A seminal question in wildlife toxicology is whether exposure to an environmental contaminant, in particular a second-generation anticoagulant rodenticide, can evoke subtle long lasting effects on body condition, physiological function and survival. Many reports indicate that non-target predators often carry residues of several rodenticides, which is indicative of multiple exposures. An often-cited study in laboratory rats demonstrated that exposure to the second-generation anticoagulant rodenticide brodifacoum prolongs blood clotting time for a few days, but weeks later when rats were re-exposed to the first-generation anticoagulant rodenticide warfarin, coagulopathy was more pronounced in brodifacoum-treated rats than naïve rats exposed to warfarin. To further investigate this phenomenon, American kestrels were fed environmentally realistic doses of chlorophacinone or brodifacoum for a week, and following a week-long recovery period, birds were then challenged with a low-level dietary dose of chlorophacinone. In the present study, neither hematocrit nor clotting time (prothrombin time, Russell’s viper venom time) were differentially affected in sequentially exposed kestrels compared to naïve birds fed low-level dietary dose of chlorophacinone. While the present findings do not reveal lasting effects of anticoagulant exposure on blood clotting ability, findings in laboratory rats and other species have demonstrated such effects on blood clotting, and even other molecular pathways associated with immune function and xenobiotic metabolism. Additional studies using an environmentally realistic route of exposure and dose are underway to further test this hypothesis.