person may be exposed using peak level, B‐duration, for varying levels of hearing protection usage. The European Union upper limit peak exposure action level is 137 dB C‐weighted for the unprotected ear and 140 dB C‐weighted for the protected ear. The U.S. Army blast overpressure studies in the early 1990's investigated the effects on the hearing of soldier subjects of simulated weapon blasts with varied levels and A‐durations. The hearing thresholds of the subjects were tested before and after exposure to blasts. Exposures ranged from 6 shots to 100 shots per day and levels from 173 to 195 dB peak SPL. As judged by information criteria (AIC, BIC), the LAeq8 index with unprotected data yielded the best fit to logistic models; all the indices produ...

Recovery of distortion product otoacoustic emissions (DPOAE) after impulse vs. continuous equal‐energy exposures

The correct assessment of impulse noise from occupational environments for hearing‐conservation purposes is still a controversial issue. Currently, no universally accepted standard defines impulse noise accurately nor does a standard method exist to measure impulses. Moreover, current impulse‐damage risk‐criteria suffer from lack of empirical data needed to quantify impulse noise exposures and assess potential damage. In this experiment human subjects are exposed to binaural recordings of noises from industrial environments. Stimuli consist of impulse noise, continuous noise, and combinations of impulse and continuous noise. Noise exposures are normalized to have the same energy (LAeq,8h= 80dB). The effects in the hearing of the subjects are monitored by measuring the recovery of the distortion product otoacoustic emissions (DPOAE) with high‐time resolution. The results can be used to investigate the validity of current assessment methods and descriptors of the temporal characteristics of sound exposures ...

Activation of JNK in the Inner Ear following Impulse Noise Exposure

Noise exposure is known to induce cell death signaling in the cochlea. Since c-Jun N-terminal kinase (JNK) signaling is known to induce both cell survival and apoptosis, the present study focused on early changes (within 24 h) after impulse noise exposure, inquiring whether cell death is always related to phosphorylation of JNK in the inner ear. Anesthetized adult albino rats were exposed to a single impulse noise exposure (194 kPa) and sacrificed 3 or 24 h later. Paraffin-embedded sections were examined for positive staining of phosphorylated JNK and the presence of cells with fragmented DNA (TUNEL staining). Positive TUNEL staining was observed at the spiral limbus and in the stria vascularis at 24 h following impulse noise exposure, but no correlation with JNK activation was found at these locations. In the hearing organ (organ of Corti) and in the lateral wall, TUNEL-reactive cells were observed at 24 h following trauma. This was preceded by p-JNK staining at 3 h, indicating JNK-activated cell death in these regions. Finally, p-JNK reactivity was observed in the spiral ganglion with no correlation to TUNEL staining within the time frame of this study. These results suggest that JNK activation following impulse noise exposure may not always be related to cell death, and conversely, some cells may die through JNK-independent signaling.

Up-regulation of prestin mRNA expression in the organs of Corti of guinea pigs and rats following unilateral impulse noise exposure

Prestin is the motor protein of the outer hair cells (OHCs) and is required for both their electromotility and for cochlear amplification. We investigated the prestin mRNA expression in guinea pigs and rats in relation to the degree of noise-induced hearing loss (NIHL) induced by unilateral impulse noise exposure (167 dB peak SPL) for 2.5–5 min. Distortion product otoacoustic emissions (DPOAE) and auditory brainstem responses were recorded before and one week post exposure. Prestin mRNA was examined by quantitative reverse transcription-polymerase chain reaction. Either the whole organs of Corti or the apical, middle and basal parts were examined separately. The specimens were pooled and grouped according to the degree of NIHL measured in the exposed ears. In rats, the number of hair cells was counted. A clear base-to-apex gradient in the prestin mRNA expression was found to exist in guinea pig and rat controls. In both species, there was an increase in the number of prestin RNA transcripts at a mean NIHL of about 15–25 dB indicating an up-regulation in the remaining intact cells. In rats, this degree of NIHL corresponded to an OHC loss of about 40%. Interestingly, the contralateral ears also revealed an up-regulation of prestin mRNA accompanied by significant DPOAE improvements.

