The Use of the Kurtosis-Adjusted Cumulative Noise Exposure Metric in Evaluating the Hearing Loss Risk for Complex Noise.

OBJECTIVE: To test a kurtosis-adjusted cumulative noise exposure (CNE) metric for use in evaluating the risk of hearing loss among workers exposed to industrial noises. Specifically, to evaluate whether the kurtosis-adjusted CNE (1) provides a better association with observed industrial noise-induced hearing loss, and (2) provides a single metric applicable to both complex (non-Gaussian [non-G]) and continuous or steady state (Gaussian [G]) noise exposures for predicting noise-induced hearing loss (dose-response curves). DESIGN: Audiometric and noise exposure data were acquired on a population of screened workers (N = 341) from two steel manufacturing plants located in Zhejiang province and a textile manufacturing plant located in Henan province, China. All the subjects from the two steel manufacturing plants (N = 178) were exposed to complex noise, whereas the subjects from textile manufacturing plant (N = 163) were exposed to a G continuous noise. Each subject was given an otologic examination to determine their pure-tone HTL and had their personal 8-hr equivalent A-weighted noise exposure (LAeq) and full-shift noise kurtosis statistic (which is sensitive to the peaks and temporal characteristics of noise exposures) measured. For each subject, an unadjusted and kurtosis-adjusted CNE index for the years worked was created. Multiple linear regression analysis controlling for age was used to determine the relationship between CNE (unadjusted and kurtosis adjusted) and the mean HTL at 3, 4, and 6 kHz (HTL346) among the complex noise-exposed group. In addition, each subject's HTLs from 0.5 to 8.0 kHz were age and sex adjusted using Annex A (ISO-1999) to determine whether they had adjusted high-frequency noise-induced hearing loss (AHFNIHL), defined as an adjusted HTL shift of 30 dB or greater at 3.0, 4.0, or 6.0 kHz in either ear. Dose-response curves for AHFNIHL were developed separately for workers exposed to G and non-G noise using both unadjusted and adjusted CNE as the exposure matric. RESULTS: Multiple linear regression analysis among complex exposed workers demonstrated that the correlation between HTL3,4,6 and CNE controlling for age was improved when using the kurtosis-adjusted CNE compared with the unadjusted CNE (R = 0.386 versus 0.350) and that noise accounted for a greater proportion of hearing loss. In addition, although dose-response curves for AHFNIHL were distinctly different when using unadjusted CNE, they overlapped when using the kurtosis-adjusted CNE. CONCLUSIONS: For the same exposure level, the prevalence of NIHL is greater in workers exposed to complex noise environments than in workers exposed to a continuous noise. Kurtosis adjustment of CNE improved the correlation with NIHL and provided a single metric for dose-response effects across different types of noise. The kurtosis-adjusted CNE may be a reasonable candidate for use in NIHL risk assessment across a wide variety of noise environments.

The value of a kurtosis metric in estimating the hazard to hearing of complex industrial noise exposures.

A series of Gaussian and non-Gaussian equal energy noise exposures were designed with the objective of establishing the extent to which the kurtosis statistic could be used to grade the severity of noise trauma produced by the exposures. Here, 225 chinchillas distributed in 29 groups, with 6 to 8 animals per group, were exposed at 97 dB SPL. The equal energy exposures were presented either continuously for 5 d or on an interrupted schedule for 19 d. The non-Gaussian noises all differed in the level of the kurtosis statistic or in the temporal structure of the noise, where the latter was defined by different peak, interval, and duration histograms of the impact noise transients embedded in the noise signal. Noise-induced trauma was estimated from auditory evoked potential hearing thresholds and surface preparation histology that quantified sensory cell loss. Results indicated that the equal energy hypothesis is a valid unifying principle for estimating the consequences of an exposure if and only if the equivalent energy exposures had the same kurtosis. Furthermore, for the same level of kurtosis the detailed temporal structure of an exposure does not have a strong effect on trauma.

Application of the kurtosis statistic to the evaluation of the risk of hearing loss in workers exposed to high-level complex noise.

