Natriumdiethyldithiocarbamat

1.1 at 68 °F (NTP, 1992) - Denser than water; will sink

1.1 g/cu cm at 20 °C/20 °C

Relative density (water = 1): 1.1

1.1 @ 20°C

Crystals from ethanol

Yellow to green liquid at 20 °C and 1013 hPa (solution in water)

greater than or equal to 100 mg/mL at 57 °F (NTP, 1992)

Soluble in water

Soluble in alcohol

Solubility in water: soluble

203 °F (NTP, 1992)

95 °C

90-102 °C

95 °C

5.9 (NTP, 1992) - Heavier than air; will sink (Relative to Air)

5.9 (Air = 1)

Relative vapor density (air = 1): 5.9

Sodium diethyldithiocarbamate appears as odorless white or slightly brown or slightly pink crystals. (NTP, 1992)

Crystals; [ICSC]

WHITE CRYSTALS.

Stable under recommended storage conditions. /Sodium diethyldithiocarbamate trihydrate/

Aqueous solutions decompose slowly.

AQUEOUS SOLN IS ALKALINE TO LITMUS & PHENOLPHTHALEIN

Solubility in water = 2.9X10+4mg/L; log Kow = 1.67; VP: 0.121 mm Hg; Henry's Law constant = 6.84X10-4 atm-cu m/mol; Hydroxyl radical reaction rate constant = 2.0X10-10 cu cm/molecule-sec (all estimated at 25 °C) /Ditiocarb/

Thin, irregular plate-like crystals from acetone, mp 94-102 °C. Also reported as 90-92 °C. Freely soluble in water; soluble in ethanol, methanol, acetone. Insoluble in ether, benzene. The aqueous solution is alkaline to litmus and phenolphthalein and slowly decomposes. (pH of 10% aqueous solution is 11.6 at room temperature). The addition of an acid to the aqueous solution produces a white turbidity due to the liberation of carbon disulfide. UV max (ethanol): 257, 290 nm (epsilon 1200, 1300) /Sodium diethyldithiocarbamate trihydrate/

Greenish-yellow liquid with a characteristic smell comprising a 23% solution in water

Warning

H302 (71.2%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P264+P265, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 66 reports by companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Warning

H302: Harmful if swallowed [Warning Acute toxicity, oral]

Chemical: Carbamodithioic acid, diethyl-, sodium salt

Status: Active Update: 30-08-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/11278

Sodium diethyldithiocarbamate: Does not have an individual approval but may be used under an appropriate group standard

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)

Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

SYMPTOMS: Symptoms of exposure to this chemical include irritation of the eyes. Continued exposure may cause mild skin irritation. The dusts of this compound are caustic to the mucous membranes. This compound is also caustic to the digestive tract.

Symptoms of exposure to this chemical include irritation of the eyes. Continued exposure may cause mild skin irritation. The dusts of this compound are caustic to the mucous membranes. This compound is also caustic to the digestive tract. [CAMEO] Danger of sensitization of the skin; [MAK] See Carba mix.

SODIUM DIETHYLDITHIOCARBAMATE is not compatible with strong oxidizing agents. Aqueous solutions slowly decompose to form carbon disulfide and an amine. Such decompositions are accelerated by acids. Addition of acid to the aqueous solution produces a white turbidity (NTP, 1992).

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Use water, foam, carbon dioxide, powder.

Fresh air, rest.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give one or two glasses of water to drink.

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.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /Sodium diethyldithiocarbamate trihydrate/

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary. /Sodium diethyldithiocarbamate trihydrate/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided; Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /Sodium diethyldithiocarbamate trihydrate/

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: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product. /Sodium diethyldithiocarbamate trihydrate/

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed. /Sodium diethyldithiocarbamate trihydrate/

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday. /Sodium diethyldithiocarbamate trihydrate/

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /Sodium diethyldithiocarbamate trihydrate/

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.

