A MODEL FOR PREDICTING CENTRAL-NERVOUS-SYSTEM OXYGEN-TOXICITY FROM HYPERBARIC-OXYGEN EXPOSURES IN HUMANS

Under certain circumstances, Navy divers breathe 100% O-2 when working underwater, Serious symptoms of central nervous system (CNS) O-2 toxi city can develop from hyperbaric O-2 exposure; immersion and exercise are also known to exacerbate toxicity. We developed risk models for qu antitative prediction of the probability of developing symptoms using a large set of human data in which occupational exposure conditions we re simulated, Exposures were 5 to 265 min at P-o2 levels from 20 to 50 feet of sea water (fsw) (1 fsw = 3.06 kPa). Approximately half of the exposures were to a single P-o2, while the remainder were more compli cated consisting of exposures to multiple levels of hyperbaric O-2. In 688 trials, there were 42 exposure-stopping symptoms. We used maximum likelihood to estimate parameters, likelihood ratios to compare model fits, and chi(2) tests to judge goodness-of-fit of model predictions to observations. The modeling shows that risk has a steep P-o2 depende nce. A model with autocatalytic features fits the data as well as a si mpler model: when P-o2 is elevated beyond 34 fsw, risk accumulates rap idly without bound while accumulating toward an asymptote at lower P-o 2 levels. This autocatalytic feature of risk accumulation implies a te stable hypothesis that substantial protection from human CNS O-2 toxic ity can be obtained from intermittent exposure (periodic exposure to l ower P-o2). The models predict that the probability of O-2 toxicity is less than 7% with current Navy limits while breathing 95% O-2. Probab ility of symptoms is <1% if FIO2 is maintained at the United States Na vy recommended level of 75%.