Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Comparative effects of inhaled diesel exhaust and ambient fine particles on inflammation, atherosclerosis, and vascular dysfunction.

Authors: Quan, Chunli; Sun, Qinghua; Lippmann, Morton; Chen, Lung-Chi

Published In Inhal Toxicol, (2010 Aug)

Abstract: Ambient air PM(2.5) (particulate matter less than 2.5 mum in diameter) has been associated with cardiovascular diseases (CVDs), but the underlying mechanisms affecting CVDs are unknown. The authors investigated whether subchronic inhalation of concentrated ambient PM(2.5) (CAPs), whole diesel exhaust (WDE), or diesel exhaust gases (DEGs) led to exacerbation of atherosclerosis, pulmonary and systemic inflammation, and vascular dysfunction; and whether DEG interactions with CAPs alter cardiovascular effects. ApoE(-/-) mice were simultaneously exposed via inhalation for 5 hours/day, 4 days/week, for up to 5 months to one of five different exposure atmospheres: (1) filtered air (FA); (2) CAPs (105 microg/m(3)); (3) WDE (DEP = 436 microg/m(3)); (4) DEG (equivalent to gas levels in WDE group); and (5) CAPs+DEG (PM(2.5): 113 microg/m(3); with DEG equivalent to WDE group). After 3 and 5 months, lung lavage fluid and blood sera were analyzed, and atherosclerotic plaques were quantified by ultrasound imaging, hematoxylin and eosin (H&E stain), and en face Sudan IV stain. Vascular functions were assessed after 5 months of exposure. The authors showed that (1) subchronic CAPs, WDE, and DEG inhalations increased serum vascular cell adhesion molecule (VCAM)-1 levels and enhanced phenylephrine (PE)-induced vasoconstriction; (2) for plaque exacerbation, CAPs > WDE > DEG = FA, thus PM components (not present in WDE) were responsible for plaque development; (3) atherosclerosis can exacerbated through mechanistic pathways other than inflammation and vascular dysfunction; and (4) although there were no significant interactions between CAPs and DEG on plaque exacerbation, it is less clear whether the effects of CAPs on vasomotor dysfunction and pulmonary/systemic inflammation were enhanced by the DEG coexposure.

PubMed ID: 20462391 Exiting the NIEHS site

MeSH Terms: Air Pollutants/toxicity*; Animals; Aorta, Abdominal/drug effects; Aorta, Abdominal/pathology; Atherosclerosis/chemically induced; Atherosclerosis/pathology; Atherosclerosis/ultrasonography; Brachiocephalic Trunk/drug effects; Brachiocephalic Trunk/pathology; Brachiocephalic Trunk/ultrasonography; Bronchoalveolar Lavage Fluid/chemistry; Bronchoalveolar Lavage Fluid/cytology; Cardiotonic Agents; Drug Synergism; Inhalation Exposure; Lung/drug effects*; Lung/metabolism; Lung/pathology; Mice; Mice, Knockout; Particulate Matter/toxicity*; Pneumonia/chemically induced; Pneumonia/pathology; Vascular Cell Adhesion Molecule-1/metabolism; Vasoconstriction/drug effects; Vasoconstriction/physiology; Vasomotor System; Vehicle Emissions/toxicity*

to Top