Auto Emissions Transform Cholesterol from Good to Bad

University of Washington researchers along with the University of California Los Angeles recently conducted an interesting study about emissions and health. The study found that the inhalation of emissions from vehicles may actually change beneficial cholesterol into the harmful, plaque causing cholesterol that blocks vessels and can cause heart disease and stroke.

The research was done with mice, and is the first of its kind to find that emissions actually transform the good HDL (high density lipoprotein), taking away its ability to rid vessels of the bad LDL type protein – low density lipoprotein. LDL causes oxidation in the bloodstream, which in turn causes inflammation there and hardening of the arteries.

Amazingly, the HDL (good cholesterol) actually switched sides and worked with the bad LDL to create more inflammation, hardening and oxidation in the vessels. Hardening of the arteries, or atherosclerosis, happened even as soon as one week after exposure to the auto emissions.

According to the Centers for Disease Control and Prevention, atherosclerosis can be deadly as one of the leading causes of heart disease. This first study was conducted on mice and will have to be repeated with human subjects in order to gather further data, say researchers.

To do the study, the researchers took two groups of mice for comparison. One was exposed to vehicle emissions, and the other was exposed to the type of diesel exhaust that mimics a more extreme exposure, such as the long term exposure of mine workers to air pollution. Robert Brook, associate professor of cardiology at University of Michigan, said that the latter type of exposure “mimics years of exposure.” After the exposure, both groups of mice were placed in a clean filtered air environment. The first group had one week of clean air, and the second had two weeks of clean air. Neither group recovered from the blood and liver damage.

Michael E. Rosenfeld, professor of environmental occupational health sciences and pathology at the University of Washington, is one of the study’s authors. He 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.”

The mice used during the study had been genetically manipulated to have a higher risk of developing atherosclerosis. Due to this, further studies will have to be done to decide if HDL damage is reversible, says Jesus Araujo, UCLA associate professor and lead author of the study.

Further testing will focus on finding the same changes in human cholesterol. Brooks says that the HDL enhancement of atherosclerosis will be studied as well as extended exposure at real world levels and its effect on HDL. At UCLA, researchers will be looking deeper into reversal of the cholesterol dysfunction and which specific particles are involved in the changes. They will also attempt to determine the smallest amount of exposure time required to cause them. Brooks says that HDL has a short life span, which may mean that reversing the harmful changes may be possible in a couple of weeks.

Research regarding air pollution and its link to heart disease has been ongoing for years. At the University of Washington and University of Michigan, air pollution was found to increase stroke risk by 2%, regardless of other risk factors. This was one of the very first studies of air pollution and cardiovascular disease.

Fen Yin, researcher at UCLA and study author, said, “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.”

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