By Janet Raloff
Cholesterol poses a cardiovascular risk once it becomes transformed into an inflammatory building block of artery-clogging plaque. That process, which happens all the time, is triggered by oxidation. A new study finds that breathing nanoscale particles spewed by diesel-fuel combustion—also a common occurrence—may turn on genes that multiply cholesterol’s inflammatory and atherosclerotic risks.
André Nel of the David Geffen School of Medicine at the University of California, Los Angeles and his colleagues subjected cells from the lining of human arteries to oxidized cholesterol or diesel particulates. Some 2,500 genes changed their activity in response to both insults. Among this group, the researchers discerned what Nel calls “a genetic footprint” of heightened activity by genes whose activity promotes inflammation.
Pairing a low concentration of diesel particles with a high concentration of oxidized cholesterol ratcheted up the unwanted activity of some of these genes to 15 times the activity triggered by either of the agents alone. Nel’s team reports similar genetic changes in mice engineered to develop high cholesterol, when they were exposed to Los Angeles traffic for 5 hours per day, 3 days a week, for 2 months.
The findings were published online July 26 in Genome Biology, an online journal.
People who eat fatty foods or who have a genetic predisposition to high cholesterol can’t completely avoid air pollution’s exacerbating impacts by moving to remote areas. “You probably will be exposed to far more ultrafine [combustion] particles in Los Angeles,” Nel says, but emerging data show that once emitted, such particles travel long distances—even across oceans. In other words, he notes, “they’re everywhere.”
