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Indium-tin oxide does not induce GM-CSF autoantibodies (authors response).

Cummings-KJ; Kreiss-K; Roggli-VL
Am J Respir Crit Care Med 2011 Sep; 184(6):741-742
As Omae and colleagues recently pointed out, it has been difficult to reconcile seven cases of interstitial pneumonia and three cases of pulmonary alveolar proteinosis among 10 published cases of lung disease in indium workers. Dr. Masuko and colleagues describe a re-evaluation of pathologic specimens from cases of interstitial pneumonia in Japanese indium workers that revealed the presence of periodic acid-Schiff-positive material not previously reported. We are pleased that the theory of disease evolution (from alveolar proteinosis to fibrosis and emphysema) initially proposed at a September 2010 workshop on indium-related lung disease sponsored by the National Institute for Occupational Safety and Health (NIOSH) of the Centers for Disease Control and Prevention has now been accepted by workshop attendees who co-authored the letter. However, we object to the characterization of alveolar proteinosis as a response "particularly in cases of massive exposure," as exposure assessment has been lacking or limited and precludes comparative analysis among cases. Furthermore, this characterization is not supported by the development of alveolar proteinosis in animals exposed to indium-tin oxide in airborne concentrations as low as the NIOSH recommended exposure limit of 0.1 mg/m3. We appreciate the information that Masuko and colleagues provide on the measurement of autoantibodies to granulocyte/ macrophage colony-stimulating factor in 17 indium workers and in rats exposed to indium-tin oxide, which suggests that if autoimmunity played a role in indium toxicity in the second case we described, the mechanism of indium's toxicity is not exclusively autoimmune. Further investigation into the mechanism of indium toxicity is warranted, and may inform preventive efforts. In describing the 17 indium workers, the authors note that the normal range of serum indium is 0.3 plus or minus 2.6 ng/ml. While not a range per se, we wonder if these numbers are derived from analyses suggesting a serum indium greater than 2.9 ng/ml is associated with elevations in KL-6 in current indium workers. If so, we question the derivation of a normal range from an exposed population and encourage the use of norms derived from unexposed populations in the future. Whether office workers in indium facilities are truly unexposed - and without long-term risk of lung disease - remains to be determined from follow-up studies.
Epidemiology; Exposure-assessment; Immune-reaction; Immune-system-disorders; Immunology; Immunotoxins; Lung-disease; Lung-disorders; Lung-fibrosis; Lung-irritants; Immune-system; Pulmonary-system; Pulmonary-system-disorders; Quantitative-analysis; Respiratory-hypersensitivity; Respiratory-irritants; Respiratory-system-disorders; Risk-factors; Statistical-analysis; Work-practices
Kristin J. Cummings, CDC, NIOSH, Morgantown, WV
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American Journal of Respiratory and Critical Care Medicine