Airborne particles less than 2.5 micrometers in diameter (PM2.5) and black carbon, a marker for traffic exhaust fumes, can adversely affect the heart’s ability to conduct electrical signals in people with serious coronary artery disease, according to a new study published online 8 September in the American Heart Association’s journal Circulation.
In a recent study of 48 Boston-area patients, all of whom had coronary artery disease, 24-hour Holter monitors were used to examine electrocardiograms for the conductivity change called an ST-segment depression, which may indicate inadequate blood flow to the heart or inflamed heart muscle. The average 24-hour levels for all pollutants included in the analysis were below accepted or proposed National Air Quality Standard thresholds—meaning patients were breathing air technically considered healthy.
We found that an elevation in fine particles, from non-traffic as well as traffic sources, and black carbon, a marker for traffic, predicted ST-segment depression. Effects were greatest within the first month after hospitalization, and for patients who were hospitalized for a heart attack or had diabetes.— Diane R. Gold, M.D., M.P.H., senior author
The ST-segment changes Gold observed were not associated with symptoms in these patients, all of whom had experienced in-hospital procedures to examine or open up their coronary arteries.
Previous studies have documented that exposure to road traffic can trigger heart attacks, and that particulate air pollution increases the risk for cardiac death or heart attack. A study in 2002, cited by Gold, found that when coal sales were banned in Dublin, Ireland, black smoke concentrations declined by 70% within the next 72 months and cardiovascular deaths fell by 10 percent.
The new findings expand the evidence that air pollution can affect heart health, either through inflaming the heart muscle or through reducing blood flow to the heart. It suggests the need for greater vigilance by physicians and heart patients in the weeks after discharge from the hospital, researchers said.
The American Heart Association and the American College of Cardiology recommend that some heart patients, particularly those who have had a heart attack, delay driving for two to three weeks after leaving the hospital and avoid driving in heavy traffic because of the stress it creates.
Our study provides additional rationale to avoid or reduce heavy traffic exposure after discharge, even for those without a heart attack, since traffic exposure involves pollution exposure as well as stress.—Diane Gold
The study’s 48 participants had been hospitalized for either a heart attack, unstable angina or worsening symptoms of stable coronary artery disease. Their median age was 57 years, 81% were male, 40% had suffered a heart attack and 25% had diabetes.
Researchers visited the patients two to four weeks after their discharge, and then three more times at approximately three-month intervals. At each visit, a portable electrocardiograph called a Holter monitor recorded the patients’ heart activity for 24 hours. All participants were monitored on the first visit, and 35 had monitoring on more than one visit. Researchers averaged monitor readings over each half-hour, providing 5,979 half-hour observations. They then examined the relation of these ECG measurements with levels of several pollutants, including black carbon, produced by the incomplete combustion of fossil fuels, and PM2.5.
Researchers obtained the PM2.5 and black carbon readings at a Harvard School of Public Health monitoring site, an average distance of 10.9 miles from the participants’ homes.
Among the study’s findings:
Increased levels of PM2.5 and black carbon were associated with ST-segment depression in the study participants.
Sulfur dioxide, a pollutant that can have non-traffic sources, also was associated with ST-segment depression.
No significant correlation was found between ST-segment depression and increased levels of carbon monoxide, but levels of this pollutant were low in this study.
Patients recovering from a heart attack had greater changes in ST segment depression on electrocardiograms compared to other participants.
How breathing air polluted by PM2.5 and black carbon might cause ST segment depression remains to be discovered.
Further research is needed to evaluate whether the pollution-related ST-segment depression that we see is related to increased heart muscle inflammation, reduced oxygen flow, oxidative stress, or increased risk of arrhythmias. We think that our findings, which are definitely subclinical, may represent a process that increases clinical risk for people with symptomatic coronary artery disease.—Diane Gold
The National Institute of Environmental Health Services, the Environmental Protection Agency, and the National Science Council funded the study.
Kai Jen Chuang, Brent A. Coull, Antonella Zanobetti, Helen Suh, Joel Schwartz, Peter H. Stone, Augusto Litonjua, Frank E. Speizer, and Diane R. Gold (2008) Particulate Air Pollution as a Risk Factor for ST-Segment Depression in Patients With Coronary Artery Disease. Circulation, Sep 2008; doi: 10.1161/CIRCULATIONAHA.108.765669