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Air Pollution Damages Arterial Function
Long-term exposure, but not short-term exposure, to pollution caused artery dilation.
By Nancy Walsh, MedPage Today
Medically Reviewed byDori F Zaleznik, MD
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FRIDAY, Oct. 26, 2012 (MedPage Today) —Long-term exposure to air pollution — and especially fine particulate matter — may be an important risk factor for atherosclerosis, a multi-city study suggested.
An interquartile increase of only 3 µg/m3in exposure to particulate matter less than 2.5 µg in diameter was associated with a decrease of 0.3 percent in flow-mediated dilation of the brachial artery, according to Ranjini M. Krishnan, MD, of the University of Washington in Seattle, and colleagues.
The magnitude of that percentage increase of flow-mediated dilation "is comparable to the effect of 5 years' increase in age, or of active tobacco smoking," the researchers explained online in theJournal of the American College of Cardiology.
Epidemiologic studies have identified an association between air pollution and cardiovascular disease, and experiments have suggested that exposure to air pollution can lead to endothelial dysfunction.
To explore the hypothesis that exposure to particulate matter can lead to persistent endothelial compromise and the attendant effects on the vasculature, Krishnan and colleagues analyzed data from the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA).
The cohort included 3,040 participants living in Chicago, Los Angeles, New York, St. Paul, and Winston-Salem, N.C.
Median age was 61, and the sexes were equally represented. One-third of the participants were white, while the remainder were African-American, Chinese, or Hispanic.
Slightly more than half had never smoked, and 34 percent were taking antihypertensive medications.
Baseline and maximum brachial artery diameter were measured ultrasonographically, and flow-mediated dilation calculated in standard fashion.
MESA employed complex modeling to estimate particulate exposures, utilizing monitoring stations and factors such as proximity to highways and seasonal trends to estimate individual short- and long-term exposures.
The researchers determined that long-term concentrations of fine particulate matter ranged from 10.6 to 24.7 µg/m3, while short-term concentrations were 1 to 74 µg/m3.
Mean baseline artery diameter was 4.3 mm, and flow-mediated dilation was 4.4 percent.
A statistically significant −0.1 percent difference was seen in flow-mediated dilation according to long-term concentration of fine particulate matter, the researchers found.
In contrast, only nonsignificant reductions in flow-mediated dilation were seen for short-term exposures.
This observation of minimal effects with short-term exposure was similar to what has been seen in previous cohort studies, where a 1-day 10 µg/m3increase in exposure was associated with a mortality increase of only 0.1 percent to 0.5 percent, compared with a 10 percent increase seen with long-term exposure.
The association between change in flow-mediated dilation and particulate matter exposure was consistent across the study locations, with the exception of St. Paul, which had lower concentrations of pollutants than the other cities.
The strongest association was seen in Chicago.
Further analysis revealed a large effect for younger age, with a reduction of −0.5 percent in brachial artery dilation.
Greater effects also were seen for women, nonsmokers, and individuals with mild hypertension.
One factor that appeared to ameliorate the influence of particulate matter on endothelial function was the use of angiotensin-converting enzyme inhibitors, possibly through effects on endothelial kinins and nitric oxide, the researchers explained.
Proposed mechanisms by which pollutants could induce changes in blood vessels include inflammation, oxidative stress, and effects on the autonomic nervous system.
"We found that long-term exposure to [fine particulate matter] might produce chronic changes in the brachial artery that negatively affects its ability to react to shear stress, primarily from [nitric oxide]-mediated endothelial dysfunction," observed Krishnan and colleagues.
In an editorial comment, Robert D. Brook, MD, of the University of Michigan in Ann Arbor, and Sanjay Rajagopalan, MD, of Ohio State University in Columbus, noted that an implication of the study was that even modest increases in air pollution levels can have significant and "clinically pertinent" negative effects on vascular function.
"This novel observation should re-awaken us to the fact that even 'invisible' elements, such as chronic exposure to low levels of air pollution commonly encountered in the United States, can have significant adverse effects on [cardiovascular] health," stated Brook and Rajagopalan.
And the health hazards may be worse elsewhere, they suggested.
"When one considers the fact that [fine particulate matter] levels often average 5- to 10-fold higher across numerous regions populated by billions of people worldwide, the grave global public health consequences of air pollution corroborated by the findings of this important study deserve serious and immediate attention," the editorialists concluded.
Limitations of the study included its cross-sectional design and the possibility of measurement errors with the modeling methods used.
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