Hydrogen Gas Protects Hearing from Loud Noise Damage in Animal Study
- Authors
- Pernilla Videhult Pierre, Anette Fransson, Marta A. Kisiel, Göran Laurell
- Journal
- Annals of Otology, Rhinology & Laryngology
- Year
- 2022
- DOI
- 10.1177/00034894221118764
- Study Type
- Guinea Pig
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Sweden
- Health Condition
- Noise-Induced Hearing Loss
- Body System
- Auditory
TL;DR
Inhaling molecular hydrogen right after loud noise exposure can reduce hearing damage in guinea pigs.
Key Finding
Guinea pigs that inhaled hydrogen gas immediately after impulse noise exposure experienced significantly less hearing damage and preserved more cochlear hair cells than those exposed to noise without hydrogen treatment.
Summary
Researchers exposed guinea pigs to very loud impulse noise (similar to gunfire) and tested whether inhaling hydrogen gas immediately afterward could protect hearing. Guinea pigs that received hydrogen gas after noise exposure showed less hearing damage and better preservation of inner and outer hair cells (the sound-sensing structures in the ear) compared to those exposed to noise alone.
Practical Takeaway
This preclinical animal study suggests hydrogen gas inhalation may help protect against acute noise-induced hearing damage when administered immediately after exposure. However, this is early-stage research in guinea pigs only—human studies would be needed to determine if these findings apply to people and whether the timing and dosage would be practical in real-world situations.
Abstract
Objective: Molecular hydrogen (H 2 ) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H 2 when inhaled immediately after impulse noise exposure. Methods: Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H 2 inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H 2 group), or to H 2 inhalation (n = 5; the H 2 group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H 2 exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells. Results: Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H 2 group; P < .05) but significantly less so in the Noise + H 2 group ( P < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H 2 group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H 2 group. The difference between the groups was significant in the basal region for OHCs ( P = .003) and apical ( P = .033) and basal ( P = .048) regions for IHCs. Conclusions: Acute acoustic trauma can be reduced by H 2 when inhaled immediately after impulse noise exposure.