<unk>  is caused by exposure to<unk>  at partial pressures greater than those to which the body is normally exposed. This occurs in three principal settings: underwater diving, hyperbaric<unk>  therapy, and the provision of supplemental<unk> , particularly to premature infants. In each case, the risk factors are markedly different. Central nervous system<unk>  Exposures, from minutes to a few hours, to partial pressures of<unk>  above —about eight times normal atmospheric partial pressure—are usually associated with central nervous system<unk>  and are most likely to occur among patients undergoing hyperbaric<unk>  therapy and divers. Since sea level atmospheric pressure is about , central nervous system<unk>  can only occur under hyperbaric conditions, where ambient pressure is above normal. Divers breathing air at depths beyond face an increasing risk of an<unk>  "hit" (seizure). Divers breathing a gas mixture enriched with<unk> , such as nitrox, can similarly suffer a seizure at shallower depths, should they descend below the maximum operating depth allowed for the mixture. Lung<unk>  The curves show typical decrement in lung vital capacity when breathing<unk> . Lambertsen concluded in 1987 that could be tolerated indefinitely. The lungs and the remainder of the respiratory tract are exposed to the highest concentration of<unk>  in the human body and are therefore the first organs to show<unk> . Pulmonary<unk>  occurs only with exposure to partial pressures of<unk>  greater than , corresponding to an<unk>  fraction of 50% at normal atmospheric pressure. The earliest signs of pulmonary<unk>  begin with evidence of tracheobronchitis, or inflammation of the upper airways, after an asymptomatic period between 4 and 22 hours at greater than 95%<unk> , with some studies suggesting symptoms usually begin after approximately 14 hours at this level of<unk> . At partial pressures of<unk>  of —100%<unk>  at 2 to 3 times atmospheric pressure—these symptoms may begin as early as 3 hours after exposure to<unk> . Experiments on rats breathing<unk>  at pressures between suggest that pulmonary manifestations of<unk>  may not be the same for normobaric conditions as they are for hyperbaric conditions. Evidence of decline in lung function as measured by pulmonary function testing can occur as quickly as 24 hours of continuous exposure to 100%<unk> , with evidence of diffuse alveolar damage and the onset of acute respiratory distress syndrome usually occurring after 48 hours on 100%<unk> . Breathing 100%<unk>  also eventually leads to collapse of the alveoli (atelectasis), while—at the same partial pressure of<unk> —the presence of significant partial pressures of inert gases, typically nitrogen, will prevent this effect. Preterm newborns are known to be at higher risk for bronchopulmonary dysplasia with extended exposure to high concentrations of<unk> . Other groups at higher risk for<unk>  are patients on mechanical ventilation with exposure to levels of<unk>  greater than 50%, and patients exposed to chemicals that increase risk for<unk>  such the chemotherapeutic agent bleomycin. Therefore, current guidelines for patients on mechanical ventilation in intensive care recommends keeping<unk>  concentration less than 60%. Likewise, divers who undergo treatment of decompression sickness are at increased risk of<unk>  as treatment entails exposure to long periods of<unk>  breathing under hyperbaric conditions, in addition to any<unk>  exposure during the dive. Ocular<unk>  Prolonged exposure to high inspired fractions of<unk>  causes damage to the retina. Damage to the developing eye of infants exposed to high<unk>  fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions. Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants. In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental<unk>  exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental<unk>  use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications. Hyperoxic myopia has occurred in closed circuit<unk>  rebreather divers with prolonged exposures. It also occurs frequently in those undergoing repeated hyperbaric<unk>  therapy. This is due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift. It is usually reversible with time.
Oxygen toxicity
Cerebral hypoxia
Nitrogen dioxide poisoning
Chromium toxicity
Histotoxic hypoxia
Fluoride toxicity
Chlorine gas poisoning
Silent hypoxia