아스코르비산 나트륨

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.

Firefighters should wear full protective clothing including self-contained breathing apparatus. If possible control runoff from fire control or dilution water to prevent environmental contamination.

Use methods for the surrounding fire including water spray, dry chemical, carbon dioxide, or foam.

Keep container tightly closed when not in use. Store containers in a cool, dry location, away from direct sunlight, sources of intense heat, or where freezing is possible. Material should be stored in secondary containers or in a diked area, as appropriate. Store containers away from incompatible chemicals. Storage areas should be made of fireresistant materials. Post warning and "NO SMOKING" signs in storage and use areas, as appropriate.

Small releases can be cleaned-up wearing gloves, goggles and suitable body protection. In case of a large spill (in which excessive dusts can be generated), clear the affected area, protect people, and respond with trained personnel. If a vacuum is used for spill clean-up, only an explosion-proof vacuum should be used, due to the possibility for dust explosion. Do not allow the spilled product to enter public drainage system or open water courses. Place all spill residues in an appropriate container and seal. Thoroughly wash the area after a spill or leak clean-up. Avoid contamination of soil, and prevent spill residue from running to groundwater or storm drains.

Stop the flow of material, if this can be done without risk. Contain the discharged material. If sweeping of a contaminated area is necessary use a dust suppressant agent, which does not react with product...

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces 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.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

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. Ensure that the local ventilation moves the contaminant away from the worker.

Handling and storage Handling Procedures All employees who handle this material should be trained to handle it safely. Do not breathe dust. Avoid all contact with skin and eyes. Wherever dust clouds may be generated, eliminate sparks, flames and other ignition sources. Use this product only with adequate ventilation. Areas in which this compound is used should be wiped down periodically so that this substance is not allowed to accumulate. Dry powders can build static electricity charges when subjected to the friction of transfer and mixing operations. Provide adequate precautions, such as electrical grounding and bonding, or inert atmospheres. Wash thoroughly after handling.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

Effects of 17 environmental chemicals on urinary bladder carcinogenesis were investigated in rats. Male F-344-rats were given orally 0.05 percent N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN). Rats were fed diets containing 5 percent sodium-saccharin, 2 percent sodium-o-phenylphenate (SOPP), 2 percent butylated-hydroxyanisole (BHA), 5 percent sodium-L-ascorbate (SA), 5 percent ascorbic-acid, 5 percent ascorbic-stearate, 5 percent sodium-erythorbate (SE), 0.8 percent ethoxyquin, 0.02 percent N-nitrosopyrrolidine, 0.2 percent methylhydroquinone, 0.2 percent hydroquinone, 0.2 percent resorcinol, 0.8 percent catechol, 0.5 percent pyrogallol, 0.6 percent carbazole, 0.1 percent quinoline, or 1 percent uric-acid. The left ureter was ligated on day 22. Animals were killed after week 24 and autopsied. Urinary bladder, both kidneys, ureter, and liver were stained for light microscopy examination. No cancer was induced in any rat. Papillary or nodular (PN) hyperplasia was induced by BBN in 7 percent of controls. PN hyperplasia incidences and quantitative values were significantly higher in BBN treated rats fed sodium-saccharin, SOPP, BHA, SA, SE, ethoxyquin, and carbazole. Significant differences in incidences and quantitative values of papillomas were observed in BBN treated rats fed sodium-saccharin, SOPP, BHA, SA, and N-nitrosopyrrolidine. Histopathological changes were found in the left kidney, and dilation in the left pelvic space and ureter were common. No changes were found in the right kidney, ureter, or liver. The authors conclude that the ureter ligation system seems to be suitable as a short term method for the screening of bladder carcinogens and promoters.

