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Diesel Fumes Help Clog Arteries
Researchers track the way particles trigger inflammation
By Ed Edelson
Posted 7/26/07
THURSDAY, July 26 (HealthDay News) -- Scientists say they've spotted the biochemical process that makes diesel exhaust so dangerous to human arteries.
An interaction between the fine particles found in diesel exhaust and the fatty acids in LDL ("bad") cholesterol activates genes that then cause inflammation in blood vessels, a team from the University of California, Los Angeles (UCLA) report.
This process accelerates atherosclerosis -- a buildup of fatty deposits that can eventually lead to complete vessel blockage, according to the study in the July 26 online issue of Genome Biology.
The mechanism is one key way that "chemicals in diesel exhaust impact the cardiovascular system," said Dr. Andre Nel, chief of nanomedicine at the UCLA David Geffen School of Medicine. "We have done an analysis of genes that respond to those chemicals in synergy with the components of bad cholesterol."
LDL cholesterol is usually described as the bad kind because it is involved in blood vessel damage, in contrast to "good" HDL cholesterol, which works to prevent such damage.
In a series of studies, the UCLA scientists combined particulate diesel pollutants with fatty acids found in LDL cholesterol, studying their interactions with free radicals -- highly reactive molecules that can damage cells. They exposed cells to this mixture and then extracted genetic material from those cells.
Genes that promote cellular inflammation were found to be highly activated in those cells. Inflammation is well known as a contributor to atherosclerosis, Nel said.
"The primary implication of our finding is that for people who have cardiovascular risk factors such as high blood cholesterol, simultaneous exposure to diesel air pollution can enhance damage by enhancing inflammation in the cardiovascular system," Nel said.
The UCLA research team now is working to develop a test, such as measurement of a protein produced in response to air pollution, that could be used to assess the safety of people working or living in areas with different levels of pollution, he said.
Nel's work is an important part of ongoing research on the damaging molecular effects of air pollution from diesel and other sources, said Dr. John Balbus, chief of health sciences of Environmental Defense, a watchdog group.
"There have been lots of studies of inflammation," Balbus said. "This one goes down to the genetic level, and finds a pattern of gene expression that is particularly associated with diesel exhaust."
While such laboratory work has been going over for the past five to 10 years, epidemiological studies have also tightened the link between cardiovascular risk and exposure to pollutants, Balbus said. He cited a recent German study that found that living near a major source of pollution, such as a highway, was associated with a higher incidence of atherosclerosis.
"That was observational data in real people," he said. "When you put that together with the laboratory work, you have a very convincing picture."
"This study is more evidence of why we need to become more aggressive in cleaning up existing diesel engines," said Frank O'Donnell, director of Clean Air Watch, a private organization.
Chances that diesel engines will be used as commonly in the United States as in Europe, where they are found in many cars, are slim, because U.S. pollution standards are tougher, O'Donnell said.
"The real big problem remains the many thousands of diesel engines in construction equipment, old trucks and buses," he said. "The biggest bang for the buck would come from cleaning up existing diesel engines."
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