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VINYL ACETATE

CASRN: 108-05-4 

Human Health Effects:

Evidence for Carcinogenicity:

Evaluation: There is inadequate evidence in humans for the carcinogenicity of vinyl acetate. 

There is limited evidence in experimental animals for the carcinogenicity of vinyl acetate. 

Overall evaluation: Vinyl acetate is possibly carcinogenic to humans (Group 2B). In making the 

overall evaluation, the working group took into account the following evidence: (1) Vinyl 

acetate is rapidly transformed into acetaldehyde in human blood and animal tissues. (2) There is 

sufficient evidence in experimental animals for the carcinogenicity of acetaldehyde. Both vinyl 

acetate and acetaldehyde induce nasal cancer in rats after administration by inhalation. (3) Vinyl 

acetate and acetaldehyde are genotoxic in human cells in vitro and on animals in vivo. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. 63 459 (1995)] **PEER REVIEWED** 

A3; Confirmed animal carcinogen with unknown relevance to humans. 

[American Conference of Governmental Industrial Hygienists TLVs and BEIs. 

Threshold Limit Values for Chemical Substances and Physical Agents and 

Biological Exposure Indices. Cincinnati, OH, 2008, p. 59] **PEER REVIEWED** 

Human Toxicity Excerpts:

/HUMAN EXPOSURE STUDIES/ To provide validation data for the application of the PBPK 

model ... in humans, controlled human exposures to inhaled vinyl acetate were conducted. Air 

was sampled by a probe inserted into the nasopharyngeal cavity of five volunteers (two women, 

three men). Volunteers were instructed to inhale and exhale through the nose. Sampling was 

carried out during exposure to labeled 13C1, 13C2-vinyl acetate during resting and light 

exercise at three exposure levels (1, 5 and 10 ppm nominally). Both, labeled vinyl acetate and 

the major metabolite acetaldehyde from the nasopharyngeal region were sampled at a calibrated 

flow rate of 12 L/hr and analyzed in real time utilizing ion trap mass spectrometry (MS/MS). 

Measurements were taken every 0.8 sec in an exposure period of 2 to 5 min resulting in data 

during all phases of the breathing. The rate of sampling was rapid enough to capture much of the 

behavior of vinyl acetate in the human nasal cavity including inhalation and exhalation. 

However, the sampling was not frequent enough to accurately capture the peak concentration in 

every breath ... 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/SIGNS AND SYMPTOMS/ Factory workers exposed to vinyl acetate showed gradual 

deterioration of heart muscles, arrhythmias, amplitude decrease in electrocardiogram, and 

recognized myocardium dystrophies, fainting spells, pain around the heart area, and a sensation 

of dying. 
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[AGARONYAN ZP, AMATUNI VA; KROVOOBRASHCHENIE 13 (4): 31-6 (1980)] **PEER 

REVIEWED** 

/SIGNS AND SYMPTOMS/ Industrial experience has revealed severe irritation of skin with 

blister formation. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the Threshold Limit Values and Biological Exposure Indices. 5th ed. 

Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 

1986., p. 621] **PEER REVIEWED** 

/CASE REPORTS/ One case of burn of a human cornea has been listed as returned to normal in 

less than forty-eight hours. 

[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. 

Thomas Publisher, 1986., p. 978] **PEER REVIEWED** 

/EPIDEMIOLOGY STUDIES/ A nested case-control study was undertaken in a cohort of 29139 

men employed in two chemical manufacturing facilities and a research and development center, 

who had died in 1940-1978 with non-Hodgkin`s lymphoma, multiple myeloma, lymphocytic or 

nonlymphocytic leukemia. Exposure odds ratios (OR) were examined in relation to 111 work 

areas, 21 specific chemicals (OR based on an ever/never basis), and 52 chemical activity groups. 

Exposure to vinyl acetate was associated with non-Hodgkin's lymphoma in seven of 52 men 

(OR 1.2), multiple myeloma in three of 20 men (OR 1.6), non-lymphocytic leukemia in two of 

39 men (OR 0.5), and with lymphocytic leukemia in two of 18 men (OR 1.8). Examination of 

OR related to the exposure duration was not done because of the OR /less than/ 1.3 or number of 

cases /less than/ 4. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/EPIDEMIOLOGY STUDIES/ A cross-sectional epidemiologic study of vinyl acetate operators 

in a chemical plant revealed that the workers were exposed to an average concentration of 5 to 

10 ppm vinyl acetate with potential acute exposures at 300 ppm. Irritation of the eyes and throat 

was reported by those employees exposed at 21 ppm, but no complaints of eye irritation were 

recorded when exposures were maintained below 10 ppm. The authors concluded that 

concentrations up to 10 ppm were unlikely to produce respiratory or ocular irritation in most 

workers; however, concentrations above 20 ppm appeared to produce irritation in the majority of 

the exposed workers. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/EPIDEMIOLOGY STUDIES/ /Researchers/ undertook a cohort study of 4806 men employed at 

a plant for the manufacture of synthetic chemicals in the United States between 1942 and 1973. 

Death certificates could not be found for 16 (3%) of the deceased. In comparison with national 

rates, the cohort had an excess risk for cancer of the respiratory system (42 observed; 

standardized mortality ratio, 1.5 [95% confidence interval, 1.1-2.0]). In a review of medical 

records, 45 men were found to have had lung cancer. Histological specimens were found for 27 

of these men, and eight showed undifferentiated large-cell lung cancer. The exposure of the 

patients with lung cancer to 19 chemicals, including vinyl acetate, was examined. The group had 
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an estimated cumulative dose of exposure to vinyl acetate below the estimated weighted mean 

expected for the members of the cohort with the same year of birth and age at commencement of 

work in the plant. The subgroup with undifferentiated large-cell lung cancer had had slightly 

higher cumulative exposure to vinyl acetate. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V63 450 (1995)] **PEER REVIEWED** 

/EPIDEMIOLOGY STUDIES/ A Texas (USA) petrochemical plant had elevated standardized 

mortality ratios for neoplasms of the brain. A case-control study examined possible associations 

between gliomas of the brain and job title, departmental employment history, chemical exposure 

history, geographic location within plant, dates of employment and residence. The greatest 

apparent risks were associated: with exposure to carbon dioxide, diethyl sulfate, diethylene 

glycol, ethanol, ethylene, isopropanol, methane, tetraethylene glycol, and vinyl acetate; with 

first employment in the 1940s or early 1950s; and with residence in La Marque, Texas. No 

significant differences between cases and controls were apparent in duration of exposure to any 

of these chemicals. 

[Leffingwell SS et al; Neuroepidemiology 2 (3-4): 179-95 (1984)] **PEER 

REVIEWED** 

/SURVEILLANCE/ In a vinyl resin plant 456 workers (313 men and 143 women) were 

examined for the presence of chronic nonspecific diseases of the respiratory tract (CNDRT). The 

% of chronic bronchitis was higher in vinyl chloride and vinyl acetate department. 

[JEDRYCHOWSKI W ET AL; PRZEGL LEK 36 (9): 679-82 (1979)] **PEER REVIEWED** 

PubMed Abstract

/SURVEILLANCE/ Abnormal pregnancies were related to chemical pollutants present in 

working atmosphere in the production of acetylene and vinyl acetate. 

[TALAKINA EI ET AL; GIG TR PROF ZABOL (3): 46-7 (1977)] **PEER REVIEWED** 

/GENOTOXICITY/ None of the treatments affected the number of micronuclei in 

normochromatic erythrocytes. In human whole-blood lymphocyte cultures, micronucleus 

induction by a 48-hr treatment with vinyl acetate (0.125, 0.25, 0.5, 1 and 2 mM; 24 hr after 

culture initiation) was studied in lymphocytes with preserved cytoplasm from smear slides 

prepared by a method involving the removal of erythrocytes at harvest by sodium cyanide 

treatment to improve preparation quality. The frequency of micronucleated lymphocytes reached 

a peak at 0.5 mM (3.2 +/- 1.0% vs. 0.9 +/- 0.1% in control cultures) and 1 mM (3.1 +/- 0.7%), 

with a decline at 2 mM probably because of a toxic effect resulting in mitotic inhibition. 

[Maki-Paakkanen J, Norppa H; Mutat Res 190 (1): 41-5 (1987)] **PEER 

REVIEWED** PubMed Abstract

/GENOTOXICITY/ ...Vinyl acetate /was/ tested for ... ability to induce chromosome aberrations 

in cultured human lymphocytes. The effects of a 24-hr treatment (48 hr after culture initiation) 

were studied both in whole-blood cultures (with 2 X 10+8 erythrocytes/mL) and in isolated 

lymphocytes (with 4000 erythrocytes/mL). ... Vinyl acetate (0.125-2 mM) ... induced a distinct 

dose-dependent increase in chromatid-type aberrations and a slight elevation in chromosometype breaks in both culture types. The lowest concentration giving a positive result was 0.25 mM. 
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The clastogenic effects of vinyl acetate were somewhat more pronounced in isolated 

lymphocytes than in whole blood. Vinyl acetate is known to be rapidly hydrolyzed in vitro to 

acetaldehyde, which probably explains the positive result. 

[Jantunen K et al; Mutat Res 159 (1-2): 109-16 (1986)] **PEER REVIEWED** 

PubMed Abstract

/GENOTOXICITY/ Human leukocytes were incubated in the presence of vinyl acetate ... (10-20 

mM) for 4 hr at 37 degrees C in vitro. DNA damage was analyzed by alkaline elution. /Vinyl 

acetate did not induce/ a detectable increase in the frequency of DNA strand breaks.

[Lambert B et al; Mutat Res 146 (3): 301-3 (1985)] **PEER REVIEWED** PubMed 

Abstract

/GENOTOXICITY/ A 48-hr treatment with vinyl acetate (0.05-1 mM) induced a drastic 

increase in sister chromatid exchanges (SCEs) and (in first division cells) structural chromosome 

aberrations in cultured human lymphocytes. The effects were more pronounced in cultures of 

isolated lymphocytes than in whole-blood cultures. 

[Norppa H et al; Cancer Res 45 (10): 4816-21 (1985)] **PEER REVIEWED** PubMed 

Abstract

/GENOTOXICITY/ The frequency of sister chromatid exchange (SCE) was studied in cultures 

of human lymphocytes exposed to vinyl acetate or acetaldehyde for various time periods and in 

different phases of the cell cycle. Equimolar concn (0.1-2.4 mM) of vinyl acetate and 

acetaldehyde induced very similar, dose-dependent increases of sister-chromatid exchange. The 

sister-chromatid exchange frequency in cells treated with vinyl acetate increased linearly with 

exposure times up to 24 hr. Cells exposed to vinyl acetate or acetaldehyde in the late G1-phase 

of the cell cycle showed a two-fold higher sister-chromatid exchange frequency than cells 

exposed in early G1. Cultures treated with vinyl acetate in the first G1-phase showed a 

significant increase of sister-chromatid exchange during 3 subsequent cell cycles. Thus, (1) 

acetaldehyde is likely to be responsible for the sister-chromatid exchange induction /noted/ in 

vinyl acetate treated cells, (2) the sister-chromatid exchange inducing activity of acetaldehyde 

persists for several cell cycles in vitro, and (3) removal of sister-chromatid exchange inducing 

acetaldehyde damage occurs during G1. Taken together, the data suggest that acetaldehyde has 

slow turn-over in human lymphocytes in vitro, and may accumulate in the cells, possibly by 

forming reversible Schiff bases, and when release gives rise to sister-chromatid exchange 

inducing DNA cross-links. 

[He SM, Lambert B; Mutat Res 158 (3): 201-8 (1985)] **PEER REVIEWED** PubMed 

Abstract

/OTHER TOXICITY INFORMATION/ CHANGES IN VITAL FUNCTION CAPACITY & 

MAX VENTILATION CAPACITY WERE FOUND IN PERSONS EMPLOYED IN 

PRODUCTION OF VINYL ACETATE. DISTURBANCES OF PULMONARY FUNCTIONS 

DEPEND ON THE INTENSITY & DURATION OF THE EFFECT OF THE CHEM CMPD. 

[AMATUNI VG, AGARONYAN ZP; ZH EKSP KLIN MED 19 (4): 72-8 (1979)] **PEER 

REVIEWED** 

Skin, Eye and Respiratory Irritations:

Vinyl acetate vapor at concn below 250 mg/cu m is a primary irritant to the upper respiratory 
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tract & eyes & the liquid may irritate the skin ... . 

[Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 

2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 917] **PEER 

REVIEWED** 

Moderate health hazard. May be harmful if inhaled. Irritating to skin, eyes and respiratory 

system. 

[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 

Fire Protection Association, 2002., p. 49-125] **PEER REVIEWED** 

Medical Surveillance:

Placement examinations shall include at least: Comprehensive medical and work histories, with 

special emphasis directed to evidence of any existing eye, respiratory, or skin disorder; Physical 

examination giving particular attention to the upper respiratory tract, eyes, and skin; A judgment 

of the employee's ability to use positive pressure air-supplied respirators. 

[NIOSH; Criteria Document: Vinyl Acetate p.2 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Periodic examinations shall be made available at least annually, except as otherwise determined 

by the responsible physician, and shall include: Interim medical and work histories and a 

physical examination. 

[NIOSH; Criteria Document: Vinyl Acetate p.2 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Pertinent medical records for all employees subject to exposure to vinyl acetate in the workplace 

shall be retained for at least 30 years after termination of employment. Records of environmental 

exposures applicable to an employee shall be included in that employee's medical records. These 

records shall be made available to the designated medical representatives of the Secretary of 

Health, /and Human Services/, of the Secretary of Labor, of the employer, and of the employee 

or former employee. 

[NIOSH; Criteria Document: Vinyl Acetate p.2 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Whole Blood: Reference Ranges: Normal - Not established; Exposed - Not established; Toxic -

Not stablished. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2268] **PEER REVIEWED** 

Serum or Plasma: Reference Ranges: Normal - Not established; Exposed - Not established; 

Toxic - Not stablished. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2268] **PEER REVIEWED** 

Urine: Reference Ranges: Normal - Not established; Exposed - Not established; Toxic - Not 

stablished. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2268] **PEER REVIEWED** 

Respiratory Symptom Questionnaires: Questionnaires have been published by the American 
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Thoracic Society and the British Medical Research Council. These questionnaires have been 

found to be useful in identification of people with chronic bronchitis, however certain pulmonary 

function tests such as FEV 1 have been found to be better predictors of chronic airflow 

obstruction. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2269] **PEER REVIEWED** 

Chest Radiography: This test is widely used for assessing pulmonary disease. Chest radiographs 

have been found to be useful for detection of early lung cancer in asymptomatic people, 

especially for detection of peripheral tumors such as adenocarcinomas. However, even though 

OSHA mandates this test for exposure to some toxicants such as asbestos, there are conflicting 

views on its efficacy in detection of pulmonary disease. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2269] **PEER REVIEWED** 

Pulmonary Function Tests: The tests that have been found to be practical for population 

monitoring include: Spirometry and expiratory flow-volume curves; Determination of lung 

volumes; Diffusing capacity for carbon monoxide; Single-breath nitrogen washout; Inhalation 

challenge tests; Serial measurements of peak expiratory flow; Exercise testing. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2269] **PEER REVIEWED** 

Sputum Cytology: Sputum cytology along with chest radiographs have been the standard 

procedures for detecting early lung cancer in asymptomatic patients. Sputum cytology has been 

found to be useful for detection of central tumors, especially squamous carcinomas. For this test 

to be effective, exfoliated respiratory mucosal cells must be present in the expectorated 

specimen. Pooling of sputum collected over 2-3 days may enhance the sensitivity of this test by 

increasing the yield of exfoliated cells in the specimen. 

[Ryan, R.P., C.E. Terry (eds.). Toxicology Desk Reference 4th ed. Volumes 1-

3. Taylor & Francis, Washington, D.C. 1997., p. 2269] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in 

particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken 

concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 23] **PEER REVIEWED** 

Populations at Special Risk:

Applicants or employees found during examinations to have medical conditions that could be 

directly or indirectly aggravated by exposure to vinyl acetate, eg, chronic irritation of the 

respiratory tract, chronic inflammatory conditions of the skin, or chronic eye irritation, shall be 

counseled on the increased risk of impairment of their health from working with the compound. 

[NIOSH; Criteria Document: Vinyl Acetate p.2 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 
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Probable Routes of Human Exposure:

NIOSH (NOES Survey 1981-1983) has statistically estimated that 129,024 workers (36,642 of 

these were female) were potentially exposed to vinyl acetate in the US(1). Occupational 

exposure to vinyl acetate may occur through inhalation and dermal contact with this compound 

at workplaces where vinyl acetate is produced or used(SRC). The general population may be 

exposed to vinyl acetate through inhalation and dermal contact with products containing vinyl 

acetate; limited exposure may occur via ingestion from its use in chewing gum and tablet 

coatings(SRC). 

[(1) NIOSH; NOES. National Occupational Exposure Survey conducted from 1981-

1983. Estimated numbers of employees potentially exposed to specific agents 

by 2-digit standard industrial classification (SIC). Available at 

http://www.cdc.gov/noes/ as of Feb 4, 2009.] **PEER REVIEWED** 

School books fabricated with a polyvinyl chloride (PVC) cover were experimentally shown to 

emit several volatile organic compounds including vinyl acetate in a temperature/relative

humidity controlled sampling chamber. One book placed with open pages in a chamber at 23 deg 

C over a 24 hour period emitted vinyl acetate at a concentration of 72 ug/cu m(1). Hexcel, a 

graphite/epoxy composite dust used in machining, following mild heating(2). 

[(1) Salthammer T; Organic Indoor Air Pollutants: Volatile Organic 

Ingredients of Household and Consumer Products. Occurrence, Measurement, 

Evaluation. Wiley-VCH: New York, NY p. 225. (1999) (2) Kalman DA; Am Ind Hyg 

Assoc J 47: 270-75 (1986)] **PEER REVIEWED** 

Emergency Medical Treatment:

Emergency Medical Treatment:

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The following Overview, *** VINYL ACETATE ***, is relevant for this HSDB record 

chemical.

Life Support:

 o This overview assumes that basic life support measures

 have been instituted.

Clinical Effects:

 0.2.1 SUMMARY OF EXPOSURE

 0.2.1.1 ACUTE 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.

 0.2.1.2 CHRONIC EXPOSURE

 A) Chronic occupational exposure has been reported to

 cause CNS symptoms, chronic bronchitis, cardiovascular

 symptoms, liver function changes, and hepatic enzyme

 induction.

 0.2.4 HEENT

 0.2.4.1 ACUTE EXPOSURE
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 A) Eye and mucous membrane irritation and reversible

 corneal injury may occur. Olfactory fatigue develops

 with continued exposure.

 0.2.4.2 CHRONIC EXPOSURE

 A) Atrophy of the olfactory epithelium with replacement

 with different cell types, and focal leukocyte exudate

 and hyperplasia in the nasal cavity may occur.

 0.2.5 CARDIOVASCULAR

 0.2.5.1 ACUTE EXPOSURE

 A) Cardiac effects are not well documented. Chronic

 exposure has resulted in dysrhythmias, chest pain, and

 syncope.

 0.2.5.2 CHRONIC EXPOSURE

 A) Cardiac effects are not well documented. Chronic

 exposure has resulted in dysrhythmias, chest pain, and

 syncope.

 0.2.6 RESPIRATORY

 0.2.6.1 ACUTE EXPOSURE

 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.

 0.2.6.2 CHRONIC EXPOSURE

 A) Chronic bronchitis and impaired ventilatory function

 have been associated with industrial exposure. Various

 lesions of the lungs, emphysema, and atelectasis may

 occur.

 0.2.7 NEUROLOGIC

 0.2.7.1 ACUTE EXPOSURE

 A) Chronic exposure is reported to cause fatigue,

 irritability, insomnia, encephalopathy, vertigo,

 weakness, and polyneuritis.

 0.2.7.2 CHRONIC EXPOSURE

 A) Chronic exposure is reported to cause fatigue,

 irritability, insomnia, encephalopathy, vertigo,

 weakness, and polyneuritis.

 0.2.9 HEPATIC

 0.2.9.1 ACUTE EXPOSURE

 A) Liver function changes and hepatic enzyme induction may

 occur after chronic exposure.

 0.2.9.2 CHRONIC EXPOSURE

 A) Liver function changes and hepatic enzyme induction may

 occur after chronic exposure.

 0.2.14 DERMATOLOGIC

 0.2.14.1 ACUTE EXPOSURE

 A) Severe skin irritation with blister formation may

 occur.

 0.2.14.2 CHRONIC EXPOSURE

 A) Severe skin irritation with blister formation has been

 reported.

 0.2.16 ENDOCRINE

 0.2.16.2 CHRONIC EXPOSURE

 A) Adenoma or carcinoma of the thyroid has been reported

 in animal studies.

 0.2.20 REPRODUCTIVE HAZARDS

 A) No human epidemiologic data could be found evaluating
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 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

 0.2.21.1 IARC CATEGORY

 A) IARC Carcinogenicity Ratings for CAS108-05-4 (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.

 0.2.21.2 HUMAN OVERVIEW

 A) Inadequate evidence exists to evaluate carcinogenicity

 of vinyl acetate in humans. Some evidence of

 carcinogenicity exists in animals.

 0.2.21.3 ANIMAL OVERVIEW

 A) In mice and rats, vinyl acetate was carcinogenic by

 inhalation, but not when administered in the drinking

 water.

 0.2.22 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:

 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 EXPOSURE

 A) DILUTION: Immediately dilute with 4 to 8 ounces (120 to

 240 mL) of water or milk (not to exceed 4 ounces/120 mL

 in a child).
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 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 Trendelenburg and

 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 inhaled

 beta2 agonist and oral or parenteral corticosteroids.

 0.4.4 EYE EXPOSURE

 A) DECONTAMINATION: Irrigate exposed eyes with copious

 amounts of room temperature water for at least 15

 minutes. If irritation, pain, swelling, lacrimation, or

 photophobia persist, the patient should be seen in a

 health care facility.

 0.4.5 DERMAL EXPOSURE

 A) OVERVIEW

 1) DECONTAMINATION: Remove contaminated clothing and wash

 exposed area thoroughly with soap and water. A

 physician may need to examine the area if irritation or

 pain persists.

Range of Toxicity:

 A) Inhalation exposure to 20 ppm or greater may produce

 symptoms of irritation.

[Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO, 

2010; CCIS Volume 143, edition expires Feb, 2010. Hall AH & Rumack BH (Eds): 

TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2010; CCIS 

Volume 143, edition expires Feb, 2010.] **PEER REVIEWED** 

Antidote and Emergency Treatment:
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Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not 

breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valvemask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush 

contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean 

patient forward or place on left side (head-down position, if possible) to maintain an open airway 

and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain 

medical attention. /Esters and related compounds/ 

[Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For 

Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 

2005, p. 253] **PEER REVIEWED** 

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). 

Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if 

necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Provide a low-stimulus 

environment. Monitor for shock and treat if necessary ... . Anticipate seizures and treat if 

necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye 

continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse 

mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a 

strong gag reflex, and does not drool ... . Treat frostbite by rapid rewarming ... . /Esters and 

related compounds/ 

[Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For

Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 

2005, p. 253] **PEER REVIEWED** 

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the 

patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. 

Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. 

Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if 

necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 

0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension 

with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is 

hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine 

hydrochloride to assist eye irrigation ... . /Esters and related compounds/ 

[Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For 

Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 

2005, p. 254] **PEER REVIEWED** 

Animal Toxicity Studies:

Evidence for Carcinogenicity:

Evaluation: There is inadequate evidence in humans for the carcinogenicity of vinyl acetate. 

There is limited evidence in experimental animals for the carcinogenicity of vinyl acetate. 

Overall evaluation: Vinyl acetate is possibly carcinogenic to humans (Group 2B). In making the 

overall evaluation, the working group took into account the following evidence: (1) Vinyl 

acetate is rapidly transformed into acetaldehyde in human blood and animal tissues. (2) There is 

sufficient evidence in experimental animals for the carcinogenicity of acetaldehyde. Both vinyl 
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acetate and acetaldehyde induce nasal cancer in rats after administration by inhalation. (3) Vinyl 

acetate and acetaldehyde are genotoxic in human cells in vitro and on animals in vivo. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. 63 459 (1995)] **PEER REVIEWED** 

A3; Confirmed animal carcinogen with unknown relevance to humans. 

[American Conference of Governmental Industrial Hygienists TLVs and BEIs. 

