PM2.5 associates with blood pressure: a Mendelian randomization analysis

The relationship between fine particulate matter (PM2.5) and blood pressure (BP) is a controversial issue. We conducted a two-sample Mendelian randomization (MR) analysis and identified 58 genome-wide significant single-nucleotide polymorphisms associated with PM2.5 as instrument variables. Inverse-variance weighted (IVW) was used as the primary analysis approach. MR-Egger, weighted median, simple model, and weighted model methods were selected for quality control. We found a significant negative causal association of higher genetically predicted PM2.5 levels with lower systolic BP (SBP), while no causal relationship was identified between PM2.5 and diastolic BP (DBP). For each 1 standard deviation increase in genetically predicted PM2.5 levels, the beta value (95% CI) of SBP was -0.14 (-0.25, -0.03) for IVW (p=0.02), and -0.13 (-0.22, -0.04) for weighted median (p=0.005). Increased PM2.5 concentrations can lead to decreased SBP levels. Our findings provided novel insights into the controversial topic on the causal relationship between PM2.5 and BP.

细颗粒物（PM2.5）与血压（BP）之间的关联是一项存在争议的研究议题。本研究开展了两样本孟德尔随机化（Mendelian randomization, MR）分析，筛选出58个与PM2.5相关的全基因组显著性单核苷酸多态性（single-nucleotide polymorphisms）作为工具变量。以逆方差加权（Inverse-variance weighted, IVW）作为主要分析方法，同时选取MR-Egger、加权中位数法、简单模型法以及加权模型法开展质量控制。研究结果显示，遗传预测的PM2.5水平升高与收缩压（systolic BP, SBP）降低存在显著的负向因果关联，但未发现PM2.5与舒张压（diastolic BP, DBP）之间存在因果关系。当遗传预测的PM2.5水平每升高1个标准差时，IVW分析得到的收缩压β值（95%置信区间）为-0.14（-0.25，-0.03）（p=0.02），加权中位数分析得到的β值为-0.13（-0.22，-0.04）（p=0.005）。PM2.5浓度升高可导致收缩压水平降低。本研究结果为PM2.5与血压之间因果关联这一争议性议题提供了全新的研究视角。