Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization

BackgroundsMany studies have shown particulate matter has emerged as one of the major environmental risk factors for diabetes; however, studies on the causal relationship between particulate matter 2.5 (PM2.5) and diabetes based on genetic approaches are scarce. The study estimated the causal relati...

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Main Authors: Joyce Mary Kim, Eunji Kim, Do Kyeong Song, Yi-Jun Kim, Ji Hyen Lee, Eunhee Ha
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-08-01
Series:Frontiers in Public Health
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fpubh.2023.1164647/full
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author Joyce Mary Kim
Joyce Mary Kim
Eunji Kim
Eunji Kim
Do Kyeong Song
Yi-Jun Kim
Ji Hyen Lee
Ji Hyen Lee
Eunhee Ha
Eunhee Ha
Eunhee Ha
Eunhee Ha
author_facet Joyce Mary Kim
Joyce Mary Kim
Eunji Kim
Eunji Kim
Do Kyeong Song
Yi-Jun Kim
Ji Hyen Lee
Ji Hyen Lee
Eunhee Ha
Eunhee Ha
Eunhee Ha
Eunhee Ha
author_sort Joyce Mary Kim
collection DOAJ
description BackgroundsMany studies have shown particulate matter has emerged as one of the major environmental risk factors for diabetes; however, studies on the causal relationship between particulate matter 2.5 (PM2.5) and diabetes based on genetic approaches are scarce. The study estimated the causal relationship between diabetes and PM2.5 using two sample mendelian randomization (TSMR).MethodsWe collected genetic data from European ancestry publicly available genome wide association studies (GWAS) summary data through the MR-BASE repository. The IEU GWAS information output PM2.5 from the Single nucleotide polymorphisms (SNPs) GWAS pipeline using pheasant-derived variables (Consortium = MRC-IEU, sample size: 423,796). The annual relationship of PM2.5 (2010) were modeled for each address using a Land Use Regression model developed as part of the European Study of Cohorts for Air Pollution Effects. Diabetes GWAS information (Consortium = MRC-IEU, sample size: 461,578) were used, and the genetic variants were used as the instrumental variables (IVs). We performed three representative Mendelian Randomization (MR) methods: Inverse Variance Weighted regression (IVW), Egger, and weighted median for causal relationship using genetic variants. Furthermore, we used a novel method called MR Mixture to identify outlier SNPs.ResultsFrom the IVW method, we revealed the causal relationship between PM2.5 and diabetes (Odds ratio [OR]: 1.041, 95% CI: 1.008–1.076, P = 0.016), and the finding was substantiated by the absence of any directional horizontal pleiotropy through MR-Egger regression (β = 0.016, P = 0.687). From the IVW fixed-effect method (i.e., one of the MR machine learning mixture methods), we excluded outlier SNP (rs1537371) and showed the best predictive model (AUC = 0.72) with a causal relationship between PM2.5 and diabetes (OR: 1.028, 95% CI: 1.006–1.049, P = 0.012).ConclusionWe identified the hypothesis that there is a causal relationship between PM2.5 and diabetes in the European population, using MR methods.
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spelling doaj.art-5025799c1496469fb6a98562e3a5d25d2023-08-11T07:27:05ZengFrontiers Media S.A.Frontiers in Public Health2296-25652023-08-011110.3389/fpubh.2023.11646471164647Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomizationJoyce Mary Kim0Joyce Mary Kim1Eunji Kim2Eunji Kim3Do Kyeong Song4Yi-Jun Kim5Ji Hyen Lee6Ji Hyen Lee7Eunhee Ha8Eunhee Ha9Eunhee Ha10Eunhee Ha11Graduate Program in System Health Science and Engineering, College of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Environmental Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of KoreaGraduate Program in System Health Science and Engineering, College of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Environmental Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Internal Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Environmental Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of KoreaInstitute of Ewha-SCL for Environmental Health (IESEH), College of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Pediatrics, College of Medicine, Ewha Womans University, Seoul, Republic of KoreaGraduate Program in System Health Science and Engineering, College of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Environmental Medicine, School of Medicine, Ewha Womans University, Seoul, Republic of KoreaInstitute of Ewha-SCL for Environmental Health (IESEH), College of Medicine, Ewha Womans University, Seoul, Republic of KoreaDepartment of Medical Science, College of Medicine, Ewha Medical Research Institute, Ewha Womans University, Seoul, Republic of KoreaBackgroundsMany studies have shown particulate matter has emerged as one of the major environmental risk factors for diabetes; however, studies on the causal relationship between particulate matter 2.5 (PM2.5) and diabetes based on genetic approaches are scarce. The study estimated the causal relationship between diabetes and PM2.5 using two sample mendelian randomization (TSMR).MethodsWe collected genetic data from European ancestry publicly available genome wide association studies (GWAS) summary data through the MR-BASE repository. The IEU GWAS information output PM2.5 from the Single nucleotide polymorphisms (SNPs) GWAS pipeline using pheasant-derived variables (Consortium = MRC-IEU, sample size: 423,796). The annual relationship of PM2.5 (2010) were modeled for each address using a Land Use Regression model developed as part of the European Study of Cohorts for Air Pollution Effects. Diabetes GWAS information (Consortium = MRC-IEU, sample size: 461,578) were used, and the genetic variants were used as the instrumental variables (IVs). We performed three representative Mendelian Randomization (MR) methods: Inverse Variance Weighted regression (IVW), Egger, and weighted median for causal relationship using genetic variants. Furthermore, we used a novel method called MR Mixture to identify outlier SNPs.ResultsFrom the IVW method, we revealed the causal relationship between PM2.5 and diabetes (Odds ratio [OR]: 1.041, 95% CI: 1.008–1.076, P = 0.016), and the finding was substantiated by the absence of any directional horizontal pleiotropy through MR-Egger regression (β = 0.016, P = 0.687). From the IVW fixed-effect method (i.e., one of the MR machine learning mixture methods), we excluded outlier SNP (rs1537371) and showed the best predictive model (AUC = 0.72) with a causal relationship between PM2.5 and diabetes (OR: 1.028, 95% CI: 1.006–1.049, P = 0.012).ConclusionWe identified the hypothesis that there is a causal relationship between PM2.5 and diabetes in the European population, using MR methods.https://www.frontiersin.org/articles/10.3389/fpubh.2023.1164647/fullparticulate matter 2.5diabetesgenetics epidemiologyenvironmental epidemiologytwo sample Mendelian randomizationGWAS
spellingShingle Joyce Mary Kim
Joyce Mary Kim
Eunji Kim
Eunji Kim
Do Kyeong Song
Yi-Jun Kim
Ji Hyen Lee
Ji Hyen Lee
Eunhee Ha
Eunhee Ha
Eunhee Ha
Eunhee Ha
Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
Frontiers in Public Health
particulate matter 2.5
diabetes
genetics epidemiology
environmental epidemiology
two sample Mendelian randomization
GWAS
title Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
title_full Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
title_fullStr Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
title_full_unstemmed Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
title_short Causal relationship between particulate matter 2.5 and diabetes: two sample Mendelian randomization
title_sort causal relationship between particulate matter 2 5 and diabetes two sample mendelian randomization
topic particulate matter 2.5
diabetes
genetics epidemiology
environmental epidemiology
two sample Mendelian randomization
GWAS
url https://www.frontiersin.org/articles/10.3389/fpubh.2023.1164647/full
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