PULMONARY AND SYSTEMIC TOXICITY OF GALLIUM-ARSENIDE (RAT, GALLIUM OXIDE, ARSENIC OXIDE).

Persistent Link:
http://hdl.handle.net/10150/187807
Title:
PULMONARY AND SYSTEMIC TOXICITY OF GALLIUM-ARSENIDE (RAT, GALLIUM OXIDE, ARSENIC OXIDE).
Author:
WEBB, DAVID RONALD.
Issue Date:
1984
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Inhalation of gallium arsenide (GaAs) particulates represent a potential health hazard in the semiconductor industry. Our results showed that GaAs was soluble under a variety of in vitro conditions. Arsenic levels in phosphate buffer filtrates indicated 78% dissolution by 36 hours. The in vivo dissolution of GaAs was dependent upon particle size, time, and route of administration. Intratracheal (i.t.) instillation of GaAs particulates (10-100 mg/kg) to rats resulted in blood arsenic levels of 5-187 ppm at 14-28 days, depending upon particle size. Dissolution doubled as the mean volume particle diameter was halved. Oral administration of GaAs particulates (10-1000 mg/kg) resulted in blood arsenic levels of 3-18 ppm at 14 days. Gallium was not detected in blood at any dose level by any route of exposure. Indices of toxicity that correlated to GaAs exposure were decreased weight gain and porphyria. These effects were maximal at 100 mg/kg GaAs i.t. Uroporphyrin replaced coproporphyrin as the major urinary metabolite. GaAs (10-100 mg/kg i.t.) resulted in an increase in the lung:body weight ratio (136-228%) at 14-28 days, depending upon particle size. Lungs retained 14-42% of the dose as gallium or arsenic. The increase in lung wet weight was not primarily due to edema although pulmonary edema increased in magnitude as particle size decreased. Lung dry weight, DNA, protein, and lipid content were also elevated 14 days after 100 mg/kg GaAs i.t. (large fraction). At this time and dose, major pathological lesions were a thickening in the alveolar wall, pneumonocyte hyperplasia, and interstitial pneumonia. Gallium, as Ga₂O₃ (65 mg/kg), accounted for the increase in lung lipids. Arsenic, as As₂O₃ (17 mg/kg), was responsible for the remaining changes in lung composition observed with GaAs administration. As₂O₃, but not GaAs, resulted in acute fibrosis at 14 days. With 100 mg/kg GaAs i.t. (smaller fraction), proteinosis, edema, mild fibrosis, and increased reticulin formation were observed over 1-28 days in addition to lesions previously described for the larger fraction. These results showed that oral and i.t. GaAs resulted in systematic arsenic intoxication. Intoxication was proportional to in vivo dissolution which was dependent upon particle size. GaAs i.t. was relatively more toxic to rats than an equivalent oral dose. The finding that urinary uroporphyrin levels were greater than coproporphyrin levels may serve as a sensitive, pretoxic indicator of GaAs exposure.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Gallium -- Toxicology.; Gallium arsenide semiconductors -- Toxicology.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Pharmacology and Toxicology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Carter, Dean

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titlePULMONARY AND SYSTEMIC TOXICITY OF GALLIUM-ARSENIDE (RAT, GALLIUM OXIDE, ARSENIC OXIDE).en_US
dc.creatorWEBB, DAVID RONALD.en_US
dc.contributor.authorWEBB, DAVID RONALD.en_US
dc.date.issued1984en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractInhalation of gallium arsenide (GaAs) particulates represent a potential health hazard in the semiconductor industry. Our results showed that GaAs was soluble under a variety of in vitro conditions. Arsenic levels in phosphate buffer filtrates indicated 78% dissolution by 36 hours. The in vivo dissolution of GaAs was dependent upon particle size, time, and route of administration. Intratracheal (i.t.) instillation of GaAs particulates (10-100 mg/kg) to rats resulted in blood arsenic levels of 5-187 ppm at 14-28 days, depending upon particle size. Dissolution doubled as the mean volume particle diameter was halved. Oral administration of GaAs particulates (10-1000 mg/kg) resulted in blood arsenic levels of 3-18 ppm at 14 days. Gallium was not detected in blood at any dose level by any route of exposure. Indices of toxicity that correlated to GaAs exposure were decreased weight gain and porphyria. These effects were maximal at 100 mg/kg GaAs i.t. Uroporphyrin replaced coproporphyrin as the major urinary metabolite. GaAs (10-100 mg/kg i.t.) resulted in an increase in the lung:body weight ratio (136-228%) at 14-28 days, depending upon particle size. Lungs retained 14-42% of the dose as gallium or arsenic. The increase in lung wet weight was not primarily due to edema although pulmonary edema increased in magnitude as particle size decreased. Lung dry weight, DNA, protein, and lipid content were also elevated 14 days after 100 mg/kg GaAs i.t. (large fraction). At this time and dose, major pathological lesions were a thickening in the alveolar wall, pneumonocyte hyperplasia, and interstitial pneumonia. Gallium, as Ga₂O₃ (65 mg/kg), accounted for the increase in lung lipids. Arsenic, as As₂O₃ (17 mg/kg), was responsible for the remaining changes in lung composition observed with GaAs administration. As₂O₃, but not GaAs, resulted in acute fibrosis at 14 days. With 100 mg/kg GaAs i.t. (smaller fraction), proteinosis, edema, mild fibrosis, and increased reticulin formation were observed over 1-28 days in addition to lesions previously described for the larger fraction. These results showed that oral and i.t. GaAs resulted in systematic arsenic intoxication. Intoxication was proportional to in vivo dissolution which was dependent upon particle size. GaAs i.t. was relatively more toxic to rats than an equivalent oral dose. The finding that urinary uroporphyrin levels were greater than coproporphyrin levels may serve as a sensitive, pretoxic indicator of GaAs exposure.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectGallium -- Toxicology.en_US
dc.subjectGallium arsenide semiconductors -- Toxicology.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePharmacology and Toxicologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorCarter, Deanen_US
dc.identifier.proquest8500479en_US
dc.identifier.oclc693324815en_US
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