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Environmental exposure is a complex mixture of hazardous compounds with different mechanisms of toxicity. In case of concomitant exposure to carcinogenic substances—such as polycyclic aromatic hydrocarbons (PAHs)—and to heavy metals—such as lead (Pb)—the level of DNA damage may be enhanced. Children are considered more vulnerable than adults to chemical toxicants because they take in more toxicants as a proportion of body mass and because of inherent biological growth and developmental factors. The objective of the study was to measure cytogenetic effects in Silesian children and to investigate their relation with the environmental exposure to PAHs and Pb. The examined population included 74 children 5–14-year-old who lived in two cities located in the most polluted centre of the Silesia province. Individual exposure to lead was assessed for each child by measuring lead in blood (PbB), and to PAH by measuring 1-hydroxypyrene in urine (1-OHP), urinary mutagenicity and DNA adducts in circulating lymphocytes. Biomarkers of genetic effects were assessed by measuring micronuclei (MN) and sister chromatid exchanges (SCE) in children's peripheral lymphocytes. The mean levels of biomarkers of exposure were as follows: PbB 7.69 μg/dl, DNA adducts 9.59 adducts per 108 nt, 1-OHP 0.54 μmol/mol creatinine, and urinary mutagenicity presented as the number of revertants per mmol of creatinine: 485 for TA 98 and 1318 for YG1024. Mean value of MN was 4.44 per 1000 binucleated cells and SCE frequency ranged between 6.24 and 10.06 with a mean value of 7.87. The results suggest the influence of exposure to environmental agents on the induction of cytogenetic effects in peripheral lymphocytes of children: namely Pb on MN and PAHs on SCE. The sources of that exposure may be outdoor and indoor. Emissions from coal-burning stoves are important contributors to the total exposure to PAHs and Pb in Silesian children. [ABSTRACT FROM AUTHOR]