Asymptotic Threshold Shift Research Articles

Prolonged noise exposure-induced auditory threshold shifts in rats

Noise-induced hearing loss (NIHL) initially increases with exposure duration, but eventually reaches an asymptotic threshold shift (ATS) once the exposure duration exceeds 18–24 h. Equations for predicting the ATS have been developed for several species, but not for rats, even though this species is extensively used in noise exposure research. To fill this void, we exposed rats to narrowband noise (NBN, 16–20 kHz) for 5 weeks starting at 80 dB SPL in the first week and then increasing the level by 6 dB per week to a final level of 104 dB SPL. Auditory brainstem responses (ABR) were recorded before, during, and following the exposure to determine the amount of hearing loss. The noise induced threshold shift to continuous long-term exposure, defined as compound threshold shift (CTS), within and above 16–20 kHz increased with noise level at the rate of 1.82 dB threshold shift per dB of noise level (NL) above a critical level (C) of 77.2 dB SPL i.e. CTS = 1.82(NL-77.2). The normalized amplitude of the largest ABR peak measured at 100 dB SPL decreased at the rate of 3.1% per dB of NL above the critical level of 76.9 dB SPL, i.e., %ABR Reduction = 3.1%(NL-76.9). ABR thresholds measured >30 days post-exposure only partially recovered resulting in a permanent threshold shift of 30–40 dB along with severe hair cell loss in the basal, high-frequency region of the cochlea. In the rat, CTS increases with noise level with a slope similar to humans and chinchillas. The critical level (C) in the rat is similar to that of humans, but higher than that of chinchillas.

Hearing-aid safety: A comparison of estimated threshold shifts for gains recommended by NAL-NL2 and DSL m[i/o] prescriptions for children

Objective: To investigate the predicted threshold shift associated with the use of nonlinear hearing aids fitted to the NAL-NL2 or the DSL m[i/o] prescription for children with the same audiograms. For medium and high input levels, we asked: (1) How does predicted asymptotic threshold shifts (ATS) differ according to the choice of prescription? (2) How does predicted ATS vary with hearing level for gains prescribed by the two prescriptions? Design: A mathematical model consisting of the modified power law combined with equations for predicting temporary threshold shift (Macrae, 1994b) was used to predict ATS. Study sample: Predicted threshold shift were determined for 57 audiograms at medium and high input levels. Results: For the 57 audiograms, DSL m[i/o] gains for high input levels were associated with increased risk relative to NAL-NL2. The variation of ATS with hearing level suggests that NAL-NL2 gains became unsafe when hearing loss > 90 dB HL. The gains prescribed by DSL m[i/o] became unsafe when hearing loss > 80 dB HL at a medium input level, and > 70 dB HL at a high input level. Conclusion: There is a risk of damage to hearing for children using nonlinear amplification. Vigilant checking for threshold shift is recommended.

Dan Johnson’s impact on hearing research

Daniel L. Johnson is well known for his many technical contributions to noise research. Throughout a long and distinguished career at Wright–Patterson Air Force Base, Dan published the results of several significant experiments, including his landmark experiments on asymptotic threshold shift and exposure to impulse noise. His work in the area of noise exposure laid much of the groundwork for a greater understanding of the physiologic response to hazardous noise, much of which has since been incorporated in national and international standards. Dan is highly regarded for his tireless work on technical and advisory committees in noise, and most recently, ototoxicity. Throughout his career, Dan has adhered to a self-imposed standard of intellectual honesty and discovery. Dan’s most recent endeavor, the development of a personal noise dosimeter designed for self-monitoring by the employee, is characteristic of his creativity and energy. Perhaps less well known are his contributions over the years to the success of his younger colleagues. He has accomplished this in an unselfish and egalitarian manner, oftentimes challenging and even contradicting his own research. The focus of this talk will elaborate on these facets of Dan’s professional contributions.

