The effects of interrupted noise exposures on the noise-damaged cochlea.

A variety of interrupted noise exposure paradigms will produce a toughening effect in the mammalian auditory system. That is, the threshold shift will gradually become smaller with each successive daily exposure. The ability of the system to be toughened has not been explored in subjects with a pre-existing noise-induced hearing loss. Using the chinchilla as the experimental animal, evoked potential audiometry to obtain thresholds, and surface preparation histology to quantify the sensory cell population, the issue of toughening was examined in the noise-damaged auditory system. Toughening was produced by a 1.0 kHz, narrow-band impact at 115 dB peak SPL for 10 days, 6 h/day, and trauma was produced by a 1.0 kHz, narrow-band impact at 121 dB peak SPL for 5 days, 24 h/day. Four groups of animals were used. Group 1: traumatic exposure followed 30 days later by the toughening exposure. Group 2: toughening exposure followed 30 days later by the traumatic exposure. Group 3: a trauma-only control. Group 4: a toughening-only control. Group 2 that received the toughening exposure 30 days prior to the traumatic exposure showed a 10 to more than 20 dB toughening effect between the 0.5 and 4.0 kHz test frequencies, while Group 1 that received the traumatic exposure followed 30 days later by the toughening exposure showed no toughening. The permanent changes in the evoked response audiograms and sensory cell populations were the same in Groups 1, 2 and 3 that were exposed to the traumatic noise, regardless of whether or not the animals were ever subjected to the toughening noise or whether the toughening noise preceded or followed the traumatic noise.

The cubic distortion product otoacoustic emissions from the normal and noise-damaged chinchilla cochlea.

A normative study of the cubic distortion product emissions from 104 monaural and binaural chinchillas was undertaken to establish criteria upon which noise exposed animals could be evaluated. From this normative group, 47 randomly selected chinchillas were exposed to various high level (150-, 155-, and 160-db peak SPL) impulse noises. Auditory evoked potentials and cubic distortion product otoacoustic emissions were measured on each animal pre- and post-exposure and related to the sensory cell populations 30 days post-exposure. Both group mean and individual animal data indicated that the distortion product emissions were more sensitive, frequency-specific indices of noise-induced cochlear effects than pure-tone threshold measures. This was particularly evident near the threshold for noise-induced damage to the outer hair cell system.

Evoked-potential thresholds and cubic distortion product otoacoustic emissions in the chinchilla following carboplatin treatment and noise exposure.

Twenty-two chinchillas were given either a single intraperitoneal (i.p.) or intravenous (i.v.) injection (50 or 75 mg/kg) of Paraplatin, an asymptotic threshold shift-producing noise or a combination of the drug and noise in series. Auditory evoked potential (pure-tone) audiograms and cubic distortion product otoacoustic emissions were obtained on each animal before and after treatment, and the sensory epithelium of the cochlea was evaluated using the surface preparation method. Anatomical analysis indicated that the carboplatin alone caused relatively severe but scattered losses of inner hair cells throughout most of the cochlea which were dependent on dose and administration route. The outer sensory cell population remained essentially intact. In animals that had up to 40% scattered losses of only inner hair cells, evoked potential thresholds were near normal and the emission functions either were normal or showed an enhanced output. The severe losses of inner hair cells produced by the drug had no effect on the threshold shift dynamics produced by a five-day uninterrupted noise exposure. In general, there was not a consistent relation between the emission data and both the permanent threshold shift and outer hair cell losses.

Audiometric and histological differences between the effects of continuous and impulsive noise exposures.

An experiment was designed to determine if, for equal SPL and power spectrum, the effects on hearing of high-kurtosis noise exposures and a Gaussian noise exposure are different and the extent to which any differences measured in terms of audiometric and histological variables are frequency specific. Three groups of chinchillas with 10 animals/group were exposed for 5 days at 90 dB SPL to one of three types of noise, each with the same power spectrum. The impulsiveness, defined by the kurtosis, and the region of the spectrum from which the impulsive components of the noise were created differed for two of the noises, while the third was a continuous Gaussian noise. The results show that the most impulsive noise produced up to 20 dB greater permanent threshold shift at the high frequencies than did the Gaussian noise exposure. However, these audiometric results were difficult to reconcile with the pattern of sensory cell losses that showed statistically significant larger losses of outer hair cells for the impulsive exposure in the 0.25-kHz region. When the impacts in a high-kurtosis noise were created from the energy in the 1- through 6-kHz region of the spectrum, the audiometric profile of hearing loss was similar to that produced by the Gaussian noise; however, inner hair cell losses were significantly greater in the 4-kHz octave band region of the cochlea.

Complex noise exposures: an energy analysis.

