Pilot 2
Lawrence Bielak, DDS, MPH
Assistant Research Scientist
Department of Epidemiology
University of Michigan
ABSTRACT
Neighborhood Change, Inflammation, and Coronary Artery Calcification in an African American Cohort
Project Description: We propose to build upon the resources of the longitudinal Genetic Epidemiology Network of Arteriopathy (GENOA) Study, part of the Family Blood Pressure Program. Phase 1 of GENOA was initiated in 1995. African-American participants from the Jackson, Mississippi Field Center are now undergoing their third study visit (Phase 3; HL085571; PI: PA Peyser). At each visit, participants are extensively characterized for anthropometric, life-style, and traditional CAD risk factors. During Phase 2 (2000-2004), markers of inflammation (e.g. fibrinogen and C-reactive protein (CRP)) also were measured. During the on-going Phase 3 visit conducted at the University of Mississippi Medical Center (Thomas Mosley, PhD, PI at the University of Mississippi), these markers of inflammation are being re-measured and participants also receive a CT scan to measure CAC quantity. Population-based, neighborhood-level measures of SES from the 2000 US Census have already been collected for participants based on their residence at the time of participation in Phase 1 (1995-1999). We propose to collect these same measures of SES for these same neighborhoods from the 1990 US Census. We would then determine on a population-based level whether these neighborhoods improved, remained stable, or declined over the 1990-2000 decade. The overall goal of the proposed study is to investigate the association between the dynamics of population-based change in neighborhood attributes and individual-based measures of inflammation and subclinical coronary atherosclerosis, as assessed by CAC quantity. The following specific aims will be accomplished: Aim 1: To test the hypothesis that change in population-based, neighborhood-level measures of SES during the 1990-2000 decade is associated with individual-based measures of inflammation measured in Phase 2 and in Phase 3, after adjusting for the concurrent individual-level measures of SES and traditional CAD risk factors. Aim 2: To test the hypothesis that change in population-based, neighborhood-level measures of SES during the 1990-2000 decade is associated with individual-based CAC quantity measured in Phase 3 after adjusting for concurrent individual-level measures of SES and traditional CAD risk factors. Aim 3: To test the hypothesis that change in population-based, neighborhood-level measures of SES during the 1990-2000 decade is associated with individual-based CAC quantity measured in Phase 3 after adjusting for concurrent individual-level measures of SES, traditional CAD risk factors, and measures of inflammation.