AM-111 protects against permanent hearing loss from impulse noise trauma

The otoprotective peptide AM-111, a cell-permeable inhibitor of JNK mediated apoptosis, was tested for its efficacy as a rescue agent following impulse noise trauma. Single dose administrations of AM-111 at 1 h or 4 h post-impulse noise exposure (155 dB peak SPL) via systemic or local routes were evaluated with a total of 48 chinchillas. The animals received the compound either by IP injection or locally onto the round window membrane (hyaluronic acid gel formulation or osmotic mini-pump). Efficacy was determined by auditory brainstem responses (ABR) as well as cytocochleograms. Three weeks after impulse noise exposure, permanent threshold shifts (PTS) were significantly lower for AM-111 treated ears compared to controls, regardless of the drug administration route and the time point of drug delivery. Even the treatments which started 4 h post-noise exposure, reduced hearing loss in the 2–8 kHz range compared to controls by up to 16–25 dB to a PTS as low as 6–17 dB, demonstrating significant protection against permanent hearing loss from impulse noise trauma. These findings suggest a key role for JNK mediated cochlear sensory cell death from oxidative stress.

Relationship between impulse noise and continuous noise inducing hearing loss by dosimeter measurement in working populations

To compare the dose-response relationship differences between impulse noise exposure workers and continuous noise exposure workers in prevalence of noise inducing hearing loss using dosimeter measurement. Thirty-two mechanical workers in a workshop were selected as impulse noise group and 163 textile workers in a textile factory as continuous noise group. SH-126 dosimeter was used to measure A weighted equal sound level of eight hours (L(Aeq.8 h)) during full working duration with equal energy rule for the selected workers. The cumulative noise exposure (CNE) was calculated by L(Aeq.8 h) and noise working years with equal energy rule for each worker. Hearing thresholds were measured by audiometer by routine method and adjusted by age and gender with GBZ49 - 2002. Hearing loss was diagnosed by GBZ49 - 2002 for each worker. CNE of impulse noise group [(103.2 +/- 4.2) dB (A) .year] was found lower than the continuous noise group [(110.6 +/- 6.0) dB (A) .year] by significance, P < 0.05. The hearing loss prevalence of impulse noise group (68.8%) was similar as continuous noise group (65%) without significance, P > 0.05. Strata analysis showed the hearing loss prevalence in 100 - 104 dB (A) .year and 105 - 109 dB (A) .year of impulse noise group was double than that of continuous noise group (76.9%, 90.9% vs 30.4%, 50.0%), P < 0.05. The chi-square test showed a relationship between CNE and hearing loss prevalence that was in high significance (P < 0.01) in both impulse noise group and continuous noise group. Logistic regression model showed the dose-response relationship curve of impulse noise group was left shift and sharp slope. The damage of impulse noise on hearing loss was much more than that of continuous noise according to equal energy rule of dosimeter data.

Prevention of noise-induced hearing loss with Src-PTK inhibitors

Studies from our lab show that noise exposure initiates cell death by multiple pathways [Nicotera, T.M., Hu, B.H., Henderson, D., 2003. The caspase pathway in noise-induced apoptosis of the chinchilla cochlea. J. Assoc. Res. Otolaryngol. 4, 466–477] therefore, protection against noise may be most effective with a multifaceted approach. The Src protein tyrosine kinase (PTK) signaling cascade may be involved in both metabolic and mechanically induced initiation of apoptosis in sensory cells of the cochlea. The current study compares three Src-PTK inhibitors, KX1-004, KX1-005 and KX1-174 as potential protective drugs for NIHL. Chinchillas were used as subjects. A 30 μl drop of one of the Src inhibitors was placed on the round window membrane of the anesthetized chinchilla; the vehicle (DMSO and buffered saline) alone was placed on the other ear. After the drug application, the middle ear was sutured and the subjects were exposed to noise. Hearing was measured before and several times after the noise exposure and treatment using evoked responses. At 20 days post-exposure, the animals were anesthetized their cochleae extracted and cochleograms were constructed. All three Src inhibitors provided protection from a 4 h, 4 kHz octave band noise at 106 dB. The most effective drug, KX1-004 was further evaluated by repeating the exposure with different doses, as well as, substituting an impulse noise exposure. For all conditions, the results suggest a role for Src-PTK activation in noise-induced hearing loss (NIHL), and that therapeutic intervention with a Src-PTK inhibitor may offer a novel approach in the treatment of NIHL.

