Physical exercise mitigates the adverse effects of PM_2.5 constituents on lung function: New evidence for inflammatory pathways from a crossover study.

Physical exercise in polluted air involves a significant trade-off. However, the interaction effects and underlying mechanisms between PM_2.5 constituents and physical exercise on lung function remain poorly understood. This crossover study was conducted among 74 adults who completed a session of outdoor physical exercise and a session of no exercise in random order. We analyzed the chemical constituents of PM_2.5 that the subjects were exposed to during each session, measured lung function, and assessed 10 biomarkers of systemic inflammation both before and after each session. We used linear mixed-effect models to assess the independent and interactive effects of PM_2.5 constituents and physical exercise on lung function and biomarkers. We also conducted a moderated mediation analysis to examine the role of inflammatory factors that mediated the effects of PM_2.5 constituents and physical exercise on lung function. We found that traffic emissions and resuspended dust may be major contributors to the adverse effects of PM_2.5 on lung function, and that physical exercise significantly attenuated these detrimental impacts. We also identified heat shock protein 70 (HSP70), granulocyte-macrophage colony stimulating factor, toll-like receptor 4 protein (TLR-4), Clara cell protein 16, and interleukin-8 as the mediators in the association. Our results support the hypothesis that PM_2.5 constituents and physical exercise interact to affect lung function through the HSP70-mediated regulation of the TLR4/NF-κB inflammatory pathway. These findings are expected to inform future control strategies targeting source-specific PM_2.5 constituents and public health decisions on exercise on air pollution days.

Duke Scholars

Author Junfeng Zhang Environmental Natural Science