Experimenting on mice, the team from the University of California in Los Angeles (UCLA), and other institutions, found that just two weeks of exposure to emission particles was enough to cause blood and liver damage that was not reversed by a week of receiving filtered air.
The researchers found vehicle emissions can trigger a change in high-density lipoprotein (HDL) cholesterol, altering its cardiovascular protective qualities.
The mice were exposed to diesel exhaust for a few hours a day, several days a week, at a particulate mass concentration within the range mine workers are usually exposed to.
The researchers analysed blood and tissue specimens and checked if the protective antioxidant and anti-inflammatory properties of the ‘good’ HDL cholesterol were still intact, and found that many of the positive properties of HDL were markedly altered after air-pollutant exposure. The exposed mice had a significantly decreased ability to protect against oxidation and inflammation induced by ‘bad’ low-density lipoprotein (LDL) cholesterol.
“This is the first study showing that air pollutants promote the development of dysfunctional, pro-oxidative HDL cholesterol and the activation of an internal oxidation pathway, which may be one of the mechanisms in how air pollution can exacerbate clogged arteries that lead to heart disease and stroke,” said senior author Dr Jesus Araujo, associate professor of medicine and director of environmental cardiology at the David Geffen School of Medicine at UCLA.
First author and researcher in the division of cardiology at the Geffen School of Medicine, Fen Yin, encouraged people to be vigilant around vehicle emissions.
“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,” Yin said.
The study was funded by the US National Institute of Environmental Health Sciences; the National Heart, Lung and Blood Institute; and the US Environmental Protection Agency.