This study was designed to investigate whether or not chronic exposure to Chornobyl radiation poses a molecular genetic risk to mammals by examining a relatively rapidly evolving genetic system, mitochondrial DNA (mtDNA). More mtDNA mutations (∼19%) and an increase in mtDNA heteroplasmy (∼5%) occurred in the cytochrome b gene of an exposed mother-embryo set when compared to a relatively unexposed mother-embryo set. However, this increase was not statistically significant (p > 0.05). Our results, in conjunction with previous molecular genetic research on small mammals from Chornobyl, suggest that chronic exposure to environmental ionizing radiation does not increase the number of nucleotide substitutions, as predicted by studies using acute or subacute exposures. Thus, cumulative models of radiation risk would not appear to follow simple linear functions derived from high doses and dose rates. The equivocal nature of research regarding the effects of the Chornobyl accident indicates that future research is warranted such that models of chronic environmental exposure can be developed or refined. Although additional study is required to properly validate mtDNA heteroplasmy as a useful effect biomarker, examination of these data does not indicate that a significant risk to mtDNA exists in native rodents chronically exposed to both internal and external radiation.