Threshold recovery functions following impulse noise trauma

An analysis of the pure-tone threshold recovery functions obtained from 118 chinchillas exposed to high-level impulse noise showed that there are at least three distinctly different types of recovery function: type I--a recovery function for which the initial threshold shift recovers monotonically with increasing postexposure time; type II--a delayed recovery; i.e., for a period as long as 6 h following removal from noise, the pure-tone threshold remains elevated and stable before thresholds begin to follow a monotonic course of recovery; and type III--the growth function; i.e., over a period of at least 6 h following removal from the noise, pure-tone thresholds continue to get worse before they begin to follow a monotonic course of recovery. There is more permanent threshold shift (PTS), more sensory cell loss, and predictions of PTS and cell loss based upon initial measures of threshold shift are less accurate at those frequencies characterized by a type III recovery process than at those frequencies characterized by a type I recovery process.     

Onset, growth, and recovery of in-air temporary threshold shift in a California sea lion (Zalophus californianus)

A California sea lion (Zalophus californianus) was tested in a behavioral procedure to assess noise-induced temporary threshold shift (TTS) in air. Octave band fatiguing noise was varied in both duration (1.5-50 min) and level (94-133 dB re 20 muPa) to generate a variety of equal sound exposure level conditions. Hearing thresholds were measured at the center frequency of the noise (2500 Hz) before, immediately after, and 24 h following exposure. Threshold shifts generated from 192 exposures ranged up to 30 dB. Estimates of TTS onset [159 dB re (20 muPa)(2) s] and growth (2.5 dB of TTS per dB of noise increase) were determined using an exponential function. Recovery for threshold shifts greater than 20 dB followed an 8.8 dB per log(min) linear function. Repeated testing indicated possible permanent threshold shift at the test frequency, but a later audiogram revealed no shift at this frequency or higher. Sea lions appear to be equally susceptible to noise in air and in water, provided that the noise exposure levels are referenced to absolute sound detection thresholds in both media. These data provide a framework within which to consider effects arising from more intense and/or sustained exposures.     

Acoustic distortion in the ear canal. I. Cubic difference tones: effects of acute noise injury

Acoustic emissions in the form of cubic difference tones (CDT's), 2f1-f2, were measured in the ear canals of gerbils and cats. The state of the cochlea was manipulated by means of acute exposure to noise and was monitored with the aid of the whole-nerve response to tone pips. The resulting shifts in the levels of emissions generated by pairs of primary tones of equal intensity were then compared to the corresponding threshold shifts of the whole-nerve response across frequency. Data obtained from normal ears before injury indicate that the absolute thresholds of the whole-nerve responses across frequency are not necessarily good predictors of the absolute levels of CDT emissions generated by 70- and 80-dB SPL primaries. While high emission levels were often linked to low whole-nerve thresholds in pre-exposed ears, instances of animals with sensitive whole-nerve thresholds coupled with very weak emissions were also found. Conversely, animals with poor whole-nerve thresholds (shifted by up to 30 dB) could occasionally have high levels of emissions. After acute noise injury, however, the shifts of emission levels as a function of the center frequency of the primary-tone pair largely corresponded to the threshold shifts seen in the whole-nerve response. In other words, the temporary level shift of an acoustic emission largely reflected the acute change to a specific cochlear region associated with the primary frequencies.     

Underwater temporary threshold shift in pinnipeds: effects of noise level and duration

Behavioral psychophysical techniques were used to evaluate the residual effects of underwater noise on the hearing sensitivity of three pinnipeds: a California sea lion (Zalophus californianus), a harbor seal (Phoca vitulina), and a northern elephant seal (Mirounga angustirostris). Temporary threshold shift (TTS), defined as the difference between auditory thresholds obtained before and after noise exposure, was assessed. The subjects were exposed to octave-band noise centered at 2500 Hz at two sound pressure levels: 80 and 95 dB SL (re: auditory threshold at 2500 Hz). Noise exposure durations were 22, 25, and 50 min. Threshold shifts were assessed at 2500 and 3530 Hz. Mean threshold shifts ranged from 2.9-12.2 dB. Full recovery of auditory sensitivity occurred within 24 h of noise exposure. Control sequences, comprising sham noise exposures, did not result in significant mean threshold shifts for any subject. Threshold shift magnitudes increased with increasing noise sound exposure level (SEL) for two of the three subjects. The results underscore the importance of including sound exposure metrics (incorporating sound pressure level and exposure duration) in order to fully assess the effects of noise on marine mammal hearing.     

