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BUTYL ACETATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) These compounds are solvents, generally in mixtures, used in the manufacture of lacquers, nail polishes and removers, adhesives, artificial leather, photographic films, plastics, and safety glass (Ashford, 1994; ACGIH, 1996a) Zaleski, 1992; (ILO, 1998).
    B) Butyl acetates are used as synthetic flavoring ingredients (i.e., fruit flavors), as extractants for flavorings, perfume and penicillin and as dehydrating agents to process oils and pharmaceuticals, and are used in food processing (Lewis, 1998; ITI, 1995; Ashford, 1994; ACGIH, 1996a; Clayton & Clayton, 1994; HSDB , 2002).
    C) Tert-butyl acetate is used as a gasoline additive (Lewis, 1997; Proctor et al, 1988).
    D) It is manufactured by the esterification of the respective alcohol with acetic acid or acetic anhydride (Clayton & Clayton, 1994).

Specific Substances

    A) N-BUTYL ACETATE
    1) 1-butyl acetate
    2) acetic acid n-butyl ester
    3) acetic acid, butyl ester
    4) acetate de butyle (French)
    5) butile (acetati de) (Italian)
    6) butylacetat (German)
    7) butylacetaten (Dutch)
    8) butyle (acetate de) (French)
    9) butylester kyseling octove (Czech)
    10) butyl ethanoate
    11) CAS 123-86-4
    12) FEMA NUMBER 2174
    13) Molecular formula: C6-H12-O2
    14) octan n-butylu (Polish)
    SEC-BUTYL ACETATE
    1) acetic acid 1-methylpropyl ester
    2) acetic acid sec-butyl ester
    3) 2-butanol acetate
    4) 2-butyl acetate
    5) 1-methylpropyl acetate
    6) Molecular formula: C6-H12-O2
    7) CAS 105-46-4
    TERT-BUTYL ACETATE
    1) acetic acid 1,1-dimethylethyl ester
    2) acetic acid tert-butyl ester
    3) tertiary butyl acetate
    4) t-butyl acetate
    5) Butyl acetate (tert)
    6) Butile (acetati di) (Italian)
    7) TLA
    8) Molecular formula: C6-H12-O2
    9) CAS 540-88-5

