Sodium Diethyldithiocarbamate

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

H315 (16.7%): Causes skin irritation [Warning Skin corrosion/irritation]

H319 (13.6%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H335 (10.6%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H400 (43.9%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

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.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

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

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

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.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (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.

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/

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

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/

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.

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.

STORAGE PRECAUTIONS: You should store this material under ambient temperatures and keep it away from oxidizing materials. (NTP, 1992)

Dry. Well closed. Keep in a well-ventilated room. Store in an area without drain or sewer access.

Keep container tightly closed in a dry and well-ventilated place. Hygroscopic. Store under inert gas. /Sodium diethyldithiocarbamate trihydrate/

2.0 [mg/m3], inhalable fraction[German Research Foundation (DFG)]

4.0 [mg/m3]

50 [mg/m3]

300 [mg/m3]

(inhalable fraction): 2 mg/m

Evaporation at 20 °C is negligible; a nuisance-causing concentration of airborne particles can, however, be reached quickly when dispersed.

The substance is irritating to the skin, eyes and upper respiratory tract.

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)

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /Sodium diethyldithiocarbamate trihydrate/

Skin protection: Handle with gloves. /Sodium diethyldithiocarbamate trihydrate/

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /Sodium diethyldithiocarbamate trihydrate/

Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /Sodium diethyldithiocarbamate trihydrate/

NO open flames.

Use local exhaust.

Protective gloves.

Wear safety spectacles.

Do not eat, drink, or smoke during work.

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

Crystals; [ICSC]

WHITE CRYSTALS.

Crystals from ethanol

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

203 °F (NTP, 1992)

90-102 °C

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

Soluble in water

Soluble in alcohol

Solubility in water: soluble

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

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

5.9 (Air = 1)

Relative vapor density (air = 1): 5.9

log Kow <1.10

Stable under recommended storage conditions. /Sodium diethyldithiocarbamate trihydrate/

Aqueous solutions decompose slowly.

When heated to decomposition it emits very toxic fumes of /nitrogen, sulfur, and sodium oxides/.

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

Pesticide -> EPA IRIS

Plastics & Rubber -> Dithiocarbamates (Rubber)

Water soluble. Thio and dithiocarbamates slowly decompose in aqueous solution to form carbon disulfide and methylamine or other amines. Such decompositions are accelerated by acids.

Thiocarbamate Esters and Salts/Dithiocarbamate Esters and Salts

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).

Incompatible materials: Strong oxidizing agents /Sodium diethyldithiocarbamate trihydrate/

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.

Sodium diethyldithiocarbamate

3 x 10 ^-2 mg/kg-day

No data are available in humans. Inadequate evidence of carcinogenicity in animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its carcinogenicity to humans.

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 12: (1976) Some Carbamates, Thiocarbamates and Carbazides

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

Sodium diethyldithio-carbamate

TR-172: Bioassay of Sodium Diethyldithiocarbamate for Possible Carcinogenicity (CASRN 148-18-5) (1979 )

12/13/78

No Evidence

It is concluded that under the conditions of this bioassay, sodium diethyldithiocarbamate was not carcinogenic for F344 rats or B6C3F1 mice of either sex.

The substance can be absorbed into the body by ingestion.

Cough. Sore throat.

Redness.

Abdominal pain. Drowsiness. Nausea.

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

IRIS Current

HEAST Current

LD50 Rat oral 2830 mg/kg /Trihydrate/

LD50 Mouse oral 1870 mg/kg /Trihydrate/

LD50 Mouse iv >1000 mg/kg /Trihydrate/

LD50 Rat oral 1500 mg/kg

For more Non-Human Toxicity Values (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (8 total), please visit the HSDB record page.

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.

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 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/

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/

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. 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 (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/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.

/LABORATORY ANIMALS: Acute Exposure/ Groups of 18 male and 18 female (C57BL/6xC3H/ANF)F1 mice and 18 male and 18 female (C57BL/6xAKR)F1 mice were given single sc injections of 464 mg/kg bw sodium diethyldithiocarbamate (mp 94-96 °C) in water on 28th day of life and were observed until they were 78 wk of age, at which time 16, 18, 18 and 16 mice in the 4 groups, respectively, were still alive. Tumor incidences were compared with those in groups of 141, 154, 161 and 157 untreated or vehicle injected controls that were necropsied. Incidences were not increased (p>0.05) for any tumor type in any sex strain subgroup or in the combined sexes of either strain (NTIS, 1968)

/LABORATORY ANIMALS: Acute Exposure/ Sodium diethyldithiocarbamate (DEDC) pretreatment of rats prevented the ethylene dibromide depression of liver glutathione (GSH) 2 hr after intoxication. The levels of cytochrome p450 seem to be unaffected by ethylene dibromide. The inhibition of glutathione-s-transferase by DEDC is noncompetitive, producing a change in Vmax without a change in Km. DEDC also inhibited the covalent binding of (14)C-ethylene dibromide to microsomal proteins in the microsomal system supplemented with NADPH.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Diethyldithiocarbamate sodium... has been tested on rabbit corneas at 0.01 to 0.05 molar concentrations by injection or application to the denuded surface and was found nontoxic. Administered systemically, it 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 administration daily for ninety days.

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.

/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.

2.00e+00

8.50e+00

2.90e-01

4.00e+00

1.80e-04

2.70e-01

3.00e-02

Volatile

2.00e+02

8.50e+02

2.90e+01

The substance is very toxic to aquatic organisms. It is strongly advised not to let the chemical enter into the environment.

Sodium diethyldithiocarbamate is not known to occur as a natural product.

Sodium diethyldithiocarbamate's production and use in colorimetric determination of small quantities of copper and for its separation from other metals(1,2) and experimental administration as a trial HIV drug(3) will result in its release to the environment through various waste streams(SRC).

The fate and transport of sodium diethyldithiocarbamate in the soil is likely to be determined by its ability to undergo biological transformation and chemical reactions. Microbial degradation of sodium diethyldithiocarbamate is likely to occur slowly in the soil environment because of the inherent microbial toxicity of the dithiocarbamates.

Sodium diethyldithiocarbamate can be converted in soils to diethylamine, a nitrosamine precursor ... however, the biodegradation half-life of this compound was not established.

AEROBIC: Sodium diethyldithiocarbamate, added to soil at 10,000 ppm, was biodegraded at a rate of 10 kg/wk(1). Sodium diethyldithiocarbamate was degraded by 99% after 14 days in acclimatised sludges (starting concentrations of 10 mg C/L); however, this substance was toxic to microorganisms in nonacclimatised sludges(2,3).

Sodium diethyldithiocarbamate may undergo hydrolysis in soils, though no quantitative estimate of the rate of this reaction was made.

Sodium diethyldithiocarbamate was found to be stable in aqueous solution at pH 7 but decomposed under slightly acidic conditions (pH 5-6.7), producing carbon disulfide and a salt of diethylamine.

According to the 2012 TSCA Inventory Update Reporting data, one reporting facility stated that the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of sodium diethyditiocarbamate in the United States may be confidential business information (CBI)(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 7,970 workers (1,982 of these are female) are potentially exposed to sodium diethyldithiocarbamate in the US(1).

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/

UN Hazard Class: 9; UN Pack Group: III