Biomarkers of genotoxicity of air pollution (the AULIS project): bulky DNA adducts in subjects with moderate to low exposures to airborne polycyclic aromatic hydrocarbons and their relationship to environmental tobacco smoke and other parameters.

The levels of bulky DNA adducts were measured by (32)P-post-labelling in lymphocytes of 194 non-smoking students living in the city of Athens and the region of Halkida, Greece, once in the winter and again in the following summer. Personal exposures to particulate-bound polycyclic aromatic hydrocarbons (PAH) were significantly higher in Athens subjects during both seasons. There was hardly any diagonal radioactive zone in the pattern of DNA adducts observed. Highest adduct levels were observed in a sub-group of subjects living in or near the Halkida Institute campus, which was located in rural surroundings with a minimal burden of urban air pollution. The remaining Halkida subjects had intermediate levels, while Athens subjects showed the lowest levels. This trend, which was observed over both monitoring seasons, consistently paralleled the variation in three markers of exposure to environmental tobacco smoke (ETS), namely (i) declared times of exposure to ETS during the 24 h prior to blood donation, (ii) plasma cotinine levels and (iii) chrysene/benzo[g,h,i]perylene ratios in the profile of personal PAH exposure. Furthermore, among the Halkida campus area subjects (but not the remaining subjects) positive correlations were observed between DNA adducts and (i) measured personal exposures to chrysene or benzo[a]pyrene, (ii) time of declared ETS exposure and (iii) chrysene/benzo[g,h,i] perylene ratios. These correlations suggest that, for a group suffering minimal exposure to urban air pollution, exposure to ETS was a significant determinant of the observed DNA damage. Gender had a consistent and significant effect on adduct levels (males having higher levels), which remained significant even after multiple regression analysis. Habitual consumption of roasted meat was significantly associated with an enhancement of adduct levels and the effect was strengthened when only individuals unexposed to ETS were taken into consideration. No significant effects were observed for other dietary parameters or factors reflecting exposure to air pollution.

Personal exposures to PM(2.5) and polycyclic aromatic hydrocarbons and their relationship to environmental tobacco smoke at two locations in Greece.

In the context of a large-scale molecular epidemiology study of biomarkers of genotoxicity of air pollution, 24-h mean personal exposures to airborne PM(2.5) (particulate matter <2.5 microm) and associated polycyclic aromatic hydrocarbon (PAHs) were measured in 194 non-smoking technical institute students living in the city of Athens, Greece (an area with moderately high levels of air pollution) and the nearby small town of Halkida anticipated to have lower pollution levels. Extensive information relevant to the assessment of long-term and recent exposure to PAH was obtained from questionnaires as well as a time-location-activity diary (TLAD) which was kept by all subjects during a 4-day observation period. During the last 24 h of this period, subjects underwent personal exposure monitoring for PM(2.5) and PAH, while a sample of blood was donated at the end of this period. All subjects were monitored in this way twice; once during a winter season (October-February) and once during the following summer season (June-September). Nine subjects with plasma cotinine levels above 20 ng/ml were considered as unreported smokers and excluded from the study. Winter PM(2.5) exposures were lower in Athens (geometric mean 39.7 microg/m(3)) than Halkida (geometric mean 56.2 microg/m(3)) (P<0.001), while there was no significant location difference during the summer (Athens: geometric mean 32.3 microg/m(3), Halkida: geometric mean 32.9 microg/m(3); P=0.79). On the other hand, PAH exposures (sum of the eight carcinogenic PAHs) were significantly higher in Athens than in Halkida during the winter (Athens: geometric mean 8.26 ng/m(3), Halkida: geometric mean 5.80 ng/m(3); P<0.001) as well as during the summer (Athens: geometric mean 4.44 ng/m(3), Halkida: geometric mean 1.48 ng/m(3); P<0.001). There was a significant difference in the profile of the PAH exposures at the two locations, the proportion of lighter PAH (benzo[a]anthracene, chrysene [CHRYS], benzo[k]fluoranthene, and benzo[b]fluoranthene) being higher, and that of heavier PAH (benzo[ghi]perylene [BPer] and indeno[1,2,3,cd]pyrene) lower, in Halkida than in Athens, regardless of season. This difference appeared to be related to individual exposure to environmental tobacco smoke (ETS), as indicated by (a) the correlation at the individual level between the CHRYS/BPer ratio and declared time of recent exposure to ETS as well as plasma cotinine levels, especially during the winter; (b) the parallel variation of the mean levels of all three markers (declared ETS exposure, cotinine levels, CHRYS/BPer ratio) among three subgroups of subjects (Athens subjects who had lowest levels of all three markers; Halkida subjects other than those living in the institute campus area; and Halkida subjects living in the institute campus area who had the highest levels of all three markers). This demonstrates that ETS can have a distinctive effect on the PAH exposure profile of subjects exposed to relatively low levels of urban air pollution.