孟德尔随机化
溃疡性结肠炎
医学
微粒
随机化
内科学
生物
遗传学
临床试验
疾病
生态学
基因
遗传变异
基因型
作者
Chong Yau Fu,Qi Wang,Chen‐Hua Yan,Y.H. Zhang
出处
期刊:PLOS ONE
[Public Library of Science]
日期:2024-03-08
卷期号:19 (3): e0300066-e0300066
标识
DOI:10.1371/journal.pone.0300066
摘要
Background Existing research has demonstrated links between airborne particulate matter and ulcerative colitis (UC) onset. Through Mendelian randomization, this study aims to further delineate the causal association between specific types of airborne particulates and UC. Methods A two-sample Mendelian randomization analysis was undertaken to investigate the causality between airborne particulate matter and UC. Genetic datasets for both airborne particulates and UC were derived from accessible genome-wide association studies (GWAS). We employed a range of MR techniques, such as inverse variance weighted (IVW), weighted median, MR-Egger, and Wald Ratio, to validate the causality. In addition, sensitivity assessments were executed to ensure result reliability. Results The data indicate a probable positive correlation between PM 2.5 exposure and UC risk (OR: 3.6; 95% CI: [1.2–11.3]; P = 0.026). The statistical strength for causal determination via the IVW approach stood at 0.87, with a Type I error rate set at 0.025. Assessments using Cochran’s Q test, MR-Egger intercept, MR-PRESSO, and leave-one-out sensitivity analyses did not identify notable heterogeneity, pleiotropy, or biases in the overall relationship between PM 2.5 and UC. Furthermore, the MR-Steiger assessment indicated that PM 2.5 exposure level determinants predominantly affect UC vulnerability. Conclusion The findings underscore the potential involvement of PM 2.5 in UC pathogenesis.
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