Hearing loss in divers: a 6-year prospective study.

Occupational diving is associated with hearing loss, but the cause is disputed. Our aim was to follow a cohort of divers through the first 6 years of their career in order to look for evidence of permanent threshold shift associated with diving activity, occupational noise exposure or acute injuries. Hearing was measured by pure tone audiometry in 67 participants at a basic course for working divers. Hearing thresholds were adjusted for age (ISO 7029). The subjects were examined and interviewed by an otologist. Additional medical and exposure data were recorded in questionnaires and personal logbooks. The procedure was repeated after 3 and 6 years. None of the subjects suffered inner ear barotrauma or inner ear decompression sickness during follow-up. Middle ear barotrauma was common. The prevalence of subjective hearing difficulties increased during follow-up, and there was a significant threshold shift at 4 kHz (mean 2.6 dB, 95% confidence interval 0.9-4.3 dB). Both subjective and objective hearing loss was associated with occupational noise exposure, but not with diving frequency or with a history of middle ear barotrauma. In the absence of manifest inner ear barotrauma or inner ear decompression sickness, noise seems to be the most important cause of long-term hearing loss in occupational divers. This study did not find evidence of long-term hearing loss caused by uneventful diving per se.

Postural control and venous gas bubble formation during hypobaric exposure.

BACKGROUND: Earlier studies have shown that acute hypoxia at simulated altitudes up to 18,000 ft affects postural control. The main objective of this study was to investigate whether this is caused by hypoxia or by other effects of reduced barometric pressure. Doppler monitoring was included to rule out venous gas emboli (VGE) as a possible cause of disturbed postural control. A secondary objective was to evaluate two conventional altitude chamber training profiles regarding release of VGE. HYPOTHESIS: Chamber flights up to 18,000 ft affect postural control due to acute hypoxia or other effects of reduced barometric pressure such as bubble formation. VGE probably will not be formed at the altitude chamber flight profiles and procedures selected for this study. METHODS: Repeated registrations of postural control and Doppler monitoring for detection of possible VGE were performed on 12 subjects before, during, and after exposure to two different altitude chamber flight profiles. In chamber flight profile 1 the subjects were first preoxygenated for 45 min and then exposed to a normoxic environment at altitudes of 25,000, 18,000, 14,000, and 8000 ft. Chamber flight profile 2 consisted of an 80 min exposure to 14,000 ft without preoxygenation or supplemental oxygen for the first 60 min. RESULTS: In chamber flight profile 1, where normoxic conditions were achieved during all balance testing, no significant changes in postural control were found. No VGE were observed and no subjective dizziness was reported during this exposure. In chamber flight profile 2, a significant influence on postural control was reported for the eyes-open condition, when breathing air at 14,000 ft. These changes normalized when reaching ground level. VGE were observed in one of the 12 subjects after 75 min at 14,000 ft. Another subject complained of severe dizziness during the initial part of the decompression to 14,000 ft, and was excluded from further experiments. CONCLUSIONS: Changes in postural control at altitudes up to 18,000 ft is probably due to acute hypoxia. VGE may form during acute altitude exposure to 14,000 ft.