Published on May 28th, 2016 | by James Ayre0
Decade-Long Study Reveals Biological Process Behind Air-Pollution-Induced Heart Disease
Originally published on CleanTechnica.
While long-term exposure to air pollution has long been known to increase the risk of heart disease, the specific mechanisms behind the association have remained somewhat opaque.
A recent decade-long study following the lives of over 6,000 US residents has shed some new light on the subject, though — revealing the way that people living in areas with “higher” levels of outdoor air pollution “accumulate deposits in the arteries that supply the heart faster than do people living in less polluted areas.”
“Higher” levels of outdoor air pollution in this case refers to levels that are actually quite common in many regions of the US nowadays. And certainly elsewhere as well.
The findings — resulting from an analysis of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) — show that even outdoor air-pollution levels below current regulatory standards accelerate the progression of atherosclerosis (hardening of the arteries, associated with heart attacks). The researchers used CT scanners to repeatedly and regularly measure calcium deposits in the heart arteries of those taking part in the study.
“The study provides important new information on how pollution affects the main biological process that leads to heart disease,” commented Dr Joel Kaufman, who directs MESA Air and is the lead author of the published paper. “The evidence supports worldwide efforts to reduce exposures to ambient air pollutants.”
“This was the most in-depth study of air pollution exposures ever applied to a large study group specifically designed to examine influences on cardiovascular health.”
The press release provides more:
The researchers calculated each participant’s exposure to ambient fine particulate matter that is less than 2.5 microns in diameter and too small to be seen by the naked eye. In addition to PM2.5, they also measured exposure to nitrogen oxide and nitrogen dioxide, and black carbon or soot.
The research team collected thousands of air pollution measurements in the study participants’ communities and at their homes. The research team developed and applied computational models that included local information on land use, roadway and traffic volumes, weather conditions, and local sources of air pollution. These models could generate accurate pollution concentrations at each person’s home. Meanwhile, between the years 2000 and 2012, participants visited study clinics several times to undergo CT scanning to determine the amount of calcium deposits in their heart arteries.
Results were strongest for fine particulate matter and the traffic-related pollutant gases called oxides of nitrogen. The study found that for every 5 µg/m3 higher concentration of PM2.5, or 35 parts per billion higher concentration of oxides of nitrogen — about the difference between more and less polluted areas of a US metropolitan area — individuals had a 4 Agatston units/year faster rate of progression of coronary artery calcium scores. This is about a 20% acceleration in the rate of these calcium deposits.
“The effects were seen even in the United States where efforts to reduce exposure have been notably successful compared with many other parts of the world,” Kaufman continued.
“Exposures were low when compared to US ambient air quality standards, which permit an annual average PM2.5 concentration of 12 µg/m3. The participants in this MESA-Air study experienced concentrations between 9.2 and 22.6 µg/m3.”
The research is outlined in a new paper published in The Lancet.