OBJECTIVE: Develop dose-response relations for two groups of industrial workers exposed to Gaussian or non-Gaussian (complex) types of continuous noises and to investigate what role, if any, the kurtosis statistic can play in the evaluation of industrial noise-induced hearing loss (NIHL). DESIGN: Audiometric and noise exposure data were acquired on a population (N = 195) of screened workers from a textile manufacturing plant and a metal fabrication facility located in Henan province of China. Thirty-two of the subjects were exposed to non-Gaussian (non-G) noise and 163 were exposed to a Gaussian (G) continuous noise. Each subject was given a general physical and an otologic examination. Hearing threshold levels (0.5-8.0 kHz) were age adjusted (ISI-1999) and the prevalence of NIHL at 3, 4, or 6 kHz was determined. The kurtosis metric, which is sensitive to the peak and temporal characteristics of a noise, was introduced into the calculation of the cumulative noise exposure metric. Using the prevalence of hearing loss and the cumulative noise exposure metric, a dose-response relation for the G and non-G noise-exposed groups was constructed. RESULTS: An analysis of the noise environments in the two plants showed that the noise exposures in the textile plant were of a Gaussian type with an Leq(A)8hr that varied from 96 to 105 dB whereas the exposures in the metal fabrication facility with an Leq(A)8hr = 95 dB were of a non-G type containing high levels (up to 125 dB peak SPL) of impact noise. The kurtosis statistic was used to quantify the deviation of the non-G noise environment from the Gaussian. The dose-response relation for the non-G noise-exposed subjects showed a higher prevalence of hearing loss for a comparable cumulative noise exposure than did the G noise-exposed subjects. By introducing the kurtosis variable into the temporal component of the cumulative noise exposure calculation, the two dose-response curves could be made to overlap, essentially yielding an equivalent noise-induced effect for the two study groups. CONCLUSIONS: For the same exposure level, the prevalence of NIHL is greater in workers exposed to non-G noise environments than for workers exposed to G noise. The kurtosis metric may be a reasonable candidate for use in modifying exposure level calculations that are used to estimate the risk of NIHL from any type of noise exposure environment. However, studies involving a large number of workers with well-documented exposures are needed before a relation between a metric such as the kurtosis and the risk of hearing loss can be refined.

Role of the kurtosis statistic in evaluating complex noise exposures for the protection of hearing.

OBJECTIVE: To highlight a selection of data that illustrate the need for better descriptors of complex industrial noise environments for use in the protection of hearing. DESIGN: The data were derived using a chinchilla model. All noise exposures had the same total energy and the same spectrum; that is, they were equal energy exposures presented at an overall 100 dB(A) SPL that differed only in the scheduling of the exposure and the value of the kurtosis, beta(t), a statistical metric. Hearing thresholds were determined before and after noise exposure using the auditory-evoked potential measured from the inferior colliculus in the brain stem. Cochlear damage was estimated from sensory-cell counts (cochleograms). RESULTS: (1) For equivalent energy and spectra, exposure to a high-kurtosis, non-Gaussian noise produced substantially greater hearing and sensory-cell loss in the chinchilla model than a low-kurtosis, Gaussian noise. (2) beta(t) computed on the amplitude distribution of the noise could clearly differentiate between the effects of Gaussian and non-Gaussian noise environments. (3) beta(t) can order the extent of the trauma as determined by hearing thresholds and sensory-cell loss. CONCLUSIONS: The noise level in combination with the statistical properties of the noise quantified by beta(t) clearly differentiate the effects between both continuous and interrupted and intermittent Gaussian and non-Gaussian noise environments. For the same energy and spectrum, the non-Gaussian environments are clearly the more hazardous. The use of both an energy and kurtosis metric can better predict the hazard of a high-level complex noise than the use of an energy metric alone (as is the current practice). These results point out the need for a new approach to the analysis and quantification of industrial noise for the purpose of hearing conservation practice.

The effectiveness of N-acetyl-L-cysteine (L-NAC) in the prevention of severe noise-induced hearing loss.

Three groups of chinchillas were exposed to a nonGaussian continuous broadband noise at an Leq=10 5dB SPL, 8h/d for 5d. One group (N=6) received only the noise. A second group (N=6) received the noise and was additionally treated with L-NAC (325 mg/kg, i.p.). Treatment was administered twice daily for 2d prior to exposure and for 2d following the exposure. During exposure the animals received the L-NAC just prior to and immediately after each daily exposure. The third group (N=4) was exposed to the noise and received saline injections on the same schedule as the L-NAC treated animals. Auditory evoked potential recordings from the inferior colliculus were used to estimate pure tone thresholds and surface preparations of the organ of Corti quantified the sensory cell population. In all three groups PTS exceeded 50 dB at 2.0k Hz and above with severe sensory cell loss in the basal half of the cochlea. There was no statistically significant difference among the three groups in all measures of noise-induced trauma. Treatment with L-NAC did not reduce the trauma produced by a high-level, long duration, broadband noise exposure.

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.

Real-time data-reusing adaptive learning of a radial basis function network for tracking evoked potentials.

Tracking variations in both the latency and amplitude of evoked potential (EP) is important in quantifying properties of the nervous system. Adaptive filtering is a powerful tool for tracking such variations. In this paper, a data-reusing non-linear adaptive filtering method, based on a radial basis function network (RBFN), is implemented to estimate EP. The RBFN consists of an input layer of source nodes, a single hidden layer of non-linear processing units and an output layer of linear weights. It has built-in nonlinear activation functions that allow learning of function mappings. Moreover, it produces satisfactory estimates of signals against a background noise without a priori knowledge of the signal, provided that the signal and noise are independent. In clinical situations where EP responses change rapidly, the convergence rate of the algorithm becomes a critical factor. A carefully designed data-reusing RBFN can accelerate the convergence rate markedly and, thus, enhance its performance. Both theoretical analysis and simulation results support the improved performance of our new algorithm.

