Two-sample mendelian randomization analysis investigates ambient fine particulate matter's impact on cardiovascular disease development

Abstract

Abstract PM2.5, a key component of air pollution, significantly threatens public health. Cardiovascular disease is increasingly associated with air pollution, necessitating more research. This study used a meticulous two-sample Mendelian randomization (MR) approach to investigate the potential causal link between elevated PM2.5 levels and 25 types of cardiovascular diseases. Data sourced from the UK Biobank, focusing on individuals of European ancestry, underwent primary analysis using Inverse Variance Weighting. Additional methods such as MR-Egger, weighted median, Simple mode, and Weighted mode provided support. Sensitivity analyses assessed instrument variable heterogeneity, pleiotropy, and potential weak instrument variables. The study revealed a causal link between PM2.5 exposure and higher diagnoses of Atherosclerotic heart disease (primary or secondary, OR [95% CI] 1.0307 [1.0103–1.0516], p-value = 0.003 and OR [95% CI] 1.0179 [1.0028–1.0333], p-value = 0.0202) and Angina pectoris (primary or secondary, OR [95% CI] 1.0303 [1.0160–1.0449], p-value = 3.04e−05 and OR [95% CI] 1.0339 [1.0081–1.0603], p-value = 0.0096). Additionally, PM2.5 exposure increased the likelihood of diagnoses like Other forms of chronic ischaemic heart disease (secondary, OR [95% CI] 1.0193 [1.0042–1.0346], p-value = 0.0121), Essential hypertension (secondary, OR [95% CI] 1.0567 [1.0142–1.1010], p-value = 0.0085), Palpitations (OR [95% CI] 1.0163 [1.0071–1.0257], p-value = 5e−04), and Stroke (OR [95% CI] 1.0208 [1.0020–1.0401], p-value = 0.0301). Rigorous sensitivity analyses confirmed these significant findings' robustness and validity. Our study revealed the causal effect between higher PM2.5 concentrations and increased cardiovascular disease risks. This evidence is vital for policymakers and healthcare providers, urging targeted interventions to reduce PM2.5 levels.