DNA-binding of polycyclic aromatic hydrocarbons in a human bronchial epithelial cell line treated with diesel and gasoline particulate extracts and benzo[a]pyrene.

S.K. Pohjola (Corresponding Author), Maija Lappi, L. Rantanen, M. Honkanen, K. Savela

Research output: Contribution to journalArticleScientificpeer-review

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Abstract

Particulate matter of vehicle exhaust is known to contain carcinogenic compounds such as polycyclic aromatic hydrocarbons (PAH) and is suggested to increase lung cancer risk in humans. This study examines the differences in diesel and gasoline‐derived PAH binding to DNA in a human bronchial epithelial cell line (BEAS‐2B). Particulate matter (PM) of gasoline exhaust was collected from passenger cars on filters and semi‐volatile compounds on polyurethane foam (PUF). The soluble organic fraction (SOF) extracted from the particles was used to expose the cells and to perform PAH analysis. Gasoline extracts, benzo[a]pyrene (B[a]P) and reference materials (SRM 1650 and 1587) were used to study dose‐dependent adduct formation in BEAS‐2B cells. The levels of DNA adducts were in good accord with the 10 DNA adduct‐forming PAH concentrations analyzed in the extracts. Gasoline extracts, SRM 1650, SRM 1587 and B[a]P formed DNA adducts dose‐dependently in BEAS‐2B cells. The time‐dependent DNA adduct formation of 5.0 µM B[a]P was lower than that of 2.5 µM B[a]P. The results of this study indicate that reformulated and standard diesel fuels formed about 11‐ and 31‐fold more adducts than gasoline, respectively, when PAH–DNA adduct levels were calculated on an emission basis (adducts/mg PM/km), whereas on a particulate basis (adducts/mg PM) no difference between the diesel and gasoline extracts was observed. We conclude that the genotoxicity of diesel fuel is based on higher particulate emission rates compared to gasoline emission and although the concentration of PAH compounds was higher in diesel particulate extracts, DNA binding by the gasoline particulate‐bound PAH compounds was more pronounced than that by the diesel particulate‐bound PAH compounds.
Original languageEnglish
Pages (from-to)429-438
Number of pages10
JournalMutagenesis
Volume18
Issue number5
DOIs
Publication statusPublished - 2003
MoE publication typeA1 Journal article-refereed

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Gasoline
Benzo(a)pyrene
Polycyclic Aromatic Hydrocarbons
Epithelial Cells
Particulate Matter
Cell Line
DNA
DNA Adducts
Diesel fuels
Particulate emissions
Passenger cars
Lung Neoplasms

Cite this

Pohjola, S.K. ; Lappi, Maija ; Rantanen, L. ; Honkanen, M. ; Savela, K. / DNA-binding of polycyclic aromatic hydrocarbons in a human bronchial epithelial cell line treated with diesel and gasoline particulate extracts and benzo[a]pyrene. In: Mutagenesis. 2003 ; Vol. 18, No. 5. pp. 429-438.
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title = "DNA-binding of polycyclic aromatic hydrocarbons in a human bronchial epithelial cell line treated with diesel and gasoline particulate extracts and benzo[a]pyrene.",
abstract = "Particulate matter of vehicle exhaust is known to contain carcinogenic compounds such as polycyclic aromatic hydrocarbons (PAH) and is suggested to increase lung cancer risk in humans. This study examines the differences in diesel and gasoline‐derived PAH binding to DNA in a human bronchial epithelial cell line (BEAS‐2B). Particulate matter (PM) of gasoline exhaust was collected from passenger cars on filters and semi‐volatile compounds on polyurethane foam (PUF). The soluble organic fraction (SOF) extracted from the particles was used to expose the cells and to perform PAH analysis. Gasoline extracts, benzo[a]pyrene (B[a]P) and reference materials (SRM 1650 and 1587) were used to study dose‐dependent adduct formation in BEAS‐2B cells. The levels of DNA adducts were in good accord with the 10 DNA adduct‐forming PAH concentrations analyzed in the extracts. Gasoline extracts, SRM 1650, SRM 1587 and B[a]P formed DNA adducts dose‐dependently in BEAS‐2B cells. The time‐dependent DNA adduct formation of 5.0 µM B[a]P was lower than that of 2.5 µM B[a]P. The results of this study indicate that reformulated and standard diesel fuels formed about 11‐ and 31‐fold more adducts than gasoline, respectively, when PAH–DNA adduct levels were calculated on an emission basis (adducts/mg PM/km), whereas on a particulate basis (adducts/mg PM) no difference between the diesel and gasoline extracts was observed. We conclude that the genotoxicity of diesel fuel is based on higher particulate emission rates compared to gasoline emission and although the concentration of PAH compounds was higher in diesel particulate extracts, DNA binding by the gasoline particulate‐bound PAH compounds was more pronounced than that by the diesel particulate‐bound PAH compounds.",
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DNA-binding of polycyclic aromatic hydrocarbons in a human bronchial epithelial cell line treated with diesel and gasoline particulate extracts and benzo[a]pyrene. / Pohjola, S.K. (Corresponding Author); Lappi, Maija; Rantanen, L.; Honkanen, M.; Savela, K.