Impact of three hours of discotheque music on pure-tone thresholds and distortion product otoacoustic emissions

The aim of this study was to investigate whether distortion product otoacoustic emissions (DPOAEs) are a suitable means for detecting changes in outer hair cell (OHC) functionality due to exposure to three hours of discotheque music and whether efferent reflex strength of the medial olivocochlear bundle is able to predict the ear's susceptibility to high-level noise. High-resolution DPOAEs (Δf(2)=47 Hz) were recorded between 3.5 and 4.5 kHz at close-to-threshold primary tone levels. For comparison, high-resolution pure-tone audiometry was conducted in the same frequency range. Efferent reflex strength was measured by means of DPOAEs at a specific frequency with and without contralateral acoustic stimulation. A significant deterioration of more than 10 dB was found for pure-tone thresholds and DPOAE levels indicating that three hours of high-level noise exert a considerable influence on hearing capability and OHC functionality. A significant correlation between shifts in pure-tone threshold and shifts in DPOAE level occurred when removing data with differing calibration across measurements. There was no clear correlation between efferent reflex strength and shifts in pure-tone threshold or shifts in DPOAE level suggesting that the applied measures of efferent reflex strength may not be suitable for quantifying individual vulnerability to noise.     

Hazard from an intense midrange impulse

It has been hypothesized that the ear would become increasingly susceptible to impulses (gunfire) as the spectral peak of the impulse approached the frequency region where the ear was tuned best (about 4 kHz for the cat ear) [G. R. Price, J. Acoust. Soc. Am. Suppl. 1 62, S95 (1977)]. This prediction was counter to the predictions of the world's damage-risk criteria for impulse noise. It has been supported by experiments using exposures to 100-Hz and 800- to 1000-Hz impulses; but no test had been run at the point of predicted maximum susceptibility. In the present experiment, three groups of cats were exposed to 50 impulses produced by a primer explosion (spectral peak at 4 kHz) at peak levels of 135, 140, or 145 dB. Auditory thresholds were electrophysiologically measured from the vertex to 2-, 4-, 8-, and 16-kHz tone pips and losses were determined 30 min after exposure and more than 2 months post-exposure. Losses were greatest at 4 kHz, began to develop at 134-dB peak pressure, and the immediate losses grew at a rate of about 7 dB for every dB increase in peak pressure. About half of the loss measured immediately became permanent. The energy required to begin producing a permanent threshold shift was only about 0.07 J/m2, far lower than that required with continuous noises at lower sound pressures. The data were interpreted as supporting the original hypothesis of greater susceptibility in the midrange.     

Effect of periodic rest on hearing loss and cochlear damage following exposure to noise

Changes in hearing sensitivity and cochlear damage were determined in two groups of chinchillas exposed to an octave band of noise (OBN) centered at 0.5 kHz, 95 dB SPL on two different schedules: 6 h per day for 36 days, or 15 min/h for 144 days. Hearing sensitivity was measured behaviorally at 1/4-oct frequency intervals from 0.125 to 16.0 kHz before, during, and for a period of 1 to 2 months after the exposure, at which time the animals' cochleas were fixed and prepared for microscopic examination. Cochlear damage was determined by counts of missing sensory cells. Both exposures produced an initial shift of thresholds of 35-45 dB; however, after a few days of exposure, thresholds began to decline and eventually recovered to within 10-15 dB of original baseline values even though the exposure continued. Measures of recovery made after completion of the exposures indicated minimal permanent threshold shifts in all animals. The behavioral and anatomical data indicated that these intermittent exposures produced less temporary and permanent hearing loss and less cochlear damage than continuous exposures of equal energy.     

