Environmental Toxicants, Race, and Cardiovascular Disease Risk in Children - DESCRIPTION (provided by applicant): Cardiovascular disease (CVD) remains the leading cause of death in the United States and disables 10 million Americans each year. However, CVD risk in the US is higher for African Americans (AAs) relative to European Americans (EAs). In addition to R/E differences in CVD risk, there is extensive data demonstrating that, relative to
EAs, AAs have higher rates of poverty and a corresponding increase in exposure to environmental toxicants, including lead (Pb), both in their blood and in their bones. Moreover, studies suggest a positive association between Pb and blood pressure, left ventricular hypertrophy, and CVD mortality. The current proposal addresses the question of whether R/E differences in CVD are partially a consequence of corresponding differences in exposure to Pb from the environment. Furthermore, this proposal considers whether these effects might be amplified by R/E differences in psychosocial background, including social control motives, background stress, and racial discrimination. Specifically, our proposal focuses on whether R/E differences in Pb exposure might produce differing rates of CVD risk through underlying alterations in cardiovascular responses to acute psychological stress, a mechanism whereby the psychosocial environment can affect CVD risk. In recent research (Gump, et al., 2011), increasing blood Pb was associated with alterations in cardiac autonomic regulation reflecting "co-inhibition" of both sympathetic and parasympathetic activity that is typically associated with greater vascular resistance, a cardiovascular pattern we had already observed in children with heightened early childhood blood Pb (Gump, et al., 2005). This vascular response to stress has also been shown to be associated with greater left ventricular mass, a significant predictor of cardiovascular morbidity. Interestingly, a number of studies have noted that AAs respond to psychological stress with a vascular pattern relative to EAs typical cardiac response and are more likely than EAs to develop left ventricular hypertrophy at similar levels of blood pressure, and have greater arterial stiffness as reflected by faster pulse wave velocity. In sum, there is evidence that: 1) AAs (relative to EAs) have higher levels of blood Pb, 2) AAs (relative to EAs) typically respond to stress with a more vascular pattern, as well as greater arterial stiffness and
left ventricular mass, and 3) increasing Pb is associated with a heightened vascular response to acute stress. This accumulated evidence provides strong support for testing the hypothesis that R/E differences in Pb exposure might account for R/E differences in cardiovascular patterns of response to acute stress and R/E differences in left ventricular mass and arterial stiffness.
