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VINYL ACETATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Vinyl acetate is a clear, flammable liquid used as an industrial chemical in polymerization, copolymerization, or as a chemical intermediate. Vinyl acetate is an important member of the unsaturated acetates. The most likely routes of occupational exposure are inhalation and dermal.

Specific Substances

    1) 1-Acetoxyethylene
    2) Acetic acid, ethenyl ester
    3) Acetic acid, vinyl ester
    4) VAC
    5) Vinyl A monomer
    6) Vinyl acetate
    7) VYAC
    8) CAS 108-05-4
    1.2.1) MOLECULAR FORMULA
    1) C4-H6-O2

Available Forms Sources

    A) FORMS
    1) Polyvinyl acetate is a clear, mobile, flammable liquid, which polymerizes in light to a colorless, transparent mass (Hurtt et al, 1995; Budavari, 1996; Lewis, 1996).
    B) SOURCES
    1) Vinyl acetate is manufactured by a reaction between ethylene and sodium acetate (Clayton & Clayton, 1994).
    C) USES
    1) Vinyl acetate is used as an industrial solvent in polymerization (Hurtt et al, 1995; Budavari, 1996). It is used in polymerized form for plastic masses, films, and lacquers (Budavari, 1996). Polymerization occurs readily to form inert polyesters, which are widely used as plastic copolymers (Clayton & Clayton, 1994).
    2) Vinyl acetate is used in polyvinyl acetate, polyvinyl alcohol, polyvinyl butyral, and polyvinyl chloride-acetate resins. It is also used in latex paints, paper coating, adhesives, textile finishing, and safety glass interlayers. A vinyl acetate-ethylene copolymer is available for specialty products (Lewis, 1993).
    a) ADHESIVES: A common use of polyvinyl acetate copolymer resins is in the production of white glues for the furniture industry. They may also be a component of spackling paste, an additive to cement mortar, concrete, or plaster, and in the assembly of cigarette filters (IARC, 1986).
    b) PAINTS: Polyvinyl acetate copolymer emulsions are a common component of latex house paints, particularly exterior paints (IARC, 1986).
    c) TEXTILES: Copolymers or emulsions are used in sizing, starch substitutes, binders in nonwoven fabrics, and nylon hosiery (IARC, 1986).
    d) PAPER: Emulsions may be binders in paper coatings (IARC, 1986).
    e) OTHER: Polyvinyl acetate copolymer is used as a chewing gum base. It is also found in hairsprays (Ellenhorn & Barceloux, 1988).
    3) Polymers contain residual amounts of vinyl acetate monomer, up to 5 g/kg (IARC, 1986).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Vinyl acetate is moderately toxic by the ingestion, inhalation, and intraperitoneal routes of exposure. It is irritating to the eyes, skin, mucous membranes, and respiratory tract. Prolonged dermal contact (clothing wet with vinyl acetate) may result in severe irritation or blistering of the skin.
    B) In a study of 21 workers exposed for an average of 15 years at concentrations between 5 and 10 ppm (with occasional excursions above 300 ppm), it produced no serious chronic effects.
    1) Chronic occupational exposure has been reported to cause CNS symptoms, chronic bronchitis, cardiovascular symptoms, liver function changes, and hepatic enzyme induction.
    C) Vinyl acetate is a questionable carcinogen with experimental carcinogenic and tumorigenic data. It causes experimental reproductive effects. Human mutation data have been reported.
    D) Populations at special risk include those with chronic irritation of the respiratory tract, chronic inflammatory conditions of the skin, and those with chronic eye irritation.
    E) Routes of human exposure primarily include occupational exposure via inhalation of the vapor and contact of the liquid or vapor with the skin and eyes.
    F) The general population may be exposed through inhalation of contaminated air in the vicinity of its commercial production and use and in the vicinity of waste disposal sites containing the compound. Dermal contact from residual monomer remaining in polyvinyl acetate products may be possible.
    1) Although never demonstrated experimentally, residual monomer (in polyvinyl acetate containers used to store food products) may leach into food products and result in ingestion. Vinyl acetate exhibits relatively low toxicity as a monomer, and more toxicity as a polymer. Primary human exposure, however, most likely results through inhalation at occupational sites.
    0.2.4) HEENT
    A) Eye and mucous membrane irritation and reversible corneal injury may occur. Olfactory fatigue develops with continued exposure.
    0.2.5) CARDIOVASCULAR
    A) Cardiac effects are not well documented. Chronic exposure has resulted in dysrhythmias, chest pain, and syncope.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation (cough, hoarseness) has been reported after exposure to 22 ppm. Chronic bronchitis and impaired ventilatory function have been associated with industrial exposure.
    0.2.7) NEUROLOGIC
    A) Chronic exposure is reported to cause fatigue, irritability, insomnia, encephalopathy, vertigo, weakness, and polyneuritis.
    0.2.9) HEPATIC
    A) Liver function changes and hepatic enzyme induction may occur after chronic exposure.
    0.2.14) DERMATOLOGIC
    A) Severe skin irritation with blister formation may occur.
    0.2.20) REPRODUCTIVE
    A) No human epidemiologic data could be found evaluating prenatal or reproductive toxicity. At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
    B) In animal studies, fertility was affected by exposure to vinyl acetate, and toxic effects on the male fertility index and sperm morphology were reported.
    0.2.21) CARCINOGENICITY
    A) Inadequate evidence exists to evaluate carcinogenicity of vinyl acetate in humans. Some evidence of carcinogenicity exists in animals.