Rats exposed to enflurane (100 ppm) or methoxyflurane (300 ppm) in a closed all glass system eliminated these anesthetics from atmosphere with half life of 6.84 hr for enflurane and 0.64 for methoxyflurane. Pretreatment with dithiocarb (100 mg/kg ip) prolonged elimination half life of both compounds.

Rat liver microsomes catalyze covalent binding of (14)C-carbon tetrachloride metabolites to the microsomal protein; this binding was inhibited by dithiocarb at an I50 (50% inhibition) of 2.3x10-5 moles. Dithiocarb effectively inhibited metabolic elimination of carbon tetrachloride at a dose of 100 mg/kg.

Dithiocarb increased T-cell associated responses in mice treated with azathioprine or hydrocortisone acetate. Such a beneficiary effect contrasted with its inefficiency to restore functions abrogated by cyclophosphamide. The results raise the possibility of developing a rational chemoimmunotherapy using dithiocarb with a compatible cytoreductive drug.

Sc injection of 0.5 mmoles dithiocarb, 30 min before an ip injection of 280 mg aniline- hydrocloric acid/kg, affected aniline toxicity to rats by increasing mortality from 41.6 to 75%, decreasing methemoglobin formation by 67.72%, and inhibiting hepatic aniline hydroxylase by 47.6%.

For more Interactions (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (15 total), please visit the HSDB record page.

LC50; Species: Poecilia reticulata (Guppy); Conditions: renewal; Concentration: 6.9 mg/L for 96 hr (95% confidence interval: 5.5-8.5 mg/L)

LC50; Species: Daphnia magna (Water flea); Conditions: renewal; Concentration: 910 ug/L for 48 hr (95% confidence interval: 710-1060 ug/L)

EC50; Species: Chlorella pyrenoidosa (Green Algae) 10+8 cells/100 mL; Conditions: freshwater, static, 20 °C; Concentration: 1400 ug/L for 96 hr; Effect: growth, general /99% purity/

LC50; Species: Cyprinodon variegatus (Sheepshead minnow); Conditions: flow through; Concentration: 107 mg/L for 24 hr

For more Ecotoxicity Values (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (18 total), please visit the HSDB record page.

IDENTIFICATION AND USE: Sodium diethyldithiocarbamate (DETC) is a solid. It is used as corrosive inhibitor, rubber accelerator, intermediate, polymerization shortstop, and chemical intermediate in production of bis(thiocarbamoyl)sulfides (rubber-processing accelerators and fungicides). It is also used for colorimetric determination of small quantities of copper and for its separation from other metals, as well as spin trap (as FeDETC complex) for nitric oxide detection. DETC has also been used as a medication and antidote in nickel carbonyl exposures. HUMAN EXPOSURE AND TOXICITY: Allergic contact dermatitis from a wet suit was related to zinc diethyldithiocarbamate. ANIMAL STUDIES: Zinc diethyldithiocarbamate and DETC were positive in the murine local lymph node assay (LLNA). Administered systemically, DETC is reported to have caused detachment of the retina in dogs, but no damage to the retina in monkeys. In albino rats and beagle dogs, it caused no impairment of vision or structural alteration in the eye after daily administration for ninety days. In a 6-wk experiment in mice, daily sc injection of 50 mg/kg bw had marked anti-thyroid activity. DETC administered to rabbits at 100, 200, and 400 mg/kg daily for 4 weeks increased triglyceride and phospholipid levels. No changes were found in serum cholesterol concentration. DETC reduces blood copper concentrations. Pregnant rabbits injected intravenously with 0.5 g sodium diethyldithiocarbamate/day on 5 days per week throughout pregnancy failed to deliver litters. DETC elevated copper levels in the brain and peripheral nerve, leading to oxidative stress and lipid peroxidation from redox cycling of copper. Lipid peroxidation appears to either be a contributing event in the development of demyelination, possibly through an increase of redox active copper, or a consequence of the myelin injury. Continued DETC exposure induced an extensive degeneration of axons and myelin sheath (Wallerian degeneration in axons). DETC was not carcinogenic to rats or mice in NTP bioassay. Sodium diethyldithiocarbamate was negative when tested using Salmonella typhimurium strains (TA1535, TA1537, TA97, TA98 and TA100) in the presence and absence of metabolic activation. However, a small but significant increase in the number of chromosome breakages and aberrations was found in Vicia faba. DETC given orally to young and adult domestic fowl produced retarded testicular development, and produced degeneration in the seminiferous epithelium of mature birds. Nerve fiber degeneration was produced in the medulla and spinal cord of chicks. ECOTOXICITY STUDIES: DETC>3 mg/L applied to developing frog embryos was lethal in 24 hr. Between 1-3 mg/L caused severely malformed embryos. Retardation of growth, curvature of body axis, general edemic condition, pigmentation disorders, and abnormal notochords were noted.

