Linking exposure to environmental pollutants with biological effects

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Linking exposure to environmental pollutants with biological effects. / Sørensen, Mette; Autrup, Herman; Møller, Peter; Hertel, Ole; Jensen, Steen Solvang; Vinzents, Peter; Knudsen, Lisbeth E; Loft, Steffen.

In: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, Vol. 544, No. 2-3, 2003, p. 255-71.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Sørensen, M, Autrup, H, Møller, P, Hertel, O, Jensen, SS, Vinzents, P, Knudsen, LE & Loft, S 2003, 'Linking exposure to environmental pollutants with biological effects', Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, vol. 544, no. 2-3, pp. 255-71.

APA

Sørensen, M., Autrup, H., Møller, P., Hertel, O., Jensen, S. S., Vinzents, P., Knudsen, L. E., & Loft, S. (2003). Linking exposure to environmental pollutants with biological effects. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 544(2-3), 255-71.

Vancouver

Sørensen M, Autrup H, Møller P, Hertel O, Jensen SS, Vinzents P et al. Linking exposure to environmental pollutants with biological effects. Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis. 2003;544(2-3):255-71.

Author

Sørensen, Mette ; Autrup, Herman ; Møller, Peter ; Hertel, Ole ; Jensen, Steen Solvang ; Vinzents, Peter ; Knudsen, Lisbeth E ; Loft, Steffen. / Linking exposure to environmental pollutants with biological effects. In: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis. 2003 ; Vol. 544, No. 2-3. pp. 255-71.

Bibtex

@article{64013660cdfb11dea1f3000ea68e967b,
title = "Linking exposure to environmental pollutants with biological effects",
abstract = "Exposure to ambient air pollution has been associated with cancer. Ambient air contains a complex mixture of toxics, including particulate matter (PM) and benzene. Carcinogenic effects of PM may relate both to the content of PAH and to oxidative DNA damage generated by transition metals, benzene, metabolism and inflammation. By means of personal monitoring and biomarkers of internal dose, biologically effective dose and susceptibility, it should be possible to characterize individual exposure and identify air pollution sources with relevant biological effects. In a series of studies, individual exposure to PM(2.5), nitrogen dioxide (NO(2)) and benzene has been measured in groups of 40-50 subjects. Measured biomarkers included 1-hydroxypyrene, benzene metabolites (phenylmercapturic acid (PMA) and trans-trans-muconic acid (ttMA)), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine, DNA strand breaks, base oxidation, 8-oxodG and PAH bulky adducts in lymphocytes, markers of oxidative stress in plasma and genotypes of glutathione transferases (GSTs) and NADPH:quinone reductase (NQO1). With respect to benzene, the main result indicates that DNA base oxidation is correlated with PMA excretion. With respect to exposure to PM, biomarkers of oxidative damage showed significant positive association with the individual exposure. Thus, 8-oxodG in lymphocyte DNA and markers of oxidative damage to lipids and protein in plasma associated with PM(2.5) exposure. Several types of DNA damage showed seasonal variation. PAH adduct levels, DNA strand breaks and 8-oxodG in lymphocytes increased significantly in the summer period, requiring control of confounders. Similar seasonal effects on strand breaks and expression of the relevant DNA repair genes ERCC1 and OGG1 have been reported. In the present setting, biological effects of air pollutants appear mainly related to oxidative stress via personal exposure and not to urban background levels. Future developments include personal time-resolved monitors for exposure to ultrafine PM and PM(2.5,) use of GPS, as well as genomics and proteomics based biomarkers.",
author = "Mette S{\o}rensen and Herman Autrup and Peter M{\o}ller and Ole Hertel and Jensen, {Steen Solvang} and Peter Vinzents and Knudsen, {Lisbeth E} and Steffen Loft",
note = "Keywords: Air Pollutants; Carcinogens; DNA Damage; Environmental Exposure; Environmental Pollutants; Humans; Models, Biological; Neoplasms",
year = "2003",
language = "English",
volume = "544",
pages = "255--71",
journal = "Mutation Research Letters",
issn = "0027-5107",
publisher = "Elsevier",
number = "2-3",

