品名

锗; Germanium; CAS:7440-56-4;

锗化氢; Germane; CAS:7782-65-2

氧化锗;Germanium dioxide; CAS:1310-53-8

氯化锗;

理化性质

银灰色脆硬金属,元素符号Ge。原子量75.29。相对密度5.35。熔点937.4 ℃。沸点2830℃。锗具有半导体性质。在600℃以下时,不与氧反应,但加热到熔点以上时,就挥发燃烧成白色氧化锗。锗不溶于盐酸,在硫酸中溶解慢,可被硝酸转变为氧化物。常见的锗化合物有氧化锗（GeO2）,氯化锗（GeCl4）及锗化氢（GeH4）。

接触机会

金属锗矿物有硫银锗矿和锗石等,也存在于含硫化锌的矿石中。工业上主要用金属锗作半导体; 制造特种玻璃及萤光材料等。在生产和使用锗及锗化合物时均可接触到。

侵入途径

可从胃肠道和呼吸道侵入。

毒理学简介

金属锗粉：人（男性）经口TDLo: 58 mg/kg/26W-I；786 mg/kg/2Y-I。儿童经口TDLo: 2 gm/kg/78W-I。大鼠吸入LCLo: 3860 mg/m3/4H。

锗化氢：小鼠经口LD50: 1250 mg/kg；吸入LC50: 1380 mg/m3。

氧化锗：大鼠经口LD50: 1250 mg/kg；吸入LC50: >1420 mg/m3/4H。小鼠经口LD50: 1250 mg/kg。

锗及其化合物属于低毒类。动物的急性毒作用表现为体温过低、倦怠、腹泻、呼吸循环衰竭。病理改变为肺水肿、出血、小肠壁点状出血、腹膜腔积液; 未见明显的神经、血液毒性作用。

锗由胃肠道吸收很快,4小时吸收给予剂量的76.3 ％; 8小时后吸收96.4 ％,皮下、肌肉、腹腔内注射时,吸收也很快,几乎全部吸收。

锗进入血液后,不与血浆蛋白结合,而广泛分布于各脏器。给狗静脉注射氧化锗后,其组织含锗量较高,依次为肾、肝、脾、胃肠道和骨骼。锗在体内无明显的蓄积作用。可由尿和粪便中排出,肾脏是主要排出途径。

有报道正常人血锗的含量为4.0μmol/L(0.29mg/L); 红细胞为8.95μmol/L(0.65mg/L); 尿为17.36μmol/L(1.26mg/L)。也有人测定尿锗的正常范围为7.71～41.33μmol/d(0.56～3mg/d)。

临床表现

氢化锗接触到眼结膜时形成锗酸,可引起刺激症状。四氯化锗对呼吸道有刺激作用,引起支气管炎或肺炎。对皮肤有刺激作用,可引起刺激症状。

美国HSDB引用文献：

*AMONG SUBGROUP IVA METALS, GERMANIUM IS CONSIDERED LEAST TOXIC... PHARMACOLOGICAL INERTNESS, DIFFUSIBILITY, & RAPID EXCRETION ARE RESPONSIBLE FOR LOW GERMANIUM TOXICITY. [R18, 179]

*GERMANIUM IS NOT CONSIDERED AN INDUSTRIAL HEALTH HAZARD; ACCIDENTAL POISONINGS IN HUMANS ARE RARE, IN SPITE OF EXPOSURE TO APPRECIABLE AMT OF GERMANIUM IN FOODS & FLUE DUST, & IN ELECTRONICS INDUSTRY. [R18, 177]

*Symptoms: Low temperature, languor, diarrhea, cyanosis, extreme depression of heart and breath, edema, lung hemorrhage, spot hemorrhage from the small intestine wall, peritoneal extravasation. [R19]

*One effect which may have human relevance is the profound ability of germanium to disturb water balance when high exposure levels are expected. This leads to hemoconcentration, a fall in blood pressure, and hypothermia. [R20, 504]

*Germanium compounds are marketed as nonprescription drugs in Europe and are recommended by the suppliers for AIDS and metastatic cancer. /A/ patient with nonmetastatic breast cancer who died because of severe lactic acidosis (plasma lactate concn = 27 mmol/l) after ingestion of 25g of elemental germanium over a 2 mo period. Renal failure and hepatotoxicity had newly developed during a germanium intake. Postmortem examination revealed severe hydropic vacuolation of tubule cells and the presence of inclusion bodies predominantly in straight proximal tubule cells with normal appearance of renal interstitium and glomeruli. The liver showed panlobular steatosis. Urine, blood and tissue (kidney, liver, muscle, pancreas) levels of germanium were high. Lactic acidosis may have been caused by the combined germanium induced renal and hepatic failure (underutilization), but it remains to be seen whether germanium can affect lactate production and/or metabolism. [R22]

*Acute renal failure (ARF) or renal dysfunction (RD) associated with germanium induced nephrotoxicity has been reported in 18 patients since 1982. In 2 of these cases the patients died of acute renal and cardiogenic failure. In 17 of 18 cases biopsies showed vacuolar degeneration in renal tubular epithelial cells in the absence of glomerular changes, without proteinuria or hematuria. Accumulated elemental germanium intake in 17 patients over a period of 4 to 36 months ranged between 16 and 328 g, or more than 100 to 2000 times the average estimated dietary intake of germanium for man (1.5 mg/day; range 0.40 to 3.40 mg/day). The biological half-life of germanium is 4.5 days for kidneys, the highest retention level of any organ. The mean concn of germanium in healthy adult kidneys is 9.0 mg/kg wet weight. In 3 patients studied with germanium induced RD or ARF, urinary germanium excretion was 9, 15, and 60 ng/ml, compared to greater than 5 ng/ml in healthy controls, and remained elevated even 12 months after discontinuing supplemental germanium intake. The mechanism for germanium induced nephrotoxicity remains unknown, although the suspected cause is the inorganic germanium salts, such as germanium dioxide. Sufficient evidence for a role of organogermanium compounds, such as carboxyethyl germanium sesquioxide or citrate-lactate germanate, In germanium induced nephrotoxicity remains lacking. The recent introduction of over the counter germanium nutritional supplements in some countries increases the risk of additional cases of germanium induced nephrotoxicity, especially if appreciable levels of inorganic germanium salts are present and consumed for long periods. ... [R23]

