Impact noise: the importance of level, duration, and repetition rate

The applicability of the equal energy hypothesis (EEH) to impact noise exposures was studied using chinchillas. Hearing thresholds were estimated by recording the evoked potentials from a chronic electrode implanted in the inferior colliculus. The animals were exposed to broadband impacts of 200-ms duration. The study was carried out in two parts. In experiment I, six exposure levels (107, 113, 119, 125, 131, and 137 dB SPL) and three repetition rates (4/s, 1/s and 1/4s) were employed. In the second experiment, the total duration of the exposure as well as the total energy were kept constant by trading level and rate. Results indicate that hearing loss resulting from exposure to impact noise does not conform to the predictions of the EEH. The permanent threshold shift as well as the hair cell loss are more or less equal across the lower peak exposure levels. However, both the hearing loss and the hair cell damage increase for exposures with higher peak levels. Furthermore, hearing loss and cochlear damage are dependent upon the rate of exposure. Thus the amount of hearing loss and hair cell damage appears to depend on the interaction of several factors including peak level, rate, and the susceptibility of the animal.     

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.     

The importance of "temporal pattern" in traumatic impulse noise exposures

The equal energy hypothesis (EEH) was evaluated for impulse noise. Specifically, the experiments evaluated the importance of the temporal distribution of impulses; the trading relation between the number of impulses and peak level and the difference between continuous and impulse noise. Monaural chinchillas were exposed to one of seven conditions. Their hearing was evaluated before, immediately after, and 30 days after the exposure. Hair cell damage was reported in the form of a cochleogram. The experiments show that the EEH is more appropriate for low-level impulse (135-dB peak); for equal amounts of energy, 150-dB impulses produce more hearing loss and hair cell damage than 135-dB impulses; for equal amounts of energy, impulses presented in rapid bursts cause less damage than impulses presented at "1/s" and 50 microseconds. Pairs of impulses presented at "1/s" produce the largest amount of damage. The results are discussed in terms of implications for the EEH.     

The effect of impulse intensity and the number of impulses on hearing and cochlear pathology in the chinchilla

Forty-one chinchillas, divided into seven groups, were exposed to 1, 10, or 100 noise impulses (one every 3s) having peak intensities of 131, 135, 139, or 147 dB. Hearing thresholds were measured in each animal before and after exposure using an avoidance conditioning procedure; a surface preparation of the cochlear sensory epithelia was performed approximately 90 days after exposure. There was generally an orderly relation between the amount of permanent threshold shift and the severity of exposure, and a general agreement between averaged histological data and the audiometric data. For the impulses used in this study, there is a range of intensities which is bounded on the high side by the intensity which just produces injury with single impulse exposures and bounded on the low side by a critical intensity below which the injury potential drops precipitously with a reduction of impulse intensity. This region is only about 10-15 dB wide for the exposure conditions of this experiment. Within this region, the threshold of injury is a constant total energy; i.e., 10-dB change of intensity implies a tenfold change in the number of impulses for threshold injury. Detailed relations between temporary and permanent threshold shift, cochlear pathology, and exposure variables are discussed, as are the implications of these data to the development of exposure criteria.     

Psychophysical tuning curves and auditory thresholds after hair cell damage in the chinchilla

Chinchillas were treated with kanamycin sulfate (150--200 mg/kg/day) to produce high-frequency hearing loss extending to about 4.0 kHz. Thresholds and psychophysical tuning curves (PTCs) were obtained before and after treatment, utilizing a shuttlebox avoidance procedure, and cochlear hair cells were evaluated under phase contrast microscopy. Hair cell loss resulting from kanamycin treatment varied from restricted lesions of the outer hair cells (OHCs) in the cochlear base, with no loss of inner hair cells (IHCs), to more extensive lesions involving both OHCs and IHCs. Threshold shift of at least 40 dB was always associated with OHC loss. PTCs obtained from frequency regions exhibiting 40--50 dB of threshold shift were normal in shape. With threshold shift in excess of 50 dB, PTCs were progressively distorted, with truncation of the tip segment and in some cases increased sensitivity of the tail segment. The results suggest that the threshold of optimally functional IHCs after kanamycin-induced OHC loss is about 40 dB higher than normal. Threshold shift in excess of 40 dB may represent IHC damage. IHCs are capable of transducing the fine-frequency information necessary for generating normally sharp PTCs in the absence of OHCs. However, with threshold shift in excess of approximately 50 dB, this frequency resolution is increasingly compromised.     

