Abstract 4368787: The Role of Accelerated Development of Cardiovascular Disease Risk Factors in the Association between High Noise Exposure and Cardiovascular Events

Abstract

Background: Noise exposure is a risk factor for the development of cardiovascular disease risk factors (CVDRFs, i.e., diabetes, hypertension, and hyperlipidemia) and major adverse cardiovascular events (MACE). Yet, it is not known how the development of CVDRFs contributes to the association between noise and MACE. Objective: We hypothesized that (1) high noise exposure (>45 dBA) increases MACE risk via the accelerated development of CVDRFs, and (2) the findings are similar across categories of MACE [overall MACE, heart failure (HF), peripheral vascular disease (PVD), acute coronary syndrome (ACS, i.e., unstable angina, myocardial infarction), stroke, and coronary MACE (i.e., ACS and coronary revascularization)]. Methods: Individuals with transportation noise exposure data without MACE before study onset were identified in the Mass General Brigham Biobank. Average 24-h transportation noise was estimated at each participant’s residence using a US Department of Transportation tool. Presence and timing of MACE and CVDRFs were determined using ICD-10 codes; air pollution exposure and median neighborhood income were assessed with US government data. Logistic regression and mediation analyses that accounted for temporal relationships were employed. Primary models were adjusted for age, sex, and baseline CVDRFs. Results: Of 25,761 participants (median age 61 years (IQR: 46-71); 51.4% female), 8,397 lived in areas with high noise exposure. Over 10-years of follow-up, high noise exposure associated with incident MACE (OR=1.10, p=0.005) and development of new CVDRFs (1.15, p<0.001). Among individual MACE endpoints, noise associated with HF (1.10, p=0.033), PVD (1.32, p =0.013), ACS (1.13, p=0.020), and stroke (1.12, p=0.018) but not coronary MACE (p=0.136, Fig 1A). Noise also associated with the development of a new CVDRF (Fig 1B). Further, the development of a CVDRF predicted MACE (Fig 1C). Most models remained robust to further separate adjustment for air pollution and neighborhood median income. Moreover, the development of a CVDRF mediated the link between noise and overall MACE (indirect pathway: log odds 0.03, p<0.05) as well as the separate MACE endpoints (Fig 1D). Conclusions: High noise exposure accelerates the development of CVDRFs, which contributes to increased MACE risk. These findings suggest that noise-exposed individuals may benefit from amplified efforts to diagnose and treat CVDRFs to prevent downstream MACE.