Threshold Limit Values for Chemical Substances and Physical Agents and 

Biological Exposure Indices. Cincinnati, OH, 2008, p. 59] **PEER REVIEWED** 

Non-Human Toxicity Excerpts:

/LABORATORY ANIMALS: Acute Exposure/ Mild irritation after 5-15 minutes of exposure 

and necrosis after 20 hours of exposure was demonstrated in a further skin irritation study: An 

unknown number of rabbits were dermally exposed to unknown amounts of undiluted vinyl 

acetate for 1, 5 and 15 minutes and for 20 hours ... . No signs of irritation were observed after 24 

hours following 1-minute exposure; slight erythema occurred 24 hours after the 5- and the 15-

minutes exposures. Mild erythema and mild edema were observed at 24 hr after the 20-hours 

exposure. Necrosis was observed 8 days after 20 hour-exposure to the compound. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Acute Exposure/ Vinyl acetate caused mild irritation in the eyes 

of rabbits which was reversible within 48 hr after application. The test was performed according 

to the current guidelines on acute eye irritation. The amount of 0.1 mL of undiluted vinyl acetate 

(purity of 99.9 %) was placed in the left conjuctival sacs of one male and two female New 

Zealand White rabbits. One hour after application mild redness and chemosis of conjunctivae 

were observed, which were fully reversible in all animals after 48 and 24 hr, respectively. No 

changes of corneal opacity and iris were observed. The mean scores determined after 24, 48 and 

72 hr and relevant for classification were 1/0/0 for redness and 0/0/0 for chemosis, corneal 

opacity and iris. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Acute Exposure/ Vinyl acetate (purity /greater than/ 99.9%) was 

tested in a Local Lymph Node Assay (LLNA). A total of seven groups each of five female mice 

(CBA strain) were used. Five groups were treated with vinyl acetate at concentrations of 5%, 

10%, 25%, 50% (w/v) in acetone: olive oil, 4:1 (v/v) and 100% (undiluted) by topical application 

to the dorsum of each ear lobe (left and right) on three consecutive days ... Five days after the 

first topical application the mice were intravenously injected into the tail vein with 3H-methyl 

thymidine (equal to 19.8 uC/mouse). Approximately five hours after the intravenous injection the 

mice were killed, auricular lymph nodes were excised and pooled per animal ... All animals had 

survived and systemic clinical were not noted. Local inflammatory reactions (increased ear 

thickness) were noted in all groups with the exception of the vehicle control group and the 5%-

group. The Stimulation Index (SI) was below a 3-fold increase in all groups with the exception 
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of the positive control group. Mean SI values were 2.0, 2.4, 1.9, 1.7, 1.3, 16.6 for the 5%, 10%, 

25% 50%, 100% test solution and the positive control (25% HCA) (5%). 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Acute Exposure/ Respiratory tract damage is characteristic of 

vinyl acetate exposure in laboratory animals following acute-, intermediate-, or chronic-duration 

inhalation exposure ... Respiratory tract damage was reported to be the cause of death in rats, 

mice, guinea pigs, and rabbits acutely exposed (4 hours) to vinyl acetate. Gasping and labored 

breathing were usually observed in these animals prior to death, and necropsy revealed lung 

congestion and hemorrhage, froth in the trachea, and excess pleural fluid. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

/LABORATORY ANIMALS: Acute Exposure/ VINYL ACETATE IS A LOW EYE 

IRRITANT, BUT INJURIES HAVE BEEN OBSERVED TO HEAL WITHIN 48 HR. IT 

DEFATS THE SKIN & IS ... /A CNS DEPRESSANT/ IN HIGH CONCN. 

[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and 

Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: 

John Wiley & Sons Inc., 1993-1994., p. 2987] **PEER REVIEWED** 

/LABORATORY ANIMALS: Acute Exposure/ The content of free non-protein thiols (-SH) was 

investigated in the livers of guinea pigs, rats, and mice after ip injection of vinyl acetate. A rapid 

change of the hepatic non-protein thiols level was found in guinea pigs after injection of 500 

mg/kg, resulting in a 50% decr in non-protein thiols content. In mice, the decr was slower and 

amounted to only 23% 4 hr after injection of 300 mg/kg. Rats responded to a single dose of 450 

mg/kg with only a 10% redn of liver non-protein thiols content. An approx 20% decr was 

observed after chronic intermittent exposure (5 hr/day for 6 mo) to 10, 100 or 500 mg/cu m vinyl 

acetate. 

[Holub I, Tarkowski S; Int Arch Occup Environ Health 51 (2): 185-9 (1982)] 

**PEER REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Acute Exposure/ ... Exposed rabbits by inhalation at 7 to 142 

ppm...for 40 min. ... At 71 ppm decreased the excitability of the CNS, whereas 142 ppm 

produced a more pronounced excitability of the CNS. 

[American Conference of Governmental Industrial Hygienists, Inc. 

Documentation of the Threshold Limit Values and Biological Exposure Indices. 

6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1685] **PEER 

REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In a 90-day inhalation study 

groups of 10 male and 10 female Sprague-Dawley rats and CD-1 mice were exposed to vinyl 

acetate vapors (purity of test substance 99.9%) at concentrations of 0, 50, 200 or 1000 ppm 

(calculated as 0, 180, 710 or 3600 mg/cu m), 6 hours/day, 5 days/week ... Exposure of rats to 

1000 ppm vinyl acetate resulted in significantly decreased body weight gain (final body weight -

19% in both sexes), clinical effects (intermittent incidence of respiratory distress, hunched 

postures and ruffled fur), increased lung-to-body weight ratio (assumed as due to lung 
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congestion), and histomorphological changes in the respiratory tract (mild histiocytic alveolitis) 

... Many rats from both groups had peribronchial/perivascular lymphoid hyperplasia, alveolar 

histiocytosis/ histiocytic pneumonia, chronic tracheitis and laryngitis, and lympadenitis. Except a 

higher incidence of alveolar histiocytosis in high dose rats (19/20 vs. 12/20 controls) no 

treatment-related toxic effect was seen in the organs examined. The olfactory regions of nasal 

sections of 4 male and 3 female rats exposed to 1000 ppm were reviewed. The most severe 

lesions were seen in the dorsal medial meatus of the anterior nasal passages (level II), lesions 

extended posteriorly to the dorsal medial meatus of levels III and IV and the dorsal scroll of the 

third ethmoturbinates. Lesions were characterized by postdegenerative atrophy of the olfactory 

epithelium and focal erosion, with associated infiltration of neutrophils and eosinophils. Some 

losses of Bowman's glands and of nerve bundles in the lamina propria were observed in the most 

severely affected areas. There was only a minimal evidence of regeneration of the affected 

epithelium. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... It was/ hypothesized that 

prolonged VA exposure at high concentrations would induce cytotoxicity and a restorative cell 

proliferation (CP). These endpoints were measured in F-344 rats and BDF1 mice administered 

drinking water containing 0, 1000, 5000, 10,000, or 24,000 ppm /vinyl acetate/ for 92 days. On 

test days, Days 1, 8, 29, and 92, upper digestive tract histopathology and oral cavity CP (pulsed 

5-bromodeoxyuridine [BrdU] to measure S-phase DNA synthesis) were evaluated. Analysis of 

test solutions showed that VA spontaneously hydrolyzed, slowly releasing acetic acid and 

thereby lowering pH. Statistically significant, concentration-related increases in CP occurred in 

basal cells of the mandibular oral cavity mucosa of mice at 10,000 and 24,000 ppm but only after 

92 days. CP increases were approximately 2.4- and 3.4-fold above controls and were considered 

to be toxicologically significant. Some statistically significant increases in CP were also 

measured in the oral cavity mucosa of rats; however, these changes were considered to be of 

equivocal biological relevance. No histopathological evidence of mucosal injury was seen in 

either species. The absence of cytotoxicity in the upper digestive tract mucosa suggests that the 

increased CP at high administered VA concentrations may be due to a mitogenic response, 

ostensibly from the loss of cell growth controls in oral cavity mucosa. 

[Valentine R et al; Toxicol Sci 67 (2): 190-7 (2002)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Groups of ten male and ten 

female rats were given drinking water containing 200, 1000, or 5000 ppm of vinyl acetate for 13 

weeks, decreased food consumption was noted at the highest dose and decreased body weight 

gain occurred in the males. Female rats excreted more concentrated and darker urine at the 

highest level. No liver pathology or any other histopathologic change was noted. In a similar 

study, groups of ten male and ten female mice were administered drinking water containing 200, 

1000, or 5000 ppm vinyl acetate for 13 weeks. No overt signs of toxicity were noted during the 

study. The no-observed-effect level (NOEL) in this study was 5000 ppm. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Groups of five male and five 

female rats were exposed by inhalation 6 hours/day, 5 days/week for 4 weeks at 50, 150, 500, or 

1000 ppm of vinyl acetate. The 50 ppm level was increased to 1500 ppm on exposure day 10. At 

500 ppm and above, vinyl acetate appeared to be a pulmonary irritant. A concentration-related 

reduction in body weight gain was seen and was more pronounced in the females. No pathologic 

lesions were noted at necropsy. Groups of five male and five female mice were also exposed by 

inhalation on a similar dosing schedule as the rats except that the 50 ppm level was increased to 

1500 ppm on exposure day 8. The findings were similar, i.e., pulmonary irritation and decreased 

body weight gain. No pathologic changes were seen at necropsy. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Exposure of four dogs 6 

hours/day, 5 days/week for a period of 6 weeks at an average concentration of 91 ppm vinyl 

acetate failed to result in any detectable physiological changes. Exposure was interrupted for 2.5 

weeks after which the dogs were exposed at an average concentration of 79 ppm for an 

additional 2 weeks. Following this period, the exposure was increased to 186 ppm for 1 week. 

No gross or microscopic pathology was noted; only irritation of the eyes and lacrimation were 

observed at the 186 ppm level. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Groups of five male and five 

female rats were given drinking water containing 50, 200, 1000, or 5000 ppm of vinyl acetate 

for 4 weeks; during the last week of treatment, the 50ppm exposure was increased to 10,000 

ppm. During the early part of the study, there was minimal and transient retardation of the body 

weight gain in the 5000 ppm group. A lower rate of body weight gain was observed in females 

administered 1000 ppm. Treatment with 10,000 ppm was associated with a decrease in water 

consumption. No deaths occurred and the animals appeared to be healthy. Absolute and relative 

liver weights were reduced for all vinyl acetate-treated rats. The toxicological significance of 

these changes was considered questionable due to the absence of any liver pathology. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ DOGS EXPOSED 6 HR 

DAILY FOR SEVERAL WK @ CONCN STARTING WITH AN AVG OF 91 PPM & 

ENDING AFTER ... 11 WK @ 186 PPM . THE DOMINANT RESPONSE ... WAS 

IRRITATION OF THE EYES WITH LACRIMATION. ... 

[American Conference of Governmental Industrial Hygienists, Inc. 

Documentation of the Threshold Limit Values and Biological Exposure Indices. 

6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1686] **PEER 

REVIEWED** 

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Following exposure for 6 hr 

on 5 days/wk over a 4 wk period, signs of irritation of the respiratory tract were observed in mice 

exposed to concn of 520 mg/cu m (150 ppm) & in rats exposed to 1760 mg/cu m (500 ppm). 
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Exposure of both species to 3500 mg/cu m (1000 ppm) for 6 hr/day on 6 days/wk over 3 mo 

caused retardation in wt gain; no specific damage to parenchymal organs was noted. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The development of 

hepatic enzyme-altered foci (ATPase, GGTase) was investigated after dosing vinyl acetate (200 

and 400 mg/kg per day, orally) to newborn rats for 3 weeks, with or without subsequent 

promotion by phenobarbital. Whereas the structurally related compounds vinyl carbamate and 

vinyl chloride induce enzyme-altered foci under comparable experimental conditions, no foci 

were observed in vinyl acetate-treated animals at the age of 14 weeks. This is consistent with 

investigations on metabolism and pharmacokinetics of vinyl acetate which show that this 

compound, after entering the organism, is immediately split by blood esterases and thus may not 

be available for epoxidation to an ultimately carcinogenic metabolite. 

[Laib RJ, Bolt HM; Carcinogenesis 7 (5): 841-3 (1986)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In animals, long-term 

inhalation and oral administration of vinyl acetate produce tumors at the primary site of 

exposure, the surface epithelium of the respiratory tract and of the upper gastrointestinal tract ... 

Vinyl acetate exposure produced tumors at the site of first contact along the exposure routes. A 

thresholded mode of carcinogenic action is thought to be active. The observed tumor responses 

are reflecting the target site-specific enzyme activities: Following inhalation and oral exposure 

vinyl acetate is rapidly hydrolyzed by carboxylesterases leading to the formation of acetic acid 

and acetaldehyde which is further converted into acetic acid in the presence of aldehyde 

dehydrogenases. Intracellular aldehyde dehydrogenase activity is limited, at higher 

concentrations of vinyl acetate it will not be sufficient for the oxidation of generated 

acetaldehyde. Thus, at high vinyl acetate concentrations non-physiologically high 

concentrations of acetaldehyde are produced ... Overall, it is considered that the critical events in 

vinyl acetate carcinogenesis do fit to the criteria for the exceptional cases where genotoxic 

action is thought to be thresholded. From animal data it is concluded that vinyl acetate might 

pose a cancer risk for humans exposed to the substance via the inhalation or oral route. 

Carcinogenicity is thought to act via a secondary mechanism and the concern may be relevant 

above threshold concentrations. The observed effects are thought to be relevant for the human. 

For the respiratory tract humans may be less sensitive than the rat due to a lower 

carboxylesterase activity in the nasal mucosa. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Carcinogenicity and 

chronic toxicity of vinyl acetate monomer (VA) were examined in male and female Crj:BDF1 

mice and F344/DuCrj Rats. Groups of 50 mice and 50 rats of each sex were orally administered 

VA in drinking water containing 0, 400, 2,000 or 10,000 ppm (g/g) VA for 104 wk. Squamous 

cell tumors were clearly evident in the upper digestive tract of treated mice and rats, and in the 

larynx of treated mice of both sexes. In mice, squamous cell carcinomas and papillomas were 
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observed in the oral cavity, esophagus, forestomach and larynx of the 10,000 ppm group, 

together with basal cell hyperplasia, squamous cell hyperplasia and epithelial dysplasia. In rats, 

incidences of squamous cell carcinomas and papillomas were increased in the oral cavity of the 

10,000 ppm group of both sexes, and an esophagus squamous cell carcinoma was observed in a 

10,000 ppm female. Pre-neoplastic hyperplasias were also noted. Mapping of the neoplastic and 

pre-neoplastic lesions in the oral cavity of the 10,000 ppm group revealed that both the lesions 

occurred predominantly at Level V in mice and at Level VI in rats. A lower confidence limit of a 

benchmark dose (BMDL10) of 477 mg/kg/d was obtained from a dose-response relationship 

between combined incidence of squamous cell carcinomas and papillomas in the oral cavity of 

mice and rats and the estimated daily VA intakes per body weight, and compared with literature 

values. 

[Umeda Y et al; J Occup Health 46 (2): 87-99 (2004); Comment in: J Occup 

Health 46 (3):249 (2004); author reply 250-1.] **PEER REVIEWED** PubMed 

Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Vinyl acetate monomer 

(VAM) was administered in drinking water supplied ad libitum at doses of 5,000, 1,000, and 0 

ppm (v/v) to 17-week-old Sprague-Dawley rats (breeders) and to 12-day embryos (offspring).

Treatment lasted for 104 weeks; thereafter, animals were kept under control conditions until 

spontaneous death. VAM was found to cause an increase in total malignant tumors and in 

carcinomas and/or precursor lesions of the oral cavity, lips, tongue, esophagus, and forestomach. 

Based on these data, VAM must be considered a multipotent carcinogen. 

[Minardi F et al; Ann N Y Acad Sci 982: 106-22 (2002)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Vinyl acetate monomer 

(VAM) was administered in drinking water at doses of 5,000, 1,000, and 0 ppm (v/v), to Swiss 

mice, 17 weeks old (breeders) or 12-day embryos (offspring) at the start of the experiment. The 

treatment lasted 78 weeks, and the animals were kept under control until spontaneous death. 

VAM has been shown to cause an increase in: (1) total malignant tumors; (2) carcinomas of the 

Zymbal glands, oral cavity, tongue, esophagus, and forestomach; (3) stomach tumors; (4) lung 

tumors; and (5) uterine tumors. A slight increase of hepatomas has been observed among male 

mice offspring treated with the higher dose. On the basis of these data VAM must be considered 

a multipotential carcinogen. 

[Maltoni C et al; Ann N Y Acad Sci 837: 209-38 (1997)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Vinyl acetate was 

evaluated for chronic toxicity and oncogenicity in male and female rats and mice in a 104-week 

study. Target concentrations were 0, 50, 200, and 600 ppm. The study included interim 

terminations at approximately 53 and 83 weeks and a group whose exposure was terminated at 

70 weeks and allowed a 15-week recovery period. Over the course of the exposures, body weight 

gain was consistently depressed in all 600 ppm groups and in the 200 ppm mice. Except for 

female rats of the 600 ppm exposure group, recovery animals showed significant improvements 

in weight gain relative to controls. There were no changes in hematological parameters of either 

species that could be unequivocally related to treatment. The only effect noted on clinical 

chemical parameters during the study were decreases in blood glucose in the 600 ppm females. 

There were no adverse effects on survival in either species. Increases in lung weight were noted 
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in rats and mice primarily in the 600 ppm groups. These changes were associated with bronchial 

exfoliation, macrophage accumulation, and fibrous plaques and buds extending into the airway 

lumen, and bronchial/bronchiolar epithelial disorganization. The most significant 

histopathological changes were noted in the nasal cavity. In the olfactory epithelium of both rats 

and mice, the main nonneoplastic changes included epithelial atrophy, regenerative effects 

(squamous metaplasia and respiratory metaplasia of olfactory epithelium), basal cell hyperplasia, 

and epithelial nest-like infolds. No nonneoplastic changes were observed in the respiratory 

epithelium of rats, while squamous metaplasia at the naso/maxilloturbinate region was prevalent 

in mice. Nonneoplastic changes were similar in the recovery groups. Oncogenic responses to 

vinyl acetate exposure were mainly confined to the nasal cavity in rats and included endo- and 

exophytic papillomas, squamous cell carcinoma, carcinoma in situ in olfactory regions, and 

endophytic papilloma in respiratory regions. Squamous cell carcinomas were also found either in 

areas normally covered by cuboidal epithelium or areas of unknown origin. One squamous cell 

carcinoma was found in the larynx of a rat of the 600 ppm groups. One squamous cell carcinoma 

was found in the lung of a mouse of the 600 ppm group. 

[Bogdanffy MS et al; Fundam Appl Toxicol 23 (2): 215-29 (1994)] **PEER 

REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The purpose of this study 

was to evaluate vinyl acetate for potential chronic toxicity and oncogenicity when given to rats 

in drinking water from the time of gestation. Target concentrations were 0, 200, 1000, and 5000 

ppm (v/v). Drinking water solutions were prepared daily and analyzed at approximately 4-week 

intervals. F0 rats were given solutions of vinyl acetate for 10 weeks and then mated. Offspring 

(F1 rats) were culled to equal group sizes of 60 main study rats and 30 rats for satellite groups. 

F1 rats were treated for up to 104 weeks with interim kills of satellite groups at 52 and 78 weeks. 

Body weights and clinical signs of toxicity were monitored in F0 and F1 rats. Food and water 

consumption were measured in F1 rats. At Weeks 52 and 78 of the test, clinical pathology and 

urine analysis examinations were conducted on 10 rats per group from satellite animals. A 

complete gross and histopathological examination of F1 rats was conducted at the interim kills 

and on main study rats at Week 104. Average vinyl acetate consumption over the course of the 

study in male rats of the 200, 1000, and 5000 ppm groups was 10, 47, and 202 mg/kg/day, 

respectively. Female rats consumed an average of 16, 76, and 302 mg/kg/day, respectively. 

Compound-related effects observed during the study included a concentration-related decrease in 

water consumption among rats of the 1000 and 5000 ppm groups and a decrease in food 

consumption among rats of the 5000 ppm groups. Concurrent body weight decrement was 

observed only in the 5000 ppm groups. 

[Bogdanffy MS et al; Fundam Appl Toxicol 23 (2): 206-14 (1994)] **PEER 

REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The scope of the study 

included ... 10-month exposure of animals to vinyl acetate at concentrations 10, 100 and 500 

mg/cu m, 5 days weekly, 5 hours daily. During the 10-month experiment the animals were 

observed and body weight controlled. In addition, periodically some hematological examinations 

and biochemical of blood serum as well as histopathological examinations of inner organs were 

carried on. Post-mortally the weight of inner organs was determined. ... The prevalence and the 

degree of intensity of the changes of ... indicators was the least in the group of animals exposed 

to vinyl acetate at concentration of 10 mg/cu m. These changes were transient /and did not 
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involve/ reticulopenia and animal body weight decrease. Histopathological examinations 

revealed some inflammatory changes in the respiratory system both in control and exposed 

animals. Only planoepithelial metaplasia of bronchi was found exclusively in animals exposed to 

vinyl acetate at all concentrations used. The changes within liver were found only in animals 

exposed to vinyl acetate at concentration of 100 and 500 mg/cu m. These changes involved fatty 

degeneration of hepatic parenchyma, proliferation and extension of smooth endoplasmatic 

reticulum and the changes within the biliary canaliculi... 

[Czajkowska T et al., Med Pr. 37(1):26-36 (1986).] **PEER REVIEWED** PubMed 

Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A chronic toxicity test was 

carried out in groups of 20 male and female F344 rats with vinyl acetate dissolved in drinking 

water at two concentrations, 2500 and 1000 mg/liter. Treatment lasted for 2 years and did not 

lead to early death of the animals compared with untreated controls. The incidence of most types 

of neoplasm was similar in the treated and control groups. However, six females receiving the 

higher dose of vinyl acetate had adenoma or carcinoma of the thyroid and five had carcinoma of 

the uterus; the latter were not seen in the controls. 

[Lijinsky W, Reuber MD; Toxicol Appl Pharmacol 68 (1): 43-53 (1983)] **PEER 

REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ CHRONIC 24 HR 

INHALATION OF 2.4 MG/CU M VINYL ACETATE BY RATS RESULTED IN SUBTLE 

HEPATIC CHANGES OF ENZYME RHYTHMS, BUT WERE MORE PRONOUNCED WITH 

13.2 & 68 MG/CU M. 

[Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and 

Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: 

John Wiley & Sons Inc., 1993-1994., p. 2987] **PEER REVIEWED** 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A GROUP OF 96 

SPRAGUE-DAWLEY RATS (SEX NOT SPECIFIED) WERE EXPOSED FOR 4 HR/DAY ON 

5 DAYS/WK FOR 52 WK TO MAX TOLERATED CONCN, 8.8 G/CU M (2500 PPM) 

VINYL ACETATE IN AIR. NO TUMORS WERE REPORTED TO HAVE OCCURRED 

DURING 135 WK. EARLY MORTALITY WAS HIGH: 49 ANIMALS SURVIVED FOR 26 

OR MORE WK. (THE WORKING GROUP NOTED THAT THE TIME OF DEATH OF

ANIMALS THAT LIVED LONGER THAN 26 WK WAS NOT INDICATED) 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V19 345 (1979)] **PEER REVIEWED** 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ CONTINUOUS 4 MO 

INHALATION BY RATS & MICE OF 13.2 OR 68.0 MG VINYL ACETATE/CU M 

CAUSED CONCN DEPENDENT EMPHYSEMA & LUNG ATELECTASIS, & DISTURBED 

BLOOD CIRCULATION IN OTHER ORGANS. THE FUNCTIONS OF CNS, HYPOPHYSIS, 

& ADRENAL GLAND WERE DISTURBED. 

[RUMYANTSEV AP ET AL; KHIM PROM-ST, SER: TOKSIKOL SANIT KHIM PLASTMASS (2): 

20-2 (1979)] **PEER REVIEWED** 
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Groups of 20 female 

Fischer F344 rats, 7 to 8 wk of age, received 0 (controls), 1000 or 2500 mg/L vinyl acetate (with 

no significant impurities) in drinking water for 100 wk & were then observed for the rest of their 

lifetime (max, 130 wk). At that time, survival in males & females was: controls, 7/20 & 5/20; 

1000 mg/L, 8/20 & 11/20; 2500 mg/L, 1/6 & 11/20, respectively. Increases in incidence of liver 

neoplastic nodules (0 control, 4 low-dose & 2 high dose males; 0 control, 0 low dose & 6 high 

dose females (p< 0.01), of uterine adenocarcinomas (0 control, 1 low dose & 5 high dose 

females) (p< 0.024) & polpys (0 control, 3 low dose, & 5 high dose females), & thyroid C-cell 

adenomas (0 control, 2 low dose & 5 high dose females) (p= 0.024) were observed in treated 

groups. No malignant neoplasm was found in liver. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 121 (1986)] **PEER REVIEWED** 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The questioning of results 

of carcinogenicity of vinyl acetate resulted in the conducting of a DNA binding assay in vivo in 

rats, using (14)C-labelled vinyl acetate. After administration of (14)C-vinyl acetate to male and 

female Fischer-344 rats, either orally (1 mCi) or by inhalation (0.45-0.75 mL injected into the 

gas phase of the exposure chamber), no specific hepatic DNA adducts, known to occur after 

administration of labelled vinyl halides or vinyl carbamates, could be detected. 

[Simon P et al; Toxicol Lett 27 (1-3): 115-20 (1985)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Chronic and reproductive 

toxicology studies were performed for vinyl acetate. Inhalation studies using rats and mice were 

conducted, with animals being exposed to 50, 200, or 600 ppm vinyl acetate in air. A small 

percentage of early deaths in mice, attributable to respiratory lesions, was possibly associated 

with inhalation of 600 ppm vinyl acetate. Body weight gain was lower in both species at higher 

concentrations. In the nasal cavity, atrophy of the olfactory epithelium with replacement with 

different cell types was noted in both species at 200 and 600 ppm. Epithelial hyperplasia of the 

trachea was noted at 200 and 600 ppm in mice only. In the lungs in both species, foamy 

histiocytes, epithelial exfoliation and fibroepithelial tags were noted at 600 ppm. Mice 

demonstrated epithelial hyperplasia at 600ppm and fibroepithelial tags were noted at 200 ppm. 