Correlations among evoked potential thresholds, distortion product otoacoustic emissions and hair cell loss following various noise exposures in the chinchilla

Changes in cubic distortion product otoacoustic emissions (ΔDPOAEs), evoked potential threshold shifts (TSs) and outer hair cell (OHC) losses were measured in a population of 95 noise-exposed chinchillas. Each animal was exposed to one of 23 different noises in an asymptotic threshold shift (ATS) producing paradigm or an interrupted noise paradigm which typically produced a toughening effect. Noises were narrow band (400 Hz) impacts with center frequencies of 0.5, 1.0, 2.0, 4.0 or 8.0 kHz presented 1 impact/s at peak SPLs of 109, 115, 121 or 127 dB. The duration of the exposures was 24 h/day for 5 days (ATS paradigm) or 6 h/day for 20 days (toughening paradigm). Based on a linear regression analysis of individual subject and group mean data, correlations among the following dependent variables were made: ΔDPOAEs, ATS, toughening or TS recovery (TS r), permanent threshold shift (PTS) and OHC loss. Correlations among these metrics were generally highest for DPOAE primary frequency levels, L 1= L 2=70 dB. Correlation between ΔDPOAE and TS r was typically low, while a considerably higher correlation was found between ΔDPOAE and ATS. Correlations among the permanent measures of noise-induced effects, i.e. for ΔDPOAE/PTS and ΔDPOAE/OHC loss were typically poor when there was only a small or a moderate noise-induced effect (PTS<25 dB and ΔDPOAE<20 dB). However, for PTS<25 dB the correlation between PTS and OHC loss was considerably better than the correlation between ΔDPOAE and OHC loss. For more severe noise-induced changes there was generally a good correspondence between OHC loss, PTS and ΔDPOAE metrics.

Sound-induced priming of the chinchilla auditory system

Exposure of the auditory system to either continuous or interrupted nontraumatic noises, often collectively referred to as priming exposures, has been shown, in a number of experimental paradigms, to reduce the susceptibility of the auditory system to noise-induced hearing and sensory cell loss from a subsequent traumatic exposure. Using auditory evoked potentials to obtain pure-tone thresholds and cochleograms to quantify sensory cell losses, the issue of priming-induced protective effects was examined in the chinchilla. Priming was accomplished with either a continuous noise or with a continuous noise followed by an interrupted noise. Trauma was induced by exposure to high-level impacts over a 5-day period that resulted in an asymptotic threshold shift. A comparison of the two groups of primed subjects with an unprimed control group showed that there were some statistically significant reductions in the asymptotic response of the primed groups to the traumatic exposure but no differences in permanent changes in thresholds among the three groups 30 days following the traumatic exposure. There were, however, some statistically significant, frequency-specific, reductions in outer hair cell loss in the primed groups. When conditioning was followed by the interrupted exposure that produced a threshold shift toughening effect, the conditioning protocol had no effect on the response of subjects to the interrupted exposure. There were also no differences in thresholds or sensory cell loss between the two primed groups 30 days post-trauma. Priming protocols may have different effects on the development of noise-induced trauma that are dependent on the nature of the traumatic stimulus, that is, long-term high-level impact noise exposure versus acute continuous noise exposure.

Susceptibility of the noise-toughened auditory system to noise-induced trauma

The auditory system ‘toughened’ by an interrupted noise exposure has been shown in several reports, to be less affected by (or protected from) a subsequent high level noise exposure. A group of chinchillas ( n=12) was exposed to an interrupted noise at 95 dB SPL, 0.5 kHz octave band, 6 h/day for 10 days. Threshold shifts measured over the 10 day exposure showed that the animals responded by either (1) developing a large toughening effect (i.e., thresholds after day 10 of the exposure were considerably better than at the end of day 1) ( n=5) or (2) not showing any toughening, instead thresholds continued to get worse over the course of the exposure ( n=7). After a 5 day interval, during which thresholds of all the animals returned to normal, they, along with a control group ( n=10) not exposed to the interrupted noise, were exposed to an asymptotic threshold shift producing traumatic noise (127 dB peak SPL narrow band impact, 1 kHz center frequency, 24 h/day for 5 days). Auditory evoked potential audiometry and surface preparation histology showed that there were no statistically significant differences in the response of any of the above groups to the traumatic noise. The interrupted noise exposure, whether it produced a toughening or not, did not provide any protection from a subsequent high-level noise.

