Polluted air causes widespread inflammation and disease

There are so many things to worry about – pollution is just one of them. If you take time to contemplate this scourge, you more than likely find yourself concerned with lung health.

The “junk” contained in the air you breathe, has the potential to get trapped in your delicate lungs, causing respiratory tract problems – asthma, COPD and lung cancer.

But epidemiological studies also implicate pollution in heart disease. The question that has puzzled researchers is how what happens in the lungs, can clog up the heart.

Pollution is upsetting more than your lungs

Researchers from Ohio State University have begun piecing together how these “junk” particles, carried on the air entering your lungs, can end up stressing your heart.

The researchers found that the fine particulate matter, typical of pollution, was able to kick off an inflammatory cascade in mice that spiralled out of control, leaving their little bodies “ON FIRE”.

The researchers found the trouble begins when the protective fluid in the lungs, undergoes a chemical alteration, in response to the pollutants. The oxidized phospholipids are what triggers an aberrant inflammatory cascade.

The inflammatory cascade

The data comes from a series of experiments, performed by the Ohio State University team.

In one experiment, two sets of mice were exposed to overloads of pollution particles, way more than would be experienced in a typical urban environment, way way more. The one group of mice were normal, but the other group, had been genetically tinkered with, so that they did not have toll-like receptor 4.

NOTE : The Toll-like receptor 4 (TLR4) is what immune cells use to recognize foreign invaders.

The polluted air was able to amplify the number of circulating immune cells in the normal mice. The dirty air had little effect on the levels of white blood cells in the mice lacking the toll-like receptor 4, implicating this receptor in the pollution problem.

More white blood cells , more free radicals

Stimulated white blood cells are on the war path – they are working hard to fight off invaders, usually bacteria, not undesired chemicals.

The way these cells “kill” invading organisms is to douse them with free radicals. So the pollution response in normal mice, saw free radical levels rise significantly.

Blood vessels and fat cells under attack

The extra white blood cells circulating in response to the pollution, did not only move into the lungs to beef up lung security, they became pests in other parts of the body.

Some stuck to blood vessels, spewing out free radicals in their vicinity. Free radicals flying around cause tiny fissures in the blood vessels, these gaps need to be repaired. Damaged blood vessels are the real problem in the lifestyle diseases, so the lungs trouble starts to impact on the heart.

The stimulated white blood cells also penetrate fat – worming their way between the fat cells. As they spit out free radicals, they injure the fat cells, creating even more unhappy fat cells. Crying fat cells are what makes being fat a health hazard.

More pollution more disease

Something more to worry about ?

Breathing in high levels of “dirty” air can increase inflammation. Of course pretty much everything causes inflammation, some of the things are within your ability to keep in check, many, like pollution, are not directly within your control.

Focus on those things you can do something about, get your body chemistry balanced, some ideas

follow the rule of thirds which will reduce the amount of inflammation caused by eating,
plant a tree or two to suck up some of that dirty air,
eat foods rich in antioxidants e.g. nuts, raw eggs and vegetables to neutralize some of those pesky free radicals.

Why not enrol in our free e-course, 31 Days to Better Body Chemistry to get tips and ideas on delivered to your inbox.

Chronic Fine Particulate Matter Exposure Induces Systemic Vascular Dysfunction via NADPH Oxidase and TLR4 Pathways. Circulation Research, 2011; 108 (6): 716.. T. Kampfrath, A. Maiseyeu, Z. Ying, Z. Shah, J. A. Deiuliis, X. Xu, N. Kherada, R. D. Brook, K. M. Reddy, N. P. Padture, S. Parthasarathy, L. C. Chen, S. Moffatt-Bruce, Q. Sun, H. Morawietz, S. Rajagopalan.