In
a continuing effort to find out if the tiniest airborne
particles pose a health risk, University of Rochester
Medical Center scientists showed that when rats breathe
in nano-sized materials they follow a rapid and efficient
pathway from the nasal cavity to several regions
of the brain, according to a study in the August
issue of Environmental Health Perspectives.
Researchers also saw changes in gene expression
that could signal inflammation and a cellular stress
response, but they do not know yet if a buildup of
ultrafine particles causes brain damage, said lead
author Alison Elder, Ph.D., research assistant professor
of Environmental Medicine.
The study tested manganese oxide ultrafine particles
at a concentration typically inhaled by factory welders.
The manganese oxide particles were the same size
as manufactured nanoparticles, which are controversial
and being diligently investigated because they are
the key ingredient in a growing industry -- despite
concerns about their safety.
Nanotechnology is a new wave of science that deals
with particles engineered from many materials such
as carbon, zinc and gold, which are less than 100
nanometers in diameter. The manipulation of these
materials into bundles or rods helps in the manufacturing
of smaller-than-ever electronics, optical and medical
equipment. The sub-microscopic particles are also
used in consumer products such as toothpaste, lotions
and some sunscreens.
Some doctors and scientists are concerned about
what happens at the cellular level after exposure
to the ultrafine or nano-sized particles, and the
University of Rochester is at the forefront of this
type of environmental health research. In 2004 the
Defense Department selected the University Medical
Center to lead a five-year, $5.5 million investigation
into whether the chemical characteristics of nanoparticles
determine how they will interact with or cause harm
to animal and human cells.
In the current study, the particles passed quickly
through the rats' nostrils to the olfactory bulb,
a region of the brain near the nasal cavity. They
settled in the striatum, frontal cortex, cerebellum,
and lungs.
After 12 days, the concentration of ultrafine particles
in the olfactory bulb rose 3.5-fold and doubled in
the lungs, the study found. Although the ultra-tiny
particles did not cause obvious lung inflammation,
several biomarkers of inflammation and stress response,
such as tumor necrosis factor and macrophage inflammatory
protein, increased significantly in the brain, according
to gene and protein analyses.
"We suggest that despite differences between human
and rodent olfactory systems, this pathway is likely
to be operative in humans," the authors conclude.
The U.S. Environmental Protection Agency, National
Institute of Environmental Health Sciences, Department
of Defense and Department of Energy funded the study. Contact:
Leslie Orr
Leslie_Orr@urmc.rochester.edu
585-275-5774
University of Rochester Medical Center
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