Studies were made on the carcinogenic activity of butylated hydroxyanisole (BHA) in rats, mice, and hamsters and the effect of the antioxidants BHA, butylated hydroxytoluene (BHT), ethoxyquin (EQ), sodium L-ascorbate (SA), ascorbic acid (AA), sodium erythorbate (SE), propyl gallate (PG), and alpha-tocopherol, on two-stage chemical carcinogenesis in rats initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 1,2-dimethylhydrazine (DMH), diethylnitrosamine (DEN), 7,12-dimethylbenz(a)anthracene (DMBA), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), N-ethyl-N-hydroxyethylnitrosamine (EHEN), or N-methylnitrosourea (MNU). BHA clearly induced squamous cell carcinomas in both the rat and hamster forestomach. The tumorigenic action of crude BHA on the forestomach is largely due to 3-tert-BHA. In two-stage chemical carcinogenesis, BHA promoted MNNG or MNU-initiated forestomach and BBN- or MNU-initiated urinary bladder carcinogenesis and inhibited DEN- or EHEN-initiated liver and DMBA-initiated mammary carcinogenesis. BHT demonstrated promotion potential for urinary bladder and MNU-initiated thyroid carcinogenesis and inhibited DMBA-initiated ear duct carcinogenesis. EQ promoted EHEN-initiated kidney carcinogenesis and inhibited DMBA-initiated mammary and EHEN-initiated liver carcinogenesis. SA promoted forestomach and urinary bladder carcinogenesis and SE likewise enhanced urinary bladder carcinogenesis. alpha-Tocopherol inhibited ear duct carcinogenesis. No effects of any of the antioxidants on glandular stomach carcinogenesis were found. The results clearly demonstrated that antioxidants have different effects (promoting or inhibitory influences) depending on the organ studied and suggest the importance of a whole body approach to their investigation.

Studies were conducted on the carcinogenic activity of butylated hydroxyanisole (BHA) in rats and hamsters. To obtain information concerning the mechanism of action of BHA on the forestomach, the following areas were examined: the effects of 12 phenolic compounds structurally related to BHA on the hamster forestomach, the effects of combinations of BHA and other antioxidants on the rat forestomach, and the metabolism of BHA in the forestomach. Also examined were the effects of several antioxidants on two-stage carcinogenesis in rats. Squamous-cell carcinomas were induced in the forestomach of rats and hamsters fed BHA. In a limited study, 1 of 13 hamsters developed a squamous-cell carcinoma. The tumorigenic action of crude BHA on the forestomach was largely due to the action of 3-tert-BHA. p-tert-Butylphenol and 2-tert-butyl-4-methylphenol induced pronounced hyperplasia and papillomas in the hamster forestomach. BHA and other antioxidants, particularly propyl gallate and ethoxyquin, showed additive effects in inducing forestomach hyperplasia and cytotoxicity. Neither BHA nor its metabolites were found in the forestomach epithelium, although small amounts of metabolites were detected in the stomach contents. Thus, a direct action on the stomach epithelium may be exerted by BHA itself or by metabolites formed on interaction of BHA with gastric juice. BHA enhanced forestomach carcinogenesis initiated in rats by N-methyl-N'-nitro-N-nitrosoguanidine or N-methylnitrosourea (MNU) and enhanced urinary bladder carcinogenesis initiated by MNU or N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). In contrast, it inhibited carcinogenesis initiated in the liver by either diethylnitrosamine or N-ethyl-N-hydroxyethylnitrosamine (EHEN) and mammary carcinogenesis initiated by 7,12-dimethylbenz[a]anthracene (DMBA). BHT promoted urinary bladder carcinogenesis initiated by BBN or MNU and thyroid carcinogenesis initiated by MNU, but inhibited ear-duct carcinogenesis initiated by DMBA. Ethoxyquin promoted EHEN-initiated kidney carcinogenesis, but inhibited both DMBA-initiated mammary and EHEN-initiated liver carcinogenesis. Sodium ascorbate promoted forestomach and urinary bladder carcinogenesis, and sodium erythorbate also enhanced urinary bladder carcinogenesis. Alpha-tocopherol inhibited ear-duct carcinogenesis. No antioxidants tested had any effect on glandular stomach carcinogenesis. Thus antioxidants have independent modifying (promoting or inhibitory) effects in different organs.

