Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
Type II diabetes is an established cause of vascular impairment. Particulate air pollution is known to exacerbate cardiovascular and respiratory conditions, particularly in susceptible populations. This study set out to determine the impact of exposure to traffic pollution, with and without particle...
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Published in | PloS one Vol. 10; no. 12; p. e0144250 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Public Library of Science
14.12.2015
Public Library of Science (PLoS) |
Subjects | |
Online Access | Get full text |
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Summary: | Type II diabetes is an established cause of vascular impairment. Particulate air pollution is known to exacerbate cardiovascular and respiratory conditions, particularly in susceptible populations. This study set out to determine the impact of exposure to traffic pollution, with and without particle filtration, on vascular endothelial function in Type II diabetes. Endothelial production of nitric oxide (NO) has previously been linked to vascular health. Reactive hyperemia induces a significant increase in plasma nitrite, the proximal metabolite of NO, in healthy subjects, while diabetics have a lower and more variable level of response. Twenty type II diabetics and 20 controls (ages 46-70 years) were taken on a 1.5 hr roadway traffic air pollution exposure as passengers. We analyzed plasma nitrite, as a measure of vascular function, using forearm ischemia to elicit a reactive hyperemic response before and after exposure to one ride with and one without filtration of the particle components of pollution. Control subjects displayed a significant increase in plasma nitrite levels during reactive hyperemia. This response was no longer present following exposure to traffic air pollution, but did not vary with whether or not the particle phase was filtered out. Diabetics did not display an increase in nitrite levels following reactive hyperemia. This response was not altered following pollution exposure. These data suggest that components of acute traffic pollution exposure diminish vascular reactivity in non-diabetic individuals. It also confirms that type II diabetics have a preexisting diminished ability to appropriately respond to a vascular challenge, and that traffic pollution exposure does not cause a further measureable acute change in plasma nitrite levels in Type II diabetics. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address: New Jersey Department of Health, Trenton, NJ, United States of America Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: HK AG RL. Performed the experiments: AP KKM CC LA SS SL. Analyzed the data: AP AG HK POS RL. Contributed reagents/materials/analysis tools: AG HK POS ZHF. Wrote the paper: AP HK AG RL. Recruited diabetic subjects and gave input on health related issues: LA SL SS. Current address: Department of Biochemistry & Molecular Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, 08854, United States of America |
ISSN: | 1932-6203 1932-6203 |
DOI: | 10.1371/journal.pone.0144250 |