Available Forms Sources

    A) SOURCES
    1) N-butyl acetate is a biosynthesis product of fermentation processes in yeasts (Budavari, 1996). It is found in apples, bananas, cheese, beer, brandy, wine, cocoa, coffee, roasted nuts and honey (Howard, 1990) Zaleski, 1992). Sec-butyl acetate and tert-butyl acetate are found in bananas and related fruits (Zaleski, 1992).
    B) USES
    1) N-butyl acetate is used in the manufacture of lacquers, nail polishes and removers, artificial leathers, perfumes, photographic films, plastics and safety glasses. It is used an an industrial solvent (e.g. oils, nitrocellulose, fats, resins, waxes, and camphor), as an extraction solvent in food processing, and in inks and thinners used in printing processes (Reynolds, 1996; (ACGIH, 1996a). It is also used as a larvicide (Harbison, 1998).
    2) Sec-butyl acetate is used mainly as a solvent, especially for nitrocellulose lacquers, thinners, nail enamels, and leather finishes and also used in the paper industries (HSDB , 2000).
    3) Tert-butyl acetate is used as a gasoline additive, and as a solvent in lacquer industries (HSDB , 2000).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Butyl acetate is used as a synthetic-flavoring ingredient in the production of fruit flavorings, as well as in manufactured products (eg, lacquers, nail polish, photographic film). Butyl acetate has a strong fruity taste and a banana-like odor, with an odor threshold in the range of 7 parts per million (ppm) to 20 ppm.
    B) TOXICOLOGY: Butyl acetate has low systemic toxicity. It can be irritating and narcotic in high concentrations. N-butyl acetate is more irritating than sec- or tert-butyl acetate.
    C) EPIDEMIOLOGY: Significant exposure is rare and severe toxicity has not been reported in humans.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Possible symptoms of overexposure may include mucous membrane irritation, headache, drowsiness, dizziness, ataxia, nausea, vomiting, diarrhea, cough, and dryness and irritation of the eyes, upper respiratory system and skin.
    2) SEVERE TOXICITY: Rare severe effects might include confusion, delirium, and coma.
    0.2.20) REPRODUCTIVE
    A) N-butyl acetate is among a group of solvents associated with spontaneous abortion in female workers employed in certain semiconductor manufacturing processes. However, experiments in animals have failed to demonstrate an effect of butyl acetate on reproduction.
    0.2.21) CARCINOGENICITY
    A) N-butyl acetate is considered not classifiable as a human carcinogen.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, liver enzymes and urinalysis is symptomatic patients.
    C) Serum concentrations of butyl acetate are not widely available or useful to guide therapy.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Care is symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) High concentrations of this material may cause CNS depression. Monitor for CNS and respiratory depression.
    C) DECONTAMINATION
    1) GI decontamination is not recommended because of the potential for CNS depression and subsequent aspiration after large ingestions and the lack of toxicity from small exposures. Dilution may ameliorate mild irritant effects. Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eyes.
    D) ANTIDOTE
    1) None
    E) ENHANCED ELIMINATION PROCEDURE
    1) There is no data to support hemodialysis or hemoperfusion.
    F) PITFALLS
    1) Significant toxicity is not expected, avoid over treatment. Consider the contribution of other xenobiotics present in commercial products (often hydrocarbons and solvent) to the potential for toxicity.
    G) DIFFERENTIAL DIAGNOSIS
    1) Exposure to other hydrocarbons or solvents.
    H) TOXICOKINETICS
    1) Absorbed orally, via inhalation and transdermally. Undergo hydrolysis in the liver and small intestine.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with small inadvertent exposures and only mild irritant symptoms can be managed at home.
    2) OBSERVATION CRITERIA: Patients with large or deliberate exposures or more than mild symptoms should be referred to a healthcare facility for evaluation.
    3) ADMISSION CRITERIA: Patients with persistent CNS depression or other symptoms should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patients with severe toxicity or in whom the diagnosis is unclear.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    0.4.4) EYE EXPOSURE
    A) 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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) 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).
    2) The butyl acetates are only mildly irritating and should not cause significant burns.

Range Of Toxicity

    A) In humans, brief exposures to 3300 parts per million (ppm) caused marked irritation to the eyes and nose. Mild irritation was reported after a brief exposure to butyl acetate at concentrations of 1400 ppm for 20 minutes, and up to 700 ppm for 4 hours.
    B) Butyl acetate has a fruity, banana-like odor with an odor threshold of 7 parts per million (ppm) to 20 ppm.
    C) The threshold limit values for an 8 hour work day of these compounds range from 710 to 950 mg/m(3), or 150 to 200 parts per million.
    D) The following concentrations are considered immediately dangerous to life and health: sec-butyl acetate 1700 ppm; tert-butyl acetate 1500 ppm; n-butyl acetate 1700 ppm.

