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The goal of this research was to compare, in the rescue mode of treatment, the effectiveness of (1) L-N-acetylcysteine (L-NAC); (2) D-Methionine (D-MET); (3) Ebselen SPI-1005; (4) Acetyl-L-carnitine (ALCAR) and (5) Src-PTK inhibitor, KX1-004 in reducing hearing and sensory cell loss as the result of an acute acoustic trauma that simulates blast injury to the auditory system. A shock tube was used to produce a blast injury to the cochlea in a chinchilla model. A secondary goal was to apply the same drug administration protocol to groups of animals exposed to a lower level continuous noise. Data from the treated and control animals consisted of: (1) auditory evoked potential hearing thresholds; (2) cubic distortion product otoacoustic emissions (DPOAE) input/output functions along with DPOAEs as a function of frequency (DPEgram) to estimate sensory cell function; (3) tympanograms to screen for conductive changes; (4) surface preparation histology to estimate the frequency specific sensory cell loss. Statistical analysis of the data employed a mixed model analyses of variance with repeated measures on one factor (frequency) using the SPSS Release 4.0 statistical package. Results: (1) There were no statistically significant differences between drug treated groups and controls. (2) There was a very large inter subject variability for all exposure groups., The original document contains color images.

Hearing loss and sensory cell loss data, obtained from 909 chinchillas exposed to one of 137 different impulse noise or blast wave exposure paradigms, were statistically analyzed. The objective was to extract relations between the effects of the exposure on the auditory system (effects metrics) and metrics used to characterize the blast wave exposure. Specifically the following two questions were asked: (a) What is the best indicator of the amount of hazard associated with an impulse noise exposure? (b) How does the hazard of an impulse noise exposure accumulate with increasing numbers of impulses? Two analytical approaches were used. Both approaches indicated that the P-weighting functions or one of its derivatives (P1-, P2- or R-weighting) best organized the effects metrics. Depending on the analytical approach, either an energy trading rule of 10 log10 N or 6 log10 N; where N is the number of impulses, best organized the data for N between 10 and 100. For exposures of between 1 and 10 impulses, a region of the parametric space that is of considerable practical significance, there is insufficient data to form any conclusions. For this region the limited data suggest that an energy trading rule i.e., 10 log N, does not work.

A health hazard assessment for blast overpressure exposures is presented.

The purpose of this contract was to support the USAARL research program on the auditory effects of blast overpressure (BOP). The statement of work for this contract identified two broad areas of responsibility; (a) to perform all the required histological work relating to the BOP projects at the USAARL and at the Albuquerque, New Mexico (EG&G) test site; (b) to assist in the on-site (USAARL) physiological and behavioral testing of experimental animals. In mid-1995, the decision was made to terminate this program (ref. Blast Program Review, Aug. 1995) and effective 30 September 1995 our on-site effort ceased, and all on-going animal experiments were terminated. The following was accomplished: (1) Atypical speaker generated impulses were shown to be suitable for modeling the effects of - blast waves. (2) Correlations between audiometry and cochlear pathology were shown to be poor and that individual susceptibility to BOP trauma is highly variable. However, cochlear emissions are a sensitive, frequency specific index of BOP auditory trauma in an individual. (3) One-third octave bands of noise are suitable stimuli for audiometric testing.

Biological Basis of Noise-Induced Hearing Loss, Sensory Cell Regeneration and Functional Recovery, The Effects of Acoustic Trauma, Other Cochlear Injury, and Death on Basilar-Membrane Responses to Sound, Excitotoxicity and Plasticity of IHC-Auditory Nerve Contributes to Both Temporary and Permanent Threshold shift, Noise-Induced Expression of Heat Shock Proteins in the Cochlea, Changes in Gene Expression Following Temporary Noise-Induced Threshold Shift, Genetic Susceptibility to Noise-Induced Hearing Loss in Mice, Effects of Acoustic Overstimulation on Distortion-Product and Transient-Evoked Otoacoustic Emissions, Physiological Correlates of Spontaneous Otoacoustic Emissions Induced by Acoustic Trauma, Cochlear Blood Flow Changes With Short Sound Stimulation,Individual Differences in Peripheral Sound Transfer Function, Relationship to NIHL, Experimental Studies of Noise-Induced Hearing Loss Underwater Hearing and Occupational Noise Exposure Threshold Shift Dynamics Following Interrupted Impact or Continuous Noise Exposure: A Review,Protection from Continuous, Impact, or Impulse Noise Provided by Prior Exposure to Low-Level Noise, Efferent and Priming Modulation of Noise-Induced Hearing Loss, Protection Against Temporary and Permanent Noise-Induced Hearing Loss by Sound Conditioning Psychophysical and Evoked Response Studies of Aged Subjects: Masking by Low-Pass Noise, Interactions Between Age-Related and Noise-Induced Hearing Loss, Application of Frequency and Time Domain Kurtosis to Assessment of Complex, Time-Varying Noise Exposures

The effects of exposure to high levels of reverberant blast waves (impulse noise) on the auditory system using an animal (chinchilla) model are reported. Blast waves were generated by two different shock tubes which produced wave signatures having different spectral distributions of energy. Intensities for each blast wave source were 150, 155, and 160 dB peak SPL with exposure to 1, 10, or 100 impulses. Repetition rates were fixed at one impulse/sec. There were 15 subjects per group. Brainstem evoked potentials were used to estimate temporary and permanent threshold shifts and conventional surface preparations of the cochlea were used to quantitatively assess sensory cell loss. In addition, pre and postexposure cubic distortion product otoacoustic emissions (3DPE) were collected on a subset of these animals for correlation with audiometric and histological indices of trauma. Trauma systematically increased with sound exposure level (SEL) and was dependent on the energy spectrum of the impulse. An application of the A and P weighting functions to the spectra improved the correlations between indices of trauma and SEL. The 3DPE data were consistent with PTS and, overall, both measures were correlated with sensory cell loss. (AN)

