Inhal Toxicol. 2005 Dec;17(13):709-16. Links
Disruption of iron homeostasis as a mechanism of biologic effect by
ambient air pollution particles.
Ghio AJ, Cohen MD.
Clinical Research Branch, Human Studies Division, Office of Research
and Development, U.S. Environmental Protection Agency, Research
Triangle Park, North Carolina.
Several features of the clinical presentation and changes in physiology
and pathology following exposure to many diverse ambient air pollution
particles are comparable, suggesting a common mechanism for their
biological effect. We propose that a mechanism of biological effect
common to many ambient air pollution particles is a disruption of iron
homeostasis in cells and tissues. Among traits shared by every
particle-related lung injury is the introduction of a solid-liquid
interface into the respiratory tract. All surfaces of particulate
matter have some concentration of oxygen-containing functional groups.
As a result of its electropositivity, Fe(3+) has a high affinity for
oxygen-donor ligands and will react with these groups at the particle
surface. Retained particles accumulate metal from available sources in
a cell and tissue, and this complexed iron mediates oxidant generation.
In addition to complexation onto the solid-liquid interface provided by
the surface of particulate matter (PM), there are several alternative
pathways by which metal homeostasis in the lower respiratory tract can
be disrupted following exposure to ambient air pollution particles to
affect an oxidative stress. Evidence suggests that disruption in iron
homeostasis following exposures to ambient air pollution particles is
an initial event in their biological effect. An association between
metal equilibrium in the lower respiratory tract and biological effect
in the lung could explain the observed differential toxicity of
ultrafine, fine, and coarse particles and disparities in host
susceptibility.
PMID: 16195206 [PubMed - in process]
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