Commenting on the results, Dr Klsch confirms that long-term exposure to fine PM air pollution and to road traffic noise are both independently associated with TAC as a measure of subclinical atherosclerosis.
"These two major types of traffic emissions help explain the observed associations between living close to high traffic and subclinical atherosclerosis," he says. "The considerable size of the associations underscores the importance of long-term exposure to air pollution and road traffic noise as risk factors for atherosclerosis."
Fine PM and traffic noise are believed to act through similar biologic pathways, thereby increasing cardiovascular risk; they both cause an imbalance in the autonomic nervous system, which feeds into the complex mechanisms regulating blood pressure, blood lipids, glucose level, clotting and viscosity.
TAC, alongside coronary artery calcification (CAC), is a reliable marker of subclinical atherosclerosis. While sharing cardiovascular risk factors with coronary atherosclerosis, TAC like TAC has been shown to be independently related to the incidence of cardiovascular events.
A further study reported at this congress from French investigators found that all the main air pollutants (carbon monoxide (CO), nitrogen dioxide (NO2), sulphur dioxide (SO2), and particulate matter measured as PM10 or PM2.5, but with the exception of ozone (O3)) were significantly associated with an increased risk of myocardial infarction.(3)
|Contact: Jacqueline Partarrieu|
European Society of Cardiology