Causal effects of various particulate matter on inflammatory bowel disease and its subtypes: insights from Mendelian randomization.

Abstract

The role of particulate matter (PM) on genetic susceptibility to inflammatory bowel disease (IBD) is a controversial topic. The study aims to evaluate the causal effect of PM on IBD using Mendelian randomization (MR). PM and IBD datasets were screened for common single nucleotide polymorphisms (SNPs) based on the MR basic assumptions. Subsequently, the effect of these SNPs on genetic susceptibility to IBD was analyzed using inverse variance weighted. Finally, the heterogeneity and robustness of the results were assessed using Cochran's Q and leave-one-out sensitivity analysis, respectively. MR analysis revealed that PM2.5 was linked to a heightened genetic predisposition to (odds ratio [OR] 1.530, 95% confidence interval [CI] 1.100-2.128, p = 0.011) and ulcerative colitis (UC) (OR 1.675, 95% CI 1.129-2.485, p = 0.010), but not to Crohn's disease (CD) (OR 1.685, 95% CI 0.883-3.216, p = 0.114). PM10 was not associated with increased genetic susceptibility to IBD (OR 1.164, 95% CI 0.650-2.083, p = 0.610), UC (OR 1.439, 95% CI 0.691-2.996, p = 0.331), or CD (OR 0.825, 95% CI 0.265-2.564, p = 0.739). MR-Egger intercept did not indicate any horizontal pleiotropy (p > 0.05). Cochran's Q revealed no evidence of heterogeneity (p > 0.05). Leave-one-out sensitivity analysis confirmed the robustness of the results. The MR analysis demonstrated that PM2.5 increased genetic susceptibility to UC, while no such association was observed for CD. Furthermore, PM10 showed no association with genetic susceptibility to IBD. Therefore, implementing protective measures, such as air purifiers and anti-haze masks, may help reduce the risk of UC.