Temporary threshold shifts in humans exposed to octave bands of noise for 16 to 24 hours.

Groups of human subjects were exposed in a diffuse sound field for 16--24 h to an octave-band noise centered at 4, 2, 1, or 0.5 kHz. Sound-pressure levels were varied on different exposure occasions. At specified times during an exposure, the subject was removed from the noise, auditory sensitivity was measured, and the subject was returned to the noise. Temporary threshold shifts (TTS) increased for about 8 h and then reached a plateau or asymptote. The relation between TTS and exposure duration can be described by a simple exponential function with a time constant of 2.1 h. In the frequency region of greatest loss, threshold shifts at asymptote increased about 1.7 dB for every 1 dB increase in the level of the noise above a critical level. Critical levels were empirically estimated to be 74.0 dB SPL at 4 kHz. 78 dB at 2 kHz, and 82 dB at 1 and 0.5 kHz. Except for the noise centered at 4.0 kHz, threshold shifts were maximal about 1/2 octave above the center frequency of the noise. A smaller second maximum was observed also at 7.0 kHz for the noise centered at 2.0 kHz, at 6.0 kHz for the noise centered at 1.0 kHz, and at 5.5 kHz for the noise centered at 0.5 kHz. After termination of the exposure, recovery to within 5 dB of pre-exposure thresholds was achieved within 24 h or less. Recovery can be described by a simple exponential function with a time constant of 7.1 h. The frequency contour defined by critical levels matches almost exactly the frequency contour defined by the E-weighting network.     

Underwater temporary threshold shift induced by octave-band noise in three species of pinniped.

Pure-tone sound detection thresholds were obtained in water for one harbor seal (Phoca vitulina), two California sea lions (Zalophus californianus), and one northern elephant seal (Mirounga angustirostris) before and immediately following exposure to octave-band noise. Additional thresholds were obtained following a 24-h recovery period. Test frequencies ranged from 100 Hz to 2000 Hz and octave-band exposure levels were approximately 60-75 dB SL (sensation level at center frequency). Each subject was trained to dive into a noise field and remain stationed underwater during a noise-exposure period that lasted a total of 20-22 min. Following exposure, three of the subjects showed threshold shifts averaging 4.8 dB (Phoca), 4.9 dB (Zalophus), and 4.6 dB (Mirounga). Recovery to baseline threshold levels was observed in test sessions conducted within 24 h of noise exposure. Control sessions in which the subjects completed a simulated noise exposure produced shifts that were significantly smaller than those observed following noise exposure. These results indicate that noise of moderate intensity and duration is sufficient to induce TTS under water in these pinniped species.     

The Okinawa study: an estimation of noise-induced hearing loss on the basis of the records of aircraft noise exposure around Kadena Air Base

Aircraft noise measurements were recorded at the residential areas in the vicinity of Kadena Air Base, Okinawa in 1968 and 1972 at the time of the Vietnam war. The estimated equivalent continuous A-weighted sound pressure level L_Aeq for 24 h was 85 dB.The time history of sound level during 24 h was estimated from the measurement conducted in 1968, and the sound level was converted into the spectrum level at the centre frequency of the critical band of temporary threshold shift (TTS) using the results of spectrum analysis of aircraft noise operated at the airfield. With the information of spectrum level and its time history, TTS was calculated as a function of time and level change. The permanent threshold shift was also calculated by means of Robinson's method and ISO's method. The results indicate the noise exposure around Kadena Air Base was hazardous to hearing and is likely to have caused hearing loss to people living in its vicinity.     

