ArticleEnvironment & health (Washington, D.C.)2025
Heat Exposure Changes Lung Function, Biomarkers of Airway Injury, and Airway Microbiota: A Randomized, Crossover Trial.
Article in Environment & health (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Short-term exposure to heat associated with lower lung function in older adults: analysis of the Lung VITAL cohort.BMJ open respiratory research · 2026Article
- Extreme temperature exposure induces lung-gut dysbiosis in healthy mice.Current research in microbial sciences · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High temperature exposure has been identified as a significant risk factor for respiratory diseases. However, causal evidence is needed to confirm the respiratory effects associated with heat exposure and to elucidate the underlying mechanisms. We conducted a randomized crossover trial among healthy adults in Shanghai, China. Participants received 2 h exposures to moderate-temperature (22 °C) and high-temperature (32 °C) conditions. Spirometry tests, fractional exhaled nitric oxide (FeNO) measurements, and collections of pharyngeal secretion and peripheral blood samples were performed before and after each session. Pharyngeal microbiota was analyzed via 16S rRNA amplicon sequencing. Serum biomarkers, including Clara cell protein (CC16) and Chitinase-3-like protein 1 (YKL-40) were also measured. Heat exposure was associated with decreases of 18.8% (95% CI: 4.7%, 32.8%) in peak expiratory flow, 9.6% (95% CI: 1.9%, 17.3%) in forced expiratory volume in the first second, and 8.8% (95% CI: 3.5%, 14.1%) in the ratio of forced expiratory volume in the first second and forced vital capacity. Corresponding increases were observed in FeNO (13.9%; 95% CI: 3.5%, 24.2%), serum CC16 (20.4%, 95% CI: 1.6%, 39.3%), and serum YKL-40 (17.1%, 95% CI: 3.9%, 30.2%). Additionally, three pathogenic pharyngeal bacteria exhibited a higher relative abundance. In summary, acute heat exposure was associated with reductions in lung function and airway injury. Potential biological mechanisms may involve lung epithelial damage, airway inflammation, and disruption of the airway microbiota.
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