The modifying effects of antioxidants were examined in a carcinogenesis system after N,N-dibutylnitrosamine treatment. Male F344 rats were given 0.05% N,N-dibutylnitrosamine in their drinking water for 4 wk and then treated with basal diet containing 2% butylated hydroxyanisole (BHA), 1% butylated hydroxytoluene (BHT) with 7 ppm vitamin K, 0.8% ethoxyquin, 5% sodium L-ascorbate, 5% sodium erythorbate, or no added chemical for 32 wk. BHA enhanced forestomach carcinogenesis but did not enhance esophageal carcinogenesis. BHT enhanced esophageal carcinogenesis but did not enhance forestomach carcinogenesis. Ethoxyquin significantly enhanced esophageal tumorigenesis. Neither esophageal nor forestomach carcinogenesis was affected by the other antioxidants evaluated. BHA significantly increased DNA synthesis of the forestomach epithelium, whereas BHT tended to increase that of the esophageal epithelium. Thus, BHA and BHT showed different modifying responses in carcinogenesis of the esophagus and forestomach.

For more Interactions (Complete) data for SODIUM ERYTHORBATE (7 total), please visit the HSDB record page.

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Sodium erythorbate forms white, free-flowing crystals. It is a synthetic antioxidant used in food and cosmetic formulations. Foliar application of sodium erythorbate sprays and dusts are used to control young tree decline in citrus trees and to reduce ozone damage to Thompson seedless grapes. It is also used in hydraulic fracturing mixtures to prevent precipitation of metal oxides (iron control). HUMAN EXPOSURE AND TOXICITY: Sodium erythorbate did not cause chromosomal aberrations or sister chromatid exchanges in cultured human embryo fibroblasts. ANIMAL STUDIES: Sodium erythorbate powder did not cause signs of dermal irritation when applied to the intact and abraded skin of rabbits. Instillation of sodium erythorbate powder to the conjunctival sac of rabbits caused slight and transient reddening of the conjunctiva that cleared within 24 hours. Sodium erythorbate did not cause maternal or fetal toxicity when administered to female rats and mice during gestation by oral intubation at dosages up to 1030 mg/kg/day. Developmental toxicity did not occur after pregnant rats were given up to 5% sodium erythorbate in feed during a 13-week teratogenesis study. It produced negative results in the Ames test, the host-mediated assay using S. typhimurium, chromosomal aberration tests using Chinese hamster ovary fibroblasts, the dominant lethal test using rats, and the B. subtilis rec assay. Sodium erythorbate did cause chromosomal aberrations in rat bone marrow cells in vivo. It did not increase the mitotic recombination frequency of S. cerevisiae D3 in vitro, and did not induce heritable translocation heterozygosity in male mice. Rats given 5% sodium erythorbate in feed for 168 days had no morphological alterations such as hyperplasias of the urinary bladder mucosa. It did not enhance the development of rare spontaneous tumors or transform benign tumors to carcinomas after administration to rats in feed at concentrations up to 2.5%. During a 24-week study, rats given 5% sodium erythorbate in feed had simple hyperplasia of the urinary bladder epithelium. The addition of 1.25-2.5% sodium erythorbate to drinking water did not significantly increase tumor incidence, time to death with tumors, or the distribution of tumors in mice after 96 weeks of treatment. It did not have modifying effects on second-stage carcinogenesis of the nonglandular and glandular stomach, colon, liver, kidneys, mammary gland, ear duct, or thyroid gland, but increased the incidence and average number of lesions of the urinary bladder after initiation with N-butyl-(4-hydroxybutyl)nitrosamine. After administration of sodium erythorbate to rats, they eliminated it in urine as erythorbic acid and dehydroerythorbic acid, whereas ascorbic acid and dehydroascorbic acid were not detected. ECOTOXICITY STUDIES: The acute toxicity of the sodium erythorbate to the freshwater fish rainbow trout (Oncorhynchus myldss) has been investigated and gave a 96-Hour LC50 of greater than 100 mg/L (semi-static).

