Fatimah Waseem, USA TODAY
Inhaling motor vehicle emissions may transform good, protective cholesterol into bad, artery-clogging cholesterol that increases the risk of heart disease and stroke, says a new study by researchers at the University of Washington and the University of California-Los Angeles.
Conducted on mice, the study is the first to suggest auto emissions strip good cholesterol - high-density lipoprotein, or HDL - of its protective ability to purge bad cholesterol - low-density lipoprotein, or LDL - from the blood and block oxidation, a process that inflames blood vessels and hardens arteries.
In fact, HDL became dysfunctional and worked with its natural enemy - LDL - to enhance the inflammation, oxidation and hardening of arteries, known as atherosclerosis, that occurs when it is exposed to auto emissions, even one week after exposure to those emissions.
Atherosclerosis is a leading cause of heart disease, according to the Centers for Disease Control and Prevention. Since the research was conducted in mice, it will need to be tested in the future in humans, the researchers say.
Researchers exposed one group of mice to vehicle emissions and another group to diesel exhaust similar to air pollution mine workers are exposed to daily, an "extreme" amount of exposure that "mimics years of exposure" to normal vehicle emissions, said Robert Brook, associate professor of cardiology at the University of Michigan.
Both groups then were exposed to clean filtered air - the first for one week, the second for two weeks - and neither recovered from blood and liver damage.
"The biggest surprise was finding that after two weeks of exposure to vehicle emissions, one week of breathing clean filtered air was not enough to reverse the damage," said study author Michael E. Rosenfeld, a professor of environmental occupational health sciences and pathology at the University of Washington.
Because the study was conducted on mice genetically manipulated to have increased risk of clogged arteries, more research is necessary to determine if HDL dysfunction is reversible, said lead author and UCLA associate professor Jesus Araujo.
Follow-up studies should examine if similar abnormalities arise in humans, if HDL directly enhances atherosclerosis, and how long-term, real-world exposure levels can affect HDL, Brooks said.
UCLA researchers plan to study the time required to reverse cholesterol dysfunction, what particles are responsible for the changes, and the minimum time exposure required to trigger changes. All HDL particles have short life spans, suggesting the immediate effects of exposure may be reversible within a couple of weeks, Brooks said.
The research adds to a growing body of evidence linking air pollution with atherosclerosis and heart disease.
For example, after examining arteries of more than 5,000 men and women over three years, researchers at the University of Washington and the University of Michigan found that exposure to air pollution increased risk of stroke by 2%. That was true even after they took into account smoking, race, education and other socioeconomic factors. Published in the April edition of PLOS Medicine, the research was one of the first to explore how air pollution may cause heart disease.
"We suggest that people try to limit their exposure to air pollutants, as they may induce damage that starts during the exposure and continues long after it ends," study author and UCLA researcher Fen Yin said.
Inflammatory diseases such as rheumatoid arthritis, lupus, diabetes and end-stage renal disease also trigger the formation of dysfunctional HDL.
The study was published in the June edition of Arteriosclerosis, Thrombosis, and Vascular Biology, a publication of the American Heart Association.