Mutagenicity and PAH-analysis of airborne particulate matter

Møller, Mona; Alfheim, Ingrid

doi:10.1016/0004-6981(80)90111-0

Cited by 128 publications

(44 citation statements)

References 11 publications

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“…Several other researchers have also reported higher rev plate À1 values for TA100 compared to TA98, both for studies with and without metabolic activation, for organic extracts from mine tailings (Madill et al, 1999) and atmospheric particulates (Matsumoto et al, 1998;Pagano et al, 1996). In contrast, Moller and Alfheim (1980) have reported a reverse trend, mutagenicity with TA98 greater than those with TA100 while characterizing the mutagenicity of airborne particulate matter in Oslo, indicating that the nature of particulate matter extract in atmospheric particulates may vary significantly from region to region.…”

Section: Resultsmentioning

confidence: 91%

“…TA98 is designed to detect frameshift mutations whereas TA100 is designed to detect base-pair mutations. Variation in the mutagenicity values obtained with the two tester strains has been reported in the literature and is interpreted as being indicative of the probability of the respective types of mutation (Madill et al, 1999;Moller and Alfheim, 1980). In this study, mutagenicity was determined both in the presence and in the absence of activating enzymes from rat liver microsomal fractions (S9), so as to determine the relative contribution of direct-acting and indirect-acting mutagens.…”

Section: Introductionmentioning

confidence: 88%

“…PAHs as well as numerous PAH derivatives, i.e., alkylated PAHs, nitro-PAHs, oxygenated PAHs, quinones, hydroxy and hydroxynitro compounds, are produced by the incomplete combustion of fuels such as coal, gasoline, diesel and biofuels (Beak et al, 1991;Matsumoto et al, 1998). The mutagenicity and carcinogenicity of PAHs associated with combustion and ambient aerosols have been conclusively demonstrated through bacterial assays, human cell mutagenicity assays, animal assays and epidemiological studies (Hannigan et al, 1998;Helmig et al, 1992;Kamens et al, 1984;Kleindienst et al, 1986;Mastrangelo et al, 1996;McCrillis et al, 1992;Moller and Alfheim, 1980). The Ames assay test, a plate incorporation test based on genetically engineered microorganisms offers a relatively quick method for mutagenicity assessment and has been widely used as a screening tool for determining health risks associated with emissions, effluents and specific chemicals (Madill et al, 1999;Maron and Ames, 1983).…”

Section: Introductionmentioning

confidence: 99%

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Comparative mutagenicity assessment of aerosols in emissions from biofuel combustion

Mukherji¹,

Swain²,

Venkataraman³

2002

Atmospheric Environment

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Section: Resultsmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Comparative mutagenicity assessment of aerosols in emissions from biofuel combustion

Mukherji¹,

Swain²,

Venkataraman³

2002

Atmospheric Environment

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“…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 ). An additional factor contributing to the increase of the BPer /B [ a] P ratios in the summer may be the relatively high photolability of B [ a] P and reactivity (as compared to that of BPer ) which leads to its selective degradation during the summer ( IARC Monographs, 1983;Nielsen, 1984;Greenbeng, 1989) .…”

Section: Variables Both Locations Athens Halkidamentioning

confidence: 99%

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

Georgiadis

Stoikidou

Topinka

et al. 2001

J Expo Sci Environ Epidemiol

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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.

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“…The mutagenic activity was shown to be most pronounced in the absence of liver microsomes, whereas conventional PAH compounds need metabolic conversion to give a positive response in the Salmonella test system. Several studies have shown that only a small part of the observed mutagenic activity in extracts of particles can be caused by such PAH compounds (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Bioassay of Extracts of Ambient Particulate Matter

Alfheim¹,

Lofroth²,

Moller³

1983

Environmental Health Perspectives

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Organic extracts from airborne particles collected at various sites in Scandinavia have been tested for mutagenicity in the Ames Salmonella/microsome assay. Extracts from particles in the respirable size fraction (diameter less than 3 R±m) were mutagenic with and without metabolic activation. The mutagenic activity varied from day to day, mainly due to variations in meteorological parameters, especially wind speed and atmospheric stability. A seasonal variation could also be observed, with the highest average values in winter time.Samples collected in urban areas were considerably more mutagenic than samples from background areas. The results suggest that exhaust from motor vehicles are the most important source of mutagenic particles in urban areas.Comparison of roof top samples with street level samples indicated that atmospheric reactions cause transformation of nonpolar compounds in the primary emission to more oxygenated mutagenic compounds. It is, however, not known to which degree this causes an overall increase of the mutagenic activity.The mutagenic activity of emissions from stationary combustion sources have also been studied, and residential heating by burning solid fuels in small combustion units have been shown to be a major contributor to mutagens in the environment.

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Mutagenicity and PAH-analysis of airborne particulate matter

Cited by 128 publications

References 11 publications

Comparative mutagenicity assessment of aerosols in emissions from biofuel combustion

Comparative mutagenicity assessment of aerosols in emissions from biofuel combustion

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

Bioassay of Extracts of Ambient Particulate Matter

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