Pollution from motor vehicles may be driving up rates of heart disease by triggering inflammation and hardening blood vessels, scientists have warned.
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 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 metre, deaths from one form of heart disease rise 6 per cent.
Arteries begin to harden when fats circulating in the bloodstream get trapped in the blood vessel walls and begin to deteriorate through oxidation.
But scientists at the University of California in Los Angeles suspected that airborne pollution may be responsible for exacerbating the damage. The team, led by Andre Nel, an expert on the health effects of pollutants, took cells from the walls of human blood vessels and exposed them to diesel exhaust particles at levels equivalent to those found in cities.
Some of the cells were exposed to blood vessel fats at the same time.
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 one and a half 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.
Studies in mice confirmed that breathing in fine particles from exhaust fumes triggered the genetic changes that drive heart disease.
Experiments that had previously been carried out on the animals had already confirmed that exposure to diesel particles increased their risk of developing hardened arteries.