Los Angeles, CA - New epidemiologic evidence suggests that long-term exposure to air pollution might lead to atherosclerosis.[1] According to investigators, a vascular response to the respiratory and systemic effects may be part of the complex processes by which ambient air-pollution exposure could lead to cardiovascular disease.

"This is the very first study supporting the hypothesis that air pollutants from fossil-fuel burning, which in the Los Angeles area is mainly from traffic, could possibly contribute to the development of atherosclerosis or would be atherogenic," said lead investigator Dr Nino Künzli (University of Southern California Keck School of Medicine, Los Angeles). "Of course, these findings need to be corroborated in more focused, more specified studies. It will be particularly important to see how specific subgroups might be affected, because there is evidence that people with a higher subclinical state of inflammation might be susceptible."

The results of the study are published in the February 2005 issue of Environmental Health Perspectives.

Künzli told heartwire that there is previous evidence supporting the hypothesis that air pollutants lead to long-term systemic inflammation. Animal studies have also shown that inhalation of ambient particulate matter promotes oxidative lung damage, including alveolar and systemic inflammatory responses. One study, in hypercholesterolemic rabbits, showed large increases in inflammatory markers in the lung and vasculature after four weeks of exposure to pollution, he noted.

To understand the association between atherosclerosis and long-term exposure to air pollution in humans, the investigators evaluated 798 participants with no clinical signs or symptoms of cardiovascular disease from two clinical trials. Used as a quantitative measure of subclinical atherosclerosis, changes in the carotid artery intima-media thickness (IMT) was the primary end point of the analysis. Air quality was collected from monitoring stations throughout the Los Angeles area, measuring ambient particulate matter up to 2.5 µg in diameter (PM_2.5). Particulate-matter concentrations ranged from 5.2 to 26.9 µg/m³, depending on the neighborhood.

Investigators report that carotid IMT increased with worsening air conditions. For individuals exposed to 10 µg/m³ of the particulate matter, carotid IMT increased by 5.9% in an unadjusted analysis. Künzli noted that adjusting for other covariates still showed robust increases in carotid IMT. When PM_2.5 levels were categorized into quartiles, greater exposure to the particulate matter resulted in greater increases in carotid IMT, a trend that was statistically significant.

He noted that among older subjects, women, never smokers, and those who reported taking lipid-lowering treatment at baseline the association between levels of PM_2.5 and carotid IMT were stronger. The next steps will involve studying how pollution may promote atherosclerosis in these specific subgroups.

One of the strengths of the study, added Künzli, was the dense network of monitoring stations that allowed investigators to construct a virtual map of air pollution throughout the Los Angeles area. Based on this information, investigators were able to assign long-term mean ambient concentrations of PM_2.5 to every individual in the study, helping them create a very reliable model of pollution exposure that they will use in future studies.

"As a rule of thumb, the more you move inland toward the mountains, which actually block movement of air, the warmer it is, and the entire mixture seems to get cooked up into quite a toxic mixture of pollutant," said Künzli. Inland regions, such as San Bernardino and Riverside, had the highest levels of pollution, he noted.