I dunno. With all due respect to Dr. Pollock, I'm still not buying the 'oxygen ear' theory.
- Virtually all of the online literature that discusses 'oxygen ear' or 'middle ear oxygen absorption' quotes other websites, notably the US Navy Diver Manual, which talks about it but doesn't reference a source.
- None of the discussions about Oxygen Ear actually reference a scientific study on the topic. I couldn't find any source study at all. (This is a big red flag for people in medical research, where common folklore supplants rigorous studies-- until it's proven wrong.)
- There is actually evidence against
the idea.https://www.ncbi.nlm.nih.gov/pubmed/3920459https://www.tandfonline.com/doi/abs/10. ... 9509139341
- For nitrox divers, the PPO2 percentage is typically ~50% higher than ambient air (for EAN32). Let's assume the middle ear (ME) is flushed with nitrox during the dive, so that on surfacing the ME contains pure nitrox. If all of the extra
oxygen were to be absorbed, this corresponds to a ~10% reduction in ambient pressure within the ME (Before O2 absorption: .68 PPN2 + .32 PPO2; After O2 absorption: .68 PPN2 + .21 PPO2 @ 1ATA). That 10% change in pressure is the equivalent of about the first 3 fsw at the beginning of a dive, a difference easily cleared with a single Valsalva maneuver -- or a yawn if you happen to be riding up in a fast elevator. And yet... the ear clearing continues on for 12, 24 hours... Note: in the course of researching this I found out that the ME does not normally contain the same mix of gasses as air; more closely the mix of gasses in venous blood: a super high concentration of CO2, low O2, and high N2. How that fits in this discussion I'm not sure. Source: https://www.tandfonline.com/doi/abs/10. ... 9009122520
So I think there's more to it, perhaps due to high PO2 levels affecting the ME chemoreceptors, which regulate ME aeration, as A. Shupak (1994)
suggests. That would explain why the problem is worse after high-O2 dives and long rebreather dives.