An international team of scientists has found that breathing car emissions triggers a change in high-density lipoprotein, sometimes called the ‘good cholesterol,’ altering its cardiovascular protective qualities so that it actually contributes to clogged arteries.

According to their paper published in the journal Arteriosclerosis, Thrombosis and Vascular Biology, in addition to changing high-density lipoprotein (HDL) from ‘good’ to ‘bad,’ the inhalation of car emissions activates other components of oxidation, the early cell and tissue damage that causes inflammation, leading to hardening of the arteries.

Emission particles such as those from vehicles are major pollutants in urban settings. These particles are coated in chemicals that are sensitive to free radicals, which have been known to cause oxidation. The mechanism behind how this leads to atherosclerosis, however, has not been well understood.

The team found that after 2 weeks of exposure to vehicle emissions, mice showed oxidative damage in the blood and liver – damage that was not reversed after a subsequent week of receiving filtered air. Altered HDL cholesterol may play a key role in this damaging process.

“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 Prof Jesus Araujo of the University of California’s David Geffen School of Medicine.

One group of mice was exposed to vehicle emissions for two weeks and then filtered air for one week, a second was exposed to two weeks of emissions with no filtered air, and a third was exposed to only clean, filtered air for two weeks.

Study co-author Prof Michael Rosenfeld from the University of Washington said: “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.”

Mice were exposed for a few hours, several days a week, to whole diesel exhaust at a particulate mass concentration within the range of what mine workers usually are exposed to.

After the exposures, the team analyzed blood and tissue specimens and checked to see if the protective antioxidant and anti-inflammatory properties of HDL were still intact. The scientists used special analytical laboratory procedures to evaluate how ‘good’ or ‘bad’ HDL had become. The team found that many of the positive properties of HDL were markedly altered after the air-pollutant exposure.

For example, the HDL of mice exposed to two weeks of vehicle emissions, including those that received a subsequent week of filtered air, had a much-decreased ability to protect against oxidation and inflammation induced by low-density lipoprotein (LDL) cholesterol, known as ‘bad’ cholesterol, than the mice that had only been exposed to filtered air.

Without HDL’s ability to inhibit LDL, along with other factors, the oxidation process may run unchecked. Moreover, not only was the HDL of the mice exposed to diesel exhaust unable to protect against oxidation, but, in fact, it further enhanced the oxidative process and even worked in tandem with the LDL to promote even more oxidative damage.

Researchers also found a twofold to threefold increase of additional oxidation products in the blood of mice exposed to vehicle emissions, as well as activation of oxidation pathways in the liver. The degree of HDL dysfunction was correlated with the level of these oxidation markers.

“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,” said study first author Dr Fen Yin fron the Geffen School of Medicine.

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Bibliographic information: Mohamad Navab et al. 2013. Diesel Exhaust Induces Systemic Lipid Peroxidation and Development of Dysfunctional Pro-Oxidant and Pro-Inflammatory High-Density Lipoprotein. Arteriosclerosis, Thrombosis, and Vascular Biology 33: 1153-1161; doi: 10.1161/ATVBAHA.112.300552