Should we be watching our exposure to airborne pollution as well as our cholesterol levels" Research now indicates that air pollution has a role to play in atherosclerosis (artery hardening), which can contribute to heart attacks or strokes. Findings published in the open access journal, Genome Biology, show how the fats that clog arteries work together with air pollution particles, triggering the genes behind inflammation.
A research team drawn from medical and environmental engineering disciplines at the Universities of California, Los Angeles, investigated the relationship between oxidized phospholipids found in the low density lipoprotein (LDL) particles, the 'bad' fats that clog arteries, and diesel exhaust particles. They exposed cells that line human blood vessels (microvascular endothelial cells) to both exhaust particles and oxidised phospholipids, and measured the effect on genes by using microarray expression profiling. This allowed the identification of gene modules containing a high number of co-expressed genes. These modules appear to be activated by a combination of phospholipids and diesel particles and are linked to vascular inflammation pathways. To confirm these findings, the team exposed mice with high cholesterol levels to the pollutant diesel particles, and saw some of the same gene modules upregulated.
The American Cancer Society has reported a six percent increase in cardiopulmonary deaths for every 10 ìg/m3 rise in particulates. Exactly how airborne pollutant particles cause cardiovascular injury is poorly understood. But it is known that these particles are generally coated with a number of chemicals such as organic hydrocarbons, transition metals, sulfates and nitrates. Organic hydrocarbons and transition metals inflame airways by generating reactive oxygen species and oxidative stress when combined with oxidised phospholipids in the arteries. This can lead to vascular inflammation, which can in turn lead to increased lesions in the clogged arteries, potentially giving rise to blood clots that trigger heart attack or stroke.
These findings bring us closer to understanding the impact our environment has on our health.
Air pollutant chemicals and oxidized lipids exhibit genome-wide synergistic effects on endothelial cells
Ke Wei Gong, Wei Zhao, Ning Li, Berenice Barajas, Michael Kleinman, Constantinos Sioutas, Steve Horvath, Aldons J Lusis, Andre E Nel and Jesus A Araujo Genome Biology (in press)
During embargo, article available at:
After the embargo, article available from the journal website at:
Please quote the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's Open Access policy.
Article citation and URL available on request at email@example.com on the day of publication
Elaine Schmidt (Press Office, UCLA) by phone (310) 794-2272 or via email firstname.lastname@example.org
BioMed Central (http://www.
BioMed Central currently publishes over 160 journals across biology and medicine. In addition to open-access original research, BioMed Central also publishes reviews, commentaries and other non-original-research content. Depending on the policies of the individual journal, this content may be open access or provided only to subscribers.