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.