Clinical Effects

Summary Of Exposure

    A) USES: Butyl acetate is used as a synthetic-flavoring ingredient in the production of fruit flavorings, as well as in manufactured products (eg, lacquers, nail polish, photographic film). Butyl acetate has a strong fruity taste and a banana-like odor, with an odor threshold in the range of 7 parts per million (ppm) to 20 ppm.
    B) TOXICOLOGY: Butyl acetate has low systemic toxicity. It can be irritating and narcotic in high concentrations. N-butyl acetate is more irritating than sec- or tert-butyl acetate.
    C) EPIDEMIOLOGY: Significant exposure is rare and severe toxicity has not been reported in humans.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Possible symptoms of overexposure may include mucous membrane irritation, headache, drowsiness, dizziness, ataxia, nausea, vomiting, diarrhea, cough, and dryness and irritation of the eyes, upper respiratory system and skin.
    2) SEVERE TOXICITY: Rare severe effects might include confusion, delirium, and coma.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) HUMAN DATA
    a) Short-term exposure to butyl acetate vapor irritates the eyes (ACGIH, 1996a). Symptoms of overexposure include dry, red, painful eyes (Budavari, 1996; ILO, 1998). Conjunctival irritation has been reported with occupational exposure (ACGIH, 1996a).
    b) In human studies, n-butyl acetate produced only minimal complaints of irritation, and only minimal changes were noted in eye redness, lipid layer thickness, and bronchial responsiveness at concentrations up to 1400 parts per million (ppm) for 20 minutes or 700 ppm for 4 hours (Iregren et al, 1993).
    c) Vapor exposure has been associated with noticeable irritation at a concentration of 300 parts per million (ppm in air, and objectionable irritation at a concentration of 3300 ppm (Nelson et al, 1943; Von Oettingen, 1960; Grant, 1993). Vapor concentrations in excess of 3300 ppm may cause tearing and hyperemia of the conjunctiva (Flury & Zernik, 1931; Grant, 1993).
    2) ANIMAL DATA
    a) Acute inhalation exposure to n-butyl acetate has resulted in irritation of the eyes in rats and cats (Korsak & Rydzynski, 1994; ACGIH, 1996a).
    b) The butyl acetates may cause conjunctivitis (Browning, 1965). Eye irritation was the first symptom reported at the lowest concentration in guinea pig tests occurring at less than 0.33% by volume (Sayers et al, 1936). Concentrations of 1600 parts per million produced eye irritation in cats (Anon, 1980).
    c) Liquid application to rabbit eyes caused superficial injury graded 5 on a scale of 1 to 10 (Grant & Schuman, 1993). A case report described one corneal burn caused by butyl acetate (unknown isomer), which healed within 48 hours (McLaughlin, 1946).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Short-term exposure to butyl acetate vapor irritates the nose (ACGIH, 1996a).
    2) One study showed that workers exposed to greater than 200 parts per million (ppm) for 8 hours developed eye, nose and throat irritation. The odor did not become objectionable until greater than 300 ppm (Silverman et al, 1946). Similarly, eye and nose irritation was reported at 300 ppm, and a sore throat at 200 to 300 ppm (Nelson et al, 1943).
    3) ANIMAL DATA: Irritation of the nose occurred immediately in animals exposed to 0.7% in air by volume (Sayers et al, 1936).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Short-term exposure to butyl acetate vapor irritates the throat, beginning at a concentration of 200 parts per million (ppm), with severe irritation at 300 ppm (ACGIH, 1996a; HSDB , 2002). Pharyngeal irritation has been reported with occupational exposure (ACGIH, 1996a).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) Disturbances in cardiac rhythm and cardiac failure may occur after exposure to butyl acetate (HSDB , 2002).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Inhalation exposure to butyl acetate results in coughing and difficulty breathing, and mild respiratory inflammation (ILO, 1998; HSDB , 2002; ITI, 1995). Dryness of the upper respiratory system is a symptom of overexposure (Budavari, 1996). Acute lung injury (pulmonary edema) has also been reported following exposure to butyl acetate (HSDB , 2002). Butyl acetate-induced death usually results from respiratory failure (Harbison, 1998).
    B) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Ingestion can cause irritation and dryness of the upper respiratory system (Harbison, 1998).
    b) In human studies, n-butyl acetate produced only minimal complaints of irritation, and only minimal changes were noted in eye redness, lipid layer thickness, and bronchial responsiveness at concentrations up to 1400 parts per million (ppm) for 20 minutes or 700 ppm for 4 hours (Iregren et al, 1993).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Upper respiratory tract irritation was reported in rats following acute inhalation exposure to n-butyl acetate (Korsak & Rydzynski, 1994).
