No abstract

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.

A study was made of the relation between tinnitus masker composition (frequency, bandwidth, intensity duration) and the time course and magnitude of residual inhibition (RI). RI was determined by methods of (a) loudness estimation - where the subject varied the pointer position on a loudness scale (b) loudness balance - where the tinnitus loudness was maintained in loudness balance in the period following masking with a tone of variable intensity presented to the opposite ear. In addition, sensitivity change (temporary threshold shift, TTS) in the tinnitus and masker frequency regions was measured by determining tone thresholds (using a tracking technique) before and after masker presentation. The key findings were as follows: (I) RI depends on masker centre frequency. The frequency producing maximal RI is usually lower than the tinnitus frequency (as determined by pitch matching). (2) In some subjects only narrow-band noise produces RI. (3) RI is proportional to the masker intensity provided the tinnitus is completely masked; little or no RI is produced by a partial masker. (4) For the masker durations used (in the range 10 s to 10 min) RI duration is linearly related to the logarithm of masker duration. (5) A second masker presentation during RI does not potentiate RI. (6) Contralateral masking did not produce RI. (7) maskers producing RI also produce TTS around the tinnitus frequency. (8) The TTS magnitude and the time course of TTS appear to be related to RI.

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.