Laboratory Monitoring

    A) An EKG, chest x-ray, and liver function tests should be obtained periodically in exposed workers, and following significant acute exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) EMESIS - Is NOT recommended due to irritant effects of vinyl acetate.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) 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.
    E) Monitor for CNS depression, respiratory irritation, cardiac dysrhythmias, and liver function changes. There is no specific treatment other than supportive care.
    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).

Range Of Toxicity

    A) Inhalation exposure to 20 ppm or greater may produce symptoms of irritation.

Clinical Effects

Summary Of Exposure

    A) Vinyl acetate is moderately toxic by the ingestion, inhalation, and intraperitoneal routes of exposure. It is irritating to the eyes, skin, mucous membranes, and respiratory tract. Prolonged dermal contact (clothing wet with vinyl acetate) may result in severe irritation or blistering of the skin.
    B) In a study of 21 workers exposed for an average of 15 years at concentrations between 5 and 10 ppm (with occasional excursions above 300 ppm), it produced no serious chronic effects.
    1) Chronic occupational exposure has been reported to cause CNS symptoms, chronic bronchitis, cardiovascular symptoms, liver function changes, and hepatic enzyme induction.
    C) Vinyl acetate is a questionable carcinogen with experimental carcinogenic and tumorigenic data. It causes experimental reproductive effects. Human mutation data have been reported.
    D) Populations at special risk include those with chronic irritation of the respiratory tract, chronic inflammatory conditions of the skin, and those with chronic eye irritation.
    E) Routes of human exposure primarily include occupational exposure via inhalation of the vapor and contact of the liquid or vapor with the skin and eyes.
    F) The general population may be exposed through inhalation of contaminated air in the vicinity of its commercial production and use and in the vicinity of waste disposal sites containing the compound. Dermal contact from residual monomer remaining in polyvinyl acetate products may be possible.
    1) Although never demonstrated experimentally, residual monomer (in polyvinyl acetate containers used to store food products) may leach into food products and result in ingestion. Vinyl acetate exhibits relatively low toxicity as a monomer, and more toxicity as a polymer. Primary human exposure, however, most likely results through inhalation at occupational sites.