    2) ACUTE LUNG INJURY
    a) Acute lung injury (pulmonary edema) was reported in rats exposed to an inhaled dose of 390 parts per million for 4 hours (RTECS , 2000). Moderate pulmonary edema was observed in animals exposed to n-butyl acetate during postmortem examination (Sayers et al, 1936).
    3) EMPHYSEMA
    a) Exposure of cats to an inhaled dose of 68 g/m(3) for 72 months resulted in emphysema (RTECS , 2000).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Butyl acetate is a CNS depressant (HSDB , 2002). Inhalation of butyl acetate results in headache, dizziness, ataxia, confusion, delirium, and coma (Harbison, 1998; ILO, 1998). Following severe exposure, butyl acetate can cause weakness, drowsiness, and unconsciousness (ACGIH, 1996a).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Butyl acetates are narcotic in high concentrations (ILO, 1998; Browning, 1965). Effects occur gradually, and disappear slowly once exposure has ceased (ILO, 1998; Zaleski, 1992). N-butyl acetate has narcotic properties estimated to be 1.7 times those of ethyl acetate (ACGIH, 1996a).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SOMNOLENCE
    a) In animals, 0.7% by volume of n-butyl acetate in air caused incoordination in 420 minutes and narcosis after 700 minutes of exposure. Concentrations of 1.4% caused death in 240 minutes (Sayers et al, 1936). Cats experienced slight narcosis after 6 hours of exposure to 6100 parts per million (Anon, 1980).
    b) CNS depression has been reported in rats following acute inhalation exposure. The authors also observed the additive neurotoxic effects of combined exposure to n-butyl alcohol and n-butyl acetate (both agents have similar chemical structures and biological effects) (Korsak & Rydzynski, 1994).
    2) EDEMA CEREBRAL
    a) Cerebral edema was observed at autopsy in animals exposed to n-butyl acetate (Sayers et al, 1936).
    3) LACK OF EFFECT
    a) CHRONIC TOXICITY
    1) Repeated subchronic (up to 13 weeks) exposure to n-butyl acetate vapors caused initial sedation and hypoactivity, but did not result in cumulative neurotoxicity in Sprague-Dawley rats (David et al, 1998).
    4) CNS DEPRESSION
    a) In neurotoxicity and operant behavior studies, rats exposed to n-butyl acetate by inhalation at up to 3000 parts per million (ppm), 6 hours per day, 65 exposures, over a 14-week period showed only decreased motor activity in males at the highest dose. Neuropathologic examinations were negative (David et al, 1998). In 20-minute acute inhalation toxicity studies, the minimally effective concentration of n-butyl acetate causing activity reduction was 8000 ppm (Bowen & Balster, 1997).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Acute exposure results in anorexia, nausea, vomiting, and diarrhea (ILO, 1998; Harbison, 1998; ITI, 1995).
    B) GASTROINTESTINAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Gastrointestinal hemorrhage has been reported following exposure to butyl acetate (HSDB , 2002).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Liver damage has been reported in humans following exposure to butyl acetate (HSDB , 2000).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Liver edema was found in animals exposed to n-butyl acetate during postmortem examination (Sayers et al, 1936).
    b) Fatty liver degeneration was found in guinea pigs exposed to an intraperitoneal dose of 1500 mg/kg (RTECS , 2000).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) GLYCOSURIA
    1) WITH POISONING/EXPOSURE
    a) Renal damage with glycosuria has been reported in humans following exposure to butyl acetate (HSDB , 2002).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) Repeated exposures to butyl acetate have produced renal changes in animals (Sittig, 1991). Kidney edema has been observed at autopsy in animals exposed to n-butyl acetate (Sayers et al, 1936).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BLOOD DYSCRASIA
    a) Repeated exposures to butyl acetate have produced hematological changes in animals (Sittig, 1991).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Dry, irritated, red skin can result from overexposure to butyl acetate (Budavari, 1996; ILO, 1998).
    B) POISONING
    1) WITH POISONING/EXPOSURE
    a) Systemic absorption can occur following dermal contact at high concentrations, which can result in narcotic effects (Zaleski, 1992; Harbison, 1998).
    C) DRY SKIN
    1) WITH POISONING/EXPOSURE
    a) Drying of the skin has been reported following direct contact (Fassett, 1963). This results in a low magnitude of injury and most cases heal in one day (Clayton & Clayton, 1994).
    D) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Dermatitis may occur following skin exposure (Clayton & Clayton, 1994; ITI, 1995).

