The Inhalation Toxicity of Indium Sesquioxide in the Rat

Lj, Leach; Jk, Scott; Rd, Armstrong; Lt, Steadman; Ea, Maynard

doi:10.2172/4046157

Cited by 13 publications

(14 citation statements)

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“…These findings are consistent with the results of animal studies that have demonstrated alveolar proteinosis and pulmonary fibrosis following exposure to a variety of indium compounds including indium oxide and ITO [Leach et al 1961;National Toxicology Program 2001;Tanaka et al 2002;Lison et al 2009;Lison and Delos 2010;Tanaka et al 2010;Nagano et al 2011].…”

Section: Health Hazard Evaluation Report 2009-0214-3153supporting

confidence: 89%

“…Furthermore, pathologists participating in the international workshop at NIOSH found histopathological evidence of alveolar proteinosis in nearly all cases of lung disease in workers exposed to indium compounds, regardless of the initial diagnosis [Cummings et al 2011]. Fourth, there is coherence between epidemiologic and laboratory findings, in that multiple experimental studies have demonstrated alveolar proteinosis in animals exposed to indium compounds [Leach et al 1961;National Toxicology Program 2001;Lison and Delos 2010;Nagano et al 2011].…”

Section: Health Hazard Evaluation Report 2009-0214-3153mentioning

confidence: 99%

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An evaluation of preventive measures at an indium-tin oxide production facility.

2012

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Section: Health Hazard Evaluation Report 2009-0214-3153supporting

confidence: 89%

Section: Health Hazard Evaluation Report 2009-0214-3153mentioning

confidence: 99%

An evaluation of preventive measures at an indium-tin oxide production facility.

2012

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“…ACGIH's recommendation of TLV-TWA 13) for indium and its compounds of 0.1 mg/m 3 was based on pulmonary toxicity of widespread alveolar edema resembling alveolar proteinosis, resulting from 3-month inhalation exposure of rats to IO aerosol 33) . JSOH recommended a BEI of 3 µg/l as a serum level of indium, below which chronic inflammation would not occur 15) .…”

Section: Discussionmentioning

confidence: 99%

Two‐ and 13‐week Inhalation Toxicities of Indium‐tin Oxide and Indium Oxide in Rats

Nagano

Gotoh

Kasai

et al. 2011

Journal of Occupational Health

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Two-and 13-week Inhalation Toxicities of Indium-tin Oxide and Indium Oxide in Rats: Kasuke NagaNo, et al. Japan Bioassay Research Center, Japan Industrial Safety and Health AssociationObjectives: Two-and 13-week inhalation toxicities of indium-tin oxide (ITO) and indium oxide (IO) were characterized for risk assessments of workers exposed to ITO. Methods: F344 rats of both sexes were exposed by inhalation to ITO or IO aerosol for 6 h/day, 5 day/wk for 2 wk at 0, 0.1, 1, 10 or 100 mg/m 3 or 13 wk at 0, 0.1or 1 mg/m 3 . An aerosol generator and inhalation exposure system was constructed. Results: Blood and lung contents of indium were elevated in a dose-related manner in the ITO-and IO-exposed rats. ITO and IO particles were deposited in the lung, mediastinal lymph node and nasal-associated lymphoid tissue. Exposures to ITO and IO induced alveolar proteinosis, infiltrations of alveolar macrophages and inflammatory cells and alveolar epithelial hyperplasia in addition to increased lung weight. ITO affected the lung more severely than IO did. Fibrosis of alveolar wall developed and some of these lesions worsened at the end of the 26-week post-exposure period. Conclusions: Persistent pulmonary lesions including alveolar proteinosis and macrophage infiltration occurred after 2-and 13-week inhalation exposures of rats to ITO and IO. Fibrosis of alveolar wall developed later. These lesions occurred after ITO exposure at the same concentration as the current occupational exposure limit in the USA and at blood indium levels below the biological exposure index in Japan for indium. (J Occup Health 2011; 53: 51-63)

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“…At the same time, this reevaluation demonstrates the problem of varying diagnoses of the same pathological lung condition by different pathologists. In some cases of animal experiments, where the description and figures presented clearly point to a PAP (among other changes), the authors do not mention this diagnosis (e.g., Leach et al 1961;Tanaka et al 2010;Warheit et al 1991).…”

Section: Diagnosis Of Papmentioning

confidence: 97%

Particle-induced Pulmonary Alveolar Proteinosis and Subsequent Inflammation and Fibrosis: A Toxicologic and Pathologic Review

Bomhard¹

2017

Toxicol Pathol

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This review analyzes the published data on cases of pulmonary alveolar proteinosis (PAP) in workers inhaling crystalline aluminum, indium, silicon, and titanium particles and possible sequelae, that is, inflammation and fibrosis, and compares these findings with those from animal experiments. In inhalation studies in rodents using crystalline indium and gallium compounds, pronounced PAP followed by inflammation and fibrosis down to very low concentration ranges have been reported. Crystalline aluminum, silicon, and titanium compounds also induced comparable pulmonary changes in animals, though at higher exposure levels. Laboratory animal species appear to react to the induction of PAP with varying degrees of sensitivity. The sensitivity of humans to environmental causes of PAP seems to be relatively low. Up to now, no cases of PAP, or other pulmonary diseases in humans, have been described for gallium compounds. However, a hazard potential can be assumed based on the results of animal studies. Specific particle properties, responsible for the induction of PAP and its sequelae, have not been identified. This review provides indications that, both in animal studies and in humans, PAP is not often recognized due to the absence of properly directed investigation or is concealed behind other forms of lung pathology.

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The Inhalation Toxicity of Indium Sesquioxide in the Rat

Cited by 13 publications

References 1 publication

An evaluation of preventive measures at an indium-tin oxide production facility.

An evaluation of preventive measures at an indium-tin oxide production facility.

Two‐ and 13‐week Inhalation Toxicities of Indium‐tin Oxide and Indium Oxide in Rats

Particle-induced Pulmonary Alveolar Proteinosis and Subsequent Inflammation and Fibrosis: A Toxicologic and Pathologic Review

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