EPA has released the first beta version (version 0.5) of the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The beta version of the iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays; See the data in Chemical Explorer/[USEPA; ICSS Dashboard Application; Available from, as of June 27, 2014: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of June 30, 2014: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=6381-77-7]

Sodium erythrobate's production and use as a preservative and antioxidant in foods and cosmetics(1) may result in its release to the environment through various waste streams(SRC); its use to control metal oxide precipitation in hydrofracking(3) will result in its direct release to the environment(SRC).

/LABORATORY ANIMALS: Acute Exposure/ Sodium Erythorbate powder was applied to the intact and abraded skin of six rabbits as a single 2 g/kg dose. A substantial amount of residual compound was observed 24 hours after dosing. No erythema, edema, or other signs of dermal irritation were observed at five of six test sites. One rabbit (abraded skin) had slight (1+) erythema at 24 hours that cleared by 48 hours.

/LABORATORY ANIMALS: Acute Exposure/ Sodium Erythorbate powder (100 mg) was instilled into the conjunctival sac of albino rabbits (10 male and 2 female). The eyes of half of the treated rabbits were rinsed after 5 seconds. Reactions were comparable in rinsed and unrinsed eyes, and were slight and transient in nature. One hour after dosing, two of six unrinsed eyes had congestion of the iris, but the iris reacted normally to light. Varying degrees of redness were observed in the lids of all unrinsed eyes. Slight redness of the nictitating membrane or palpebral conjunctiva at the medial canthus was observed in two unrinsed eyes. At one hour, 1+ iritis was observed in one rinsed eye. Five of six rinsed eyes had slight redness that was limited to only the nictitating membrane in three cases. At 24 hours, all eyes were normal, with the exception of one that had slight reddening of the conjunctiva at the medial canthus. All eyes, rinsed and unrinsed, were normal at 48 hours. The mean ocular irritation scores were 0.33/110 (unrinsed eyes) and 0.17/110 (rinsed eyes)

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male and female B6C3F1 mice (10 per sex per group) were given drinking water containing 0.625%, 1.25%, 2.5%, 5.0%, or 10% Sodium Erythrobate for 10 weeks. Water and feed were available ad libitum. The untreated control group consisted of 20 male and 20 female mice. By the end of the 1st week of treatment, six male mice and one female mouse of the 10% dosing group had died. Of the male mice given 5.0% Sodium Erythrobate, the average weekly body weight gain was slightly less than 90% that of the control female mice. Body weight gain was increased in female mice given Sodium Erythrobate at a concentration of 5.0%, compared to that of control mice. The maximum tolerated dose (MTD) of Sodium Erythrobate in drinking water was 2.5% for male mice and 5.0% for female mice. Mice given doses greater than the MTD had marked atrophy of both hepatocytes and splenic lymphoid follicles, as well as hydropic degeneration of the renal tubular epithelium. No significant changes were observed in the visceral organs of untreated mice or mice given the dose less than or equal to the MTD of Sodium Erythrobate.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Sodium Erythorbate powder (2 g/kg) was applied to the intact and abraded skin of six rabbits. Each test site was moistened with physiological saline just prior to dosing. After application of the test material, the exposure area was covered with a double layer of surgical gauze and a piece of rubber dam. The trunk of each rabbit was wrapped in a stockinette, which was secured to the body with tape. The dressings were removed after 24 hour, and the amount of residual sample and signs of localized irritation were noted. The exposure area was cleaned by thorough wiping, and the rabbits were observed for signs of toxicity for 14 days. At 72 hours, a significant amount of residual compound was found at the exposure site of each rabbit. Behavior, body weight gain, and consumption of feed and water were normal, and no signs of toxicity were observed.

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of sodium erythrobate is 100 to 999; the data may be greatly underestimated(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 19,468 workers (6,527 of these were female) were potentially exposed to sodium erythorbate in the US(1). Occupational exposure to sodium erythorbate may occur through inhalation and dermal contact with this compound at workplaces where sodium erythorbate is produced or used. Use data indicate that the general population may be exposed to sodium erythorbate via ingestion of some food products and dermal contact with consumer products containing sodium erythorbate(SRC).

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. 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 ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/