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Environ Res. 2017 Jan;152:165-174. doi: 10.1016/j.envres.2016.10.012. Epub 2016 Oct 20.

Environmental exposure to human carcinogens in teenagers and the association with DNA damage.

Author information

1
Flemish Institute for Technological Research (VITO), Mol, Belgium; Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium. Electronic address: carmen.franken@vito.be.
2
Flemish Institute for Technological Research (VITO), Mol, Belgium.
3
Interuniversity Institute for Biostatistics and Statistical Bioinformatics, Hasselt University, Hasselt, Belgium.
4
Political and Social Sciences, University of Antwerp, Antwerp, Belgium.
5
Provincial Institute for Hygiene, Antwerp, Belgium.
6
Department of Public Health, Ghent University, Ghent, Belgium; Department of Food Safety and Food Quality, Ghent University, Ghent, Belgium.
7
Centre for Environmental Sciences, Hasselt University, Diepenbeek, Belgium; Department of Public Health & Primary Care, Leuven University, Leuven, Belgium.
8
Department of Analytical and Environmental Chemistry, Vrije Universiteit Brussel, Brussels, Belgium.
9
Department of Analytical and Environmental Chemistry, Vrije Universiteit Brussel, Brussels, Belgium; Department of Radiotherapy and Experimental Cancerology, Ghent University, Ghent, Belgium.
10
Toxicological Centre, Department of Pharmaceutical Sciences, University of Antwerp, Antwerp, Belgium.
11
Department of Occupational and Social Medicine, RWTH Aachen University, Aachen, Germany.
12
Flemish Institute for Technological Research (VITO), Mol, Belgium; Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium; University of Southern Denmark, Institute of Public Health, Department of Environmental Medicine, Odense, Denmark.

Abstract

BACKGROUND:

We investigated whether human environmental exposure to chemicals that are labeled as (potential) carcinogens leads to increased (oxidative) damage to DNA in adolescents.

MATERIAL AND METHODS:

Six hundred 14-15-year-old youngsters were recruited all over Flanders (Belgium) and in two areas with important industrial activities. DNA damage was assessed by alkaline and formamidopyrimidine DNA glycosylase (Fpg) modified comet assays in peripheral blood cells and analysis of urinary 8-hydroxydeoxyguanosine (8-OHdG) levels. Personal exposure to potentially carcinogenic compounds was measured in urine, namely: chromium, cadmium, nickel, 1-hydroxypyrene as a proxy for exposure to other carcinogenic polycyclic aromatic hydrocarbons (PAHs), t,t-muconic acid as a metabolite of benzene, 2,5-dichlorophenol (2,5-DCP), organophosphate pesticide metabolites, and di(2-ethylhexyl) phthalate (DEHP) metabolites. In blood, arsenic, polychlorinated biphenyl (PCB) congeners 118 and 156, hexachlorobenzene (HCB), dichlorodiphenyltrichloroethane (DDT) and perfluorooctanoic acid (PFOA) were analyzed. Levels of methylmercury (MeHg) were measured in hair. Multiple linear regression models were used to establish exposure-response relationships.

RESULTS:

Biomarkers of exposure to PAHs and urinary chromium were associated with higher levels of both 8-OHdG in urine and DNA damage detected by the alkaline comet assay. Concentrations of 8-OHdG in urine increased in relation with increasing concentrations of urinary t,t-muconic acid, cadmium, nickel, 2,5-DCP, and DEHP metabolites. Increased concentrations of PFOA in blood were associated with higher levels of DNA damage measured by the alkaline comet assay, whereas DDT was associated in the same direction with the Fpg-modified comet assay. Inverse associations were observed between blood arsenic, hair MeHg, PCB 156 and HCB, and urinary 8-OHdG. The latter exposure biomarkers were also associated with higher fish intake. Urinary nickel and t,t-muconic acid were inversely associated with the alkaline comet assay.

CONCLUSION:

This cross-sectional study found associations between current environmental exposure to (potential) human carcinogens in 14-15-year-old Flemish adolescents and short-term (oxidative) damage to DNA. Prospective follow-up will be required to investigate whether long-term effects may occur due to complex environmental exposures.

KEYWORDS:

8-hydroxydeoxyguanosine (8-OHdG); Carcinogen; Comet assay; DNA damage; Environmental exposure; Human biomonitoring

PMID:
27771571
DOI:
10.1016/j.envres.2016.10.012
[Indexed for MEDLINE]

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