Exhaust fumes from motor vehicles reacts with cholesterol to choke the arteries thus raising the `risk of heart diseases. The fumes trigger the inflammation and harden blood vessels.
Researchers found that fine particles released in exhaust fumes combine with natural fats in arteries to spark a cascade of genetic changes which are capable of inducing cardiovascular atherosclerosis, the leading cause of death in the western world. The study done by the UCLA team of scientist appeared in the online issue of Genome Biology.
AdvertisementLead researcher Dr André Nel, an expert in nanomedicine, said the impact of diesel particles and cholesterol fats combined was much greater than the impact of each in isolation. He said "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."
The researchers investigated the interaction between diesel exhaust particles and the fatty molecules found in low-density lipoprotein (LDL), the "bad" form of cholesterol. The researchers combined the pollutants and fats and cultured them with cells taken from the inner lining of human blood vessels. A few hours later, they extracted DNA from the cells for genetic analysis.
Laboratory tests showed that the particles and fats worked in tandem to active genes that promote cellular inflammation. 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."
When the scientists screened the cells to see how their genes had reacted to the exposure, they found that 1,555 genes had been made more than 1.5 times more active in the cells. The effect was more pronounced when the cells were exposed to diesel particles and the fatty deposits. Further analysis revealed that most of the boosted genes belonged to three distinct groups that all play crucial roles in arterial blood vessel disease.
Previous experiments with the animals have already confirmed that exposure to diesel particles increased their risk of developing hardened arteries.
"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 finding points to an underlying explanation for the significant rise in hospital admissions and deaths from heart disease that coincides with greater levels of pollution. Previous studies have shown that when levels of airborne particles rise by 10 micrograms per cubic meter, deaths from one form of heart disease rise 6%.
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.
"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.
Cathy Ross, cardiac nurse at the British Heart Foundation, said anyone with chronic lung disease or coronary heart disease should avoid staying outside for long periods when pollution levels are high.