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Vehicular Particulate Matter (PM) Characteristics Impact Vascular Outcomes Following Inhalation

  • Katherine E. ZychowskiEmail author
  • Christina R. Steadman Tyler
  • Bethany Sanchez
  • Molly Harmon
  • June Liu
  • Hammad Irshad
  • Jacob D. McDonald
  • Barry E. Bleske
  • Matthew J. Campen
Article
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Abstract

Roadside proximity and exposure to mixed vehicular emissions (MVE) have been linked to adverse pulmonary and vascular outcomes. However, because of the complex nature of the contribution of particulate matter (PM) versus gases, it is difficult to decipher the precise causative factors regarding PM and the copollutant gaseous fraction. To this end, C57BL/6 and apolipoprotein E knockout mice (ApoE−/−) were exposed to either filtered air (FA), fine particulate (FP), FP+gases (FP+G), ultrafine particulate (UFP), or UFP+gases (UFP+G). Two different timeframes were employed: 1-day (acute) or 30-day (subchronic) exposures. Examined biological endpoints included aortic vasoreactivity, aortic lesion quantification, and aortic mRNA expression. Impairments in vasorelaxation were observed following acute exposure to FP+G in C57BL/6 animals and FP, UFP, and UFP+G in ApoE−/− animals. These effects were completely abrogated or markedly reduced following subchronic exposure. Aortic lesion quantification in ApoE−/− animals indicated a significant increase in atheroma size in the UFP-, FP-, and FP+G-exposed groups. Additionally, ApoE−/− mice demonstrated a significant fold increase in TNFα expression following FP+G exposure and ET-1 following UFP exposure. Interestingly, C57BL/6 aortic gene expression varied widely across exposure groups. TNFα decreased significantly following FP exposure and CCL-5 decreased in the UFP-, FP-, and FP+G-exposed groups. Conversely, ET-1, CCL-2, and CXCL-1 were all significantly upregulated in the FP+G group. These findings suggest that gas–particle interactions may play a role in vascular toxicity, but the contribution of surface area is not clear.

Keywords

Cardiovascular Particulate matter Pulmonary Diesel exhaust Vascular toxicity Vehicle emissions 

Notes

Acknowledgments

We thank Dr. Jesse Denson for manuscript editing and assistance in preparation.

Funding

This work has been supported by the ASERT-IRACDA program at UNM (K12GM088021) and NIEHS (K99ES029104; R01 ES014639).

Compliance with Ethical Standards

Conflicts of interest

The authors confirm that they have no conflicts of interest, financial or otherwise, with the contents of this manuscript.

Ethical Approval

Studies were conducted with full approval by the Institutional Animal Care and Use Committees of both the University of New Mexico and Lovelace Respiratory Research Institute.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Katherine E. Zychowski
    • 1
    Email author
  • Christina R. Steadman Tyler
    • 2
  • Bethany Sanchez
    • 1
  • Molly Harmon
    • 1
  • June Liu
    • 3
  • Hammad Irshad
    • 3
  • Jacob D. McDonald
    • 3
  • Barry E. Bleske
    • 4
  • Matthew J. Campen
    • 1
  1. 1.Department of Pharmaceutical SciencesThe University of New Mexico, College of PharmacyAlbuquerqueUSA
  2. 2.Biosciences DivisionLos Alamos National LaboratoriesLos AlamosUSA
  3. 3.Lovelace Respiratory Research InstituteAlbuquerqueUSA
  4. 4.Department of Pharmacy Practice & Administrative SciencesThe University of New Mexico, College of PharmacyAlbuquerqueUSA

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