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A Study on the Effect of Cadmium on Human Lung Fibroblasts*

Xiang-der Liu, MD; T. Umino; Yun Kui Zhu, MD; Hangjun Wang, MD; John R. Spurzem, MD; Debra J. Romberger, MD, FCCP; Stephen I. Rennard, MD, FCCP
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*From the University of Nebraska Medical Center, Pulmonary and Critical Care Medical Section, Omaha, NE.

Correspondence to: Xiang-der Liu, MD, Pulmonary and Critical Care Medical Section, Department of Internal Medicine, University of Nebraska Medical Center, 600 South 42nd Street, Omaha, NE 68198-5300



Chest. 2000;117(5_suppl_1):247S. doi:10.1378/chest.117.5_suppl_1.247S
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Abbreviations: CdCl2 = cadmium chloride; HFL-1 = human fetal lung fibroblast

Cadmium is one of the contaminants of tobacco and may play a role in cigarette smoking-related emphysema. Consistent with such a role, chronic inhalation of cadmium in the workplace is also associated with emphysema. We hypothesized that the action of cadmium may be via direct effects on fibroblasts, leading to decreased proliferation and compromised repair. In this study, we investigated the effect of cadmium chloride (CdCl2) on fibroblast proliferation, attachment to extracellular matrix, chemotaxis in the Boyden blindwell chamber, contraction of native type I collagen gels, fibronectin production, and type I procollagen messenger RNA expression by reverse transcriptase-polymerase chain reaction. CdCl2-inhibited human fetal lung fibroblast (HFL-1) proliferation in a dose-dependent manner in response to 4% serum (concentration of 50% inhibition = 10–12.5 μm). Cadmium also decreased cell adhesion to fibronectin (reduced 62.18 ± 0.85%; p < 0.01) and chemotaxis towards fibronectin (35.7 ± 5.7 vs 3.3 ± 1.1 cells/high-powered field; p < 0.01). Contractility of type I collagen gels was significantly decreased in the CdCl2-pretreated HFL-1 cells (final size 28.7 ± 1.5% vs 68.5 ± 0.5% of original size; p < 0.001). However, cadmium (20 μm for 48 h in the absence of serum) did not affect fibronectin production or type I procollagen messenger RNA expression. These data thus indicate that cadmium may directly impair connective tissue repair processes and may contribute to the development of emphysema associated with cigarette smoking or chronic inhalation of cadmium fumes.

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