21 January 2008
A new academic study led by researchers from the University of California, Los Angeles (UCLA) concluded that ultrafine particles from vehicle emissions may be the most damaging components of air pollution in triggering plaque buildup in the arteries, which can lead to heart attack and stroke. The findings have been published in the Circulation Research journal.
It is the first study that demonstrates the ability of nano-sized air pollutants to promote atherosclerosis in an animal model. The scientists identified a way in which pollutant particles may promote hardening of the arteries—by inactivating the protective qualities of high density lipoprotein (HDL) cholesterol.
In the study, conducted over a five-week period, researchers exposed mice with high cholesterol to one of two sizes of air pollutant particles from downtown Los Angeles freeway emissions and compared them with mice that received filtered air that contained very few particles. It was found that mice exposed to ultrafine particles of diameters below 0.18 µm exhibited 55% greater atherosclerotic plaque development than animals breathing filtered air, and 25% greater plaque development than mice exposed to fine particles (< 2.5 µm). This suggests that ultrafine particles are the more toxic air pollutants in promoting events leading to cardiovascular disease. (The authors of the study refer to the 0.18 µm particles as “ultrafine”, but ultrafine particles are more commonly defined as those below 0.10 µm).
Pollutant particles are coated in chemicals sensitive to free radicals, which damage the cell and tissue through oxidation, which leads to the inflammation that causes clogged arteries. Samples from polluted air revealed that ultrafine particles have a larger concentration of these chemicals and a larger surface area where these chemicals can be adsorbed, compared with larger particles. The researchers suggested that the key mechanism behind how these air pollutants are able to affect the atherosclerotic process is through a reduction of the anti-inflammatory protective properties of HDL cholesterol, known as “good” cholesterol.
To explore if air particle exposure caused oxidative stress throughout the body—which is an early process triggering the inflammation that causes clogged arteries—researchers checked for an increase in genes that would have been activated to combat this inflammatory progression. Greater levels of gene activation was found in mice exposed to ultrafine particles, compared to the other groups.
Previous studies assessing the cardiovascular impact of air pollution have taken place over longer periods of exposure time, such as five to six months. The current study demonstrated that ill effects can occur more quickly, in just five weeks.
Vehicle exhaust is an important source of ultrafine particle emissions. The highest levels of ultrafines are found in exhaust gases from diesel engines that are not equipped with particulate filters, but they are also present in gasoline exhaust, especially in directly injected gasoline engines.
Existing PM emission regulations from internal combustion engines are expressed in terms of particle mass—a metric that is not sensitive to ultrafine particles which represent only a small fraction of the total PM mass, but are a major contributor to particle number emissions. However, diesel particulate filters of the wall-flow design that are being introduced on diesel engines to comply with the mass-based PM emission limits are also very effective in controlling emissions of ultrafine particles and in reducing PM number emissions. Therefore, some environmental authorities, including the US EPA, have currently no plans to introduce particle number emission standards. In Europe, on the other hand, particle number limits are to be introduced at the Euro 6 stage for both light- and heavy-duty diesel engines, to prevent the possibility that the mass-based PM standards are met in the future using other technologies, such as flow-though (“open”) filters, which may allow large numbers of ultrafine particles to pass.