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Impact Of A Chemical Component Of Diesel Exhaust Particles

ScienceDaily (May 4, 2007) — A new study finds that exposure to a chemical component of diesel exhaust particles can compromise the ability of resistance arteries to regulate blood flow to bone marrow. Post-menopausal females, the elderly and males are most likely to be impacted, according to a new vascular biology study using an animal model.

Background

Diesel exhaust contributes significantly to the U.S. ambient air pollution burden. This form of air pollution is the product of diesel fuel combustion, commonly generated by buses, trucks, trains and ferries. The particles can remain airborne for extended time periods, and travel long distances prior to being inhaled. When inhaled, chemical components such as polyaromatic hydrocarbons (PAH) attached to the particles can interact with the body. Quinones are PAHs and are among the more toxic components of diesel exhaust. In the current study, the investigators used phenanthraquinone (PQ) because previous research found PQ to compromise the ability of larger blood vessels to relax. They have also noted that in certain populations, exposure to particle pollution may exacerbate various cardiovascular diseases.

The principal nutrient artery (PNA) is the major resistance vessel that regulates blood blow to the femoral bone marrow. The ability of arteries to dilate (widen) declines with age and this corresponds with reduced blood flow in an artery¡¦s target organ. Impaired blood flow regulation in the bone marrow can have wide- and long-reaching health consequences. It is unclear what PQ does to the ability of this artery to dilate, and how age or gender alters any such effect.

Summary of Methodology

Against this backdrop the research team sought to determine whether PQ impairs vasodilation in the PNA and identify whether age, gender or estrogen alters the presumed effects of PQ. The researchers isolated and cannulated femoral PNAs from intact and ovariectomized (OVX) female rats (6, 14 and 24 months) and male rats (6 and 24 months). To evaluate the ability of the PNA to dilate when it was incubated with PQ, researchers used the chemical acetylcholine (ACh). A series of ACh doses were administered over time, starting with low doses and graduating to higher doses to produce maximum dilation of the artery.

Results

The researchers found that:

  • exposure to PQ had greatly compromised -- by approximately 65 percent -- the ability of the blood vessels to effectively dilate in six month old male rats, but had no effect in female rats;
  • at 14 months (female rats) and 24 months (female and male rats), PQ had impaired and abolished vasodilatation, respectively;
  • in all OVX rats (i.e., the young females who had lost estrogen due to menopausal status), PQ abolished vasodilatation;
  • following the loss of estrogen, particularly at six months where a cardioprotective effect was previously observed, PQ exposure had obliterated vasodilation.

Conclusion

This study demonstrates that exposure to the diesel particle component PQ, can compromise the ability of the PNA to regulate bone marrow blood flow in males, the elderly and post-menopausal females in an animal model. These findings may provide an important link to other discoveries involving the protective effects of estrogen to environmental pollutants. Physiology is the study of how molecules, cells, tissues and organs function to create health or disease. The American Physiological Society (APS) has been an integral part of the scientific discovery process since it was established in 1887.

Further Information: The study, Effects of Age, Gender, and Estrogen on Endothelium-Dependent Vasodilation Subsequent to Phenanthraquinone Exposure, was conducted by Rhonda D. Prisby, Judy Muller-Delp and Timothy R. Nurkiewicz, all of the Center for Interdisciplinary Research in Cardiovascular Sciences at the West Virginia University School of Medicine in Morgantown, WV, USA. Dr. Nurkiewicz is presenting the findings on behalf of the University¡¦s interdisciplinary cardiovascular research team. The research was funded by the Health Effects Institute and the National Institutes of Health. This study was one of several related studies presented at the 120th Annual Meeting of The American Physiological Society from April 28-May 2, 2007 in Washington, DC.


Adapted from materials provided by American Physiological Society, via EurekAlert!, a service of AAAS.
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