Chromic nitrate

Liquid; Liquid; Other Solid; Large Crystals; Other Solid

Pale green solid; Extremely deliquescent; Soluble in water; [Merck Index]

This chemical does not meet GHS hazard criteria for 13.8% (41 of 297) of reports.

Danger

H272 (76.8%): May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

P210, P220, P261, P264, P264+P265, P271, P272, P273, P280, P302+P352, P304+P340, P305+P351+P338, P317, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P370+P378, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 297 reports by companies from 18 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Nitric acid, chromium(3+) salt

Nitric acid, chromium(3+) salt (3:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Nitric acid, chromium(3+) salt (3:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 13-07-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/13746

Nitric acid, chromium(3+) salt: HSNO Approval: HSR001320 Approved with controls

Chromium (III) nitrate normally crystallizes with 9 molecules of water; [Ullmann] A strong oxidizing agent; May cause fire on contact with organic material; May cause irritation to skin, eyes, and mucous membranes; [CAMEO] May cause skin and respiratory sensitization after prolonged contact; [eChemPortal: ERMA] See Chromium III nitrate nonahydrate. See NITRATES and NITRITES. See Cr(III) compounds in Chromium.

0.041 [mg/m3]

110 [mg/m3]

640 [mg/m3]

There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (L1613, L16)

Chromium in its trivalent state is not very toxic. It may be oxidized to hexavalent chromium, a known carcinogen. Hexavalent chromium has also been shown to affect reproduction and development. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (L1137, A12)

Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613, A12, L16, A34, A35, A36)

Chromium in its trivalent state is not very toxic, but it may be oxidized to hexavalent chromium. Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (L1137, L16)

In the blood, 95% of chromium (III) is bound to large molecular mass proteins, such as transferrin, while a small proportion associates with low molecular mass oligopeptides. Serum chromium is bound to transferrin in the beta globulin fraction.

Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.

Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein. As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells. Chromium attenuates the activity of PTP-1B _in vitro,_ which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling. Transient upregulation of AMPK by chromium also leads to increased glucose uptake.

The metabolism of Cr (VI) involves reduction by small molecules and enzyme systems to generate Cr (III) and reactive intermediates. During this process, free radicals can be generated, which is thought to induce damage of cellular components and cause toxicity of chromium. The metabolites bind to cellular constituents.

Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (L1137, A12, L16)

Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form. Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed. Vitamin C and the vitamin B niacin is reported to enhance chromium absorption. Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids. Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration. Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF).

Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile. Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter.

Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form. Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone.

Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day. The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day.

Used to make catalysts; Also used as a corrosion inhibitor and in textile printing; [Merck Index] Used as a mordant in cotton printing; [Ullmann]

Textiles (Printing, Dyeing, or Finishing) [Category: Industry]

Chromium nitrate is used in the production of alkali metal-free catalysts and in pickling. (L517)

All Other Basic Inorganic Chemical Manufacturing

Nitric acid, chromium(3+) salt (3:1): ACTIVE