Abstract
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.
Highlights
Exposure to hyperbaric hyperoxic conditions can lead to pulmonary oxygen toxicity
There was a significant decrease in DLNO after both the air and oxygen dives, i.e., −2.19 mmol min−1 kPa−1 (p = 0.026) and −2.36 mmol min−1 kPa−1 (p = 0.003), respectively
Combining these seven components revealed a significant increase after oxygen diving, which was at its peak 3 h postdive
Summary
Exposure to hyperbaric hyperoxic conditions can lead to pulmonary oxygen toxicity. 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. Exposure to higher than normal partial pressures of oxygen can lead to pulmonary oxygen toxicity (POT) (van Ooij et al, 2016). The first, caused by local inflammation with capillary and endothelial edema, leads to tracheobronchial irritation, coughing and retrosternal pain (Miller and Winter, 1981). This inflammatory process is reversible, while the irreversible proliferative phase develops when oxygen exposure is continued. The end state of this disease is proliferation of fibroblasts and type II alveolar cells, leading to fibrosis (Kapanci et al, 1972; Robinson et al, 1974)
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