Energy-independent factors influencing noise-induced hearing loss in the chinchilla model.

The effects on hearing and the sensory cell population of four continuous, non-Gaussian noise exposures each having an A-weighted L(eq)=100 dB SPL were compared to the effects of an energy-equivalent Gaussian noise. The non-Gaussian noise conditions were characterized by the statistical metric, kurtosis (beta), computed on the unfiltered, beta(t), and the filtered, beta(f), time-domain signals. The chinchilla (n=58) was used as the animal model. Hearing thresholds were estimated using auditory-evoked potentials (AEP) recorded from the inferior colliculus and sensory cell populations were obtained from surface preparation histology. Despite equivalent exposure energies, the four non-Gaussian conditions produced considerably greater hearing and sensory cell loss than did the Gaussian condition. The magnitude of this excess trauma produced by the non-Gaussian noise was dependent on the frequency content, but not on the average energy content of the impacts which gave the noise its non-Gaussian character. These results indicate that beta(t) is an appropriate index of the increased hazard of exposure to non-Gaussian noises and that beta(f) may be useful in the prediction of the place-specific additional outer hair cell loss produced by non-Gaussian exposures. The results also suggest that energy-based metrics, while necessary for the prediction of noise-induced hearing loss, are not sufficient.     

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.     

The kurtosis metric as an adjunct to energy in the prediction of trauma from continuous, nonGaussian noise exposures

Data from an earlier study [Hamernik et al. (2003). J. Acoust. Soc. Am. 114, 386-395] were consistent in showing that, for equivalent energy [Leq= 100 dB(A)] and spectra, exposure to a continuous, nonGaussian (nonG) noise could produce substantially greater hearing and sensory cell loss in the chinchilla model than a Gaussian (G) noise exposure and that the statistical metric, kurtosis, computed on the amplitude distribution of the noise could order the extent of the trauma. This paper extends these results to Leq= 90 and 110 dB(A), and to nonG noises that are generated using broadband noise bursts, and band limited impacts within a continuous G background noise. Data from nine new experimental groups with 11 or 12 chinchillas/group is presented. Evoked response audiometry established hearing thresholds and surface preparation histology quantified sensory cell loss. At the lowest level [Leq=90 dB(A)] there were no differences in the trauma produced by G and nonG exposures. For Leq >90 dB(A) nonG exposures produced increased trauma relative to equivalent G exposures. Removing energy from the impacts by limiting their bandwidth reduced trauma. The use of noise bursts to produce the nonG noise instead of impacts also reduced the amount of trauma.     

Cochlear toughening,protection, and potentiation of noise-induced trauma by non-Gaussian noise