Recent studies of temporary threshold shift (TTS) and permanent threshold shift (PTS) in animals

It is well known that excessive exposure to noise results in temporary and/or permanent changes in hearing sensitivity in both human and animal subjects. The purpose of this review is to describe the major findings from laboratory studies of experimentally induced hearing losses, both temporary and permanent, resulting from exposure to noise in animal subjects which have been published since the report of Kryter et al. (1966). The data reviewed support the following general statements: (1) The chinchilla is the most widely used and most appropriate animal model for studies of noise-induced hearing loss; (2) with continuous exposures to moderate-level noise, thresholds reach asymptotic levels (ATS) within 18-24 h; (3) permanent threshold shifts, however, depend upon the level, frequency, and the duration of exposure; (4) below a "critical level" of about 115 dB, permanent threshold shift (PTS) and cell loss are generally related to the total energy in continuous exposures; (5) periodic rest periods inserted in an exposure schedule are protective and result in less hearing loss and cochlear damage than equal energy continuous exposures; and (6) under some schedules of periodic exposure, threshold shifts increase over the first few days of exposure, then recover as much as 30 dB as the exposure continues.     

Summation bandwidths at threshold in normal and hearing-impaired listeners

The bandwidths for summation at threshold were measured for subjects with normal hearing and subjects with sensorineural hearing loss. Thresholds in quiet and in the presence of a masking noise were measured for complex stimuli consisting of 1 to 40 pure-tone components spaced 20 Hz apart. The single component condition consisted of a single pure tone at 1100 Hz; additional components were added below this frequency, in a replication of the G?ssler [Acustica 4, 408-414 (1954)] procedure. For the normal subjects, thresholds increased approximately 3 dB per doubling of bandwidth for signal bandwidths exceeding the critical bandwidth. This slope was less for the hearing-impaired subjects. Summation bandwidths, as estimated from two-line fits, were wider for the hearing-impaired than for the normal subjects. These findings provide evidence that hearing-impaired subjects integrate sound energy over a wider-than-normal frequency range for the detection of complex signals. A second experiment used stimuli similar to those of Spiegel [J. Acoust. Soc. Am. 66, 1356-1363 (1979)], and added components both above and below the frequency of the initial component. Using these stimuli, the slope of the threshold increase beyond the critical bandwidth was approximately 1.5 dB per doubling of bandwidth, thus replicating the Spiegel (1979) experiment. It is concluded that the differences between the G?ssler (1954) and Spiegel (1979) studies were due to the different frequency content of the stimuli used in each study. Based upon the present results, it would appear that the slope of threshold increase is dependent upon the direction of signal expansion, and the size of the critical bands into which the signal is expanded.     

Psychophysical correlates of contralateral efferent suppression. I. The role of the medial olivocochlear system in "central masking" in nonhuman primates

An extensive physiological literature, including experimental and clinical studies in humans, demonstrates that activation of the medial olivocochlear (MOC) efferent system, by either contralateral sound or electrical stimulation, can produce significant alterations in cochlear function and suggests a role for the MOC system in influencing the auditory behavior of binaural hearing. The present data are from psychophysical studies in nonhuman primates which seek to determine if the noted physiological changes in response to contralateral acoustic stimulation have a perceptual counterpart. Four juvenile Japanese macaques were trained to respond to the presence of 1-s sinusoids, presented to the test ear, in an operant reinforcement paradigm. Thresholds were compared for frequencies ranging from 1.0 to 4.0 kHz in quiet, with thresholds measured when continuous, two octave-band noise, centered on the test tone frequency, was presented in the contralateral ear. Contralateral noise was presented at levels of 10-60 dB above detection threshold for the test-tone frequency. While some variability was evident across subjects, both in the frequency distribution and magnitude (as a function of contralateral noise level), all subjects exhibited an increase, or suppression of thresholds in the presence of contralateral noise. On average, thresholds increased systematically with contralateral noise level, to a peak of 7 dB. In one subject, the threshold increase seen with contralateral noise was significantly reduced when the MOC was surgically sectioned on the floor of the IVth ventricle. The characteristics of the measured shifts in behavioral thresholds, in the presence of contralateral noise reported here, are qualitatively and quantitatively similar to both efferent physiological suppression effects and psychophysical central masking threshold shifts which have been reported previously. These data suggest that at least some aspects of "central masking" are efferent-mediated peripheral processes, and that the term "central masking" may be incorrect.     

Speech reception in quiet and in noisy conditions by individuals with noise-induced hearing loss in relation to their tone audiogram.

