Numerous studies have linked heart disease and air pollution, particularly smog. Smog--a toxic brew of chemicals and molecules such as ozone--seems to exacerbate heart disease, leading to an increase in heart attacks and fatalities. But researchers have yet to discover the pathway by which smog impacts the cardiovascular system. Now a new study shows how ozone's byproducts in the body can harden arteries and cause heart disease.
Chemist Paul Wentworth, Jr., of the Scripps Research Institute and his colleagues tested such byproducts--known as atheronals--in vitro. These molecules form when ozone and cholesterol interact. "Cholesterol makes up 40 percent of most of your membranes, including those in your lungs," Wentworth explains. "If you inspire smog, there directly is the interaction."
The team's previous research had shown that the white blood cells responsible for inflaming arterial walls also produce ozone and, ultimately, the atheronals: atheronal-a and atheronal-b. These compounds are present in the plaque removed from clogged arteries. The new research shows that when the atheronals interact with various blood cells, they produce some of the effects known to lead to heart disease, such as causing a malfunction in the cells that line arterial walls. "The atheronals can actually cause all the relative aspects that are known to promote cardiovascular disease," Wentworth notes.
On supporting science journalism
If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.
It remains unclear whether the atheronals typically derive from interactions in the bloodstream or in the lungs. "My sense is that it's a combination of both," Wentworth says. And more research will be needed to determine whether atheronal levels in the blood speed the onset of heart disease such as atherosclerosis. Nevertheless, the scientists write: "the atheronals may be a heretofore unrecognized chemical player in the known linkage between environmental pollution and cardiovascular disease." The research will appear in the June 13 issue of Biochemistry.
