The clearance of cadmium aerosols after I inhalation exposure

Oberdoerster, G.; Baumert, H.-P.; Hochrainer, D.; Stoeber, W.

doi:10.1080/15298667991429813

Cited by 44 publications

(9 citation statements)

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“…The induction of metallothionein synthesis by cadmium in liver and kidneys might be responsible for the retention of cadmium in these organs. A similar pulmonary clearance and extrapulmonary tissue distribution of inhaled cadmium aerosol and of intratracheally instilled cadmium oxide have been observed earlier (Boisset et al 1978;Henderson et al 1979;Oberdoerster 1979;Hadley et al 1980 appears to be due to haemorrhage and inflammatory oedema followed by reparative proliferative processes in lungs (Cross e t a / . 1979).…”

Section: Discussionsupporting

confidence: 74%

Distribution of Intratracheally Administered Cadmium in Rats

Tandon

Asokan

1981

Acta Pharmacologica et Toxicologica

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Cadmium chloride cleared rapidly from the lungs and translocated mainly into the liver within 24 hrs of an intratracheal instillation. Further pulmonary clearance and hepatic accumulation were very slow during the remaining observation period of 24 days. Though, the uptake of cadmium by kidneys was lower but the level increased consistently with the time after instillation. The induction of metallothionein synthesis by cadmium might be responsible for accumulation and retention of cadmium in liver and kidneys significantly.

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Section: Discussionsupporting

confidence: 74%

Distribution of Intratracheally Administered Cadmium in Rats

Tandon

Asokan

1981

Acta Pharmacologica et Toxicologica

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“…However, the same study reported significantly reduced liver-to-body weight ratios in the food-restricted animals, while the heart-, spleen-, and kidney-to-body weight ratios were unchanged from control values, indicating the changes observed after Cd exposure may be treatmentrelated. Although effects of Cd on the spleen have not been reported, Cd accumulation in the liver, kidneys, and heart has been documented (Fischer and Thind, 1971;Amacher and Ewing, 1975;Boisset et al, 1978;Ohanian et al, 1978;Prigge, 1978;Oberdoerster et al, 1979). In one of these studies (Boisset et al, 1978) Cd accumulation in the liver and kidney was accompanied by increased organ-to-body weight ratios, while in another (Ohanian et al, 1978) this did not appear to be the case.…”

Section: Discussionmentioning

confidence: 88%

Pulmonary changes resulting from subchronic exposure to cadmium chloride aerosol

Kutzman

Drew

Shiotsuka

et al. 1986

Journal of Toxicology and Environmental Health

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Fischer-344 rats were exposed to 0.0, 0.3, 1.0, or 2.0 mg Cd/m3 as CdCl2 aerosol for 6 h/d, 5 d/wk, for 62 exposure days. Exposure to 2.0 mg Cd/m3 resulted in rapid weight loss, and all of the animals died within the first 45 exposure days. As a group, female rats survived significantly longer than the males. Exposure to Cd resulted in dose-dependent increases in lung weight. The increased weight was the result of additional tissue mass rather than edema. Both connective-tissue components, elastin and collagen, were significantly increased in the 1.0-mg/m3 group when these components were expressed on the basis of dry weight. Dose-dependent changes at the terminal bronchioles consisted of hyperplasia and flattening of type II cells, inflammation, and the proliferation of fibroblasts. Exposure to Cd also resulted in the development of intralymphatic microgranulomas in the perivascular and peribronchiolar lymphoid tissues.

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“…Toxicity is affected not only by Cd concentration but also by the form, this is probably related to solubility. The bioavailability of Cd is dependent on the solubility 11) . On acute exposure, the bioavailabilities and the toxicity of more soluble Cd compounds are higher than those of less soluble Cd compounds after rapid absorption in blood by inhalation exposure 12) .…”

Section: Discussionmentioning

confidence: 99%

Acute Lethal Toxicity, Hyperkalemia Associated with Renal Injury and Hepatic Damage after Intravenous Administration of Cadmium Nitrate in Rats

Dote

Shimizu

et al. 2007

Journal of Occupational Health

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(CdN) is commonly used in Ni-Cd battery factories. The possibility of accidental exposure to CdN is great. CdN is very soluble in water compared to other Cd compounds. Therefore, acute toxicity would be expected to be quick due to rapid absorption after exposure. However, the mechanisms of CdN toxicity have not been fully elucidated. We investigated the acute lethal toxicity and harmful systemic effects of acute exposure to large doses of CdN. The lethal dose and dose-response study of the liver and kidney were determined after intravenous administration of CdN in rats. The LD 50 of CdN was determined to be 5.5 mg/ kg. Doses of 2.1, 4.2, 6.3 mg/kg were selected for the dose-response study. Liver injury was induced at doses greater than 4.2 mg/kg. Severe hepatic injury occurred in the 6.3 mg/kg group, which would have been caused by acute exposure to the high concentration of Cd that exceeded the critical concentration in hepatic tissue. A remarkable decrease in urine volume in the 6.3 mg/ kg group indicated acute renal failure. A decrease in creatinine clearance suggested acute glomerular dysfunction at doses greater than 4.2 mg/kg. Increases in urinary N-acetyl-β-D-glucosaminidase/creatinine, β 2 -microglobulin and glucose in the 6.3 mg/kg group indicated proximal tubular injury. Secretion of K ion was also severely affected by proximal tubular injury and severe decreases in urine volume, and an increase in serum K ion was identified at doses greater than 4.2 mg/kg. Thus severe hyperkalemia might be associated with the cardiac-derived lethal toxicity of CdN. (J Occup Health 2007; 49: 17-24)

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The clearance of cadmium aerosols after I inhalation exposure

Cited by 44 publications

References 0 publications

Distribution of Intratracheally Administered Cadmium in Rats

Distribution of Intratracheally Administered Cadmium in Rats

Pulmonary changes resulting from subchronic exposure to cadmium chloride aerosol

Acute Lethal Toxicity, Hyperkalemia Associated with Renal Injury and Hepatic Damage after Intravenous Administration of Cadmium Nitrate in Rats

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