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BCES was first used during World War I as a chemical weapon. Sufficient epidermal exposure results in selective destruction of the epidermal basal cell layer resulting in blister formation. Like many neoplastic and anti-neoplastic compounds, BCES is a bifunctional alkylating agent capable of alkylating DNA, RNA, and proteins, although DNA is the primary target. The literature has reported the appearance and disappearance of single strand breaks (SSB) in the DNA of rat keratinocytes after exposure to low levels of BCES. Since SSB are a consequence of depurination/depyrimidination followed by excision of the apurinic/apyrimidinic site and deoxyguanosine (GdR) is the major alkylation site in DNA exposed to BCES, it was hypothesized that repair occurred by a GdR specific base-replacement and not by large section repair. To test this hypothesis, cultures of human keratinocytes were pre-incubated with 5-bromo-$2\sp\prime$deoxyuridine (BUdR), a heavy analog of thymidine (TdR) incorporated into replicating DNA, immediately before exposure to BCES. Cultures were incubated post-exposure with BUdR, radiolabeled GdR and/or deoxyadenosine (AdR), as a measure of base-specific repair, and/or radiolabeled TdR, as a measure of DNA replication and large section repair. A CsCl density gradient was used to remove any BUdR containing, post-exposure DNA replication. Each gradient was assayed for radioactivity (CPM) and DNA content $\rm (A\sb{260}).$ The peak $\rm A\sb{260}$ fractions were pooled and rebanded in another CsCl gradient. If DNA repair had occurred, the specific activity (CPM/$\rm A\sb{260})$ of the peak $\rm A\sb{260}$ fraction in the gradient would be greater than control. After exposure to BCES, there was a dose-dependent increase in the specific activity for $\rm\lbrack \sp3H\rbrack GdR$ but not $\rm\lbrack \sp{14}C\rbrack TdR$ over the dose range used $\rm (20\mu M{-}50\mu M$ BCES). A dose-dependent increase in specific activity was also detected when using $\rm\lbrack \sp{14}C\rbrack AdR$ and $\rm\lbrack \sp3 H\rbrack AdR.$ The literature has shown the removal of damaged DNA bases after alkylation via glycosylases. In this series of experiments, we have demonstrated that cultures of HK exposed to an alkylating agent, in this case BCES, repair their damaged DNA by the replacement of only the damaged base. In the case of BCES exposure, this is the GdR base and to a lesser extent the AdR base.