Short time exposure to ambient ozone and associated cardiovascular effects: A panel study of healthy young adults

The evidence that exposure to ambient ozone (O₃) causes acute cardiovascular effects appears inconsistent. A repeated-measure study with 61 healthy young volunteers was conducted in Xinxiang, Central China. Real-time concentrations of O₃ were monitored. Cardiovascular outcomes including blood pressure (BP), heart rate (HR), serum levels of high sensitivity C-reactive protein (hs-CRP), 8-hydroxy-2'-deoxyguanosine (8-OHdG), tissue-type plasminogen activator (t-PA), and platelet-monocyte aggregation (PMA) were repeated measured. Linear mixed-effect models were used to analyze the association of ambient O₃ with these cardiovascular outcomes. Additionally, the modifying effects of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) polymorphisms were estimated to explore the potential mechanisms and role of the association between O₃ exposure and the above cardiovascular outcomes. A 10 μg/m³ increase in O₃ was associated with increases of 9.2 mmHg (95% confidence interval [CI]: 2.5, 15.9), 7.2 mmHg (95% CI: 0.8, 13.6), and 21.2 bpm (95% CI: 5.8, 36.6) in diastolic BP (DBP, lag1), mean arterial BP (MABP, lag1), and HR (lag01), respectively. Meanwhile, the serum concentrations of hs-CRP, 8-OHdG, and t-PA were all increased by O₃ exposure, but the PMA level was decreased. Stratification analyses showed that the estimated effects of O₃ on DBP, MABP, and HR in GSTM1-sufficient subjects were significantly higher than in GSTM1-null subjects. Moreover, GSTM1-null genotype enhanced O₃-induced increases, albeit insignificant, in levels of serum hs-CRP, 8-OHdG, and t-PA compared with GSTM1-sufficient genotype. Insignificant increases in hs-CRP and t-PA were also detected in GSTT1-null subjects. Taken together, our findings indicate that acute exposure to ambient O₃ induces autonomic alterations, systemic inflammation, oxidative stress, and fibrinolysis in healthy young subjects. GSTM1 genotype presents the trend of modifying O₃-induced cardiovascular effects.