Many researchers have focused attention on problem in view of the increase of noise in the environment and its possible deleterious effects on the hearing organ. However, several questions still remain to be clarified, including those related to : 1) mechanism(s) involved in the damage to hearing organ caused by various noise, 2) the healing patterns of the hearing organ after noise trauma, 3) more accurate damage risk criteria and 4) discrepancies between histopathological findings and functional deteriorations. The purposes of this study are to 1) clarify mechanism(s) involved in the damage of Corti's organ caused by various noise, 2) correlate the hair cell damage to ABR(auditory brainstem response) threshold shift, 3) verify the healing patterns of Croti's organ and 4) revise the damage risk criteria currently in use in the world. As experimental animals, 115 cats(weighing 2 to 3kg) and 40 chinchillas(weighing about 1kg) showing a positive preyer reflex, were used. For the revision of damage risk criteria currenty in use and to see the correlation of the hair-cell loss with ABR threshold shift, M-16 rifle and 105 mm howitzer were mounted on the ground and fired 60 rounds with three and 5 second intervals at the peak levels ranging 140 to 166 dB SPL, respectively. ABRs were picked up at the vertex 30 to 60 days after the noise exposure and the temporal bones were processed for the SEM(scanning electron microscopy) and LM(light microscopy) examination immediately. For the observation of healing patterns of Corti's organ, animals were exposed to the narrow-band noise of 1 kHz at the level of 110 dB SPL for 5 hours continuously. Animals were sacrificed 1 to 3 hours, 1 to 3 days, 7 to 14 days, and 30 days following the noise exposure. The temporal bones were processed for the LM and EM(SEM, TEM) studies. For the study of the early changes of inner ear following the exposure of infrasound, chinchillas were exposed to continuous or intermittent infrasound(1, 10, 20 Hz) at levels of 150 to 170 dB SPL. Serial sections of the temporal bones were examined by light microscopy. The losses of hair cells in both impulse noises tended to be in the middle of the cochlea in focused lesions, enven though the spectral peaks of the acoustic stimuli had been at about 80 Hz(howitzer) and 1,000 Hz(M-16). Two impulse noises were equally hazardous when the peak pressure of M-16 impulse was lower than the peak pressure of the howitzer impulse by about 10 dB. The outer hair-cell losses were closely correlated to the ABR threshold shift(γ-=0.83 in M-16 exposure, γ=0.86 in howitzer exposure). Continuous infrasound was more damaging than intermittent. Pathologies noted were tympanic membrane perforation, stapes subluxation, bleeding from the middle ear mucosa and tensor tympani muscle, strial edema, Reissner's membrane rupture, endolymphatic hydrops, and hair cell damage. The healing of the organ of Corti became complete 30 days after noise exposure. Nevertheless, a few stereocilia remained damaged at this time. The sites of hair cell loss-lesions were sealed by the hypertrophy and migration of the supporting cells which remained, surrounding them.