Impact noise and the equal energy hypothesis

The equal energy hypothesis (EEH) was evaluated over a limited range of conditions by exposing four groups of chinchillas to impact noise (200-ms B duration) presented at a fixed rate of four impacts per second. The intensity of the impacts (107-125 dB peak SPL) and the duration (120-1.87 h) of the four exposure conditions were counterbalanced so that the four groups received the same total energy. The traumatic power of the exposures was assessed by measuring the threshold shift of the auditory evoked response and the amount of hair cell loss. Exposure between 107 and 119 dB were consistent with the EEH in that they produced roughly the same amount of permanent threshold shift (less than 20 dB) and hair cell loss (less than 20%). However, the 125-dB exposure produced substantially more threshold shift and hair cell loss than the three lower intensities. Thus, the EEH may be applicable only at lower impact intensities; above a "critical intensity" the amount of damage increases significantly.     

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.     

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.     

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 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.     

Impulse noise: critical review

A review of the last 10 years of research on impulse noise reveals certain insights and perspectives on the biological and audiological effects of exposures to impulse noise. First, impulse noise may damage the cochlea by direct mechanical processes. Second, after exposure to impulse noise, hearing may recover in an erratic, nonmonotonic pattern. Third, even though the existing damage-risk criteria evaluate impulse noise in terms of level, duration, and number, often parameters such as temporal pattern, waveform, and rise time are also important in the production of a hearing loss. Fourth, the effects of impulse noise are often inconsistent with the principle of the equal energy hypothesis. Fifth, impulse noise can interact with background continuous noise to produce greater hearing loss than would have been predicted by the simple sum of the individual noises.     

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.     

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.     

Hearing loss from interrupted, intermittent, and time varying non-Gaussian noise exposure: The applicability of the equal energy hypothesis

Sixteen groups of chinchillas (N=140) were exposed to various equivalent energy noise paradigms at 100 dB(A) or 103 dB(A) SPL. Eleven groups received an interrupted, intermittent, and time varying (IITV) non-Gaussian exposure quantified by the kurtosis statistic. The IITV exposures, which lasted for 8 hday, 5 daysweek for 3 weeks, were designed to model some of the essential features of an industrial workweek. Five equivalent energy reference groups were exposed to either a Gaussian or non-Gaussian 5 days, 24 hday continuous noise. Evoked potentials were used to estimate hearing thresholds and surface preparations of the organ of Corti quantified the sensory cell population. For IITV exposures at an equivalent energy and kurtosis, the temporal variations in level did not alter trauma and in some cases the IITV exposures produced results similar to those found for the 5 day continuous exposures. Any increase in kurtosis at a fixed energy was accompanied by an increase in noise-induced trauma. These results suggest that the equal energy hypothesis is an acceptable approach to evaluating noise exposures for hearing conservation purposes provided that the kurtosis of the amplitude distribution is taken into consideration. Temporal variations in noise levels seem to have little effect on trauma.     

Conditioning-induced protection from impulse noise in female and male chinchillas

Sound conditioning (pre-exposure to a moderate-level acoustic stimulus) can induce resistance to hearing loss from a subsequent traumatic exposure. Most sound conditioning experiments have utilized long-duration tones and noise at levels below 110 dB SPL as traumatic stimuli. It is important to know if sound conditioning can also provide protection from brief, high-level stimuli such as impulses produced by gunfire, and whether there are differences between females and males in the response of the ear to noise. In the present study, chinchillas were exposed to 95 dB SPL octave band noise centered at 0.5 kHz for 6 h/day for 5 days. After 5 days of recovery, they were exposed to simulated M16 rifle fire at a level of 150 dB peak SPL. Animals that were sound conditioned showed less hearing loss and smaller hair cell lesions than controls. Females showed significantly less hearing loss than males at low frequencies, but more hearing loss at 16 kHz. Cochleograms showed slightly less hair cell loss in females than in males. The results show that significant protection from impulse noise can be achieved with a 5-day conditioning regimen, and that there are consistent differences between female and male chinchillas in the response of the cochlea to impulse noise.     

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.     

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.     

