Heat Exposure Changes Lung Function, Biomarkers of Airway Injury, and Airway Microbiota: A Randomized, Crossover Trial

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.