Since epidemiological studies have firmly implied the co-exposition between
iron oxides and
polycyclic aromatic hydrocarbons (PAH) as potential etiological factor involved in the excess of mortality by
lung cancer in miners, experimental studies have been performed to investigate the role of
iron particles on
benzo[a]pyrene (B[a]P)-induced lung pathogenesis. In the present study, the alkaline single-cell gel electrophoresis (SCGE; Comet Assay) was used to measure
DNA single-strand breaks in four cell types (alveolar macrophages, lung cells, peripheral lymphocytes and hepatocytes) of OFA Sprague-Dawley rats 24h after endotracheal administration of a single dose of an
iron oxide (
hematite; Fe(2)O(3)) (0.75mg) or B[a]P (0.75mg) or B[a]P (0.75mg) coated onto
hematite particles (0.75mg). No damage was observed in cell from the four investigated organs in rats treated with
iron oxide alone, while a statistically significant increase in DNA damage was observed compared with control animals in all tested cell types of rats treated with B[a]P alone or in association with
hematite. The highest levels of damage were observed in lung cells and peripheral lymphocytes; the levels of damage in alveolar macrophages and hepatocytes were increased, but to a lesser extent compared with the first two cell types. The main finding was to notice a statistically significant increase of the damage in all organs of rats treated with B[a]P coated onto
hematite (approximately two-fold increases; P<0.001), versus B[a]P alone. The current study shows that
iron particles increase the genotoxic properties of B[a]P in the respiratory tract of endotracheally treated OFA Sprague-Dawley rats. Hence, our data may contribute to explain the excess mortality by
lung cancer in epidemiological studies and overall why exposures to B[a]P coated onto Fe(2)O(3) particles resulted in higher toxicity in rodents compared with exposure to B[a]P alone.