Changes were noted at 53 weeks into the study and showed little progression for the remainder 

of the time. Eleven tumors was found in the nasal cavities of rats at the 600 ppm exposures; eight 

were benign papillomas of various cell types and three were squamous carcinomas. There was no 

evidence that vinyl acetate exposure caused adverse systemic effects and 50ppm was a clear no 

observable effect level. A chronic 2 year toxicity/carcinogenicity study following in-utero 

exposure in rats via drinking water exposure was undertaken. Dose related reductions in water 

and food intake, and body weight gain were seen. An increase in relative kidney weight in high 

dose males was the only treatment related organ effect. 

[Clary JJ; Annals of the New York Academy of Sciences 534: 255-60 (1988)] 

**PEER REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Newborn Wistar (4-5 

animals per sex per group) rats were exposed orally to 100 or 200 mg/kg bw/day vinyl acetate 

(99% pure, impurity: 100 ppm hydroquinone) in condensed milk twice a day for three weeks. A 
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subgroup of animals was additionally treated with phenobarbital in drinking water for 8 weeks to 

stimulate the growth of potentially occurring preneoplastic liver foci. 14 weeks after the start of 

the study livers were dissected. No ATPase-free and gamma-GT-positive areas in the liver as 

indication for the development of liver nodules could be found. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Groups of 24 mated 

female Crl:CD(SD)BR rats were exposed to vinyl acetate vapors from day 6 to day 15 of 

gestation at concentrations of 0 (control), 50, 200, or 1000 ppm (equivalent to about 100, 205, 

and 1025 mg/kg bw/day, based on a respiratory rate of 0.8 L/min/kg for rats) for 6 hr/day. At 

1000 ppm, severe maternal toxicity (marked reduction in body weight gain, congestion of the 

lungs) and some signs of fetotoxicity occurred. Fetal toxicity was evident by a statistically 

significant decrease in mean fetal weight and mean crown-rump length in the fetuses of the 1000 

ppm group. In addition, there was a statistically significant increase in the incidence of minor 

skeletal alterations (mainly delayed ossification) in fetuses from dams exposed to 1000 ppm. In 

summary, vinyl acetate did adversely affect both the dam and the conceptus at an inhaled 

concentration of 1000 ppm, but not at lower exposure levels. The NOAEC for the inhalation 

study was considered to be 200 ppm. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... Groups of male and 

female Crl:CD(SD)BR rats were given 0, 200, 1000, or 5000 ppm vinyl acetate (VA) via the 

drinking water over two generations. In addition, a cross-mating trial of control and 5000-ppm 

male and female rats was conducted in the F1 generation to investigate the slightly decreased 

litter production in the high-dose group. No treatment-related mortality was observed in any of 

the groups. Water consumption was significantly reduced in the 5000-ppm groups in both 

generations and in the 1000-ppm F1 female rats. The body weights of the F0 and F1 male rats 

and the F1 female rats in the 5000-ppm group tended to be slightly lower than those of the 

control group. Body weight gain was significantly decreased during lactation in the F0 females at 

5000 ppm and in the F1 females at 1000 and 5000 ppm. Pup weights in the F1 generation, but 

not in the F2 generation, were significantly lower than those of the control on lactation Day 21. 

The number of litters produced in the F1 generation in the 5000-ppm group was slightly lower 

than that of the control group and was attributed to lower fertility. Fewer pups were produced 

when control females were mated with the 5000-ppm males; however, the decrease was due to 

poor mating performance rather than decreased fertility. No decrease was apparent when the 

5000-ppm females were mated with the control group males. Under the conditions of this study, 

the no-observed adverse effort level was considered to be 1000 ppm. 

[Mebus CA et al; Fundam Appl Toxicol 24 (2): 206-16 (1995)] **PEER REVIEWED** 

PubMed Abstract

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... To assess the 

potential of vinyl acetate (V)A causing developmental toxicity in rodents, groups of 23 or 24 

Crl:CD(SD)BR rats were given 0, 200, 1000, or 5000 ppm VA in drinking water or exposed 6 

hr/day to 0, 50, 200, or 1000 ppm VA vapors on Days 6-15 of gestation (both routes 
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approximately 0, 25, 100, or 500 mg/kg/day). Administration of VA in the drinking water 

produced no evidence of maternal or developmental toxicity. A significantly lowered water 

intake was observed in dams from the 5000 ppm VA group and probably reflected unpalatability 

of the VA water solution at the highest dose level. In the inhalation study, maternal toxicity was 

evident by a marked reduction in weight gain of dams exposed to 1000 but not 200 or 50 ppm 

VA. Fetal toxicity was evident by a statistically significant decrease in mean fetal weight and 

mean crown-rump length in fetuses from the 1000-ppm VA group. In addition, there was a 

statistically significant increase in the incidence of minor skeletal alterations in fetuses from 

dams exposed to 1000 ppm VA. Delayed ossification was the main skeletal alteration. In 

summary, pregnant rats were relatively insensitive to the effects of VA administered in the 

drinking water at a concentration level as high as 5000 ppm. However, VA did adversely affect 

both the dam and the conceptus at an inhaled concentration of 1000 ppm, but not at lower 

exposure levels. These results indicate that VA is not uniquely toxic to the conceptus. The noobserved-effect level for the dam and conceptus under these experimental conditions was greater 

than 5000 ppm for the drinking water study and was 200 ppm for the inhalation study. 

[Hurtt ME et al; Fundam Appl Toxicol 24 (2): 198-205 (1995)] **PEER 

REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Inhalation studies using 

rats and mice were conducted, with animals being exposed to 50, 200, or 600 ppm vinyl acetate 

in air. A two generation reproduction study was conducted in rates exposed via drinking water. A 

decrease in fertility was seen in the 5000 ppm group, attributable to males. 

[Clary JJ; Annals of the New York Academy of Sciences 534: 255-60 (1988)] 

**PEER REVIEWED** PubMed Abstract

/LABORATORY ANIMALS: Neurotoxicity/ In the 3-month mouse study, hunched posture and 

ruffled fur were observed from days 1 through 9 in mice exposed to 200 ppm and intermittently 

through day 34 in mice exposed to 1,000 ppm. In the 3-month rat study, these clinical signs were 

consistently observed for the first 13 days of the study and intermittently thereafter in the 

animals exposed to 1,000 ppm only. A dose-related increase in the incidence of head tilt was also 

noted in some rats and mice exposed to vinyl acetate for 104 weeks. These neurological signs 

were noted only intermittently throughout the chronic studies. It is possible that these 

neurological signs were secondary to the poor health of the animals and may not be indicative of 

a primary effect of vinyl acetate on the nervous system. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

/GENOTOXICITY/ An increase in the induction of micronuclei was detected following a single 

intraperitoneal injection of 250 to 2000 mg/kg in male C57B1/6 mice. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/GENOTOXICITY/ Vinyl acetate increased the frequency of sperm abnormalities in mice 

following five intraperitoneal injections of 500 mg/kg; no effects were seen at 125 or 250 mg/kg. 

Thus, vinyl acetate has demonstrated mutagenic activity in a number of test systems. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-
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ROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

/GENOTOXICITY/ Eighteen compounds structurally related to the mutagenic carcinogen vinyl 

chloride have been tested for mutagenicity in five strains of Salmonella typhimurium. ... Vinyl 

acetate /was/ not mutagenic. The mutagenicity tests were performed both without and with 

activation by rat and hamster liver microsomal preparations (S9). /Vinyl acetate was/ tested in 

the plate incorporation and/or liquid preincubation tests except vinyl bromide, which was tested 

as a gas. 

[Lijinsky W, Andrews AW; Teratog Carcinog Mutagen 1 (3): 259-67 (1980).] 

**PEER REVIEWED** PubMed Abstract

/GENOTOXICITY/ A mouse lymphoma assay was reported to be positive with and without S-9 

mix; however, a full report with detailed data is lacking. Vinyl acetate was tested in 

concentrations ranging, with S-9 mix, from 1.8 to 5 uL/mL and, without S-9 mix, from 1.9 to 4 

uL/mL; the highest dose of 5 uL/mL corresponds to 4650 ug/mL or 54 mmol/L. With S-9 mix, 

induced mutant frequencies were 2.4- to 7.4-fold that of the concurrent negative control; relative 

total growths ranged from 10 to 62%. Without S-9 mix, 5- to 10.3-fold increases in mutation

frequencies were observed; relative total growths were between 5 and 26%. Further details on 

the investigation are not available. Therefore, the relationship between genotoxicity and 

cytotoxicity cannot be evaluated. Furthermore, it cannot be deduced whether the genetic effects 

were preferentially due to gene or chromosome mutations. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/GENOTOXICITY/ ... /It was/ demonstrated /that/ the potential of vinyl acetate for induction of 

DNA-protein crosslinks (DPX) with purified plasmid DNA and calf thymus histone proteins. 

Doses ranging from 10 to 100 mmol/L were used. Induction of DPX was bound to the presence 

of rat liver microsomes. Induction of DPX was also found in isolated cells from rat nasal tissues. 

With treatment times of 1 to 2 hr, very high doses ranging from 25 to 75 mmol/L were needed 

for induction of DPX rates over the background level. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/GENOTOXICITY/ Vinyl acetate induced sister-chromatid exchanges (SCE) in bone marrow 

cells of male BDF rats (3 per group) after single intraperitoneal application. Weak effects were 

found at doses from 370 mg/kg upwards in non-hepatectomised rats and from 470 mg/kg 

upwards in hepatectomized rats. The maximum effect was ca. a doubling of the spontaneous 

SCE frequency at 560 mg/kg. The treatments were without clear influence on cell proliferation 

behavior. Data on general toxicity were not given; it can be estimated that 370 and 470 mg/kg 

correspond to half of the LD50. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

/GENOTOXICITY/ The testicular genotoxic effects of vinylacetate (VA) and its hydrolysis 

product, acetaldehyde (AA), were studied in mice by analyzing the induction of morphologically 

abnormal sperm and meiotic micronuclei. VA significantly increased the frequency of sperm 
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abnormalities at 500 mg/kg/day while lower doses were ineffective. AA did not induce abnormal 

sperm. Neither of the compounds influenced the frequency of meiotic micronuclei. VA, but not 

AA, caused a dose-dependent decrease in sperm production and a reduction of testicular weight 

at 500 and 125 mg/kg/day. 

[Lahdetie J; Mutat Res 202 (1): 171-8 (1988)] **PEER REVIEWED** PubMed 

Abstract

/GENOTOXICITY/ A dose-dependent increase in micronucleated polychromatic erythrocytes 

was observed in the bone marrow of male C57B1/6 mice 30 hr after a single intraperitoneal 

injection of vinyl acetate (250, 500, 1000 or 2000 mg/kg bwt; (9-14 animals per group). The 

effect was statistically significant at 1000 mg/kg (1.33 +/- 0.29% vs. 0.6 +/- 0.10% in olive oiltreated controls) and at 2000 mg/kg (1.57 +/- 0.19%) of vinyl acetate. These doses were fatal to 

6 (1000 mg/kg) and 8 (2000 mg/kg) out of 14 animals in both groups. The ratio of polychromatic 

to normochromatic cells decreased as a function of vinyl acetate dose. Cyclophosphamide (20 

mg/kg), used as a positive control chemical, induced a clear increase in micronucleated 

polychromatic erythrocytes (2.07 +/- 0.20%). 

[Maki-Paakkanen J, Norppa H: Mutat Res 190 (1): 41-5 (1987)] **PEER 

REVIEWED** PubMed Abstract

/GENOTOXICITY/ A distinct dose-dependent induction of SCEs similarly occurred in Chinese 

hamster ovary cells after a 24-hr vinyl acetate treatment (0.125-1 mM). A pulse treatment of 

Chinese hamster ovary cells for 4 hr also yielded a clear increase in SCEs, but at higher 

concentrations (0.3-5 mM). The presence of rat liver S9 mix enhanced the SCE-inducing effect 

of vinyl acetate in Chinese hamster ovary cells. 

[Norppa H et al; Cancer Res 45 (10): 4816-21 (1985)] **PEER REVIEWED** PubMed 

Abstract

/GENOTOXICITY/ Vinyl acetate was tested in the Ames Salmonella test with Salmonella 

typhimurium strains TA1537, TA1538, TA1535, TA98, and TA100 with and without rat or 

hamster S9 mix from animals pretreated with Aroclor 1254. The cmpd was not mutagenic and 

was not toxic to the cells at doses up to 1000 ug/plate. 

[Lijinsky W; Teratog Carcinog Mutagen 1: 259-67 (1980)] **PEER REVIEWED** 

PubMed Abstract

/ALTERNATIVE and IN VITRO TESTS/ The induction of DNA-protein crosslink (DPXL) 

formation by acetaldehyde and vinyl acetate in rat nasal epithelial tissues was detected using a 

sodium dodecyl sulfate/KCl precipitation technique. Endogenous crosslink levels ranged from 

0.5 to 2.0% of total DNA and were considered background. Epithelial cells isolated from both 

olfactory and respiratory turbinates exhibited dose- and time-dependent increases in DPXL 

formation when exposed to 10-150 mM acetaldehyde for 1-2 hr at 37 degrees C. Similarly, 

respiratory and olfactory epithelial cells exposed to 5-75 mM vinyl acetate for 1-2 hr 

accumulated up to 12- and 15-fold higher crosslink levels than untreated cells, respectively. 

However, vinyl acetate appears to induce much higher levels of DPXLs at equimolar doses than 

acetaldehyde. This is thought to be related to stimulation of acetaldehyde-induced DPXL 

formation by the pH lowering effect of acetic acid production (via vinyl acetate hydrolysis). 

Pretreatment of the nasal turbinates with 1 mM BNPP reduced 25 mM vinyl acetate-induced 

DPXL formation by over 75% in both tissues. These data support a hypothesis that 

carboxylesterase-mediated hydrolysis of vinyl acetate is necessary to generate the active 
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intracellular cross-linking agent, acetaldehyde, and the cytotoxic metabolite, acetic acid. 

[Kuykendall JR et al; Toxicol Appl Pharmacol 123 (2): 283-92] **PEER 

REVIEWED** PubMed Abstract

/ALTERNATIVE and IN VITRO TESTS/ To determine whether exposure to vinyl acetate 

affects the intracellular pH of intact oral cavity tissue, isolated mouse oral buccal epithelium was 

loaded with the pH-sensitive dye BCECF, and then exposed to vinyl acetate concentrations 

ranging from 10 to 1000 um for up to 4 min. Extracellular vinyl acetate exposure induced a 

progressive intracellular acidification that was reversible upon removal of the vinyl acetate. The 

rate of the acidification was concentration-dependent and increased exponentially within the 

concentration range tested. The magnitude of the vinyl acetate-induced acidification was 

inhibited by pretreatment with the carboxylesterase inhibitor bis(p-nitrophenyl)phosphate. These 

results are consistent with the hypothesis that vinyl acetate contributes to the generation and 

progression of oral cavity tumors via a process of intracellular acidification... 

[Nakamoto T et al; Toxicol Lett 158 (2): 116-21 (2005)] **PEER REVIEWED** 

PubMed Abstract

/ALTERNATIVE and IN VITRO TESTS/ ... While vinyl acetate-induced decreases in 

intracellular pH (pHi) have been demonstrated in rat hepatocytes, comparable data from nasal 

epithelial cells do not exist. ...An in vitro assay system /was used to determine/ the effects of 

vinyl acetate exposure on pHi in respiratory and olfactory nasal epithelial cells from rats. The 

respiratory and olfactory epithelial cells were isolated from dissected maxillo- and 

ethmoturbinates by enzyme digestion. The cells were plated; loaded with the pH-sensitive dye, 

carboxyseminaphthorhodafluor-1 (SNARF-1); and observed using confocal microscopy. 

Individual cellular analysis demonstrated that both respiratory and olfactory epithelial cells 

responded to vinyl acetate exposures with a dose-dependent decrease in pHi. Changes occurred 

at 100 uM but reached a plateau above 250 uM. Maximal decreases in pHi were 0.3 pH unit in 

respiratory epithelial cells. While pHi values were normally distributed for the respiratory 

epithelial cells, the olfactory epithelial cells demonstrated a bimodal distribution, indicating at 

least two populations of cells, with only one population of cells responding to vinyl acetate. 

Acidification in these cells did not plateau but continued to increase at 1000 uM. Bis(pnitrophenyl)phosphate (BNPP), a carboxylesterase inhibitor, was able to attenuate the vinyl 

acetate-induced decrease in pHi. ... These results are consistent with the proposed mode of 

action for vinyl acetate and supply further data for developing appropriate risk assessments for 

vinyl acetate exposure. 

[Lantz RC et al; Toxicol Sci 75 (2): 423-31 (2003).] **PEER REVIEWED** PubMed 

Abstract

/ALTERNATIVE and IN VITRO TESTS/ ... Freshly isolated rat hepatocytes were used as a 

model system to test the concept that exposure of cells to vinyl acetate causes a reduction in 

pH(i). Quantitative fluorescence imaging ratio microscopy showed that exposure of hepatocytes 

to vinyl acetate concentrations ranging from 10 to 1000 uM caused rapid and sustained 

reductions of approximately 0.03 to 0.65 pH units. Cellular acidification was rapidly reversed to 

control pH(i) upon removal of vinyl acetate. There was minimal accumulation of protons during 

the exposure period, as suggested by minor differences in pH(i) of cells with or without prior 

exposure to vinyl acetate. The effect of vinyl acetate on pH(i) was attenuated by prior exposure 

to the carboxylesterase inhibitor bis(p-nitrophenyl)phosphate. These results support the concept 

that intracellular acidification is a sentinel pharmacodynamic response of cells to vinyl acetate 
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exposure and that pH(i) is an appropriate metric dose for use in quantitative risk assessments of 

cancer and noncancer human health risk assessment. 

[Bogdanffy MS; Toxicol Sci 66 (2): 320-6 (2002)] **PEER REVIEWED** PubMed 

Abstract

/IMMUNOTOXICITY/ Reductions in relative thymus and/or spleen weight were consistently 

noted in rats and mice exposed to vinyl acetate for 4 weeks and 3 months at exposure 

concentrations of 1,000 ppm, but no gross or histopathological effects were noted in these 

organs. In rats chronically exposed to vinyl acetate, only males exposed to 50 or 600 ppm 

exhibited a decrease in relative spleen weight. The biological significance of these changes is not 

known. They may be suggestive of an immunosuppressive action of vinyl acetate, but the 

appropriate parameters were not investigated to delineate this possibility. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

Ecotoxicity Excerpts:

/AQUATIC SPECIES/ ...Three species of Lecane, a littoral rotifer, /were analyzed/ for 

susceptibility to six metals and four organic toxicants using a fluorometric assay based on 

inhibition of activity of the enzyme phospholipase A2. The metallic toxicants that we tested 

included Cd, Cr, Cu, Pb, Hg (as HgCl2), and Ti; the organic toxicants included benzene, ethyl 

acetate, toluene, and vinyl acetate. The three species differed greatly with respect to their 

susceptibility to the various toxicants. Lecane quadridentata, for example, was particularly 

sensitive to the four organic compounds (median effective concentration values [EC50] ranged 

from 6.6 x 10-4 to 0.987 mg/L). Lecane luna, in contrast, seemed particularly sensitive to metals 

(EC50 values ranged from 2 x 10-6 to 1.92 mg/L). Lecane hamata was relatively insensitive to 

organic solvents (EC50 values ranged from 4.25 to 126.5 mg/L). 

[Perez-Legaspi IA, Rico-Martinez R; Environ Toxicol Chem 22 (10): 2349-53 

(2003)] **PEER REVIEWED** PubMed Abstract

Non-Human Toxicity Values:

LC50 Rat inhalation 3680 ppm/4 hr 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 

LC50 Mouse inhalation 5150 ppm/4 hr 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 

LC50 Guinea pig inhalation 21800 ppm/4 hr 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

LC50 Rabbit inhalation 8800 ppm/4 hr 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 

LD50 Rat oral 2920 mg/kg 

[Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and 

Biologicals. Rahway, NJ: Merck and Co., Inc., 1989., p. 1572] **PEER 

REVIEWED** 

LC50 Mouse inhalation 1550 ppm/4hr 

[Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. 

Louis, MO., 1994, p. 710] **PEER REVIEWED** 

LC50 Rabbit inhalation 2500 ppm/4hr 

[Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. 

Louis, MO., 1994, p. 710] **PEER REVIEWED** 

LD50 Mice oral 1613 mg/kg 

[American Conference of Governmental Industrial Hygienists, Inc. 

Documentation of the Threshold Limit Values and Biological Exposure Indices. 

6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1685] **PEER 

REVIEWED** 

LC50 Guinea pig inhalation 6215 ppm/4 hr 

[American Conference of Governmental Industrial Hygienists, Inc. 

Documentation of the Threshold Limit Values and Biological Exposure Indices. 

6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1685] **PEER 

REVIEWED** 

LC50 Rabbits inhalation 2511 ppm / 4 hr 

[American Conference of Governmental Industrial Hygienists, Inc. 

Documentation of the Threshold Limit Values and Biological Exposure Indices. 

6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1685] **PEER 

REVIEWED** 

LD50 Rabbit dermal 2335 mg/kg 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

LD50 Rat ip 0.71 mL/kg Kg. 

[European Commission, ESIS; IUCLID Dataset, Vinyl acetate (108-05-4) p 105 

(2000 CD-ROM edition). Available from, as of March, 3 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

LD50 Mouse ip 595 mg/kg 

[European Commission, ESIS; IUCLID Dataset, Vinyl acetate (108-05-4) p 106 

(2000 CD-ROM edition). Available from, as of March, 3 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Ecotoxicity Values:

LC50; Species: Carassius auratus (Goldfish, length 3.8-6.4 cm, weight 1-2 g); Conditions: 

freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L CaCO3, 

dissolved oxygen 7.8 mg/L; Concentration: 42330 ug/L for 24-96 hr (95% confidence interval: 

33520-53470 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Lepomis macrochirus (Bluegill, length 3.8-6.4 cm, weight 1-2 g); Conditions: 

freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L CaCO3, 

dissolved oxygen 7.8 mg/L; Concentration: 18530 ug/L for 24 hr (95% confidence interval: 

15730-22070 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Lepomis macrochirus (Bluegill, length 3.8-6.4 cm, weight 1-2 g); Conditions: 

freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L CaCO3, 

dissolved oxygen 7.8 mg/L; Concentration: 18000 ug/L for 48 and 96 hr (95% confidence 

interval: 15040-21540 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1 day); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 172 mg/L CaCO3, alkalinity 144 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 14000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 2 day); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 172 mg/L CaCO3, alkalinity 144 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 15000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1 day); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 164 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 16000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1 day); Conditions: freshwater, 

static, 25 deg C, pH 8.6, hardness 170 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

oxygen saturated; Concentration: 18000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 2 day); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 164 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 18000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, length 3.8-6.4 cm, weight 1-2 g); 

Conditions: freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L 

CaCO3, dissolved oxygen 7.8 mg/L; Concentration: 22170 ug/L for 24 hr (95% confidence 

interval: 19210-27100 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009:

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, length 3.8-6.4 cm, weight 1-2 g); 

Conditions: freshwater, static, 25 deg C, pH 8.2, hardness 360 mg/L CaCO3, alkalinity 300 mg/L 

CaCO3, dissolved oxygen 7.8 mg/L; Concentration: 36810 ug/L for 24 hr (95% confidence 

interval: 32640-42690 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 24000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 4 days); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 164 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 25000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 7.5, hardness 24 mg/L CaCO3, alkalinity 20 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 25000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 4 days); Conditions: freshwater, 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

static, 25 deg C, pH 8.3, hardness 156 mg/L CaCO3, alkalinity 126 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 28000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 8.1, hardness 362 mg/L CaCO3, alkalinity 302 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 42000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 8.2, hardness 312 mg/L CaCO3, alkalinity 260 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 44000 ug/L for 24 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1 day); Conditions: freshwater, 

static, 25 deg C, pH 8.6, hardness 170 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 14000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1 day); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 172 mg/L CaCO3, alkalinity 144 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 14000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 1,2 days); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 164 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 15000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 2 days); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 172 mg/L CaCO3, alkalinity 144 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 15000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, length 3.8-6.4 cm, weight 1-2 g); 

Conditions: freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

CaCO3, dissolved oxygen 7.8 mg/L; Concentration: 19730 ug/L for 96 hr (95% confidence 

interval: 16280-25110 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 7.5, hardness 24 mg/L CaCO3, alkalinity 20 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 20000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 4 days); Conditions: freshwater, 

static, 25 deg C, pH 8.2, hardness 164 mg/L CaCO3, alkalinity 136 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 23000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 24000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, age 4 days); Conditions: freshwater, 

static, 25 deg C, pH 8.3, hardness 156 mg/L CaCO3, alkalinity 126 mg/L CaCO3, dissolved 

oxygen saturated; Concentration: 26000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, length 3.8-6.4 cm, weight 1-2 g); 

Conditions: freshwater, static, 25 deg C, pH 8.2, hardness 360 mg/L CaCO3, alkalinity 300 mg/L 

CaCO3, dissolved oxygen 7.8 mg/L; Concentration: 35750 ug/L for 96 hr (95% confidence 

interval: 31440-41710 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 

deg C, pH 8.1, hardness 362 mg/L CaCO3, alkalinity 302 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 41000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Pimephales promelas (Fathead minnow, adult); Conditions: freshwater, static, 25 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

deg C, pH 8.2, hardness 312 mg/L CaCO3, alkalinity 260 mg/L CaCO3, dissolved oxygen 

saturated; Concentration: 44000 ug/L for 96 hr /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

LC50; Species: Poecilia reticulata (Guppy, age 6 months, length 1.9-2.5 cm, weight 0.1-0.2 g; 

Conditions: freshwater, static, 25 deg C, pH 7.5, hardness 20 mg/L CaCO3, alkalinity 18 mg/L 

CaCO3, dissolved oxygen 7.8 mg/L; Concentration: 31080 ug/L for 24, 48, 96 hr (95% 

confidence interval: 26100-36630 ug/L) /formulation/ 

[Pickering QH, Henderson C; J Water Pollut Control Fed 38 (9): 1419-29 (1966) 

Available from, as of January 26, 2009: 

http://cfpub.epa.gov/ecotox/quick_query.htm ] **PEER REVIEWED** 

Toxicity threshold (cell multiplication inhibition test): Entosiphon sulcatum (protozoa) 81 mg/l 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1185] **PEER REVIEWED** 

Toxicity threshold (cell multiplication inhibition test): Uronema parduczi Chatton-Lwoff 

(protozoa) 91 mg/l 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1185] **PEER REVIEWED** 

Toxicity threshold (cell multiplication inhibition test): Pseudomonas putida (Bacteria) 6 mg/l 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1185] **PEER REVIEWED** 

Toxicity threshold (cell multiplication inhibition test): Microcystis aeruginosa (Algae) 35 mg/l 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1185] **PEER REVIEWED** 

Toxicity threshold (cell multiplication inhibition test): Scenedesmus quadricauda (Green algae) 

370 mg/l 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1185] **PEER REVIEWED** 

LC50; Species: Artemia salina (Brine shrimp, nauplii); Conditions: saltwater, static, 24 deg C; 

Concentration: 45000 ug/L for 24 hr /formulation/ 

[Price KS et al; J Water Pollut Control Fed 46 (1): 63-77 (1974) Available 

from, as of January 26, 2009: http://cfpub.epa.gov/ecotox/quick_query.htm ] 

**PEER REVIEWED** 

LC50; Species: Daphnia magna (Water flea, age <or =24 hr); Conditions: freshwater, static, 20-

22 deg C, pH 7.6-7.7; Concentration: 330000 ug/L for 24 hr /formulation/ 

[Bringmann G, Kuhn R; Z Wasser-Abwasser-Forsch 10 (5): 161-6 (1977) Available 

from, as of January 26, 2009: http://cfpub.epa.gov/ecotox/quick_query.htm ] 

**PEER REVIEWED** 

TSCA Test Submissions:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Teratogenicity was evaluated in mated female Sprague Dawley rats (23/group) orally exposed to 

vinyl acetate in their drinking water at concentrations of 0, 200, 1000 or 5000 ppm on gestation 

days (GD) 6-15. There was a significant difference observed between treated and control animals 

in increased mean pregnancy rates (high-dose group). There were no significant differences 

observed between treated and control animals in the following: maternal mortality, body weight, 

body weight gain and food intake, mean pregnancy rates, numbers of corpora lutea/dam and fetal 

sex ratio, pre- or post-implantation losses, macroscopic fetal changes, mean litter weight and 

fetal weight, external/visceral and skeletal defects and crown rump length.

[Hazelton Laboratories Europe Ltd.; Vinyl Acetate Oral and Inhalation 

Teratology Studies in the Rat. (1980), EPA Document No. FYI-OTS-0184-0278, 

Fiche No. 0000278-0] **UNREVIEWED** 

Teratogenicity was evaluated in mated female Sprague Dawley rats (24/group) orally exposed to 

vinyl acetate in their drinking water at nominal concentrations of 0, 50, 200 or 1000 ppm on 

gestation days (GD) 6-15. There was a significant difference observed between high-dose treated 

group animals and control animals in the following: decreased maternal body weight gain, 

increased incidence of congestion of the lungs, decreased pre-implantation losses and mean litter 

and fetal weights and crown rump length, and increased minor skeletal fetal defects/variants (due 

to retarded sternebral ossification). There were no significant differences observed between 

treated and control animals in the following: maternal mortality, body weight, mean pregnancy 

rates, numbers of corpora lutea/dam and fetal sex ratio, post-implantation losses, and 

external/visceral fetal defects.

[Hazelton Laboratories Europe Ltd.; Vinyl Acetate Oral and Inhalation 

Teratology Studies in the Rat. (1980), EPA Document No. FYI-OTS-0184-0278, 

Fiche No. 0000278-0] **UNREVIEWED** 

The fate of vinyl acetate (VA) was studied using male and female Sprague-Dawley CD rats (2 

and 3/sex for excretion and whole body radiography studies, respectively) exposed by inhalation 

at a dose level of 5000 ppm aqueous solution of 14C-VA. In the excretion study, the rats were 

placed into metabolism cages following dosing and feces, urine, and expired CO2 collected for 

96 hrs, the rats were sacrificed and the carcasses analyzed for radioactivity. Expiration of 14CO2 

accounted for 81.4% of the dose after 24 hrs, 84.6% after 96 hrs. The radioactivity excreted in 

the urine was 3.03% of the dose in 24 hrs, 3.40% in 96 hrs. Fecal excretion accounted for 1.13% 

of the dose and 7.1% was recovered form the carcasses. Elimination was similar for both male 

and female rats. In the radiography study, the rats were placed into Roth-type metabolism cages 

and at 1, 6 and 72 hrs, pairs of rats were sacrificed, the carcasses frozen and cut longitudinally 

into sections, and autoradiographs made at -78 degC for 5 weeks. One hr after dosing, high 

concentrations of radioactivity were found in the Harderian and salivary glands and 

gastrointestinal mucosa, and radioactivity was also readily detected in the liver, lungs, kidneys, 

bone marrow, and the region of the larynx. Six hrs after dosing the distribution of radioactivity 

appeared unchanged but the levels had clearly declined, and at 72 hrs nearly all the radioactivity 

had been eliminated.

[Hazelton Labs. Europe Ltd.; Investigations into the Fate of Vinyl Acetate in 

the Rat and Mouse Part 1. (1979), EPA Document No. FYI-OTS-0184-0278, Fiche 

No. OTS0000278-0] **UNREVIEWED** 

The fate of vinyl acetate (VA) was studied using male and female Sprague-Dawley CD rats (2 

and 8/sex for the excretion and tissue distribution studies, respectively) exposed by gavage to 6 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

hourly 1 ml doses of 10,000 ppm aqueous solution of 14C-VA. In the excretion study, the rats 

were placed into metabolism cages following dosing and feces, urine, and expired CO2 collected 

for 96 hrs. The rats were then sacrificed and the carcasses analyzed for radioactivity. Expiration 

of 14CO2 accounted for 61.2% of the dose during dosing period, 14.3% after 24 hrs, and 61% 

after 96 hrs. The radioactivity excreted in the urine and feces in 96 hrs were 1.8 and 1.4% of the 

dose, respectively, and 5.4% was recovered from the carcasses. Elimination was similar for both 

male and female rats. In the tissue distribution study, the rats were placed in wire cages and at 1, 

2, 7 and 73 hrs after the last dosing, pairs of rats were sacrificed and their tissues analyzed for 

radioactivity. One hr after dosing, high concentrations of radioactivity were found in the 

Harderian (1455 ug Eq 14C-VA/g) and salivary glands (449 ug Eq 14C-VA/g) and ovaries (340 

ug Eq14C-VA/g), and radioactivity was also readily detected (100-200 ug Eq 14C-VA/g) in the 

liver, kidney, stomach, ileum, colon and gastrointestinal contents. At 7 hrs, the levels had clearly 

declined in most tissues, and had markedly reduced in the salivary gland, and at 72 hrs 

radioactivity was highest in the Harderian and adrenal glands, skin and ovaries (female rat). 

[Hazelton Labs. Europe Ltd.; Investigations into the Fate of Vinyl Acetate in 

the Rat and Mouse Part 2. (1980), EPA Document No. FYI-OTS-0184-0278, Fiche 

No. OTS0000278-0] **UNREVIEWED** 

The fate of vinyl acetate (VA) was studied using male and female Sprague-Dawley CD rats (2 

and 4/sex for excretion and whole body radiography studies, respectively) exposed by nose-only 

inhalation to a nominal concentration of 1000 ppm 14C-VA for 6 hrs. In the excretion study, the 

rats were placed into metabolism cages following dosing and feces, urine, and expired CO2 

collected for 96 hrs, the rats were sacrificed and the carcass analyzed for radioactivity. 

Expiration of 14CO2 accounted for 70% of the dose. The radioactivity excreted in the urine, 

feces and carcass in 96 hrs were 7.1, 3.9, and 18.7% of the dose, respectively. Elimination was 

similar for both male and female rats. In the radiography study, the rats were placed into Rothtype metabolism cages and at 0, 1, 6 and 72 hrs, pairs of rats were sacrificed, the carcasses frozen 

and cut longitudinally into sections, and autoradiographs made at -78 degC for 96 hrs. 

Immediately following dosing, high concentrations of radioactivity were found in the Harderian, 

lacrimal and salivary glands and gastrointestinal mucosa, nasoturbinates, kidneys and region of 

the larynx. Radioactivity was also readily detected in the liver, bone marrow, brain and spinal 

cord, and brown fat. One hr after dosing the levels of radioactivity appeared unchanged, at 6 hrs 

they were noticeably lower, and at 72 hrs they had declined markedly but were still detectable in 

the brain, spinal cord, Harderian and adrenal glands, turbinates, maxillary sinuses and kidneys.

[Hazelton Labs. Europe Ltd.; Investigations into the Fate of Vinyl Acetate in 

the Rat and Mouse Part 1. (1979), EPA Document No. FYI-OTS-0184-0278, Fiche 

No. OTS0000278-0] **UNREVIEWED** 

The fate of vinyl acetate (VA) was studied using male and female Sprague-Dawley CD rats (2 

and 8/sex for excretion and tissue distribution studies, respectively) exposed by nose-only 

inhalation to a nominal concentration of 750 ppm 14C-VA for 6 hrs. In the excretion study, the 

rats were placed into metabolism cages following dosing and feces, urine, and expired CO2 

collected for 96 hrs, the rats were sacrificed and the carcass analyzed for radioactivity. 

Expiration of 14CO2 accounted for 74.6% of the dose (most was excreted within 24 hrs). The 

radioactivity excreted in the urine, feces and that remaining in the carcass at 96 hrs were 4.8, 3.6 

and 16.4% of the dose, respectively. In the tissue distribution study, the rats were placed into 

metal cages and at 1, 2, 7 and 73 hrs pairs of rats were sacrificed. At 1 hr after dosing, high 

concentrations (up to 178.7 ugEq/g) of radioactivity were found in the Harderian and salivary 
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glands and gastrointestinal contents, liver, ileum, kidneys, lungs, brain, stomach, colon and 

ovaries. At 2 hrs, the levels of radioactivity appeared marginally reduced, at 7 hrs the distribution 

was similar to that at 1 and 2 hrs. At 72 hrs, they had declined markedly but were > 70 ugEq/g in 

the Harderian and adrenal glands, ovaries and liver.

[Hazelton Labs. Europe Ltd.; Investigations into the Fate of Vinyl Acetate in 

the Rat and Mouse Part 2. (1980), EPA Document No. FYI-OTS-0184-0278, Fiche 

No. OTS0000278-0] **UNREVIEWED** 

The fate of vinyl acetate (VA) was studied using male and female Sprague-Dawley CD rats 

(3/sex for excretion and whole body radiography studies, respectively) exposed by gavage at a 

dose level of 0.25 ml of a 5000 ppm aqueous solution of 14C-VA. The rats were placed into 

Roth-type metabolism cages and at 1, 6 and 72 hrs, 1 male and 1 female rat were sacrificed, the 

carcasses frozen and cut longitudinally into sections, freeze-dried, and autoradiographs made at -

30 degC for 2 weeks. One hr after dosing, high concentrations of radioactivity were found in the 

Harderian, lingual and salivary glands, gastrointestinal mucosa, liver and brown fat and low 

levels radioactivity were also detected in the blood, muscle, fat and testes. Six hrs after dosing 

the distribution of radioactivity appeared unchanged but the levels had clearly declined. At 72 

hrs, radioactivity was still widely distributed at much reduced concentrations, except in the 

gastric mucosa in which a relatively high concentration was still present.

[Hazelton Labs. Europe Ltd.; Investigations into the Fate of Vinyl Acetate in 

the Rat and Mouse Part 2. (1980), EPA Document No. FYI-OTS-0184-0278, Fiche 

No. OTS0000278-0] **UNREVIEWED** 

Metabolism/Pharmacokinetics:

Metabolism/Metabolites:

... /On/ hydrolysis /in the blood/, vinyl acetate yields acetic acid, a normal body constituent, and 

vinyl alcohol, which should rapidly tautomerize to yield acetaldehyde, another normal body 

constituent. 

[Filov VA; Gig Tr Prof Zabol 3: 42-6 (1959) as cited in NIOSH; Criteria 

Document: Vinyl Acetate p.24 (1978) DHEW Pub. NIOSH 78-205] **PEER REVIEWED** 

The hydrolysis of vinyl acetate was studied in vitro with rat liver and lung microsomes, rat and 

human plasma and purified esterases (acetylcholine esterase, butyrylcholine esterase, carboxyl 

esterase). Characterization of the kinetic parameters revealed that rat liver microsomes and 

purified carboxyl esterase (from porcine liver) displayed the highest activity. In order to establish 

the rate of metab of vinyl acetate in vivo, rats were exposed in closed desiccator jar chambers, 

and gas uptake kinetics were studied. The decay of vinyl acetate was dose-dependent, indicating 

possible satn of metabolic pathway(s). The maximal clearance (at lower concn) of vinyl acetate 

from the system (30,000 mL/hr/kg) was similar to the maximal ventilation rate in this species. 

The exposure of rats to vinyl acetate resulted in a transient exhalation of significant amts of 

acetaldehyde into the closed exposure system. 

[Simon P et al; Arch Toxicol 57 (3): 191-5 (1985)] **PEER REVIEWED** PubMed 

Abstract

Gas chromatographic analysis of human whole-blood lymphocyte cultures treated for 10 seconds 

to 20 min with vinyl acetate (5.4 mM) revealed a rapid degradation of vinyl acetate and 
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formation of acetaldehyde. During the 20 min observation period, no degradation of vinyl 

acetate or formation of acetaldehyde were observed in complete culture medium without blood, 

which suggested that the reaction was enzymatic. 

[Norppa H et al; Cancer Res 45 (10): 4816-21 (1985)] **PEER REVIEWED** PubMed 

Abstract

Vinyl acetate hydrolysis has been studied in vitro in the oral mucosal tissues from the oral cavity 

of rats and mice. The hydrolysis activity of the oral tissues is at least 100-fold lower than that of 

the nasal tissues. A physiologically based pharmacokinetic model was developed which 

describes the deposition of vinyl acetate in the nasal cavity of the rat. This model predicts steady 

state concentrations of the metabolite acetic acid after continuing 6 hr-exposure in respiratory 

tissue which are approximately 13 times greater and in olfactory tissue which are approximately 

2 times greater than those of acetaldehyde, the second metabolite. As the concentration of acids 

is indicative for the concentration of protons the model predicts the greatest reduction in 

intracellular pHi for respiratory mucosa. Hence, pH effects should be more pronounced in this 

tissue as compared to other tissues. This physiologically based toxicokinetic/toxicodynamic 

model for rat was modified for the olfactory epithelium of the both human and rat nasal cavity. 

The change in intracellular pH is predicted to be slightly greater for human olfactory epithelium, 

than that of rats. To provide validation data for this model, controlled human exposures at 

exposure levels of 1, 5 and 10 ppm to inhaled vinyl acetate were conducted. Air was sampled by 

a probe inserted into the nasopharyngeal cavity of five volunteers at bi-directional breathing 

through the nose. Data from ion trap mass spectrometry measurements of labeled vinyl acetate 

and acetaldehyde were compared with data from the human nasal model simulation. For the 

vinyl acetate data a good fit was demonstrated (r = 0.9). 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

... Since carboxylesterase-dependent hydrolysis of vinyl acetate (VA) to acetic acid and 

acetaldehyde has been implicated in the nasal inhalation carcinogenesis of this ester, the potential 

for oral mucosa of the F344 rat and BDF mouse to hydrolyze VA was examined. Homogenates 

were prepared by scraping the mucosa from four regions of the oral cavity: dorsal interior (all 

tissues interior to the teeth), dorsal tongue surface, ventral interior (sublingual area and lower 

interior tissues) and exterior (all tissues exterior to the teeth). The oral cavity was rinsed once 

with saline prior to dissection to determine if oral secretions possessed metabolic capacity. 

Aliquots of the homogenates or rinse fluid were incubated for 30 min with varying 

concentrations of vinyl acetate (0.05-10 mM), and the production of acetaldehyde was 

quantitated by HPLC. All tissue regions possessed VA hydrolysis activity. In both species the 

hydrolysis activity was greatest in the dorsal interior region (Vmax of 90 and 6 nmol/min in the 

rat and mouse, respectively, Km values of 0.5 and 0.9 mM). Activity in the other oral regions 

was 2-15-fold lower. Activity was observed in the rinse fluid, but was 20-fold or more lower 

than the dorsal interior region. Finally, solutions of vinyl acetate were placed in the mouth of 

anesthetized rats for 10 min and then analyzed for acetaldehyde concentrations. Acetaldehyde 

was detected in these solutions providing evidence that metabolism of this ester occurs in vivo in 

oral tissues. 

[Morris JB et al; Toxicol Lett 126 (1): 31-9 (2002)] **PEER REVIEWED** PubMed 

Abstract
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The metabolism of vinyl acetate has been studied in animals ... Vinyl acetate is rapidly 

hydrolyzed by esterases in the blood to acetate and the unstable intermediate, vinyl alcohol. 

Vinyl alcohol is rapidly converted to acetaldehyde, which in turn is metabolized to acetate in the 

liver. This in turn is incorporated into the "2 carbon pool" of normal body metabolism and 

eventually forms CO2 as the major breakdown product. Therefore, the metabolism of vinyl 

acetate results in two acetate molecules that enter the 2 carbon pool. This has been confirmed in 

excretion studies that have documented 14CO2 in exhaled air as the major metabolite and source 

of radioactivity recovered following either inhalation or oral exposure to 14C-VA. A very small 

amount also appears to be excreted in the urine as urea and several other unidentified 

metabolites. The metabolic pattern was not influenced by the route of administration. Similar 

results were found in rats exposed to concentrations of vinyl acetate (200-2,000 ppm) in the air 

for 1.4 hours or less. The results show that vinyl acetate is rapidly metabolized by blood 

esterases and that hepatic monooxygenases have a minor role, if any, in the metabolism of vinyl 

acetate. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

In vitro metabolic studies show that vinyl acetate added to preparations of rat liver supernatant 

did conjugate (although not to a large degree) with glutathione. The reaction is mediated by 

glutathione S-transferase and further metabolism produces mercapturic acid derivatives that are 

eliminated in the urine. Rats exposed for 5 hours a day for 6 months to vinyl acetate in the air 

(10, 100, or 500 mg/cu m) showed a significant depletion of free non-protein thiols in the liver 

but not in a dose-dependent pattern. According to the authors, the thiol depletion indicates that 

conjugation with glutathione plays an important role in the detoxification of this chemical. 

Similar results were seen in rats, guinea pigs, and mice given single intraperitoneal doses of 

vinyl acetate. The highest decrease (50%) in SH content was seen in guinea pigs following a 

single intraperitoneal injection of 500 mg/kg vinyl acetate. Glutathione conjugation may 

decrease the toxicity of potentially harmful electrophiles by facilitating excretion into the bile. 

These studies show that vinyl acetate quickly undergoes hydrolysis in the body through several 

intermediate steps to form the principal end products, carbon dioxide and water. The metabolic 

pattern was not influenced by the route of vinyl acetate exposure, but did show nonlinear kinetic 

patterns at high concentrations, indicating that the metabolic processes are saturable. In vivo and 

in vitro tests indicate that vinyl acetate may bind to various degrees with glutathione in different 

species, which may help to detoxify vinyl acetate or its metabolites and enhance their 

elimination. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

Vinyl acetate is hydrolyzed by carboxylesterases to acetic acid and acetaldehyde which is 

subsequently oxidized to acetic acid by aldehyde dehydrogenases. Acetate enters the citric cycle 

in an activated form as acetyl coenzyme A. Vinyl acetate metabolism not only takes place in the 

liver but also in several tissues... 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 
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Absorption, Distribution & Excretion:

... /The/ fate of inhaled vinyl acetate in rabbits /was studied/. ... Vinyl acetate tended to remain 

in the body after it was inhaled; 70% of the vinyl acetate administered was retained, and an 

equilibrium was established in the first few min after exposure began. ... No vinyl acetate /was 

found/ in the blood, either during or after its inhalation, which suggested ... that vinyl acetate is 

rapidly metabolized when it enters the body through the lungs. 

[Filov VA; Gig Tr Prof Zabol 3: 42-6 (1959) as cited in NIOSH; Criteria 

Document: Vinyl Acetate p.24 (1978) DHEW Pub. NIOSH 78-205] **PEER REVIEWED** 

When mice were exposed to (14)C-vinyl acetate, the radioactivity excretion pattern was similar 

to that observed with (14)C-acetaldehyde. In both cases, the majority of radioactivity was 

exhaled as (14)C-carbon dioxide. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 122 (1986)] **PEER REVIEWED** 

Two male Wistar Rats exposed to vinyl acetate (stabilized with 0.01% hydroquinone) 

concentrations varying between 200 and 2000 ppm in closed chambers with an exposure time of 

1.4 hr or less demonstrated dose dependent elimination kinetics. The authors concluded that the 

metabolic pathways became saturated when vinyl acetate exposure levels exceeded 650 ppm 

(2320 mg/cu m). Vinyl acetate deposition was measured in the isolated upper respiratory tract 

(URT) of anaesthetized adult male CrlCD:BR rats at exposure concentrations ranging from 73 to 

2190 ppm during 1 hr inhalation under unidirectional flow conditions (flow rate 100 mL/min) ... 

Preliminary experiments showed that approximately 8 min of exposure was required for vinyl 

acetate to achieve a steady state in nasal tissues. After 8 min of equilibration, impinger samples 

were collected, approximately every 4 min, for up to 40 min and analyzed for vinyl acetate and 

acetaldehyde by gas chromatography ... Acetaldehyde was found in expired air at all vinyl 

acetate exposure concentrations. With increasing the vinyl acetate exposure, concentration of 

acetaldehyde in expired air increased. At vinyl acetate exposure of approximately 1000 ppm the 

concentration of acetaldehyde in the expired air was 277 ppm (499 mg/cu m). 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

Rats were administered oral doses of 14C-vinyl acetate (labeled at the vinyl moiety, 1 mL of a 

10000 ppm (v/v) aqueous solution, overall dose level 297 mg/kg bw) by gastric intubation. The 

dosing regimen was 6 times 1 hour apart. During the dosing regime and subsequent 96 hr 

collection period, a mean of 64.4% of the administered radioactivity was excreted (1.4% in feces, 

1.8% in urine and 61.2% in exhaled air). In addition a mean of 5.4% was found in the carcass at 

96 hr. The major portion of the urinary radioactivity was excreted within the first 24 hr. Most of 

the radioactivity eliminated by the expired air was recovered during the 6 hr dosing regime and 

the first 6 hr after dosing. This portion of radioactivity was recovered from the traps designed for 

collecting carbon dioxide. The authors of the study suppose, that the unaccounted 30.1% of the 

dose were most likely lost in the expired air, which escaped from the metabolism cages when the 

animals were removed for dosing. There was a wide tissue distribution of radioactivity following 

administration of 14C-vinyl acetate by the oral route. One hour after the sixth dose the highest 
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mean concentrations of radioactivity were found in the harderian gland and the submaxillary 

salivary gland. High levels were also found in the liver, kidney, stomach, ileum, colon and 

gastrointestinal tract contents. Low concentrations of radioactivity were found in fat. Attempts 

have been undertaken to determine vinyl acetate metabolites in urine and feces. No radiolabeled 

carbonates or bicarbonates were found in urine or feces. Thin layer chromatography of urine 

indicated that there was one major radioactive fraction and several minor fractions. Exhaled 

radioactivity was entirely present as 14C carbon dioxide. Therefore it can be concluded, that 63 

% of orally applied 14C vinyl acetate is excreted as metabolites. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

... To establish the rate of metabolism of vinyl acetate in vivo, rats were exposed in closed 

desiccator jar chambers, and gas uptake kinetics were studied. The decay of vinyl acetate was 

dose-dependent, indicating possible saturation of metabolic pathway(s). The maximal clearance 

(at lower concentrations) of vinyl acetate from the system (30000 mL/hr per kg body weight) 

was similar to the maximal ventilation rate in this species. This indicated that under conditions 

when metabolic enzymes are not saturated the metabolic rate is mainly determined by pulmonary 

uptake. The exposure of rats to vinyl acetate resulted in a transient exhalation of significant 

amounts of acetaldehyde into to the closed exposure system. This indicates the presence of this 

metabolic intermediate of vinyl acetate in the organism in vivo. 

[Simon P et al; Arch Toxicol 57 (3): 191-5 (1985)] **PEER REVIEWED** PubMed 

Abstract

Wholebody autoradiograms revealed wide tissue distribution with concentration in the Harderian 

and salivary glands. During a 96-hour collection period following exposure, the mean proportion 

of the recovered radioactivity was highest in expired air, with lesser amounts found in urine and 

the least in feces. Seventy-five percent of the radioactivity was eliminated in the first 12 to 24 

hours. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

Biological Half-Life:

... The half-life of /200 uM/ vinyl acetate elimination in human whole blood was 4.1 minutes as 

compared to /less than/ 1 minute in rat whole blood. 

