水素ガス吸入による騒音性難聴の予防：活性酸素種の低減を介した内耳保護効果
Reactive oxygen species (ROS) generated in the inner ear are central to the development of noise-induced hearing loss (NIHL). This animal study investigated whether H2 gas inhalation could mitigate NIHL in guinea pigs exposed to noise, followed by daily 5-hour inhalation of 0.5%, 1.0%, or 1.5% H2 for five consecutive days. Auditory brainstem response measurements showed that threshold shifts improved significantly in the 1.0% and 1.5% H2 groups relative to untreated controls. Outer hair cell (OHC) survival assessed 7 days post-exposure was markedly higher in the 1.0% and 1.5% groups, particularly in the basal cochlear turn. Immunohistochemical staining for 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, revealed substantially reduced immunoreactivity in H2-inhaled animals compared with controls. These findings indicate that H2 inhalation at concentrations of 1.0% and above confers meaningful protection against noise-induced cochlear injury through ROS suppression.
Inhaled H2 selectively scavenges ROS produced in the inner ear following noise exposure, reducing oxidative DNA damage (measured by 8-OHdG immunoreactivity) in outer hair cells and thereby limiting cochlear injury.
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/25196919