Tone thresholds and speech-reception thresholds were measured in 200 individuals (400 ears) with noise-induced hearing loss. The speech-reception thresholds were measured in a quiet condition and in noise with a speech spectrum at levels of 35, 50, 65, and 80 dBA. The tone audiograms could be described by three principal components: hearing loss in the regions above 3 kHz, from 1 to 3 kHz and below 1 kHz; the speech thresholds could be described by two components: speech reception in quiet and speech reception in noise at 50-80 dBA. Hearing loss above 1 kHz was related to speech reception in noise; hearing loss at and below 1 kHz to speech reception in quiet. The correlation between the speech thresholds in quiet and in noise was only R = 0.45. An adequate predictor of the speech threshold in noise, the primary factor in the hearing handicap, was the pure-tone average at 2 and 4 kHz (PTA2,4, R = 0.72). The minimum value of the prediction error for any tone-audiometric predictor of this speech threshold was 1.2 dB (standard deviation). The prediction could not be improved by taking into account the critical ratio for low-frequency noise nor by its upward spread of masking. The prediction error is due to measurement error and to a factor common to both ears. The latter factor is ascribed to cognitive skill in speech reception. Hearing loss above 10 to 15 dB HL (hearing level) already shows an effect on the speech threshold in noise, a noticeable handicap is found at PTA2,4 = 30 dB HL.     

Differential responses to acoustic damage and furosemide in auditory brainstem and otoacoustic emission measures

Characteristics of distortion product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs) were measured in Mongolian gerbil before and after the introduction of two different auditory dysfunctions: (1) acoustic damage with a high-intensity tone, or (2) furosemide intoxication. The goal was to find emission parameters and measures that best differentiated between the two dysfunctions, e.g., at a given ABR threshold elevation. Emission input-output or "growth" functions were used (frequencies f1 and f2, f2/f1 = 1.21) with equal levels, L1 = L2, and unequal levels, with L1 = L2 + 20 dB. The best parametric choice was found to be unequal stimulus levels, and the best measure was found to be the change in the emission threshold level, delta x. The emission threshold was defined as the stimulus level required to reach a criterion emission amplitude, in this case -10 dB SPL. (The next best measure was the change in emission amplitude at high stimulus levels, specifically that measured at L1 x L2 = 90 x 70 dB SPL.) For an ABR threshold shift of 20 dB or more, there was essentially no overlap in the emission threshold measures for the two conditions, sound damage or furosemide. The dividing line between the two distributions increased slowly with the change in ABR threshold, delta ABR, and was given by delta x(t) = 0.6 delta ABR + 8 dB. For a given delta ABR, if the shift in emission threshold was more than the calculated dividing line value, delta x(t), the auditory dysfunction was due to acoustic damage, if less, it was due to furosemide.     

A simple mathematical model for TTS

Published data on Temporary Threshold Shift (TTS) suggest that in many cases the rms pressure at threshold during and after exposure to noise varies in a simple exponential manner, and that the ultimate shift of pressure threshold for exposure to steady noise is dependent on the mean square pressure of that noise. This response could occur if some part of the hearing mechanism were heated by exposure to noise and were at the same time subject to Newtonian cooling, and if the change in the pressure threshold were proportional to the change of temperature. This model can explain the shapes of many growth and recovery curves given in dB, why time constants found for recovery from TTS appear greater than those for growth and why threshold shifts on ears with elevated thresholds appear smaller than those for ears with low thresholds. Because of individual variation, averaged dB results mask the nature of the processes involved. Hence, for a better understanding of TTS, individual ears should be studied separately, and, if possible, measurements should be made in rms Pa instead of dB.     