[ATSDR; Toxicological Profile for Vinyl acetate (C4H6O2) Available from, as 

of March, 9 2009: http://www.astdr.cdc.gov/toxprofiles/tp59.html ] **PEER 

REVIEWED** 

Mechanism of Action:

/It has been suggested that/ vinyl acetate disturbs glutathione metabolism, ... by acting as a 

substrate for glutathione transferase. 

[NIOSH; Criteria Document: Vinyl Acetate p.26 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Acetaldehyde is a metabolite of vinyl acetate through esterase-mediated metabolism. It is 
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discussed that vinyl acetate exhibits its genotoxicity via acetaldehyde. For example /researchers/ 

demonstrated that vinyl acetate induces /DNA protein crosslinking/ via acetaldehyde, and ... 

chromosomal damage induced by vinyl acetate in mammalian cell cultures is through formation 

of acetaldehyde ... Acetaldehyde is a naturally occurring substance in the metabolic pathways of 

animals and humans (metabolism of ethanol and sugars). It occurs in small quantities in human 

blood. Therefore, it may well be that acetaldehyde expresses its genotoxic potential in case of 

metabolic overload. 

[European Chemicals Bureau; European Union Risk Assessment Report Draft, 

Vinyl Acetate (108-05-4) (2005). Available from, as of February 27, 2009: 

http://ecb.jrc.ec.europa.eu/esis/ ] **PEER REVIEWED** 

Interactions:

... Previous studies from our laboratory suggest that rat liver microsome-activated vinyl acetate 

induces plasmid DNA-histone crosslinks, in vitro, through esterase-mediated metabolism. Since 

nasal tissues contain high levels of carboxylesterase, tumorigenesis may be related to in situ 

production of the hydrolysis products acetaldehyde and acetic acid. Vinyl acetate was cytotoxic 

to both respiratory and olfactory tissues in vitro at 50-200 mM, but not 25 mM, after 2 hr 

exposure. Pretreatment of rats with the carboxylesterase inhibitor, bis-(p-nitrophenyl) phosphate 

(BNPP), attenuated the cytotoxic effects and metabolism of vinyl acetate in both tissue types. 

Semicarbazide, an aldehyde scavenger, was unable to protect the tissues from vinyl acetateinduced cytotoxicity. When the metabolites were tested, acetic acid, but not acetaldehyde, was 

cytotoxic to both tissues. 

[Kuykendall JR et al; Toxicol Appl Pharmacol 123 (2): 283-92 (1993)] **PEER 

REVIEWED** PubMed Abstract

Pharmacology:

Interactions:

... Previous studies from our laboratory suggest that rat liver microsome-activated vinyl acetate 

induces plasmid DNA-histone crosslinks, in vitro, through esterase-mediated metabolism. Since 

nasal tissues contain high levels of carboxylesterase, tumorigenesis may be related to in situ 

production of the hydrolysis products acetaldehyde and acetic acid. Vinyl acetate was cytotoxic 

to both respiratory and olfactory tissues in vitro at 50-200 mM, but not 25 mM, after 2 hr 

exposure. Pretreatment of rats with the carboxylesterase inhibitor, bis-(p-nitrophenyl) phosphate 

(BNPP), attenuated the cytotoxic effects and metabolism of vinyl acetate in both tissue types. 

Semicarbazide, an aldehyde scavenger, was unable to protect the tissues from vinyl acetateinduced cytotoxicity. When the metabolites were tested, acetic acid, but not acetaldehyde, was 

cytotoxic to both tissues. 

[Kuykendall JR et al; Toxicol Appl Pharmacol 123 (2): 283-92 (1993)] **PEER 

REVIEWED** PubMed Abstract

Environmental Fate & Exposure:
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Environmental Fate/Exposure Summary:

Vinyl acetate's production and use as a monomer for making poly(vinyl acetate) and vinyl 

acetate copolymers, in the production of paints, sealants, coatings, and binders and in 

miscellaneous uses such as chewing gum and tablet coatings may result in its release to the 

environment through various waste streams. If released to air, a vapor pressure of 90.2 mm Hg at 

20 deg C indicates vinyl acetate will exist solely as a vapor in the ambient atmosphere. Vaporphase vinyl acetate is expected to be degraded in the atmosphere by reaction with 

photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to 

be 14 hours. If released to soil, vinyl acetate is expected to have high mobility based upon an 

estimated Koc of 60. Although leaching is possible, concurrent hydrolysis will decrease its 

importance. Volatilization from moist soil surfaces is also expected to be an important fate 

process based upon an estimated Henry's Law constant of 5.1X10-4 atm-cu m/mole. Vinyl 

acetate may volatilize from dry soil surfaces based upon its vapor pressure. Polymerization may 

occur in sunlight. Biodegradation of vinyl acetate may be an important environmental fate 

process in soil under both aerobic (51 to 62% biodegradation reached in 5 day BOD test using 

sewage inoculum) and anaerobic conditions (nearly complete degradation in 26 hrs); reaction 

products of acetaldehyde and acetate are formed under both oxygen conditions. If released to 

water, Vinyl acetate is not expected to adsorb to suspended solids and sediment in water based 

on the estimated Koc value. Volatilization from water surfaces is expected to be an important 

fate process based on its estimated Henry's Law constant. Estimated volatilization half-lives for a 

model river and model lake are 4 hours and 4 days, respectively. A 98% of theoretical BOD was 

reported using activated sludge in the Japanese MITI test, suggesting that biodegradation may be 

an important environmental fate process in water. An estimated BCF of 3.2 suggests the potential 

for bioconcentration in aquatic organisms is low. Degradation by hydrolysis (half-life of 7.3 days 

at 25 deg C and pH 7) and by photochemically produced oxidants will occur. Occupational 

exposure to vinyl acetate may occur through inhalation and dermal contact with this compound 

at workplaces where vinyl acetate is produced or used. The general population may be exposed 

to vinyl acetate through inhalation and dermal contact with products containing vinyl acetate; 

limited exposure may occur via ingestion from its use in chewing gum and tablet coatings. (SRC) 

**PEER REVIEWED** 

Probable Routes of Human Exposure:

NIOSH (NOES Survey 1981-1983) has statistically estimated that 129,024 workers (36,642 of 

these were female) were potentially exposed to vinyl acetate in the US(1). Occupational 

exposure to vinyl acetate may occur through inhalation and dermal contact with this compound 

at workplaces where vinyl acetate is produced or used(SRC). The general population may be 

exposed to vinyl acetate through inhalation and dermal contact with products containing vinyl 

acetate; limited exposure may occur via ingestion from its use in chewing gum and tablet 

coatings(SRC). 

[(1) NIOSH; NOES. National Occupational Exposure Survey conducted from 1981-

1983. Estimated numbers of employees potentially exposed to specific agents 

by 2-digit standard industrial classification (SIC). Available at 

http://www.cdc.gov/noes/ as of Feb 4, 2009.] **PEER REVIEWED** 

School books fabricated with a polyvinyl chloride (PVC) cover were experimentally shown to 
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emit several volatile organic compounds including vinyl acetate in a temperature/relative 

humidity controlled sampling chamber. One book placed with open pages in a chamber at 23 deg 

C over a 24 hour period emitted vinyl acetate at a concentration of 72 ug/cu m(1). Hexcel, a 

graphite/epoxy composite dust used in machining, following mild heating(2). 

[(1) Salthammer T; Organic Indoor Air Pollutants: Volatile Organic 

Ingredients of Household and Consumer Products. Occurrence, Measurement, 

Evaluation. Wiley-VCH: New York, NY p. 225. (1999) (2) Kalman DA; Am Ind Hyg 

Assoc J 47: 270-75 (1986)] **PEER REVIEWED** 

Natural Pollution Sources:

With the exception of an isolated report of an occurrence in trace quantities in plants 

/watercress/, it is not known whether vinyl acetate is a natural product. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39: 119 (1986)] **PEER REVIEWED** 

Artificial Pollution Sources:

Vinyl acetate's production and use as a monomer for making poly(vinyl acetate) and vinyl 

acetate copolymers, in the production of paints, films, sealants, lacquers, coatings, food 

packaging, and binders, in chewing gum and as a tablet coating(1,2) and safety glass(3) may 

result in its release to the environment through various waste streams(SRC). Vinyl acetate can 

be released to the environment from industrial sources and biomass combustion(4). Waste gases 

from scrubbers (generated during the industrial manufacture of vinyl acetate) may contain trace 

levels of vinyl acetate(5). 

[(1) Cordeiro CF; Kirk-Othmer Encycl Chem Tech 4th Ed. New York, NY: JohnWiley 24: 943 (1997) (2) O'Neil MJ, ed; The Merck Index. 14th ed. Whitehouse 

Station, NJ: Merck and Co., Inc., p. 1719 (2006) (3) Lewis RJ Sr; Hawley's 

Condensed Chemical Dictionary 15th ed New York, NY: Van Nostrand Reinhold Co. 

p. 1317 (2007) (4) Graedel TE et al; Atmospheric Chemical Compounds. Sources, 

Occurrence, and Bioassay. Orlando, FL: Academic Press p. 324 (1986) (5) 

Liepins R et al; Industrial Process Profiles for Environmental Use. USEPA600/2-77-023f Chpt 6 p. 6-261 (1977)] **PEER REVIEWED** 

Environmental Fate:

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 

60(SRC), determined from a log Kow of 0.73(2) and a regression-derived equation(3), indicates 

that vinyl acetate is expected to have high mobility in soil(SRC). Volatilization of vinyl acetate 

from moist soil surfaces is expected to be an important fate process(SRC) given an estimated 

Henry's Law constant of 5.1X10-4 atm-cu m/mole(SRC), derived from its vapor pressure, 90.2 

mm Hg(4), and water solubility, 20,000 mg/L(5). However, a hydrolysis half-life of 7.3 days (25 

deg C and pH 7)(6) indicates that hydrolysis may occur in moist soils and is expected to 

attenuate leaching in the soil column(SRC). Vinyl acetate is expected to volatilize from dry soil 

surfaces(SRC) based upon its vapor pressure(4). Vinyl acetate readily polymerizes; therefore, if 

vinyl acetate is released to the environment, polymerization may occur(SRC). Complete 

biodegradation of vinyl acetate occurred using a soil inoculum within 26 hours under both 
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anaerobic and aerobic conditions; acetaldehyde and acetate were formed as reaction products 

under both oxygen conditions(7). This suggests that biodegradation may be an important 

environmental fate process in soil(SRC). 

[(1) Swann RL et al; Res Rev 85: 17-28 (1983) (2) Hansch C et al; Exploring 

QSAR. Hydrophobic, Electronic, and Steric Constants. ACS Prof Ref Book. 

Heller SR, consult. ed., Washington, DC: Amer Chem Soc p. 9 (1995) (3) Lyman 

WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: 

Amer Chem Soc pp. 4-9 (1990) (4) Daubert TE, Danner RP; Physical and 

Thermodynamic Properties of Pure Chemicals: Data Compilation. Design 

Institute Phys Prop Data, Amer Inst Chem Eng. New York, NY: Hemisphere Pub 

Corp (1989) (5) Riddick JA et al; Techniques of Chemistry: Organic Solvents, 

Physical Properties and Methods of Purification. 4th edition. New York, NY: 

John Wiley & Sons (1986) (6) Mabey W, Mill T; J Phys Chem Ref Data 7: 383-415 

(1978) (7) Nieder M et al; Appl Environ Microbiol 56: 3023-28 (1990)] **PEER 

REVIEWED** 

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 60(SRC), 

determined from a log Kow of 0.73(2) and a regression-derived equation(3), indicates that vinyl

acetate is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from 

water surfaces is expected(3) based upon an estimated Henry's Law constant of 5.1X10-4 atm-cu 

m/mole(SRC), derived from its vapor pressure, 90.2 mm Hg(4), and water solubility, 20,000 

mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives 

for a model river and model lake are 4 hours and 4 days, respectively(SRC). According to a 

classification scheme(6), an estimated BCF of 3.2(SRC), from its log Kow(2) and a regressionderived equation(7), suggests the potential for bioconcentration in aquatic organisms is 

low(SRC). Vinyl acetate is degraded in natural water by hydrolysis with an estimated hydrolysis 

half-life at 25 deg C and pH 7 of 7.3 days(8); the hydrolysis rate increases as the pH increases(8). 

Reaction with hydroxyl radicals and singlet oxygen in natural water may proceed with half-lives 

of approximately 13 and 8 days, respectively, based on rates determined for olefinic

structures(9). A 98% of theoretical BOD was reported using activated sludge in the Japanese 

MITI test(10), suggesting that biodegradation may be an important environmental fate process in 

water(SRC). 

[(1) Swann RL et al; Res Rev 85: 17-28 (1983) (2) Hansch C et al; Exploring 

QSAR. Hydrophobic, Electronic, and Steric Constants. ACS Prof Ref Book. 

Heller SR, consult. ed., Washington, DC: Amer Chem Soc p. 9 (1995) (3) Lyman 

WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: 

Amer Chem Soc pp. 4-9, 15-1 to 15-29 (1990) (4) Daubert TE, Danner RP; 

Physical and Thermodynamic Properties of Pure Chemicals: Data Compilation. 

Design Institute Phys Prop Data, Amer Inst Chem Eng. New York, NY: Hemisphere 

Pub Corp (1989) (5) Riddick JA et al; Techniques of Chemistry: Organic 

Solvents, Physical Properties and Methods of Purification. 4th edition. New 

York, NY: John Wiley & Sons (1986) (6) Franke C et al; Chemosphere 29: 1501-

14 (1994) (7) Meylan WM et al; Environ Toxicol Chem 18: 664-72 (1999) (8) 

Mabey W, Mill T; J Phys Chem Ref Data 7: 383-415 (1978) (9) Mill T, Mabey W; 

p. 208-10 in Environ Exposure from Chemicals Vol I; Neely WB, Blau GE eds 

Boca Raton,FL: CRC Press (1985) (10) NITE; Chemical Risk Information Platform 

(CHRIP). Biodegradation and Bioconcentration. Tokyo, Japan: Natl Inst Tech 

Eval. Available at http://www.safe.nite.go.jp/english/db.html as of May 27, 

2009.] **PEER REVIEWED** 

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile 

organic compounds in the atmosphere(1), vinyl acetate, which has a vapor pressure of 90.2 mm 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Hg at 20 deg C(2), is expected to exist solely as a vapor in the ambient atmosphere(SRC). 

Vapor-phase vinyl acetate is degraded in the atmosphere by reaction with photochemicallyproduced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 14 

hours(SRC) calculated from its rate constant of 2.50X10-11 cu cm/molecule-sec at 25 deg C(3). 

Vapor-phase vinyl acetate may also be degraded in the atmosphere by reaction with ozone(4); 

the half-life for this reaction in air is estimated to be 3.9 days(SRC). 

[(1) Bidleman TF; Environ Sci Technol 22: 361-367 (1988) (2) Daubert TE, 

Danner RP; Physical and Thermodynamic Properties of Pure Chemicals: Data 

Compilation. Design Institute Phys Prop Data, Amer Inst Chem Eng. New York, 

NY: Hemisphere Pub Corp (1989) (3) Saunders SM et al; Proc Spie-int Soc Opt 

Eng 1715: 88-99 (1993) (4) Grosjean E; in Amer Chem Soc, Div Environ Chem 

Preprint. 207th ACS Natl Mtg. 34: 705-7 (1994)] **PEER REVIEWED** 

Environmental Biodegradation:

AEROBIC: Values of 42% and 51.3% theoretical of BOD for vinyl acetate were reached in 5 

days when incubated in marine water and sewage inoculum, respectively(1). 62% and 72% of 

theoretical BOD values were measured in 5 and 20 days, respectively, using an acclimated 

sewage inoculum(2); 51 and 69% of theoretical BOD values were measured in 5 and 15 days, 

respectively, in marine water containing a synthetic sewage seed(2). CO2 evolution of 27 and 

49% over 19 and 38 days incubation, respectively, was obtained using a non-acclimated sewage 

inoculum(3); 58% CO2 evolution in 22 days was obtained using an acclimated sewage 

inoculum(3). CO2 evolution of 42% in 10 days was measured using an acclimated sewage 

inoculum(4). Vinyl acetate, initial concentration of 20 mM, was readily degraded using aerobic 

sewage (nearly complete degradation in 7.5 hrs) with reaction products of acetaldehyde and 

acetate formed(5). Vinyl acetate, present at 100 mg/L, reached 98% of its theoretical BOD in 

two weeks using an activated sludge inoculum at 30 mg/L in the Japanese MITI test(6). 

[(1) Takemoto S et al; Suishitsu Odaku Kenkyu 4: 80-90 (1981) (2) Price KS et 

al; J Water Pollut Control Fed 46: 63-77 (1974) (3) Pahren HR, Bloodgood DE; 

Water Pollut Control Fed J 33: 233-8 (1961) (4) Ludzack FJ, Ettinger MB; J 

Water Pollut Control Fed 32: 1173-1200 (1960) (5) Nieder M et al; Appl 

Environ Microbiol 56: 3023-28 (1990) (6) NITE; Chemical Risk Information 

Platform (CHRIP). Biodegradation and Bioconcentration. Tokyo, Japan: Natl 

Inst Tech Eval. Available at http://www.safe.nite.go.jp/english/db.html as of 

May 27, 2009.] **PEER REVIEWED** 

ANAEROBIC: 100% degradation of vinyl acetate was observed following a 3-day lag period 

using the Hungate Serum Bottle technique (anaerobic conditions) and enriched methane 

cultures(1). Vinyl acetate, initial concentration of 20 mM, was readily degraded under anaerobic 

conditions using soil, with nearly complete degradation observed in 26 hrs; using an anaerobic 

sludge inocula nearly complete degradation was observed in 5 hrs(2). Biodegradation products of 

acetaldehyde and acetate were formed(2). 

[(1) Chou WL et al; Biotechnol Bioeng Symp 8: 391-414 (1979) (2) Nieder M et 

al; Appl Environ Microbiol 56: 3023-28 (1990)] **PEER REVIEWED** 

Environmental Abiotic Degradation:

The rate constant for the vapor-phase reaction of vinyl acetate with photochemically-produced 

hydroxyl radicals has been measured as 2.50X10-11 cu cm/molecule-sec at 25 deg C(1). This 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

corresponds to an atmospheric half-life of about 14 hours at an atmospheric concentration of 

5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of vinyl 

acetate with ozone has been measured as 2.92X10-18 cu cm/molecule-sec at 18 deg C(2). This 

corresponds to an atmospheric half-life of about 3.9 days at an atmospheric concentration of 

7X10+11 ozone molecules per cu cm(1). 

[(1) Saunders, SM et al; Proc Spie-int Soc Opt Eng 1715: 88-99 (1993)(2) 

Grosjean D, Grosjean E; in Amer Chem Soc, Div Environ Chem Preprint. 207th 

ACS Natl Mtg. 34: 705-7 (1994)] **PEER REVIEWED** 

The aqueous hydrolysis half-life of vinyl acetate at 25 deg C and pH 7 has been reported to be 

7.3 days(1); the hydrolysis rate will increase as the pH increases(1). A second-order rate constant 

for the basic hydrolysis of vinyl acetate in water at 25 deg C was reported as 4.25 L/molesec(2), corresponding to a half-life of about 2 days at pH 8(SRC). The hydrolysis rate at pH 4.4 

has been reported to be minimal(4). The half-lives for olefinic structures in sunlit natural waters 

are about 13 and 8 days with respect to reaction via hydroxyl radicals and singlet oxygen, 

respectively(3). Vinyl acetate does not absorb UV light above 250 nm in ethanol solvent(4), and 

therefore it may not be susceptible to direct photolysis in sunlight. Vinyl acetate readily 

polymerizes(4,5). 

[(1) Mabey W, Mill T; J Phys Chem Ref Data 7: 383-415 (1978) (2) Drossman H 

et al; Chemosphere 17: 1509-30 (1988) (3) Mill T, Mabey W; p. 208-10 in 

Environ Exposure from Chemicals Vol I; Neely WB, Blau GE eds Boca Raton,FL: 

CRC Press (1985) (4) Daniels W; Kirk-Othmer Encycl Chem Tech 3rd ed NY: Wiley 

23: 817-20 (1983) (5) O'Neil MJ, ed; The Merck Index. 14th ed. Whitehouse 

Station, NJ: Merck and Co., Inc.,p 1719 (2006)] **PEER REVIEWED** 

Environmental Bioconcentration:

An estimated BCF of 3.2 was calculated for vinyl acetate(SRC), using a log Kow of 0.73(1) and 

a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the 

potential for bioconcentration in aquatic organisms is low(SRC). 

[(1) Hansch C et al; Exploring QSAR, Hydrophobic, Electronic, and Steric 

Constants. ACS Prof Ref Book. Washington,DC: Amer Chem Soc (1995) (2) Lyman 

WJ et al; Handbook of Chemical Property Estimation Methods. Washington DC: 

Amer Chem Soc pp. 5-4, 5-10 (1990) (3) Franke C et al; Chemosphere 29: 1501-

14 (1994)] **PEER REVIEWED** 

Soil Adsorption/Mobility:

The Koc of vinyl acetate is estimated as approximately 60(SRC), using a log Kow of 0.73(1) 

and a regression-derived equation(2). According to a classification scheme(3), this estimated 

Koc value suggests that vinyl acetate is expected to have high mobility in soil(SRC). 

[(1) Hansch C et al; Exploring QSAR, Hydrophobic, Electronic, and Steric 

Constants. ACS Prof Ref Book. Washington,DC: Amer Chem Soc (1995) (2) Lyman 

WJ et al; Handbook of Chemical Property Estimation Methods. Washington DC: 

Amer Chem Soc pp. 4-9 (1990) (3) Swann RL et al; Res Rev 85: 23 (1983)] 

**PEER REVIEWED** 

Volatilization from Water/Soil:

The Henry's Law constant for vinyl acetate is estimated as 5.1X10-4 atm-cu m/mole(SRC) 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

derived from its vapor pressure, 90.2 mm Hg at 20 deg C(1), and water solubility, 20,000 

mg/L(2). This Henry's Law constant indicates that vinyl acetate is expected to volatilize rapidly 

from water surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a 

model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 4 

hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind 

velocity of 0.5 m/sec)(3) is estimated as 4.2 days(SRC). The Henry's Law constant of vinyl 

acetate indicates that volatilization from moist soil surfaces may occur(SRC). The potential for 

volatilization of vinyl acetate from dry soil surfaces may exist based upon its vapor pressure(1). 

[(1) Daubert TE, Danner RP; Physical and Thermodynamic Properties of Pure 

Chemicals: Data Compilation. Design Institute Phys Prop Data, Amer Inst Chem 

Eng. New York, NY: Hemisphere Pub Corp (1989) (2) Riddick JA et al; 

Techniques of Chemistry: Organic Solvents, Physical Properties and Methods of 

Purification. 4th edition. New York, NY: John Wiley & Sons (1986) (3) Lyman 

WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: 

Amer Chem Soc pp. 15-1 to 15-29 (1990)] **PEER REVIEWED** 

Environmental Water Concentrations:

SURFACE WATER: Vinyl acetate was detected not quantified in a river water sample from 

Great Britain(1). 

[(1) Fielding M et al; Organic Micropollutants in Drinking Water. TR-159. 

Medmenham, England: Water Research Center (1981)] **PEER REVIEWED** 

GROUND WATER: Vinyl acetate was not detected (detection limit not reported) in 

groundwater samples in EPA region 1-6 and 8-10; no results were given for region 7(1). 

[(1) Plumb RH Jr; in Environ Sci Pollut Control Ser, 4(Groundwater 

Contamination and Analysis at Hazardous Waste Sites): 173-197 (1992)] **PEER 

REVIEWED** 

Effluent Concentrations:

Vinyl acetate was qualitatively detected in wastewater effluents collected from the advanced 

waste treatment facility in Lake Tahoe, CA in Oct 1974(1). A concentration of 50 ppm was 

detected in a wastewater effluent from a polyvinyl acetate plant(2). Vinyl acetate was identified 

in municipal landfill gas at an average concentration of 5663 ppbV(3). Vinyl acetate emission 

factors (based on mass of fuel consumed) were measured in smoke condensates of Ponderosa 

pine wood (3 g/kg, smoldering; 0.05 g/kg, flaming), needles (2.0 g/kg, smoldering), bark (1 g/kg, 

smoldering; 0.5 g/kg, self-substained smoldering), litter (0.7 g/kg, smoldering; 0.5 g/kg, selfsubstained smoldering), duff (0.15 g/kg, smoldering; 0.3 g/kg, self-substained smoldering), and 

humus (not detected, detection limit not specified)(4). Pulverized coal combustion emission 

factors using a small-scale down-fired combustor were reported as follows: not detected to 

4.179X10-7 lb/10+6 Btu for baseline conditions; not detected to 4.274X10-7 lb/10+6 Btu for 

stoichiometric ratio conditions; and 2.081X10-8 to 3.684X10-7 lb/10+6 Btu for low NOx 

conditions (detection limit = 10 ng per sample)(5). 

