Link Between Exhaust Emissions to Increased Rate of Heart Disease

Scientists at the University of California have recently completed a survey which shows that pollution from motor vehicles may be driving up the rates of heart disease by triggering inflammation and hardening blood vessles.

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 artherosclerious, the leading cause of death in the western world.

The findings 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 by as much as 6 per cent.

Arteries begin to harden when fats circulating in the blood-stream get trapped in the blood vessle walls and begin to deteriorate through oxidation. The Scientists at the University of California in Los Angeles suspect 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 human blood vessles and exposed them to diesel emission particles at levels equivalent to those found in cities. Some of the cells were exposed to blood vessel fats at the same time.

The overall effect was more pronounced when the cells were exposed to diesel particles and the fatty deposits. Further analysis reveals 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 diesel or petrol emissions triggered the genetic changes that drive heart disease. Experiments that had presiously been carried out on the animals had already confirmed that exposure to diesel particles incresased their risk of developing hardened arteries.