121-19-7O=[N+]([O-])c1cc([As](=O)(O)O)ccc1OXMVJITFPVVRMHC-UHFFFAOYSA-N4-hydroxy-3-nitrophenyl arsonic acid appears as pale yellow crystals or light tan powder. (NTP, 1992)
121-19-7DTXSID9020956CHEMBL1321154CHEBI:35817greater than 572 °F (NTP, 1992)
300 °C
4-hydroxy-3-nitrophenyl arsonic acid appears as pale yellow crystals or light tan powder. (NTP, 1992)
Pale yellow solid; [Merck Index] Fine yellow crystals; [MSDSonline]
Solid
145.0 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: TOXCAST; Source Identifier: DTXSID9020956]
145.5 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]
This chemical does not meet GHS hazard criteria for 55.9% (52 of 93) of all reports.
Danger
H301 (44.1%): Toxic if swallowed [Danger Acute toxicity, oral]
P261, P264, P270, P271, P273, P301+P316, P304+P340, P316, P321, P330, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 93 reports by companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Restricted substance: Roxarsone
Roxarsone: Does not have an individual approval but may be used under an appropriate group standard
SYMPTOMS: This compound may cause irritation. Symptoms of exposure to this class of compounds include restlessness, nausea, vomiting, headache, dizziness, chills, cramps, irritability and variable paralysis that may progress over a period of several weeks. Ventricular arrhythmias may occur. Inhalation of dusts may cause acute pulmonary edema, restlessness, dyspnea, cyanosis, cough with foamy sputum, and rales. The principle manifestations are gastrointestinal disturbances. Chronic poisoning can result in polyneuritis, optic neuritis, anesthesias, paresthesias, bronzing of the skin, alopecia, localized edema, dermatitis, liver cirrhosis, abdominal pain, salivation, anemia, weight loss, chronic nephritis, cardiac failure and dependent edema. Ingestion of lethal doses of this type of compound can cause violent gastroenteritis, convulsions and coma. Death may occur from circulatory failure.
Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (L20)
Agents useful in the treatment or prevention of COCCIDIOSIS in man or animals.
Substances that inhibit the growth or reproduction of BACTERIA.
Used as an antimicrobial agent (growth promoter) for poultry and swine, a reagent for zirconium, formerly in the manufacture of arsphenamines, and as a veterinary medicine for control of enteric infections; [HSDB]
Farming (Feed Additives) [Category: Industry]
3-nitro-4-hydroxy-phenyl-arsonic acid is found in poultry feed.
용도antiinfective, preservative
일반 설명Pale yellow crystals or light tan powder.
현재 필터 조건에 해당하는 반응 기록이 없습니다.
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BEIGE-BROWN FINE CRYSTALLINE POWDER
May cause arsenic poisoning; [CAMEO] Almost nothing is known regarding health effects of organic arsenic compounds in humans. Studies in animals show that some simple organic arsenic compounds are less toxic than inorganic forms. Ingestion of methyl and dimethyl compounds can cause diarrhea and damage to the kidneys. [ATSDR ToxProfiles] Marginally increased incidence of pancreatic adenomas in 2-year feeding studies of rats; Repeated oral doses (0.87-5.8 mg/kg/day for 1 month) to pigs causes neurotoxicity with axonal degeneration and partial paralysis. Causes kidney injury in animals in acute toxicity testing; Oral LD50 (rat) = 81 mg/kg; [HSDB] In order of decreasing toxicity are inorganic trivalent, organic trivalent, inorganic pentavalent, and organic pentavalent compounds. [Sullivan, p. 858] Arsenic and arsenic compounds are carcinogenic in humans (not necessarily to all individuals chemicals within the group). [IARC] May cause irritation; Targets pancreas, kidneys, and nerves; Effects in high-dose animal studies include diffuse hepatitis (hepatocellular necrosis) and kidney damage; [MSDSonline] See Arsanilic acid.
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with 60-70% ethanol and transfer the dampened material to a suitable container. Use absorbent paper dampened with 60-70% ethanol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.
Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (L20)
Hypovolemia from capillary leakage (third-spacing of fluids) is a common, serious, early effect. Muscle cramps, facial edema, bronchitis, dyspnea, chest pain, dehydration, intense thirst, and fluid-electrolyte disturbances are also common following significant exposures. A garlic-like odor of the breath and feces may also occur. After absorption, arsenic may cause multi-organ failure by inhibiting sulfhydryl-containing enzymes. Encephalopathy, with headache, lethargy, mental confusion, hallucinations, emotional lability, memory loss and delirium may occur; seizures, stupor, convulsions, coma, and death may follow within 24 hours of a severe acute exposure. Dysrhythmias (particularly QTc prolongation and torsade de pointes), cardiomyopathy, ARDS, hepatitis, rhabdomyolysis, hemolysis, and renal failure may develop over several days. The sequence of chronic poisoning involves hyperpigmentation, and eczematoid and allergic dermatitis. muscle fasciculations; gross tremors; ataxia; incoordination; and mental confusion. Muscular weakness, limb tenderness and difficulty walking may follow. The final phase consists of peripheral sensory neuropathy of the hands and feet. That may be associated with a motor neuropathy as well (T36).
Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carcinogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (T1, A17)
Initial signs and symptoms of arsenic ingestion include burning lips, throat constriction and dysphagia, followed by excruciating abdominal pain, hemorrhagic gastritis, gastroenteritis, severe nausea, projectile voting, profuse "rice water-like" diarrhea, with hypovolemia that may result in hypotension and an irregular pulse. The sequence of chronic poisoning involves weakness, anorexia, hepatomegaly, jaundice, and gastrointestinal complaints, followed by conjunctivitis, irritation of the throat and respiratory tract. ther effects of chronic exposure include conjunctivitis with irritation and lacrimation; hair, skin and nail changes; hyperkeratosis of feet and hands; and melanosis, with pigment spots in corneal and conjunctival epithelium. Peripheral nervous system symptoms may include numbness, burning, and tingling of the hands and feet; pain; paresthesias; tenderness (T36).
Roxarsone
TR-345: Toxicology and Carcinogenesis Studies of Roxarsone (CASRN 121-19-7) in F344/N Rats and B6C3F1 Mice (Feed Studies) (1989 )
11/06/87
Equivocal Evidence
No Evidence
No Evidence
정의ChEBI: An organoarsonic acid where the organyl group is 4-hydroxy-3-nitrophenyl.