Nano Air Pollution: Hazardous to Your Heart Health
prone to heart disease may one day be told by physicians to avoid not
only fatty foods and smoking but air pollution, too.
academic study led by UCLA researchers reveals that the smallest
particles from vehicle emissions may be the most damaging components of
air pollution in triggering plaque buildup in the arteries, which can
lead to heart attack and stroke. The findings appear in the Jan. 17
online edition of the journal Circulation Research.
The scientists identified a way in which pollutant particles may
promote hardening of the arteries — by inactivating the protective
qualities of high-density lipoprotein cholesterol, known as "good"
A multicampus team from UCLA, the University of Southern California,
the University of California, Irvine, and Michigan State University
contributed to the research, which was led by Andre Nel, UCLA's chief
of nanomedicine. The study was primarily funded by the National
Institute of Environmental Health Sciences and the U.S. Environmental
"It appears that the smallest air pollutant particles, which are the
most abundant in an urban environment, are the most toxic," said first
author Jesus Araujo, assistant professor of medicine and director of
environmental cardiology at the David Geffen School of Medicine at
UCLA. "This is the first study that demonstrates the ability of
nano-sized air pollutants to promote atherosclerosis in an animal
Nanoparticles are the size of a virus or molecule — less than 0.18
micrometers, or about one-thousandth the size of a human hair. The EPA
currently regulates fine particles, which are the next size up, at 2.5
micrometers but doesn't monitor particles in the nano or ultrafine
These particles are too small to capture in a filter, so new technology
must be developed to track their contribution to adverse health effects.
"We hope our findings offer insight into the impact of nano-sized air
pollutant particles and help explore ways for stricter air quality
regulatory guidelines," said Nel, principal investigator and a
researcher at UCLA's California NanoSystems Institute.
Nel added that the consequences of air pollution on cardiovascular health may be similar to the hazards of secondhand smoke.
Pollution particles emitted by vehicles and other combustion sources
contain a high concentration of organic chemicals that could be
released deep into the lungs or even spill over into the systemic
The UCLA research team previously reported that diesel exhaust
particles interact with artery-clogging fats in low-density lipoprotein
cholesterol to activate genes that cause the blood-vessel inflammation
that can lead to heart disease.
In the study, researchers exposed mice with high cholesterol to one of
two sizes of air pollutant particles from downtown Los Angeles freeway
emissions and compared them with mice that received filtered air that
contained very few particles.
The study, conducted over a five-week period, required a complex
exposure design that was developed by teams led by Michael Kleinman,
professor of community and environmental medicine at UC Irvine, and
Constantinos Sioutas, professor of civil and environmental engineering
Researchers found that mice exposed to ultrafine particles exhibited 55
percent greater atherosclerotic-plaque development than animals
breathing filtered air and 25 percent greater plaque development than
mice exposed to fine-sized particles.
"This suggests that ultrafine particles are the more toxic air
pollutants in promoting events leading to cardiovascular disease,"
Pollutant particles are coated in chemicals sensitive to free radicals,
which cause the cell and tissue damage known as oxidation. Oxidation
leads to the inflammation that causes clogged arteries. Samples from
polluted air revealed that ultrafine particles have a larger
concentration of these chemicals and a larger surface area where these
chemicals thrive, compared with larger particles, Sioutas noted.
"Ultrafine particles may deliver a much higher effective dose of
injurious components, compared with larger pollutant particles," Nel
Scientists also identified a key mechanism behind how these air
pollutants are able to affect the atherosclerotic process. Using a test
developed by Mohamad Navab, study co-author and a UCLA professor of
medicine, researchers found that exposure to air pollutant particles
reduced the anti-inflammatory protective properties of high-density
lipoprotein (HDL) cholesterol.
"HDL normally helps reduce the vascular inflammation that is part of
the atherosclerotic process," said Jake Lusis, study co-author and a
UCLA professor of cardiology, human genetics and microbiology,
immunology and molecular genetics. "Surprisingly, we found that
exposure to air pollutant particles, and especially the ultrafine size,
significantly decreased the positive effects of HDL."
To explore if air particle exposure caused oxidative stress throughout
the body — which is an early process triggering the inflammation that
causes clogged arteries — researchers checked for an increase in genes
that would have been activated to combat this inflammatory progression.
"We found greater levels of gene activation in mice exposed to
ultrafine particles, compared to the other groups," Lusis said. "Our
next step will be to develop a biomarker that could enable physicians
to assess the degree of cardiovascular damage caused by air pollutants
or measure the level of risk encountered by an exposed person."
Researchers added that previous studies assessing the cardiovascular
impact of air pollution have taken place over longer periods of
exposure, such as five to six months. The study demonstrated that ill
effects can occur in just five weeks.
"Further study will pinpoint critical chemical and toxic properties of ultrafine particles that may affect humans," Nel said.
The research team included investigators from the fields of
nanomedicine, cardiology and genetics. Additional co-authors included
Berenice Barajas, Xuping Wang, Brian J. Bennett and Ke Wei Gong of the
David Geffen School of Medicine at UCLA, and Jack Harkema from the
department of pathobiology and diagnostic investigation at Michigan
Additional grant support was provided by the National Institute of
Allergy and Infectious Diseases; the National Heart, Lung and Blood
Institute; and the Robert Wood Johnson Foundation.