|Volume 6 Issue 313 Published - 14:00 UTC 08:00 EST 8-Nov-2004 Next Update - 14:00 UTC 08:00 EST 9-Nov-2004||Editor: Susan K. Boyer, RN
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Air pollution may cause and speed up artery disease
Air pollution may trigger and accelerate narrowing of carotid arteries, according to a study presented at the American Heart Association's Scientific Sessions 2004.
Researchers found an association between long-term air pollution exposure and the early stages of atherosclerosis (hardening of the arteries).
"We knew that people in more polluted areas die earlier from cardiovascular disease, but it was not clear how early in the disease process air pollution contributes. Our study found that air pollution may contribute to cardiovascular problems at a very early stage of the disease, similar to smoking, and enhances atherosclerosis, which is the underlying disease process of cardiovascular diseases," said study author Nino Kuenzli, M.D., Ph.D., associate professor, division of environmental health, Keck School of Medicine at the University of Southern California in Los Angeles.
Researchers reviewed data from two clinical trials on 798 people age 40 and older who lived in the Los Angeles area. The data included baseline measurements of the thickness of the inner lining of participants' neck arteries (carotid artery intima-media thickness or CIMT). CIMT is measured by ultrasound and used to determine the level of subclinical atherosclerosis.
Researchers then assigned a PM2.5 particle level to the study subjects' home ZIP codes. PM2.5 particles are pollutants with a diameter of 2.5 micrometers or less. They are commonly produced by burning fossil fuels such as driving cars, and smelting and processing metals. They are tiny enough to be inhaled into the smallest airways.
PM2.5 levels are measured in micrograms per meter cubed (ug/m3). In this study, readings ranged from 5.2 to 26.9 ug/m3.
For every 10 ug/m3 increase of PM2.5, CIMT increased by 5.9 percent. After adjusting for age, socio-demographic, lifestyle (including active and passive smoking) and physiological factors, researchers determined that CIMT rose by 3.9 percent to 4.3 percent for every 10 ug/m3 increase in PM2.5. The association between air pollution and CIMT was even greater among people over age 60, women and people taking cholesterol-lowering medication.
Overall, the strongest association was seen in women age 60 or older, with a 15.7 percent increase in CIMT for every 10 ug/m3 increase of PM2.5.
Kuenzli said that the air pollution causes the body to produce oxidants (unstable molecules) that cause inflammatory reactions in both the respiratory tract and blood vessels, triggering artery damage. Some air particles find their way into the blood or even the brain, he said. Other constituents of air pollution may be neutralized locally, but secondary reaction products may still cause systemic responses. "The responses may involve both the autonomic nervous system (which controls breathing and blood pressure) and inflammation in the blood. Both pathways together can lead to a state of subclinical chronic inflammation, causing adverse consequences in the blood vessels where oxidized lipids damage the artery walls. This can lead to thickening of the artery wall, calcification and plaques – and ultimately ruptures," Kuenzli said.
"It is interesting that the effects of air pollution were particularly strong in older women. Also, those with increased cardiovascular risk profiles appeared to be at higher risk of an association between air pollution and narrowing of the arteries," he said.
"However, the study is too small and not designed to clarify whether effects are truly different in men and women, old and young, or whether part of the differences are caused by uncertainties such as in how exposure was assessed," Kuenzli said.
"Given that cardiovascular disease is the leading cause of death, and that large populations are exposed to ambient PM2.5 at the levels observed in this study, these findings need to be corroborated. The public health implications could be immense," he said.
Co-authors are Wendy J. Mack, Ph.D.; Howard N. Hodis, M.D.; Michael Jerrett, Ph.D.; Laurie LaBree, M.S.; Frank Gilliland, M.D., Ph.D.; Duncan Thomas, Ph.D.; John Peters, M.D., Sc.D.; and doctoral student Bernardo Beckermann.
Statements and conclusions of study authors that are published in the American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect association policy or position. The American Heart Association makes no representation or warranty as to their accuracy or reliability.
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