Hydrogen gas inhalation protects against cigarette smoke-induced COPD development in mice
Lu W, Li D, Hu J, Mei H, Shu J, Long Z, Yuan L, Li D, Guan R, Li Y, Xu J, Wang T, Yao H, Zhong N, Zheng Z. · Journal of Thoracic Disease. 2018;10(6):3232–3243.
Study at a glance
Preclinical
Male C57BL/6J mice exposed to cigarette smoke for 90 days and cultured 16HBE human bronchial epithelial cells exposed to hydrogen peroxide.
After 60 days of cigarette-smoke exposure, mice inhaled the final H₂/O₂/N₂ mixture for one hour twice daily, with a 6–8 hour interval, through day 90. · The delivered mixture contained 42% H₂, 21% O₂ and 37% N₂ at a reported total flow of 3.8 L/min.
One hour per session, twice daily with a 6–8 hour interval, during the final 30 days of a 90-day cigarette-smoke protocol; assessment on day 91.
H₂ exposure was associated with less emphysema, airway remodeling, inflammation and mucus and favorable changes in several lung-function and signaling outcomes. Forced vital capacity and resistance index did not differ significantly between smoke-only and H₂ groups. The experiment tested prevention/development in mice, not treatment of established human COPD.
Preclinical prevention model with small assay-specific groups, high-concentration chamber exposure, numerous outcomes and no adverse-event assessment. Component flows are calculations from the chamber mixture, not direct inspired dose per mouse. Multiple Chinese public grants funded the work; authors declared no conflicts of interest.
What kind of evidence is this?
Preclinical
Randomized cigarette-smoke mouse experiment with complementary human bronchial-epithelial-cell assays
Respiratory health
Inhaled H₂
Information not yet classified
Some editorial classification fields are still pending. The source-reported outcomes and result are shown below; Hydrogenology does not infer a positive or negative signal from prose automatically.
Methods
Male C57BL/6J mice exposed to cigarette smoke for 90 days and cultured 16HBE human bronchial epithelial cells exposed to hydrogen peroxide.
Main in-vivo groups were normal-air control n=10, cigarette smoke n=8 and cigarette smoke plus H₂ n=8; histology used n=5/group, signaling assays n=4/group and cell assays n=3–5/group.
One hour per session, twice daily with a 6–8 hour interval, during the final 30 days of a 90-day cigarette-smoke protocol; assessment on day 91.
After 60 days of cigarette-smoke exposure, mice inhaled the final H₂/O₂/N₂ mixture for one hour twice daily, with a 6–8 hour interval, through day 90.
Diluted Brown's gas / oxyhydrogen — co-generated 66.7% H₂/33.3% O₂ was diluted with nitrogen before delivery.
The delivered mixture contained 42% H₂, 21% O₂ and 37% N₂ at a reported total flow of 3.8 L/min.
1,596 mL/min H₂, calculated from the reported 3,800 mL/min total flow × 42% H₂.
21% O₂; 798 mL/min O₂, calculated from 3,800 mL/min × 21%. The remaining 1,406 mL/min was N₂.
Cigarette-smoke mice without H₂ and normal-air controls; matched H₂O₂-treated cell controls were used in vitro.
Outcomes and reported result
Forced lung-function measures, hematocrit, emphysema, collagen deposition, airway goblet cells, bronchoalveolar inflammatory cells and cytokines, mucins, ERK1/2 and NF-κB signaling and cell-culture cytokines.
H₂ exposure was associated with less emphysema, airway remodeling, inflammation and mucus and favorable changes in several lung-function and signaling outcomes. Forced vital capacity and resistance index did not differ significantly between smoke-only and H₂ groups. The experiment tested prevention/development in mice, not treatment of established human COPD.
The complete open-access publisher/PMC article, randomization, assay-specific sizes, gas generation, final composition and flow, schedule, positive and null results, funding and conflict statement were checked.
A reported association, difference or mechanism is not automatically a clinical benefit.
Limitations and applicability
Preclinical prevention model with small assay-specific groups, high-concentration chamber exposure, numerous outcomes and no adverse-event assessment. Component flows are calculations from the chamber mixture, not direct inspired dose per mouse. Multiple Chinese public grants funded the work; authors declared no conflicts of interest.
Cigarette-smoke-induced COPD-like changes in mice and oxidative-stress assays in cells; it does not establish efficacy or safety in people with COPD.
No single-study GRADE certainty rating is assigned. Read how records and evidence assessments are prepared.
Sources and record status
PMID: 30069319 · DOI: 10.21037/jtd.2018.05.93
Open-access publisher article and PubMed Central copy.
Complete Journal of Thoracic Disease/PMC article and PubMed metadata; full-text extraction checked 9 August 2026.
10 August 2026
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