大気中PM2.5への亜急性曝露ラットモデルにおける水素の肺傷害軽減効果とアリール炭化水素受容体を介したメカニズムの検討
Using a rat model of subacute concentrated ambient PM2.5 exposure (1328 ± 730 µg/m³, 5 h/day, 5 days/week for 4 weeks), this study examined whether 66.7% hydrogen inhalation (2 h/day post-exposure) could protect against pulmonary damage. PM2.5-exposed animals showed deteriorated lung function, histopathological changes, airway mucus hypersecretion (elevated MUC5AC expression by immunohistochemistry and RT-qPCR), increased pro-inflammatory cytokines (TNF-α, IL-8, IL-1β), and elevated oxidative stress markers (MDA and 8-isoprostane F2α). Hydrogen inhalation significantly attenuated all these parameters. Western blot analysis revealed that PM2.5 exposure reduced aryl hydrocarbon receptor (AhR) protein levels in lung tissue, and hydrogen inhibited this AhR downregulation. These findings suggest that hydrogen exerts its pulmonary protective effects at least partly through AhR-dependent signaling.
H2 inhalation prevents PM2.5-induced downregulation of aryl hydrocarbon receptor (AhR) in lung tissue, thereby suppressing downstream oxidative stress and pro-inflammatory cytokine production, which collectively reduces pulmonary 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/31718930