Otoacoustic emissions in early noise-induced hearing loss.

OBJECTIVE: To follow changes in transient evoked and distortion product otoacoustic emissions (TEOAEs, DPOAEs) as they relate to pure-tone audiometry (PTaud) thresholds during the first 2 years of occupational noise exposure. DESIGN: Prospective controlled. METHODS: Pure-tone audiometry thresholds, TEOAE and DPOAE amplitudes, and contralateral medial olivocochlear reflex strength were repeatedly evaluated during 2 years and compared between and within a cohort of 135 ship engine room recruits and a control group of 100 subjects with no noise exposure. RESULTS: Pure-tone audiometry thresholds for 2,000, 3,000 and 4,000 Hz in both ears were significantly elevated in the study group after 2 years of noise exposure. Significantly lower TEOAE amplitudes were found at 2,000 Hz in the right ear and 2,000 and 4,000 Hz in the left ear. Longitudinal intrasubject analysis of the study group revealed significant reductions of TEOAE amplitudes at 2,000 to 4,000 Hz in both ears and reduced DPOAE amplitudes for 5,957 Hz in the right ear and 3,809, 4,736, and 5,957 Hz in the left ear in the second follow-up evaluation. Baseline medial olivocochlear reflex strength showed no correlation to PTaud thresholds after 2 years of noise exposure. Poor to moderate negative linear correlations (r = -0.07 to -0.37) were found between the DPOAE-averaged amplitudes at 2,979 to 5,957 Hz and PTaud threshold means at 3,000 to 6,000 Hz. Abnormal TEOAE parameters after the first year of noise exposure had high sensitivity (86-88%) and low specificity (33-35%) for the prediction of noise-induced hearing loss (NIHL) after 2 years. CONCLUSION: The DP-gram is not significantly correlated with PTaud and cannot be used as an objective measure of pure-tone thresholds in early NIHL. Medial olivocochlear reflex strength before the beginning of chronic exposure to occupational noise has no relation to individual vulnerability to NIHL. Although TEOAEs changes after 1 year showed high sensitivity in predicting NIHL after 2 years of exposure, they cannot be recommended as an efficient screening tool due to high false-positive rates.

Underwater hearing and sound localization with and without an air interface.

HYPOTHESIS: Underwater hearing acuity and sound localization are improved by the presence of an air interface around the pinnae and inside the external ear canals. BACKGROUND: Hearing threshold and the ability to localize sound sources are reduced underwater. The resonance frequency of the external ear is lowered when the external ear canal is filled with water, and the impedance-matching ability of the middle ear is significantly reduced due to elevation of the ambient pressure, the water-mass load on the tympanic membrane, and the addition of a fluid-air interface during submersion. Sound lateralization on land is largely explained by the mechanisms of interaural intensity differences and interaural temporal or phase differences. During submersion, these differences are largely lost due to the increase in underwater sound velocity and cancellation of the head's acoustic shadow effect because of the similarity between the impedance of the skull and the surrounding water. METHODS: Ten scuba divers wearing a regular opaque face mask or an opaque ProEar 2000 (Safe Dive, Ltd., Hofit, Israel) mask that enables the presence of air at ambient pressure in and around the ear made a dive to a depth of 3 m in the open sea. Four underwater speakers arranged on the horizontal plane at 90-degree intervals and at a distance of 5 m from the diver were used for testing pure-tone hearing thresholds (PTHT), the reception threshold for the recorded sound of a rubber-boat engine, and sound localization. For sound localization, the sound of the rubber boat's engine was randomly delivered by one speaker at a time at 40 dB HL above the recorded sound of a rubber-boat engine, and the diver was asked to point to the sound source. The azimuth was measured by the diver's companion using a navigation board. RESULTS: Underwater PTHT with both masks were significantly higher for frequencies of 250 to 6000 Hz when compared with the thresholds on land (p <0.0001). No differences were found in the PTHT or the reception threshold for the recorded sound of a rubber-boat engine for dry or wet ear conditions. There was no difference in the sound localization error between the regular mask and the ProEar 2000 mask. CONCLUSIONS: The presence of air around the pinna and inside the external ear canal did not improve underwater hearing sensitivity or sound localization. These results support the argument that bone conduction plays the main role in underwater hearing.

Attenuation of cerebral oxygen toxicity by sound conditioning.

HYPOTHESIS: Sound conditioning might reduce cerebral oxygen toxicity. BACKGROUND: Cerebral oxygen toxicity is related to high levels of reactive oxygen species. Noise-induced hearing loss has been shown to result from ischemia-reperfusion, in which reactive oxygen species play a major role. Repeated exposure to loud noise at levels below that which produces permanent threshold shift prevented noise-induced hearing loss and was associated with significant elevation of the antioxidant enzymes measured in the inner ear. We tested the hypothesis that sound conditioning might reduce cerebral oxygen toxicity. METHODS: Forty-five guinea pigs were prepared for electroencephalography and auditory brainstem recording. The auditory brainstem recording detection threshold was determined to confirm baseline normal hearing. The animals were divided into three equal groups and subjected to the following procedures: Group 1, electroencephalography electrode implantation and auditory brainstem recording only; Group 2, exposure to oxygen at 608 kPa (the latency to the first electrical discharge in the electroencephalogram preceding the appearance of seizures was measured); and Group 3, sound conditioning followed by oxygen exposure. The animals were killed, and the brains were excised and homogenized. Brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, and thiobarbituric acid reactive substances were compared among the groups. RESULTS: Latency to the first electrical discharge was compared between Groups 2 and 3, and was found to be significantly longer in Group 3 (27.9 +/- 11 versus 20.4 +/- 7.6 min, p < 0.03). No significant changes were found in brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, or thiobarbituric acid reactive substances. CONCLUSION: Our data show that sound conditioning prolongs the latency to oxygen-induced convulsions. This effect was not accompanied by significant changes in whole-brain antioxidant enzyme activity or the magnitude of lipid peroxidation.