HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Part 4. Assessment of plasma markers and cardiovascular responses in rats after chronic exposure to new-technology diesel exhaust in the ACES bioassay.

Abstract
Although epidemiologic and experimental studies suggest that chronic exposure to diesel exhaust (DE*) emissions causes adverse cardiovascular effects, neither the specific components of DE nor the mechanisms by which DE exposure could induce cardiovascular dysfunction and exacerbate cardiovascular disease (CVD) are known. Because advances in new technologies have resulted in cleaner fuels and decreased engine emissions, uncertainty about the relationship between DE exposure and human cardiovascular health effects has increased. To address this ever-changing baseline of DE emissions, as part of the larger Advanced Collaborative Emissions Study (ACES) bioassay studying the health effects of 2007-compliant diesel engine emissions (new-technology diesel exhaust), we examined whether plasma markers of vascular inflammation, thrombosis, cardiovascular aging, cardiac fibrosis, and aorta morphometry were changed over 24 months in an exposure-level-, sex-, or exposure-duration-dependent manner. Many plasma markers--several recognized as human CVD risk factors--were measured in the plasma of rats exposed for up to 24 months to filtered air (the control) or DE. Few changes in plasma markers resulted from 12 months of DE exposure, but significant exposure-level-dependent increases in soluble intercellular adhesion molecule 1 (sICAM-1) and interleukin-6 (IL-6) levels, as well as decreases in total and non-high-density-lipoprotein cholesterol (non-HDL) levels in plasma, were observed in female rats after 24 months of DE exposure. These effects were not observed in male rats, and no changes in cardiac fibrosis or aorta morphometry resulting from DE exposure were observed in either sex. Collectively, the significant changes may reflect an enhanced sensitivity of the female cardiovascular system to chronic DE exposure; however, this conclusion should be interpreted within both the context and limitations of the current study.
AuthorsDaniel J Conklin, Maiying Kong, HEI Health Review Committee
JournalResearch report (Health Effects Institute) (Res Rep Health Eff Inst) Issue 184 Pg. 111-39; discussion 141-71 (Jan 2015) ISSN: 1041-5505 [Print] United States
PMID25842618 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)
Chemical References
  • Biomarkers
  • Cytokines
  • Inflammation Mediators
  • Interleukins
  • Lipids
  • Proteins
  • Vehicle Emissions
  • Intercellular Adhesion Molecule-1
Topics
  • Aging (metabolism)
  • Animals
  • Biomarkers
  • Cardiovascular Diseases (chemically induced, physiopathology)
  • Cytokines (metabolism)
  • Female
  • Inflammation Mediators (metabolism)
  • Intercellular Adhesion Molecule-1 (metabolism)
  • Interleukins (metabolism)
  • Lipids (blood)
  • Male
  • Proteins (metabolism)
  • Rats
  • Sex Factors
  • Time Factors
  • Vehicle Emissions (toxicity)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: