N-BUTYL ACETATE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
ACETATE DE BUTYLE (French) ACETIC ACID, BUTYL ESTER ACETIC ACID n-BUTYL ESTER BUTILE (ACETATI DE) (Italian) BUTYLACETAT (German) BUTYL ACETATE n-BUTYL ACETATE 1-BUTYL ACETATE BUTYLACETATEN (Dutch) BUTYLE (ACETATE DE) (French) BUTYLESTER KYSELINY OCTOVE (Czech) n-BUTYL ESTER of ACETIC ACID BUTYL ETHANOATE OCTAN n-BUTYLU (Polish)
IDENTIFIERS
BEILSTEIN HANDBOOK REFERENCE:4-02-00-00143 IMO CLASSIFICATION:3.2 - Butyl acetates STANDARD INDUSTRIAL TRADE CLASSIFICATION NUMBER:51372
SYNONYM REFERENCE
- (CHRIS , 2002; HSDB , 2002; NIOSH , 2002; OHM/TADS , 2002; RTECS , 2002)
USES/FORMS/SOURCES
n-Butyl acetate is used as a solvent for adhesives, nitrocellulose, resins, waxes, oils, fats, printing inks, and camphor. It is also used in the manufacture of perfumes and as a flavoring ingredient (Ashford, 1994; Hathaway et al, 1996; HSDB, 2002). It is also used as a solvent in the production of lacquer, leather, photographic films, safety glass, and plastics (Budavari, 2000). It is used as a solvent in the manufacture of airplane dopes (Sittig, 1991a). n-Butyl acetate is used as a synthetic raw material, as larvicide, and in the fabrication of circuits in the semiconductor industry (Bingham et al, 2001). It is a component of the binder system used for the inside coating of fluorescent lamps and it is a component of the semi-paste ink used in screen printing (ILO, 1998a). It is also used to dehydrate oils and pharmaceuticals; as a solvent for fingernail polishes, paper coatings and other types of protective coatings; as solvent for the extraction of penicillin; to split influenza viruses in the manufacturing of vaccines; and as an agent to remove lacquers (HSDB, 2002).
n-Butyl acetate is a colorless liquid, with a strong, pleasant, fruity odor (Lewis, 2000a; Sittig, 1991a). Its odor and taste have been described as banana-like. The initial burning taste is later perceived as sweet and pineapple-like (HSDB, 2002). GRADES OF PURITY (ACGIH, 1996; CHRIS, 2002):
It occurs naturally in apples and bananas. It is synthetically produced by contact of butyl alcohol with acetic acid or acetic anhydride, followed by esterification and distillation in the presence of a catalyst (Ashford, 1994; Bingham et al, 2001; Lewis, 1997a).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- n-Butyl acetate may be irritating to the eyes, skin, and mucous membranes. Effects of overexposure may include nausea, vomiting, diarrhea, difficulty breathing, and cough. Dryness of the eyes, upper respiratory tract, and skin has also been observed. Exposure to high concentrations may cause CNS depression and narcosis, headache, dizziness, drowsiness, ataxia, and confusion. Death occurs from respiratory failure.
- Prolonged or repeated exposure may cause conjunctival irritation, coughing, sensation of chest constriction, and drying of the skin.
- Effects of exposure in experimental animals include ocular and respiratory irritation, lacrimation, excessive salivation, dyspnea, ataxia, and CNS depression.
- Signs of toxicity in experimental animals that died as a result of exposure included ocular and respiratory irritation, tachypnea, tremors, and decreased motor activity. Gross lesions in these animals included discoloration of the lungs and liver, congestion, alveolar hemorrhage, sloughing of the bronchiolar mucosa, necrosis of the alveolar epithelial cells, and pulmonary edema.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
May cause toxic effects if inhaled or absorbed through skin. Inhalation or contact with material may irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution.
ACUTE CLINICAL EFFECTS
- Butyl acetate is an eye and upper respiratory tract irritant and a central nervous system depressant considered to have low toxicity to humans (Harbison, 1998).
- Exposure to butyl acetate vapor irritates the eyes, nose, throat, pharynx and mucous membranes (ACGIH, 1996a). Inhalation exposure results in coughing and difficulty breathing, and mild respiratory inflammation (ILO, 1998; HSDB , 2000; ITI, 1995). Exposure symptoms may also include anorexia, nausea, vomiting, diarrhea, gastrointestinal hemorrhage, liver damage, and renal damage with glycosuria (ILO, 1998; Harbison, 1998; ITI, 1995; HSDB , 2000).
- Toxicity can occur with inhalation or ingestion; absorption after dermal contact with high concentrations can produce a narcotic effect (Lewis, 1998; Zaleski, 1992; Harbison, 1998). The central nervous system depression and narcotic effects include headache, dizziness, ataxia, confusion, delirium, weakness, and decreased level of consciousness ranging from drowsiness to coma (HSDB , 2000; Harbison, 1998; ILO, 1998; ACGIH, 1996a; ILO, 1998).
- Pulmonary edema has also been reported as a symptom of exposure to butyl acetate (HSDB , 2000). Exposure to n-butyl acetate resulted in pulmonary edema in rats, and in emphysema in cats (RTECS , 2000). Butyl acetate-induced death usually results from respiratory failure (Harbison, 1998).
- Silverman et al (1946) found that workers exposed to greater than 200 ppm for 8 hours developed eye, nose and throat irritation. The odor did not become objectionable until greater than 300 ppm. Vapor exposure has been associated with noticeable irritation at a concentration of 300 ppm in air and objectionable irritation at a concentration of 3,300 ppm in humans (Nelson et al, 1943; von Oettingen, 1960; (Grant, 1993).