This research is directed at studying the effects on the auditory system of exposure to high levels of reverberant impulse noise using an animal (chinchilla) model. The blast waves were generated by a three inch diameter shock tube (source III), which produced wave signatures having spectral energy concentrated in the 12 kHz region. The waves were discharged into a reverberant chamber within which animals were individually exposed. Animals were exposed to either 150, 155 or 160 dB peak SPL impulses. The number of impulses presented at each intensity was 1, 10 or 100, with repetition rates fixed at 1 impulse/sec. This parametric design yielded 9 groups of animals. There were 15 animals in each group. Brainstem evoked potentials were used to estimate temporary and permanent threshold shifts and conventional surface preparations of the cochlea were used to quantitatively assess sensory cell loss. This midterm report presents the audiometric data and a portion of the histological data for the 136 animals that completed the exposure protocol. The audiometric and available histological data showed that damage to the auditory system systematically increased as the energy of the exposure was increased through manipulation of number of presentations or peak SPL. Hearing loss, Impulse noise, Blast waves, RADIII.

Limits for exposure to hazardous agents are set by defining some specific acceptable effect (the response) and then determining what exposure conditions (the dose) produce that effect. In 1968, the Committee on Hearing, Bioacoustics, and Biomechanics (CHABA) proposed a limit for exposure to impulse noise (gunfire) in which the response was a specific amount of temporary threshold shift (TTS) and dose was specified in terms of the peak pressure and two aspects of the duration of a particular impulse, with correction factors for number of impulses and for the angle of incidence on the ear. The proposal was basically an endorsement of one advanced by an Anglo-American team of investigators (Coles, Garinther, Hodge, and Rice, 1968) that was based on the very limited pool of information then available about the auditory hazard of gunfire. Coles, Garinther, and Hodge were members of the Working Group on Proposed Damage-Risk Criterion for Impulse Noise (Gunfire).

The energy spectrum of a noise is known to be an important variable in determining the effects of a traumatic exposure. However, existing criteria for exposure to impulse noise do not consider the frequency spectrum of an impulse as a variable in the evaluation of the hazards to the auditory system. This report presents the results of a study that was designed to determine the relative potential that impulsive energy concentrated at different frequencies has in causing auditory system trauma. One hundred and eighteen (118) chinchilla, divided into 20 groups with 5 to 7 animals per group, were used in these experiments. Pre- and post-exposure hearing thresholds were measured at 10 test frequencies between 0.125 and 8 kHz on each animal using avoidance conditioning procedures. Quantitative histology (cochleograms) was used to determine the extent and pattern of the sensory cell damage. The noise exposure stimuli consisted of six different computer-generated narrow band tone bursts having center frequencies located at 0.260, 0.775, 1.350, 2.450, and 3.550 kHz. Each narrow band exposure stimulus was presented at two to four different intensities. An analysis of the audiometric and histological data allowed frequency weighing functions to be derived.

A previous report by Patterson et al., (1991) derived a frequency weighting function from audiometric and histological data gathered on 118 chinchillas exposed to a variety of narrow band impulses at various peak intensities. The weighting function clearly demonstrated that equivalent amounts of impulsive energy concentrated at different frequencies is not equally hazardous to the auditory system. However, on the basis of a preliminary analysis of a large amount of audiometric data obtained from chinchillas exposed to high level blast waves (Patterson and Hamernik, 1991), there appeared to be some inconsistencies between the narrow band impulse data and the blast wave data in the region of 2.0 kHz. To resolve this discrepancy, two additional groups of animals were exposed to narrow band impulses with a center frequency of 2.075 kHz and peak intensities of 134 dB and 139 dB. The results of these two additional groups confirm the shape of the original P-weighting function and indicate that changes must be made in our approach to the analysis of the blast wave data referred to above.

Existing criteria for exposure to impulse noise do not provide any explicit means for evaluating exposures for which the peak SPL (Sound Pressure Level) of the impulses varies in any given exposure day. Approaches to evaluating such exposures have included the application of a 'proportional dose' method such as used with continuous noise or use of an average level. Implicit in these approaches is the assumption that the order in which a sequence of variable intensity impulses is presented is not important. This same assumption is also implicit in any energy-based exposure criteria. This report presents results of a pilot experiment designed to test the validity of this assumption. Two groups of chinchillas were exposed to a sequence of 100 impulses. One group received 90 exposures at 138-dB peak SPL impulses followed by 10 exposures at 146-dB peak SPL impulses; the second group received the same series of impulses but in reverse order. Results from these two groups were compared to results of 100 exposures at 147-dB peak SPL impulses from a report by Patterson et al., (1986). The 139-dB peak SPL exposure had the same total energy as the two variable intensity exposures. Results of the three equivalent energy exposures showed that exposures having equal energies could produce statistically different levels of hearing trauma. However, while the mean data were very suggestive in showing an effect of the presentation order, this result did not hold up to statistical analysis because of a large intersubject variability., Prepared in cooperation with Auditory Research Laboratory, State University of New York at Plattsburgh.