Lung inflammation after exposure to nonfibrous silicates increases with chelatable [Fe3+].

Lung exposures to complexes of coordinated iron can be associated with a neutrophilic alveolitis. We tested the hypothesis that lung inflammation after intratracheal instillation of mineral oxides in rats increases with surface-complexed [Fe3+]. The 10 mineral oxides employed had measurable [Fe3+] complexed to the dust surface. The metal was incompletely coordinated, as demonstrated by the ability of the particles to catalyze electron transfer and generate thiobarbituric acid (TBA) reactive products of deoxyribose. After exclusion of those silicates containing structural iron within the crystal lattice, there was a significant correlation between the concentration of chelatable metal and TBA-reactive products (r = 0.82; p = .04). Four days after intratracheal instillation of the 10 mineral oxide particles into rats, lavage neutrophils and protein were significantly increased for all dusts compared to injected saline. Among those dusts with no structural iron, the correlation between chelatable iron concentrations and percentage neutrophils did not reach significance (r = 0.73; p = .10), but that between metal and lavage protein did (r = 0.80; p = .05). We conclude that (1) mineral oxides complex iron cations at the surface, (2) in vitro measures of oxidant generation increase with the concentration of surface iron among those dusts with no structural iron, and (3) acute inflammation following introduction of these particles into the lower respiratory tract also increases with surface iron concentrations among those mineral oxides with no structural iron.

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