The Smog to Heart Connection
It is well known that certain concentrations of air pollution can adversely affect human respiratory condition. What is not as well-known is how air pollution can affect the heart. A new study presented at the American Heart Association's Basic Cardiovasular Sciences 2010 Scientific Session by researchers from Texas A&M links ground-level ozone (smog) to cell deaths in the heart.
Ozone (O3) is extremely beneficial to the planet while it is in the upper atmosphere. From there, it blocks damaging ultraviolet light from reaching the planet surface. However, near the ground, it is a harmful and reactive air pollutant. It is created from the reaction of sunlight on air containing NOx or hydrocarbons. These pollutants are cause be vehicle exhaust or other fossil fuel burning operations. Therefore, ozone is a not a direct product, but an indirect product of fuel emissions. Ozone is one of the primary constituents of smog which also includes particulate matter, volatile organic compounds, and water vapor (fog).
The researchers indicate that chronic ozone exposure increases the sensitivity to myocardial (heart muscle) dysfunction. The heart muscle is one of three main types of muscle in the human body along with skeletal and smooth muscle. It is well adapted to be resistant to fatigue and are assured of a constant and abundant blood supply.
To test their theory, the researchers used rats exposed to clean air or air containing 0.8 ppm ozone for eight hours per day. The experiment was also conducted over varying durations — 28 days and 56 days. After completion, the cardiac functions of the rats exposed to ozone were significantly less than those exposed to clean air.
The ozone-exposed rats had higher levels of TNF α (tumor necrosis factor-alpha). The increase in TNF α has been shown to cause a decrease in Cav1 (Caveolin-1) levels. Cav1 is a protein that is the main component of the caveolae membranes found in most cell types. It acts as a tumor suppressor and serves an important function in promoting the cell cycle progression. Decreases in Cav1 can lead to cell dysfunction and possibly cell death.
This is the first time a link has been made connecting ozone to Cav1 in the heart muscle. Researchers hope this information will help to better understand the mechanisms behind ozone-caused cardiac dysfunction. Then it can be used to guide policies to determine property air quality standards in order to protect the millions of citizens living in smoggy, urban environments.
For more information: http://www.americanheart.org/presenter.jhtml