Even low levels of traffic pollution tied to heart damage
Air pollution has long been linked to increased risk of heart ailments, yet less is known about how they alter structure, function of heart.
People exposed to even low levels of air pollution are more likely to develop structural changes in the heart that can be a precursor to heart failure, a UK study suggests.
While exposure to air pollution has long been linked to an increased risk of heart attacks and strokes, less is known about how pollutants might alter the structure and function of the heart, the study team writes in Circulation.
Researchers looked at data on exposure to traffic-related air pollution and results from heart MRIs for 3,920 adults who did not have cardiovascular disease. They found that previous exposure to tiny particles known as PM2.5, which include dust, dirt, soot and smoke, and to nitrogen dioxide, a poisonous gas in car exhaust, were associated with enlargement on both sides of the heart.
“Air pollution appears to be damaging for cardiovascular health even at a relatively low exposure level,” said lead study author Nay Aung of Queen Mary University of London.
Individuals exposed to higher level of air pollutants were more likely to have larger cardiac ventricles (main pumping chambers) after accounting for potential factors that can independently influence the size of these chambers, Aung said by email.
“This is important because these observed changes in the heart were similar to the patterns seen in heart failure development,” Aung said.
To assess exposure to traffic fumes, researchers examined data on average annual air pollution levels at participants’ home addresses at the start of the study.
Half of the participants were exposed to average annual concentrations of less than 9.9 micrograms of PM2.5 particles per cubic meter of air (ug/m3) and 28.2 ug/m3 of nitrogen dioxide.
For fine particulate matter, that’s well within UK guidelines limiting average exposure to no more than 25 ug/m3 of PM2.5, although the World Health Organization (WHO) has said there are no safe limits for PM2.5 exposure, Aung and colleagues note in Circulation.
Researchers measured participants’ heart structure with MRIs a median of 5.2 years after assessing their air pollution exposure.
For every extra 1 ug/m3 of PM2.5 and every additional 10 ug/m3 of nitrogen dioxide people were exposed to near their homes, their hearts were enlarged by approximately 1 percent, the study found.
The type of enlargement seen in the study is a “well-recognized . . . adaptation heralding heart failure development,” the authors note.
Heart failure happens when the heart muscle is too weak to pump enough blood through the body. Symptoms can include fatigue, weight gain from fluid retention, shortness of breath and coughing or wheezing. Medications can help strengthen the heart and minimize fluid buildup in the body.
The study wasn’t a controlled experiment designed to prove whether or how air pollution might directly cause enlargement in the heart.
It’s possible that when people inhale polluted air it causes inflammation in the lungs and blood vessels and fine particulate matter enters the bloodstream, said Benjamin Horne, director of cardiovascular and genetic epidemiology at Intermountain Medical Center Heart Institute in Salt Lake City, Utah.
This can overwork the heart, Horne, who wasn’t involved in the study, said by email.
“Even people who are free from cardiovascular disease may, over time, develop diseases due to chronic exposure to air pollution,” Horne said.