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 g/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
Contact: Charlotte Webber