Oxidative stress markers in bus drivers

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Exposure to ambient air pollution is associated with many diseases. Oxidative stress is believed to be the major source of particulate matter (PM)-mediated adverse health effects. PM in ambient air arises from industry, local heating, and vehicle emissions and poses a serious problem mainly in large cities. Among other compounds PM contains carcinogenic polycyclic aromatic hydrocarbons (cPAHs). In the present study we analyzed the level of oxidative stress among 50 bus drivers from Prague, Czech Republic, and 50 matching controls. Samples from the same individuals were collected in two seasons with different levels of air pollution: in winter 2005 and in summer 2006. We assessed simultaneously the levels of 15-F_2t-isoprostane (15-F_2t-IsoP) and 8-oxodeoxyguanosine (8-oxodG) in urine and protein carbonyl groups in blood plasma. For the analysis of all markers we used ELISA techniques. In samples collected in winter 2005 we observed significantly increased levels of oxidative stress in bus drivers. The median levels (min, max) of individual markers in bus drivers vs. controls were as follows: 8-oxodG: 7.79 (2.64-12.34) vs. 6.12 (0.70-11.38) nmol/mmol creatinine (p<0.01); 15-F_2t-IsoP: 0.81 (0.38-1.55) vs. 0.68 (0.39-1.79) nmol/mmol creatinine (p<0.01); carbonyl levels: 14.1 (11.8-19.0) vs. 12.9 (9.8-16.6) nmol/ml plasma (p<0.001). In samples collected in summer 2006 only 8-oxodG levels were significantly higher in bus drivers. The following median levels (min, max) of analyzed markers were observed in bus drivers vs. controls: 8-oxodG: 6.91 (1.30-10.68) vs. 5.11 (2.34- 12.32) nmol/mmol creatinine (p<0.05); 15-F_2t-IsoP: 0.62 (0.24-1.14) vs. 0.60 (0.28-3.40) nmol/mmol creatinine (p=0.89); carbonyl levels: 17.5 (12.0-23.2) vs. 16.6 (13.0-25.6) nmol/ml plasma (p=0.28). Exposure to air pollution was measured by personal monitors used by all participants of the study for 48 hours. As expected, exposure to cPAHs and to benzo[a]pyrene (B[a]P) was significantly higher in winter 2005; median levels (min, max) in winter 2005 vs. summer 2006 among all subjects were following: B[a]P: 1.34 (0.25-6.71) vs. 0.13 (0.13-0.92) ng/m³ (p<0.001); cPAHs: 7.56 (1.85-35.35) vs. 1.69 (1.55-6.93) ng/m³ (p<0.001). In concordance with these observations levels of both 8-oxodG and 15-F_2t-IsoP were significantly increased among all subjects in winter 2005; median levels (min, max) in winter 2005 vs. summer 2006 were as follows: 8-oxodG: 6.65 (0.70-12.34) vs. 5.75 (1.87-12.32) nmol/mmol creatinine (p<0.05); 15-F_2t-IsoP: 0.76 (0.39-1.79) vs. 0.61 (0.24-3.40) nmol/mmol creatinine (p<0.001). In conclusion, our study indicates that exposure to B[a]P and c-PAHs increases oxidative damage to DNA and lipids.

Acknowledgements:The study was supported by the Czech Ministry of Environment grant VaV-SL/5/160/05.