TABLE 1

Time of onset of pathological findings of pulmonary oxygen toxicity (POT) in primates and humans

DayPOT phasePrimatesDayPOT phaseHumans
11Tracheobroncholitis, mucous flow decreased
2ExudationAlveolar oedema, septal wall oedema, distention lymphatic vessels, decrement alveolar type 1 cells2–5ExudationDenuded alveolar type 1 cells, oedematous endothelial capillary cell swelling, necrosis respiratory epithelium, squamous metaplasia tracheal and bronchial mucosa, deposition eosinophilic slough, alveolar and interstitial oedema, formation hyaline membrane, cilial loss, decreased mucociliary transport
4Resolution, formation hyaline membrane, influx inflammatory cells
5ProliferationIncrement alveolar type 2 cells, fibroblast infiltration5–88ProliferationProliferation of alveolar type 2 replacing alveolar type 1 cells, derangement of collagen and elastin, incorporation of hyaline membranes into the septal walls, fibroblastic proliferation, collagen fibre deposition, fibro-proliferative organisation of intra-alveolar exudate, infiltration with inflammatory cells, interstitial lung fibrosis, emphysematous alveoli with areas of fibrosis, cilial loss
8Intra-alveolar hyaline membranes, thickening of the alveolar-capillary membrane, leukocytic infiltration, marked cellular proliferation of abnormal alveolar type 2 cells, haemorrhagic areas, accumulation of intracellular water
12Extravascular lung water within the pulmonary parenchyma and interstitial space, invasion of fibroblasts and macrophages
56Air-blood barrier thickened, increase in collagen content, intra-alveolar septal scarring, alveolar air volume diminished