We recently reported that passive exposure for at least 4 months of adult cats to a two-octave-wide tone pip ensemble at 80 dB SPL, decreased the responsiveness of primary auditory cortex (AI) to sound frequencies in the exposure band, and increased the responsiveness to frequencies at the outer edges of the band. Here we expand on this by demonstrating qualitatively similar plasticity for a 6-week exposure level of 68 dB SPL. Though no peripheral hearing loss is induced by the exposure, the resulting reorganization of the AI tonotopic map resembles that following a restricted lesion of the sensory epithelium. Most exposure-induced effects were likely present in the thalamus, as deduced from changes in local field potentials, but were further modified in AI. We then examined the potential for the reversal of these changes, given recovery in a quiet laboratory environment for up to 12 weeks after the cessation of exposure. While frequency tuning returned to near-normal, other neuronal response properties, as well as tonotopic map organization, remained abnormal at the end of our 12-week window. This could have implications for persistently noisy work/recreation/living environments, even at levels considerably below those presently considered unacceptable.