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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

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

Authors: Zychowski, Katherine E; Tyler, Christina R Steadman; Sanchez, Bethany; Harmon, Molly; Liu, June; Irshad, Hammad; McDonald, Jacob D; Bleske, Barry E; Campen, Matthew J

Published In Cardiovasc Toxicol, (2020 06)

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.

PubMed ID: 31410643 Exiting the NIEHS site

MeSH Terms: Animals; Aorta/drug effects*; Aorta/metabolism; Aorta/pathology; Aorta/physiopathology; Aortic Diseases/chemically induced*; Aortic Diseases/metabolism; Aortic Diseases/pathology; Aortic Diseases/physiopathology; Atherosclerosis/chemically induced*; Atherosclerosis/metabolism; Atherosclerosis/pathology; Atherosclerosis/physiopathology; Chemokine CCL2/genetics; Chemokine CCL2/metabolism; Chemokine CCL5/genetics; Chemokine CCL5/metabolism; Chemokine CXCL1/genetics; Chemokine CXCL1/metabolism; Disease Models, Animal; Endothelin-1/genetics; Endothelin-1/metabolism; Inhalation Exposure/adverse effects*; Male; Mice, Inbred C57BL; Mice, Knockout, ApoE; Particulate Matter/toxicity*; Risk Assessment; Tumor Necrosis Factor-alpha/genetics; Tumor Necrosis Factor-alpha/metabolism; Vasodilation/drug effects; Vehicle Emissions/toxicity*

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