衝撃性騒音外傷に対する水素ガス吸入の保護効果：前臨床動物実験
This preclinical study examined whether hydrogen gas inhalation administered immediately after impulse noise exposure could reduce cochlear damage in guinea pigs (n=26). Animals were exposed to 400 impulse noise stimuli at 156 dB SPL, followed or not by H2 inhalation at 2 mol% (500 ml/min for 1 hour). Auditory brainstem response (ABR) thresholds were measured at five frequencies (3.15–30.0 kHz) before and 4 days after exposure, and cochleae were harvested for hair cell quantification. ABR threshold elevations were significantly smaller in the noise-plus-hydrogen group compared with the noise-only group across all tested frequencies. Outer hair cell loss in the mid-cochlear region was 53% in the noise-only group versus 22% in the hydrogen group, and inner hair cell loss was similarly reduced. Statistically significant differences were observed in the basal region for outer hair cells and in both apical and basal regions for inner hair cells, supporting a protective role of H2 inhalation against acute acoustic cochlear injury.
H2 inhalation is thought to scavenge reactive oxygen species generated by acute impulse noise exposure, thereby reducing oxidative damage to cochlear hair cells and limiting auditory threshold shifts.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/35962590