ACGIH: TWA 0.1 mg/m3NIOSH: IDLH 10 mg/m3; TWA 0.015 mg/m3
物理描述：
Anhydrous nickel sulfate is a yellow-green crystalline solid. Nickel sulfate can also be obtained as a hexahydrate (NiSO4.6H2O (CAS: 10101-97-0) which is blue to emerald green, and as a heptahydrate (NiSO4.7H2O) (CAS: 10101-98-1) , which is green. Samples can contain variable quantities of water, depending on their previous exposure to moisture or conditions. All forms are mildly toxic and are carcinogenic. All are denser than water. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. Used to make other nickel compounds, in printing, and in dyeing of textiles.
颜色/状态：
Green-yellow crystals
气味：
Odorless
稳定性/保质期：
STABLE @ 40 °C /HEXAHYDRATE/
自燃温度：
Not flammable (USCG, 1999)
分解：
848 °C. This produces toxic fumes of sulfur trioxide and nickel monoxide. See ICSC 0926. See ICSC 1202. Reacts with oxidants. This generates fire and explosion hazard. The solution in water is a weak acid.
Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and _2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, wherease unabsorbed nickel is excreted in the faeces. (L41)
Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. (L41, A40)
CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Human data in which exposure to nickel refinery dust caused lung and nasal tumors in sulfide nickel matte refinery workers in several epidemiologic studies in different countries and on animal data in which carcinomas were produced in rats by inhalation and injection. HUMAN CARCINOGENICITY DATA: Sufficient. /Nickel refinery dust/
Evaluation: There is sufficient evidence in humans for the carcinogenicity of nickel sulfate, and of the combinations of nickel sulfides and oxides encountered in the nickel refining industry. There is inadequate evidence in humans for the carcinogenicity of metallic nickel and nickel alloys. There is sufficient evidence in experimental animals for the carcinogenicity of metallic nickel, nickel monoxides, nickel hydroxides and crystalline nickel sulfides. There is limited evidence in experimental animals for the carcinogenicity of nickel alloys, nickelocene, nickel carbonyl, nickel salts, nickel arsenides, nickel antimonide, nickel selenides and nickel telluride. There is inadequate evidence in experimental animals for the carcinogenicity of nickel trioxide, amorphous nickel sulfide and nickel titanate. The Working Group made the overall evaluation on nickel compounds as a group on the basis of the combined results of epidemiological studies, carcinogenicity studies in experimental animals, and several types of other relevant data, supported by the underlying concept that nickel compounds can generate nickel ions at critical sites in their target cells. Overall evaluation: Nickel compounds are carcinogenic to humans (Group 1). Metallic nickel is possibly carcinogenic to humans (Group 2B). /Nickel compounds/
Nickel concentration in serum and whole blood and excretion in urine was assayed at different time intervals before and after ingestion of nickel sulfate in 8 healthy volunteers for 3 days. The peak level of nickel in blood was reached 2.5 hours after nickel ingestion, and maximal urinary excretion of nickel occured during the first 8 hours after ingestion.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
硫酸镍可以通过豚鼠、兔子和老鼠的皮肤被吸收。
Absorption of nickel sulfate from the skin has been found to occur in guinea pigs, rabbits, and rats.
The relationship between dose level of nickel sulfate and lung clearance, tissue distribution, and excretion of the metal was examined. F344N rats were given intratracheal injections of 17, 190, or 1800 nm (63)nickel labelled nickel sulfate. Tissues containing the highest concentrations of (63)nickel after 4, 24, and 96 hr were the lung, trachea, larynx, kidney, urinary bladder, adrenals, blood, large intestine, and thyroid. (63)Nickel was rapidly cleared from the lungs to the blood. Eight to 49% of the nickel sulfate remained in the lungs at 4 hr post treatment depending upon the original dose. Urine was the major form of (63)nickel excretion and accounted for 50% of the doe at the 17 and 190 nm levels and 80% at the 1800 nm level. The half time for urinary clearance was 4.6 hours at the highest dose and 23 hours at the lowest dose. Over 50% of the (63)nickel remaining 96 hours post treatment was in the lungs, and the half time for lung (63)nickel clearance ranged from 36 hr at the lowest dose to 21 hr at the highest dose. Urinary and pulmonary clearance of (63)nickel were both dose dependent.
