Biomarkers for exposure to ambient air pollution--comparison of carcinogen-DNA adduct levels with other exposure markers and markers for oxidative stress.

Autrup, Herman; Daneshvar, Bahram; Dragsted, LO; Gamborg, Michael; Hansen, Max; Loft, Steffen; Okkels, Henrik; Nielsen, Finn Årup; Nielsen, Patricia Switten; Raffn, Edith; Wallin, Håkan; Knudsen, Lisbeth B.

doi:10.1289/ehp.99107233

Cited by 53 publications

(43 citation statements)

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“…Kuusimaki et al 43) found the concentration of 1-OHP was higher among bus-garage and waste-collection workers exposed to PAH (0.125 µmol/mol creatinine) than in a control group (0.055 µmol/mol creatinine). Autrup et al 44) found that the average urinary 1-OHP value for non-smoking Danish bus drivers in a city center (0.25 µmol/mol creatinine) was similar to that in rural/suburban areas (0.24 µmol/mol creatinine), but higher than that for postal workers (0.15 µmol/mol creatinine). Merlo et al 37) found that the average urinary 1-OHP levels for traffic police officers were 0.102 µmol/mol creatinine for non-smokers and 0.201 µmol/mol creatinine for smokers; office employees had lower average corresponding measurements, 0.067 and 0.179 µmol/mol creatinine, respectively.…”

Section: Discussionmentioning

confidence: 98%

Urinary 1‐Hydroxypyrene Level Relative to Vehicle Exhaust Exposure Mediated by Metabolic Enzyme Polymorphisms

Chuang

Chang

2007

Journal of Occupational Health

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Urinary 1-Hydroxypyrene Level Relative to Vehicle Exhaust Exposure Mediated by MetabolicEnzyme Polymorphisms: Chun-Yu CHUANG, et al. Department of Biomedical Engineering andEnvironmental Sciences, National Tsing-Hua University, Taiwan-Polycyclic aromatic hydrocarbons (PAH) are common air pollutants generated from incomplete combustion. The inhalation of exhaust fumes in urban areas has been suggested to be an additional contributing factor. This study investigated the influence of urban traffic exposure, personal lifestyle factors and metabolic enzyme polymorphisms on the urinary 1-hydroxypyrene (1-OHP) level, approximating exposure to PAH. With consents, 95 male taxi drivers exposed to vehicle exhaust in traffic and 75 male office employees received health interviews and provided urine samples. The results showed taxi drivers had higher urinary 1-OHP than the office employees (mean ± standard deviation were 0.17 ± 0.10 vs. 0.10 ± 0.07 µmol/mol creatinine, p<0.001). The average urinary 1-OHP level increased from 0.07 µmol/mol creatinine for non-smoking office employees to 0.17 µmol/mol creatinine for those who smoked more than 20 cigarettes daily. The values for taxi drivers with similar smoking statuses were 0.12 and 0.25 µmol/mol creatinine, respectively. Among non-smokers, taxi drivers still had higher 1-OHP level than office employees (0.12 ± 0.05 vs. 0.07 ± 0.03 µmol/mol creatinine). The subjects with the m1/m2 or m2/m2 genotype of CYP1A1 MspI or GSTM1 deficiency had significantly higher urinary 1-OHP levels than those with other CYP1A1 MspI and GSTM1 genotypes. Multivariate logistic regression analysis showed that taxi drivers (adjusted odds ratio (OR)=5.1, 95% confidence interval (CI)=1.1-13.6), smokers (OR=5.5, 95% CI=1.6-18.4) and subjects with the m1/m2 or m2/ m2 genotype of CYP1A1 MspI (OR=9.7, 95% CI=2.7-35.0) had elevated urinary 1-OHP (greater than the overall median value, 0.11 µmol/mol creatinine). The results of this study suggest smoking contributes to the elevated urinary 1-OHP levels in taxi drivers in addition to taxi driving, and the excess level contributed from traffic exhaust and smoke was regulated by the CYP1A1 MspI genotype. Traffic exhaust exposure, smoking and CYP1A1 MspI genotype contributed to the variation in levels of urinary 1-OHP excretion.