Reproductive

    3.20.1) SUMMARY
    A) N-butyl acetate is among a group of solvents associated with spontaneous abortion in female workers employed in certain semiconductor manufacturing processes. However, experiments in animals have failed to demonstrate an effect of butyl acetate on reproduction.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) N-butyl acetate reportedly failed to produce malformations, resorptions or deaths of fetuses in rats or rabbits (ACGIH, 1996a).
    3.20.5) FERTILITY
    A) LACK OF EFFECT
    1) N-butyl acetate reportedly had no adverse effect on fertility in rats or rabbits (ACGIH, 1996a).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS105-46-4 (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):
    1) Not Listed
    B) IARC Carcinogenicity Ratings for CAS540-88-5 (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):
    1) Not Listed
    C) IARC Carcinogenicity Ratings for CAS123-86-4 (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):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) N-butyl acetate is considered not classifiable as a human carcinogen.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) N-butyl acetate is considered not classifiable as a human carcinogen (ACGIH, 1996a).
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) N-butyl acetate is considered not classifiable as a human carcinogen (ACGIH, 1996a).

Genotoxicity

    A) N-butyl acetate was non-mutagenic in the Ames test and did not induce chromosomal aberrations in Chinese hamster fibroblasts. Negative results were obtained for n-butyl acetate for tests of mitotic aneuploidy in Saccharomyces cerevisiae (Zaleski, 1992; ACGIH, 1996a)

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, liver enzymes and urinalysis is symptomatic patients.
    C) Serum concentrations of butyl acetate are not widely available or useful to guide therapy.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) No therapeutic or toxic levels of the butyl acetates have been determined.
    B) Serum concentrations of butyl acetate are not widely available or useful to guide therapy.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Generally, urine is not considered a useful medium for measuring n-butyl acetate in humans (ACGIH, 1996a).
    4.1.4) OTHER
    A) OTHER
    1) Patients should be monitored for CNS depression after exposure to butyl ketones (Harbison, 1998).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with persistent CNS depression or other symptoms should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with small inadvertent exposures and only mild irritant symptoms can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center for patients with severe toxicity or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with large or deliberate exposures or more than mild symptoms should be referred to a healthcare facility for evaluation.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor serum electrolytes, renal function, liver enzymes and urinalysis is symptomatic patients.
    C) Serum concentrations of butyl acetate are not widely available or useful to guide therapy.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Prehospital GI decontamination is not recommended because of the potential for CNS depression and subsequent aspiration after large ingestions and the lack of toxicity from small exposures. Dilution may ameliorate mild irritant effects. Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eyes.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) GI decontamination is not recommended because of the potential for CNS depression and subsequent aspiration after large ingestions and the lack of toxicity from small exposures. Dilution may ameliorate mild irritant effects.
    B) DILUTION
    1) 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 (Caravati, 2004).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY: Care is symptomatic and supportive.
    2) MANAGEMENT OF SEVERE TOXICITY: High concentrations of this material may cause CNS depression. Monitor for CNS and respiratory depression.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor serum electrolytes, renal function, liver enzymes and urinalysis is symptomatic patients.
    3) Serum concentrations of butyl acetate are not widely available or useful to guide therapy.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) CEREBRAL EDEMA
    1) CLINICAL IMPLICATIONS
    a) Cerebral edema and elevated intracranial pressure (ICP) may occur. Emergent management includes head elevation and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.
    2) MONITORING
    a) Patients will usually require endotracheal intubation and mechanical ventilation. Monitor intracranial pressure, cerebral perfusion pressure and cerebral blood flow.
    3) TREATMENT
    a) Most information on the treatment of cerebral edema is derived from studies of traumatic brain injury.
    4) MANNITOL
    a) ADULT/PEDIATRIC DOSE: 0.25 to 1 gram/kilogram intravenously over 10 to 15 minutes (None Listed, 2000).
    b) AVAILABLE FORMS: Mannitol injection (5%, 10%, 15%, 20%, 25%).
    c) MAJOR ADVERSE REACTIONS: Congestive heart failure, hypernatremia, hyponatremia, hyperkalemia, renal failure, pulmonary edema, and allergic reactions.
    d) PRECAUTIONS: Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia. Do not add to whole blood for transfusions; enhanced neuromuscular blockade has occurred with tubocurarine. Keep serum osmolarity below 320 mOsm.
    e) MONITORING PARAMETERS: Renal function, urine output, fluid balance, serum potassium levels, serum osmolarity, and CVP.
    5) HYPERTONIC SALINE
    a) Preliminary studies suggest that hypertonic saline (7.5% saline/6% dextran) 100 ml reduced ICP more effectively than 200 mL of 20% mannitol in adults with elevated ICP after traumatic brain injury(Battison et al, 2005).
    6) ELEVATION
    a) Elevation of the head of the bed to approximately 30 degrees decreases ICP and improves cerebral perfusion pressure (Meixensberger et al, 1997; Schneider et al, 1993; Feldman et al, 1992).
    7) MECHANICAL DECOMPRESSION
    a) Early surgical decompression, ventriculostomy with CSF drainage, or craniectomy may be useful in patients with persistent elevation of ICP (Sahuquillo & Arikan, 2006; Sakai et al, 1998; Polin et al, 1997; Taylor et al, 2001). Most experience with these modalities has been in patients with traumatic brain injury.
    8) HYPERVENTILATION
    a) SUMMARY: Hyperventilation has been associated with adverse outcomes and should not be performed routinely (Muizelaar et al, 1991). It is indicated in patients who have clinical evidence of herniation or if there is intracranial hypertension refractory to sedation, paralysis, CSF drainage and osmotic diuretics (None Listed, 2000a).
    b) RECOMMENDATION:
    1) The PCO2 must be controlled in the range of 25 torr; further lowering of PCO2 may create undesirable effects secondary to local tissue hypoxia.
    2) End-tidal CO2 tension, correlated with an initial ABG measurement, provides a noninvasive means of monitoring PCO2 (Mackersie & Karagianes, 1990).
    3) Most authorities advise that hyperventilation should be considered a temporizing measure only; SUSTAINED hyperventilation should be avoided (Am Acad Neurol, 1997; Bullock et al, 1996; Kirkpatrick, 1997).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Abstracts

