Sustained efficacy of aluminum to reduce quartz toxicity in the lung.

In a recent study of the sheep tracheal lobe model, we have demonstrated that surface chemistry modification of quartz by aluminum lactate significantly alters the biological activity of quartz for at least 2 months after exposure. In the present study, we have extended our observations of the biological reaction of the lung tissue to aluminum treated quartz and to untreated quartz, added lung lavage analyses of surfactant and glycosaminoglycans as additional indicators of activity of the quartz-induced lung injury and analyzed lung lavage and tissue retention of the minerals. The tracheal lobe of 8 sheep was exposed to either 11 mg of aluminum lactate in 100 ml saline (Al group), 100 mg of quartz (Minusil-5) in 100 ml saline (Si group) or 100 mg of quartz treated with 11 mg of Al lactate in 100 ml saline (Si-Al group). The 24 sheep were studied by lung lavage at month 9, 0.13, 1, 2, 3, 5, 7, 9, and 10 and by autopsy at month 10. In the Al group, we found no significant change over time, the pathologic score was 0.38 +/- 0.15 and Si undetectable. In the Si group, we found significant sustained increases in total lavage cells, macrophages, lymphocytes, neutrophils, glycosaminoglycans, lactate dehydrogenase, phosphatidylcholine and phosphatidylglycerol. Histologically we found a macrophagic lymphocytic alveolitis with early nodular silicotic lesions; the pathological score was 3.0 +/- 0.8 at month 10 with an average quartz tissue level of 1.4 +/- 0.4 micrograms/mg. In the Si-Al group, all these changes were significantly reduced early and remained so up to 10 months after exposure; the pathological score was 1.1 +/- 0.4 and lung levels of quartz were undetectable. The data thus demonstrated that Al treatment of quartz significantly reduces the biological activity of quartz and increases its clearance with essentially no detectable particle retention in the lung 10 months after exposure.