Inhalation of House Dust and Ozone Alters Systemic Levels of Endothelial Progenitor Cells, Oxidative Stress, and Inflammation in Elderly Subjects.

Journal article

Jantzen K, Jensen A, Kermanizadeh A, Elholm G, Sigsgaard T, Møller P, Roursgaard M and Loft S 2018. Inhalation of House Dust and Ozone Alters Systemic Levels of Endothelial Progenitor Cells, Oxidative Stress, and Inflammation in Elderly Subjects. Toxicological sciences : an official journal of the Society of Toxicology. Vol 163 (Issue 2), p. 353–363. https://doi.org/10.1093/toxsci/kfy027
AuthorsJantzen K, Jensen A, Kermanizadeh A, Elholm G, Sigsgaard T, Møller P, Roursgaard M and Loft S
Abstract

Ambient air pollution including ozone and especially particulate matter represents important causes of cardiovascular disease. However, there is limited knowledge on indoor air dust with respect to this risk and the potential interactions between dust and ozone. Here, we exposed 23 healthy elderly subjects for 5.5 h, to either clean air, house dust at 275 µg/m3 (diameter < 2.5 µm), ozone at 100 ppb or combined house dust and ozone in a double-blinded randomized cross-over study. The combined house dust and ozone exposure was associated with a 48% (95% CI 24%–65%) decrease as compared with the clean air exposure, in CD34+KDR+ late endothelial progenitor cells (EPCs) per leukocyte in the blood shortly after exposure, whereas none of the single exposures resulted in a significant effect. The combined exposure also increased reactive oxygen species production capacity in granulocytes and monocytes as well as an up-regulation of interleukin-8 mRNA levels in leukocytes. Ozone alone reduced the gene expression of tumor necrosis factor and C-C motif chemokine ligand 2, while dust alone showed no effects. The combined exposure to house dust and ozone also reduced levels of oxidized purines in DNA consistent with concomitant up-regulation of mRNA of the repair enzyme 8-oxoguanine DNA glycosylase. The reduction in late EPCs can be an indicator of cardiovascular risk caused by the combination of pulmonary oxidative stress induced by ozone and the inflammatory potential of the house dust. These data were corroborated with in vitro findings from exposed human macrophages and endothelial cells.

KeywordsEndothelial progenitor cells; House dust; Inflammation; Oxidative stress; Ozone
Year2018
JournalToxicological sciences : an official journal of the Society of Toxicology
Journal citationVol 163 (Issue 2), p. 353–363
PublisherOxford Academic
ISSN1096-0929
1096-6080
Digital Object Identifier (DOI)https://doi.org/10.1093/toxsci/kfy027
Web address (URL)http://europepmc.org/abstract/med/29767793
Output statusPublished
Publication datesJun 2018
Publication process dates
Deposited12 Jun 2023
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