Polluted air impairs neurons that regulate heart rate in mice.

Pham, H, AC Bonham, KE Pinkerton and CY Chen. 2009. Central neuroplasticity and decreased heart rate variability following particulate matter exposure in mice. Environmental Health Perspectives doi: 10.1289/ehp.0900674.

In mice, short-term exposure to fine particulate matter reduces responsiveness of specialized neurons that regulate cardiac rhythm. Scientists at the University of California Davis believe that this reduced activity may be responsible for the cardiovascular disease associated with air pollution.

Fine particulate matter known as PM2.5 is a mixture of particles that are smaller than 2.5 micrometers (about one third of the diameter of a human hair). PM2.5 is the product of combustion and is released into the environment by forest fires and by gasses emitted by power plants, factories and automobiles.

Small particles are more damaging because they pass through the nose and throat and enter the lungs. Exposure to fine particles is associated with respiratory problems, heart disease and premature death.

According to estimations by EPA, each year approximately 20,000 people die as the result of exposure to PM2.5 and many more are hospitalized. Surprisingly, deaths due to PM2.5 exposure have stronger association with cardiovascular disorders such as heart failure, arrhythmia and ischemic heart disease rather than respiratory problems. This is the first study to show that exposure to PM2.5 increases the risk of cardiovascular disease by altering neuronal activity.

In order to understand the effects of PM2.5 air pollution on heart function, researchers exposed mice to PM2.5 in the form of soot or soot containing iron for three days. Soot and iron are typical environmental pollutants.

These mice had special implants that allowed researchers to monitor the beat-to-beat alterations in heart rate or HRVs (Heart Rate Variations). Reduced HRVs are a sign of cardiovascular problems.

In a parallel study, they also chemically inhibited different set of neurons in the brains of unexposed mice to pinpoint which neurons are important for reducing HRVs. Then, isolated the same section of brain in the PM2.5 exposed mice and recorded neuronal activity.

Mice, breathing air containing soot or soot-iron for 3 days, had significantly lowered levels of vagal neuron activity and reduced HRVs that lasted for 48 hours. Presence of iron exacerbated the effects of PM2.5.

Researchers believe that metals trigger lung inflammation that contributes to the reduction of HRVs. Their findings suggest that short term exposure to PM2.5 alters the activity of vagal neurons that control cardiac output.

In this study, mice were exposed to PM2.5 levels that were about six times higher than the recommended maximum daily exposure set by the Clean Air Scientific Advisory Committee (CASAC). In rare occasions, air pollution does reach these levels. For example, in June of 2008, agencies designated by EPA recorded similar high levels of PM2.5 in areas near the wildfires of California.