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Section: Discussionmentioning

confidence: 98%

Urinary 1‐Hydroxypyrene Level Relative to Vehicle Exhaust Exposure Mediated by Metabolic Enzyme Polymorphisms

Chuang

Chang

2007

Journal of Occupational Health

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“…The level of DNA adducts in colon and liver were determined by 32 P-postlabelling with a standard method usually used to determine PAH adducts [20]. In liver and colon cell proliferation was assayed by immunohistochemistry of PCNA staining and apoptosis was detected by the TUNEL assay [5].…”

Section: Dna Adducts Proliferation and Apoptosismentioning

confidence: 99%

Sucrose and IQ induced mutations in rat colon by independent mechanism

Hansen¹,

Hald²,

Autrup

et al. 2004

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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“…1-OH-pyrene levels were determined to be biomarker of exposure to PAHs, in 4 studies (57,63,64,77). No effects of exposure to PAHs in ambient air on 1-OH-pyrene levels in urine were observed for exposure to PAHs in ambient air.…”

Section: Discussionmentioning

confidence: 99%

“…8-oxodG in urine was determined in bus drivers (57,60). One study found a negative association (57), another a positive one (60 (60) in pmol/kg 24 hr.…”

Section: Discussionmentioning

confidence: 99%

“…Autrup et al (57) and nasal epithelial cells (p < 0.001) in young adults from the southern part of the city who were exposed to high levels of ozone compared with young adults from the northern part who were exposed to hydrocarbons and particles. These differences were not observed in buccal epithelial cells.…”

Section: Environmental Exposure To Mutagens and Carcinogensmentioning

confidence: 97%

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Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

Srám¹,

Binková²

2000

Environmental Health Perspectives

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Molecular epidemiology is a new and evolving area of research, combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and influence of individual susceptibility with epidemiologic methodologies. Biomarkers evaluated were selected according to basic scheme: biomarkers of exposure-metabolites in urine, DNA adducts, protein adducts, and Comet assay parameters; biomarkers of effect-chromosomal aberrations, sister chromatid exchanges, micronuclei, mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, and the activation of oncogenes coding for p53 or p21 proteins as measured on protein levels; biomarkers of susceptibility-genetic polymorphisms of genes CYP1A1, GSTM1, GSTT1, NAT2. DNA adducts measured by 32P-postlabeling are the biomarker of choice for the evaluation of exposure to polycyclic aromatic hydrocarbons. Protein adducts are useful as a biomarker for exposure to tobacco smoke (4-aminobiphenyl) or to smaller molecules such as acrylonitrile or 1,3-butadiene. Of the biomarkers of effect, the most common are cytogenetic end points. Epidemiologic studies support the use of chromosomal breakage as a relevant biomarker of cancer risk. The use of the Comet assay and methods analyzing oxidative DNA damage needs reliable validation for human biomonitoring. Until now there have not been sufficient data to interpret the relationship between genotypes, biomarkers of exposure, and biomarkers of effect for assessing the risk of human exposure to mutagens and carcinogens. Key words: air pollution, benzene, biomarkers, coke oven, genotypes, occupational exposure, PAHs, pesticides, tobacco smoke. -Envwron Health Perspect 1 08(suppl 1):57-70 (2000). http.//ehpnetl. niehs. nih.gov/docs/2000/suppl-1/57-70sram/abstract. html A new and evolving area of research termed molecular epidemiology attempts to merge sophisticated and highly sensitive laboratory methods (many of them developed during the recent revolution in molecular biology) with analytical epidemiologic methods. Molecular epidemiology bridges basic research in molecular biology and studies of human cancer causation by combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and the influence of individual susceptibility with epidemiologic methodologies (1). The most common view is that the approach represents a natural convergence of molecular biology and epidemiology (2).The number of biomarkers available for evaluating genetic and cancer risk in humans is quite large. Their utility-for human biomonitoring is suggested by the well-known paradigm of environmentally induced cancer, which represents end points for assessing the entire spectrum of human-genotoxicant interactions (3). These biomarkers begin with exposure and include absorption, metabolism, distribution, critical target interaction (i.e., DNA damage and repair), genetic changes, and finally, disease, which is the province of traditional epidemiology. The development of biomarkers has given rise to the field of ...

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Biomarkers for exposure to ambient air pollution--comparison of carcinogen-DNA adduct levels with other exposure markers and markers for oxidative stress.

Cited by 53 publications

References 40 publications

Urinary 1‐Hydroxypyrene Level Relative to Vehicle Exhaust Exposure Mediated by Metabolic Enzyme Polymorphisms

Urinary 1‐Hydroxypyrene Level Relative to Vehicle Exhaust Exposure Mediated by Metabolic Enzyme Polymorphisms

Sucrose and IQ induced mutations in rat colon by independent mechanism

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

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