Frequency-specific cochlear damage in guinea pig after exposure to different types of realistic industrial noise

For the causal evaluation of occupational hearing damage it is important to identify definitely the noise source. Here we tested, whether recordings of distortion product otoacoustic emissions (DPOAEs) in awake guinea pigs can distinguish the effects of different industrial noises. Six groups of 12 animals each were investigated before and over four months after a single 2 h exposure to specific, played-back industrial noise as well as before and for 2 months after impulse noise exposure. We compared broadband noise (buzz saw, bottle washing machine), low frequency noise (drawing press), and mid-frequency noise (bottle filling machine). All animals had stable DPOAE levels before noise exposure. Frequency specific decreases in DPOAEs were found after exposure to the different noises. Broadband noise diminished mostly all frequencies tested, whereas low- or mid-frequency noise had a greater effect on DPOAE evoked by middle and higher frequencies, respectively. DPOAE evoked by middle and higher frequencies were obliterated after impulse noise. Morphological analysis of the cochleae confirmed these alterations. OHC loss was found in the middle turns of the cochleae corresponding to the diminution of DPOAE. We conclude that different kinds of industrial noise tend to produce typical changes in DPOAE levels.

Moderate variations of mood/emotional states related to alterations in cochlear otoacoustic emissions and tinnitus onset in young normal hearing subjects exposed to gun impulse noise

This study was designed to test whether under impulse noise exposure mood and emotional states could play a role in the onset of tinnitus and/or could modify cochlear sensitivity objectively measured with distortion product otoacoustic emissions (DPOAEs). The experimental design consisted in a short follow-up study of 54 young military subjects (20 ± 2 years old), psychologically normal, with normal hearing, during two consecutive days of target practice rounds. Data collection included an abbreviated version of the profile of mood states (POMSs) inventory [Profile of Mood States, Educational and Industrial Testing Service, San Diego, 1971], questionnaires on tinnitus perception (previous history and after shooting) and DPOAEs measurements before and after shooting. Higher scores of tension-anxiety were found in subjects having previous history of tinnitus. Association between tinnitus previous history and tinnitus after shooting was found significant. Perception of tinnitus after target practice rounds was associated with significantly lower DPOAEs at 3 kHz. The most tense-anxious subjects were found to have DPOAEs decreases of 3.35 ± 6 dB at 3 kHz after shooting. This study clearly shows that, in young healthy population, psychologically normal and with normal hearing, moderate variations in mood and emotional states were related to tinnitus onset and DPOAEs alterations. It is possible that stronger variations in mood and/or emotional condition would increase risks of tinnitus and alterations of cochlear sensitivity.

Effect of Superoxide Dismutase and Allopurinol on Impulse Noise-exposed Guinea Pigs--Electrophysiological and Biochemical Study

To investigate the protective effect of two anti-reactive oxygen species (ROS) substances, copper-zinc superoxide dismutase (CuZn-SOD) and allopurinol, in impulse noise-exposed guinea pigs. Allopurinol or CuZn-SOD were administered intraperitoneally before exposure to 125 dB SPL noise centered at 2.0-3.0 kHz, with a repetition rate of 4/s, for 1.8 h. Hearing thresholds were tested by means of electrocochleography after implanting the animals with permanent electrodes. The presence of lipoperoxides in the guinea pig cochleae exposed to noise-induced oxidative stress was determined by means of the dosage of malondialdhyde, evaluated by measuring the content of thiobarbituric acid reactive substances in perilymph samples. Acoustic stress induced ROS formation and both allopurinol and CuZn-SOD exerted a protective effect on the cochlea. Comparison of compound action potential thresholds in different animal groups showed that the temporary threshold shift was significantly lower in treated animals than in those without pharmacological protection. The protective effect of the antioxidant agents demonstrates that, even at a high level of impulse noise exposure, a metabolic mechanism of cochlear damage may still play an important role in noise-exposed sensorineural hearing loss.

Impulse noise transiently increased the permeability of nerve and glial cell membranes, an effect accentuated by a recent brain injury.

