(NaturalNews) Fine particulate matter, the kind that comes from vehicle exhaust (PM2.5), has recently been found to cause inflammation beyond the lungs. Through specific protein pathways in the immune system, fine particulate matter invites inflammation into the cells, eliciting insulin resistance and heart disease. Moreover, the research finds that a high-fat diet, when coupled with exposure to particulate matter, increases a person's risk for these conditions. Lead researcher Sanjay Rajagopalan, from the University of Maryland Medical Center, singled out complex cellular mechanisms that help explain how particulate matter and a high-fat diet cause inflammation and insulin resistance.
Studying inflammation and insulin resistance through protein pathways
The study centered on a specific protein - CCR2. This protein beckons innate immune cells toward visceral fat cells and liver cells. These insulin-sensitive tissue sites in the body can be inflamed when these immune cells are overworked. This inflammation is observed in animal models of obesity and type 2 diabetes.
The researchers investigated various wild-type mice that produce the CCR2 protein, comparing them with mice that do not produce the protein. All the mice in each group studied were fed a high-fat diet to observe the coupled effects. Then, for 17 weeks, these mice were exposed to either filtered air or air containing 117 µg/m^3 of PM2.5.
Particulate matter exposure associated with increased inflammation and insulin resistance
Wild-type mice exposed to fine particulate matter showed increased levels of liver lipids and inflammation. This was witnessed through elevated SREBP-1c activity, which is protein regulation of fatty acid synthesis. This also translated to increased insulin resistance.
Observations also showed that abnormal insulin signaling was taking place through the AKT pathway. A reduction of phosphorylation of the AKT enzyme caused further inflammation. The researchers noticed that more of this reduction occurred in the mice group exposed to particulate matter. This brought higher levels of inflammation, as seen in elevated levels of F4/80 macrophages in visceral fat storage.
The researchers basically isolated particulate matter as a cause of inflammation in the body and linked it to the recruiting of inflammatory cells through the CCR2 protein pathways.
Rajagopalan says, "This mechanism directly ties a known inflammatory mechanism in the pathogenesis of type 2 diabetes to exposure to environmental air pollution."
The observed inflammatory damage can create a cycle that welcomes other health issues including cardiovascular disease and obesity. Vehicle exhaust particulate matter can now be singled out as a major cause of inflammation in the body which leads to further complications like insulin resistance.
"We should look more closely at these kinds of associations in human epidemiological studies," says Rajagopalan.
Solutions to airborne toxicity may involve the study of superfood antioxidants
The fine particulate matter used in this study can be generated not only from vehicle exhaust but from industrial coal burning as well. This inflammation-causing matter exists at disturbing levels now in major cities around the world. Whole countries, including China, India and some in Latin America, can easily average 100-150 µg/m^3, which translates to similar regional amounts used in this study.
Now, scientists and environmentalists can better understand how intrusive these particles really are in the human body. Pollution goes beyond the lungs; this matter is transported by innate immune cells and carried through specific protein pathways. The toxicity of polluted air definitely has a penetrating power and becomes a significant source of inflammation and insulin resistance.
Changing human behavior and the further spread of fine particulate matter will be an enormous challenge, as many scientists agree. That's why solution should center more on the study of antioxidants in superfoods for their ability to capture specific toxins, protect cells and bring down inflammation.