Diisopropylcarbodiimide

126.2

126.20

878281

211-743-7

OQO20I6TWH

42080

DTXSID4025086

Colorless liquid

29252000

24.7

4.11 (est)

Clear colorless to yellow Liquid

0.806 g/cu cm at 25 deg C

147 °C

147 °C

93 °F

1.445

soluble in chloroform, methylene chloride, acetonitrile, dioxane, dimethylformamide andtetrahydrofuran.

2-8°C

5.1 mm Hg at 25 deg C

Henry's Law constant = 9.92X10-6 atm-cu m/mol at 25 °C (est)

Flammable; Reacts with water to form 1,3-diisopropylurea|Hydroxyl radical reaction rate constant = 4.55X10-12 cu cm/molecule-sec at 25 °C (est)

II

6.1

UN 2929 6.1/PG 1

3

10-26-36/37/38-41-42/43-37/38

26-36/37/39-45-38-28A-16-22

FF2175000

T+,T,F,Xn

Flammable/Highly Toxic/

Stable under normal temperatures and pressures.

P260-P280-P284-P305 + P351 + P338-P310

H315-H317-H318-H330-H334-H335

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.

|Danger|H226 (100%): Flammable liquid and vapor [Warning Flammable liquids]|P210, P233, P240, P241, P242, P243, P260, P261, P264, P271, P272, P280, P284, P285, P302+P352, P303+P361+P353, P304+P340, P304+P341, P305+P351+P338, P310, P312, P320, P321, P332+P313, P333+P313, P342+P311, P362, P363, P370+P378, P403+P233, P403+P235, P405, and P501|Aggregated GHS information provided by 198 companies from 22 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Warning|H226: Flammable liquid and vapor [Warning Flammable liquids]|P210, P233, P240, P241, P242, P243, P260, P261, P272, P280, P302+P352, P303+P361+P353, P314, P321, P333+P313, P363, P370+P378, P403+P235, and P501

LD50 Mouse intravenous 36 mg/kg

Groups of 50 male and 50 female F344/N rats were dermally administered 0, 10, 20, or 40 mg/kg diisopropylcarbodiimide in anhydrous ethanol 5 days per week for 2 years. Survival of 20 mg/kg males was significantly greater than that of the vehicle controls; survival of all dosed groups of females was similar to that of the vehicle controls. Body weights of 40 mg/kg rats were generally less than those of the vehicle controls after week 13. Clinical findings frequently observed in 40 mg/kg males included ataxia, excitability, impaired gait, low muscle tone, abnormal breathing, lethargy, vocalization, and seizures. Because of severe neurological signs exhibited by the 40 mg/kg males, a neuropathological review of these animals was performed. The principal pathological findings of the brain included neuronal necrosis, hemorrhage, and/or fibrinoid arteriole necrosis. Incidences of hemorrhage in the lung of 40 mg/kg males, chronic lung inflammation in 10 and 20 mg/kg females, and alveolar epithelium hyperplasia in 20 mg/kg females were significantly greater than those of the vehicle controls. At the site of application, the incidences of epidermal hyperplasia in all dosed groups of males and 20 and 40 mg/kg females and chronic inflammation in all dosed groups of males and 40 mg/kg females were significantly increased. There were no increased incidences of neoplasms related to diisopropylcarbodiimide administration.|Groups of 50 male and 50 female B6C3F1 mice were dermally administered 0, 10, 20, or 40 mg/kg diisopropylcarbodiimide in anhydrous ethanol, 5 days per week for 2 years. Survival of all dosed groups was similar to that of the vehicle control groups. Mean body weights of dosed groups of mice were generally similar to those of the vehicle control groups throughout the study. There were no increased incidences of neoplasms that were attributed to the administration of diisopropylcarbodiimide. Significantly increased incidences of epidermal hyperplasia and focal dermal inflammation of the skin at the site of application occurred in 20 mg/kg male mice.|Groups of five male and five female F344/N rats were dermally administered 0.3 mL ethanol containing 0, 3, 9, 27, or 81 mg diisopropylcarbodiimide or 0.3 mL of the neat chemical containing 242 mg per animal, 5 days a week for 2 weeks. All rats in the 27, 81, and 242 mg groups died before the end of the study. Of the surviving groups, final body weights were similar to those of the vehicle controls. Clinical findings included convulsions/seizures, nasal/eye discharge, tremors, and comatose conditions in 81 and 242 mg rats and lethargy, ataxia, and abnormal breathing in 27 mg rats. The incidences of epidermal hyperplasia at the site of application in 9 and 27 mg males and 27 mg females were significantly greater than those in the vehicle controls; the incidences of hyperkeratosis in 3 and 9 mg males and 9 mg females were also significantly increased.|Groups of five male and five female B6C3F1 mice were dermally administered 0.1 mL ethanol containing 0, 1, 3, 9, or 27 mg diisopropylcarbodiimide or 0.1 mL of the neat chemical containing 81 mg per animal, 5 days a week for 2 weeks. All 9, 27, and 81 mg mice died before the end of the study. Final body weights of the surviving groups were similar to those of the vehicle controls. Clinical findings in 9, 27, and 81 mg mice included comatose conditions, convulsions/seizures, tremors, abnormal breathing, nasal/eye discharge, lethargy, and irritation at the site of application. Incidences of chronic active inflammation at the site of application in 9 mg males and females were significantly greater than those in the vehicle control groups.|For more National Toxicology Program Studies (Complete) data for 1,3-Diisopropylcarbodiimide (7 total), please visit the HSDB record page.

