## 1 Introduction  
Prolonged occupational exposure to high doses of ionizing radiation (IR) can cause DNA alterations, such as single-strand breaks (SSBs), double-strand breaks (DSBs), damage to purine and pyrimidine bases, and DNA-protein crosslinking, that can result in cell death or neoplastic transformation [1].  
In fact, IR is classified in group 1 by the International Agency Research on Cancer (IARC) as carcinogenic to humans [2].  
Increased genotoxic damage has also been observed in workers with occupational exposure to IR at lower doses than the authorized dose limits, consisting of an increased frequency of chromosome aberrations (CAs) and micronuclelei (MN), as compared to control groups with no occupational exposure [3; 4; 5]. However, these genotoxic effects were not shown to be correlated to the cumulative dose of IR exposure [6]. The Comet assay also yielded discordant results in regards to increased DNA damage in workers exposed to IR, although no influence was observed when considering specific parameters of oxidative damage to the purine or pyrimidine bases using the Fpg and Endo III enzymes [7; 8; 9; 10; 11].  
Genetic polymorphisms of the DNA repair enzymes can play a fundamental role in the expression of the effects of exposure to low doses of IR. In this regard, [PERSON] et al. [4] observed a significant increase in the frequency of MN in workers exposed to a mean equivalent IR cumulative dose of 40.61 mSv, with allelic variants for _XRCC1_, _XRCC3_ and _XPD_, as compared to controls with the same genotype, while [PERSON] et al. [12] found an increased frequency of MN in workers exposed to IR, with allelic variants for _XRCC3_ compared to workers with the same exposure but with the wild-type genotype.  
Polymorphisms of the glutathione-S-transferases (GSTs) genes M1 and T1 also seem to affect DNA damage induced by IR, eliciting a greater susceptibility by interfering with the detoxification processes of the intermediate reactive species produced by the cells in response to the IR effects [13]. Nevertheless, the role of these polymorphisms remains controversial. In fact, [PERSON] et al. [14] demonstrated a greater frequency of CAs correlated to the GST1 positive phenotype in peripheral lymphocytes of smokers, irradiated in vitro with \(\gamma\) rays, while [PERSON] et al. [15] showed that these polymorphisms do not significantly alter the potential genotoxic effect of IR.  
In workers exposed to low doses of IR, chromatid damage induced in peripheral lymphocytes following in vitro exposure to bleomycin (BLM), defined as mutagen sensitivity, can be indicative of individual variability in the response capacity to genotoxic IR actions [16; 17; 18]. Individual mutagen sensitivity seems to be influenced by the presence of polymorphisms in enzymes responsible for both the DNA repair and the detoxification of reactive intermediates, as shown in healthy subjects not exposed to IR. Up to now, however, the relation between mutagen sensitivity and the presence of enzyme polymorphisms has never been studied in workers exposed to low doses of IR [19; 20; 21].  
The aim of this study was, therefore, to verify whether the genotoxic effects and mutagen sensitivity in workers with occupational exposure to very low doses of IR can be modulated by genetic polymorphisms of the enzymes involved in DNA repair and detoxification of reactive intermediates induced by IR.