Exposure to diesel exhaust may render friendly, cholesterol-fighting molecules incapable of performing their important job. A new study suggests that the traffic air pollutant may prevent good cholesterol from battling the bad, artery-clogging cholesterol that promotes heart attack and stroke.
The study’s team included environmental health scientists led by Michael E. Rosenfeld at the UW School of Public Health and heart disease specialist Jesus Araujo and his colleagues in the Division of Cardiology at the University of California, Los Angeles. Their paper, published in the June issue of Arteriosclerosis, Thrombosis, and Vascular Biology, is the first to report that exposure to traffic sources of air pollution — diesel exhaust from combustion engines — can alter the protective nature of normal high-density lipoprotein, or HDL, and set in motion biological mechanisms that lead to cardiovascular disease.
Best known for its ability to scavenge harmful “bad” cholesterol from blood vessels and excrete it from the body, HDL is also an antioxidant powerhouse. Set against bad cholesterol — low-density lipoprotein or LDL — HDL blocks oxidation, a process that induces inflammation in the blood vessels and leads to the hardening of arteries, explained Rosenfeld, professor of environmental and occupational health sciences. But that’s not all. An additional virtue of HDL’s “goodness” lies in its ability to prevent inflammation caused by white blood cell patrols honing in tissues antagonized by air pollution particulates.
All of this adds up. Scoring high levels of HDL in blood tests at the doctor’s office has generally been accepted as protective against cardiovascular disease. Higher levels of HDL mean less risk of heart attack and stroke. That is, until now.
Researchers found that exposure to diesel exhaust led to the loss of the anti-oxidant and anti-inflammatory properties of the HDL.
“It turned the good cop into a bad cop,” said study co-author Timothy Larson, UW professor of environmental and occupational health sciences.
HDL normally performs protective functions, but if the molecules are exposed to pollution, they lose their protective quality.
In the arm of the study completed at the UW, mice were exposed to diesel exhaust over a two-week period at levels comparable to those we encounter everyday. The lab is one of the few in the country that can accurately simulate ambient air pollution exposures in a controlled environment. Results of the mice’s exposure were compared to a control group that received only clean filtered air. In a second experiment, a third group was exposed to diesel exhaust for two weeks and filtered air for an additional week. Researchers wanted to assess whether a week was sufficient time for the HDL to return to normal.
“What was really surprising: the one week of recovery time was not sufficient,” said Rosenfeld, who is also a UW professor of pathology. “This has some pretty significant implications for how exposure to air pollution can impact development of cardiovascular disease. Even short-term exposures to pollution can have pretty long-term effects.”
The National Institute of Environmental Health Sciences, one of the National Institutes of Health, supported the research through grant number R01 ES016959/ES/NIEHS.