Heent

    3.4.1) SUMMARY
    A) Eye and mucous membrane irritation and reversible corneal injury may occur. Olfactory fatigue develops with continued exposure.
    3.4.3) EYES
    A) CORNEAL INJURY has been described, with recovery within 48 hours (McLaughlin, 1946; Grant & Schuman, 1993).
    B) Eye irritation was noted in the human using the Standard Draize test (RTECS , 2000).
    3.4.5) NOSE
    A) Normal volunteers reported olfactory fatigue after 0.5 to 4 hours exposure to air concentrations ranging from 19.5 to 71.5 parts per million (NIOSH , 1996). The olfactory fatigue cleared within a few minutes of termination of each exposure (NIOSH , 1996).
    B) RATS - In a study of inhalation exposure in rats, atrophy of the olfactory epithelium with replacement with different cell types was observed; focal leukocyte exudate and hyperplasia were noted in the nasal cavity of mice (Clary, 1988).
    3.4.6) THROAT
    A) IRRITATION of mucous membranes can occur at ambient concentrations as low as 20 ppm (NIOSH , 1996).

Cardiovascular

    3.5.1) SUMMARY
    A) Cardiac effects are not well documented. Chronic exposure has resulted in dysrhythmias, chest pain, and syncope.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) Chronic exposure was reported to produce gradual deterioration of heart muscle, with symptoms of abnormal heart beat, chest pain, and syncope (EPA, 1985). These effects are not well documented.

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation (cough, hoarseness) has been reported after exposure to 22 ppm. Chronic bronchitis and impaired ventilatory function have been associated with industrial exposure.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Slight respiratory tract irritation (cough, hoarseness) has resulted from exposure to 22 ppm, with no evidence of irritation from chronic exposure to levels of 5 to 10 ppm (Deese & Joyner, 1969).
    2) When vinyl acetate is heated to decomposition, it emits acrid fumes (EPA, 1985).
    B) BRONCHITIS
    1) Symptoms of chronic bronchitis, with impaired ventilatory function, were reported in workers exposed to up to 40 ppm; however, other chemicals were also present in the workplace (Amatouni & Aharonian, 1980; Aharonian & Amatouni, 1982).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) EMPHYSEMA
    a) Experimental inhalation exposure in rats and/or mice has produced epithelial hyperplasia and concentration-dependent emphysema and atelectasis (Clary, 1988; HSDB , 2000).
    2) RESPIRATORY DISORDER
    a) At 200 and 600 ppm, epithelial hyperplasia of the trachea was noted in mice. In the lungs of both mice and rats, foamy histocytes, epithelial exfoliation, and fibroepithelial tags were noted at 600 ppm; in mice, epithelial hyperplasia was noted at 600 ppm and fibroepithelial tags at 200 ppm (Clary, 1988).

Neurologic

    3.7.1) SUMMARY
    A) Chronic exposure is reported to cause fatigue, irritability, insomnia, encephalopathy, vertigo, weakness, and polyneuritis.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) At high acute concentrations, vinyl acetate is reported to have a narcotic-like effect (Clayton & Clayton, 1994).
    2) Chronic exposure is reported to result in fatigue, irritability, insomnia, encephalopathy, vertigo, weakness, and polyneuritis (Finkel, 1983) IARC, 1985).

Hepatic

    3.9.1) SUMMARY
    A) Liver function changes and hepatic enzyme induction may occur after chronic exposure.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) Liver function changes were noted in the majority (unspecified) of 558 workers in a polyvinyl acetate production plant (Nargizyan et al, 1978).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ENZYME ABNORMALITY
    a) RATS - A dose dependent increase in hepatic cytochrome P-450 occurred in rats exposed to 2.9 to 143 ppm for 6 months (IARC, 1986).