CHRONIC CLINICAL EFFECTS
- Evidence that n-butyl acetate has chronic systemic toxicity is so far inconclusive (Lewis, 2000). Chronic occupational exposure to butyl acetate has been reported to cause skin irritation and cracking, allergic contact dermatitis, other dermatoses and anemia (ACGIH, 1996a; Roed-Peterson, 1980; Elizarov & Lapina, 1971) Makshanova & Omelyanchik, 1973). It may cause corneal damage or eye inflammation (Schmid, 1956).
- Occupational exposure to n-butyl acetate has resulted in conjunctival irritation, chest constriction and coughing; however, related lesions were only found in workers exposed to a mixture of solvents that included n-butyl acetate (ACGIH, 1996a). Hepatotoxicity has also been reported after occupational exposure (HSDB , 2000). Repeated exposures to butyl acetate have produced renal and hematological changes in animals (Sittig, 1991).
- Long-term inhalation of butyl acetate affected protein and lipid metabolism in rats, but multivitamin therapy normalized these effects (Makshanova & Omelyanchik, 1977).
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID EYE EXPOSURE - Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. DERMAL EXPOSURE - Flush the contaminated skin with water promptly. If this chemical penetrates the clothing, immediately remove the clothing and flush the skin with water promptly. If irritation persists after washing, get medical attention. INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE - If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS - Eyes, skin, respiratory system, and central nervous system (National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000).
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
DERMAL EXPOSURE DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE Because of the potential for gastrointestinal tract irritation or CNS depression, DO NOT induce emesis. DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002). In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis. The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- The minimum lethal human dose to this agent has not been delineated.
Exposure to an airborne concentration of 14,000 ppm of n-butyl acetate for 4 hours (at 30 degrees C) was lethal to guinea pigs (ACGIH, 1996a; Clayton & Clayton, 1994; Hathaway et al, 1996a). Exposure to an airborne concentration of approximately 10,000 ppm of n-butyl acetate was fatal to rats in 8 hours. Rats exposed to 2.2 or 5.2 mg/L for 4 hours died within 24 hours of exposure. Mortality in rats also occurred following exposure to an aerosol concentration of 540 ppm (ACGIH, 1996a).
MAXIMUM TOLERATED EXPOSURE
- The maximum tolerated human exposure to this agent has not been delineated.
- Human exposure to airborne concentrations between 70 and 1400 mg/m(3) for 20 minutes, or to 70 and 700 mg/m(3) for 4 hours caused slight irritation of eyes and respiratory system, based on the results of rating scales, measures of eye irritation, and pulmonary function tests (ACGIH, 1996a) Bingham et al, 2001; Hathaway, 1996).
- No sensitization occurred following repeated insult patch-testing using 0.5 mL of n-butyl acetate. Patches were applied 9 times for 24 hours over a 3 week period (ACGIH, 1996a).
- Human data suggests that inhalation exposure to 300 ppm of n-butyl acetate may be irritating to the eyes and the upper respiratory system, and that direct contact with the chemical may cause dermatitis. Nervous, respiratory, and cardiovascular disorders have been described in one report about the effects of human exposure to polyester lacquer. Interpretation of epidemiological data is difficult because most reports are based on exposure to solvent mixtures containing n-butyl acetate (Bingham et al, 2001).
- Exposure of six paint factory workers in Taiwan to solvents containing n-butyl acetate, toluene, xylene, n-hexane, and methyl isobuytl ketone was associated with prolonged response latencies in tests of continuous performance, pattern comparison, and pattern memory (Bingham et al, 2001).
- The following effects were reported following exposure to n-butyl acetate (Bingham et al, 2001):
- Acute toxicity was reported in mice exposed to 8000 ppm of n-butyl acetate for 20 minutes. The neurobehavioral effects included changes in posture, decreased arousal, increased tonic/clonic movements, disturbances in gait, delayed righting reflex, and increased sensorimotor activity. Following discontinuation of the exposure, the animals recovered quickly (Bingham et al, 2001).
- Dose-dependent effects were reported in a study where rats and mice were exposed to butyl alcohol and n-butyl acetate, either individually or as a mixture. The results showed changes in the rotarod performance of the animals at median concentrations of 7559 ppm n-buytl alcohol, 8339 ppm n-buytl acetate and a 5:50 mixture of the two solvents at a concentration of 10,672 ppm. Other effects observed in this study included decreased pain sensitivity in the hot-plate behavior test (Bingham et al, 2001).
- Decreased maternal body weight and decreased size of the rat fetuses were reported in a study where pregnant rabbits and rats were exposed to 1500 ppm of n-butyl acetate vapor. Rabbits were exposed from gestation day 1-19, rats from gestation day 1-16 (Bingham et al, 2001).
- Rats experimentally exposed to n-butyl acetate vapors for 6h/day for 65 exposures over 14 days showed transient sedation and hypoactivity at concentrations of 1500 and 3000 ppm. No effect was seen at 500 ppm. There was no indication that neurotoxicity was cumulative (Bingham et al, 2001).
- Cats exposed via inhalation to 17,500 ppm (83 mg/L of diluent) for 30 minutes showed signs of CNS depression. This concentration was lethal to some animals (Bingham et al, 2001).
- Cats exposed via inhalation to 4200 ppm (20 mg/L of diluent) for 6 hours over 6 days developed weakness, weight loss and showed minor blood changes (Bingham et al, 2001).
- Guinea pigs exposed via inhalation to 14,000 ppm (66 mg/L of diluent) for 4 hours developed eye irritation, showed signs of CNS depression. This concentration was lethal to some animals (Bingham et al, 2001).
- Guinea pigs exposed via inhalation to 7,000 ppm (33 mg/L of diluent) for 13 hours developed eye irritation and showed signs of CNS depression, but they recovered after exposure ceased (Bingham et al, 2001).
- Experimental inhalation exposure of rats to n-butyl acetate at concentrations of 0, 500, 1500 and 3000 ppm was evaluated in one study. Following exposure for 6 hours per day, 5 days per week (65 exposures over 13 weeks) showed effects only in the groups exposed to 1500 and 3000 ppm. Compared to the control group, animals in these two exposure groups displayed a decrease in feed consumption and a reduced body weight. The group exposed to 3000 ppm also showed changes in absolute and relative organ weights. Degeneration of olfactory epithelium was seen in areas with carboxylesterase activity. There was no evidence for hepatotoxicity in any exposure group. Sperm counts in exposed animals were lower than in the control group, but the effect was not statistically significant (David et al, 2001).
- Carcinogenicity Ratings for CAS123-86-4 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: n-Butyl acetate EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: n-Butyl acetate MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS123-86-4 (U.S. Environmental Protection Agency, 2011):
ACGIH, 1996a Budavari, 2000 Clayton & Clayton, 1994 Lewis, 2000 OHM/TADS, 2002 RTECS, 2002 LC50- (INHALATION)MOUSE: LC50- (INHALATION)RAT: 2000 ppm for 4H (ACGIH, 1996a; Lewis, 2000) 160 ppm for 4H (ACGIH, 1996a) 391 ppm for 4H (ACGIH, 1996a) 390 ppm for 4H -- Change in motor activity; acute pulmonary emphysema; hemorrhage
LCLo- (INHALATION)CAT: LCLo- (INHALATION)GUINEA_PIG: 67 g/m(3) for 4H (Lewis, 2000) 67 g/m(3) for 4H -- Antipsychotic; effects on sense organs and special senses
LD- (INHALATION)GUINEA_PIG: LD50- (INTRAPERITONEAL)GUINEA_PIG: LD50- (ORAL)GUINEA_PIG: LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: LD50- (ORAL)RABBIT: 3200 mg/kg 7.4 g/kg (ACGIH, 1996a)
LD50- (SKIN)RABBIT: LD50- (ORAL)RAT: 10,768 mg/kg -- Somnolence; effects on respiratory system and liver 13,100 mg/kg (Lewis, 2000) 14.0 g/kg (Clayton & Clayton, 1994) 14.13 g/kg (ACGIH, 1996a; Budavari, 2000) 4130 mg/kg (OHM/TADS, 2002) 14,300 mg/kg for 14D (OHM/TADS, 2002)
LDLo- (INTRAMUSCULAR)GUINEA_PIG: LDLo- (INTRAPERITONEAL)GUINEA_PIG: TCLo- (INHALATION)HUMAN: TCLo- (INHALATION)RAT: Female, 1500 ppm for 7H at 7-16D of pregnancy -- Fetotoxicity; musculoskeletal abnormalities 1500 ppm for 6H/13W-intermittent -- Somnolence; weight loss or decreased weight gain
CALCULATIONS
1 mg/m(3) = 0.21 ppm (at 25 degrees C) (ACGIH, 1996a) 1 ppm = 4.75 mg/m(3) (at 68 degrees F and 760 mmHg) (NIOSH , 2002)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS123-86-4 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS123-86-4 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS123-86-4 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS123-86-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS123-86-4 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS123-86-4 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS123-86-4 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS123-86-4 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS123-86-4 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS123-86-4 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS123-86-4 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS123-86-4 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1123 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1123 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS123-86-4 (NFPA, 2002):
Listed as: Butyl Acetate Hazard Ratings: Health Rating (Blue): 2 Flammability Rating (Red): 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
Instability Rating (Yellow): 0 Oxidizer/Water-Reactive Designation: Not Listed
-HANDLING AND STORAGE
SUMMARY
This compound should be stored in tightly closed containers in an area that is cool and well-ventilated. It should be kept away from sources of ignition and explosives, oxidizing materials, organic peroxides, readily odor-impregnable material, and food products (ITI, 1995; Sittig, 1991).
HANDLING
- Appropriate personal protective equipment should always be worn when handling broken packages (AAR, 2000).
- This compound remains stable during transport (CHRIS , 2002).
STORAGE
- ROOM/CABINET RECOMMENDATIONS
This compound should be kept in a cool, well-ventilated area away from heat and other sources of ignition, explosives, oxidizing materials, organic peroxides, readily odor-impregnable material, and food products (ITI, 1995; Sittig, 1991).
n-Butyl acetate is incompatible with nitrates, strong oxidizers, strong alkalis, and strong acids (NIOSH , 2002; Pohanish & Greene, 1997; Sittig, 1991). This compound reacts violently with oxidants, possibly leading to fire or explosion. It attacks various plastics and resins (ILO, 1998; Pohanish & Greene, 1997). It dissolves rubber and some coatings (Pohanish & Greene, 1997).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
- Wear appropriate rubber protective clothing and eye protection, including boots, gloves, goggles, and a chemical cartridge mask, when working with n-butyl acetate. Appropriate personal protective equipment should always be worn when handling broken packages. Contaminated clothing and shoes should be removed and isolated at the site (AAR, 2000; (ITI, 1995; NIOSH , 2002; Sittig, 1991).
- Immediately wash contaminated skin and immediately remove work clothing that becomes wet or contaminated due to its flammability hazard (AAR, 2000; (NIOSH , 2002; Sittig, 1991).
EYE/FACE PROTECTION
- Appropriate eye protection should be worn to prevent eye contact when working with this compound (AAR, 2000; NIOSH, 200; (Sittig, 1991).
- Use an all-purpose canister mask, chemical safety goggles and rubber gloves (CHRIS, 200).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 123-86-4.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004) HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water.
n-Butyl acetate is a flammable liquid with a moderate explosion risk. Fight fires involving this compound with alcohol foam, dry chemical, carbon dioxide, or flooding quantities of water as fog. Solid streams of water may be ineffective or spread the fire (AAR, 2000; (CHRIS , 2002; Lewis, 1997; Lewis, 2000; Sittig, 1991). Vapors of this compound may ignite due to accumulation of static electricity (Pohanish & Greene, 1997). This compound presents a moderate fire hazard when exposed to heat or open flame (OHM/TADS , 2002). Ignition occurred following contact of 1.5 g of solid potassium tert-butoxide with butyl acetate vapor for 2 minutes (Urben, 2000).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS123-86-4 (NFPA, 2002):
Listed as: Butyl Acetate Flammability Rating: 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
Dry chemical, CO2, water spray or alcohol-resistant foam. Do not use dry chemical extinguishers to control fires involving nitromethane or nitroethane.
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
Water spray, fog or alcohol-resistant foam. Do not use straight streams. Move containers from fire area if you can do it without risk.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS123-86-4 (NFPA, 2002):
- A self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode should be used when fighting a fire involving n-butyl acetate (HSDB , 2002).
- Fire should not be extinguished unless flow of the liquid can be stopped. Apply water from as far a distance as possible in flooding quantities as fog to extinguish fire and cool affected containers (AAR, 2000; (Sittig, 1991).
- Alcohol foam, carbon dioxide, or dry chemical extinguishers may be used to combat fires (AAR, 2000; (Lewis, 2000; Sittig, 1991).
- Carbon tetrachloride is also a suitable fire extinguishing agent (OHM/TADS , 2002).
- Solid streams of water may be ineffective for fire control, as they may spread the fire (AAR, 2000; (NFPA, 1997).
EXPLOSION HAZARD
- This compound is moderately explosive when exposed to flame (Lewis, 2000; OHM/TADS , 2002).
- Fire and explosion may occur if n-butyl acetate comes in contact with nitrates, strong acids, strong alkalis, or strong oxidizers (ACGIH, 1996a; Pohanish & Greene, 1997).
- Explosion may also occur if n-butyl acetate is ignited in an enclosed area (CHRIS , 2002).
- A vapor trail of this compound can result in flashbacks (CHRIS , 2002).
- n-Butyl acetate forms explosive mixtures with air (Pohanish & Greene, 1997).
DUST/VAPOR HAZARD
- Acrid and irritating fumes and toxic gases, such as carbon monoxide, are emitted when n-butyl acetate is involved in a fire (ACGIH, 1996a; Lewis, 2000).
- In spill situations, knock down vapors with water spray (AAR, 2000).
REACTIVITY HAZARD
- n-Butyl acetate ignites when in contact with potassium tert-butoxide (Lewis, 2000; NFPA, 1997; Pohanish & Greene, 1997).
- Fire and explosion may occur if n-butyl acetate comes in contact with nitrates, caustics, strong acids, strong alkalis, or strong oxidizers (ACGIH, 1996a; Pohanish & Greene, 1997).
- This chemical is reactive under extreme conditions. Reaction with oxidizing agents should be expected (OHM/TADS , 2002).
- n-Butyl acetate reacts over time with water, generating acetic acid and n-butyl alcohol in the process. It attacks rubber, many plastics, resins and certain coatings (Pohanish & Greene, 1997).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
If tank, rail car or tank truck 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.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
- Keep upwind and avoid breathing vapors (AAR, 2000).
- Ventilate the area after all ignition sources have been removed. Reduce vapors using water spray (AAR, 2000; (CHRIS , 2002).
- In emergency spill situations, notify fire department, local health and pollution control agencies and operators of nearby water intakes (CHRIS , 2002).
- AIHA ERPG Values for CAS123-86-4 (AIHA, 2006):
Listed as n-Butyl Acetate ERPG-1 (units = ppm): 5 ERPG-2 (units = ppm): 200 ERPG-3 (units = ppm): 3000 Under Ballot, Review, or Consideration: No Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS123-86-4 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Butyl acetate, n- TEEL-0 (units = ppm): 5 TEEL-1 (units = ppm): 5 TEEL-2 (units = ppm): 200 TEEL-3 (units = ppm): 3000 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS123-86-4 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS123-86-4 (National Institute for Occupational Safety and Health, 2007):
IDLH: 1700 ppm Note(s): [10%LEL]
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. Use clean non-sparking tools to collect absorbed material.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 129 (ERG, 2004) Only persons wearing protective clothing, including boots, gloves, and goggles should be allowed in the contaminated area (AAR, 2000). If it is not a hazard to personnel, attempt to stop or control any leaks and prevent the compound from entering water supplies. If necessary, build dikes to contain the flow of the liquid (AAR, 2000). Reduce vapors and dilute liquid spill using water spray (AAR, 2000; (Sittig, 1991). Sittig (1991) reports that material spilled on land or water should be absorbed using activated carbon and then removed for disposal. ITI (1995) reports that spills should be absorbed on paper and then evaporated on glass or an iron dish in a hood. The paper should then be burned. LAND SPILL: Dig a holding area to contain liquid or solid material and build dikes to contain any surface flow using sand bags, soil, foamed polyurethane, or foamed concrete. Vapor and fire hazard may be diminished using an appropriate foam. Cement powder or fly ash should be used to absorb the liquid (AAR, 2000). WATER SPILL: Travel of the spill should be controlled using natural barriers or oil spill control booms. A surface active agent, such as alcohol, detergent, or soap, may be used if it is approved by the EPA. The effectiveness of the booms may be increased by using a universal gelling agent. Mechanical dredges or lifts may be used to remove immobilized masses of the spilled material. Use suction hoses to remove trapped material. Activated carbon should be applied at ten times the spilled amount if the spilled material is dissolved in an area of 10 ppm or greater concentration (AAR, 2000; (HSDB , 2002). For in situ amelioration, booms or skimming procedures can be used to limit movement of the slick. The slick can also be sorbed on foam. Carbon or peat are suitable materials to pack the soluble portion (OHM/TADS , 2002). Spilled material can be thickened through the application of surface active agents, such as detergents, snaps and alcohols. A universal gelling agent may be solidify the spilled material (HSDB , 2002).
Butyl acetate and butanol may be present in waste waters from antibiotic- manufacturing plants. A highly efficient method for removal of these compounds from waste waters containing solids that tend to settle has been described (HSDB , 2002). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
Incineration is the suggested disposal method (Sittig, 1991). Large quantities of this compound may be collected for atomization in a suitable combustion chamber (HSDB , 2002). Dispose of this chemical by spraying it into incinerator or by burning it in paper packaging. Incineration may be facilitated by the addition of flammable solvents (OHM/TADS , 2002). This compound can be burned off under controlled conditions to cleanup and restore beaches or shores (OHM/TADS , 2002). Proposed methods of disposal should be used on statutory requirements of the state where disposal is to occur. The usual methods would be expected to include: 1) Absorbing in vermiculite, dry sand, earth or a similar material. 2) Atomization in a suitable combustion chamber" (HSDB, 2002).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- n-Butyl acetate is a naturally occurring component of apples, bananas, and other fruit. It has also been detected as a volatile flavor component of roasted filbert nuts and baked potatoes (Bingham et al, 2001; Howard, 1990).
- It is primarily released to the environment by evaporation during its use as a solvent or through waste streams associated with its use (Howard, 1990; HSDB, 2004).
- Because of danger to human health and aquatic life, this compound should be prevented from entering water supplies (CHRIS , 2002; AAR, 2000).
ENVIRONMENTAL FATE AND KINETICS
n-Butyl acetate has a relatively high vapor pressure and thus should exist almost entirely as a vapor in the ambient atmosphere. The primary removal mechanism should be the vapor-phase reaction of n-butyl acetate with photochemically produced hydroxyl radicals which corresponds to a half-life of approximately 4 days (HSDB, 2004; Howard, 1990). A half-life of approximately 4 days has been estimated for the vapor phase reaction of n-butyl acetate with photochemically produced hydroxyl radicals, assuming an average atmospheric hydroxyl radical concentration of 5 x 10(5) molecules/cm(3). Hydrolysis half-lives of n-butyl acetate are estimated to be 3.1 years at pH 7.0, 114 days at pH 8.0, and 11 days at pH 9.0 (HSDB , 2002; Howard, 1990). The half-life for the reaction with photochemically produced hydroxyl radicals in the atmosphere is 4 days (HSDB, 2004). The calculated half-life for reaction with atmospheric hydroxyl radicals is 45 hours (Verschueren, 2001).
SURFACE WATER Significant biodegradation of n-butyl acetate may occur in natural water. Hydrolysis is likely to occur in alkaline waters, but should not be an important removal process in neutral or acidic waters. Based on an approximate Henry's Law constant of 3.2x10(-4) atm-m(3)/mol (at 25 degrees C), volatilization from environmental waters should be significant. Bioconcentration and aquatic adsorption, however, should not be significant (Howard, 1990). Based on the estimated Koc value of 200, adsorption of n-butyl acetate to suspended solids or sediments is unlikely to occur in water. Based on Henry's Law constant of 2.8X10(-4) atm-m(3)/mole, volatilization from the water surface is expected (HSDB, 2004). Based on experimentally derived hydrolysis half-lives, hydrolysis is expected to be the most important environmental fate process for this compound (HSDB, 2004). Results from experiments showed hydrolysis half-lives of 114 days for water at pH 8, and 11 days for water at pH 9 (HSDB, 2004). Estimated half-life for volatilization from a model river is 7 hours; from a model lake, it is 127 hours (HSDB, 2004).
TERRESTRIAL n-Butyl acetate in moist alkaline soils is expected to undergo chemical hydrolysis, however hydrolysis should not be important in neutral or acidic soils. Rapid volatilization should occur from dry soil surfaces. Microbial decomposition may occur. The estimated Koc value of 200 indicates that moderate movement in soil may occur (HSDB, 2004; Howard, 1990) . Based on a calculated Koc value of 200, moderate soil motility is expected. Based on Henry's Law constant of 2.8X10(-4) atm-m(3)/mole, volatilization is likely to occur from moist soil surfaces. Based on a measured vapor pressure of 11.5 mmHg, volatilization from dry soil surfaces can be expected (HSDB, 2004).
ABIOTIC DEGRADATION
- n-Butyl acetate has a relatively high vapor pressure and thus should exist almost entirely as a vapor in the ambient atmosphere, with the primary removal mechanism being vapor-phase reaction with photochemically produced hydroxyl radicals. Significant degradation of n-butyl acetate may occur in natural water through hydrolysis (in alkaline waters only) or volatilization. In moist alkaline soils, butyl acetate will likely undergo chemical hydrolysis or microbial decomposition. Hydrolysis is not as important a process in moist, neutral or acidic soils. Rapid volatilization should occur from dry soil surfaces. Bioconcentration in aquatic organisms is expected to be low and not significant (Howard, 1990)
BIODEGRADATION
- A concentration of 0.1 mg/L or higher can affect the capability of surface water to self-purify(Verschueren, 2001).
- Theoretical oxygen demand (ThOD): 2.207 Chemical oxygen demand (COD): 78% of theoretical oxygen demand, using potassium dichromate (K2Cr2O7) (Verschueren, 2001).
- Percent theoretical BODs are reported as follows:
23.5% (after 5 days) (< 1 lb/lb) (standard dilution water tests using a settled sewage seed) (HSDB, 2004; OHM/TADS, 2002) 57.4% (after 20 days) (> 1 lb/lb) (standard dilution water tests using a settled sewage seed) (HSDB, 2004; OHM/TADS, 2002) 58% (after 5 days) (> 1 lb/lb) (fresh water dilution tests using a filtered sewage seed) (HSDB, 2004; OHM/TADS, 2002) 83% (after 20 days) (> 1 lb/lb) (fresh water dilution tests using a filtered sewage seed) (HSDB, 2004; OHM/TADS, 2002) 40% (after 5 days) (< 1 lb/lb) (in saltwater using a filtered sewage seed) (HSDB, 2004; OHM/TADS, 2002) 61% (after 20 days) (> 1 lb/lb) (in saltwater using a filtered sewage seed) (HSDB, 2004; OHM/TADS, 2002) 20.9% (after 5 days) (river water using the standard dilution method) (HSDB, 2004) 55.4% (after 20 days) (river water using the standard dilution method) (HSDB, 2004) 56.8% (after 5 days) (distilled water using the standard dilution method) (HSDB, 2004) 51.8% (after 5 days) (sea water using the standard dilution method) (HSDB, 2004) 68% (after 10 days) (> 1 lb/lb) (BOD using sewage seed) (HSDB, 2004; OHM/TADS, 2002) 70% (after 15 days) (> 1 lb/lb) (BOD using sewage seed) (HSDB, 2004; OHM/TADS, 2002) 52% (after 10 days) (> 1 lb/lb) (saltwater BOD using sewage seed) (OHM/TADS, 2002) 56% (after 15 days) (> 1 lb/lb) (saltwater BOD using sewage seed) (OHM/TADS, 2002) 0.15 - 0.5 lb/lb (after 5 days) (standard dilution water tests using a settled sewage seed) (OHM/TADS, 2002) 52% (after 5 days) (CHRIS, 2002) 0.15 - 0.5 lb/lb (after 5 days) (CHRIS, 2002) 7% of ThOD (after 5 days at 20 degrees C) (test condition not specified) (Verschueren, 2001) 24% of ThOD (after 5 days at 20 degrees C) (test condition not specified) (Verschueren, 2001) 46% of ThOD (after 5 days at 20 degrees C) (test condition not specified) (Verschueren, 2001) 60% of ThOD (after 20 days) (test condition not specified) (Verschueren, 2001)
BIOACCUMULATION
Bioconcentration should not be significant based on estimated BCF values of 14 and 4 (Howard, 1990). Based on a Kow value of 1.78, the bioconcentration is estimated to be 10, hence bioconcentration in aquatic organisms is expected to be low (HSDB , 2002).
