The first objective, to better understand the relation between the parameters of impact noise and noise-induced hearing loss, stems from the ambiguity (and inadequacy) of the current noise standards. Currently, exposures of 115 dBA are permitted for 15 minutes, but no exposure to impulse or impact noise over 140 dBA is permitted. However, it is relatively common in industry to find impacts ranging from 100 to 140 dBA, but there is limited guidance on what is a safe exposure. An impact is evaluated in terms of the peak level equivalent, but the spectral content, duration of the impact, the rate of presentation and the total number of the impacts are ignored. Thus, the first aim was to provide a perspective on the role of spectral content, repetition rate, and duration as factors in noise-induced hearing loss. A unifying principle of all the experiments is that the level, duration and number of exposures are counterbalanced so each experimental condition had the same total acoustic energy (power/time). The first major finding is that the duration, spectral content, and rate of presentation all influence the degree of hearing. This is an important finding because current noise standards are based solely on the peak level of the impact and the duration of time the impacts are presented. Second, a more general significant result is the demonstration of the "critical level" phenomenon for impact noise. Specifically, for exposures below a certain peak level, the hearing loss results were consistent with the Equal Energy Hypothesis; however, for exposures with peak levels above the "critical level", hearing loss grew proportionately to the peak level of the impact. Above the "critical level" the ear is damaged by direct mechanical failure and below the "critical level" the mode of damage is more metabolic. The second specific aim, to better understand the biological changes in the cochlea associated with exposure to high level impact noise, is based on the assumption that an understanding of the mechanisms of noise-induced hearing loss will provide insights into the practical problem of identifying individuals who are unusually susceptible or resistant to the effects of noise. Since impact noise causes mechanical damage to the cochlea, several of our experiments were directed at understanding the changes in F -actin, a key structural protein in the cochlea. With exposures over the "critical level", the structural elements of pillar cells, and Deiter cells, as well as, tight cell junction at the cuticular plate/reticular lamina, are interrupted leading to a possible mixing of perilymph and endolymph and fundamental change in the vibratory characteristics of the organ of Corti.