“…A seasonal increase in this ratio has been also reported elsewhere (Greenberg et al, 1985 ), while similar summer values were observed for ambient levels in cities of northern Greece ( Papageorgopoulou et al, 1999 ), and even higher values have been reported for Stockholm (Colomsjo et al, 1986 ) and Toronto (Katz et al, 1978 ) . The increase of BPer /B [ a] P ratios (which are believed to reflect the contribution of gasoline exhaust ) during the summer could be attributed to the contribution during winter to the PAH emission profile of dieselpowered central heating ( Moller and Afheim, 1980 ).…”
Section: Variables Both Locations Athens Halkidasupporting
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 m ) 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 g / m 3 ) than Halkida ( geometric mean 56.2 g / m 3 ) (P < 0.001 ) , while there was no significant location difference during the summer ( Athens: geometric mean 32.3 g / m 3 , Halkida: geometric mean 32.9 g / 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 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.
“…A seasonal increase in this ratio has been also reported elsewhere (Greenberg et al, 1985 ), while similar summer values were observed for ambient levels in cities of northern Greece ( Papageorgopoulou et al, 1999 ), and even higher values have been reported for Stockholm (Colomsjo et al, 1986 ) and Toronto (Katz et al, 1978 ) . The increase of BPer /B [ a] P ratios (which are believed to reflect the contribution of gasoline exhaust ) during the summer could be attributed to the contribution during winter to the PAH emission profile of dieselpowered central heating ( Moller and Afheim, 1980 ).…”
Section: Variables Both Locations Athens Halkidasupporting
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 m ) 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 g / m 3 ) than Halkida ( geometric mean 56.2 g / m 3 ) (P < 0.001 ) , while there was no significant location difference during the summer ( Athens: geometric mean 32.3 g / m 3 , Halkida: geometric mean 32.9 g / 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 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.
“…Since coal combustion is often used as an electricity source for mining operations (Katz et al, 1978), the co-variance of total PAHs with 56 the trace metals in Fairbanks Lake may reflect electric power production in the mine in question.…”
The utility of lead isotopes as particulate contaminant tracers and chronostratigraphic markers was assessed in six lakes from the Great Lakes region. The geographic range of the 19 th
“…Estimation of the Adsorption Coefficient of the Spherical Particle Typical urban air has a total content of both free and particle-associated BaP of 0.6 to 3.5 ng/m3 (24). If about 3% of this amount is estimated to be free in the gas phase (1), this gives a concentration in the gas phase of BaP of, say, 0.05 ng/m3.…”
Section: Appendixmentioning
confidence: 99%
“…If it is further assumed that the concentration of BaP constitutes 5% of the total concentration of the model PAH, which represents the multitude of components present in reality, then the free gas-phase concentration of the model PAH will be CG = 1 ng/m3. A typical concentration of particle-bound BaP in urban air is 5 to 50 ,ug/g (24). Assume that this constitutes 5% of the total concentration of the model PAH.…”
This paper presents a mathematical model of how rapidly polycyclic aromatic hydrocarbons (PAHs) adsorb onto initially clean micron-size particles in the ambient air and how fast these substances are likely to be desorbed from the particles after deposition on the surface lining layer of the lung. Results show that, on the one hand, the very low gas-phase concentrations of PAHs in the ambient air should result in a comparatively slow transfer of such compounds to micron-size particles, a process that may last from minutes to hours. On the other hand, the comparatively high solubilities of PAHs in the lining layer of the lung should promote an almost instantaneous release of PAHs onto nonporous particles, and a release within a matter of minutes of most PAHs reversibly adsorbed onto the interior surfaces of porous particles. Two important conclusions can be drawn from this. First, the PAHs in tobacco smoke do not have time enough to interact in the gas phase with other airborne particles before these agents are inhaled into the smoker's lungs. Therefore, adsorption in the gas phase of PAHs onto asbestos fibers can hardly be a characteristic parameter in the mechanism behind the synergistic effect between tobacco smoking and asbestos exposure for the induction of bronchial cancer. Second, the release rate of reversibly adsorbed PAHs from their carrier particles in the lung seems to be so fast that this cannot be a parameter of importance in directly influencing the residence times of such substances in the lung.
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