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Indium (In) compounds are poorly absorbed when ingested and moderately so when inhaled. Muscle, skin, and bone constitute the main storage sites, but the excretion routes vary depending on the form: ionic indium is excreted primarily in urine; and fecal elimination is the predominant route for removal of colloidal indium. A biphasic pattern of excretion and a whole-body biological half-time in the order of 2 weeks have been reported for both forms of indium. Ionic indium is concentrated in the kidneys, producing renal failure; colloidal indium is taken up by the reticuloendothelial system, causing damage to the liver and spleen. Ionic indium has been shown to produce marked ultrastructural damage to the endoplasmic reticulum of both hepatocytes and renal proximal tubule cells, with associated disruption of heme metabolism and hemoprotein function. The intravenous administration of ionic indium to pregnant hamsters is reported to produce malformations of the fetal digits. The most common routes of exposure for the general population are inhalation and ingestion; for occupationally exposed persons, it is inhalation. The use of In for nanotechnology may increase the possibility of dermal absorption in work environments. The toxicology of indium has been reviewed by Izrael’son, 1973; Smith et al., 1978; Fowler, 1979 ; Fowler, 1986, and Fowler and Sexton (2002).

Animal experimental data show that germanium compounds, both inorganic and organic, are rapidly and almost completely absorbed from the lungs and the gastrointestinal tract. The distribution among the organs and tissues is fairly uniform, but there is evidence of an initial preference for kidney and liver, followed by rapid urinary excretion and long-term accumulation in the bone. Data on biological half-times are inadequate, but for the rat the whole-body retention half-time is estimated to be approximately 1.5 days. Germanium tetrachloride is a strong irritant of the respiratory system, skin, and the eye, possibly because it is easily hydrolyzed, producing hydrogen chloride; in mice, high-level inhalation exposures cause necrosis of the tracheal mucosa, bronchitis, and interstitial pneumonia. Systemic toxicity of germanium compounds is comparatively uncommon; however, when overexposure occurs, nephropathy, neuropathy, and hepatotoxicity are usually observed. Trialkylgermanium compounds are less toxic than the corresponding lead or tin alkyls, and current evidence suggests that germanium is not carcinogenic. Dimethylgermanium oxide is teratogenic in chickens, but sodium germanate has not produced malformations in hamsters. Cell culture studies show that water-soluble nanoparticle germanium may be more toxic than germanium dioxide (GeO2), but may not directly damage DNA; however, more research is needed. There is little information on the toxicity of inorganic germanium compounds to humans, except that germanium tetrachloride may produce skin irritation and germanium health supplements have been linked to serious health effects in humans. In clinical trials, spirogermanium, an organogermanium antitumor agent, has been shown to be neurotoxic. For these and other reasons, the U.S. Food and Drug Administration (FDA) authorized the detention of germanium products labeled to claim human health benefits. In addition, the American Cancer Society considers that germanium supplements may be harmful and that delaying conventional medical care to take germanium compounds could seriously impact health. High doses of germanium compounds (taken as supplements) induced remarkable lactic acidosis, hydropic degeneration of the proximal convoluted tubules with presence of inclusion bodies, and some cellular necrosis and subsequent renal failure; however, the renal glomeruli and the renal interstitial tissue seemed normal. Neurological effects involved negative deep tendon reflexes in the lower extremities and a persistent tingling sensation of the palms and soles. In addition to severe cardiac dilation, vacuolar degeneration of myocardial cells and interstitial edema were observed. Inhalation is the main route of occupational exposure to germanium during its production and that of related products; the main source of exposure for the general population is germanium naturally present in food. Short reviews on the toxicology of germanium and its compounds have been published by Mogilevskaja Ja, 1973; Underwood, 1977; Aldridge, 1978 ; Ohri et al., 1993, and Tao and Bolger (1997).