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Polluted air leads to disease by promoting widespread inflammation (#1950)
Chronic inhalation of polluted air appears to activate a protein that triggers the release of white blood cells, setting off events that lead to widespread inflammation, according to new research in an animal model.
This finding narrows the gap in researchers' understanding of how prolonged exposure to pollution can increase the risk for cardiovascular problems and other diseases.
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The research group, led by Ohio State University scientists, has described studies in mice suggesting that chronic exposure to very fine particulate matter triggers events that allow white blood cells to escape from bone marrow and work their way into the bloodstream.
Their presence in and around blood vessels alters the integrity of vessel walls and they also collect in fat tissue, where they release chemicals that cause inflammation.
The cellular activity resembles an immune response that has spiraled out of control. A normal immune response to a pathogen or other foreign body requires some inflammation, but when inflammation is excessive and has no protective or healing role, the condition can lead to an increased risk for cardiovascular diseases, diabetes and obesity, as well as other disorders.
Though many questions about the beginning of this process remain unanswered, the scientists predict that the damage may originate in fluid that lines the lung.
Tiny molecules in this fluid change structure after being exposed to polluted air, and that change appears to set off this cascade of damaging white blood cell behavior by activating a receptor called "toll-like receptor 4."
The job of toll-like receptor 4, or TLR4, is to recognize specific characteristics of pathogens and then send out signals to activate other players in the immune system.
Mice that lack this molecule don't produce as much inflammation after exposure to pollution as do normal mice, suggesting that TLR4 has a prominent role in the body's response to chronic exposure to particulate matter.
The research is published in a recent issue of the journal Circulation Research.
Many of these researchers already have documented the link between chronic exposure to polluted air and high blood pressure, diabetes and obesity. They now aim to pinpoint how and where the earliest damage occurs.
For this study, the scientists exposed different groups of mice to either filtered air or air containing between eight and 10 times more fine particulates than the ambient air in an urban environment – an average of approximately 111 micrograms per cubic meter. The mice were exposed for six hours per day for five days per week for at least 20 weeks.
The polluted air contained fine particulates that are so tiny – 2.5 micrometers or smaller in diameter, or about 1/30th of the average width of a human hair – that they can reach deep areas of the lungs and other organs in the body.
For most of the experiments, the effects of exposure to pollution were compared in normal mice and mice deficient in TLR4.
"After exposure, there is an increase in oxidized phospholipids in the lung fluid. We know it happens, but we don't know how," Thomas Kampfrath said. "What we do know is that the increase in oxidized phospholipids in turn promotes inflammation."
In an editorial in the same issue of Circulation Research, Daniel Conklin of the University of Louisville wrote, "Is the mystery solved regarding the mechanism how inhaled [fine particulate matter] exposure stimulates vascular inflammation and injury? Well, probably not completely, but the present scenario laid out … connects findings from their study with many disparate human and animal epidemiological/exposure studies into a plausible story."
For more information, contact Sanjay Rajagopalan at firstname.lastname@example.org.
Editor’s note: This public release has been edited for length.
Source: Ohio State University
Author: Emily Caldwell