Noise levels and hearing thresholds in the drop forging industry

A-weighted equivalent continuous noise levels for hammer and press operations in a drop-forging industry were determined using both tape recordings of the noise and personal noise dosimeters. The results indicated average A-weighted Leq values of 108 dB for hammer operators and 99 dB for press operators. Comparison of hearing level statistics for 716 hammer and press operators and 293 control subjects indicated the severe hazard to hearing of impact noise exposures. For mean exposure times of less than 10 years, hearing levels for the press (99 dB) and hammer (108 dB) operator age groups are nearly identical, and in the latter case are less than those predicted for exposure to equivalent continuous noise. For long-term exposures of 10 years or more, the results of this study indicate that hearing losses resulting from impact noise in the drop-forging industry are as great or greater than those resulting from continuous noise.     

Cubic distortion product otoacoustic emissions in young and aged chinchillas exposed to low-frequency noise.

The aim of this study was to examine susceptibility to noise-induced hearing loss in animals with and without age-related hearing loss (AHL), using cubic distortion product otoacoustic emissions (CDPs) to assess the functional status of the outer hair cell (OHC) system. Subjects were young (< or = 3-yr-old) and aged (10- to 15-yr-old) chinchillas. CDP thresholds and input/output (I/O) functions were measured before and after exposure to 95 dB or 106 dB SPL low-frequency noise. The results indicate that (a) aging in the chinchilla is associated with significant elevations of CDP thresholds and depression of CDP I/O functions, (b) noise exposures cause equivalent CDP threshold elevations and amplitude reductions in young animals with normal hearing and older animals with AHL, and (c) CDP threshold and amplitude measures provide information that complements evoked potentials measured from the auditory midbrain.     

Attenuation of high-level impulses by earmuffs

Attenuation of high-level acoustic impulses (noise reduction) by various types of earmuffs was measured using a laboratory source of type A impulses and an artificial test fixture compatible with the ISO 4869-3 standard. The measurements were made for impulses of peak sound-pressure levels (SPLs) from 150 to 170 dB. The rise time and A duration of the impulses depended on their SPL and were within a range of 12-400 mus (rise time) and 0.4-1.1 ms (A duration). The results showed that earmuff peak level attenuation increases by about 10 dB when the impulse's rise time and the A duration are reduced. The results also demonstrated that the signals under the earmuff cup have a longer rise and A duration than the original impulses recorded outside the earmuff. Results of the measurements were used to check the validity of various hearing damage risk criteria that specify the maximum permissible exposure to impulse noise. The present data lead to the conclusion that procedures in which hearing damage risk is assessed only from signal attenuation, without taking into consideration changes in the signal waveform under the earmuff, tend to underestimate the risk of hearing damage.     

Attenuation and protection provided by ossicular removal

Behavioral studies of hearing loss produced by exposure to ototraumatic agents in experimental animals, combined with the anatomical evaluation of end-organ pathology, have provided useful information about the relation between dysfunction and pathology. However, in order to attribute a given hearing loss to some pattern of cochlear damage, it is necessary to test each ear independently. The objective of the present study was to evaluate attenuation measured behaviorally and protection to the cochlea provided by removal of the malleus and incus in noise-exposed chinchillas. Results from one behaviorally trained chinchilla with ossicular removal indicated a conductive hearing loss that varied from 41 dB at 0.125 kHz to 81 dB at 4.8 kHz and averaged 60 dB. Counts of missing sensory cells in ears of seven chinchillas with unilateral ossicular removal and exposure to noise (octave band centered at 0.5 kHz, 95 dB SPL, for durations up to 216 days, or centered at 4.0 kHz, 108 dB SPL, for 1.75 h) showed no more cell loss on the protected side than in age-matched control ears. From these data it is concluded that ossicular removal provides enough attenuation to protect the chinchilla cochlea from damage during these noise exposures, and that it will insure monaural responses behaviorally as long as the hearing loss in the test ear does not exceed that in the ear with ossicular removal by approximately 50 dB at any frequency.     

Effects of peak pressure and energy of impulses

Peak pressure has been one of the key parameters of impulse noise used to assess the hazard to hearing. It is used in most international noise exposure limits. France uses an A-weighted energy limit. There is a rough correspondence between peak pressure and the hazard to hearing for a given type of impulse noise. However, when the effects of different types of impulses are compared, this correspondence breaks down. One of the alternate measures of impulse intensity is weighted energy. Weighted energy is appealing for a number of reasons. It does not depend on details of the pressure-time history such as the peak pressure and the more common duration measures. It should be easier to integrate with continuous or intermittent noise standards. It would make it easier to use standard hearing protector attenuation to estimate the hazard when a specific hearing protector is worn. Results of previously published articles and reports will be discussed. These reports lead to the conclusion that weighted energy is a more potent determiner of hearing hazard than peak pressure if spectral effects are controlled.