Black individuals are predisposed to an earlier onset and higher prevalence of cardiovascular disease, such as hypertension. Hypertension may be caused by inflammation and heightened levels of reactive oxygen species (ROS). At rest, Black and White individuals exhibit divergent in vivo and in vitro inflammation, ROS production, and ROS clearance. This study investigated racial differences in ROS production and ROS clearance following induced inflammation in human plasma and HUVECs from Black (B HUVECs) and White (W HUVECs) individuals. W HUVECs, but not B HUVECs, exhibited significantly greater ROS production with increased exposure to TNF-α. Further, W HUVECs alone experienced a significant increase in SOD activity with increased time that was abolished with TNF-α. The HUVEC data were also analyzed for sex differences. HUVECs from females exhibited significantly lower ROS production than HUVECS from males basally and following TNF-α treatment. Female HUVECs alone exhibited significantly greater SOD activity with increased exposure to TNF-α. The findings suggest a ‘priming’ for lower ROS production via greater total antioxidant status (from non-SOD antioxidants) in B HUVECs. Further, male HUVECs may be predisposed to a pro-inflammatory state due to higher androgen exposure in fetal umbilical cord blood.