Global heart · 2024
Causal Associations of Environmental Pollution and Cardiovascular Disease: A Two-Sample Mendelian Randomization Study.
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Gao Hui, Li Jiahai, Ma Qiaoli, Zhang Qinghui, Li Man, Hu Xiaoliang
Аннотация
BACKGROUND: There is growing evidence that concentrations of environmental pollutants are previously associated with cardiovascular disease; however, it is unclear whether this association reflects a causal relationship.
METHODS: We utilized a two-sample Mendelian randomization (MR) approach to investigate how environmental pollution affects the likelihood of developing cardiovascular disease. We primarily employed the inverse variance weighted (IVW) method. Additionally, to ensure the robustness of our findings, we conducted several sensitivity analyses using alternative methodologies. These included maximum likelihood, MR-Egger regression, weighted median method and weighted model methods.
RESULTS: Inverse variance weighted estimates suggested that an SD increase in PM2.5 exposure increased the risk of heart failure (OR = 1.40, 95% CI 1.02-1.93, p = 0.0386). We found that an SD increase in PM10 exposure increased the risk of hypertension (OR = 1.45, 95% CI 1.02-2.05, p = 0.03598) and atrial fibrillation (OR = 1.41, 95% CI 1.03-1.94, p = 0.03461). Exposure to chemical or other fumes in a workplace was found to increase the risk of hypertension (OR = 3.08, 95% CI 1.40-6.78, p = 0.005218), coronary artery disease (OR = 1.81, 95% CI 1.00-3.26, p = 0.04861), coronary heart disease (OR = 3.15, 95% CI 1.21-8.16, p = 0.0183) and myocardial infarction (OR = 3.03, 95% CI 1.13-8.17, p = 0.02802).
CONCLUSION: This study reveals the causal relationship between air pollutants and cardiovascular diseases, providing new insights into the protection of cardiovascular diseases.
METHODS: We utilized a two-sample Mendelian randomization (MR) approach to investigate how environmental pollution affects the likelihood of developing cardiovascular disease. We primarily employed the inverse variance weighted (IVW) method. Additionally, to ensure the robustness of our findings, we conducted several sensitivity analyses using alternative methodologies. These included maximum likelihood, MR-Egger regression, weighted median method and weighted model methods.
RESULTS: Inverse variance weighted estimates suggested that an SD increase in PM2.5 exposure increased the risk of heart failure (OR = 1.40, 95% CI 1.02-1.93, p = 0.0386). We found that an SD increase in PM10 exposure increased the risk of hypertension (OR = 1.45, 95% CI 1.02-2.05, p = 0.03598) and atrial fibrillation (OR = 1.41, 95% CI 1.03-1.94, p = 0.03461). Exposure to chemical or other fumes in a workplace was found to increase the risk of hypertension (OR = 3.08, 95% CI 1.40-6.78, p = 0.005218), coronary artery disease (OR = 1.81, 95% CI 1.00-3.26, p = 0.04861), coronary heart disease (OR = 3.15, 95% CI 1.21-8.16, p = 0.0183) and myocardial infarction (OR = 3.03, 95% CI 1.13-8.17, p = 0.02802).
CONCLUSION: This study reveals the causal relationship between air pollutants and cardiovascular diseases, providing new insights into the protection of cardiovascular diseases.