Abstract
With the single exception of mercury, all metals in the atmosphere are associated with particles. The lungs are subsequently exposed to metals present in air pollution particles on a continuous basis. Because metal exposure can be associated with an oxidative stress, a mechanism that isolates the metal in a chemically less reactive form would be of benefit. We tested the hypothesis that the concentrations of both lactoferrin and ferritin in the rat lung increase after exposure to a metal-rich emission source air pollution particle. Using immunohistochemistry, we characterized changes in the concentrations of ferritin and lactoferrin after exposure of rats to an emission source air pollution particle. Lavage metal concentrations, measured by inductively coupled plasma emission spectroscopy, increased 4 hr after exposure to an oil fly ash. After exposure to this metal-rich emission source air pollution particle, ferritin concentrations in the lower respiratory tract increased. Comparable to the iron-storage protein, concentrations of both lactoferrin and transferrin were elevated after exposure. The greatest concentrations of ferritin, lactoferrin, and transferrin occurred at approximately 24 hr after exposure to the air pollution particle. Levels then decreased, and by 96 hr after instillation of the oil fly ash, ferritin, lactoferrin, and transferrin were not elevated relative to those animals exposed to saline. We conclude that, in response to an emission source air pollution particle with high concentrations of metals, there is an increase in ferritin, lactoferrin, and transferrin concentrations in the lungs of the host. The function of these increases in iron-binding proteins may be to control the oxidative stress associated with the exposure to metals.