Chronic exposure to air pollution triggers systemic inflammation.
Cardiovascular diseases (Risk factors)
|Publication:||Name: Townsend Letter Publisher: The Townsend Letter Group Audience: General; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2012 The Townsend Letter Group ISSN: 1940-5464|
|Issue:||Date: April, 2012 Source Issue: 345|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Chronic inhalation of fine particulate matter (PM) has long been
linked to increased morbidity and mortality from ischemic cardiovascular
events; however, until now the precise reasons for this have remained
elusive. Sanjay Rajagopalan, professor of cardiovascular medicine at
Ohio State, and colleagues exposed different groups of mice to filtered
air or air containing from 8 to 10 times more PM than urban ambient air.
The mice were exposed for 6 hours a day, 5 days a week, for at least 20
weeks. Some of the mice used in the experiment lacked a molecule called
toll-like receptor 4 (TLR4), which recognizes specific characteristics
of pathogens and then sends out signals to activate other immune system
component. It is known that mice that lack TLR4 do not produce as much
inflammation after exposure to pollution as do normal mice, thus
suggesting that TLR4 plays an important role in the body's response
to chronic exposure to PM. Results of the experiment showed that normal
mice chronically exposed to air containing PM had higher levels of
inflammatory monocytes in their spleens and bloodstream than mice
breathing filtered air. Mice with TLR4-deficiency exhibited a diminished
response to breathing PM, thus suggesting that if the receptor is not
present, the monocytes will not be released. Results also showed that
the increase in monocytes was accompanied by an increase in superoxides
in the blood vessels. Again, the TLR4-deficient mice produced fewer
oxygen free radicals in response to polluted air than did normal mice.
The results of these and other experiments led Rajagopalan to conclude:
"PM stimulates inflammation in the lung, and products of that
inflammation spill over into the body's circulation, traveling to
fat tissue to promote inflammation and causing vascular dysfunction. We
haven't identified the entire mechanism, but we have evidence now
that activation of TLR4 influences this response."
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Kampfrath T, Maiseyeu A, Ying Z, et al. Chronic fine particulate matter exposure induces systemic vascular dysfunction via NADPH oxidase and TLR4 pathways. Ore Res. 2011; 108:716-726.
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