In guinea pigs exposed to 100-percent oxygen at normal air pressure for 48 hours, fluid accumulated in the lungs (
pulmonary edema) and the epithelial cells lining the alveolus and pulmonary capillaries were damaged. This damage was probably caused by a highly reactive form of the oxygen molecule called the
oxygen free radical, which destroyed
proteins and
membranes in the epithelial cells. In humans breathing 100-percent oxygen at normal pressure, the following effects were observed:
- Pulmonary edema (intensive-care patients on breathing machines at 30 hours or more exposure)
- Decreases in the rate of gas exchange across the alveoli (intensive-care patients on breathing machines at 30 hours of exposure)
- Chest pains that were worse during deep breathing (volunteers with 24 hours of exposure)
- Decrease in the total volume of exchangeable air in the lung (vital capacity) by 17 percent (volunteers with 24 hours of exposure)
- Local areas of collapsed alveoli when plugged by mucus, a condition called atelectasis (patients, volunteers). The oxygen entrapped in the plugged alveolus gets absorbed into the blood, no gas is left to keep the plugged alveolus inflated and it collapses. Mucus plugs happen normally but are cleared by coughing. Also, if alveoli become plugged during air breathing, the nitrogen entrapped in the alveoli keeps them inflated.
- blindness caused by inadequate development of the capillaries in the lens and retina of the eye (premature infants). Reducing the oxygen to 40 percent can prevent this blindness.