[(1) Lucas SV; GC/MS Analysis of Organics in Drinking Water Concentrates and 

Advanced Waste Treatment Concentrates: Vol 1. USEPA-600/1-84-020a p. 46,175 

(1984) (2) IARC; Monographs on the Evaluation of the Carcinogenic Risk of 

Chemicals to Humans 39: 113-31 (1986) (3) Brosseau J, Heitz M; Atmos Environ 

28: 285-93 (1994) (4) McKenzie LM et al; Environ Sci Technol 29: 2047-54 

(1995) (5) Miller CA et al; Environ Sci Technol 28: 1150-58 (1994)] **PEER 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

REVIEWED** 

Vinyl acetate can be released to the environment from industrial sources and biomass 

combustion(1). Waste gases from scrubbers (generated during the industrial manufacture of 

vinyl acetate) may contain trace levels of vinyl acetate(2). An emission factor of 6.22 ug/g 

vinyl acetate from extruded ethylene-vinyl acetate and vinyl acetate copolymer (28% vinyl 

acetate) was determined experimentally at 435 deg C under laboratory conditions. All low 

density polyethylene and ethylene-methyl acrylate copolymers with vinyl acetate emitted >0.01 

ug/g vinyl acetate at 435 deg C(3). 

[(1) Graedel TE et al; Atmospheric Chemical Compounds. Sources, Occurrence, 

and Bioassay. Orlando, FL: Academic Press p. 324 (1986) (2) Liepins R et al; 

Industrial Process Profiles for Environmental Use. USEPA-600/2-77-023f Chpt 6 

p. 6-261 (1977) (3) Barlow A et al; J Air Waste Manage Assoc 47: 1111-18 

(1997)] **PEER REVIEWED** 

Atmospheric Concentrations:

URBAN/SUBURBAN: Ambient vinyl acetate air levels of 0.07-0.57 ppm were detected in 

Houston, TX air during June and July 1974(1). Samples of ambient air collected in the vicinity of 

the Kin-Buc waste disposal site (Edison, NJ) between Jun 29 and Jul 1, 1976 contained 0.5 ug/cu 

m vinyl acetate(2). Vinyl acetate was not detected in 8 of 8 urban air samples in Lima, OH, 

1990-91 (detection limit = 7 ug/cu m); not detected in 22 of 22 air samples collected in Houston, 

TX during 1990-91 (detection limit = 7 ug/cu m); and not detected in 22 of 22 air samples 

collected in Boston, MA during 1990-91 (detection limit = 7 ug/cu m)(3). 

[(1) Gordon SJ, Meeks SA; AICHE Symp Ser 73: 84-94 (1977) (2) Pellizzari ED; 

Environ Sci Technol 16: 781-5 (1982) (3) Kelly TJ et al; Ambient concn 

Summaries for Clean Air Act. Title III. Hazardous Air Pollutants. USEPA 

Contract No 68-D80082, EPA/600/R-94/090, Final Report Research Triangle Park 

(1993)] **PEER REVIEWED** 

INDOOR AIR: Vinyl acetate was emitted by a carpet with a PVC backing in an environmental 

chamber at a rate of 853 ug/sq m-hr in a 24 hr period(1). In a field study using an occupied 

townhouse, vinyl acetate was again reported as a major compound emitted from the carpet with 

a PVC backing(1). 

[(1) Hodgson AT et al; J Air Waste Manage Assoc 43: 316-24 (1993)] **PEER 

REVIEWED** 

SOURCE DOMINATED: In a vinyl acetate production plant, air concentrations ranged from 

nondetectable to 173 mg/cu m with a mean of 30 mg/cu m. During hopper cleaning, short-term 

concentration as high as 1150 mg/cu m were measured. Air levels have also been detected in 

various paint, adhesive production and polymerization plants. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. 39: 119 (1986)] **PEER REVIEWED** 

Other Environmental Concentrations:

Drums of chemical waste collected from the North Sea were found to contain vinyl acetate(1). 

[(1) Greve PA; Science 173: 1021-2 (1971)] **PEER REVIEWED** PubMed Abstract
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Environmental Standards & Regulations:

TSCA Requirements:

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting 

Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed 

chemical substances and mixtures to submit to EPA copies and lists of unpublished health and 

safety studies. Vinyl acetate is included on this list. Effective date 2/10/86; Sunset date: 2/10/96. 

[40 CFR 716.120 (USEPA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

CERCLA Reportable Quantities:

Persons in charge of vessels or facilities are required to notify the National Response Center 

(NRC) immediately, when there is a release of this designated hazardous substance, in an amount 

equal to or greater than its reportable quantity of 5000 lb or 2270 kg. The toll free number of the 

NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 

CFR 302.4 (section IV. D.3.b). 

[40 CFR 302.4 (USEPA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

Releases of CERCLA hazardous substances are subject to the release reporting requirement of 

CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR 

part 355. Vinyl Acetate Monomer is an extremely hazardous substance (EHS) subject to 

reporting requirements when stored in amounts in excess of its threshold planning quantity 

(TPQ) of 1,000 lbs. 

[40 CFR 355 (USEPA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

Atmospheric Standards:

This action promulgates standards of performance for equipment leaks of Volatile Organic 

Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The 

intended effect of these standards is to require all newly constructed, modified, and reconstructed 

SOCMI process units to use the best demonstrated system of continuous emission reduction for 

equipment leaks of VOC, considering costs, non air quality health and environmental impact and 

energy requirements. Vinyl acetate is produced, as an intermediate or final product, by process 

units covered under this subpart. 

[40 CFR 60.489 (USEPA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major 

sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and 

phase in specific performance based standards for all air emission sources that emit one or more 

of the listed pollutants. Vinyl acetate is included on this list. 

[Clean Air Act as amended in 1990, Sect. 112 (b) (1) Public Law 101-549 Nov. 

15, 1990] **PEER REVIEWED** 

Clean Water Act Requirements:

Vinyl acetate is designated as a hazardous substance under section 311(b)(2)(A) of the Federal 

Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 

and 1978. These regulations apply to discharges of this substance. This designation includes any 

isomers and hydrates, as well as any solutions and mixtures containing this substance. 

[40 CFR 116.4 (USEPA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

State Drinking Water Guidelines:

(FL) FLORIDA 250 ug/l

[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee 

(FSTRAC). Summary of State and Federal Drinking Water Standards and 

Guidelines (11/93) To Present] **PEER REVIEWED** 

FDA Requirements:

Vinyl acetate is an indirect food additive for use only as a component of adhesives. 

[21 CFR 175.105 (USFDA); U.S. National Archives and Records Administration's 

Electronic Code of Federal Regulations. Available from, as of February 23, 

2009: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

Chemical/Physical Properties:

Molecular Formula:

C4-H6-O2 

[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. 

Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V1 432] **PEER 

REVIEWED** 

Molecular Weight:

86.09 

[Lide, D.R. CRC Handbook of Chemistry and Physics 88TH Edition 2007-2008. CRC 

Press, Taylor & Francis, Boca Raton, FL 2007, p. 3-518] **PEER REVIEWED** 

Color/Form:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

COLORLESS, MOBILE LIQUID 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

Clear, colorless liquid 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

Odor:

An initially pleasant odor which quickly becomes sharp and irritating ... Not unpleasant , 

sweetish smell in small quantities 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

Boiling Point:

72.8 deg C 

[Lide, D.R. CRC Handbook of Chemistry and Physics 88TH Edition 2007-2008. CRC 

Press, Taylor & Francis, Boca Raton, FL 2007, p. 3-518] **PEER REVIEWED** 

Melting Point:

-93.2 deg C 

[Lide, D.R. CRC Handbook of Chemistry and Physics 88TH Edition 2007-2008. CRC 

Press, Taylor & Francis, Boca Raton, FL 2007, p. 3-518] **PEER REVIEWED** 

Critical Temperature & Pressure:

Critical temperature: 486 deg F = 252 deg C = 525 K; critical pressure: 617 atm = 42 PSIA = 

4.25 mN/sq m 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Density/Specific Gravity:

0.932 at 20 deg C/4 deg C 

[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, 

and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 

1719] **PEER REVIEWED** 

Heat of Combustion:

-9754 BTU/lb = -5419 cal/g = -226.9X10+5 J/kg 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

**PEER REVIEWED** 

Heat of Vaporization:

163 BTU/lb = 90.6 cal/g = 3.79X10+5 J/kg 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Octanol/Water Partition Coefficient:

log Kow = 0.73 

[Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - Hydrophobic, Electronic, 

and Steric Constants. Washington, DC: American Chemical Society., 1995., p. 

9] **PEER REVIEWED** 

Solubilities:

Sol in ethane, acetone, chloroform 

[Lide, D.R. CRC Handbook of Chemistry and Physics 88TH Edition 2007-2008. CRC 

Press, Taylor & Francis, Boca Raton, FL 2007, p. 3-518] **PEER REVIEWED** 

Soluble in organic liquids 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

> 10% in ethyl ether; > 10% in ethanol; > 10% in benzene 

[Weast, R.C. and M.J. Astle. CRC Handbook of Data on Organic Compounds. 

Volumes I and II. Boca Raton, FL: CRC Press Inc. 1985., p. V1: 432] **PEER 

REVIEWED** 

At 20 deg C, a saturated solution of vinyl acetate in water contains 2.0-2.4 wt % vinyl acetate, 

whereas a saturated solution of water in vinyl acetate contains 0.9-1.0 wt % water; at 50 deg C, 

the solubility of vinyl acetate in water is 0.1 wt % more than at 20 deg C, but the solubility of 

water in vinyl acetate doubles to about 2 wt % 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

4.0 wt % in dilute (2.0 wt %) solution of sodium lauryl sulfate at 30 deg C 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

In water, 27 g/L at 50 deg C 

[Yalkowsky, S.H., He, Yan., Handbook of Aqueous Solubility Data: An Extensive 

Compilation of Aqueous Solubility Data for Organic Compounds Extracted from 

the AQUASOL dATAbASE. CRC Press LLC, Boca Raton, FL. 2003., p. 95] **PEER 

REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

In water, 20,000 mg/L at 20 deg C 

[Riddick, J.A., W.B. Bunger, Sakano T.K. Techniques of Chemistry 4th ed., 

Volume II. Organic Solvents. New York, NY: John Wiley and Sons., 1985.] 

**PEER REVIEWED** 

Spectral Properties:

MAX ABSORPTION (HEXANE): 258 NM (SHOULDER) (LOG E= -0.3) 

[Weast, R.C. (ed.). Handbook of Chemistry and Physics. 60th ed. Boca Raton, 

Florida: CRC Press Inc., 1979., p. C-86] **PEER REVIEWED** 

Index of refraction: 1.3926 at 25 deg C 

[Olson, K.R. (Ed.); Poisoning & Drug Overdose. 5th ed. Lange Medical 

Books/McGraw-Hill. New York, N.Y. 2007., p. 3-518] **PEER REVIEWED** 

IR: 8112 (Sadtler Research Laboratories IR Grating Collection) 

[Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. 

Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V1: 132] **PEER 

REVIEWED** 

UV: 1-29 (Phillips et al, Organic Electronic Spectral Data, Phillips et al, John Wiley & Sons, 

New York) 

[Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. 

Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V1: 132] **PEER 

REVIEWED** 

1H NMR: 65 (Varian Associates NMR Spectra Catalogue) 

[Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. 

Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V1: 132] **PEER 

REVIEWED** 

MASS: 27875 (NIST/EPA/MSDC Mass Spectral Database 1990 version), 158 (Atlas of Mass 

Spectral Data, John Wiley & Sons, New York) 

[Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. 

Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V1: 132] **PEER 

REVIEWED** 

Surface Tension:

23.95 DYNES/CM= 0.02395 N/M @ 20 DEG C 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Vapor Density:

3.0 (Air = 1) 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Vapor Pressure:

90.2 mm Hg at 20 deg C /extrapolated/ 

[Daubert, T.E., R.P. Danner. Physical and Thermodynamic Properties of Pure 

Chemicals Data Compilation. Washington, D.C.: Taylor and Francis, 1989.] 

**PEER REVIEWED** 

Relative Evaporation Rate:

8.9 (n-Butyl acetate = 1) 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

Viscosity:

0.43 cPs at 20 deg C 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

Other Chemical/Physical Properties:

Wt/gal: 7.79 lb 

[Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John 

Wiley & Sons, Inc. New York, NY 2007., p. 1316] **PEER REVIEWED** 

RATIO OF SPECIFIC HEATS OF VAPOR (GAS): 1.103; HEAT OF POLYMERIZATION: -

439 BTU/LB= -244 CAL/G= -10.2X10+5 J/KG 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Saturation concentration in air: 398 g/cu m at 20 deg C, 634 g/cu m at 30 deg C 

[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. Volumes 

1-2. 4th ed. John Wiley & Sons. New York, NY. 2001, p. 2176] **PEER 

REVIEWED** 

LIQ-WATER INTERFACIAL TENSION: 30 DYNES/CM= 0.03 N/M @ 20 DEG C (EST) 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Polymerizes in light to a colorless transparent mass 

[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, 

and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 

1719] **PEER REVIEWED** 

Polymerizes in light;...may polymerize violently; vapor forms explosive mixtures with air; 

hydrolysis catalyzed by acid- or base-forming acetic acid and acetaldehyde 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39: 114 (1986)] **PEER REVIEWED** 

Stabilized from polymerization with hydroquinone or diphenylamine inhibitors 

[Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John 

Wiley & Sons, Inc. New York, NY 2007., p. 1316] **PEER REVIEWED** 

Henry's Law constant = 5.11X10-4 atm-cu m/mol at 25 deg C (est) 

[SRC; The Physical Properties Database (PHYSPROP). Syracuse, NY: Syracuse Res 

Corp. Available from, as of Jan 29, 2009: 

http://www.syrres.com/esc/physprop.htm ] **PEER REVIEWED** 

Hydroxyl radical reaction rate constant = 2.5X10-11 cu cm/molec-sec at 25 deg C (est) 

[US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.0. Jan, 2009. 

Available from, as of Jan 15, 2009: 

http://www.epa.gov/oppt/exposure/pubs/episuitedl.htm ] **PEER REVIEWED** 

Chemical Safety & Handling:

DOT Emergency Guidelines:

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ Fire or 

Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors 

may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. 

Most vapors are heavier than air. They will spread along ground and collect in low confined 

areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those 

substances designated with "P" may polymerize explosively when heated or involved in a fire. 

Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. 

Many liquids are lighter than water. /Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ Health: 

May cause toxic effects if inhaled or absorbed through skin. Inhalation or contact with material 

may irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. 

Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause 

pollution. /Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ Public 

Safety: CALL Emergency Response Telephone Number ... As an immediate precautionary 

measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep 

unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces 

before entering. /Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ 

Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). 

Structural firefighters' protective clothing will only provide limited protection. /Vinyl acetate, 

stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ 

Evacuation: Large spill: Consider initial downwind evacuation for at least 300 meters (1000 

feet). Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) 

in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. 

/Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ Fire: 

Caution: All these products have a very low flash point: Use of water spray when fighting fire 

may be inefficient. Small fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Do 

not use dry chemical extinguishers to control fires involving nitromethane or nitroethane. Large 

fires: Water spray, fog or alcohol-resistant foam. Do not use straight streams. Move containers 

from fire area if you can do it without risk. Fire involving tanks or car/trailer loads: Fight fire 

from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with 

flooding quantities of water until well after fire is out. Withdraw immediately in case of rising 

sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks 

engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is 

impossible, withdraw from area and let fire burn. /Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ Spill or 

Leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). 

All equipment used when handling the product must be grounded. Do not touch or walk through 

spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, 

basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Absorb or 

cover with dry earth, sand or other non-combustible material and transfer to containers. Use 

clean non-sparking tools to collect absorbed material. Large spills: Dike far ahead of liquid spill 

for later disposal. Water spray may reduce vapor; but may not prevent ignition in closed spaces. 

/Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

/GUIDE 129P: FLAMMABLE LIQUIDS (POLAR/WATER-MISCIBLE/NOXIOUS)/ First Aid: 

Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if 

victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate 

contaminated clothing and shoes. In case of contact with substance, immediately flush skin or 

eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim 

warm and quiet. In case of burns, immediately cool affected skin for as long as possible with 

cold water. Do not remove clothing if adhering to skin. Effects of exposure (inhalation, ingestion 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the 

material(s) involved and take precautions to protect themselves. /Vinyl acetate, stabilized/ 

[U.S. Department of Transportation. 2008 Emergency Response Guidebook. 

Washington, D.C. 2008] **PEER REVIEWED** 

Odor Threshold:

0.12 ppm 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

50% recognition threshold /the concn at which 50% of the odor panel defined the odor as being 

representive of the odorant being studied/: 0.40 ppm; 100% recognition threshold: 0.55 ppm. 

[Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. 

New York, NY: Van Nostrand Reinhold Co., 1983., p. 1184] **PEER REVIEWED** 

Skin, Eye and Respiratory Irritations:

Vinyl acetate vapor at concn below 250 mg/cu m is a primary irritant to the upper respiratory 

tract & eyes & the liquid may irritate the skin ... . 

[Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 

2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 917] **PEER 

REVIEWED** 

Moderate health hazard. May be harmful if inhaled. Irritating to skin, eyes and respiratory 

system. 

[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 

Fire Protection Association, 2002., p. 49-125] **PEER REVIEWED** 

Fire Potential:

It is a highly flammable liq and a dangerous fire hazard. 

[International Labour Office. Encyclopedia of Occupational Health and Safety. 

Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 2260] 

**PEER REVIEWED** 

Highly dangerous fire hazard when exposed to heat, flame or oxidizers. 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

NFPA Hazard Classification:

Health: 2. 2= Materials that, on intense or continued (but not chronic) exposure, could cause 

temporary incapacitation or possible residual injury, including those requiring the use of 

respiratory protective equipment that has an independent air supply. These materials are 

hazardous to health, but areas may be entered freely if personnel are provided with full-face 

mask self-contained breathing apparatus that provides complete eye protection. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

Flammability: 3. 3= This degree includes Class IB and IC flammable liquids and materials that 

can be easily ignited under almost all normal temperature conditions. Water may be ineffective 

in controlling or extinguishing fires in such materials. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

Reactivity: 2. 2= This degree includes materials that are normally unstable and readily undergo 

violent chemical change, but are not capable of detonation. This includes materials that can 

undergo chemical change with rapid release of energy at normal temperatures and pressures and 

materials that can undergo violent chemical changes at elevated temperatures and pressures. This 

also includes materials that may react violently with water or that may form potentially explosive 

mixtures with water. In advanced or massive fires involving these materials, fire fighting should 

be done from a safe distance or from a protected location. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

Flammable Limits:

% BY VOL: LOWER FLAMMABLE LIMIT: 2.6, UPPER FLAMMABLE LIMIT: 13.4 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

Flash Point:

-8 DEG C, 18 DEG F (CLOSED CUP) 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

0.5-0.9 deg C (open cup) 

[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New 

York, NY: John Wiley and Sons, 1978-1984., p. V23 818 (1983)] **PEER 

REVIEWED** 

Autoignition Temperature:

402 DEG C, 756 DEG F 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 325-92] **PEER REVIEWED** 

Fire Fighting Procedures:

Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid 

streams of water may spread fire. Apply water from as far a distance as possible. Cool all 

affected containers with flooding quantities of water. Use "alcohol" foam, dry chemical, or 

carbon dioxide. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Evacuation: If fire becomes uncontrollable or container is exposed to direct flame--consider 

evacuation of 0.5 (1/2) mile radius. If material leaking (not on fire) consider evacuation from 

downwind area based on amount of material spilled, location & weather conditions. /Vinyl 

acetate, inhibited/ 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 

Fight fire from protected location or maximum possible distance. Use water spray, dry chemical, 

"alcohol resistant" foam, or carbon dioxide. Water may be ineffective. Use water only in 

flooding quantities as fog. Use water spray to keep fire-exposed containers cool. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use 

water in flooding quantities as fog. Solid streams of water may spread fire. Cool all affected 

containers with flooding quantities of water. Apply water from as far a distance as possible. Use 

"alcohol" foam, dry chemical or carbon dioxide. 

[Association of American Railroads; Bureau of Explosives. Emergency Handling 

of Hazardous Materials in Surface Transportation. Association of American 

Railroads, Pueblo, CO. 2005, p. 946] **PEER REVIEWED** 

Toxic Combustion Products:

Combustion may produce irritants and toxic gases. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 

Firefighting Hazards:

Vapors are heavier than air and may travel to a source of ignition and flash back. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 

Flammable liquid. Moderate health hazard. 

[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 

Fire Protection Association, 2002., p. 49-152] **PEER REVIEWED** 

Explosive Limits & Potential:

2.6 TO 13.4% 

[International Labour Office. Encyclopedia of Occupational Health and Safety. 

Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 2260] 

**PEER REVIEWED** 

Flammable liquid. Vapors are heavier than air and may travel to a source of ignition and flash 

back. Combustion may produce irritants and toxic gases. Closed containers may rupture violently 

when heated. Liquid floats on water and may spread fire. 

[Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Fire Protection Association, 2002., p. 49-152] **PEER REVIEWED** 

...Reaction with air or water to form peroxides that catalyze an exothermic polymerization 

reaction has caused several large industrial explosions. Reaction with hydrogen peroxide forms 

the explosive peracetic acid. Reacts with oxygen above 50 deg C to form an unstable explosive 

peroxide. Reacts with ozone to form the explosive vinyl acetate ozonide. Solution 

polymerization of the acetate dissolved in toluene has resulted in large industrial explosions. 

Polymerization reaction with dibenzoyl peroxide + ethyl acetate may release ignitalbe and 

explosive vapors. The vapor may reat vigorously with desiccants (e.g., silica gel or alumina). 

Incompatable (explosive) with 2-amino ethanol, chlorosulfonic acid, ethylenediamine, 

ethyleneimine, [hydrochloric acid, hydrofluoric acid, nitric acid], oleum, peroxides, [sulfuric 

acid]. 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

Hazardous Reactivities & Incompatibilities:

Vinyl acetate vapor may react vigorously in contact with silica gel or alumina. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 447] **PEER REVIEWED** 

Reaction with air or water to form peroxides... has caused several large industrial explosions. 

Reaction with hydrogen peroxide forms the explosive peracetic acid. Reacts with oxygen above 

50 deg Celsius... . Reacts with ozone to form the explosive vinyl acetate ozonide.... The vapor 

may react vigorously with desiccants (e.g., silica gel or alumina). Incompatable (explosive) with 

2-amino ethanol, chlorosulfonic acid, ethylenediamine, ethyleneimine, HCl, HF, HNO3, oleum, 

peroxides, H2SO4. 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

MIXING VINYL ACETATE /WITH EACH OF THE FOLLOWING CMPD, 2-

AMINOETHANOL, CHLOROSULFONIC ACID, ETHYLENEIMINE, 36% 

HYDROCHLORIC ACID, 48.7% HYDROFLUORIC ACID, 70% NITRIC ACID, OLEUM, 

96% SULFURIC ACID, & ETHYLENE DIAMINE/ IN A CLOSED CONTAINER CAUSED 

TEMP & PRESSURE TO INCREASE. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 491-205] **PEER REVIEWED** 

POLYMERIZATION OF THE ESTER WITH DIBENZOYL PEROXIDE IN ETHYL 

ACETATE ACCELERATED OUT OF CONTROL & LED TO DISCHARGE OF LARGE 

VOL OF VAPOR WHICH IGNITED & EXPLODED. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 447] **PEER REVIEWED** 

UNSTABILIZED POLYMER EXPOSED TO OXYGEN @ 50 DEG C GENERATED AN 

ESTER-OXYGEN INTERPOLYMERIC PEROXIDE WHICH, WHEN ISOLATED, 
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EXPLODED VIGOROUSLY ON GENTLE HEATING. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 447] **PEER REVIEWED** 

VINYL ACETATE HAD BEEN HYDROXYLATED BY TREATMENT WITH EXCESS 

HYDROGEN PEROXIDE IN PRESENCE OF OSMIUM TETRAOXIDE CATALYST. AN 

EXPLOSION OCCURRED WHILE EXCESS VINYL ACETATE & SOLVENT WERE 

BEING REMOVED BY VACUUM DISTILLATION. THIS WAS ATTRIBUTED TO 

PRESENCE OF PERACETIC ACID, FORMED BY INTERACTION OF EXCESS 

HYDROGEN PEROXIDE WITH ACETIC ACID PRODUCED BY HYDROLYSIS OF THE 

VINYL ACETATE. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 1214] **PEER REVIEWED** 

THE INITIAL EXOTHERM OF SOLN POLYMERIZATION OF THE ESTER IN BOILING 

TOLUENE IN 10 CU M REACTOR WAS TOO GREAT FOR THE COOLING & VENTING 

SYSTEMS, & THE REACTION BEGAN TO ACCELERATE OUT OF CONTROL. FAILURE 

OF A GASKET RELEASED A QUANTITY OF FLAMMABLE REACTION MIXT WHICH ... 

IGNITED & DESTROYED THE CONTAINING BUILDING. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 448] **PEER REVIEWED** 

Acids, bases, silica gel, alumina, oxidizers, azo compounds, ozone [Note: Usually contains a 

stabilizer (e.g., hydroquinone or diphenylamine) to prevent polymerization.]

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Hazardous Decomposition:

WHEN HEATED TO DECOMP, BURNS & EMITS FUMES WITH AN ACRID ODOR. 

[Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, 

NY: Van Nostrand Reinhold, 1984., p. 85] **PEER REVIEWED** 

Hazardous Polymerization:

... TOO LOW A LEVEL OF INHIBITOR & WARM, MOIST STORAGE CONDITIONS MAY 

LEAD TO SPONTANEOUS POLYMERIZATION. THIS PROCESS INVOLVES 

AUTOOXIDATION OF ACETALDEHYDE ... TO PEROXIDE, WHICH INITIATES 

EXOTHERMIC POLYMERIZATION AS IT DCMP. ... OTHER PEROXIDES OR RADICAL 

SOURCES WILL INITIATE EXOTHERMIC POLYMERIZATION. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 447] **PEER REVIEWED** 

Polymerization can be initiated by organic and inorganic peroxides; azo compounds; redox 

systems, which may include organometallic components; light; and high energy radiation. 