Case Reports

    A) ADVERSE EFFECTS
    1) A case report describes a worker with signs and symptoms reported as nervousness, respiratory distress, and cardiovascular system disorders after exposure to polyester lacquer. Recovery followed symptomatic care. Details are not available. It is unknown if this was pure butyl acetate or a combined lacquer-lacquer solvent mixture (Titova & Zakirova, 1977; Clayton & Clayton, 1994a).

Range Of Toxicity

Summary

    A) In humans, brief exposures to 3300 parts per million (ppm) caused marked irritation to the eyes and nose. Mild irritation was reported after a brief exposure to butyl acetate at concentrations of 1400 ppm for 20 minutes, and up to 700 ppm for 4 hours.
    B) Butyl acetate has a fruity, banana-like odor with an odor threshold of 7 parts per million (ppm) to 20 ppm.
    C) The threshold limit values for an 8 hour work day of these compounds range from 710 to 950 mg/m(3), or 150 to 200 parts per million.
    D) The following concentrations are considered immediately dangerous to life and health: sec-butyl acetate 1700 ppm; tert-butyl acetate 1500 ppm; n-butyl acetate 1700 ppm.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) A concentration of 10,000 parts per million of butyl acetate for 8 hours was fatal in all animals tested. However, a 4-hr exposure to the same concentration level resulted in no fatalities (Anon, 1980).
    2) In guinea pigs, inhalation of butyl acetate at a concentration of 14,000 parts per million (ppm) for 4 hours was reported to be lethal. In rats, the lethal concentration was 21,000 ppm for 2.5 hours of inhalation (Zaleski, 1992).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Brief exposures of humans to 3300 parts per million (ppm) caused marked irritation to eyes and nose. Mild irritation was reported after brief exposure to concentrations of 200 to 300 ppm (Clayton & Clayton, 1994).
    2) However, in other studies, workers complained that concentrations of greater than 100 parts per million (ppm) were unpleasant, and that greater than 200 ppm for 3 to 5 minutes irritated the eyes, nose and throat, whereas 300 ppm for 3 to 5 minutes irritated the eyes and nose and caused severe irritation to the throat (Silverman et al, 1946; ACGIH, 1996).
    3) In human studies, n-butyl acetate produced only minimal complaints of irritation, and only minimal changes were noted in eye redness, lipid layer thickness, and bronchial responsiveness at concentrations up to 1400 parts per million (ppm) for 20 minutes or 700 ppm for 4 hours (Iregren et al, 1993).
    4) Butyl acetate has a fruity, banana-like odor with an odor threshold of 7 parts per million (ppm) to 20 ppm (HSDB , 2002).
    5) The following concentrations are considered immediately dangerous to life and health: sec-butyl acetate 1700 ppm; tert-butyl acetate 1500 ppm; n-butyl acetate 1700 ppm (National Institute for Occupational Safety and Health, 2007).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) A concentration of 900 to 1000 parts per million given for 10 repeated 2- to 3-hr periods resulted in minimal effects (Smyth & Smyth, 1928).