An interrupted noise exposure of sufficient intensity, presented on a daily repeating cycle, produces a threshold shift (TS) following the first day of exposure. TSs measured on subsequent days of the exposure sequence have been shown to decrease relative to the initial TS. This reduction of TS, despite the continuing daily exposure regime, has been called a cochlear toughening effect and the exposures referred to as toughening exposures. Four groups of chinchillas were exposed to one of four different noises presented on an interrupted (6 h/day for 20 days) or noninterrupted (24 h/day for 5 days) schedule. The exposures had equivalent total energy, an overall level of 100 dB(A) SPL, and approximately the same flat, broadband long-term spectrum. The noises differed primarily in their temporal structures; two were Gaussian and two were non-Gausssian, nonstationary. Brainstem auditory evoked potentials were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. The experimental results presented here show that: (1) Exposures to interrupted high-level, non-Gaussian signals produce a toughening effect comparable to that produced by an equivalent interrupted Gaussian noise. (2) Toughening, whether produced by Gaussian or non-Gaussian noise, results in reduced trauma compared to the equivalent uninterrupted noise, and (3) that both continuous and interrupted non-Gaussian exposures produce more trauma than do energy and spectrally equivalent Gaussian noises. Over the course of the 20-day exposure, the pattern of TS following each day's exposure could exhibit a variety of configurations. These results do not support the equal energy hypothesis as a unifying principal for estimating the potential of a noise exposure to produce hearing loss.     

Noise level, inner hair cell damage, audiometric features, and equal-energy hypothesis

Rabbits were exposed to 2- to 7-kHz noise either for a short duration at a high sound-pressure level (15 or 30 min at 115 dB SPL), or a long duration at a low level (512 h at 85 dB SPL). The high-level exposure produced a hearing loss in the frequency range 2-6 kHz, whereas the low-level exposure gave maximum hearing loss at 12-20 kHz. The 115-dB exposure caused significantly more damage to inner hair cells than the 85-dB exposure. The implications of the present results for evaluating audiograms, equal-energy hypothesis, risk criteria, and subjective auditory features are pointed out.     

Frequency patterns of TTS for different exposure intensities

Temporary threshold shift (TTS) was measured for several different test frequencies following exposure to a 2500-Hz tone. The intensity of the exposure tone was varied from 82 to 97 dB SPL; its duration was 5 or 10 min. In each post-exposure session, TTS was followed for four test frequencies using a method of adjustment. In all cases, the "center of balance" of the TTS pattern moved upward in frequency as exposure intensity increased. This outcome is consistent with the idea of a basalward migration of the traveling-wave envelope with increasing exposure intensity, but the evidence is not unequivocal.     

The effects of the amplitude distribution of equal energy exposures on noise-induced hearing loss: the kurtosis metric

Seventeen groups of chinchillas with 11 to 16 animals/group (sigmaN = 207) were exposed for 5 days to either a Gaussian (G) noise or 1 of 16 different non-Gaussian (non-G) noises at 100 dB(A) SPL. All exposures had the same total energy and approximately the same flat spectrum but their statistical properties were varied to yield a series of exposure conditions that varied across a continuum from G through various non-G conditions to pure impact noise exposures. The non-G character of the noise was produced by inserting high level transients (impacts or noise bursts) into the otherwise G noise. The peak SPL of the transients, their bandwidth, and the intertransient intervals were varied, as was the rms level of the G noise. The statistical metric, kurtosis (beta), computed on the unfiltered noise beta(t), was varied 3 < or = beta(t) < or = 105. Brainstem auditory evoked responses were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. Trauma, as measured by asymptotic and permanent threshold shifts (ATS, PTS) and by sensory cell loss, was greater for all of the non-G exposure conditions. Permanent effects of the exposures increased as beta(t) increased and reached an asymptote at beta(t) approximately 40. For beta(t) > 40 varying the interval or peak histograms did not alter the level of trauma, suggesting that, in the chinchilla model, for beta(t) > 40 an energy metric may be effective in evaluating the potential of non-G noise environments to produce hearing loss. Reducing the probability of a transient occurring could reduce the permanent effects of the non-G exposures. These results lend support to those standards documents that use an energy metric for gauging the hazard of exposure but only after applying a "correction factor" when high level transients are present. Computing beta on the filtered noise signal [beta(f)] provides a frequency specific metric for the non-G noises that is correlated with the additional frequency specific outer hair cell loss produced by the non-G noise. The data from the abundant and varied exposure conditions show that the kurtosis of the amplitude distribution of a noise environment is an important variable in determining the hazards to hearing posed by non-Gaussian noise environments.     