ENVIRONMENTAL TOXICITY
EC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 18 mg/L for 96H (HSDB, 2004) TLm - (WATER) DAPHNIA: 44 ppm for 48H -- fresh water at 23 degrees (CHRIS, 2002; OHM/TADS, 2002) TLm - (WATER) SCENEDESMUS: 320 ppm for 96H -- fresh water at 24 degrees (OHM/TADS, 2002) TLm - (WATER) BRINE SHRIMP: 150 ppm for 24H -- saltwater, static test environment (OHM/TADS, 2002) TLm - (WATER) BRINE SHRIMP: 32 ppm for 48H -- saltwater, static test environment (OHM/TADS, 2002) TL50 - (WATER) ATLANTIC SILVERSIDE: 185 ppm for 96H -- saltwater, static test environment, mg/L added (OHM/TADS, 2002) TL50 - (WATER) BLUEGILL: 100 ppm for 96H -- fresh water, static test environment, mg/L added (OHM/TADS, 2002) LC0 - (WATER) IDE (Leuciscus idus): 44 mg/L for 48H (Verschueren, 2001) LC0 - (WATER) IDE (Leuciscus idus): 70 mg/L for 48H (Verschueren, 2001) LC0 - (WATER) IDE (Leuciscus idus): 80 mg/L for 48H (Verschueren, 2001) LC50 - (WATER) BLUEGILL: 100 mg/L for 96H -- static bioassay in fresh water at 23 degrees C, mild aeration applied after 24H (Verschueren, 2001) LC50 - (FRESHWATER) FATHEAD MINNOW (Pimephales promelas): 18 mg/L for 96H; flow-through bioassay (Verschueren, 2001) LC50 - (WATER) IDE (Leuciscus idus): 70 mg/L for 48H (Verschueren, 2001) LC50 - (WATER) IDE (Leuciscus idus): 90 mg/L for 48H (Verschueren, 2001) LC50 - (WATER) IDE (Leuciscus idus): 141 mg/L for 48H (Verschueren, 2001) LC50 - (WATER) ISLAND SILVERSIDE: 185 ppm for 96H -- static bioassay in synthetic sea water at 23 degrees C, mild aeration applied after 24H (HSDB, 2002) LC100 - (WATER) IDE (Leuciscus idus): 72 mg/L for 48H (Verschueren, 2001) LC100 - (WATER) IDE (Leuciscus idus): 176 mg/L for 48H (Verschueren, 2001)
EC0 - (SALTWATER) CHILOMONAS PARAMECIUM: 670 mg/L for 48H (Verschueren, 2001) EC0 - (SALTWATER) ENTOSIPHON SULCATUM: 321 mg/L for 72H; static bioassay (Verschueren, 2001) EC0 - (SALTWATER) URONEMA PARDUCZI: 574 mg/L for 20H; static bioassay (Verschueren, 2001) EC0 - (WATER) URONEMA PARDUCZI (Chatton Lwoff): 574 mg/L (Verschueren, 2001)
EC0 - (SALTWATER) DAPHNIA MAGNA: 93 mg/L for 24H; static bioassay (Verschueren, 2001) EC50 - (SALTWATER) ARTEMIA SALINA: 150 mg/L for 24H; static bioassay (Verschueren, 2001) EC50 - (SALTWATER) ARTEMIA SALINA: 32 mg/L for 24H; static bioassay (Verschueren, 2001) EC50 - (SALTWATER) DAPHNIA MAGNA: 24 mg/L for 24H; static bioassay (Verschueren, 2001) EC50 - (SALTWATER) DAPHNIA MAGNA: 73 mg/L for 24H; static bioassay (Verschueren, 2001) EC50 - (SALTWATER) DAPHNIA MAGNA: 205 mg/L for 24H; static bioassay (Verschueren, 2001) EC100 - (SALTWATER) DAPHNIA MAGNA: 500 mg/L for 24H; static bioassay (Verschueren, 2001) LC50 - (WATER) DAPHNIA: 44 mg/L for 48H; static bioassay (Verschueren, 2001)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- n-Butyl acetate is a colorless liquid with a strong, fruity odor. (AAR, 2000; (HSDB , 2002; Lewis, 1997).
Its odor is sometimes described as pleasant or banana-like. It also has a pleasant, banana or pineapple-like taste. n-Butyl acetate vapor is heavier than air (AAR, 2000; (HSDB , 2002; Lewis, 1997).
VAPOR PRESSURE
- 8 mmHg (at 20 degrees C) (OHM/TADS , 2002)
- 8.7 mmHg (at 20 degrees C) (Lewis, 1997)
- 10 mmHg (at 20 degrees C) (ACGIH, 1996a; Verschueren, 2001)
- 11.5 mmHg (based on experimentally-derived coefficients) (HSDB , 2002)
- 12.48 mmHg (at 25 degrees C) (Howard, 1990)
- 15 mmHg (at 25 degrees C) (Clayton & Clayton, 1994; Lewis, 2000; OHM/TADS , 2002; Verschueren, 2001)
- 13 hPa (at 20 degrees C) (Verschueren, 2001)
- 2 kPa (at 25 degrees C) (ILO, 1998)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
0.8826 (at 20/20 degrees C) (Bingham et al, 2001; (Budavari, 2000; ILO, 1998; Lewis, 1997) 0.88 (at 20/20 degrees C) (Lewis, 2000) 0.88 (at 20/4 degrees C) (ITI, 1995; NIOSH , 2002; Verschueren, 2001)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
0.88 kg/L (at 20 degrees C) (Ashford, 1994a) 0.8826 kg/L (at 20 degrees C) (ACGIH, 1996a) 0.875 kg/L (at 20 degrees C) (CHRIS , 2002)
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
-73.5 degrees C; -100 degrees F; 199.7 K (CHRIS , 2002; Clayton & Clayton, 1994) -75 degrees C (Lewis, 1997) -77 degrees C (ACGIH, 1991; (Lewis, 2000) -107 degrees F (NIOSH , 2002)