Workplace Standards

    A) ACGIH TLV Values for CAS105-46-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Under Study
    1) sec-Butyl acetate
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Adopted Value
    1) sec-Butyl acetate
    a) TLV:
    1) TLV-TWA: 200 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 116.16
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) ACGIH TLV Values for CAS540-88-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Adopted Value
    1) tert-Butyl acetate
    a) TLV:
    1) TLV-TWA: 200 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 116.16
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    C) ACGIH TLV Values for CAS123-86-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Adopted Value
    1) n-Butyl acetate
    a) TLV:
    1) TLV-TWA: 150 ppm
    2) TLV-STEL: 200 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 116.16
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    D) NIOSH REL and IDLH Values for CAS105-46-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: sec-Butyl acetate
    2) REL:
    a) TWA: 200 ppm (950 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1700 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    E) NIOSH REL and IDLH Values for CAS540-88-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: tert-Butyl acetate
    2) REL:
    a) TWA: 200 ppm (950 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1500 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    F) NIOSH REL and IDLH Values for CAS123-86-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: n-Butyl acetate
    2) REL:
    a) TWA: 150 ppm (710 mg/m(3))
    b) STEL: 200 ppm (950 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1700 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    G) Carcinogenicity Ratings for CAS105-46-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: sec-Butyl acetate
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: sec-Butyl acetate
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: sec-Butyl acetate
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    H) Carcinogenicity Ratings for CAS540-88-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: tert-Butyl acetate
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: tert-Butyl acetate
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    I) Carcinogenicity Ratings for CAS123-86-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: n-Butyl acetate
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: n-Butyl acetate
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    J) OSHA PEL Values for CAS105-46-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: sec-Butyl acetate
    2) Table Z-1 for sec-Butyl acetate:
    a) 8-hour TWA:
    1) ppm: 200
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 950
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

    K) OSHA PEL Values for CAS540-88-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: tert-Butyl acetate
    2) Table Z-1 for tert-Butyl acetate:
    a) 8-hour TWA:
    1) ppm: 200
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 950
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

    L) OSHA PEL Values for CAS123-86-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: n-Butyl-acetate
    2) Table Z-1 for n-Butyl-acetate:
    a) 8-hour TWA:
    1) ppm: 150
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 710
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (Zaleski, 1992; Norris et al, 1997 RTECS, 2000 HSDB, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 1.23 g/kg
    2) LD50- (ORAL)MOUSE:
    a) 7.1 g/kg
    b) 6 g/kg
    3) LD50- (ORAL)RAT:
    a) 10.8 g/kg
    b) 14.1 g/kg
    4) TCLo- (INHALATION)HUMAN:
    a) 200 parts per million
    5) TCLo- (INHALATION)RAT:
    a) Female, 1500 parts per million for 7 hr for 7 to 16 days of pregnancy -- REP
    b) 1500 parts per million for 6 hr/13W intermittent
    B) References: (Zaleski, 1992; Norris et al, 1997 RTECS, 2000 HSDB, 2000
    1) LD50- (ORAL)RAT:
    a) 4100 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) These compounds seem to have little physiologic activity. The initial effect is irritation of eyes, nose, throat, and mucous membranes and, in much higher concentration, narcosis (Hathaway et al, 1996).

Physicochemical

Physical Characteristics

    A) All three of the isomers in low concentrations have a strong pleasant fruity (banana-like) odor; in high concentrations, the odor is irritating (Ashford, 1994; ACGIH, 1996a; HSDB , 2000).
    B) All of the isomers are clear colorless liquids (Lewis, 1996; ILO, 1998).

Molecular Weight

    A) 116.18

Other

    A) ODOR THRESHOLD
    1) 10 parts per million (CHRIS , 2002)

References

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