Aluminium lactate treatment of DQ12 quartz inhibits its ability to cause inflammation, chemokine expression, and nuclear factor-kappa B activation

In 1997, an IARC Working Group classified quartz (crystalline silica) as a Group 1 lung carcinogen, but only in some industries, i.e., the quartz haza rd is a variable entity. The reactivity of the quartz surface may underlie its ability to cause inflammation, and treatments that ameliorate this reac tivity will reduce the quartz hazard. In this study we treated quartz (Q) w ith aluminium, lactate (AL), a procedure that is reported to decrease the q uartz hazard, and explored the effect this had on the highly reactive quart z surface and on proinflammatory events in rat lungs. Aluminium lactate-tre ated quartz showed a reduced surface reactivity as measured by, electron sp in resonance and the hemolysis assay. Eighteen hours after instillation of Q into the rat lung, there was massive inflammation as indicated by the num ber of neutrophils in the bronchoalveolar lavage (BAL). In addition, Q indu ced an increase in BAL macrophage inflammatory protein-2 (MIP-2) while ALQ had no significant effect compared to control. Epithelial damage, as indica ted by, BAL protein and gamma glutamyl transpeptidase, also increased with Q but not with ALQ. Furthermore, Q induced an increase in MIP-2 mRNA by BAL cells while ALQ had no effect compared to controls. There was an increase in nuclear binding of the transcription nuclear factor kappaB (N-F-kappaB) in the Q-exposed BAL cells and again no effect on nuclear NF-KB binding in BAL cells from ALQ-exposed rats. In conclusion, treatment of the quartz sur face with aluminium lactate reduced the reactivity of the particles both in terms of hydroxyl radical generation and in terms of the induction of mole cular signaling events leading to inflammation. (C) 2001 Academic Press.