Noise-induced hearing loss in the noise-toughened auditory system

The auditory system, toughened by an interrupted noise exposure, has been shown in several reports to be less affected by (or protected from) a subsequent high-level noise exposure. Exposure to 115 dB peak SPL, 1 kHz narrow band (400 Hz) transients presented 1/s, 6 h/day, to four groups of chinchillas produced a 10–28 dB toughening effect across the 0.5–8.0 kHz test frequency range. Following either a 30 day or an 18 h recovery period the animals were exposed to the same impulses but presented at 121 or 127 dB peak SPL for five uninterrupted days, thus producing an asymptotic threshold shift (ATS) condition. Comparisons between toughened and untoughened control subjects showed: (1) During the 121 dB exposure there was a statistically significant reduction of 10–25 dB in ATS across the entire test frequency range. Thirty days following the 121 dB exposure there were no significant differences in the postexposure permanent effects on thresholds and sensory cell loss. (2) During the 127 dB exposure only the group with the 30 day interval between the toughening and traumatic exposures showed a small (∼10 dB), statistically significant, frequency-specific (8 kHz), reduction in ATS. Thirty days following the 127 dB exposure a statistically significant protective effect on threshold was measured only at 16.0 kHz. However, both toughened groups showed less inner hair cell loss at and above 1.0 kHz, while only the group with the 18 h interval between the toughening and traumatic exposures showed less outer hair cell loss at and above 1.0 kHz. There were no systematic differences in the response of the toughened animals that could be attributed to the 30 day or 18 h post-toughening interval.

The major historical events in the relating of noise-induced hearing loss to noise exposure

One event was the recognition of ‘‘boilermaker’s disease.’’ Another was some of the threshold shift studies during and after WWII that led to the BENOX report. After these developments, there were a series of key events and decisions that have led up to our current state of knowledge and procedures. How Henning von Gierke was influential in most of these and how his decisions have consistently proven to be correct will be demonstrated. For example, he contributed to the 1953 BENOX report, promoted the ‘‘equal energy concept,’’ conceived and patented the first noise dosimeter, oversaw the EPA ‘‘levels’’ and criteria documents, and was the chair of the working group that wrote the current international standard (ISO-R1999) that relates noise exposure to noise-induced hearing loss. He was also instrumental in supporting many key research issues such as fetal noise exposure, asymptotic temporary threshold shift, and the longitudinal hearing of children. Henning’s perseverance and dedication has provided society with an answer to one of his favorite questions, ‘‘how much noise is too much?’’

Otoacoustic emissions and threshold shift correlations following asymptotic threshold shift producing noise exposures

Cubic distortion product emissions (3DPE) were measured in four groups of chinchillas (N=4 or 5/group) exposed for 5 days, 24 h/d, to 121-dB peak SPL, narrow-band (400 Hz) impacts having center frequencies (CF) of 1.0, 2.0, 4.0, or 8.0 kHz. The noise exposure produced an asymptotic threshold shift (ATS) at audiometric test frequencies showing a threshold shift (TS). Levels of ATS up to 80 dB were measured at and above the CF of the impact. Surprisingly, the 1.0- and 2.0-kHz CF impacts produced the largest ATS at 16 kHz. There was, in general, a congruence between the ATS and 3DPE changes following exposures to CFs ≥2.0 kHz. However, with the 1.0-kHz CF impact exposure, the two metrics were not in general agreement. Relations among permanent thresholds shifts (PTS), 3DPEs and outer hair cell (OHC) losses were quite variable for low- and mid-frequency (≤2.0 kHz) biased lesions. For the 4.0- and 8.0-kHz CF impacts, 3DPE changes reflected OHC losses and PTS rather closely. DPEgrams using primary levels of 40 through 70 dB SPL in 10-dB increments were found to be most effective in the evaluation of OHC lesions than was any single DPEgram. [Research supported by NIOSH Grant No. R01 OH02317.]

