A new study which was just published makes the connection between air pollution and high cholesterol. A research team working out of UCLA is the first to find a collaboration between air pollution and artery clogging fats.
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study conducted by a research team at UCLA has made a connection between diesel exhaust and atherosclerosis or hardening of the arteries. The study is published in the July 26 online edition of Genome Biology.
This is the first time that a research team has found how the fine particles in air pollution collude with artery clogging fats and switch on the genes that cause blood vessel inflammation and lead to cardiovascular disease.
According to Dr. André Nel, chief of nanomedicine at the David Geffen School of Medicine at UCLA and a researcher at UCLA’s California NanoSystems Institute, “
When you add one plus one, it normally totals two, But we found that adding diesel particles to cholesterol fats equals three. Their combination creates a dangerous synergy that wreaks cardiovascular havoc far beyond what’s caused by the diesel or cholesterol alone.”
In order to investigate the interaction between diesel exhaust particles and the fatty acids that are found in low-density lipoprotein (LDL) cholesterol, the researchers focused on how oxidation contributes to inflammation and artery disease. LDL is referred to in lay-person's terms as the bad cholesterol which leads to artery blockage.
Ke Wei Gong, a UCLA cardiology researcher said
“Diesel particles are coated in chemicals containing free radicals, and the fatty acids in LDL cholesterol generate free radicals during metabolism in the cells. We wanted to measure what happens when these two sources of oxidation come into contact.”
The research team first combined the pollutants and oxidized fats and then cultured them with cells from the inner lining of human blood vessels. After a few hours had passed DNA was extracted from the cells for genetic analysis.
What the team saw then was,
according to Dr. Jesus Araujo, UCLA assistant professor of medicine and director of environmental cardiology at the Geffen School of Medicine, that the diesel particles and oxidized fats had worked in tandem to activate the genes that promote cellular inflammation. This is a major risk factor for atherosclerosis
“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.
Mice, which had high cholesterol levels, were exposed to the diesel particles in an attempt to duplicate the teams’ findings in living cells. The result was that they witnessed activation of some of the same gene groups in the animals’ tissue.
Nel said that
“Exactly how air pollutants cause cardiovascular injury is poorly understood. 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 next step is to convert the genes’ responses to the pollutant-cholesterol combination into a biomarker. This will enable physicians to easily evaluate the effect that air pollution has on health, especially cardiovascular disease.
The team reported that once a biomarker is developed, all that would be needed would be to test a blood sample.
This test would to measure a person’s exposure to particulate matter and thus determine whether it has reached levels that require medical intervention.
