Ambient air pollution exposure is linked to increased cardiovascular disease risk and adverse imaging phenotypes

Abstract Background Ambient air pollution, specifically fine particulate matter (PM2.5), has been linked to an increased risk of cardiovascular diseases (CVDs). Poor air quality is closely intertwined with other important health determinants, such as deprivation and urban living, making it challenging to disentangle its distinct role in driving adverse health outcomes. Purpose This study investigated the relationship between PM2.5 exposure and the long-term risk of incident CVDs in the UK Biobank, adjusting for demographic, lifestyle, and health-related confounders. Furthermore, alterations in cardiac structure and function related to PM2.5 exposure were examined using cardiovascular magnetic resonance (CMR). Methods The analysis sample included 299,323 participants with a median age of 56.6 years and included 53% women. Land Use Regression modelling was used to calculate estimates for annual average exposure to PM2.5 (µg/m³) at baseline recruitment. Non-sensical measurements (negative values) were excluded. Incident myocardial infarction, heart failure, and stroke were ascertained from linked hospital episode statistics and death registration records. Participants with pre-existing CVD were excluded. Logistic regression models were used to assess the association between PM2.5 exposure and incidence CVDs, adjusting for age, sex, ethnicity, residential setting (urban/rural), deprivation index, educational attainment, smoking status, and alcohol consumption. The association of PM2.5 exposure with cardiac structure and function metrics was examined in 17,907 participants where CMR data were available. Linear regression models were applied to assess the associations between PM2.5 exposure and aortic distensibility, left ventricular mass, mass, LV volumes, LV global longitudinal strain, and left ventricular ejection fraction. Results In fully adjusted models, higher PM2.5 levels were associated with a significantly increased risk of incident heart failure (OR:1.07, 95% CI: 1.052, 1.09, p < 0.0001) and stroke (OR:1.05, 95% CI: 1.04, 1.06, p < 0.0001). There was a positive but non-significant association with incident myocardial infarction (OR:1.02, 1.00, 1.04, p =0.08). Greater PM2.5 levels were linked to significantly lower LV mass (b =-0.29, 95% CI: -0.49, -0.08, p =0.01) and smaller left ventricular end-diastolic volume (b =-0.35, 95% CI: -0.76, 0.05, p =0.09), in keeping with age-related ventricular remodelling. Conclusion Higher PM2.5 exposure is linked with increased risk of incident heart failure and stroke, and with adverse left ventricular remodelling, independent of confounding variables. These findings underscore the critical role of air pollution in cardiovascular pathology and highlight its broader implications for public health.Participants characteristics  Logistic and Linear Regression models