Behavioral avoidance threshold level of a harbor porpoise (Phocoena phocoena) for a continuous 50 kHz pure tone

The use of ultrasonic sounds in alarms for gillnets may be advantageous, but the deterring effects of ultrasound on porpoises are not well understood. Therefore a harbor porpoise in a large floating pen was subjected to a continuous 50 kHz pure tone with a source level of 122+/-3 dB (re 1 microPa, rms). When the test signal was switched on during test periods, the animal moved away from the sound source. Its respiration rate was similar to that during baseline periods, when the sound was switched off. The behavior of the porpoise was related to the sound pressure level distribution in the pen. The sound level at the animal's average swimming location during the test periods was approximately 107+/-3 dB (re 1 microPa, rms). The avoidance threshold sound pressure level for a continuous 50 kHz pure tone for this porpoise, in the context of this study, is estimated to be 108+/-3 dB (re 1 microPa, rms). This study demonstrates that porpoises may be deterred from an area by high frequency sounds that are not typically audible to fish and pinnipeds and would be less likely masked by ambient noise.     

Hearing loss from simulated work-week exposure to impulse noise.

Six monaural chinchillas were exposed to a repetitive, reverberant, impulse noise for a total of five days, 8 h per day. The average peak overpressure within the holding cage was 113 dB. The reverberation time (pressure fluctuation envelope within 20 dB of peak) was 160 ms. Auditory thresholds were measured at 0.25, 0.5, 1, 2, 4, and 8 kHz before and after each day's exposure using either the average-evoked response technique or shock avoidance conditioning. After the last exposure, recovery was monitored for five successive days. Final thresholds were obtained starting at 30 days postexposure after which the animals were sacrificed for cochlear histology. The high frequencies (4, 8 kHz) showed a daily median shift of 40 dB and a 27 dB recovery before the following day's exposure. The low frequencies (0.25, 0.5 kHz) were shifted 35 dB after each day's exposure with a 15 dB recovery overnight. Final median audiograms showed little permanent threshold shift. The cochleagrams for two test animals were found to be normal while the remaining four displayed 10%--40% losses in hair cells at specific cochlear sites.     

Noise-induced threshold shift and cochlear pathology in the Mongolian gerbil

Groups of six mongolian gerbils were exposed to two-octave (1414-5656 Hz) band noise for 1 h at 100, 110, and 120 dB SPL. Threshold shift at several frequencies was measured 0.5, 3, 6, and 12 h, and 1-28 days after exposure. Final thresholds were determined at least two months postexposure. Extensive threshold shift was observed in all groups 0.5 h after exposure (TS0.5h). Where threshold shift increased in the initial hours after exposure, such increases were correlated with eventual permanent threshold shift (PTS). Recovery of thresholds from 1-28 days after exposure was approximately exponential, and slowest at the edges of the exposure band. PTS was seen in the 110 and 120 dB SPL groups. With TS0.5h of 50 dB or less, no PTS resulted. With TS0.5h above 50-60 dB, eventual PTS increased linearly with a slope of about 1.25 PTS/TS0.5h. Cochlear damage was evaluated by light microscopy. The relationship between hair cell loss and PTS was consistent with an inner hair cell threshold about 40 dB higher than that of outer hair cells. It is suggested that recovery from noise-induced threshold shift may involve different mechanisms in the two types of hair cells.     

Low-level otoacoustic emissions may predict susceptibility to noise-induced hearing loss

In a longitudinal study with 338 volunteers, audiometric thresholds and otoacoustic emissions were measured before and after 6 months of noise exposure on an aircraft carrier. While the average amplitudes of the otoacoustic emissions decreased significantly, the average audiometric thresholds did not change. Furthermore, there were no significant correlations between changes in audiometric thresholds and changes in otoacoustic emissions. Changes in transient-evoked otoacoustic emissions and distortion-product otoacoustic emissions were moderately correlated. Eighteen ears acquired permanent audiometric threshold shifts. Only one-third of those ears showed significant otoacoustic emission shifts that mirrored their permanent threshold shifts. A Bayesian analysis indicated that permanent threshold shift status following a deployment was predicted by baseline low-level or absent otoacoustic emissions. The best predictor was transient-evoked otoacoustic emission amplitude in the 4-kHz half-octave frequency band, with risk increasing more than sixfold from approximately 3% to 20% as the emission amplitude decreased. It is possible that the otoacoustic emissions indicated noise-induced changes in the inner ear, undetected by audiometric tests. Otoacoustic emissions may therefore be a diagnostic predictor for noise-induced-hearing-loss risk.