In human volunteers who ingested nickel sulfate in the drinking water or food, at doses of between 12 and 50 ug/kg body weight (one treatment), the amt of nickel absorbed avg 27 plus or minus 17% of the dose ingested in water compared with 0.7 plus or minus 0.4% of the same dose ingested in food ... .
NICKEL METAL COMPOSITIONS AND NICKEL COMPLEXES DERIVED FROM BASIC NICKEL CARBONATES
申请人：OSTERMAIER JOHN J.
公开号：US20110196168A1
公开（公告）日：2011-08-11
Nickel-metal-containing solids for use in manufacturing nickel metal complexes are disclosed. The nickel-metal-containing solids are made by reducing basic nickel carbonates. By varying the molar ratios of carbonates and bicarbonates to nickel salts, the methods provide basic nickel carbonates that produce superior nickel metal-containing solids that react more effectively with phosphorous-containing ligands. The phosphorous containing ligands can be both monodentate and bidentate phosphorous-containing ligands.
Electrochemical Quartz Crystal Microgravimetry Study of Metal Deposition from EDTA Complexes
作者：Eimutis Juzeliunas、Howard W. Pickering、Konrad G. Weil
DOI：10.1149/1.1393318
日期：——
The electrochemicaldeposition of metalsfrom Me II (ethylenediaminetetraacetic acid, EDTA) complexes was studied by electrochemicalquartzcrystalmicrogravimetry. These investigations are important for the development of environmental clean-up processes, such as remediation of metal-contaminated soils by EDTA and subsequent electrochemical recovery of metal, in situ electrokinetic soil remediation
Me II（乙二胺四乙酸，EDTA）配合物的金属电化学沉积通过电化学石英晶体微重量法进行了研究。这些研究对于环境清理过程的发展具有重要意义，例如 EDTA 修复金属污染土壤和随后的金属电化学回收、原位电动土壤修复、电化学气体净化等。对 Pb、Cu、Cd、Zn 和 Ni 等废物位点进行了调查。从电极质量的明显增加中检测到金属沉积的潜在区域。我们观察到质子化和非质子化 EDTA 络合物中 Pb、Cu、Cd 和 Zn 的还原。没有发现镍沉积的迹象。而 Cu、Cd 的扩散限制电流，并且可以实现 Pb 沉积，Zn 沉积电流要低得多。这可以用锌沉积过程中的电极钝化来解释。确定了副反应，即质子还原、EDTA 还原和水分解。
Fluorine-containing acetophenones optionally halogenated on the CH.sub.3
申请人：Bayer Aktiengesellschaft
公开号：US05142092A1
公开（公告）日：1992-08-25
Fluorine-containing acetophenones, optionally halogenated on the CH.sub.3 group, of the formula ##STR1## in which X represents hydrogen, chlorine or bromine and the radicals R.sub.1 to R.sub.5 have the following meaning, a) R.sub.1 and R.sub.4 denote fluorine, R.sub.2 and R.sub.5 denote chlorine and R.sub.3 denotes CF.sub.3, or b) R.sub.1, R.sub.3 and R.sub.4 denote fluorine and R.sub.2 and R.sub.5 denote hydrogen, or c) R.sub.1, R.sub.4 and R.sub.5 denote hydrogen, R.sub.2 denotes chlorine and R.sub.3 denotes CF.sub.3, or d) R.sub.1, R.sub.4 and R.sub.5 denote hydrogen, R.sub.2 denotes chlorine and R.sub.3 denotes OCF.sub.3, or e) R.sub.1, R.sub.4 and R.sub.5 denote hydrogen and R.sub.2 and R.sub.3 denote CF.sub.3, or f) R.sub.1 denotes chlorine, R.sub.2 denotes CF.sub.3 and R.sub.3, R.sub.4 and R.sub.5 denote hydrogen, or g) R.sub.1 denotes chlorine, R.sub.2, R.sub.3 and R.sub.4 denote hydrogen and R.sub.5 denotes CF.sub.3, or h) R.sub.1 denotes chlorine, R.sub.2, R.sub.4 and R.sub.5 denote hydrogen and R.sub.3 denotes CF.sub.3 and a process for their preparation from the corresponding fluorinated benzonitriles or benzyl halides by reaction with an organomagnesium compound capable of introducing methyl groups and subsequent hydrolysis, if appropriate followed by a chlorination or bromination.