[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New 

York, NY: John Wiley and Sons, 1978-1984., p. V23 817 (1983)] **PEER 

REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

VINYL ACETATE IN CONTACT WITH PEROXIDES MAY POLYMERIZE VIOLENTLY. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 491-205] **PEER REVIEWED** 

Hazardous polymerization may occur. Usually contains an inhibitor to prevent selfpolymerization. Polymerization may be caused by elevated temperature, oxidizing. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 

Polymerizes in light;...may polymerize violently; vapor forms explosive mixtures with air; 

hydrolysis catalyzed by acid- or base-forming acetic acid and acetaldehyde 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 114 (1986)] **PEER REVIEWED** 

...it may undergo spontaneous exothermic polymerization. Reaction with air or water to form 

peroxides that catalyze an exothermic polymerization reaction has caused several large industrial 

explosions...Solution polymerization of the acetate disolved in toluene has resulted in large 

industrial explosions. Polymerization reaction with dibenzoyl peroxide + ethyl acetate may react 

release ignitable and explosive vapor ... [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

Other Hazardous Reaction:

THE OZONIDE FORMED BY VINYL ACETATE IS EXPLOSIVE WHEN DRY. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

Butterworth-Heinemann Ltd., 1990, p. 454] **PEER REVIEWED** 

Protective Equipment & Clothing:

/NIOSH/ APPROVED CANISTER OR AIR-SUPPLIED MASK ... RUBBER OR PLASTIC 

GLOVES. 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Respirator selection guide for vinyl acetate: Less than or equal to 140 mg/cu m; type C 

supplied-air respirator with half-mask facepiece operated in pressure-demand mode. Less than or 

equal to 1,400 mg/cu m; gas mask with full facepiece and chin-type organic vapor canister 

(maximum service life, 2 hr), gas mask will full facepiece and chest or back mounted organic 

vapor canister, type C supplied air respirator with full facepiece operated in positive pressure 

mode, self-contained breathing apparatus with full facepiece operated in positive pressure mode. 

Less than or equal to 14,000 mg/cu m; type C supplied-air respirator with half mask or full 

facepiece operated in continuous flow pressure-demand, or other positive pressure mode, type C 

supplied-air respirator with hood, helmet, or suit operated in continuous flow mode. Greater than 
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14,000 mg/cu m; self-contained breathing apparatus with full facepiece operated in pressuredemand or other positive pressure mode, combination type C supplied-air respirator with full 

facepiece operated in pressure demand mode with auxiliary self-contained air supply. Emergency 

(entry into area of unknown concentration); self-contained breathing apparatus with full 

facepiece operated in pressure-demand or other positive pressure mode. 

[NIOSH; Criteria Document: Vinyl acetate p.6 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Wear appropriate personal protective clothing to prevent skin contact. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Wear appropriate eye protection to prevent eye contact. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Eyewash fountains should be provided in areas where there is any possibility that workers could 

be exposed to the substance; this is irrespective of the recommendation involving the wearing of 

eye protection. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Facilities for quickly drenching the body should be provided within the immediate work area for

emergency use where there is a possibility of exposure. [Note: It is intended that these facilities 

provide a sufficient quantity or flow of water to quickly remove the substance from any body 

areas likely to be exposed. The actual determination of what constitutes an adequate quick 

drench facility depends on the specific circumstances. In certain instances, a deluge shower 

should be readily available, whereas in others, the availability of water from a sink or hose could 

be considered adequate.]

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Wear positive-pressure SCBA and protective equipment specified by references such as the DOT 

Emergency Response Guidebook or the CANUTEC Initial Emergency Response Guide. If 

special chemical protective clothing is required, consult the chemical manufacturer or specific 

protective clothing compatibility charts. Delay entry until trained personnel and proper protective 

equipment are available. Remove patient from contaminated area. Quickly remove and isolate 

patient's clothing, jewelry, and shoes. Gently blot excess liquids with absorbent material. Rinse 

patient with warm water, 30 deg C/86 deg F, if possible. Wash patient with Tincture of Green 

Soap or a mild liquid soap and large quantities of water. 

[Bronstein, A.C., P.L. Currance; Emergency Care for Hazardous Materials 

Exposure. 2nd ed. St. Louis, MO. Mosby Lifeline. 1994., p. 221] **PEER 
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REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": ... Dispensers of liq detergent /should be available./ 

... Safety pipettes should be used for all pipetting. ... In animal laboratory, personnel should ... 

wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), 

gloves, hair covering & overshoes. ... In chemical laboratory, gloves & gowns should always be 

worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks 

or respirators may be necessary when working with particulates or gases, & disposable plastic 

aprons might provide addnl protection. ... Gowns ... /should be/ of distinctive color, this is a 

reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 8] **PEER REVIEWED** 

Respirator Recommendations: Up to 40 ppm 

Assigned Protection 

Factor (APF) Respirator Recommendation 

APF = 10 

Any chemical cartridge respirator with organic vapor cartridge(s). 

Substance reported to cause eye irritation or damage; may require eye 

protection. 

APF = 10 Any supplied-air respirator. Substance reported to cause eye irritation or 

damage; may require eye protection. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Respirator Recommendations: Up to 100 ppm 

Assigned Protection 

Factor (APF) Respirator Recommendation 

APF = 25 

Any supplied-air respirator operated in a continuous-flow mode. 

Substance reported to cause eye irritation or damage; may require eye 

protection. 

APF = 25 

Any powered, air-purifying respirator with organic vapor cartridge(s). 

Substance reported to cause eye irritation or damage; may require eye 

protection. 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Respirator Recommendations: Up to 200 ppm 

Assigned 

Protection Factor 

(APF) 

Respirator Recommendation 

APF = 50 Any chemical cartridge respirator with a full facepiece and organic vapor 

cartridge(s). 

APF = 50 Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, 

front- or back-mounted organic vapor canister. 

APF = 50 

Any powered, air-purifying respirator with a tight-fitting facepiece and 

organic vapor cartridge(s). Substance reported to cause eye irritation or 

damage; may require eye protection. 

APF = 50 Any self-contained breathing apparatus with a full facepiece. 

APF = 50 Any supplied-air respirator with a full facepiece. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Respirator Recommendations: Up to 4000 ppm 

Assigned 

Protection Factor 

(APF) 

Respirator Recommendation 

APF = 1000 

Any supplied-air respirator operated in a pressure-demand or other 

positive-pressure mode. Substance reported to cause eye irritation or 

damage; may require eye protection. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Respirator Recommendations: Emergency or planned entry into unknown concentrations or 

IDLH conditions: 

Assigned 

Protection Factor 

(APF) 

Respirator Recommendation 

APF = 10,000 Any self-contained breathing apparatus that has a full facepiece and is 

operated in a pressure-demand or other positive-pressure mode. 

APF = 10,000 

Any supplied-air respirator that has a full facepiece and is operated in a 

pressure-demand or other positive-pressure mode in combination with an 

auxiliary self-contained positive-pressure breathing apparatus. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Respirator Recommendations: Escape conditions: 

Assigned 

Protection Factor 

(APF) 

Respirator Recommendation 

APF = 50 

Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, 

front- or back-mounted organic vapor canister/Any appropriate escape-type, 

self-contained breathing apparatus. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Preventive Measures:

Avoid breathing vapors. Keep upwind. ... Do not handle broken packages unless wearing 

appropriate personal protective equipment. Wash away any material which may have contacted 

the body with copious amt of water or soap & water. Wear appropriate chemical protective 

gloves, boots and goggles. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 

If material not on fire & not involved in fire: Keep sparks, flames, & other sources of ignition 
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away. Keep material out of water sources & sewers. Build dikes to contain flow as necessary. 

Attempt to stop leak if without undue personnel hazard. Use water spray to disperse vapors & 

dilute standing pools of liquid. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 

Keep away from sources of ignition - No smoking. 

[Commission of the European Communities. Legislation on Dangerous Substances 

- Classification and Labelling in the European Communities. Vol. II. London 

and Trotman Ltd., 1989., p. 583] **PEER REVIEWED** 

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit 

or detrimental effects of wearing contact lenses depend not only upon the substance, but also on 

factors including the form of the substance, characteristics and duration of the exposure, the uses 

of other eye protection equipment, and the hygiene of the lenses. However, there may be 

individual substances whose irritating or corrosive properties are such that the wearing of contact 

lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In 

any event, the usual eye protection equipment should be worn even when contact lenses are in 

place. 

**PEER REVIEWED** 

... Chemical safety goggles or face shields (8 inch minimum) with goggles ... /in/ the likelihood 

of exposure to liquid vinyl acetate. ... Protective clothing including gloves, aprons, suits, and 

boots. 

[NIOSH; Criteria Document: Vinyl acetate p.4 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

The worker should immediately wash the skin when it becomes contaminated. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Work clothing that becomes wet or significantly contaminated should be removed and replaced. 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Dike surface flow using 

soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, 

cement powder, or commercial sorbents. Apply "universal" gelling agent to immobilize spill. 

Apply appropriate foam to diminsh vapor and fire hazard. /vinyl acetate, inhibited/ 

[Association of American Railroads. Emergency Handling of Hazardous Materials

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 

Land spill - Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Dike surface 

flow using soil, sand bags, foamed polyurethane, or foamed concrete. /Vinyl acetate, butyl 
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acrylate blend/ 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1107] **PEER REVIEWED** 

Water spill - Use natural barriers or oil spill control booms to limit spill travel. Use surface active 

agent, if approved by EPA. Inject "universal" gelling agent to solidify encircled spill and 

increase effectiveness of booms. If dissolved in region of 10 ppm or greater concentration, apply 

activated carbon at ten times the spilled amount. Remove trapped material with suction hoses. 

Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. 

/Vinyl acetate, inhibited/ 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1108] **PEER REVIEWED**

Air spill - Apply water spray or mist to knock down vapors. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, DC: Association of American Railroads, 

Bureau of Explosives, 1994., p. 1108] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of 

food & beverage containers or utensils, & the application of cosmetics should be prohibited in 

any laboratory. All personnel should remove gloves, if worn, after completion of procedures in 

which carcinogens have been used. They should ... wash ... hands, preferably using dispensers of 

liq detergent, & rinse ... thoroughly. Consideration should be given to appropriate methods for 

cleaning the skin, depending on nature of the contaminant. No standard procedure can be 

recommended, but the use of organic solvents should be avoided. Safety pipettes should be used 

for all pipetting. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 8] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their 

outdoor clothes & wear protective suits (preferably disposable, one-piece & close-fitting at 

ankles & wrists), gloves, hair covering & overshoes. ... Clothing should be changed daily but ... 

discarded immediately if obvious contamination occurs ... /also,/ workers should shower 

immediately. In chemical laboratory, gloves & gowns should always be worn ... however, gloves 

should not be assumed to provide full protection. Carefully fitted masks or respirators may be 

necessary when working with particulates or gases, & disposable plastic aprons might provide 

addnl protection. If gowns are of distinctive color, this is a reminder that they should not be worn 

outside of lab. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 8] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": ... Operations connected with synth & purification ... 
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should be carried out under well-ventilated hood. Analytical procedures ... should be carried out 

with care & vapors evolved during ... procedures should be removed. ... Expert advice should be 

obtained before existing fume cupboards are used ... & when new fume cupboards are installed. 

It is desirable that there be means for decreasing the rate of air extraction, so that carcinogenic 

powders can be handled without ... powder being blown around the hood. Glove boxes should be 

kept under negative air pressure. Air changes should be adequate, so that concn of vapors of 

volatile carcinogens will not occur. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 8] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Vertical laminar-flow biological safety cabinets may 

be used for containment of in vitro procedures ... provided that the exhaust air flow is sufficient 

to provide an inward air flow at the face opening of the cabinet, & contaminated air plenums that 

are under positive pressure are leak-tight. Horizontal laminar-flow hoods or safety cabinets, 

where filtered air is blown across the working area towards the operator, should never be used ... 

Each cabinet or fume cupboard to be used ... should be tested before work is begun (eg, with 

fume bomb) & label fixed to it, giving date of test & avg air-flow measured. This test should be 

repeated periodically & after any structural changes. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 9] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Principles that apply to chem or biochem lab also 

apply to microbiological & cell-culture labs ... Special consideration should be given to route of 

admin. ... Safest method of administering volatile carcinogen is by injection of a soln. Admin by 

topical application, gavage, or intratracheal instillation should be performed under hood. If chem 

will be exhaled, animals should be kept under hood during this period. Inhalation exposure 

requires special equipment. ... Unless specifically required, routes of admin other than in the diet 

should be used. Mixing of carcinogen in diet should be carried out in sealed mixers under fume 

hood, from which the exhaust is fitted with an efficient particulate filter. Techniques for cleaning 

mixer & hood should be devised before expt begun. When mixing diets, special protective

clothing &, possibly, respirators may be required. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 9] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": When ... admin in diet or applied to skin, animals 

should be kept in cages with solid bottoms & sides & fitted with a filter top. When volatile 

carcinogens are given, filter tops should not be used. Cages which have been used to house 

animals that received carcinogens should be decontaminated. Cage-cleaning facilities should be 

installed in area in which carcinogens are being used, to avoid moving of ... contaminated 

/cages/. It is difficult to ensure that cages are decontaminated, & monitoring methods are 
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necessary. Situations may exist in which the use of disposable cages should be recommended, 

depending on type & amt of carcinogen & efficiency with which it can be removed. /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 10] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": To eliminate risk that ... contamination in lab could 

build up during conduct of expt, periodic checks should be carried out on lab atmospheres, 

surfaces, such as walls, floors & benches, & ... interior of fume hoods & airducts. As well as 

regular monitoring, check must be carried out after cleaning-up of spillage. Sensitive methods 

are required when testing lab atmospheres. ... Methods ... should ... where possible, be simple & 

sensitive. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 10] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Rooms in which obvious contamination has 

occurred, such as spillage, should be decontaminated by lab personnel engaged in expt. Design 

of expt should ... avoid contamination of permanent equipment. ... Procedures should ensure that

maintenance workers are not exposed to carcinogens. ... Particular care should be taken to avoid 

contamination of drains or ventilation ducts. In cleaning labs, procedures should be used which 

do not produce aerosols or dispersal of dust, ie, wet mop or vacuum cleaner equipped with highefficiency particulate filter on exhaust, which are avail commercially, should be used. Sweeping, 

brushing & use of dry dusters or mops should be prohibited. Grossly contaminated cleaning 

materials should not be re-used ... If gowns or towels are contaminated, they should not be sent 

to laundry, but ... decontaminated or burnt, to avoid any hazard to laundry personnel. /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 10] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Doors leading into areas where carcinogens are used 

... should be marked distinctively with appropriate labels. Access ... limited to persons involved 

in expt. ... A prominently displayed notice should give the name of the Scientific Investigator or 

other person who can advise in an emergency & who can inform others (such as firemen) on the 

handling of carcinogenic substances. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 11] **PEER REVIEWED** 

Evacuation: If fire becomes uncontrollable or container is exposed to direct flame-consider 
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evacuation of one-half (1/2) mile radius. If material leaking (not on fire) consider evacuation 

from downwind area based on amount of material spilled, location and weather conditions. 

[Association of American Railroads; Bureau of Explosives. Emergency Handling 

of Hazardous Materials in Surface Transportation. Association of American 

Railroads, Pueblo, CO. 2005, p. 946] **PEER REVIEWED** 

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or 

contaminated sites should be contained and evaluated for subject chemical or decomposition 

product concentrations. Concentrations shall be lower than applicable environmental discharge 

or disposal criteria. Alternatively, pretreatment and/or discharge to a POTW is acceptable only 

after review by the governing authority. Due consideration shall be given to remediation worker 

exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and 

disposal. If it is not practicable to manage the chemical in this fashion, it must meet Hazardous 

Material Criteria for disposal. 

**PEER REVIEWED** 

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no 

direct personal contact by personnel who handle, dispose, or clean the clothing. Quality 

assurance to ascertain the completeness of the cleaning procedures should be implemented 

before the decontaminated protective clothing is returned for reuse by the workers. Contaminated 

clothing should not be taken home at end of shift, but should remain at employee's place of work 

for cleaning. 

**PEER REVIEWED** 

Take precautionary measures against static discharges. 

[Commission of the European Communities. Legislation on Dangerous Substances 

- Classification and Labelling in the European Communities. Vol. II. London 

and Trotman Ltd., 1989., p. 587] **PEER REVIEWED** 

Stability/Shelf Life:

... Polymerizes in light ... 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V19 342 (1979)] **PEER REVIEWED** 

Shipment Methods and Regulations:

No person may /transport,/ offer or accept a hazardous material for transportation in commerce 

unless that person is registered in conformance ... and the hazardous material is properly classed, 

described, packaged, marked, labeled, and in condition for shipment as required or authorized by 

... /the hazardous materials regulations (49 CFR 171-177)./ 

[49 CFR 171.2 (7/1/96)] **PEER REVIEWED** 

The International Air Transport Association (IATA) Dangerous Goods Regulations are published 

by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute 

a manual of industry carrier regulations to be followed by all IATA Member airlines when 

transporting hazardous materials. 
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[International Air Transport Association. Dangerous Goods Regulations. 47th 

Edition. Montreal, Quebec Canada. 2006., p. 270] **PEER REVIEWED** 

The International Maritime Dangerous Goods Code lays down basic principles for transporting 

hazardous chemicals. Detailed recommendations for individual substances and a number of 

recommendations for good practice are included in the classes dealing with such substances. A 

general index of technical names has also been compiled. This index should always be consulted 

when attempting to locate the appropriate procedures to be used when shipping any substance or 

article. 

[International Maritime Organization. International Maritime Dangerous Goods 

Code. London, UK. 2004., p. 56] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should be 

avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or 

ampoules, which should themselves be placed inside strong screw-cap or snap-top container that 

will not open when dropped & will resist attack from the carcinogen. Both bottle & the outside 

container should be appropriately labelled. ... National post offices, railway companies, road 

haulage companies & airlines have regulations governing transport of hazardous materials. These 

authorities should be consulted before ... material is shipped. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 13] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure 

must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container 

(primary container), which should be enclosed in a second, unbreakable, leakproof container that 

will withstand chem attack from the carcinogen (secondary container). The space between 

primary & secondary container should be filled with absorbent material, which would withstand 

chem attack from the carcinogen & is sufficient to absorb the entire contents of the primary 

container in the event of breakage or leakage. Each secondary container should then be enclosed 

in a strong outer box. The space between the secondary container & the outer box should be 

filled with an appropriate quantity of shock-absorbent material. Sender should use fastest & most 

secure form of transport & notify recipient of its departure. If parcel is not received when 

expected, carrier should be informed so that immediate effort can be made to find it. Traffic 

schedules should be consulted to avoid ... arrival on weekend or holiday ... /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 13] **PEER REVIEWED** 

Storage Conditions:

It can be stored in steel, aluminum, or stainless steel containers under nitrogen. It is not 

necessary to add stabilizers at lower temperatures. If the vinyl acetate is to be warmed, 

stabilizers, such as hydroquinone, hydroquinone monomethyl ether, or diphenylamine are added. 
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The quantity of stabilizer used is small, e.g., 3 -20 ppm hydroquinone, so that it does not 

generally need to be removed during the later polymerization. 

[Ullmann's Encyclopedia of Industrial Chemistry. 6th ed.Vol 1: Federal 

Republic of Germany: Wiley-VCH Verlag GmbH & Co. 2003 to Present, p. V38 68 

(2003)] **PEER REVIEWED** 

Storage Temperature: Ambient. Inert Atmosphere: No requirement. 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Take precautionary measures against static discharges. 

[Commission of the European Communities. Legislation on Dangerous Substances 

- Classification and Labelling in the European Communities. Vol. II. London 

and Trotman Ltd., 1989., p. 587] **PEER REVIEWED** 

Vinyl acetate shall be stored at temperatures less than 37.8 deg C (100 deg F) in well-ventilated 

areas and kept away from ignition sources such as heat and direct sunlight. No heating apparatus 

capable of exceeding 80% of the autoignition temperature of vinyl acetate (427 deg C) shall be 

used in vinyl acetate storage areas. The storage of vinyl acetate in glass containers should not 

be in the same areas as oxidizing agents or other incompatible chemicals. Containers of vinyl 

acetate shall be kept tightly closed when not in use and shall be stored so as to minimize 

accidental ruptures and spills. 

[NIOSH; Criteria Document: Vinyl acetate p.8-9 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

... VERY SMALL AMT OF HYDROQUINONE ARE ADDED TO IT BUT THEY ARE NOT 

ENOUGH TO AFFECT ITS INTRINSIC TOXICITY (AMT NEEDED TO ACT AS AN 

INHIBITOR IS AT THE MOST 15 PPM). 

[Lefaux, R. Practical Toxicology of Plastics. Cleveland: CRC Press Inc., 

1968., p. 327] **PEER REVIEWED** 

Store in a cool, dry, well ventilated location. Separate from oxidizing materials, peroxides. 

Outside or detached storage is preferred. Inside storage should be in a standard flammable liquid, 

storage warehouse, room, orcabinet. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in 

which carcinogens are to be used, so that only small quantities required for ... expt need to be 

carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof 

refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. 

An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... 

Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 13] **PEER REVIEWED** 
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A storage hazard, it may undergo spontaneous exothermic polymerization. 

[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 

3672] **PEER REVIEWED** 

Cleanup Methods:

Environmental considerations: land spill: Dig a pit, pond, lagoon, holding area to contain liquid 

or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should 

be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, 

foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, 

sawdust, or commercial sorbents. Apply "universal" gelling agent to immobilize spill. Apply 

fluorocarbon-water foam to diminish vapor and fire hazard. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, D.C.: Assoc. of American Railroads, 

Hazardous Materials Systems (BOE), 1987., p. 715] **PEER REVIEWED** 

Environmental considerations: water spill: Use natural barriers or oil spill control booms to limit 

spill travel. Use surface active agent (eg detergent, soaps, alcohols), if approved by EPA. Inject 

"universal" gelling agent to solidify encircled spill and increase effectiveness of booms. If 

dissolved, in region of 10 ppm or greater concn, apply activated carbon @ ten times the spilled 

amount. Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove 

immobilized masses of pollutants and precipitates. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, D.C.: Assoc. of American Railroads, 

Hazardous Materials Systems (BOE), 1987., p. 715] **PEER REVIEWED** 

Notify local health and wildlife officals /in case of spill/. Notify operaters of nearby water 

intakes /in case of spill/. 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Environmental considerations--air spill: Apply water spray or mist to knock down vapors. 

[Association of American Railroads. Emergency Handling of Hazardous Materials 

in Surface Transportation. Washington, D.C.: Assoc. of American Railroads, 

Hazardous Materials Systems (BOE), 1987., p. 715] **PEER REVIEWED** 

Absorb on paper. Evaporate on a glass or iron dish in hood. Burn the paper. 

[ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: 

The International Technical Information Institute, 1988., p. 553] **PEER 

REVIEWED** 

Eliminate all ignition sources. Stop or control the leak, if this can be done without undue risk. 

Use water spray to cool and disperse vapors, protect personnel, and dilute spills to form 

nonflammable mixtures. Control runoff and isolate discharged material for proper disposal. 

Report any release in excess of 5000 lb. 

[Fire Protection Guide to Hazardous Materials. 12 ed. Quincy, MA: National 

Fire Protection Association, 1997., p. 49-135] **PEER REVIEWED** 
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PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or 

charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety 

cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used 

filters can be transferred into plastic bag without contaminating maintenance staff is avail 

commercially. Filters should be placed in plastic bags immediately after removal ... The plastic 

bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids 

... should be placed or collected in proper containers for disposal. The lid should be secured & 

the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer 

surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken 

glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in 

specially designed incinerators. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 15] **PEER REVIEWED** 

Disposal Methods:

SRP: The most favorable course of action is to use an alternative chemical product with less 

inherent propensity for occupational exposure or environmental contamination. Recycle any 

unused portion of the material for its approved use or return it to the manufacturer or supplier. 

Ultimate disposal of the chemical must consider: the material's impact on air quality; potential 

migration in soil or water; effects on animal, aquatic, and plant life; and conformance with 

environmental and public health regulations. 

**PEER REVIEWED** 

The following wastewater treatment technologies have been investigated for vinyl acetate: 

Concentration process: Activated Carbon. 

[USEPA; Management of Hazardous Waste Leachate, EPA Contract No.68-03-2766 

p.E-136 (1982)] **PEER REVIEWED** 

Do not empty into drains. 

[Commission of the European Communities. Legislation on Dangerous Substances 

- Classification and Labelling in the European Communities. Vol. II. London 

and Trotman Ltd., 1989., p. 587] **PEER REVIEWED** 

Vinyl acetate is a waste chemical stream constituent which may be subjected to ultimate 

disposal by controlled incineration. 

[USEPA; Engineering Handbook for Hazardous Waste Incineration p.2-10 (1981) 

EPA 68-03-3025] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has 

been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction 

... published have not been tested on all kinds of carcinogen-containing waste. ... summary of 

avail methods & recommendations ... /given/ must be treated as guide only. /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 
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Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 14] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": ... Incineration may be only feasible method for 

disposal of contaminated laboratory waste from biological expt. However, not all incinerators are 

suitable for this purpose. The most efficient type ... is probably the gas-fired type, in which a 

first-stage combustion with a less than stoichiometric air:fuel ratio is followed by a second stage 

with excess air. Some ... are designed to accept ... aqueous & organic-solvent solutions, 

otherwise it is necessary ... to absorb soln onto suitable combustible material, such as sawdust. 