The effect of the level of impact noise on hearing loss

Impulse and impact noise found in industry may be particularly dangerous for workers’ hearing. This study examines the effect of the level of impact noise on hearing loss. Twenty four adult chinchillas were exposed to impact noise for 7.5 h. The subjects were divided into four groups and exposed to impulses delivered at 1/s at one of four different intensities: 113, 119, 125, and 131 dB. As the level of exposure increased, the permanent hearing loss of the animals increased. At lower levels, 113–125 dB hearing loss increased at approximately 1.8 dB for each dB of noise. These findings are consistent with studies using continuous noise which report a 1.7‐dB increase in asymptotic threshold shift for every dB increase in exposure. However, as the level of the impact increases beyond a critical level, (125 dB) the resulting threshold shift increases dramatically i.e., 6 dB for each dB increase in exposure level. It has been shown in prior research [Hamernik et al., Hear. Res. 13, 229–247 (1984) and Henderson et al., Hear. Res. 76, 101–117 (1994)] that the anatomical damage to the cochlea at this critical level changes from metabolic to mechanical. [Research supported by NIOSH Grant No. 15034470.]

Prediction of asymptotic threshold shift caused by hearing aid use.

This study used a well-verified mathematical model to predict asymptotic temporary threshold shift (ATS) caused by hearing aid use. The model determined the amounts of ATS to be expected if real ear insertion gains (REIGs) recommended by the current National Acoustic Laboratories (NAL) procedure are used. It also determined the consequences of use of excess REIG and of high input levels to hearing aids. If recommended REIGs are used and input levels are normal (average A-weighted input levels of about 61 dB SPL), ATS is unlikely to occur for clients who have typical audiograms with three-frequency average pure-tone thresholds (PTAs) less than 60 dB HL. For people with PTAs greater than 60 dB HL, small amounts of ATS can be expected to occur during hearing aid use, but these amounts of ATS are safe, that is, unlikely to be associated with permanent threshold shift (PTS) for individuals with all PTAs except those greater than about 100 dB HL. If REIGs are 15 dB greater than those recommended, the amounts of ATS will be unsafe for people with PTAs greater than about 80 dB HL. It appears unwise for clients who have this degree of hearing loss to use excess REIG. The use of excess REIG in high ambient levels of sound (average A-weighted input levels of about 75 dB SPL) is likely to cause PTS for hearing aid users with PTAs of about 50 dB HL or greater. Clients who prefer to use excess REIG should therefore avoid high ambient sound levels.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of primed and interrupted noise exposure paradigms on hearing loss

Exposure to low-level noise (priming) produces a protective effect on the auditory system evidenced by a reduced permanent threshold shift (PTS) from a subsequent high-level exposure. Similarly, regularly interrupting a high-level noise exposure causes the threshold shift following daily repeated exposures to the noise to be reduced with a concomitant lowering of PTS. These effects, collectively referred to as ‘‘toughening,’’ can exceed 35 dB. If the toughening mechanism elicited during both types of exposure paradigms has a common origin, then combining the paradigms should yield predictable results. Results from nine exposure paradigms with five to six chinchillas in each paradigm are reported. Impacts of 113 or 119 dB peak SPL and pink noise of 72 or 78 dB SPL presented over five or 20 days in an interrupted or noninterrupted paradigm were used. Results suggest that priming can affect the PTS but has little or no effect on the toughening produced during interrupted exposures or the asymptotic threshold shift (ATS) produced by an uninterrupted exposure. Similarly, the toughening produced during an interrupted exposure affects PTS but not ATS from an uninterrupted exposure. These results suggest independent mechanisms for the two toughening phenomena. [Research sponsored by NIOSH.]