Sensitivity of distortion product otoacoustic emissions in noise-exposed chinchillas.

The present study investigates the effect of small amounts of outer hair cell (OHC) loss on distortion product otoacoustic emission (DPOAE) levels and evoked potential permanent threshold shifts (PTS) in a population of 12 noise-exposed chinchillas. The group mean DPOAE level, which decreased by up to approximately 15 dB in the presence of less than 8 dB PTS and 15% OHC loss, indicates that DPOAEs can detect an underlying cochlear pathology (i,e., OHC damage/loss) despite the presence of normal to near normal thresholds. The sensitivity of DPOAEs in detecting OHC loss makes this test measure suited for diagnosing sensorineural hearing impairment, particularly when abnormal auditory symptoms (i.e., speech discrimination problems) are associated with a normal audiogram in the clinical setting and as part of a hearing conservation program.

The use of distortion product otoacoustic emissions in the estimation of hearing and sensory cell loss in noise-damaged cochleas.

Distortion product otoacoustic emissions (DPOAE), permanent threshold shifts (PTS) and outer hair cell (OHC) losses were analyzed in a population of 187 noise-exposed chinchillas to determine the predictive accuracy (sensitivity and specificity) of the DPOAE for PTS and OHC loss. Auditory evoked potentials (AEP) recorded from the inferior colliculus of the brainstem were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. The overlapping cumulative distributions and high variability in emission responses for both PTS and OHC loss made it difficult to predict AEP threshold and OHC loss from DPOAE level measurements alone. Using a strict criterion (i.e. emissions better than the 5th percentile of the preexposure DPOAE level, and PTS< or = 5 dB or OHC loss< or = 5%), it was found that the postexposure DPOAE level could be used with reasonable confidence to determine if the status of peripheral auditory system was either normal (i.e. PTS< or = 5 dB) or abnormal (PTS>30 dB or OHC loss>40%). However, the high variability of individual DPOAE responses resulted in a broad region of 'uncertainty' (i.e. 5 or = 50%) or PTS (> or = 35 dB) in noise-exposed chinchillas. Based on an exponential regression analysis of individual subjects, correlations were higher for PTS/DPOAE than for OHC loss/DPOAE.

Adaptive filtering of evoked potentials with radial-basis-function neural network prefilter.

Evoked potentials (EPs) are time-varying signals typically buried in relatively large background noise. To extract the EP more effectively from noise, we had previously developed an approach using an adaptive signal enhancer (ASE) (Chen et al., 1995). ASE requires a proper reference input signal for its optimal performance. Ensemble- and moving window-averages were formerly used with good results. In this paper, we present a new method to provide even more effective reference inputs for the ASE. Specifically, a Gaussian radial basis function neural network (RBFNN) was used to preprocess raw EP signals before serving as the reference input. Since the RBFNN has built-in nonlinear activation functions that enable it to closely fit any function mapping, the output of RBFNN can effectively track the signal variations of EP. Results confirmed the superior performance of ASE with RBFNN over the previous method.

Considerations on assessing the risk of work-related hearing loss.

The large intersubject variability observed in demographic studies of noise-induced hearing loss illustrates how difficult it can be to estimate with precision the risk posed by exposure to noise. One possible source of the variability is the result of evaluating a diverse set of acoustic conditions with a simple metric A-weighted energy. In this paper the limitations of the energy-based criteria are reviewed. The benefits of evaluating a noise exposure in terms of energy and the metrics of frequency and time-domain kurtosis are discussed. A second source of variability in industrial noise studies may be related to non-acoustic factors such as chemical exposures that contribute to hearing loss acquired on the job

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.

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.

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.

Relations among early postexposure noise-induced threshold shifts and permanent threshold shifts in the chinchilla.

Threshold shifts (TS) were measured at various times following a wide variety of noise exposures on over 900 chinchillas. An analysis of postexposure TS measures and noise-induced permanent threshold shift (PTS) showed that, across audiometric test frequency, there was a consistent relation between these variables of the form PTS (dB) = alpha(e(TS/beta) - 1), where, for a given test frequency, alpha (dB) and beta (dB) are constants. TSs were measured immediately following exposure (TS0), 24 h after exposure (TS24), and at several intermediate times in order to estimate the maximum TS (TSmax). Correlation between TS and PTS at the various test frequencies was highest for TS24. An analysis of the 90th-percentile PTS showed a linear growth of PTS with TS24 of approximately 0.7 dB PTS/dB TS24. These data provide some support, in the chinchilla model, for a variation of the three postulates originally presented by Kryter et al. [J. Acoust. Soc. Am. 39, 451 (1966)]. Specifically: (i) TS24 is a consistent measure of the effects of a traumatic noise exposure. (ii) All exposures that produce a given TS24 will be equally hazardous. (iii) Noise-induced PTS in the most susceptible animals, following many years of exposure, is approximately equal to (0.7)TS24 measured after an 8-h exposure to the same noise.