/AQUATIC SPECIES/ The effects of intraperitoneal injection of diethyldithiocarbamate (DDC) on free radical processes were examined in brain, liver and kidney of goldfish (Carassius auratus). Levels of oxidatively modified lipids and proteins as well as the activities of antioxidant and associated enzymes were measured. Intraperitoneal injection of DDC at a concentration of 0.01 mg/g wet mass decreased SOD activities by about 30-50% after 48 and 168 hr compared to corresponding sham-injected values. This treatment resulted in transient oxidative stress. Lipid peroxide content increased after DDC injection at all time points in the kidney, after 48 hr in the liver and was elevated in most experimental groups in the brain. Thiobarbituric-acid reactive substances (end products of lipid peroxidation) rose within the first 48 hr after injection, but returned to initial levels after 168 hr. Two other indices of oxidative stress were also transiently modified: protein carbonyl levels in the brain and kidney increased 24 hr post-injection, and the low-molecular mass thiol content was reduced over the same period in all tissues examined. Activities of catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase showed differential responses to DDC treatment that rebounded by 168 hr post-injection. Glutathione peroxidase activities were reduced by 60, 45 and 65% in the brain, liver and kidney, respectively, after 24 hr but rebounded thereafter. After 48 hr post-injection with DDC significant decreases were also seen in liver and kidney catalase, GST activities in all three tissues, and kidney GR and G6PDH activities. In some cases, catalase, GST, GR and G6PDH activities transiently increased after 24 hr. It was concluded that DDC injection depleted SOD and simultaneously stimulated lipid peroxidation, but did not require compensatory enhancement of other enzymatic defenses. Different actions of the superoxide anion in cellular metabolism and possible consequences of the impairment of superoxide dismutase are discussed.

/AQUATIC SPECIES/ Sodium diethyldithiocarbamate concentration >3 mg/L applied to developing frog embryos were lethal in 24 hr. Between 1-3 mg/L caused severely malformed embryos. Retardation of growth, curvature of body axis, general edemic condition, pigmentation disorders, and abnormal notochords were noted.

Cough. Sore throat.

Redness.

Redness.

Abdominal pain. Drowsiness. Nausea.

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. 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/[USEPA; ICSS Dashboard Application; Available from, as of December 17, 2015: 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: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=148-18-5]

Sodium diethyldithiocarbamate

3 x 10 ^-2 mg/kg-day

/CASE REPORTS/ Rubber materials are common causes of contact dermatitis. Neoprene is a special synthetic rubber used in many products (eg, wet suits, elastic supports, gloves, shoes, and orthopedic devices). A 31-year-old man was admitted to our dermatoallergologic clinic with the development of a generalized itching erythematovesicular eruption. He reported that clinical manifestations occurred after he wore a neoprene wet suit that he was used to wearing for water sports. Although allergic contact dermatitis from a wet suit is not uncommon, it is usually due to thiourea derivatives whereas our patient presented with contact allergy to p-tert-butylphenol formaldehyde resin and zinc diethyldithiocarbamate. /Zinc diethyldithiocarbamate/

