Amine-based CO2 capture is a prime contender for the first full-scale implementation of CO2 capture at fossil fuel-fired power plants postcombustion. However, the formation of potentially carcinogenic N-nitrosamines and N-nitramines from reactions of flue gas NOx with the amines presents a potential risk for contaminating airsheds and drinking water supplies. Setting regulatory emission limits is hampered by the dearth of toxicity information for the N-nitramines. This study employed quantitative in vitro bioassays for mutagenicity in Salmonella typhimurium, and chronic cytotoxicity and acute genotoxicity in Chinese hamster ovary (CHO) cells to compare the toxicity of analogous N-nitrosamines and N-nitramines relevant to CO2 capture. Although the rank order was similar for genotoxicity in CHO cells and mutagenicity in S. typhimurium, the Salmonella assay was far more sensitive. In general, mutagenicity was higher with S9 hepatic microsomal activation. The rank order of mutagenicity was N-nitrosodimethylamine (NDMA)>N-nitrosomorpholine>N-nitrodimethylamine>1,4-dinitrosopiperazine>N-nitromorpholine>1,4-dinitropiperazine>N-nitromonoethanolamine>N-nitrosodiethanolamine>N-nitrodiethanolamine. 1-Nitrosopiperazine and 1-nitropiperazine were not mutagenic. Overall, N-nitrosamines were ∼15-fold more mutagenic than their N-nitramine analogues.