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DNA repair enzymes could modulate the individual susceptibility to the genotoxic effect of exposure to ionising radiation (IR).The influence of polymorphisms of XRCC1, XRCC3 and XPD genes on the onset of chromosomal and DNA damage has been investigated in 43 workers exposed to low levels of IR, including 36 healthcare professionals and 7 industrial radiologists (exposed workers), and 43 subjects not occupationally exposed to IR (controls), matched for age. Chromosomal aberrations (CA) and micronuclei (MN) frequencies in peripheral blood lymphocytes were measured according to standard procedures and used as cytogenetic biomarkers, while Tail Intensity (TI) was the parameter of the Comet test used to evaluate oxidative DNA damage. Genotypic variants Arg194Trp, Arg280His and Arg399Gln for XRCC1, Thr241Met for XRCC3 and Lys751Gln for the XPD genes were analysed using the restriction fragment length polymorphism technique.Both total CA and chromosome breaks frequencies were significantly higher in the exposed workers than controls (p<0.05 and p<0.01 respectively), while no significant differences between the two groups were observed in terms of chromatid breaks and MN frequencies as well as the TI. In the controls only, TI was significantly higher in females than males, whereas a smoking habit did not affect the biomarkers investigated. The genetic polymorphisms of XRCC1, XRCC3 and XPD, individually analysed, did not influence any of the genotoxicity and oxidative damage biomarkers studied, either in the exposed workers or the controls.Chromosome breaks frequency resulted a valid cytogenetic biomarker for the monitoring of workers exposed to low doses of IR. The presence of single genetic variants reducing the activity of DNA repair enzymes does not seem to determine an increased risk of genotoxic effects of low doses of IR.