A single exposure to intense impulse noise may cause diffuse brain injury, revealed by increased expression of immediate early gene products, transiently altered distribution of neurofilaments, accumulation of beta-amyloid precursor protein, apoptosis, and gliosis. Neither hemorrage nor any gross structural damage are seen. The present study focused on whether impulse noise exposure increased the permeability of nerve and glial cell membranes to proteins. Also, we investigated whether a preceding, minor focal surgical brain lesion accentuated the leakage of cytosolic proteins. Anaesthetized rats were exposed to a single impulse noise at either 199 or 202 dB for 2 milliseconds. Transiently elevated levels of the cellular protein neuron specific enolase (NSE) and the glial cytoplasmic protein S-100 were recorded in the cerebrospinal fluid (CSF) during the first hours after the exposure to 202 dB. A surgical brain injury, induced the day before the exposure to the impulse noise, was associated with significantly increased concentrations of both markers in the CSF. It is concluded that intense impulse noise damages both nerve and glial cells, an effect aggravated by a preexisting surgical lesion. The impulse of the shock wave, i.e. the pressure integrated over time, is likely to be the injurious mechanism. The abnormal membrane permeability and the associated cytoskeletal changes may initiate events, which eventually result in a progressive diffuse brain injury.

Effect of superoxide dismutase and allopurinol on impulse noise-exposed guinea pigs--electrophysiological and biochemical study

Objective: To investigate the protective effect of two anti-reactive oxygen species (ROS) substances, copper-zinc superoxide dismutase (CuZn-SOD) and allopurinol, in impulse noise-exposed guinea pigs.Material and Methods: Allopurinol or CuZn-SOD were administered intraperitoneally before exposure to 125 dB SPL noise centered at 2.0-3.0 kHz, with a repetition rate of 4/s, for 1.8 h. Hearing thresholds were tested by means of electrocochleography after implanting the animals with permanent electrodes. The presence of lipoperoxides in the guinea pig cochleae exposed to noise-induced oxidative stress was determined by means of the dosage of malondialdhyde, evaluated by measuring the content of thiobarbituric acid reactive substances in perilymph samples.Results: Acoustic stress induced ROS formation and both allopurinol and CuZn-SOD exerted a protective effect on the cochlea. Comparison of compound action potential thresholds in different animal groups showed that the temporary threshold shift was significantly lower in treated animals than in those without pharmacological protection.Conclusion: The protective effect of the antioxidant agents demonstrates that, even at a high level of impulse noise exposure, a metabolic mechanism of cochlear damage may still play an important role in noise-exposed sensorineural hearing loss.

Dan Johnson the mentor

I first met Dan Johnson in early 1975 as I was interviewing for an engineering job with Henning von Gierke’s bioengineering and bionics laboratory at Wright–Patterson Air Force Base. From the very beginning Dan was always direct and forthright. Over the ensuing next 27 years my knowledge and respect of Dan constantly grew. This presentation will review Dan’s technical and personal contributions while at the laboratory at Wright–Patterson Air Force Base. He was instrumental in the development of a national noise exposure criteria with the equal-energy-rule, an accurate single number hearing protector attenuation measure based on ‘‘C-A,’’ an impulse noise exposure criteria, a longitudinal study of hearing loss in children, development of noise dosimeters, and description of hearing damage risk from nonoccupational noise exposures such as disco’s, bowling alleys, lawn mowers, and school buses. Dan has had a significant effect on my career. I and the many people who knew him at the laboratory miss him greatly.

Functional impairment of the vestibular end organ resulting from impulse noise exposure.

To assess the effect of exposure t o impulse noise, known to cause damage tothe cochlea, on the vestibular part of the inner ear using short latency vestibular evoked potentials (VsEPs), which is a direct and objective test for evaluating the function of the vestibular end organs. Prospective animal study. Sand rats (Psammomys obesus) underwent baseline measurements of VsEPs in response to linear and angular acceleration stimuli and measurement of the auditory nerve and brainstem evoked response (ABR). The animals were then exposed to 10 gunshots generating impulse noise at an intensity of approximately 160 dB sound pressure level (SPL). Repeat measurements of the evoked potentials were conducted 2 to 4 hours, 1 week, and 6 weeks after the exposure. The amplitude and latency of the first wave of VsEPs in response to linear and angular acceleration stimuli, reflecting the function of the otolith organs and semicircular canals respectively, were compared between baseline and post-exposure measurements, as were ABR thresholds. The amplitude of the first wave of the VsEPs in response to linear acceleration was significantly (P <.001) reduced and the latency significantly (P <.005) prolonged 2 to 4 hours after the exposure in comparison to baselinemeasurements. The latency prolongation persisted in follow-up measurements, whereas the amplitude showed partial recovery. The first wave of VsEPs in response to angular acceleration was unchanged long-term. ABR thresholds were elevated in the long-term by 60 dB. It seems that impulse noise not only damages the cochlea, but also causes clear functional impairment to the vestibular end organs, mainly the otolith organs.