/ALTERNATIVE and IN VITRO TESTS/ Tumor necrosis factor-alpha (TNF-alpha) and etoposide both trigger a large and rapid production of reactive oxygen species (ROS) in HeLa cells. This occurs before translocations of the proapoptotic Bax and cytochrome c proteins, the loss of mitochondrial membrane potential (DeltaPsim), and apoptosis. We have used diethyldithiocarbamate (DDC), a well-known inhibitor of Cu, Zn superoxide dismutase to study the role of ROS in this system. We report that DDC strongly inhibits caspase activation, loss of DeltaPsim, and cell death induced by TNF-alpha or etoposide. Surprisingly, DDC does not inhibit Bax and cytochrome c translocations. On the contrary, we have observed that DDC can trigger the translocations of these proteins by itself, without altering DeltaPsim. Here, we report that DDC has at least two antagonistic apoptosis regulation functions. First, DDC triggers ROS-dependent Bax and cytochrome c translocations, which are potentially proapoptotic, and second, DDC inhibits caspase activation and activity, loss of DeltaPsim, and cell death, in a ROS-independent manner. Our results suggest an interesting model in which ROS-dependent Bax and cytochrome c translocations can be studied without interference from later apoptotic events.

/ALTERNATIVE and IN VITRO TESTS/ Antimycin A (AMA) inhibits mitochondrial electron transport between cytochrome b and c. We recently demonstrated that AMA inhibits the growth of lung cancer Calu-6 cells and the changes of reactive oxygen species (ROS) and glutathione (GSH) levels affect apoptosis in Calu-6 cells. Here, we examined the effects of N-acetyl-cysteine (NAC, a well known antioxidant), L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyl-dithiocarbamate (DDC, an inhibitor of Cu, Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on AMA-treated Calu-6 cells in relation to cell death, ROS and GSH levels. Treatment with AMA induced cell growth inhibition, apoptosis and the loss of mitochondrial membrane potential (MMP) (DeltaPsim) in Calu-6 cells. While the intracellular ROS level was decreased in 50 microM AMA-treated Calu-6 cells, O2.- levels among ROS were significantly increased. AMA also induced GSH depletion in Calu-6 cells. Treatment with NAC showed decreasing effect on O2.- levels in AMA-treated cells preventing apoptosis, MMP (DeltaPsim) loss and GSH depletion in these cells. BSO significantly increased GSH depletion and apoptosis in AMA-treated cells. While both DDC and AT increased ROS levels in AMA-treated Calu-6 cells, only DDC intensified GSH depletion and apoptosis. BSO and AT increased the ROS level in Calu-6 control cells, but these agents did not induce apoptosis and GSH depletion. In conclusion, our results suggest that GSH depletion rather than ROS level in AMA-treated Calu-6 cells is more tightly related to apoptosis.

/ALTERNATIVE and IN VITRO TESTS/ Propyl gallate (PG) as a synthetic antioxidant is widely used in processed food and medicinal preparations. It also exerts a variety of effects on tissue and cell functions. In the present study, we investigated the effects of L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyldithiocarbamate (DDC, an inhibitor of Cu/Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on PG-treated HeLa cells in relation to cell growth, reactive oxygen species (ROS) and glutathione (GSH). Treatment with PG induced growth inhibition, the loss of mitochondrial membrane potential [MMP (DeltaPsim)] and apoptosis in HeLa cells. ROS levels including O2.- were increased or decreased in PG-treated HeLa cells depending on the incubation times. PG caused depletion in GSH content in HeLa cells. While BSO enhanced the growth inhibition of PG-treated HeLa cells at 4 hr, DDC and AT did not. All the agents down-regulated MMP (DeltaPsim) levels in PG-treated cells. Although BSO, DDC or AT slightly increased ROS or O2.- levels in PG-treated cells at 1 hr, these enhancements of ROS did not intensify apoptosis in these cells. In addition, BSO, DDC or AT slightly reduced GSH level in PG-treated HeLa cells at 1 hr, but this reduction did not affect cell death of HeLa. Furthermore, PG induced a G1 phase arrest of the cell cycle. BSO, DDC or AT significantly inhibited the G1 phase arrest in PG-treated cells. Conclusively, the changes of ROS and GSH levels by BSO, DDC or AT in PG-treated HeLa cells did not strongly affect the cell growth and death.