*The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and saturation level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to any of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Franconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus. [R26]

*Of the semiconductor metals only arsenic has been extensively studied as a human carcinogen and systemic toxicant. Recent studies have shown however that gallium, arsenic and indium are capable of producing marked alterations in cellular gene products. After acute in vivo admin of indium and thallium have been shown to produce decreases in the activity of some drug metabolizing enzymes dependent on cytochrome p450; therefore these metals would be capable of interfering with the metabolism of organic carcinogens. Selenium is essential for the activity of the enzyme glutathione peroxidase which modulates the active intermediates generated by drug metabolizing enzyme systems. Germanium produces toxicity in a number of organ systems. Antimony produces lung and circulatory system effects. Overall available data suggest that these metals or metalloids are capable of biologically altering several cellular defense mechanisms involved in the carcinogenic process and that further studies are needed to determine the associated risks. [R27]

处理

对症处理。

标准

车间空气卫生标准:

四氢化锗：

美国ACGIH TLV-TWA 0.63 mg/m3 (0.2 ppm)

美国MSHA STANDARD-air: TWA 0.2 ppm (0.6 mg/m3)

澳大利亚: TWA 0.2 ppm (0.6 mg/m3) JAN 1993;

比利时: TWA 0.2 ppm (0.63 mg/m3) JAN 1993;

丹麦: TWA 0.2 ppm (0.6 mg/m3) JAN 1993;

芬兰: STEL 0.2 ppm (0.6 mg/m3) JAN 1993;

法国: TWA 0.2 ppm (0.6 mg/m3) JAN 1993;

荷兰: TWA 0.2 ppm (0.6 mg/m3) JAN 1993;

俄罗斯: STEL 5 mg/m3 JAN 1993;

瑞士: TWA 0.2 ppm (0.6 mg/m3) JAN 1993;

英国: TWA 0.2 ppm (0.6 mg/m3), STEL 0.6 ppm JAN 1993;

保加利亚，哥伦比亚，约旦，韩国 参照美国 ACGIH TLV;

新西兰，新加坡，越南 参照美国 ACGIH TLV

氧化锗：

俄罗斯: STEL 2 mg/m3 JAN 1993

病例报告

*A report /of/ an autopsy case of chronic germanium intoxication with major pathological changes in the central and peripheral sensory nervous systems. The patient was a 4 yr old girl who had suffered from gait disturbance and generalized muscle weakness for 22 months. She had been given orally germanium compounds (containing germanium dioxide 225-450 mg/day) for the previous 28 months. In addition to the findings of chronic renal failure and anemia she presented characteristic neurological symptoms exemplified by diffuse muscle atrophy,tongue fasciculation, sensory impairment and truncal ataxia as well as areflexia. Median and ulnar sensory nerve conduction velocities were also reduced. On the 17th hospital day she died of renal failure. In addition to conspicuous degeneration of renal tubular cells pathological studies revealed marked nerve fiber loss degeneration and gliosis in the dorsal column of the spinal cord which were most conspicuous in the thoracic and cervical cord. Axonal degenerative changes were also conspicuous in the sural and sciatic nerves. High concn of germanium was detected in the brain cerebellum spinal cord sciatic nerve, liver and kidney. It was suggested that the neural involvement in the current case was caused by chronic toxicity of germanium. [R21]

*... Five patients who have taken inorganic germanium preparations over a prolonged period /are reported/. In all cases, the renal function deteriorated with no proteinuria or hematuria. Histological examination of the kidneys showed widespread tubular degeneration and interstitial fibrosis with minor glomerular abnormalities. Most patients had gastrointestinal symptoms such vomiting, anorexia and weight loss; one patient had peripheral neuropathy and myopathy. A considerable amount of germanium was detected in the hair or nails of these patients. These cases clearly show that abuse of inorganic germanium compounds can induce renal damage with various extrarenal manifestations. [R24]

*A 55 year old woman was admitted to our hospital, complaining of general malaise, muscular weakness, anorexia and weight loss. She had a history of ingesting of a certain germanium cmpd over the preceding 19 months, with a total dose of 47g as germanium element. She was found to have renal failure (blood urea nitrogen, 44 mg/dl; serum creatinine, 2.6 mg/dl) without abnormal findings in urinalysis, and muscular and nervous damage. Initially, polymyositis was diagnosed and prednisolone admin. However, no improvement was seen, and neuromuscular symptoms and signs steadily worsened, ending in death. Microscopic study of the kidney showed that lipofuscin granules incr in the cells of the thick ascending limb of Henle loop to the distal convoluted tubule accompanying mild tubular atrophy and that sole of the tubules of these segments had vacuolar degeneration or desquamation. No apparent glomerular and vascular changes were observed. High germanium content was found in serum, urine and various tissues, e.g., spleen, liver, kidney, and adrenal gland and myocardium, while in controls germanium could not be detected in sera, urine or tissues. ... Also reviewed are case reports about germanium toxicity, and discuss the pathogenesis of renal failure induced by germanium compounds. [R25]

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