Dermatologic

    3.14.1) SUMMARY
    A) Severe skin irritation with blister formation may occur.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Vinyl acetate has a defatting action and exposures have resulted in severe skin irritation with formation of blisters following industrial exposure (ACGIH, 1986; Clayton & Clayton, 1994; HSDB , 2000).
    B) DERMATITIS
    1) Occupational dermatosis was diagnosed in 28.9% (n=22) of workers in a plant producing binders for glues and paints which were based on vinyl acetate and/or acrylates. Irritant and allergic contact dermatitis was shown in 11.8% (n=9) and 17.1% (n=13) of the workers, respectively. Dermatitis was limited to the hands in most of the workers (Gruvberger et al, 1998).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RASH
    a) RABBITS - Skin irritation was observed using the Open Draize Test in rabbits (RTECS , 1991).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) THYROID CARCINOMA
    a) RATS given vinyl acetate in drinking water for 2 years developed adenoma or carcinoma of the thyroid (Lijinsky & Reuber, 1983).

Reproductive

    3.20.1) SUMMARY
    A) No human epidemiologic data could be found evaluating prenatal or reproductive toxicity. At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
    B) In animal studies, fertility was affected by exposure to vinyl acetate, and toxic effects on the male fertility index and sperm morphology were reported.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) Human epidemiologic data evaluating prenatal or reproductive toxicity is lacking. Abnormal pregnancies have been reported following exposures to chemical pollutants present in the workplace during the production of acetylene and vinyl acetate (HSDB , 2000).
    B) ANIMAL STUDIES
    1) No significant differences between rats exposed to vinyl acetate in drinking water and controls were observed in macroscopic fetal changes, mean litter weight and fetal weight, external/visceral and skeletal defects, and crown rump length (HSDB , 2000).
    2) Mated female rats received high-dose oral vinyl acetate on gestation days 6 to 15. A significant difference was observed between treated animals and controls in the following: decreased mean litter and fetal weights and crown rump length and increased minor skeletal fetal defects/variants. There were no significant differences in external/visceral fetal defects (HSDB , 2000).
    3) Mated female rats, exposed to vapor containing 1000 ppm vinyl acetate between days 6-15 of gestation, had fetuses with decreased mean fetal weight and crown-rump length and an increased incidence of minor skeletal alterations, with ossification as the main skeletal alteration. This dose was also associated with maternal toxicity (marked reduction in weight gain). Dams and their offspring, exposed to as much as 5000 ppm in drinking water, did not have these effects (Hurtt et al, 1995).
    4) It induced minor skeletal defects and lower birth weights in fetal rats exposed to levels up to 1000 ppm in the drinking water on days 6 to 15 of gestation (Anon, 1983). Maternal toxicity occurred at 1000 ppm by inhalation exposure or with 5000 ppm in the drinking water (Proctor et al, 1988).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Pregnant rats were exposed to levels as high as 1000 ppm by inhalation or 5000 ppm in water on days 6 to 15 of gestation; significantly reduced weight gain was noted during exposure (Proctor et al, 1988).
    2) Pregnant rats were exposed to vinyl acetate in their drinking water; no significant difference was noted between exposed animals and controls in maternal mortality, body weight, body weight gain, food intake, mean pregnancy rates, numbers of corpora lutea/dam, fetal sex ratio, and pre- or post-implantation mortality (HSDB , 2000).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) HUMANS
    1) LACK OF INFORMATION
    a) At the time of this review, no data were available to assess the potential effects of exposure to this agent during lactation.
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) TESTIS DISORDER
    a) Experimental studies in rats and mice have shown effects on male fertility index, changes in sperm morphology, decreased sperm production, and reduced testicular weight (RTECS , 2000; Lahdetie, 1988).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS108-05-4 (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) IARC Classification
    a) Listed as: Vinyl acetate
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) Inadequate evidence exists to evaluate carcinogenicity of vinyl acetate in humans. Some evidence of carcinogenicity exists in animals.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) Exposure to vinyl acetate was not associated with excess risk of lung cancer incidence in one occupational study (Waxweiler et al, 1981).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) In the rat, vinyl acetate was found to be carcinogenic by RTECS criteria with thyroid tumors and uterine tumors in one study. It was found to be an equivocal tumorigenic agent by RTECS criteria with sense organ tumors in another study.
    a) In the mouse, vinyl acetate was termed an equivocal tumorigenic agent by RTECS criteria with lung, thorax, or respiratory tumors in one study (RTECS , 2000).
    2) In mice and rats, vinyl acetate was carcinogenic by inhalation, but not when administered in the drinking water (Bogdanffy et al, 1994a) 1994b).
    3) Rats given vinyl acetate at 2500 mg/L in the drinking water for two years developed adenomas or carcinomas of the thyroid gland and also adenomas of the uterus (Lijinsky & Reuber, 1983; Lijinsky, 1988). Vinyl acetate was an equivocal tumorigenic agent in the mouse for induction of tumors of the lung, thorax, and respiratory tract (RTECS , 2000). Rats exposed to 600 ppm developed squamous cell carcinomas of the nasal cavities and larynx (Clary, 1988). In another study, none of the rats exposed to 2500 ppm for 52 weeks developed specific toxic effects or tumors; there was increased mortality in the exposed rats (Proctor et al, 1988).
    4) Vinyl acetate induced tumors of the nasal cavity in rats and mice exposed by inhalation to concentrations up to 600 ppm for 104 weeks (Bogdanffy et al, 1994a). Vinyl acetate was not carcinogenic in rats or mice when administered in the drinking water at levels up to 5000 ppm from the time of gestation through 104 weeks of age (Bogdanffy et al, 1994b).
    5) Exposure to vinyl acetate vapor has induced tumors of the nasal cavity in rats, but not mice. This may be partially explained by the ability of nasal tissue to metabolize vinyl acetate to form acetaldehyde, a known carcinogen, via the action of the enzyme carboxylesterase (Bogdanffy & Taylor, 1993).