Lipid peroxidation inhibitor attenuates noise-induced temporary threshold shifts

The purpose of this study was to investigate the protective effects of U74389F (Upjohn Co. Kalamazoo, MI), a 21-aminosteroid/lipid peroxidation inhibitor, and a member of the lazaroid drug class, on temporary threshold shifts in animals exposed to prolonged noise stimulation. Animals treated with U74389F and exposed to noise showed attenuated cochlear action potential threshold (CAP) shifts and cochlear microphonic (CM) when compared to non-drug treated noise-exposed subjects. These data suggest that inhibition of FOR induced lipid peroxidation is an important mechanism in noise-induced asymptotic temporary threshold shifts.

Human temporary threshold shift (TTS) and damage risk

Information regarding the relation of human temporary threshold shift (TTS) to properties of steady-state and intermittent noise published since the 1966 appearance of the CHABA damage risk contours is reviewed. The review focuses on results from four investigative areas relevant to potential revision of the CHABA contours including effects of long-duration exposure and asymptotic threshold shifts (ATS); equivalent quiet and/or safe noise levels; effects of intermittency; and use of noise-induced temporary threshold shift (NITTS) to predict susceptibility to noise-induced permanent threshold shift (NIPTS). These data indicate that two of three major postulates on which the original contours were based are not valid. First, recovery from TTS is not independent of the conditions that produced the TTS as was assumed. Second, the assumption that all exposures that produce equal TTS2 are equally hazardous is not substantiated. The third postulate was that NIPTS produced by 10 years of daily exposure is approximately equal to the TTS2 produced by the same noise after an 8-h exposure. Based upon several TTS experiments showing that TTS reaches an asymptote after about 8 h of exposure, the third CHABA postulate can be reworded to state the hypothesis that ATS produced by sound of fixed level and spectrum represents an upper bound on PTS produced by that sound regardless of the exposure duration or the number of times exposed. This hypothesis has a strong, logical foundation if ATS represents a true asymptote for TTS, not a temporary plateau, and if threshold shifts do not increase after the noise exposure ceases.

Kurtosis measurements: Implications for noise exposure criteria

Two conventional measures of an industrial noise environment are the overall sound-pressure level (SPL) and the power spectrum. While these two measures are necessary, they may not be sufficient to describe a noise environment for the purposes of evaluating the hazard to hearing. This presentation will describe the results of an experiment designed to test the hypothesis that for equal SPL and power spectrum a high-kurtosis noise exposure is more hazardous to hearing than is a low-kurtosis noise. Two groups of chinchillas, with two animals per group, were exposed continuously for 5 days, to one of two classes of noise at a 90 dB SPL. The power spectrum of both noises was identical but the noises had different values of kurtosis. The results clearly showed that there was up to a 20 dB greater permanent hearing loss for the animals exposed to the high-kurtosis noise. Detailed results of asymptotic and permanent threshold shifts and sensory cell losses will be presented. These results would appear to be a clear indication that, even for moderate levels of exposure, energy is not a sufficient variable upon which to base noise exposure standards. [Work supported by NIOSH.]

Prediction of noise-induced temporary threshold shift

This paper reports the state of the art of the method for predicting TTS following exposure to noise having an arbitrary spectrum and temporal characteristics. Existence of the critical band for TTS was proved by two of the present authors from the results of their experiment. The center frequency and the width of the critical band were calculated, together with their 95% confidence limits. The theory of critical band enabled us to estimate TTS at a given test frequency due to noise having any spectrum content. In order to estimate the growth of TTS with the exposure time, new empirical formulae of TTS growth were determined based on the results obtained in the 8-h TTS experiments with exposure levels from 85 to 95 dB and those obtained in the 24-h TTS experiments with exposure levels from 65 to 86 dB. The formulae assume an asymptotic threshold shift and are expressed as a function of the exposure duration and the spectrum level of the exposure noise at the center frequency of critical band with respect to TTS. TTS due to steady state noise can be estimated by means of the critical band theory and the formulae of TTS growth. For the non-steady noise exposure, application of the method of unit step function is proved useful to estimate the TTS produced. The idea of the method is to approximate the temporal level change of the noise by a step function and then apply the formula of TTS growth to each of the steps where the level of noise is regarded as steady.

