Air pollution may be a top cause of heart ills - oxidative stress

[Guest guest]

As we know, elevations of oxidative stress markers are reported in many

autistic children. How many infants and toddlers who managed to escape

thimerosal injections continued to live in locales with high levels of

air pollutants? Palmer RF et al and Windham et al report associations

between autism and various airborne toxins. " Nano-size pollutants from

vehicles " seem yet another factor contributing to the epidemic of autism

and other ASDs.

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01.18.2008

Air pollution may be a top cause of heart ills

BLOOMBERG NEWS

http://www.azstarnet.com/sn/printDS/221024

Unregulated air pollution particles about one-thousandth the width of a

human hair may be a leading cause of heart disease and stroke, according

to a new study.

Nano-size pollutants from vehicles can lead to plaque buildup in the

arteries, putting people at risk of cardiovascular problems, researchers

said in a study published today in Circulation Research, a journal of

the American Heart Association. The pollutants may cause arteries to

harden by impairing the protective qualities of so-called good cholesterol.

The U.S. Environmental Protection Agency doesn't regulate the nano-size

particles, which can't be captured using current filtering technology.

The pollutants, abundant in urban areas, are less than 0.18 micrometers

in size and cause four times more artery buildup than particles four

times larger, said Jesus Araujo, director of environmental cardiology at

University of California, Los Angeles.

Public-health implications

" People who are living around and are exposed to high air pollution have

a higher risk of developing heart disease, " Araujo, the study's lead

author, said in an interview Thursday. " This has serious implications

from a public-health standpoint. "

The EPA regulates " fine particles " that are about 2.5 micrometers in

size. Araujo said people with a history of heart disease should be

especially cautious about being exposed to high levels of pollution.

Such Web sites as www.airnow.gov can be used to check air quality in

particular areas at specific times of the day, he said.

The study's findings could mean current estimates about the risk of

heart problems caused by pollution are too low. Previous studies

indicated a 25 percent increase in the risk of having a cardiovascular

event for each 10 micrograms per cubic meter of fine particulate, and

the latest findings mean the risk may actually be greater than that,

Araujo said.

" People may not be aware of the risk they have, " he said.

Researchers plan to develop a way for doctors to assess the amount of

cardiovascular damage caused by air pollutants and measure people's risk

of developing heart problems.

All content copyright © 1999-2008 AzStarNet, Arizona Daily Star

Ambient Particulate Pollutants in the Ultrafine Range Promote Early

Atherosclerosis and Systemic Oxidative Stress

Jesus A. Araujo... Andre E. Nel *

*Circulation Research. 2008*

Published online before print January 17, 2008, doi:

10.1161/CIRCRESAHA.107.164970

http://circres.ahajournals.org/cgi/content/abstract/CIRCRESAHA.107.164970v1

Air pollution is associated with significant adverse health effects,

including increased cardiovascular morbidity and mortality. Exposure to

particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5)

increases ischemic cardiovascular events and promotes atherosclerosis.

Moreover, there is increasing evidence that the smallest pollutant

particles pose the greatest danger because of their high content of

organic chemicals and prooxidative potential. To test this hypothesis,

we compared the proatherogenic effects of ambient particles of <0.18 µm

(ultrafine particles) with particles of <2.5 µm in genetically

susceptible (apolipoprotein E--deficient) mice. These animals were

exposed to concentrated ultrafine particles, concentrated particles of

<2.5 µm, or filtered air in a mobile animal facility close to a Los

Angeles freeway. Ultrafine particle--exposed mice exhibited

significantly larger early atherosclerotic lesions than mice exposed to

PM2.5 or filtered air. Exposure to ultrafine particles also resulted in

an inhibition of the antiinflammatory capacity of plasma high-density

lipoprotein and greater systemic oxidative stress as evidenced by a

significant increase in hepatic malondialdehyde levels and upregulation

of Nrf2-regulated antioxidant genes. We conclude that ultrafine

particles concentrate the proatherogenic effects of ambient PM and may

constitute a significant cardiovascular risk factor.

* To whom correspondence should be addressed. E-mail:

ANel{at}mednet.ucla.edu.

*

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