Augmented acoustic environment (AAE) is a paradigm in which animals are exposed to a non-traumatic noise and was first introduced by Turner and Willott (1998) to ameliorate progressive genetic hearing loss (HL) in mice by initiating the treatment around the time of the manifestation of HL. AAE is also known as "acoustic enrichment" which has been shown to ameliorate noise-induced hearing loss (NIHL, Norena and Eggermont, 2005; Niu et al., 2004). We have used the AAE paradigm to examine the protective effects against NIHL and age related HL (ARHL) and the influence on outer hair cell (OHC) death. To examine the AAE effects on NIHL and OHC death, chinchillas (n=5) were exposed to a traumatic noise (one octave-band with the center frequency at 4 kHz at 107 dB SPL) for 1 hour and then immediately exposed to a nontraumatic continuous noise (4 - 20 kHz at 80 dB SPL) for 3 days. An acoustically-deprived group (n=5) wore earplugs for 3 days starting immediately after the same noise exposure. The results showed that the AAE/acoustic enrichment group showed significantly smaller ABR threshold shifts at 4 and 8 kHz and fewer numbers of deteriorated OHC (apoptotic, necrotic, and missing OHCs) compared to the deprived animals. In order to investigate whether the AAE/acoustic enrichment ameliorates ARHL when it was initiated after the manifestation of HL, 16-month-old Fischer 344/NHsd rats (n=5) were exposed to the non-traumatic noise (4-20 kHz and 80 dB SPL), for 12 hours/day for 3 months. Six unexposed rats were used as controls. ABR thresholds were obtained before the treatment, and re-tested at 2, 6, 9, and 13 weeks after the initiation of the treatment. The results showed that the "vector" for ARHL was essentially stopped by the introduction of AAE and by 13 weeks of the treatment, the control group had 10-20 dB larger ABR threshold shifts at 20-40 kHz compared to the AAE group. Additionally, fewer numbers of deteriorated OHCs were observed in the AAE group compared to the control group. In conclusion, our results from both studies demonstrated that non-traumatic noise exposure can prevent deterioration of OHCs caused by a traumatic noise and aging. This study was supported by NIOSH grant 1R01OH008113-01A1.