From the Los Angeles Times
Pollution-cholesterol link to heart disease seen
The combination activates genes that can cause clogged arteries, UCLA researchers say.
By Marla Cone
Times Staff Writer
July 26, 2007
Strengthening the link between air pollution and cardiovascular
disease, new research suggests that people with high cholesterol are
especially vulnerable to heart disease when they are exposed to diesel
exhaust and other ultra-fine particles that are common pollutants in
particles in diesel exhaust combine with cholesterol to activate genes
that trigger hardening of the arteries, according to a study by UCLA
scientists to be published today.
"Their combination creates a
dangerous synergy that wreaks cardiovascular havoc far beyond what's
caused by the diesel or cholesterol alone," said Dr. André Nel, chief
of nanomedicine at the David Geffen School of Medicine at UCLA and a
researcher at UCLA's California NanoSystems Institute. He led a team of
10 scientists who conducted the study, published in an online version
of the journal Genome Biology.
Although diet, smoking and other
factors contribute to the risk of cardiovascular disease — the leading
cause of death in the Western world — scientists have long believed
that air pollution, particularly tiny pieces of soot from trucks and
factories, plays a major role, too.
For years, scientists around
the world have reported that on days when fine-particle pollution
increases, deaths from lung diseases, heart attacks and strokes rise
substantially. Riverside County and the San Gabriel Valley have among
the worst fine-particle pollution in the nation.
say their study, conducted on human cells as well as on mice, is the
first to explain how particulates in the air activate genes that can
cause heart attacks or strokes.
The researchers exposed human
blood cells to a combination of diesel particles and oxidized fats,
then extracted their DNA. Working together, the particles and fats
switched on genes that cause inflammation of blood vessels, which leads
to clogged arteries, or atherosclerosis.
The team then
duplicated the findings in living animals by exposing mice to a
high-fat diet and freeway exhaust in downtown Los Angeles. The same
artery-clogging gene groups were activated in the mice.
scientists reported that diesel particles may enter the body's
circulatory system from the lungs, and then react with fats in the
arteries to alter how genes are activated, triggering inflammation that
causes heart disease.
Other research has shown similar
inflammatory damage in lungs exposed to fine particles. Diesel exhaust
has also been linked to lung cancer, asthma attacks and DNA damage.
results emphasize the importance of controlling air pollution as
another tool for preventing cardiovascular disease," said Ke Wei Gong,
a UCLA cardiology researcher who was one of the study's authors.
many urban areas, including the Los Angeles region, ultra-fine
particles are the most concentrated near freeways, mostly from diesel
exhaust, which is spewed by trucks, buses, off-road vehicles and other
For decades, California and local air-quality
regulators have been ratcheting down particulate emissions from trucks
and other sources, but the airborne levels in most of the Los Angeles
region still frequently exceed federal health standards.
are a few hot spots throughout the country that compete with Los
Angeles from time to time, but in general, we tend to have the highest
levels here," Nel said.
Exposed in a mobile laboratory moving
down the freeway, the mice breathed a concentration of fine particles,
362 micrograms per cubic meter of air. That was five times higher than
the peak that people in the San Gabriel Valley were exposed to last
However, humans breathe polluted air every day for
decades, whereas the mice in the study were exposed five hours per day,
three days per week, for eight weeks.
"The levels were high, but
they came from real freeway exhaust so they were not artificially
high," Nel said. "It was almost within the realm of what we are exposed
Diesel particles contain free radicals, which damage tissues, and so do the fatty acids in cholesterol.
The study aimed to find out what happened when these two sources of oxidation came in contact.
the cells exposed to just the cholesterol or just the diesel, the
effects on the genes were much less pronounced. More than 1,500 genes
were turned on, and 759 were turned off, when diesel particles were
combined with the fats.
"Now that we see this genetic footprint,
we have a better understanding of how the injury occurs due to air
pollution particles," Nel said.
The UCLA scientists hope to
transform the gene changes to a biomarker, which experts can then use
to predict which people are most susceptible to heart disease from air
The smaller the particle, the more harm it can
cause. More artery-clogging genes were activated in mice exposed to the
ultra-fine particles in diesel exhaust than in those exposed to larger
particles in the air. Smaller particles generally come from sources of
combustion — mostly vehicles.
Contributing Correspondent, Science
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