Alternatively, chem destruction may be used, esp when small quantities ... are to be destroyed in 

laboratory. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 15] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": HEPA (high-efficiency particulate arrestor) filters ... 

can be disposed of by incineration. For spent charcoal filters, the adsorbed material can be 

stripped off at high temp & carcinogenic wastes generated by this treatment conducted to & 

burned in an incinerator. ... LIQUID WASTE: ... Disposal should be carried out by incineration 

at temp that ... ensure complete combustion. SOLID WASTE: Carcasses of lab animals, cage 

litter & misc solid wastes ... should be disposed of by incineration at temp high enough to ensure 

destruction of chem carcinogens or their metabolites. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 15] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": ... Small quantities of ... some carcinogens can be 

destroyed using chem reactions ... but no general rules can be given. ... As a general technique ... 

treatment with sodium dichromate in strong sulfuric acid can be used. The time necessary for 

destruction ... is seldom known ... but 1-2 days is generally considered sufficient when freshly 

prepd reagent is used. ... Carcinogens that are easily oxidizable can be destroyed with milder 

oxidative agents, such as saturated soln of potassium permanganate in acetone, which appears to 

be a suitable agent for destruction of hydrazines or of compounds containing isolated carboncarbon double bonds. Concn or 50% aqueous sodium hypochlorite can also be used as an 

oxidizing agent. /Chemical Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 16] **PEER REVIEWED** 

PRECAUTIONS FOR "CARCINOGENS": Carcinogens that are alkylating, arylating or 

acylating agents per se can be destroyed by reaction with appropriate nucleophiles, such as 

water, hydroxyl ions, ammonia, thiols & thiosulfate. The reactivity of various alkylating agents 

varies greatly ... & is also influenced by sol of agent in the reaction medium. To facilitate the 
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complete reaction, it is suggested that the agents be dissolved in ethanol or similar solvents. ... 

No method should be applied ... until it has been thoroughly tested for its effectiveness & safety 

on material to be inactivated. For example, in case of destruction of alkylating agents, it is 

possible to detect residual compounds by reaction with 4(4-nitrobenzyl)-pyridine. /Chemical 

Carcinogens/ 

[Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. 

Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical 

Carcinogens in the Laboratory: Problems of Safety. IARC Scientific 

Publications No. 33. Lyon, France: International Agency for Research on 

Cancer, 1979., p. 17] **PEER REVIEWED** 

Occupational Exposure Standards:

Threshold Limit Values:

8 hr Time Weighted Avg (TWA): 10 ppm; 15 min Short Term Exposure Limit (STEL): 15 ppm. 

[American Conference of Governmental Industrial Hygienists TLVs and BEIs. 

Threshold Limit Values for Chemical Substances and Physical Agents and 

Biological Exposure Indices. Cincinnati, OH, 2008, p. 59] **PEER REVIEWED** 

A3; Confirmed animal carcinogen with unknown relevance to humans. 

[American Conference of Governmental Industrial Hygienists TLVs and BEIs. 

Threshold Limit Values for Chemical Substances and Physical Agents and 

Biological Exposure Indices. Cincinnati, OH, 2008, p. 59] **PEER REVIEWED** 

NIOSH Recommendations:

Recommended Exposure Limit: 15-Min Ceiling Value: 4 ppm (15 mg/cu m). 

[NIOSH. NIOSH Pocket Guide to Chemical Hazards & Other Databases CD-ROM. 

Department of Health & Human Services, Centers for Disease Prevention & 

Control. National Institute for Occupational Safety & Health. DHHS (NIOSH) 

Publication No. 2005-151 (2005)] **PEER REVIEWED** 

Other Standards Regulations and Guidelines:

The maximum allowable concentrations (MAC's) for Australia, Belgium, Finland, the 

Netherlands, Sweden, and Switzerland for vinyl acetate is 10 ppm, or 30 mg/cu m. The MAC in 

the USSR, Poland, and Yugoslavia is 10 mg/cu m (2.8 ppm). The Romanian limits consist of avg 

and max concn of 50 and 100 mg/cu m (14 and 28 ppm). 

[NIOSH; Criteria Document: Vinyl Acetate p.46 (1978) DHEW Pub. NIOSH 78-205] 

**PEER REVIEWED** 

Emergency Response Planning Guidelines (ERPG): ERPG(1) 5 ppm (no more than mild, 

transient effects) for up to 1 hr exposure; ERPG(2) 75 ppm (without serious, adverse effects) for 

up to 1 hr exposure; ERPG(3) 500 ppm (not life threatening) up to 1 hr exposure. 

[American Induustrial Hygiene Association. AIHA Emergency Response Planning 

Guidelines (ERPG) & Workplace Environmental Exposure Levels (WEEL). Fairfax, 

VA. 2008, p. 27] **PEER REVIEWED** 
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Manufacturing/Use Information:

Major Uses:

In polymerized form for plastic masses, films, and lacquers; in plastic form for food packaging; 

as a modifier for food starch 

[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, 

and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 

1719] **PEER REVIEWED** 

CHEMICAL INTERMEDIATE IN SYNTH OF POLYVINYL ACETATE EMULSIONS, 

RESINS & POLYVINYL ALCOHOL; INTERMEDIATE IN SYNTH OF OTHER 

POLYMERS, RESINS, AND EMULSIONS. 

[SRI] **PEER REVIEWED** 

Safety glass interlayers 

[Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John 

Wiley & Sons, Inc. New York, NY 2007., p. 1317] **PEER REVIEWED** 

Its chief use is as a monomer for making poly(vinyl acetate) and vinyl acetate copolymers, 

which are used as components in coatings, paints, and sealants, binders (adhesives, nonwovens, 

construction products, and carpet-backing) and in miscellaneous uses such as chewing gum and 

tablet coatings. Vinyl acetate is also copolymerized as the minor constituent with vinyl chloride 

and with ethylene to form commercial polymers and with acrylonitrile to form acrylic fibers. 

[Corfeiro CF, Petrocellli FP; Kirk-Othmer Encyclopedia of Chemical 

Technology. (2001). NY, NY: John Wiley & Sons; Vinyl Acetate Polymers. Online 

Posting Date:Jan 14, 2005.] **PEER REVIEWED** 

Used in hair sprays 

[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and 

Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., 

Inc. 1988., p. 906] **PEER REVIEWED** 

Vinyl acetate has been used primarily to produce polyvinyl acetate emulsions and polyvinyl 

alcohol. The principle use of these emulsions has been in adhesives, paints, textiles, and paper 

products. 

[American Conference of Governmental Industrial Hygienists. Documentation of 

the TLV's and BEI's with Other World Wide Occupational Exposure Values. CDROM Cincinnati, OH 45240-1634 2007.] **PEER REVIEWED** 

PRODUCT PROFILE: Vinyl acetate: Polyvinyl acetate accounts for about 48% of vinyl acetate 

monomer (VAM) use, with applications including water-based paints, adhesives, acrylic fibres, 

paper coatings or non-woven binders. Polyvinyl alcohol (PVOH), used in packaging film and 

glass laminates, accounts for about 35% of demand. The remainder goes into ethylene vinyl 

acetate (EVA) polymers, ethylene vinyl alcohol (EVOH) barrier resins. 

[Burridge E; European Chemical News, 75 (1985): 16 (2001); 10-16 December 

2001] **PEER REVIEWED** 
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PRODUCT PROFILE: Vinyl acetate: Vinyl acetate monomer's (VAM) main use is polyvinyl 

acetate which accounts for about 47% of consumption and has applications in water-based 

paints, adhesives, acrylic fibres, paper coatings or non-woven binders. Polyvinyl alcohol 

(PVOH), which is used in packaging film and glass laminates, accounts for about 29% of VAM 

demand. Remaining volumes go into ethylene vinyl acetate (EVA) polymers, ethylene vinyl 

alcohol (EVOH) barrier resins and polyvinyl butyral (PVB). EVA and EVOH are finding new 

uses as copolymers in speciality adhesives and packaging films. 

[Burridge E; European Chemical News, 79 (2069): 14 (2003); 22-28 September 

2003] **PEER REVIEWED** 

CHEMICAL PROFILE: Vinyl Acetate: Vinyl acetate monomer (VAM) is mainly used in 

polyvinyl acetate which has applications in water-based paints, adhesives, acrylic fibres, paper 

coatings and non-woven binders. Polyvinyl alcohol (PVOH), used in packaging film and glass 

laminates, is the second largest consumer. The remaining volumes go into ethylene vinyl acetate 

(EVA) polymers, ethylene vinyl alcohol (EVOH) barrier resins and polyvinyl butyral (PVB). 

[Burridge E; European Chemical News, 83 (2169): 38 (2005); 31 October-6 

November 2005] **PEER REVIEWED** 

Manufacturers:

Celanese Ltd., 1601 West LBJ Freeway, Dallas, TX 75234, (972) 443-4000; Chemicals 

Division; Production sites: Bay City, TX 77404; Clear Lake, TX 77058 

[SRI Consulting. 2008 Directory of Chemical Producers United States. Menlo 

Park, CA 2008, p. 913] **PEER REVIEWED** 

The Dow Chemical Company, 2030 Dow Center, Midland, MI 48642, (989) 636-1000; 

Production site: 3301 Fifth Ave. South, Texas City, TX (409) 945-7411 /Monomer/ 

[SRI Consulting. 2008 Directory of Chemical Producers United States. Menlo 

Park, CA 2008, p. 913] **PEER REVIEWED** 

E.I. Du Pont De Nemours & Company, Inc., 1007 Market Street, Wilmington, DE 19898, (302) 

774-1000; DuPont Performance Materials, DuPont Bldg., Wilmington, DE 19898, (800) 441-

0575; DuPont Packaging and Industrial Polymers; Production site: La Porte, TX 77571 

[SRI Consulting. 2008 Directory of Chemical Producers United States. Menlo 

Park, CA 2008, p. 913] **PEER REVIEWED** 

Millennium Petrochemicals Inc., 11603 Strang Road, La Porte, TX 77571, (713) 767-1071; 

Production site: La Porte, TX 77571 

[SRI Consulting. 2008 Directory of Chemical Producers United States. Menlo 

Park, CA 2008, p. 913] **PEER REVIEWED** 

Methods of Manufacturing:

Addition of acetic acid to acetylene ... in the gas phase in the presence of heterogeneous catalysts 

containing zinc salts. 

[Ullmann's Encyclopedia of Industrial Chemistry. 6th ed.Vol 1: Federal 

Republic of Germany: Wiley-VCH Verlag GmbH & Co. 2003 to Present, p. V38 60 

(2003)] **PEER REVIEWED** 
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Reaction of ethylene with acetic acid and oxygen ... in the gas phase on heterogeneous catalysts 

containing palladium. 

[Ullmann's Encyclopedia of Industrial Chemistry. 6th ed.Vol 1: Federal 

Republic of Germany: Wiley-VCH Verlag GmbH & Co. 2003 to Present, p. V38 60 

(2003)] **PEER REVIEWED** 

REACTION OF ETHYLENE WITH SODIUM ACETATE 

[SRI] **PEER REVIEWED** 

VINYL ACETATE CAN BE MADE BY REACTION OF GLACIAL ACETIC ACID & 

ACETYLENE IN PRESENCE OF MERCURY SALTS. 

[International Labour Office. Encyclopedia of Occupational Health and Safety. 

Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 2260] 

**PEER REVIEWED** 

(a) Vapor-phase reaction of ethylene, acetic acid, and oxygen with a palladium catalyst. (b) 

Vapor-phase reaction of acetylene, acetic acid, & oxygen with zinc acetate catalyst. (c) From 

synthesis gas. 

[Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John 

Wiley & Sons, Inc. New York, NY 2007., p. 1317] **PEER REVIEWED** 

HALCO CONSIDERED A CARBONYLATION PROCESS CONVERTING SYNTHESIS 

GAS TO METHANOL WHICH REACTS WITH CARBON MONOXIDE TO GENERATE 

ACETIC ACID. METHYL ACETATE, MADE FROM METHANOL AND ACETIC ACID, IS 

SUBJECTED TO ANOTHER CARBONYLATION TO YIELD ETHYLIDENE DIACETATE 

TO BE PYROLIZED TO VINYL ACETATE AND ACETIC ACID. 

[CHEMICAL PRODUCTS SYNOPSIS: VINYL ACETATE, 1984] **PEER REVIEWED** 

The acetaldehyde/acetic anhydride process reacts acetic anhydride to yield ethylidene diacetate, 

which then cleaves to form vinyl acetate and acetic acid. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 116 (1986)] **PEER REVIEWED** 

Preparation: Schnizer, US 2859241 (1958 to Celanese); Sharp, Steitz, US 2860159 (1958 to Pan 

Am. Petroleum)... 

[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, 

and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 

1719] **PEER REVIEWED** 

CHEMICAL PROFILE: Vinyl acetate: Ethylene is now the preferred feedstock for VAM /vinyl 

acetate monomer/, largely replacing the earlier acetylene-based process. VAM is usually 

produced by the catalysed vapour phase reaction of acetic acid with ethylene and oxygen in a 

fixed bed tubular reactor using a supported noble metal catalyst. The reaction is carried out at 

175-200 deg C and 5-9 bar pressure. VAM is recovered by condensation, scrubbed and purified 

by distillation. 

[Burridge E; European Chemical News, 83 (2169): 38 (2005); 31 October-6 

November 2005] **PEER REVIEWED** 
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General Manufacturing Information:

Vinyl acetate is polymerized either alone or mixed with vinyl chloride ..., acrylic esters, maleic 

acid and vinyl benzoate. 

[Lefaux, R. Practical Toxicology of Plastics. Cleveland: CRC Press Inc., 

1968., p. 80] **PEER REVIEWED** 

... stabilized with either hydroquinone or diphenylamine inhibitors. The hydroquinone-stabilized 

material can be polymerized without redistillation. The diphenylamine-stabilized material must 

be distilled prior to polymerization. 

[Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John 

Wiley & Sons, Inc. New York, NY 2007., p. 1317] **PEER REVIEWED** 

Saponified copolymers of vinyl acetate are used as emulsifying agents for oil/water type 

cosmetics, agrochemical formulations, paints, and pharmaceuticals. 

[Jpn Kokai Tokyo Koho PATENT NO 8300234 (01/05/83) (Kuraray Co, Ltd)] **PEER 

REVIEWED** 

Polymerization is inhibited or strongly retarded by aromatic hydroxyl, nitro, or amine 

compounds and by oxygen, quinone, crotonaldehyde, copper salts, sulfur, conjugated 

polyolefins. ... Vinyl acetate has been polymerized in bulk, suspension, solution, and emulsion. 

It copolymerizes readily with some monomers but not with others. 

[Kirk-Othmer Encyclopedia of Chemical Technology. 4th ed. Volumes 1: New 

York, NY. John Wiley and Sons, 1991-Present., p. V24: 944] **PEER REVIEWED** 

Vinyl acetate is normally inhibited with hydroquinone to prevent polymerization. 

[Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: 

Butterworths, 1985., p. 430] **PEER REVIEWED** 

The preparation of ethylene-vinyl acetate copolymer matrices for use as drug carriers on 

intrauterine devices is described. /Ethylene-vinyl acetate copolymer/ 

[Burns JW et al; Contraception 26: 521-33 (1982)] **PEER REVIEWED** PubMed 

Abstract

A soil fumigant (eg, chloropicrin, methyl bromide, ethyl bromide, dibromopropane) is applied to 

soil and then the soil surface is sprayed with a soil-aggregating agent (e.g., vinyl acetate, vinyl 

propionate, methyl acrylate, poly(vinyl alcohol), CM-cellulose) to cover the soil surface for 

sealing the fumigant gas. 

[Jpn Kokai Tokkyo Koho Patent No 81110601 (09/01/81) (Mitsubishi 

Petrochemical Co, Ltd)] **PEER REVIEWED** 

Vinyl acetate was treated with dicyclopentadiene under nitrogen atm at 185-90 deg for 10 hr to 

give 2-acetoxynorbornene, which was treated with potassium hydroxide soln at 150-5 deg for 2 

hr to form 2-hydroxynorborn-5-ene. A solid fragrance and deodorant cmpd was prepd containing 

10.0 g 2-hydroxynorborn-5-ene. 

[Jpn Tokkyo Koho Patent No 8316900 (04/02/83) (Nippon Zeon Co, Ltd)] **PEER 

REVIEWED** 

Vinyl acetate, acetic anhydride, ethanol, methanol, and formaldehyde were formed in aq extracts 
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of polyvinyl acetate films only in some cases and in insignificant quantities. The difference 

between pH of aq extracts of polyvinyl acetate films and pH of the control (distilled water) the 

extracts from unsterilized films are more alk and those from sterilized films are more acidic than 

the distilled water control. Bromo cmpd were present up to 6.4 mg bromide/L in polyvinyl 

acetate film extracts and up to 12.3 mg bromide/L in inactivated extracts. The oxidizability of the 

polyvinyl acetate films was around 324-1310 mg/L and was highly dependent on the time of 

contact of the films with water. Aq extracts of various films contained 80-360 mg/L polyvinyl 

acetate. Sterilization by gamma-rays did not lead to substantial changes in hygienic-chem 

properties of the films. An increase in the irradiation dose up to 0.3 megagray decreased the 

oxidizability of aq extracts and the polyvinyl acetate content in the films. The quantities of 

formaldehyde and methanol formed are lower than the accepted quantities of migration of these 

substances into food products. Thus, polyvinyl acetate has satisfactory properties for medicinal 

use. 

[Boikova ZK et al; Plast Massy (5): 19-21 (1985)] **PEER REVIEWED** 

A cmpd, containing allethrin and vinyl acetate resin emulsion (1 part) was mixed with silica gel 

powder (4 parts) to yield a slow-release insecticide. 

[Jpn Kokai Tokkyo Koho Patent No 83113102 (07/05/83) (Earth Chemical Co, 

Ltd)] **PEER REVIEWED** 

Makeups contain film-forming copolymers of ... vinyl acetate. 

[Jpn Kokai Tokkyo Koho Patent No 8538312 (02/27/85) (Pola Chemical 

Industries, Inc)] **PEER REVIEWED** 

Microcapsules (diam 1-40 um) for makeup containing polyethylene glycol, alcs, 

polysaccharides, amino acids, etc which hold moisture in the skin. The capsules are made of 

polymers of acrylic acid, vinyl acetate, vinyl chloride, etc. 

[Horino M et al; Jpn Kokai Tokkyo Koho Patent No 85224609 (11/09/85) (Pola 

Chemical Industries, Inc)] **PEER REVIEWED** 

Formulations/Preparations:

Various commercial grades of vinyl acetate are available in USA, which differ only in the amt 

of inhibitor added: 3-5 mg/L (ppm) hydroquinone are present when use is expected within 2 mo 

of delivery; 14-17 mg/L (ppm) hydroquinone for up to 4 mo of storage; & 200-300 mg/L (ppm) 

diphenylamine when indefinite storage is anticipated. 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 114 (1986)] **PEER REVIEWED** 

GRADES OR PURITY: GRADE A (DIPHENYLAMINE-INHIBITED): 99.8%; GRADE H 

(HYDROQUINONE-INHIBITED): 99.8% 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Impurities:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

Typical /USA/ specifications are: ... acidity (as acetic acid), aldehydes (as acetaldehyde), 0.005% 

max, water, 0.04% max ... 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 114 (1986)] **PEER REVIEWED** 

In western Europe, vinyl acetate produced by the gas-phase ethylene process has the following 

typical specifications: ... ethyl acetate, 323 mg/kg (ppm): water, 240 mg/kg (ppm); methyl 

acetate, 175 mg/kg (ppm); acetaldehyde, 6 mg/kg (ppm); & acrolein, 1 mg/kg (ppm). 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 115 (1986)] **PEER REVIEWED** 

Typical specifications for vinyl acetate in Japan are as follows: ... free acid (as acetic acid), 

0.01% max; free aldehydes (as acetaldehyde), 0.05% max ... moisture, 0.2% max ... 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 115 (1986)] **PEER REVIEWED** 

Consumption Patterns:

60% FOR POLYVINYL ACETATE EMULSIONS AND RESINS; 15% FOR POLYVINYL 

ALCOHOL; 9% FOR VINYL CHLORIDE COPOLYMERS; 8% FOR POLYVINYL 

BUTYRAL; 3% FOR ETHYLENE-VINYL ACETATE RESINS AND EMULSIONS; 1% 

FOR POLYVINYL FORMAL; 4% FOR MISC APPLICATIONS AS A COPOLYMER (1971) 

[SRI] **PEER REVIEWED** 

20% FOR ADHESIVE EMULSIONS; 17% FOR PAINT EMULSIONS; 12% FOR TEXTILE 

AND PAPER EMULSIONS; 23% FOR POLYVINYL ALCOHOL; 10% FOR 

ETHYLENE/VINYL/VINYL ACETATE; 8% FOR POLYVINYL BUTYRAL; 5% FOR 

POLYVINYL CHLORIDE COPOLYMERS; 5% FOR MISC (1984 EST) 

[CHEMICAL PRODUCTS SYNOPSIS: VINYL ACETATE, 1984] **PEER REVIEWED** 

CHEMICAL PROFILE: Vinyl acetate. Polyvinyl acetate emulsions and resins, 40%; (this area 

is divided evenly between paints and adhesives); polyvinyl alcohol, 15%; polyvinyl butyral, 8%; 

ethylene-vinyl acetate resins, 6%; polyvinyl chloride copolymers, 3%; miscellaneous, 1%; 

exports, 27%. 

[Kavaler AR; Chemical Marketing Reporter 235 (16): 50 (1989)] **PEER 

REVIEWED** 

CHEMICAL PROFILE: Vinyl acetate. US Demand: 1988: 2.56 billion pounds; 1989: 2.62 

billion pounds; 1993: 2.9 billion pounds /projected/ (Includes exports, but not imports, which 

averaged 6 million lb over the last three years.) 

[Kavaler AR; Chemical Marketing Reporter 235 (16): 50 (1989)] **PEER 

REVIEWED** 

CHEMICAL PROFILE: Vinyl Acetate: Polyvinyl acetate emulsions and resins, 57%; polyvinyl 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

alcohol, 19%; polyvinyl butyral, 10%; ethylene-vinyl acetate resins, 8%; ethylene vinyl alcohol, 

2%; miscellaneous, including polyvinyl chloride copolymers, 4%. 

[Anonymous; Chemical Marketing Reporter. May 8, 1995] **PEER REVIEWED** 

CHEMICAL PROFILE: Vinyl Acetate: US Demand: 1994: 3 billion pounds; 1995: 3.1 billion 

pounds (includes exports, which were 885 million pounds in 1993, but not imports, which were 

100 million pounds). 

[Anonymous; Chemical Marketing Reporter. May 8, 1995] **PEER REVIEWED** 

PRODUCT PROFILE: VAM /vinyl acetate monomer/: World demand was 4.11 million tonnes 

last year against a capacity of about 4.7 million tonnes ... . The US is the world's largest exporter 

and Asia is the biggest importer, followed by Europe. 

[Burridge E; European Chemical News, 75 (1985): 16 (2001); 10-16 December 

2001] **PEER REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Demand: 2003: 4.3 million 

tonnes. Polyvinyl acetate, 44%; polyvinyl acetate, 40%; ethylene vinyl alcohol, 12%. 

[Anonymous; Chemical Week, 165 (23): 31 (2003); 25 June 2003] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Demand: 2004: 4.4 million 

tonnes. Polyvinyl acetate, 44%; polyvinyl acetate, 41%; ethylene-vinyl acetate copolymers, 9%; 

Other, 6%. 

[Anonymous; Chemical Week, 167 (23): 39 (2005); 13 July 2005] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Demand: 2006: 4.8 million 

tonnes. Polyvinyl acetate, 43%; polyvinyl acetate, 42%; ethylene-vinyl acetate copolymers, 9%; 

Other, 6%. 

[Anonymous; Chemical Week, 169 (20): 41 (2007); 13 June 2007] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Capacity: 2003: 5 million tonnes. 

Asia, 43%; North America, 34%; Western Europe, 18%; Others, 5%. 

[Anonymous; Chemical Week, 165 (23): 31 (2003); 25 June 2003] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Capacity: 2005: 5.3 million 

tonnes. Asia/Pacific, 48%; North America, 31%; Western Europe, 17%; Other, 4%. 

[Anonymous; Chemical Week, 167 (23): 39 (2005); 13 July 2005] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global Capacity: 2006: 5.8 million 

tonnes. Asia/Pacific, 50%; North America, 29%; Western Europe, 16%; Other, 5%. 

[Anonymous; Chemical Week, 169 (20): 41 (2007); 13 June 2007] **PEER 

REVIEWED** 

U. S. Production:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

(1972) 5.50X10+11 g 

[SRI] **PEER REVIEWED** 

(1975) 5.86X10+11 g

[SRI] **PEER REVIEWED** 

(1984) 9.17X10+11 g 

[USITC. SYN ORG CHEM-U.S.A. PROD/SALES 1984 p.257] **PEER REVIEWED** 

(1985) 2.11X10+9 lb 

[USITC. SYN ORG CHEM-U.S.A. PROD. PRELIMINARY Mar 31, 1987 (SERIES C/P-87-1)] 

**PEER REVIEWED** 

(1986) 2.24x10+9 lb 

[USITC. SYN ORG CHEM-U.S.A. PROD. PRELIMINARY Feb 26, 1988 (SERIES C/P-87-5)] 

**PEER REVIEWED** 

(1987) 2.205 billion lb 

[Chem & Eng News; 65 (23): 30 (1987)] **PEER REVIEWED** 

(1988) 2.56 billion lb 

[United States International Trade Commission. