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...

Full description

Bibliographic Details
Main Authors:	Pettit, Ashley P., Kipen, Howard, Laumbach, Robert, Ohman-Strickland, Pamela, Kelly-McNeill, Kathleen, Cepeda, Clarimel, Fan, Zhi-Hua, Amorosa, Louis, Lubitz, Sara, Schneider, Stephen, Gow, Andrew
Format:	Online
Language:	English
Published:	Public Library of Science 2015
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4682772/

id	pubmed-4682772
recordtype	oai_dc
spelling	pubmed-46827722015-12-31 Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution Pettit, Ashley P. Kipen, Howard Laumbach, Robert Ohman-Strickland, Pamela Kelly-McNeill, Kathleen Cepeda, Clarimel Fan, Zhi-Hua Amorosa, Louis Lubitz, Sara Schneider, Stephen Gow, Andrew Research Article 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 1.5hr 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. Public Library of Science 2015-12-14 /pmc/articles/PMC4682772/ /pubmed/26656561 http://dx.doi.org/10.1371/journal.pone.0144250 Text en © 2015 Pettit et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Pettit, Ashley P. Kipen, Howard Laumbach, Robert Ohman-Strickland, Pamela Kelly-McNeill, Kathleen Cepeda, Clarimel Fan, Zhi-Hua Amorosa, Louis Lubitz, Sara Schneider, Stephen Gow, Andrew
spellingShingle	Pettit, Ashley P. Kipen, Howard Laumbach, Robert Ohman-Strickland, Pamela Kelly-McNeill, Kathleen Cepeda, Clarimel Fan, Zhi-Hua Amorosa, Louis Lubitz, Sara Schneider, Stephen Gow, Andrew Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
author_facet	Pettit, Ashley P. Kipen, Howard Laumbach, Robert Ohman-Strickland, Pamela Kelly-McNeill, Kathleen Cepeda, Clarimel Fan, Zhi-Hua Amorosa, Louis Lubitz, Sara Schneider, Stephen Gow, Andrew
author_sort	Pettit, Ashley P.
title	Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
title_short	Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
title_full	Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
title_fullStr	Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
title_full_unstemmed	Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution
title_sort	disrupted nitric oxide metabolism from type ii diabetes and acute exposure to particulate air pollution
description	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 1.5hr 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.
publisher	Public Library of Science
publishDate	2015
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4682772/
_version_	1613513901621641216

Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution

Similar Items