Industrial noise environments usually present a complex stimulus to the exposed individual. These environments often contain mixtures of multiply reflected impact noises and a relatively Gaussian broadband noise. Noise exposure standards do not consider the possibility of interactions between the two classes of noise that can exacerbate the amount of hearing trauma. This paper presents the results of a large series of experiments designed to document the hazard posed to hearing from complex noise exposures. Twenty-three groups of chinchillas with 5 to 11 animals per group (total N = 135) were exposed for 5 days to either octave bands of noise, impacts alone, or combinations of impact and octave bands of noise. Evoked potential measures of hearing thresholds and cochleograms were used to quantify the noise-induced trauma. The results show that, for sound exposure levels (SEL) which produce less than approximately 10 dB PTS (permanent threshold shift) or 5% total sensory cell loss, equal-energy exposures tend to produce equivalent effects on hearing. However, there is a range of at least 10 dB in the SEL parameter where hearing loss from equal-energy exposures at a particular SEL can be exacerbated by increasing the repetition rate of the impacts or by the addition of a Gaussian low-level noise. The exacerbation of trauma from the addition of a Gaussian continuous noise is dependent upon the spectrum of that noise.

The relation among hearing loss, sensory cell loss and tuning characteristics in the chinchilla.

Evoked-potential tuning curves were obtained on over 150 chinchillas before and after acoustic overstimulation in order to relate the effects of changes in frequency selectivity to sensory cell loss over a wide range of hearing loss. Pre- and post-exposure measures of auditory thresholds and masked thresholds (simultaneous tone-on-tone paradigm) were obtained in each animal at 0.5, 1.0, 2.0, 4.0, 8.0 and 11.2 kHz, using the auditory evoked potential recorded from the inferior colliculus. Three tuning curve variables (Q10dB, low-frequency slope and high-frequency slope) were compared to the amount of noise-induced permanent threshold shift and to the percent sensory cell loss produced by a variety of noise exposures. Based upon large sample averages, frequencies showing permanent threshold shifts in excess of 10 dB also showed statistically significant differences between pre- and post-exposure measures of all three tuning curve variables. Shifts of less than 10 dB were not accompanied by statistically significant changes in the tuning curve variables. The percentage of outer hair cell loss, and percentage change in tuning curve characteristics showed systematic and parallel increases as threshold shifts increased at all probe tone frequencies except 8.0 and 11.2 kHz. In general, the results were consistent in showing that there is a systematic change in the variables which define the quality of tuning as hearing loss progressively increases and that these changes are clearly related to outer hair cell losses.

Threshold recovery functions following impulse noise trauma.

An analysis of the pure-tone threshold recovery functions obtained from 118 chinchillas exposed to high-level impulse noise showed that there are at least three distinctly different types of recovery function: type I--a recovery function for which the initial threshold shift recovers monotonically with increasing postexposure time; type II--a delayed recovery; i.e., for a period as long as 6 h following removal from noise, the pure-tone threshold remains elevated and stable before thresholds begin to follow a monotonic course of recovery; and type III--the growth function; i.e., over a period of at least 6 h following removal from the noise, pure-tone thresholds continue to get worse before they begin to follow a monotonic course of recovery. There is more permanent threshold shift (PTS), more sensory cell loss, and predictions of PTS and cell loss based upon initial measures of threshold shift are less accurate at those frequencies characterized by a type III recovery process than at those frequencies characterized by a type I recovery process.

Detection of sinusoidally amplitude modulated noise by the chinchilla.

Amplitude modulation thresholds for sinusoidally amplitude modulated noise were obtained from four monaural chinchillas using shock-avoidance conditioning procedures. The noise was band limited at either 10 or 20 kHz, amplitude modulated at frequencies between 2 and 4096 Hz and presented at levels between 52 and 73 dB SPL. The modulation thresholds of the chinchilla were approximately 9% (-- 2 dB) at modulation frequencies below 32 Hz. At higher modulation frequencies, thresholds increased at the rate of 1.9 dB/octave. Modulation thresholds were also measured in human listeners using the same experimental apparatus. Amplitude modulation functions for both subject groups exhibited low-pass characteristics; however, the thresholds for humans were better than those of the chinchilla at modulation frequencies below 64 Hz.

Discharge patterns in the cochlear nucleus of the chinchilla following noise induced asymptotic threshold shift.

Chinchillas were exposed to an 86 dB SPL octave band of noise centered at 4.0 kHz for 3.5--5 days. The noise elevated the hearing thresholds between 4.0 and 16.0 kHz to between 60 and 75 dB SPL. Measurements from single neurons in the cochlear nucleus revealed abnormalities in the response properties of neurons with characteristic frequencies (CF) above 2.0 kHz. Units above 2.0 kHz had elevated thresholds (between 50 and 90 dB SPL) and broad tuning curves due to a greater loss in sensitivity near CF than at lower frequencies. The tuning curve Q10dB values for high frequency neurons were generally less than 3.0 and approached the Q10dB values for basilar membrane displacement. Spontaneous activity rates in units above 2.0 kHz were also low. In a few units, the threshold for single tone inhibition was significantly lower than that for excitation; the best inhibitory frequencies were always below 2.0 kHz. Two-tone inhibition was present in both low and high threshold neurons, but its strength was not assessed. Cochleagrams obtained 12 hours postexposure revealed discrete hair cell lesions in the basal third of the cochlea. The locations of the lesions were consistent with the frequencies of maximum hearing loss. The behavioral thresholds and the thresholds at CF of the most sensitive units were within 10--15 dB of each other. The results indicate that intense sounds reduce the sensitivity, frequency selectivity and spontaneous activity of units in the cochlear nucleus. The findings are similar to those obtained in auditory nerve fibers with ototoxic drugs and hypoxia.