Potentiation of octave-band noise induced auditory impairment by carbon monoxide.
Hear Res 1999 Jun; 132(1-2):149-159
In previous studies from our lab, broadband noise induced hearing loss has been found to be potentiated by simultaneous carbon monoxide (CO) exposure. In the present study, octave-band noise induced auditory impairment was studied with the presence of CO at levels of 1500, 1200, 700, 500 and 300 ppm and zero (noise alone). Four octave-band noises (1.2-2.4, 2.4-4.8, 4.8-9.6 and 9.6-19.2 kHz) were used. Experimental subjects (rats) were grouped for the exposure (8 h) to each noise, CO and their combinations. The compound action potential (CAP) and cochlear microphonics (CM) were recorded 4 weeks after the exposure. The noise induced elevation of the CAP threshold and the CM iso-amplitude curve were potentiated by the simultaneous CO exposure when the CO level reached 500 ppm or higher. CO exposure alone had no effect on CAP or CM. The CO potentiation can occur in any frequency region depending on the noise band. The combined exposure can also induce threshold shifts in some cases in which both the noise and the CO alone did not cause threshold shifts. The size of the potentiation shown by CAP and CM was similar, indicating a possible origin of the CO potentiation from the damage to the outer hair cells. Interestingly, the hearing loss induced by noise alone gradually recovered (partially), but the hearing loss caused by the combined exposure did not. The potentiation may be due to the reduction of the cell's ability to repair noise induced damage by CO.
Hearing-protection; Noise-induced-hearing-loss; Synergistic-effects; Organic-solvents; Ototoxicity; Audiofrequency; Audiological-testing; Audiometry; Auditory-system; Hearing; Hearing-disorders; Hearing-impairment; Hearing-loss; Hearing-threshold
University of Oklahoma Health Sciences Center, Department of Pharmacology and Toxicology, Oklahoma City, Oklahoma 73190
Disease and Injury: Hearing Loss
University of Oklahoma, Health Sciences Center, Oklahoma Center for Toxicology, Oklahoma City, Oklahoma