## 3 Results
As reported previously, the MCDS code does not involve the process of repair in its results and thus, we take into account the existing literature in order to translate the numbers of lesions shown in the above diagrams into cancer risk information. Figure 2: Absorbed dose to the cell (target) as a function of height (on the water phantom used in our simulations) induced by different \({}^{137}\)Cs surface activities for the exposure time of one week, using MCNP6.1 code. In the dose range related to a REI, as in our study, the associated cancer risk cannot be deduced from epidemiological data, due to a lack of sensitivity. Such estimates for persons exposed to an environmental IR incident have been based on a linear extrapolation of high-dose data obtained from the study of atomic bomb survivors of Hiroshima and Nagasaki through the years; the linear-no-threshold (LNT) model assumes that the DNA damage is proportional to the dose and that the response of the irradiated cell functions equal efficiently from high to low doses [68]. However, the validity of such an extrapolation is questioned by phenomena such as the low-dose hypersensitivity, the adaptive and hormetic response, the bystander effects, and the threshold hypothesis [69; 70; 71; 72]. In attempting to  
Figure 3: Estimation of the number of (**a**) DSBs and (**b**) SSBs per cell, respectively, induced by different levels of \({}^{137}\)Cs contamination in the ground, for the exposure time of one week, according to our MCDS simulations. associate a low dose irradiation with cancer risk, it is important to make the distinction between acute exposures over a very short period of time and protracted ones [73]. Clearly, the atomic bomb survivor risks represent the average of all those exposed to an REI population. Considering the existing data, the fact that individuals are at lower or greater risk than the average, depends on genetic status, age, age of exposure and other factors [74]. Deep sequencing studies have confirmed that biomarkers (such as the micronucleassay and scoring of chromosome aberrations) are important tools for the detection of the early stages of radiation-induced carcinogenesis. These validated techniques, however, do not have the sensitivity to study the effects of IR on cells at doses below 100 mGy [75; 76]. For this reason, phosphorylated histone H2 AX (\(\gamma\)-H2 AX) foci immunodetection has become the internationally accepted quantitative biomarker of human low-level IR exposure [77]. DSBs activate histone H2 AX right after their induction by phosphorylating a highly conserved serine (Ser-139). The phosphorylated \(\gamma\)-H2 AX forms foci in the cell nucleus. In this way, a \(\gamma\)-H2 AX focus represents a DSB [77; 78]. Focused on the range of low doses (i.e., doses <0.05 Gy [79]), as this very low (\(\leq\)1 mGy, see Figure 2) in our study, [PERSON] and [PERSON] have shown that in non-dividing primary human fibroblasts cultured in vitro, irradiated by doses \(\sim\) 1 mGy of IR, the induced DSBs remain unrepaired for many days and the cells with unrepaired DSBs are eventually eliminated [80]. Similar results were observed by [PERSON] et al. in a study conducted on human MSCs, isolated from oral mucosa, where for the lower doses, after the initial rise in \(\gamma\)H2 AX foci number, there was no decrease observed [81]. It appears that, in cellular responses at low compared to high doses, different pathways may be activated, and non-linear responses prevail that are not compatible with the LNT model. Unrepaired or mis-repaired DSBs may give rise to chromosomal aberrations and alterations, micronucleI formation, gene amplification, sister chromatid exchange and other genetic instability hallmarks. In vitro observations show the induction of unstable chromosomal aberrations in cells irradiated in G1 phase and chromatid-type aberrations in the ones exposed to IR at the G2 phase of the cell cycle [82].