In: Mutagenesis, Vol. 18, No. 5, 2003, p. 429-438.

Research output: Contribution to journalArticleScientificpeer-review

TY - JOUR

T1 - DNA-binding of polycyclic aromatic hydrocarbons in a human bronchial epithelial cell line treated with diesel and gasoline particulate extracts and benzo[a]pyrene.

AU - Pohjola, S.K.

AU - Lappi, Maija

AU - Rantanen, L.

AU - Honkanen, M.

AU - Savela, K.

PY - 2003

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N2 - Particulate matter of vehicle exhaust is known to contain carcinogenic compounds such as polycyclic aromatic hydrocarbons (PAH) and is suggested to increase lung cancer risk in humans. This study examines the differences in diesel and gasoline‐derived PAH binding to DNA in a human bronchial epithelial cell line (BEAS‐2B). Particulate matter (PM) of gasoline exhaust was collected from passenger cars on filters and semi‐volatile compounds on polyurethane foam (PUF). The soluble organic fraction (SOF) extracted from the particles was used to expose the cells and to perform PAH analysis. Gasoline extracts, benzo[a]pyrene (B[a]P) and reference materials (SRM 1650 and 1587) were used to study dose‐dependent adduct formation in BEAS‐2B cells. The levels of DNA adducts were in good accord with the 10 DNA adduct‐forming PAH concentrations analyzed in the extracts. Gasoline extracts, SRM 1650, SRM 1587 and B[a]P formed DNA adducts dose‐dependently in BEAS‐2B cells. The time‐dependent DNA adduct formation of 5.0 µM B[a]P was lower than that of 2.5 µM B[a]P. The results of this study indicate that reformulated and standard diesel fuels formed about 11‐ and 31‐fold more adducts than gasoline, respectively, when PAH–DNA adduct levels were calculated on an emission basis (adducts/mg PM/km), whereas on a particulate basis (adducts/mg PM) no difference between the diesel and gasoline extracts was observed. We conclude that the genotoxicity of diesel fuel is based on higher particulate emission rates compared to gasoline emission and although the concentration of PAH compounds was higher in diesel particulate extracts, DNA binding by the gasoline particulate‐bound PAH compounds was more pronounced than that by the diesel particulate‐bound PAH compounds.

AB - Particulate matter of vehicle exhaust is known to contain carcinogenic compounds such as polycyclic aromatic hydrocarbons (PAH) and is suggested to increase lung cancer risk in humans. This study examines the differences in diesel and gasoline‐derived PAH binding to DNA in a human bronchial epithelial cell line (BEAS‐2B). Particulate matter (PM) of gasoline exhaust was collected from passenger cars on filters and semi‐volatile compounds on polyurethane foam (PUF). The soluble organic fraction (SOF) extracted from the particles was used to expose the cells and to perform PAH analysis. Gasoline extracts, benzo[a]pyrene (B[a]P) and reference materials (SRM 1650 and 1587) were used to study dose‐dependent adduct formation in BEAS‐2B cells. The levels of DNA adducts were in good accord with the 10 DNA adduct‐forming PAH concentrations analyzed in the extracts. Gasoline extracts, SRM 1650, SRM 1587 and B[a]P formed DNA adducts dose‐dependently in BEAS‐2B cells. The time‐dependent DNA adduct formation of 5.0 µM B[a]P was lower than that of 2.5 µM B[a]P. The results of this study indicate that reformulated and standard diesel fuels formed about 11‐ and 31‐fold more adducts than gasoline, respectively, when PAH–DNA adduct levels were calculated on an emission basis (adducts/mg PM/km), whereas on a particulate basis (adducts/mg PM) no difference between the diesel and gasoline extracts was observed. We conclude that the genotoxicity of diesel fuel is based on higher particulate emission rates compared to gasoline emission and although the concentration of PAH compounds was higher in diesel particulate extracts, DNA binding by the gasoline particulate‐bound PAH compounds was more pronounced than that by the diesel particulate‐bound PAH compounds.

U2 - 10.1093/mutage/geg021

DO - 10.1093/mutage/geg021

M3 - Article

VL - 18

SP - 429

EP - 438

JO - Mutagenesis

JF - Mutagenesis

SN - 0267-8357

IS - 5

ER -