Published ahead of print on March 15, 2007, doi:10.1164/rccm.200601-134OC Am. J. Respir. Crit. Care Med., Volume 176, Number 1, July 2007, 70-77 A more recent version of this article appeared on July 1, 2007
Submitted on January 31, 2006 Two-Dimensional Analysis of Elements and Mononuclear Cells in Hard Metal Lung DiseaseHiroshi Moriyama1,1 Division of Respiratory Medicine, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan, 2 EPMA Laboratory, Center of Instrumental Analysis, Niigata University, Niigata, Japan, 3 Department of Internal Medicine, JA niigata kouseiren UONUMA Hospital, Ojiya, Japan, 4 EPMA Laboratory, Center of Instrumental Analysis, Niigata University, Niigata, Japan; Division of Dental Biomaterial Science, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan, 5 Department of General Medicine, Niigata University Medical and Dental Hospital, Niigata, Japan * To whom correspondence should be addressed. E-mail: ttakada{at}med.niigata-u.ac.jp.
Rationale: Hard metal lung disease is caused by exposure to hard metal, a synthetic compound that combines tungsten carbide with cobalt as well as a number of other metals. Interstitial lung disease caused by hard metal is uniquely characterized by giant cell interstitial pneumonia. The pathogenesis of hard metal lung disease is unclear. Objective: To elucidate the distribution of inhaled hard metal and reactive inflammatory cells in biopsy lung tissue from patients with hard metal lung disease. Methods: Seventeen patients with interstitial lung disease in which tungsten was detected and five controls were studied. Detection and mapping of elements were performed using an electron probe microanalyzer equipped with a wavelength dispersive spectrometer. We immunohistochemically stained mononuclear cells in tissues from five available cases with anti-human CD4, CD8, CD20, CD68, and CD163 antibodies, and compared the distribution of positive cells with hard metal elements. Measurements and Main Results: Thirteen out of 17 patients were pathologically diagnosed as having giant cell interstitial pneumonia. Tungsten and cobalt were accumulated in the centrilobular fibrotic lesions, but never found in the control lungs. CD8+ lymphocytes and CD163+ monocyte-macrophages were predominantly distributed in centrilobular fibrotic lesions around the hard metal elements, and some of them were likely to colocalize with tungsten element. Small numbers of CD8+ and CD163+ cells were also immunohistochemically shown in peribronchiolar areas and alveolar walls. Conclusions: Macrophages may phagocytose inhaled tungsten via CD163 and play an important role in forming the fibrotic lesion of hard metal lung disease with cytotoxic T lymphocytes. Key words: Electron probe microanalysis, hard metal, interstitial lung disease, CD163 antigen, CD8-Positive T-Lymphocytes
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