We saw that the diesel particles and oxidized fats had worked in tandem to activate the genes that promote cellular inflammation a major risk factor for atherosclerosis, said Dr. Jesus Araujo, UCLA assistant professor of medicine and director of environmental cardiology at the Geffen School of Medicine.
The interaction left a genetic footprint that reveals how interaction between the particles and cholesterol accelerates the narrowing and blockage of the blood vessels, Araujo noted.
To duplicate these findings in living cells, the UCLA team exposed mice with high cholesterol to the diesel particles and saw activation of some of the same gene groups in the animals tissue.
Exactly how air pollutants cause cardiovascular injury is poorly understood, Nel said. But we do know that these particles are coated with chemicals that damage tissue and cause inflammation of the nose and lungs. Vascular inflammation in turn leads to cholesterol deposits and clogged arteries, which can give rise to blood clots that trigger heart attack or stroke.
The researchers next step will be to convert the genes responses to the pollutant-cholesterol combination into a biomarker that will enable physicians to easily evaluate air pollutions effect on health, especially cardiovascular disease.
Once a biomarker is developed, wed simply need to test a blood sample in order to measure a persons exposure to particulate matter and determine whether it has reached levels that require medical intervention, Araujo said.
The American Cancer Society has reported a 6 percent increase in heart- and lung-related deaths for every 10 micrograms per cubic meter rise in particulates.
Our results emphasize the importance of controlling air pollution as another tool for preventing car
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Contact: Elaine Schmidt
eschmidt@mednet.ucla.edu
310-794-2272
University of California - Los Angeles
25-Jul-2007