Personal exposures to PM2.5 and polycyclic aromatic hydrocarbons and their relationship to environmental tobacco smoke at two locations in Greece

Abstract

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.

Analysis of Polycyclic Aromatic Hydrocarbons in Amniotic Fluid Samples From Smokers and Nonsmokers

“…Concentrations of many PAH have been determined to be in automobile as well as diesel exhaust emissions, as well as in industrial emissions (7,8). Tobacco smoke (both mainstream and sidestream) contains thousands of chemicals including many of the more carcinogenic as well as toxic PAHs (9)(10)(11)(12). Human exposures to PAH via tobacco use continues to remain one of the single most concentrated routes by which individuals are exposed to PAH.…”

Ambient concentrations and personal exposure to polycyclic aromatic hydrocarbons (PAH) in an urban community with mixed sources of air pollution

“…Some studies have been conducted to characterize PAH exposure in community settings (Lioy et al, 1988; Chuang et al, 1999; Fiala et al, 2001; Georgiadis et al, 2001; Naumova et al, 2002; Fromme et al, 2004; Tonne et al, 2004; Ohura et al, 2005; Choi et al, 2008; Saborit et al, 2009). For example, Lioy et al (1988) measured indoor concentrations of benzo(a)pyrene (BaP) in homes in Phillipsburg, New Jersey (NJ), and estimated personal exposure to BaP based on the indoor concentrations and the outdoor concentrations measured concurrently.…”

“…This is because indoor sources are dominant of personal PAH exposure in most cases (Fiala et al, 2001; Georgiadis et al, 2001; Naumova et al, 2002; Tonne et al, 2004; Ohura et al, 2005; Saborit et al, 2009). As reported by Tonne et al (2004), personal exposures of pregnant women to benzo(b)fluoranthene (BbFA), benzo(k)fluoranthene (BkFA), BaP, benzo(g,h,i)perylene and the sum of B2 PAH (PAH compounds that have been identified as probable human carcinogens by the USEPA Integrated Risk Information System) were not associated with the time spent outdoors but with indoor sources, that is, residential heating and indoor burning of incense.…”

“…Further, personal and concurrent community PAH air pollution data for the 16 USEPA priority PAH species are still scarce. The target PAH in previous studies are often limited to BaP and 6–8 carcinogenic species (Lioy et al, 1988; Georgiadis et al, 2001; Tonne et al, 2004; Choi et al, 2008; Saborit et al, 2009). Such knowledge background limits the ability to conduct an accurate assessment of the health risks resulting from exposure to PAH in ambient air, particularly for people living in areas with mixed emission sources.…”

Lung Cancer: Mechanisms of Carcinogenesis

“…The highest occupational exposures are found in petrochemical industry workers, especially in cokeoven workers, and in workers of metal plants and foundries [ 93 ]. Sources of indoor PAH exposure include tobacco smoke, meat and fi sh roasting and frying, and charcoal grilling in poorly ventilated environments [ 94 ]. Examples of occupations with PAH exposure are given in Table 10.1 .…”