Otoacoustic Emissions and Medial Olivocochlear Suppression during Auditory Recovery from Acoustic Trauma in Humans

It is well known that the large inter-individual susceptibility to noise exposure makes it impossible to predict the degree of hearing loss which will develop after any given intense noise exposure. The acoustic trauma which sometimes occurs affects cochlear mechanisms, the damage being most probably due to deactivation of the active processes of the outer hair cells (OHCs), which receive direct efferent innervation. The present report is of a follow-up study involving young military personnel recovering auditively from impulse noise exposure, and seeks to assess changes in cochlear status by means of otoacoustic emissions (OAEs) and their modulation by the medial olivocochlear (MOC) system. The study investigated the relationship between recovery of cochlear function and variables that could serve as predictors of vulnerability to noise-induced hearing loss (NIHL). Thirty-six subjects with unilateral NHIL above 4 kHz were included. Normal and affected ears were compared with respect to click-evoked and spontaneous OAEs (CEOAEs and SOAEs, respectively) and for contralateral CEOAE suppression. Measurements were obtained: (i) just after the traumatic exposure (D0); (ii) 3 days after this first measurement (D3); and (iii) 30 days after (D30). Significant improvement in the 4, 6 and 8 kHz thresholds was observed for the affected ear, with large inter-subject variability. No significant change was observed in CEOAE amplitude or MOC suppression, whereas incidence of SOAE was found to increase in the affected ear, leading to higher SOAE prevalence on this side 1 month after the intense noise exposure. There was no significant correlation between NIHL at 4, 6 and 8 kHz and MOC functioning on D0, but significant correlations were obtained between audiometric threshold improvement by D3 and contralateral CEOAE suppression, with better recovery in subjects with greater MOC suppressive action. The MOC system could be an underlying mechanism in post-traumatic auditory threshold recovery.

Antioxidant loading reduces oxidative stress induced by high-energy impulse noise (blast) exposure

Detonation of explosives, firing of large caliber weapons and occupational explosions, professional or accidental, produce high-energy impulse noise (blast) waves characterized by a rapid rise in atmospheric pressure (overpressure) followed by gradual decay to ambient level. Exposure to blast waves causes injury, predominantly to the hollow organs such as ears and lungs. We have previously reported that blast exposure can induce free radical-mediated oxidative stress in the lung characterized by antioxidant depletion, lipid peroxidation, and hemoglobin (Hb) oxidation. In this study, we examined whether pre-loading, adequately fed rats, with pharmacological doses of antioxidants would reduce the response to blast. Sprague–Dawley rats weighing 300–350 g were loaded with either 800 IU vitamin E (VE), 1000 mg vitamin C (VC) or 25 mg lipoic acid (LA) for 3 consecutive days by gavage before exposure to blast. Both VE, and LA were dissolved in 2 ml corn oil, but VC in 2 ml water. After the 3-day antioxidant loading, the rats were divided into six groups (five rats per group), deeply anesthetized with sodium pentobarbital (60 mg/kg body weight), then exposed to a low-level blast (62±2 kPa peak pressure and 5 ms duration). A matched number of groups were sham exposed and served as controls. One hour after exposure, all rats were euthanized then blood, and lung tissue was analyzed. We found that antioxidant loading resulted in restored Hb oxygenation, and reduced lipid peroxidation. Lung tissue VE content was elevated after loading but VC did not change possibly due to their different bioavailability and saturation kinetics. These observations, suggest that brief antioxidant loading with pharmacological doses can reduce blast-induced oxidative stress, and may have occupational and clinical implications.

The effect of impulse noise exposure on distortion product otoacoustic emissions in the awake guinea pig.

Distortion product otoacoustic emissions (DPOAE) are a sensitive detector of outer hair cell (OHC) function and were monitored in awake guinea pigs before and after impulse noise damaging the cochlea (peak intensity 153 dB SPL, rise time < 0.1 ms). Animals had stable DPOAE levels before noise exposure. In the first hours after noise exposure DPOAE levels were reduced significantly. Three different patterns of recovery of DPOAE were seen in the post-exposure period:restitution exceeding controls, partial recovery and no recovery. In general, DPOAE levels declined and types of recovery closely corresponded to changes in amplitudes of cochlear microphonics after noise exposure. These data suggest that the monitoring of DPOAE is a suitable method for diagnosing impaired OHC function.