Mutation Research 662 (2009) 37–43 Contents lists available at ScienceDirect Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis journal homepage: www.elsevier.com/locate/molmut Community address: www.elsevier.com/locate/mutres Urinary 8-oxodeoxyguanosine levels in children exposed to air pollutants Vlasta Svecova, Pavel Rossner Jr., Miroslav Dostal, Jan Topinka, Ivo Solansky, Radim J. Sram ∗ Laboratory of Genetic Ecotoxicology, Institute of Experimental Medicine AS CR, v.v.i., Videnska 1083, 142 20 Prague 4, Czech Republic article info Article history: Received 2 September 2008 Received in revised form 28 November 2008 Accepted 2 December 2008 Available online 9 December 2008 Keywords: Air pollution Child health Oxidative stress Particulate matter PM2.5 PM10 Polycyclic aromatic hydrocarbons 8-Oxodeoxyguanosine abstract Oxidative stress is believed to be one of the mechanisms of effects of air pollution to human health. We investigated levels of 8-oxodeoxyguanosine (8-oxodG), a marker of oxidative damage to DNA, in urine samples of 894 children from two districts in the Czech Republic: Teplice and Prachatice. We assessed the association between 8-oxodG levels and exposure to particulate matter of different size: ≤10 m (PM10), ≤2.5 m (PM2.5) and carcinogenic polycyclic aromatic hydrocarbons (c-PAHs); as well as between 8- oxodG levels and individual lifestyle, health and pregnancy outcomes. An ELISA technique was used for analysis of 8-oxodG levels. Median levels (range) of 8-oxodG in children from Teplice vs. Prachatice were as follows: 14.6 (3.1–326.5) nmol/mmol vs. 15.2 (3.0–180.8) nmol/mmol creatinine (p = 0.34). Levels of 8- oxodG were elevated in children exposed to environmental tobacco smoke (ETS) (p < 0.05) and among the Gypsy population (p <0.01). Levels of 8-oxodG decreased with the child’s age (p < 0.001) and increasing level of the mother’s education (p < 0.01). Multivariate statistical analyses confirmed the effect of the child’s age and ETS exposure on 8-oxodG levels. The exposure to PM10 and PM2.5 measured by stationary monitors during a 7-day period before urine collection, as well as the exposure to c-PAHs measured during 3-day periods 1–3 and 7–9 days before urine collection were identified as factors affecting 8-oxodG levels in multivariate models. The obtained results indicate that 8-oxodG is a sensitive biomarker for measuring the exposure of children to air pollution. © 2008 Elsevier B.V. All rights reserved. 1. Introduction There is a growing body of evidence linking serious health con- sequences with exposure to ambient air pollution. The complexity of exposure patterns, changes in the vulnerability of children at var- ious stages of prenatal and postnatal development, and the practical limitations of research mean that understanding of the effect of air pollution on child health is incomplete [1]. The effect of exposure of ambient fine particles on child health is associated with intrauterine growth retardation (IUGR), infant mor- tality [2], and with increased bronchitis in pre-school children [3]. Exposure to respirable particulate matter of aerodynamic diameter ≤10 m (PM10) is strongly and consistently associated with post- natal respiratory mortality, and less consistently associated with sudden infant death [4]. Respirable particulate matter of aerody- Abbreviations: 8-oxodG, 8-oxodeoxyguanosine; APs, air pollutants; B[a]P, benzo[a]pyrene; c-PAHs, carcinogenic polycyclic aromatic hydrocarbons; ELISA, enzyme-linked immunosorbent assay; ETS, environmental tobacco smoke; IUGR, intrauterine growth retardation; LBW, low birth weight, <2500g; PM, particulate matter; PM2.5, respirable particulate matter of aerodynamic diameter ≤2.5 m; PM10, respirable particulate matter of aerodynamic diameter ≤10 m; RNS, reac- tive nitrogen species; ROS, reactive oxygen species; VAPS, versatile air pollution samplers; VOC, volatile organic compounds. ∗ Corresponding author. Tel.: +420 24106 2596; fax: +420 24106 2785. E-mail address: sram@biomed.cas.cz (R.J. Sram). namic diameter ≤2.5 m (PM2.5; fine PM) could be a major threat to children. This is because of their higher exposure to PM com- pared with adults, the immature state of lungs in childhood, and immune functions at birth. The mechanisms of air pollution effects are incompletely understood, but pregnant women, infants and children need specific protection against exposure to fine particles [5]. PM consists of dust, soot, other solid, liquid and aerosol particles, as well as various chemicals bound to them. Carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) are among the most important compounds in PM10 [6]. c-PAHs adsorbed onto PM2.5 are mainly derived from incomplete combustion, including mobile sources (e.g., motor vehicles) and stationary sources (e.g., residential heat- ing or power plants). These compounds exhibit carcinogenic and/or mutagenic properties. c-PAHs are metabolized into reactive inter- mediates that bind to DNA and form PAH–DNA adducts that, if unrepaired, could lead to mutations. Apart from carcinogenic- ity, c-PAHs may contribute to induction of oxidative stress via their metabolism by CYP1A1 and subsequent formation of reac- tive quinones [7]. PM contains other components with higher potency to induce oxidative stress – transition metals, benzene and other volatile organic compounds (VOC)—as well as solid particles that cause inflammation [8,9]. Nitrated polycyclic aro- matic hydrocarbons are another important component of PM, which have been shown to have carcinogenic/mutagenic activity [10]. 0027-5107/$ – see front matter © 2008 Elsevier B.V. All rights reserved. doi:10.1016/j.mrfmmm.2008.12.003