1,3-Diisopropylcarbodiimide's production and use as a reagent for peptide syntheses, chemical intermediate, and stabilizer for military nerve agents(1) may result in its release to the environment through various waste streams.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 560(SRC), determined from a structure estimation method(2), indicates that 1,3-diisopropylcarbodiimide is expected to have low mobility in soil(SRC). However, 1,3-diisopropylcarbodiimide reacts with water(3); in moist soils, dicyclohexylcarbodiimide can hydrate to form diisopropylurea which has an estimated Koc of about 30(2,SRC) indicating high mobility in soil(1) for this degradation product(SRC). Volatilization of 1,3-diisopropylcarbodiimide from moist soil surfaces is expected to occur given an estimated Henry's Law constant of 9.92X10-4 atm-cu m/mole(SRC), using a fragment constant estimation method(2). 1,3-Diisopropylcarbodiimide is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 5.1 mm Hg at 25 °C(3).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 560(SRC), determined from a structure estimation method(2), indicates that 1,3-diisopropylcarbodiimide is expected to adsorb to suspended solids and sediment(SRC). However, 1,3-diisopropylcarbodiimide reacts with water to form diisopropylurea(3). Therefore, adsorption to sediment is not expected to be an important fate processes(SRC). 1,3-Diisopropylcarbodiimide hydration with water is a pseudo-first reaction and is both acid and base catalyzed(3); depending upon conditions (pH, buffering agents, etc), the hydration half-life may vary from less than one hour to several days(3,SRC). At slow hydration rates, some volatilization from water may occur(SRC) based upon an estimated Henry's Law constant of 9.92X10-4 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 4 hours and 5 days, respectively(SRC). According to a classification scheme(6), an estimated BCF of 240(SRC), from an estimated log Kow of 4.11(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is high(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1,3-diisopropylcarbodiimide, which has a vapor pressure of 5.1 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 1,3-diisopropylcarbodiimide is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 3.5 days(SRC), calculated from its rate constant of 4.55X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). 1,3-Diisopropylcarbodiimide reacts with water(2); therefore, removal from air may occur through contact with water vapor or precipitation(SRC).

The rate constant for the vapor-phase reaction of 1,3-diisopropylcarbodiimide with photochemically-produced hydroxyl radicals has been estimated as 4.55X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 3.5 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 1,3-Diisopropylcarbodiimide hydrolyzes (hydrates) in water to form diisopropylurea(2); the hydration is a pseudo-first reaction that is both acid and base catalyzed(2); depending upon conditions (pH, buffering agents, etc), the hydration half-life may vary from less than one hour to several days(SRC).

An estimated BCF of 240 was calculated in fish for 1,3-diisopropylcarbodiimide(SRC), using an estimated log Kow of 4.11(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC), provided the compound is not metabolized by the organism(SRC). 1,3-Diisopropylcarbodiimide hydrolyzes (hydrates) in water to form diisopropylurea(3), therefore, bioconcentration in aquatic organisms is not expected to be an important fate process(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 1,3-diisopropylcarbodiimide can be estimated to be 560(SRC). According to a classification scheme(2), this estimated Koc value suggests that 1,3-diisopropylcarbodiimide is expected to have low mobility in soil. 1,3-Diisopropylcarbodiimide hydrates in water(3); in moist soils, 1,3-diisopropylcarbodiimide can hydrate to form diisopropylurea which has an estimated Koc of about 30(1) indicating very high mobility in soil for the hydration product(2).

The Henry's Law constant for 1,3-diisopropylcarbodiimide is estimated as 9.92X10-4 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 1,3-diisopropylcarbodiimide is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 4 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 5 days(SRC). The importance of volatilization from water will be lessened because 1,3-Diisopropylcarbodiimide hydrolyzes (hydrates) in water to form diisopropylurea(3) with a half-life that may vary from less than one hour to several days(SRC). 1,3-Diisopropylcarbodiimide's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). 1,3-Diisopropylcarbodiimide is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 5.1 mm Hg at 25 °C(3).

Occupational exposure to 1,3-diisopropylcarbodiimide may occur primarily through dermal contact with this compound at workplaces where diisopropylcarbodiimide is produced or used, but exposure through inhalation of vapor can also occur(SRC). Human exposure to diisopropylcarbodiimide could occur during the extensive handling of the compound that occurs during the synthesis of peptides and other compounds in the chemical, pharmaceutical, and recombinant DNA industries(1).

/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 /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's 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/

1,3-diisopropylcarbodiimide

2-Propanamine, N,N'-methanetetraylbis-: ACTIVE