Enhancement of Noise Induced Permanent Hearing Loss by Carbon Monoxide (CO)
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1999/01/01
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Description:Intense noise could induce a series of structural and functional changes in auditory hair cells. Failure to repair the damage could lead to a permanent hearing loss. Behavioral and physiological experiments show that the permanent hearing loss caused by broad-band-noise can be enhanced by carbon monoxide (CO), especially at high frequencies. In the present study, the ability of CO to enhance noise-induced hearing loss was examined in subjects exposed to one of 4 octave-band-noises (1.2-2.4, 2.4-4.8, 4.8-9.6 & 9.6-19.2 kHz) at levels of 100-115 dB SPL. The experiment subjects (pigmented rats) received CO exposure, noise exposure, or combined exposure to both the CO and the noise. Compound action potentials (CAPs) and cochlear microphonics (CM), to tones from 2 kHz to 40 kHz, were recorded from the round window following a four-week recovery from the exposure. The simultaneous exposure to both the noise and CO caused a much greater hearing loss than the sum of those to the noise alone and to the CO alone, no matter at which frequency the impairment occurred. The exposure to the CO alone did not cause any threshold shift. The high-frequency noise induced greater hearing loss than the low-frequency noise a the same intensity level. The CAP and the CM had a similar change pattern to the noise exposure, but the CM changes was usually less than the CAP change. This indicates that the impairment caused by the noise is not limited to the outer hair cells. We propose that the CO might reduce the hair cells' ability to repair the noise-induced damage during the recovery. Interestingly, this process seems mainly to occur in the outer hair cells, since the enhancement of the CAP-change was similar to that of the CM-change, though the noise-induced CM-change was much smaller. [Description provided by NIOSH]
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Volume:22
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NIOSHTIC Number:nn:20000188
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Citation:ARO Abstracts 1999 Jan; 22:153
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Contact Point Address:University of Oklahoma Health Sciences Center, Department of Pharmacology and Toxicology, Oklahoma City, Oklahoma 73190
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Email:fechter@ouhsc.edu
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Federal Fiscal Year:1999
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Performing Organization:University of Oklahoma, Health Sciences Center, Oklahoma Center for Toxicology, Oklahoma City, Oklahoma
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Peer Reviewed:False
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Start Date:19970901
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Source Full Name:ARO Abstracts
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End Date:20000831
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Main Document Checksum:urn:sha-512:86cae27025e80de8d5d9c982179f798b764efc1f4377e3c0730079db231a41ea12c92a24fbb9c42efc2690b84a22205329e6ba8689320c30bc95a3bab0c16209
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