}

RIS

TY - JOUR

T1 - Linking exposure to environmental pollutants with biological effects

AU - Sørensen, Mette

AU - Autrup, Herman

AU - Møller, Peter

AU - Hertel, Ole

AU - Jensen, Steen Solvang

AU - Vinzents, Peter

AU - Knudsen, Lisbeth E

AU - Loft, Steffen

N1 - Keywords: Air Pollutants; Carcinogens; DNA Damage; Environmental Exposure; Environmental Pollutants; Humans; Models, Biological; Neoplasms

PY - 2003

Y1 - 2003

N2 - Exposure to ambient air pollution has been associated with cancer. Ambient air contains a complex mixture of toxics, including particulate matter (PM) and benzene. Carcinogenic effects of PM may relate both to the content of PAH and to oxidative DNA damage generated by transition metals, benzene, metabolism and inflammation. By means of personal monitoring and biomarkers of internal dose, biologically effective dose and susceptibility, it should be possible to characterize individual exposure and identify air pollution sources with relevant biological effects. In a series of studies, individual exposure to PM(2.5), nitrogen dioxide (NO(2)) and benzene has been measured in groups of 40-50 subjects. Measured biomarkers included 1-hydroxypyrene, benzene metabolites (phenylmercapturic acid (PMA) and trans-trans-muconic acid (ttMA)), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine, DNA strand breaks, base oxidation, 8-oxodG and PAH bulky adducts in lymphocytes, markers of oxidative stress in plasma and genotypes of glutathione transferases (GSTs) and NADPH:quinone reductase (NQO1). With respect to benzene, the main result indicates that DNA base oxidation is correlated with PMA excretion. With respect to exposure to PM, biomarkers of oxidative damage showed significant positive association with the individual exposure. Thus, 8-oxodG in lymphocyte DNA and markers of oxidative damage to lipids and protein in plasma associated with PM(2.5) exposure. Several types of DNA damage showed seasonal variation. PAH adduct levels, DNA strand breaks and 8-oxodG in lymphocytes increased significantly in the summer period, requiring control of confounders. Similar seasonal effects on strand breaks and expression of the relevant DNA repair genes ERCC1 and OGG1 have been reported. In the present setting, biological effects of air pollutants appear mainly related to oxidative stress via personal exposure and not to urban background levels. Future developments include personal time-resolved monitors for exposure to ultrafine PM and PM(2.5,) use of GPS, as well as genomics and proteomics based biomarkers.

AB - Exposure to ambient air pollution has been associated with cancer. Ambient air contains a complex mixture of toxics, including particulate matter (PM) and benzene. Carcinogenic effects of PM may relate both to the content of PAH and to oxidative DNA damage generated by transition metals, benzene, metabolism and inflammation. By means of personal monitoring and biomarkers of internal dose, biologically effective dose and susceptibility, it should be possible to characterize individual exposure and identify air pollution sources with relevant biological effects. In a series of studies, individual exposure to PM(2.5), nitrogen dioxide (NO(2)) and benzene has been measured in groups of 40-50 subjects. Measured biomarkers included 1-hydroxypyrene, benzene metabolites (phenylmercapturic acid (PMA) and trans-trans-muconic acid (ttMA)), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine, DNA strand breaks, base oxidation, 8-oxodG and PAH bulky adducts in lymphocytes, markers of oxidative stress in plasma and genotypes of glutathione transferases (GSTs) and NADPH:quinone reductase (NQO1). With respect to benzene, the main result indicates that DNA base oxidation is correlated with PMA excretion. With respect to exposure to PM, biomarkers of oxidative damage showed significant positive association with the individual exposure. Thus, 8-oxodG in lymphocyte DNA and markers of oxidative damage to lipids and protein in plasma associated with PM(2.5) exposure. Several types of DNA damage showed seasonal variation. PAH adduct levels, DNA strand breaks and 8-oxodG in lymphocytes increased significantly in the summer period, requiring control of confounders. Similar seasonal effects on strand breaks and expression of the relevant DNA repair genes ERCC1 and OGG1 have been reported. In the present setting, biological effects of air pollutants appear mainly related to oxidative stress via personal exposure and not to urban background levels. Future developments include personal time-resolved monitors for exposure to ultrafine PM and PM(2.5,) use of GPS, as well as genomics and proteomics based biomarkers.

M3 - Journal article

C2 - 14644327

VL - 544

SP - 255

EP - 271

JO - Mutation Research Letters

JF - Mutation Research Letters

SN - 0027-5107

IS - 2-3

ER -

ID: 15712254