Genotoxicity

    A) Vinyl acetate induced DNA cross-links in human leukocytes (Lambert et al, 1985). Chromosomal aberrations have been observed in animal studies (RTECS , 2000). The genotoxic effects of vinyl acetate are thought to be due to its acetaldehyde metabolite (Norppa et al, 1985). At the time of this review, no data were available to assess the mutagenic potential of this agent in humans.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) An EKG, chest x-ray, and liver function tests should be obtained periodically in exposed workers, and following significant acute exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Liver function tests should be monitored periodically in workers and following significant acute exposure.
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) An EKG should be obtained periodically in exposed workers and following significant acute exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) A chest x-ray should be obtained in patients with respiratory symptoms. A chest x-ray and pulmonary function tests should be performed periodically on exposed workers.

Methods

    A) CHROMATOGRAPHY
    1) Vinyl acetate may be assayed in air using gas chromatography/flame ionization detection or gas chromatography/mass spectrometry. The limit of detection using the NIOSH method is 0.3 mg/m(3) (adsorb on Chromosorb 107; desorb into a sample reservoir; inject aliquot onto GC).
    a) Another method, which requires a lower sample volume, uses Ambersorb XE-347 as absorbent, solvent extraction, and analysis by capillary gas chromatography. Samples collected at a high relative humidity (>50%) had to be stored in a freezer for 12 days to achieve an acceptable recovery rate, however (Andersson & Andersson, 1990).
    2) Analysis of vinyl acetate in water can be performed using gas chromatography/mass spectrometry (IARC, 1985).
    B) OTHER
    1) A colorimetric method to determine vinyl acetate in air has been described (Suwalska & Lipinska, 1984).
    2) At the time of this review, no data were available regarding the determination of vinyl acetate in human and biological samples.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) An EKG, chest x-ray, and liver function tests should be obtained periodically in exposed workers, and following significant acute exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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).
    B) EMESIS/NOT RECOMMENDED -
    1) Emesis is not recommended due to the irritant effects of vinyl acetate.
    C) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) 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).
    1) 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.
    2) 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).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) 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).
    B) EMESIS/NOT RECOMMENDED
    1) Emesis is not recommended due to the irritant effects of vinyl acetate.
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    D) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) There is no specific treatment other than supportive care. Monitor for CNS depression, respiratory irritation, cardiac arrhythmias, and liver function changes.
    B) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    C) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

