부산대학교 도서관

Simple Summary: Epidemiological studies have identified associations between fine particulate matter (with an aerodynamic diameter of less than 2.5 μm (PM2.5)) and ozone exposure with cardiovascular disease; however, studies linking ambient air pollution and premature coronary artery disease (pCAD) in Latin America are nonexistent. We leveraged data from the Genetics of Atherosclerotic Disease (GEA) Mexican study to address the question of the extent to which long-term exposure to ozone and PM2.5 exposure was associated with the risk of pCAD. We showed for the first time a higher risk of pCAD associated with 1 ppb increase in ozone (1-year, 2-year, 3-year, and 5-year) and 5μg/m3 of PM2.5 (5-year) compared to controls. This study provides evidence that ozone and PM2.5 may be a modifiable risk factor for pCAD. (1) Background: Epidemiological studies have identified associations between fine particulate matter (PM2.5) and ozone exposure with cardiovascular disease; however, studies linking ambient air pollution and premature coronary artery disease (pCAD) in Latin America are non-existing. (2) Methods: Our study was a case–control analysis nested in the Genetics of Atherosclerotic Disease (GEA) Mexican study. We included 1615 participants (869 controls and 746 patients with pCAD), recruited at the Instituto Nacional de Cardiología Ignacio Chávez from June 2008 to January 2013. We defined pCAD as history of myocardial infarction, angioplasty, revascularization surgery or coronary stenosis > 50% diagnosed before age 55 in men and age 65 in women. Controls were healthy individuals without personal or family history of pCAD and with coronary artery calcification equal to zero. Hourly measurements of ozone and PM2.5 from the Atmospheric Monitoring System in Mexico City (SIMAT in Spanish; Sistema de Monitero Atmosférico de la Ciudad de México) were used to calculate annual exposure to ozone and PM2.5 in the study participants. (3) Results: Each ppb increase in ozone at 1-year, 2-year, 3-year and 5-year averages was significantly associated with increased odds (OR = 1.10; 95% CI: 1.03–1.18; OR = 1.17; 95% CI: 1.05–1.30; OR = 1.18; 95% CI: 1.05–1.33, and OR = 1.13; 95% CI: 1.04–1.23, respectively) of pCAD. We observed higher risk of pCAD for each 5 µg/m3 increase only for the 5-year average of PM2.5 exposure (OR = 2.75; 95% CI: 1.47–5.16), compared to controls. (4) Conclusions: Ozone exposure at different time points and PM2.5 exposure at 5 years were associated with increased odds of pCAD. Our results highlight the importance of reducing long-term exposure to ambient air pollution levels to reduce the burden of cardiovascular disease in Mexico City and other metropolitan areas. [ABSTRACT FROM AUTHOR]