Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (L6)
Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (L8, A18, A19, A28)
Evaluation: There is sufficient evidence in humans for the carcinogenicity of cadmium and cadmium compounds. There is sufficient evidence in experimental animals for the carcinogenicity of cadmium compounds. There is limited evidence in experimental animals for the carcinogenicity of cadmium metal. In making the overall evaluation, the Working Group took into consideration the evidence that ionic cadmium causes genotoxic effects in a variety of types of eukaryotic cells, including human cells. Overall evaluation: Cadmium and cadmium compounds are carcinogenic to humans (Group 1). /Cadmium and cadmium compounds/
CLASSIFICATION: B1; probable human carcinogen. BASIS FOR CLASSIFICATION: Limited evidence from occupational epidemiologic studies of cadmium is consistent across investigators and study populations. There is sufficient evidence of carcinogenicity in rats and mice by inhalation and intramuscular and subcutaneous injection. Seven studies in rats and mice wherein cadmium salts (acetate, sulfate, chloride) were administered orally have shown no evidence of carcinogenic response. HUMAN CARCINOGENICITY DATA: Limited. /Classification based on former EPA guidelines/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A2;可疑的人类致癌物。/镉及其化合物,如Cd/
A2; Suspected human carcinogen. /Cadmium and compounds, as Cd/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
镉及其化合物:已知是人类致癌物。
Cadmium and Cadmium Compounds: known to be human carcinogens.
AFTER A YR OF FEEDING 1 PPM CADMIUM (AS CADMIUM SULFIDE (CDS) OR CD CONTAINED IN ROLL SHELL LIVER) IN CA DEFICIENT DIET OF FEMALE RATS, ACCUM RATE IN LIVER & KIDNEY WAS 0.33-0.48%, WHEREAS THAT OF WATER SOL CD CMPD & CD FED AS CD POLLUTED RICE WAS 0.43-0.57%.
Rats were exposed 6 hr/day over 10 days to 0.3 mg/cu m of water soluble cadmium chloride and 0.2, 1.0 and 8.0 mg/cu m of insoluble cadmium sulfide, then killed at intervals over a 3-month period for serial measurements of lung, renal and fecal cadmium. Cadmium chloride and high-dose cadmium sulfide animals showed a transient increase in lung weight. Clearance of both compounds was biphasic. Approximately 40% of deposited material was cleared during the 10-day exposure period. For cadmium chloride, only 9% of the lung burden was cleared rapidly after the last exposure (half-life 1.0 days) and 47%. slowly (half-life 87 days), leaving a residual lung burden of 44%. For cadmium sulfide, 41% of the lung burden was cleared rapidly (half-life 1.4 days) and 40% slowly (half-life 42 days), leaving a final residue 19%. In the cadmium sulfide high-dose group, the retention of cadmium sulfide in the lung was greater than that in the cadmium sulfide low-dose groups, indicating that clearance mechanisms may possibly have been impaired in the high-dose group by too great a lung burden. For both compounds, fecal cadmium was initially high. Renal accumulation of cadmium was substantial for cadmium chloride during the exposure period and continued over the following months until it represented approximately 35% of the total cadmium cleared from the lung. For cadmium sulfide, renal accumulation was only 1% of the amount cleared from the lung. The bioavailability of cadmium from cadmium sulfide is thus poor, the majority being cleared from the lungs and excreted in the feces. However, the bioavailability of inhaled cadmium sulfide measured as cadmium in the kidney is greater than the bioavailability of orally ingested cadmium sulfide.
1.周国泰,化学危险品安全技术全书,化学工业出版社,1997 2.国家环保局有毒化学品管理办公室、北京化工研究院合编,化学品毒性法规环境数据手册,中国环境科学出版社.1992 3.Canadian Centre for Occupational Health and Safety,CHEMINFO Database.1998 4.Canadian Centre for Occupational Health and Safety, RTECS Database, 1989
experimental results. The complexes 1 and 2 have been used as singlesourceprecursors for the synthesis of ethyleneglycol capped CdS 1 and CdS 2 nanoparticles, respectively. CdS 1 and CdS 2 nanoparticles have been synthesized by solvothermal method. PXRD, SEM, Elemental colour mapping, EDAX, TEM and UV–Vis spectroscopy have been used to characterize the as-prepared CdSnanoparticles. The X-ray diffraction