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.
    6.7.2) TREATMENT
    A) SUPPORT
    1) There is no specific treatment other than supportive care. Monitor for CNS depression, respiratory irritation, cardiac arrhythmias, and liver function changes.
    B) IRRITATION SYMPTOM
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.8.2) TREATMENT
    A) SUPPORT
    1) There is no specific treatment other than supportive care. Monitor for CNS depression, respiratory irritation, cardiac arrhythmias, and liver function changes.
    2) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.9.2) TREATMENT
    A) SUPPORT
    1) There is no specific treatment other than supportive care. Monitor for CNS depression, respiratory irritation, cardiac arrhythmias, and liver function changes.
    B) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    C) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Inhalation exposure to 20 ppm or greater may produce symptoms of irritation.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) OCCUPATIONAL
    1) Industrial workplace concentrations of 5 to 10 ppm are well tolerated. Signs of mucous membrane irritation are evident at around 20 ppm (Deese & Joyner, 1969).
    B) ANIMAL DATA
    1) The No Observed Effect Level (NOEL) in rats is 200 ppm on inhalation. Administration in drinking water at 5,000 ppm gave no evidence of toxicity (ECIETC, 1991).
    2) Dogs exposed 6 hours daily for several weeks starting at 91 ppm and ending after 11 weeks at 186 ppm exhibited eye irritation and lacrimation (Hathaway et al, 1991).
    3) Rats exposed repeatedly to 100 ppm showed no effects (Hathaway et al, 1991).

Workplace Standards

    A) ACGIH TLV Values for CAS108-05-4 (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) Vinyl acetate
    a) TLV:
    1) TLV-TWA: 10 ppm
    2) TLV-STEL: 15 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Not Listed
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    c) TLV Basis - Critical Effect(s): URT, eye, and skin irr; CNS impair
    d) Molecular Weight: 86.09
    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) Under Study
    1) Vinyl 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) NIOSH REL and IDLH Values for CAS108-05-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Vinyl acetate
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 4 ppm (15 mg/m(3)) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS108-05-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Vinyl acetate
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Vinyl acetate
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Vinyl acetate
    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): 2B ; Listed as: Vinyl acetate
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Vinyl acetate
    6) MAK (DFG, 2002): Category 3A ; Listed as: Vinyl Acetate
    a) Category 3A : Substances for which the criteria for classification in Category 4 or 5 are fulfilled but for which the database is insufficient for the establishment of a MAK value.
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS108-05-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000 Lewis, 1996 Note: All values are from RTECS 2000, unless otherwise noted.
    1) LD50- (ORAL)MOUSE:
    a) 1613 mg/kg
    2) LD50- (ORAL)RAT:
    a) 2920 mg/kg
    3) TCLo- (INHALATION)RAT:
    a) 600 ppm for 6H/5D/2Y -- I, ETA (Lewis, 1996)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Poisoning may occur from inhalation, dermal, and oral exposure. When vinyl acetate is heated to decomposition, it emits acrid fumes (EPA, 1985).
    B) Vinyl acetate may act as a substrate for glutathione transferase, thus disturbing glutathione metabolism (HSDB , 2000).

Physicochemical

Physical Characteristics

    A) Vinyl acetate is a colorless, mobile liquid which polymerizes to solid on exposure to light (Lewis, 1996). It has a pleasant and sweet characteristic fruity odor (HSDB , 2000).
    B) It polymerizes in light to a colorless, transparent mass (Budavari, 1996). It may polymerize violently. The vapor forms explosive mixtures with air (HSDB , 2000).
    C) The liquid is usually stabilized with either hydroquinone or diphenylamine inhibitors (Lewis, 1993).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 86.09 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) 0.12 ppm (CHRIS , 2002)

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