Abstract
BACKGROUND: Air pollution (AP) has become a substantial environmental issue affecting human cardiorespiratory health. Physical exercise (PE) is widely accepted to promote cardiorespiratory health. There is a paucity of research on the point at which the level of polluted environment engaged in PE could be used as a preventive approach to compensate for the damages of AP. OBJECTIVES: To assess the effects of acute moderate-intensity PE on the cardio-respiratory and inflammatory responses of young adults in varying levels of AP, and to determine the pollution level at which engaging in short-term PE is considered safe. METHODS: We constructed a real-world crossover study of 30 healthy young adults with repeated measures. Participants participated in 90 min of moderate-intensity PE in different (low, medium, high) AP exposure scenarios. Cardiorespiratory health was measured by assessing systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow (PEF), mean forced expiratory flow between 25% and 75% of FVC (FEF(25-75%)), and fractional exhaled nitric oxide (FeNO) before and after the intervention. Blood samples were also collected simultaneously. The percentage changes in cardiorespiratory health markers after exercise in the three AP levels environments were compared using linear mixed-effects models. RESULTS: Compared to the changes observed post-exercise in the low-level AP environment, only PEF (-9.36, P = 0.018) showed a significant decrease, and eosinophils showed a significant increase in the medium-level environment (25.64, P = 0.022), with no significant differences in other indicators. Conversely, post-exercise in the high-level AP environment resulted in a significant increase in DBP (6.5, P = 0.05), lung inflammation (FeNO: 13.3, p < 0.001), inflammatory cell counts (WBC: 27.0, p < 0.001; neutrophils: 26.8, p < 0.001; lymphocytes: 32.2, p < 0.001; monocytes: 28.2, p < 0.001; and eosinophils: 48.9, p < 0.001), and inflammatory factors (IL-1β: 0.76, P = 0.003; IL-10: 0.17, P = 0.02; IL-6: 0.1, P = 0.17; TNF-α: 0.97, P = 0.011; CRP: 0.17, P = 0.003). Additionally, there were significant declines in lung function parameters, including FVC (-6.84, P = 0.04), FEV1 (-8.97, P = 0.009), and PEF (-9.50, P = 0.013). CONCLUSIONS: Acute PE in low and medium-level AP environments is generally secure concerning short-term effects on cardiorespiratory health among healthy young adults. However, acute PE in high-level AP environments can be detrimental to cardiorespiratory health, significantly increasing the body's inflammatory response. TRIAL REGISTRATION: ChiCTR2000031851; Registered 12.04.2020.