To study extension of O2 tolerance by interruption of hyperoxic exposure, as compared to previous studies of continuous oxygen exposure, five healthy volunteers were exposed to oxygen at 2 ATA on an intermittent schedule of 20 min breathing O2, alternating with 5 min on a normoxic N2-O2 mixture. The cycle was repeated until symptoms or signs of O2 toxicity caused cessation of the experiment. Tracheal irritation and burning on inspiration occurred after 6-9 "oxygen hours" of exposure and progressed to severe tracheobronchial burning sensation, chest pain, and dyspnea after 11-15 h of O2. Average duration of exposure was 13.7 O2 h, inducing a mean vital capacity decrease of 10.3%. The decrease began soon after onset of symptoms. With intermittent O2 administration, nearly a doubling of the average duration of actual oxygen breathing was required to induce marked vital capacity change (greater than 10%) as compared to the previous studies of continuous O2 exposure. The increased duration of tolerable O2 exposure in man resembles the extension of O2 tolerance known to occur in animals exposed to intermittent hyperoxia.

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Experiments were conducted to test the hypothesis that intermittent exposure to oxygen at two atmospheres absolute (2 ATA) could delay the onset of pulmonary toxicity. This paper reports effects of 2 ATA O2 (total exposure time of 14.1–19.3 h) upon the auditory and vestibular systems of five diver volunteers and effects of a normoxic N2O2 mix on a sixth. Immediately after exposure four subjects had increased acuity by air conduction in the mid-frequency range. Bone conduction sensitivity increased for all six subjects. Middie-ear reflexes were depressed or absent with only partial recovery one month after the experiment for the O2-breathing subjects, but were more sensitive after exposure for the subject breathing N2O2. Middle-ear pressures grew markedly more variable for O2 subjects up to 72 h postexposure, implying decreased eustachian tube function from oxygen. Vestibular systems of four O2-exposed subjects and the N2O2 subject were markedly suppressed to caloric stimulation after exposure, implying pressure as the contributory cause. Operational application may be found in possibly sensitizing certain frequencies to improve the listener's ability to detect signals in noise. [Work supported by CIC, NRMC. and COMSUBDEVGRU ONE.]

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