Hearing loss from interrupted, intermittent, and time varying Gaussian noise exposures: the applicability of the equal energy hypothesis

Eight groups of chinchillas (N=74) were exposed to various equivalent energy [100 or 106 dB(A) sound pressure level (SPL)] noise exposure paradigms. Six groups received an interrupted, intermittent, time varying (IITV) Gaussian noise exposure that lasted 8 h/d, 5 d/week for 3 weeks. The exposures modeled an idealized workweek. At each level, three different temporal patterns of Gaussian IITV noise were used. The 100 dB(A) IITV exposure had a dB range of 90-108 dB SPL while the range of the 106 dB(A) IITV exposure was 80-115 dB SPL. Two reference groups were exposed to a uniform 100 or 106 dB(A) SPL noise, 24 h/d for 5 days. Each reference group and the three corresponding IITV groups comprised a set of equivalent energy exposures. Evoked potentials were used to estimate hearing thresholds and surface preparation histology quantified sensory cell populations. All six groups exposed to the IITV noise showed threshold toughening effects of up to 40 dB. All IITV exposures produced hearing and sensory cell loss that was similar to their respective equivalent energy reference group. These results indicate that for Gaussian noise the equal energy hypothesis for noise-induced hearing loss is an acceptable unifying principle.     

Measurement of sensitivities for the thermal recording of laser beams

A simple technique for determining the energy sensitivities for the thermographic recording of laser beams is described. The principle behind this technique is that, if a laser beam with a known spatial distribution such as a Gaussian profile is used for imaging, the radius of the thermal image formed depends uniquely on the intensity of the impinging beam. Thus by measuring the radii of the images produced for different incident beam intensities the minimum intensity necessary (that is, the threshold) for thermographic imaging is found. The diameter of the laser beam can also be found from this measurement. A simple analysis based on the temperature distribution in the laser heated material shows that there is an inverse square root dependence on pulse duration or period of exposure for the energy fluence of the laser beam required, both for the threshold and the subsequent increase in the size of the recording. It has also been shown that except for low intensity, long duration exposure on very low conductivity materials, heat losses are not very significant.     

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 hearing damage caused by metabolic exhaustion: a mathematical model

A mathematical model for noise-induced hearing loss is based on the assumption that hair cells are damaged, temporarily or permanently, by metabolic exhaustion, and that the number of damaged hair cells and the hearing loss are monotonically increasing functions of an energy deficiency. The purpose of the model is to focus on the influence of sound intensity, exposure duration, and temporal pattern of the sound exposure on the noise-induced hearing loss from long-duration exposures. The model is restricted to the range of sound levels where metabolic exhaustion probably is the main reason for the hair cell damage. Only exposures with similar frequency spectra and producing moderate hearing losses are considered; frequency dependence is not discussed.     

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.     

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.     

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.     

AP threshold elevation in the guinea pig following exposure to a broadband noise

Sixty guinea pigs were exposed to a steady-state broadband noise with a falling frequency spectrum. The sound-pressure level was varied between 96 and 117 dB SPL, and the duration of the exposure was varied from 3 to 12 h. After 4-5 weeks, the auditory thresholds were determined by electrocochleography at 14 frequencies, and the results were compared with a control group. With increasing sound-pressure level, the thresholds became elevated at all frequencies. The maximum threshold elevation also exhibited a slight shift toward higher frequencies. With increasing exposure time, the threshold elevations increased and shifted into the high-frequency region, whereas the low-frequency region was less affected. Linear regression analysis showed that the average threshold elevation between 1 and 20 kHz did not deviate from that predicted by the equal-energy hypothesis. However, the high-frequency loss at 5-20 kHz was very dependent on the exposure time, whereas the 1- to 4-kHz loss was not. There was no sign of any critical intensity with sudden increments in threshold elevation.