Water Contaminants and Cardiovascular Risk: the Jackson Heart Study - In Jackson, MS, decades of inadequate public water system infrastructure have resulted in disruptions to water access and diminished water quality. Jackson has been under a consent decree since 2012 for failing to meet operational and maintenance standards and continues to have boil water notices issued regularly, eliciting concern about the health effects of chronic water contaminant exposures. Despite emerging recognition of the importance of environmental exposures in cardiometabolic-cardiovascular disease (CM-CVD) risk, few epidemiologic studies have investigated the CM-CVD effects of public water contaminants, even though these data can prioritize policy-based solutions to limit their impact. In this context, the Jackson Heart Study (JHS), a prospective cohort study of 5,306 adults, offers a rare opportunity to evaluate the effects of chronic water contaminant exposures on CM-CVD. In preparation for this application, we extracted all 165,580 compliance monitoring records (2000-2023) collected by the Mississippi Department of Health for 74 water systems serving Madison, Hinds, and Rankin counties comprising JHS (encompassing 38 unique ZIP codes), demonstrating (1) substantial temporal variability (seasonal/yearly) in prioritized water contaminants (e.g., total trihalomethanes, haloacetic acids, lead) across these water systems; (2) lead, disinfection byproducts, and chromium (all linked to CM-CVD) are higher in water systems serving JHS communities compared to those nationwide. Strikingly, disinfection byproducts and lead are largely unrelated to source water and are directly related to the deterioration and management of water system infrastructure, relevant to the ongoing water issues in Jackson. Our central hypothesis is that water toxicants (captured by water system monitoring records and quantification of ≈1000 circulating chemicals in the blood [“molecular exposome”] pioneered by our group) will be associated with CM-CVD phenotypes over ≈2 decades in JHS. In Aim 1, we quantify 26 public water contaminant exposures (including disinfection byproducts, inorganic metals, radionuclides, organic compounds) for all JHS participants over ≈2 decades and measure their association with key CM-CVD risk factors (e.g., blood pressure, insulin resistance, obesity). Aim 2 provides a complementary biochemical approach, quantifying the relation of the molecular exposome–and its changes over time–with these environmental exposures over ≈2 decades and measuring their relation to CM-CVD phenotypes. In Aim 3, we examine the association of both water monitoring records and biochemical exposures (molecular exposome) with 20-year incident CVD risk, including how these relations may be mediated by the effect of water contaminant exposures on traditional CM-CVD risk factors. If successful, this application will define the importance of water contaminant exposures to CM-CVD over 2 decades in a local community, with direct implications for policy. Resources generated here will be accessible to the scientific community for future discovery and comparison in broader populations.
