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Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes
Epidemiologic observations suggest that exposure to ambient fine particulate matter (PM(2.5)) is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CKD. We evaluated whether diabetes mediates the association between PM(2.5) and CKD. A cohort of 2,444,157...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067761/ https://www.ncbi.nlm.nih.gov/pubmed/32165691 http://dx.doi.org/10.1038/s41598-020-61115-x |
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author | Bowe, Benjamin Xie, Yan Yan, Yan Xian, Hong Al-Aly, Ziyad |
author_facet | Bowe, Benjamin Xie, Yan Yan, Yan Xian, Hong Al-Aly, Ziyad |
author_sort | Bowe, Benjamin |
collection | PubMed |
description | Epidemiologic observations suggest that exposure to ambient fine particulate matter (PM(2.5)) is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CKD. We evaluated whether diabetes mediates the association between PM(2.5) and CKD. A cohort of 2,444,157 United States veterans were followed over a median 8.5 years. Environmental Protection Agency data provided PM(2.5) exposure levels(.) Regression models assessed associations and their proportion mediated. A 10 µg/m(3) increase in PM(2.5) was associated with increased odds of having a diabetes diagnosis (odds ratio: 1.18, 95% CI: 1.06–1.32), use of diabetes medication (1.22, 1.07–1.39), and increased risk of incident eGFR <60 ml/min/1.73 m(2) (hazard ratio:1.20, 95% CI: 1.13–1.29), incident CKD (1.28, 1.18–1.39), ≥30% decline in eGFR (1.23, 1.15–1.33), and end-stage renal disease (ESRD) or ≥50% decline in eGFR (1.17, 1.05–1.30). Diabetes mediated 4.7% (4.3–5.7%) of the association of PM(2.5) with incident eGFR <60 ml/min/1.73 m(2), 4.8% (4.2–5.8%) with incident CKD, 5.8% (5.0–7.0%) with ≥30% decline in eGFR, and 17.0% (13.1–20.4%) with ESRD or ≥50% decline in eGFR. Diabetes minimally mediated the association between PM(2.5) and kidney outcomes. The findings will help inform more accurate estimates of the burden of diabetes and burden of kidney disease attributable to PM(2.5) pollution. |
format | Online Article Text |
id | pubmed-7067761 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-70677612020-03-19 Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes Bowe, Benjamin Xie, Yan Yan, Yan Xian, Hong Al-Aly, Ziyad Sci Rep Article Epidemiologic observations suggest that exposure to ambient fine particulate matter (PM(2.5)) is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CKD. We evaluated whether diabetes mediates the association between PM(2.5) and CKD. A cohort of 2,444,157 United States veterans were followed over a median 8.5 years. Environmental Protection Agency data provided PM(2.5) exposure levels(.) Regression models assessed associations and their proportion mediated. A 10 µg/m(3) increase in PM(2.5) was associated with increased odds of having a diabetes diagnosis (odds ratio: 1.18, 95% CI: 1.06–1.32), use of diabetes medication (1.22, 1.07–1.39), and increased risk of incident eGFR <60 ml/min/1.73 m(2) (hazard ratio:1.20, 95% CI: 1.13–1.29), incident CKD (1.28, 1.18–1.39), ≥30% decline in eGFR (1.23, 1.15–1.33), and end-stage renal disease (ESRD) or ≥50% decline in eGFR (1.17, 1.05–1.30). Diabetes mediated 4.7% (4.3–5.7%) of the association of PM(2.5) with incident eGFR <60 ml/min/1.73 m(2), 4.8% (4.2–5.8%) with incident CKD, 5.8% (5.0–7.0%) with ≥30% decline in eGFR, and 17.0% (13.1–20.4%) with ESRD or ≥50% decline in eGFR. Diabetes minimally mediated the association between PM(2.5) and kidney outcomes. The findings will help inform more accurate estimates of the burden of diabetes and burden of kidney disease attributable to PM(2.5) pollution. Nature Publishing Group UK 2020-03-12 /pmc/articles/PMC7067761/ /pubmed/32165691 http://dx.doi.org/10.1038/s41598-020-61115-x Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Bowe, Benjamin Xie, Yan Yan, Yan Xian, Hong Al-Aly, Ziyad Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title | Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title_full | Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title_fullStr | Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title_full_unstemmed | Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title_short | Diabetes Minimally Mediated the Association Between PM(2.5) Air Pollution and Kidney Outcomes |
title_sort | diabetes minimally mediated the association between pm(2.5) air pollution and kidney outcomes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7067761/ https://www.ncbi.nlm.nih.gov/pubmed/32165691 http://dx.doi.org/10.1038/s41598-020-61115-x |
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