Studies show that, in the long term, a robust recovery from most types of oxygen toxicity is possible. Oxygen toxicity is managed by reducing the exposure to increased oxygen levels. Prolonged exposure to above-normal oxygen partial pressures, or shorter exposures to very high partial pressures, can cause oxidative damage to cell membranes, collapse of the alveoli in the lungs, retinal detachment, and seizures. Symptoms may include disorientation, breathing problems, and vision changes such as myopia. Pulmonary and ocular toxicity result from longer exposure to increased oxygen levels at normal pressure. Central nervous system toxicity is caused by short exposure to high partial pressures of oxygen at greater than atmospheric pressure. The body is affected in different ways depending on the type of exposure. The result of breathing increased partial pressures of oxygen is hyperoxia, an excess of oxygen in body tissues. Oxygen toxicity is a concern for underwater divers, those on high concentrations of supplemental oxygen (particularly premature babies), and those undergoing hyperbaric oxygen therapy. Historically, the central nervous system condition was called the Paul Bert effect, and the pulmonary condition the Lorrain Smith effect, after the researchers who pioneered the discoveries and descriptions in the late 19th century. Severe cases can result in cell damage and death, with effects most often seen in the central nervous system, lungs, and eyes.
Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen ( OĢ) at increased partial pressures. The subject in the centre is breathing 100% oxygen from a mask. The chamber is pressurised with air to 3.7 bar. In 1942–43 the UK Government carried out extensive testing for oxygen toxicity in divers. Oxygen toxicity syndrome, oxygen intoxication, oxygen poisoning