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The current impulse noise criteria for the protection against impulse noise injury do not incorporate an objective measure of hearing protection. A new biomechanically-based model has been developed based on improvement of the Auditory Hazard Assessment Algorithm for the Human (AHAAH) using the integrated cochlear energy (ICE) as the damage risk correlate (DRC). The model parameters have been corrected using the latest literature data. The anomalous dose-response inversion behavior of the AHAAH model was eliminated. The modeling results show that the annular ligament (AL) parameters are the dominant cause of the non-monotonic dose-response behavior of AHAAH. Based on parametric optimization analysis, a 40% reduction of the AL compliance from the AHAAH default value removed the dose-response inversion problem, and this value was found to be within the physiological range when compared with experimental data. The transfer functions from the new model are in good agreement with those of the human ear. A dose-response curve based on ICE was developed using the human walk-up temporary threshold shift (TTS) data. Furthermore, the ICE values calculated for the German rifle noise tests show excellent comparison with the injury outcomes, hence providing a significant independent validation of the improved model. The ICE was found to be the best DRC to both large weapons and small arms noise injury data, covering both protected and unprotected exposures, respectively. The new AHAAH model with ICE as the dose metric is adequate for use as a medical standard against impulse noise injury.

The spatial distribution of outer hair cells that participate in generating transient-EOE frequency-components has been investigated in man. According to several models (e.g. Wilson (1990) Hear. Res. 2, 527-532; Zwicker (1986) J. Acoust. Soc. Am. 80, 154-162; Wilson and Kemp (Eds.), Cochlear Mechanisms, Structures, Functions and Models, Plenum Press, NY), EOEs result from interferences between broadly distributed contributions, responsible for their long frequency-dependent delay. This work presents an analysis of the temporal patterns of click- and tone-burst-EOEs in human ears when contributions to EOEs are reduced by noise-induced lesions with audiometric notches centred around 4 kHz (N = 46). Although the auditory thresholds at the frequencies of the studied EOE-components were always normal, these components exhibited drastic and predictable changes compared to normal control ears (N = 40). (1) Their temporal pattern at the highest EOE frequency f(max) just below the audiometric notch appeared to be determined by the cochlear state at high frequencies (6 to 8 kHz). Either it was normal and the EOE exhibited a complicated beat-structure, or it was impaired and the time envelope of the EOE was simple. In contrast, any type of time pattern could be observed in normal ears. (2) The temporal patterns of EOEs one octave below f(max). always presented many beats and short delays. The proposed interpretation is that contributions to a transient-EOE component at frequency f can come from distant basal cochlear areas, i.e. more than 1 and sometimes 1.5 octaves from the place tuned to f. Therefore, the possible relationships between transient-EOEs and tuning mechanisms which presumably involve only a small number of OHC need further investigations.

The spatial distribution of outer hair cells that participate in generating transient-EOE frequency-components has been investigated in man. According to several models (e.g. Wilson (1990) Hear. Res. 2, 527–532; Zwicker (1986) J. Acoust. Soc. Am. 80, 154–162; Wilson and Kemp (Eds.), Cochlear Mechanisms, Structures, Functions and Models, Plenum Press, NY), EOEs result from interferences between broadly distributed contributions, responsible for their long frequency-dependent delay. This work presents an analysis of the temporal patterns of click- and tone-burst-EOEs in human ears when contributions to EOEs are reduced by noise-induced lesions with audiometric notches centred around 4 kHz (N = 46). Although the auditory thresholds at the frequencies of the studied EOE-components were always normal, these components exhibited drastic and predictable changes compared to normal control ears (N = 40). (1) Their temporal pattern at the highest EOE frequency ƒ max just below the audiometric notch appeared to be determined by the cochlear state at high frequencies (6 to 8 kHz). Either it was normal and the EOE exhibited a complicated beat-structure, or it was impaired and the time envelope of the EOE was simple. In contrast, any type of time pattern could be observed in normal ears. (2) The temporal patterns of EOEs one octave below ƒ max always presented many beats and short delays. The proposed interpretation is that contributions to a transient-EOE component at frequency ƒ can come from distant basal cochlear areas, i.e. more than 1 and sometimes 1.5 octaves from the place tuned to ƒ. Therefore, the possible relationships between transient-EOEs and tuning mechanisms which presumably involve only a small number of OHC need further investigations.

The purpose of this study was to compare distortion-product otoacoustic emissions (DPOEs) and click-evoked otoacoustic emissions (CEOEs) for normally-hearing human adults. The statistical analysis consisted of computing the DPOE and CEOE levels versus frequency corresponding to the 10th, 25th, 50th, 75th, and 90th percentiles among normal adult ears. The mean and standard deviations of the DPOEs and CEOEs were computed. A direct comparison of the DPOE and CEOE data obtained from the same ears showed that, in a 1–4 kHz frequency region, there was a statistically significant correlation between the levels of the two types of otoacoustic emissions. This finding supports the hypothesis that DPOEs and CEOEs arise from some common mechanisms of the cochlea such as active nonlinear biomechemical mechanisms of the outer hair cells.

Experimental results are given dealing with various aspects of the evoked cochlear mechanical response (ECMR). Measured multiple responses are compared with the output signal of an analogue feedback model. Response latency was measured for different response frequencies and compared with travel times on the humanbasilar membrane.

A number of reports have described a relatively high incidence of spontaneous otoacoustic emissions (SOAEs) in recordings made from the sealed human ear canal. Our attempt to detect similar emissions in 122 presumably normal-hearing ears from 61 monkeys revealed SOAEs in 5% of the primates and 2.5% of the ears tested.