Mangandi(acetat)

1.74

Red monoclinic crystals; MP 80 °C; density 1.59 g/cu cm; soluble in water and ethanol. /Tetrahydrate/

1.59 @25 °C

Large Crystals; Dry Powder; Liquid; Large Crystals; Liquid

Brown crystals; [HSDB]

Cinnamon brown crystal solid; decomposes in water. /Dihydrate/

Pink crystals; soluble in methanol; dehydrates between 80-130 °C; decomposes at 350 °C to manganese(III) oxide. /Tetrahydrate/

This chemical does not meet GHS hazard criteria for 13.6% (99 of 729) of reports.

Warning

H315 (86.1%): Causes skin irritation [Warning Skin corrosion/irritation]

P264, P264+P265, P280, P302+P352, P305+P351+P338, P321, P332+P317, P337+P317, and P362+P364 (click each P-code to see the statement)

Aggregated GHS information provided per 729 reports by companies from 16 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Not Classified

Chemical: Acetic acid, manganese(2+) salt

Acetic acid, manganese(2+) salt (2:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Acetic acid, manganese(2+) salt (2:1) 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: 06-05-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/13305

Acetic acid, manganese(2+) salt: Does not have an individual approval but may be used under an appropriate group standard

Manganese acetate is an indirect food additive for use only as a component of adhesives.

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. Element: Manganese; Source compound: manganese acetate. (All substances listed may be in anhydrous or hydrated form.)

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Manganous acetate is included on this list.

... Substances for which a Federal Register notice has been published that included consideration of the serious health effects, including cancer, form ambient air exposure to the substance. Manganese (50 FR 32627; Aug. 13, 1985) is included on this list. /Manganese/

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m. /Manganese compounds and fume (as Mn)/

Recommended Exposure Limit: 15 Min Short-Term Exposure Limit: 3 mg/cu m. /Manganese compounds and fume (as Mn)/

Skin Irrit. 2 (86.1%)

Acute toxicity - category 4

Acute toxicity (Oral) - Category 4

(IL) ILLINOIS 150 ug/l /Manganese/

(NC) NORTH CAROLINA 50 ug/l /Manganese/

(NY) NEW YORK 300 ug/l /Manganese/

(CT) CONNECTICUT 500 ug/l /Manganese/

(ME) MAINE 200 ug/l /Manganese/

(MN) MINNESOTA 300 ug/L /Manganese/

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.

9.4 [mg/m3]

16 [mg/m3]

96 [mg/m3]

Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. (L228)

This work has identified the relative toxicity of four forms of manganese, using biogenic amine levels, tissue retention, weight gain, & activity scores as criteria. Male mice were chronically treated with four forms of manganese administered orally, mixed with the diet, for 12 months. The food intake for the control mice & the mice exposed to manganese was similar, but the manganese treatment reduced normal weight gain in the mice. The Mn levels were higher in some parts of brain after feeding insoluble salts than after the soluble salts. The concn of manganese was significantly increased in the liver & spleen of the manganese carbonate-exposed group, compared with the concn in the control group. Manganese dioxide feeding lowered dopamine & increased homovanilic acid. Since manganese dioxide is a powerful oxidizing agent in organic chemistry, it possibly enhanced the oxidative metabolite of dopamine. Accumulation of manganese in the brain correlated with reduced hypothalamic dopamine levels in the manganese acetate-exposed group; & the amount of manganese accumulated correlated with the intensity of suppression of motor activity. These findings indicate that manganese dioxide is more toxic than divalent manganese. Of the divalent manganese cmpds, manganese acetate seemed to have the greatest toxic effect.

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . /Manganese and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or in severe respiratory distress. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors for hypotension with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Manganese and related compounds/

Manganese acetate is an indirect food additive for use only as a component of adhesives.

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. Element: Manganese; Source compound: manganese acetate. (All substances listed may be in anhydrous or hydrated form.)

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Manganous acetate is included on this list.

... Substances for which a Federal Register notice has been published that included consideration of the serious health effects, including cancer, form ambient air exposure to the substance. Manganese (50 FR 32627; Aug. 13, 1985) is included on this list. /Manganese/

(IL) ILLINOIS 150 ug/l /Manganese/

(NC) NORTH CAROLINA 50 ug/l /Manganese/

(NY) NEW YORK 300 ug/l /Manganese/

(CT) CONNECTICUT 500 ug/l /Manganese/

(ME) MAINE 200 ug/l /Manganese/

(MN) MINNESOTA 300 ug/L /Manganese/

Manganese is absorbed mainly via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. Manganese is capable of existing in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. (L228)

The subcellular distribution of The subcellular distribution of manganese in brains of mice chronically administered manganese in different chemical forms with food was examined using gel chromatography. Male ddY-mice were divided into five groups of six animals each, and Groups 1 to 4 were given 2 g/kg manganese of standard laboratory mouse chow) in the form of manganese chloride, manganese acetate, manganese carbonate, or manganese oxide, in the diets for 12 months, while Group 5 served as control. Twenty four hours after the last feed, animals were decapitated and brains were rapidly removed for study of the different regions (corpus striatum, hypothalamus, midbrain, cerebral cortex, hippocampus, cerebellum, and medulla oblongata). Subcellular fractions (mitochondrial, microsomal and cytosolic) and gel chromatography fractions were analyzed for manganese contents using flame atomizer absorption spectrophotometry. Results showed that cerebral cortex levels of manganese in mice exposed to the nearly insoluble manganese carbonate and manganese oxide were higher than in controls, while manganese concentrations in the corpus striatum were similar to those in controls. Microsomal manganese in treated mice was also higher than in controls. The gel chromatographic profile of corpus striatum showed that 20% manganese was in the high molecular weight fractions, 45% was in the middle molecular weight fractions, while 32% was in the low molecular weight fractions. The percent manganese in high molecular weight fractions was higher (29% to 49%) in the manganese treated groups, than in controls. The percentage of manganese in low molecular weight fractions of the manganese oxide exposed group (9%) was lower than in the manganese chloride, manganese acetate, and manganese carbonate exposed groups (42%, 36%, and 38%, respectively).

Used as a dye mordant and varnish drier; [Merck Index] Used in fertilizers, food packaging, and feed additives; [Hawley]

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

Textile dyeing; oxidation catalyst; paint and varnish (drier, boiled oil manufacture); fertilizers; food packaging; feed additive /Tetrahydrate/

As mordant in dyeing; manuf bister; drier for paints and varnishes (1-1.5:1000).

As a catalyst (either alone or in combination with cobalt) in liquid-phase air oxidation of hydrocarbons to carboxylic acids.

All Other Basic Organic Chemical Manufacturing

Acetic acid, manganese(2+) salt (2:1): ACTIVE