Key Point

Air pollution may be linked to subclinical atherosclerosis, thus increasing the risk for heart disease in urban populations.

LOS ANGELES—Air pollution adversely affects lung health and is a known contributor to asthma and COPD exacerbations. New research suggests that air pollution may also be associated with artery thickening and hardening, and thus with cardiovascular disease (CVD).¹

Nino Künzli, MD, PhD, and colleagues analyzed the association between carotid intima-media thickness (CIMT), a marker of subclinical atherosclerosis, and long-term exposure to ambient particulate matter up to 2.5 μm in diameter (PM_2.5) in 798 participants in Los Angeles. Participants were free of CVD at baseline, but they had biomarkers such as slightly elevated levels of LDL cholesterol or homocysteine—indicating that they were at risk for future CVD. According to Dr. Künzli, an Associate Professor of Preventive Medicine at the Keck School of Medicine in Los Angeles, “Our study suggests that pollutants have chronic long-term effects on processes that ultimately lead to CVD. The burden of CVD is large, and air pollution affects almost the entire population; therefore, the public health burden of air pollution on CVD may be substantial.”

SMOGGY AIR, BAD NEWS

Annual mean PM2.5 concentrations in the Los Angeles study area ranged from 5.2 to 26.9 μg/m³. Overall, for each 10-μg/m³ increase in fine particles around the home, the two inner layers of the carotid artery thickened by about 4% to 5%, after adjustment for confounding variables. Participants with the highest exposure had a 10% increase in CIMT compared with participants who had the lowest exposure. Dr. Künzli hypothesized that “air pollutants initiate pulmonary and systemic inflammation. This subclinical inflammation may be chronically sustained given that exposure to these pollutants happens 24 hours a day.” The association between CIMT and air pollution was strongest in women, who had an increase of 6% to 9% per 10 μg/m³ PM_2.5. Women older than 60 were particularly affected: Their CIMTs increased by 14% to 19%. Dr. Künzli believes that the gender difference could be due to the fact that women spend more time around the home than men do. Alternatively, he speculated that “the postmenopausal phase is a period with higher susceptibility to atherogenesis, and the additional inflammatory stress [from pollution] amplifies this susceptibility.” Participants taking lipid-lowering medication were also at significant risk, with CIMT values that increased by 12% to 16%.

WHAT'S NEXT?

Dr. Künzli’s study evaluated healthy people, and it is not known how pollution affects CVD risk in patients who have preexisting heart disease or other disorders that involve a cardiac component, such as pulmonary hypertension or advanced COPD. However, Dr. Künzli acknowledged that studies suggest that these patients are at a higher risk of CVD events on days when pollution levels are high.

It is difficult to give useful advice to patients about air pollution. However, Dr. Künzli urged people to “give strong support to all those who promote strong and sustained clean air policies.” He believes that his team’s atherogenesis hypothesis must be investigated in different populations and that prospective studies must be done to evaluate whether atherosclerosis develops faster among those exposed to higher levels of pollution. Because atherogenesis is a process that occurs over the course of a lifetime, he believes that the hypotheses must be evaluated in young people, “to understand how early pollution contributes to these subclinical processes.”

—Tamara Gibb

Reference
1. Künzli N, Jerrett M, Mack WJ, et al. Ambient air pollution and atherosclerosis in Los Angeles. Environ Health Perspect. 2005;113:201-206.

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