Introduction: Exposure to hyperbaric hyperoxic conditions can lead to pulmonary oxygen toxicity. Although a decrease in vital capacity has long been the gold standard, newer diagnostic modalities may be more accurate. In pulmonary medicine, much research has focussed on volatile organic compounds (VOCs) associated with inflammation in exhaled breath. In previous small studies after hyperbaric hyperoxic exposure several methyl alkanes were identified. This study aims to identify which VOCs mark the development of pulmonary oxygen toxicity.Methods: In this randomized crossover study, 12 divers of the Royal Netherlands Navy made two dives of one hour to 192.5 kPa (comparable to a depth of 9 msw) either with 100% oxygen or compressed air. At 30 min before the dive, and at 30 min and 1, 2, 3, and 4 h post-dive, exhaled breath was collected and followed by pulmonary function tests (PFT). Exhaled breath samples were analyzed using gas chromatography–mass spectrometry (GC–MS). After univariate tests and correlation of retention times, ion fragments could be identified using a standard reference database [National Institute of Standards and Technology (NIST)]. Using these fragments VOCs could be reconstructed, which were then tested longitudinally with analysis of variance.Results: After GC–MS analysis, seven relevant VOCs (generally methyl alkanes) were identified. Decane and decanal showed a significant increase after an oxygen dive (p = 0.020 and p = 0.013, respectively). The combined intensity of all VOCs showed a significant increase after oxygen diving (p = 0.040), which was at its peak (+35%) 3 h post-dive. Diffusion capacity of nitric oxide and alveolar membrane capacity showed a significant reduction after both dives, whereas no other differences in PFT were significant.Discussion: This study is the largest analysis of exhaled breath after in water oxygen dives to date and the first to longitudinally measure VOCs. The longitudinal setup showed an increase and subsequent decrease of exhaled components. The VOCs identified suggest that exposure to a one-hour dive with a partial pressure of oxygen of 192.5 kPa damages the phosphatidylcholine membrane in the alveoli, while the spirometry and diffusion capacity show little change. This suggests that exhaled breath analysis is a more accurate method to measure pulmonary oxygen toxicity.

Wingelaar et al. Pulmonary Oxygen Toxicity in HBOT why emission of methyl alkanes (which could originate from the phosphatidylcholine membrane in the alveoli) are reduced after HBOT. This suggests that HBOT might not be as damaging to the pulmonary tract as previously assumed. Future research on POT should focus on the identified VOCs (inflammation and methyl alkanes).

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.