Oxygen Toxicity and Special Operations Forces Diving: Hidden and Dangerous

Abstract

In Special Operations Forces (SOF) closed-circuit rebreathers with 100% oxygen are commonly utilized for covert diving operations. Exposure to high partial pressures of oxygen (PO₂) could cause damage to the central nervous system (CNS) and pulmonary system. Longer exposure time and higher PO₂ leads to faster development of more serious pathology. Exposure to a PO₂ above 1.4 ATA can cause CNS toxicity, leading to a wide range of neurologic complaints including convulsions. Pulmonary oxygen toxicity develops over time when exposed to a PO₂ above 0.5 ATA and can lead to inflammation and fibrosis of lung tissue. Oxygen can also be toxic for the ocular system and may have systemic effects on the inflammatory system. Moreover, some of the effects of oxygen toxicity are irreversible. This paper describes the pathophysiology, epidemiology, signs and symptoms, risk factors and prediction models of oxygen toxicity, and their limitations on SOF diving.

Keywords: CNS-toxicity; closed-circuit rebreather; diving; oxygen toxicity; pulmonary toxicity.

Figure 1

Schematic representation of the normal alveolocapillary region. 1, alveolar type 1 cell; 2, alveolar type 2 cell; 3, basement membrane; 4, interstitium; 5, capillary endothelial cell; 6, fibroblast; 7, alveolar macrophage; 8, surfactant layer; 9, red blood cell; 10, capillary base membrane. Adapted with permission from van Ooij et al. (2013).

Figure 2

Exsudative stage (left) and proliferative stage (right) in pulmonary oxygen toxicity. 1, type 1 alveolar cell; 2, type 2 alveolar cell; 3, alveolar edema; 4, neutrophil; 5, hyaline membrane; 6, edematous interstitium; 7, fibroblast; 8, fibrin thrombus; 9, swollen capillary endothelial cell; 10, denuded basement membrane; 11, alveolar fibrin formation; 12, collagen fibers deposition; 13, incorporation of hyaline membrane; 14, fibroblastic proliferation; 15, interstitial fibrin.