For more Human Toxicity Excerpts (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.

Although the ability of disulfiram to inactivate CYP2E1 has been known for more than 20 years, the mechanism has not yet been elucidated. A metabolite of disulfiram, diethyldithocarbamate (DDC), is converted by CYP2E1 to a reactive intermediate that subsequently inactivates the protein, leading to mechanism-based inactivation. Mass spectral analysis of the inactivated human 2E1 protein demonstrates that the inactivation is due to the formation of an adduct of the reactive metabolite of DDC with the apoprotein. These data, along with mass spectral analysis of a reactive intermediate trapped with GSH, indicate the involvement of a reactive intermediate with a molecular mass of 116 Da. Our results suggest that this binding involves formation of a disulfide bond with one of the eight cysteines in CYP2E1. The inactivation of wild-type CYP2E1 as well as two of its polymorphic mutants, CYP2E1*2 and CYP2E1*4, was also investigated. For wild-type CYP2E1, the K(I) was 12.2 uM and the k(inact) was 0.02 min(-1). The K(I) values for the two polymorphic mutants were 227.6 and 12.4 uM for CYP2E1.2 and CYP2E1.4, and the k(inact) values were 0.0061 and 0.0187 min(-1), respectively. These data indicate that DDC is a much less efficient inactivator of CYP2E1.2 than it is of either the wild-type or the CYP2E1.4 variant.

... DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found. The membranes of pneumocytes type II were injured.

Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity.

Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.

Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.

Rats receiving levels of 500 mg of dithiocarb in 1-2 mL water/kg body weight by gavage reached plasma levels of 2 mg/L dithiocarb in 3 hours.

A half life for absorption of 26 minutes was determined when S-dithiocarb dissolved in 2M phosphate buffer was injected into the small intestinal lumen of adult male Wistar rats at a dose of 25 mg/kg.

Within 15 minutes of dosing rats with 25 mg (222 moles S)/rat S-dithiocarb i.p., nonprotein bound radiolabel was detected in the plasma (1561 nmoles/mL plasma) and in the liver (3211 nmoles/g liver). A substantial amount (>45% within 15 minutes of dosing) of radioactivity also was found to be bound reversibly to soluble proteins of liver and plasma.

A small amount (<0.1%) of unchanged dithiocarb was detected in the urine of rats receiving ip injections of 25 mg (35)S-dithiocarb/rat. One hr after dosing, 96.1% of the radiolabeled urinary metabolites was of S-glucuronide conjugate and 3.9% inorganic sulfate. Within 1 hr after dosing, 7% of the administered (35)S-dithiocarb was recovered as carbon disulfide in the expired air.

For more Absorption, Distribution and Excretion (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.

Used as a corrosive inhibitor, rubber accelerator, chemical intermediate, medication; and laboratory reagent; [HSDB]

Adjuvants, Immunologic; Antiviral Agents; Chelating Agents

Chelating agent. /from table/

For colorimetric determination of small quantities of copper and for its separation from other metals.

... Used as a chemical intermediate in the production of other diethyldithiocarbamate metal salts, such as the zinc, selenium and tellurium salts, and of bis(thiocarbamoyl)sulfides, which are used as rubber-processing accelerators ... .

For more Uses (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (6 total), please visit the HSDB record page.

(1977) PROBABLY GREATER THAN 2.27X10+6 G

(1978) PROBABLY GREATER THAN 2.27X10+6 G

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Carbamodithioic acid, N,N-diethyl-, sodium salt. National Production Volume: 31,900 lb/yr.

Carbamodithioic acid, N,N-diethyl-, sodium salt (1:1): ACTIVE

Sodium diethyldithiocarbamate is available in the US for use in rubber processing as a 25% active aqueous solution... .