1,2,3-프로판트리올, 모노아세테이트

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you should spill this chemical, use absorbent paper to pick up all liquid spill material. Seal the absorbent paper, as well as any of your clothing which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Wash any surfaces you may have contaminated 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: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

The effects of single and combined treatment with monoacetin and calcium-chloride against sodium-fluoroacetate poisoning was investigated in cats. Cats received a single intravenous injection of 3.3 mg /kg sodium fluoroacetate and 1% calcium-chloride or 0.5 mg/kg monoacetin every 30 min or combined monoacetin and calcium-chloride therapy. Controls received no treatment. Monoacetin alone extended average survival time of animals poisoned with sodium fluoroacetate from 94 to 166 minutes. The combined treatment with monoacetin and calcium-chloride did not prolong mean survival time above 166 minutes. Monoacetin therapy aggrevated the metabolic acidosis in sodium-fluoroacetate treated animals in groups that received monoacetin alone or in combination with calcium-chloride; the serum ionized calcium values at 40 and 80 min in these groups was 0.84 and 0.80 and 0.79 and 1.03 mmol/kg, respectively, compared to control values of 0.80 and 0.65 mmol/kg. The controls showed a pH of 7.25 80 min after sodium-fluoroacetate injection and 6.96 after monoacetin. Blood carbon-dioxide pressure was 18 and 28.6 mm of mercury in these groups, respectively, while the biocarbonate concetration was 7.7 mEq/L in controls and 4.4 mEq/L in treated animals. The lactate/pyruvate ratio did not change significantly during the first 40 minutes, but increased significantly threreafter. There was no change in serum sodium or potassium concentrations. /It was/ concluded tha combined monoacetin and calcium-chloride therapy does not prolong survival time against sodium-fluoroacetate poisoning in cats.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 5.0(SRC), determined from an estimated log Kow of -1.2(2,SRC) and a regression-derived equation(3), indicates that acetin is expected to have very high mobility in soil(SRC). Volatilization of acetin from moist soil surfaces is not expected to be important(SRC) given an estimated Henry's Law constant of 4.1X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Acetin is not expected to volatilize from dry soil surfaces based on an estimated vapor pressure of 3.9X10-3 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation of acetin in soil may be important(SRC), based upon glycerin acetate's biodegradation in an activated sludge inoculum(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 5.0(SRC), determined from an estimated log Kow of -1.2(2,SRC) and a regression-derived equation(3), indicates that acetin is not expected to adsorb to suspended solids and sediment(SRC). Acetin is not expected to volatilize from water surfaces(3,SRC) based on an estimated Henry's Law constant of 4.1X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3.2(3,SRC), from an estimated log Kow(2,SRC), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Estimated hydrolysis half-lives of 1.8 years and 66 days at pH values of 7 and 8, respectively(6), suggest that hydrolysis is not expected to be an important process(SRC). Acetin is expected to biodegrade in aquatic systems based upon glycerin acetate's (approx 28% acetin) biodegradation in an activated sludge inoculum; 91 to 94% over a 4-week period(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acetin, which has an estimated vapor pressure of 3.9X10-3 mm Hg at 25 °C(2,SRC), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase acetin 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 23 hours(3,SRC).

The Koc of acetin is estimated as approximately 5.0(SRC), using an estimated log Kow of -1.2(1,SRC) and a regression-derived equation(2,SRC). According to a classification scheme(3), this estimated Koc value suggests that acetin is expected to have very high mobility in soil(SRC).

An estimated BCF of 3.2 was calculated for acetin(SRC), using an estimated log Kow of - 1.2(1,SRC) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for acetin is estimated as 4.1X10-10 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that acetin is expected to be essentially nonvolatile from water surfaces(2,SRC). Acetin's Henry's Law constant(1,SRC) indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Acetin is not expected to volatilize from dry soil surfaces based on an estimated vapor pressure of 3.9X10-3 mm Hg(SRC), determined from a fragment constant method(3).

...IV TOXICITY IN DOGS & RABBITS. LD50...ARE 5 ML/KG /6.03 G/ & 4 ML/KG, /4.82 G/ RESPECTIVELY. SYMPTOMS ARE THOSE OF SEVERE DYSPNEA, TREMORS, RETRACTION OF NECK, & TERMINAL CONVULSIONS, OCCURRING 2-20 MIN AFTER INJECTION. PATHOLOGICAL FINDINGS WERE HEMORRHAGIC AREAS IN LUNG.

...LD50 IN RATS & MICE BY SC INJECTIONS USING 50% WATER SOLN BUFFERED WITH PHOSPHATE TO PH 7. IN MICE...DILUTED 1:5 OR 1:10. LD50 IN RATS WAS 5.5 ML/KG /6.633 G/ & IN MICE 3.5 ML/KG /4.221 G/. ...PROSTRATION, LABORED RESP, &... TERMINAL CONVULSIONS. ... AUTOPSY SHOWS MARKED PULMONARY CONGESTION & RIGHT HEART DILATATION.

MAY DISTURB ACID-BASE BALANCE. GIVEN SC OR IM TO LAB ANIMALS (INCL MONKEYS), IT PRODUCES VASODILATION, CENTRAL NERVOUS DEPRESSION, & DEATH FROM RESP FAILURE...

Acetin was tested for the induction of sex-linked recessive lethal mutations in Drosophila melanogaster using a standard protocol approved by the National Toxicology Program. Canton-S wild-type males were treated with concentrations of acetin that resulted in approximately 30% mortality. Following treatment, males were mated individually to 3 harems of Basc virgin females to produce 3 broods for analysis. Acetin was positive at a dose of 50,000 ppm when administered to males by feeding.

The rate constant for the vapor-phase reaction of acetin with photochemically-produced hydroxyl radicals has been estimated as 1.6X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1,SRC). This corresponds to an atmospheric half-life of about 23 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1,SRC). A base-catalyzed second-order hydrolysis rate constant of 0.12 L/mol-sec(SRC) was estimated using a structure estimation method(2); this corresponds to half-lives of 1.8 years and 66 days at pH values of 7 and 8, respectively(2,SRC).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,223 workers (241 of these are female) are potentially exposed to acetin in the US(1). Occupational exposure to acetin may occur through dermal contact with this compound at workplaces where acetin is produced or used(SRC). The general population may be exposed to acetin via ingestion of food products containing acetin(SRC).