Pneumotoxicity of dust from aluminum foundry and pure alumina: a comparative study of morphology and biomarkers in rats.

OBJECTIVES The overall objective was to assess the role of aluminum dust and fumes in the aluminum foundry (Al-F) in generating local inflammation in the respiratory tract, which may lead to induction and elicitation of occupational asthma and fibrosis. To understand the underlying mechanisms of involving particles from foundry, a long-term study was performed on rats. MATERIALS AND METHODS Pure alpha-alumina (Al-P) or (Al-F) was intratracheally instillated to rats in doses of 20 mg suspended in 0.5 ml of saline. After 3, 6 and 9 months since instillation, the following biomarkers were assessed in lung tissues: Clara cell protein (CC16), hyaluronic acid (HA), total protein, metaloproteinases (MMP) in bronchoalveolar lavage fluid (BALF), and GSH-S-transferase (GST). Morphological study of lungs and cells in BALF sediment was also performed. RESULTS In the long-term study, Al-F dust induced marked changes in both epithelial cells and lung tissues, leading to important remodeling in collagen deposit and elastase fibres after 6 and 9 months. By contrast, the same dose of Al-P caused an increase in the number of polymorphonuclear leukocytes in the lung and fibrosis, but the latter was manifested by only slight signs. The lung BALF showed a decreasing level of Clara cell protein and a markedly increased expression of MMP-2 and MMP-9. These findings suggest that there is an upregulation of MMP and an increase in epithelial cell death and Clara cells proliferation, which may contribute to the respiratory symptoms through remodeling of airways and alveolar structures. CONCLUSIONS In conclusion, it must be said that CC16 is the most sensitive biomarker. Decreasing levels of this biomarker in BALF was observed in an early phase (3 months PE) of our study with serum aluminum (Al-S) concentration not exceeding 30 microg/L(-1). Foundry dust causes marked irritation and inflammation in the rat lung. In occupational exposure it may therefore be active in the human lung, and thus contribute to the chronic obturative pulmonary disease (COPD).