-78 degrees C (Clayton & Clayton, 1994; HSDB , 2002) -77 degrees C (Bingham et al, 2001; (Budavari, 2000; Howard, 1990; ILO, 1998) -76.8 degrees C (ITI, 1995; OHM/TADS , 2002; Verschueren, 2001)
BOILING POINT
- 127 degrees C; 260 degrees F (NFPA, 1997)
- 126-127 degrees C (Sittig, 1991)
- 124-127 degrees C (Ashford, 1994a; Verschueren, 2001)
- 126.5 degrees C (Clayton & Clayton, 1994; ITI, 1995)
- 126.3 degrees C (Lewis, 1997)
- 126 degrees C; 259 degrees F; 399 K (at 1 atm) (CHRIS , 2002)
- 125-126 degrees C (Budavari, 2000; Howard, 1990)
- 258 degrees F (NIOSH , 2002)
- 126 degrees C (ACGIH, 1991; Bingham et al, 2001; (ILO, 1998; Lewis, 2000)
- 126.1 degrees C (HSDB , 2002)
- 117.5 degrees C (OHM/TADS , 2002)
FLASH POINT
- 22 degrees C (closed cup) (ILO, 1998)
- 22 degrees C; 72 degrees F (Closed Cup) (Budavari, 2000; NFPA, 1997; Pohanish & Greene, 1997)
- 23 degrees C (Closed Cup) (ITI, 1995)
- 24 degrees C (Closed Cup) (ACGIH, 1996a) Bingham et al, 2001)
- 25 degrees C (Tagliabue Closed Cup) (Ashford, 1994a)
- 29 degrees C (OHM/TADS , 2002)
- 36.6 degrees C; 98 degrees F (Tagliabue Open Cup) (Lewis, 1997)
- 37 degrees C (Open Cup) (ACGIH, 1996a) Bingham et al, 2001)
- 38 degrees C (Open Cup) (ITI, 1995)
- 81 degrees F (Closed Cup) (CHRIS , 2002)
- 72-88 degrees F (AAR, 2000)
- 72 degrees F (Lewis, 2000; NIOSH , 2002)
AUTOIGNITION TEMPERATURE
- 365 degrees C (OHM/TADS , 2002)
- 421.1 degrees C (ACGIH, 1996a)
- 425 degrees C; 797 degrees F (NFPA, 1997)
- 421 degrees C; 790 degrees F (Lewis, 1997)
- 420 degrees C (ILO, 1998)
- 760 degrees F (CHRIS , 2002)
- 797 degrees F (Lewis, 2000)
- 421 degrees C (ITI, 1995)
EXPLOSIVE LIMITS
1.7% (CHRIS , 2002; ILO, 1998; ITI, 1995; NFPA, 1997; NIOSH , 2002; OHM/TADS , 2002; Sittig, 1991) 1.4% (Lewis, 2000)
7.6% (ACGIH, 1996a; CHRIS , 2002; ILO, 1998; NFPA, 1997; NIOSH , 2002; Sittig, 1991) 7.5% (Lewis, 2000) 15% (ITI, 1995; OHM/TADS , 2002)
SOLUBILITY
This compound is slightly soluble in water (AAR, 2000; (ACGIH, 1996a) Bingham et al, 2001; (ILO, 1998; ITI, 1995; Lewis, 1997; NFPA, 1997). It is insoluble in water (Lewis, 2000). 7 g/L (at 20 degrees C) (Ashford, 1994a) 0.68 g/100 g (at 20 degrees C) (ACGIH, 1996a) 6710 mg/L (at 25 degrees C) (Howard, 1990) 14,000 mg/L (at 20 degrees C) (Verschueren, 2001) 5000 mg/L (at 25 degrees C) (Verschueren, 2001) 6700 ppm (at 25 degrees C) (HSDB , 2002) 7,000 ppm (at 25 degrees C) (OHM/TADS , 2002) Soluble in approximately 120 parts water (at 25 degrees C) (Budavari, 2000) 1% (NIOSH , 2002) 0.68 g/100mL (Bingham et al, 2001)
It is soluble in acetone, alcohol, diethylether, dimethylether, ethanol, ether, propylene glycol, and most hydrocarbons (Budavari, 2000; ITI, 1995; Lewis, 2000; Lewis, 1997). n-Butyl acetate is very soluble in ethanol and ether, soluble in acetone and most hydrocarbons (Budavari, 2000). It is miscible with alcohol, ether, ethanol, propylene glycol, and most organic solvents (ACGIH, 1996a; Ashford, 1994a; Budavari, 2000; ITI, 1995; Lewis, 2000).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow = 1.82 (Howard, 1990; HSDB , 2002)
- log Poct = 1.81 (measured) (Verschueren, 2001)
HENRY'S CONSTANT
- 3.2x10(-4) atm-m(3)/mol (at 25 degrees C) (Howard, 1990)
- 2.8X10(-4) atm-m(3)/mole (HSDB , 2002)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
7 ppm (ACGIH, 1996a) Bingham et al, 2001) 10 ppm (CHRIS , 2002) 20 ppm (ACGIH, 1996a) Bingham et al, 2001) 33.13 mg/m(3) (odor low) (HSDB , 2002) 94.66 mg/m(3) (odor high) (HSDB , 2002) Detection in water 0.066 mg/kg (Verschueren, 2001) 0.043 mg/kg (Verschueren, 2001)
Distinct odor: 55 mg/m(3) = 11 ppm (Verschueren, 2001) Recognition in air: 0.6 ppm (OHM/TADS , 2002) 0.6 mg/m(3) (Verschueren, 2001) 0.13 mg/m(3) (adverse reflex) (Verschueren, 2001)
Odor threshold in animals: 20 mg/m(3) (adverse effects) (Verschueren, 2001)
306 degrees C (ITI, 1995) 305.9 degrees C; 582.6 degrees F; 579.1 K (CHRIS , 2002)
1.3951 (at 20 degrees C) (Budavari, 2000) 1.3942 (at 20 degrees C) (ITI, 1995) 1.3941 (at 20 degrees C) (HSDB , 2002) 1.393-1.396 (Lewis, 2000) 1.2951 (at 20 degrees C) (Lewis, 1997)
- LIQUID WATER INTERFACIAL TENSION
- NUCLEAR MAGNETIC RESONANCE
1.004 cP (at 0 degrees C) (HSDB , 2002) 0.732 cP (at 20 degrees C) (HSDB , 2002) 0.563 cP (at 40 degrees C) (HSDB , 2002)
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