The interaction of impulse and continuous noise: Energy and spectral considerations in the production of hearing loss

Realistic industrial noise environments containing impulsive and continuous noise were modeled using a 5‐day exposure paradigm that produces an asymptotic threshold shift (ATS). Pre‐ and postexposure measures of hearing thresholds were obtained on 96 chinchillas using evoked auditory responses (EAR). Six control groups were exposed to octave bands of noise at 0.5, 2.0, and 4.0 kHz at 95, 90, and 86 dB SPL, respectively, or impacts of 113, 119, or 125 dB peak SPL presented once per 1, 4, or 16 s, respectively. Nine interaction groups were exposed to combinations of an impulse and continuous noise. The greatest spectral overlap of energy occurs between the impulse and the 0.5 kHz octave band of noise. Although each of the different impulse noise exposures were balanced to produce an equal energy exposure, an exacerbation of hearing loss was produced in animals exposed to the 119‐ and 125‐dB impacts in combination with the low‐frequency (0.5‐kHz) continuous noise. This synergistic effect gradually disappears when the spectral overlap between noises is reduced. [Research supported by NIOSH.]

Evoked response “forward‐masking” functions in hearing‐impaired chinchillas

Previous research in psychophysics has shown that the time course of recovery from forward masking is prolonged in listeners with sensorineural hearing loss (Nelson and Turner, 1980). In order to evaluate the physiological basis for the change in the time course of forward masking, evoked response recordings were obtained from the inferior colliculus of the chinchilla both before and after noise induced hearing loss. Evoked response “forward‐masking” functions were obtained by measuring the masker level required to produce a 50% reduction in the response to a probe tone (re: probe response alone) which followed the masker at various time intervals (2 to 100 ms). The time course of “forward masking” was estimated by fitting a time constant to the data. Animals were exposed to a pure tone that produced either 30–50 dB of asymptotic threshold shift or 25–30 dB of permanent threshold shift. The time constants fit to the “forward‐masking” function were found to be prolonged in the region of hearing loss. In general there was a strong correlation between the time constant of recovery from “forward masking” and hearing loss. The implications of these results will be discussed. [Work supported by NIH 5‐R01‐NS16761‐06 and NIOSH 1‐R01‐OH00364.]

The influence of moderate-intensity noise on the click-evoked compound action potential of the guinea pig, Cavia porcellus.

Noise-induced alterations of the click-evoked compound potential (CAP) were studied by means of electrodes chronically implanted near the round window in 15 pigmented guinea pigs aged 3-6 months. The potentials were recorded before, during and after exposure to continuous pink noise maintained at an intensity of 80, 90 or 100 dB SPL for 120 h. During the exposure phase the CAP thresholds of all the animals tested increased exponentially, nearly leveling out by approximately 48 h to form an asymptotic threshold shift. Recovery after the end of exposure also occurred exponentially, with a return to the original threshold for neural excitation after at most 72 h. There was no detectable change in amplitude, latency or inter-peak interval of the CAP when correlated with the change in threshold.

The growth of TTS as a function of the peak level and the duration of exposure to an impact noise

The influence of the peak level and the duration of exposure on the growth of TTS was measured using an impact noise having a decay time of approximately 500 ms. Four normal hearing subjects participated in the experiment. For each subject, TTS was measured 2 min after exposure at the most affected ear and audiometric frequency for this particular noise. The subjects were exposed to series of impacts at peak levels of 102, 108, 114, and 120 dBA. The repetititon rate of 1 pps was kept constant throughout the experiment. Exposure durations of 0.5, 1, 2, 4, 8, 16, 32, and 60 min were tested. For the higher peak levels, the exposure was limited to durations that induced amounts of TTS inferior to 20 dB. Individual and median data relating TTS to exposure duration were fitted with a high degree of accuracy using Gumpertz functions. The median rate of growth of TTS doubled for each 6‐dB increase in the peak level between 102 and 114 dBA. Asymptotic threshold shift appeared to be reached or approached within 60 ...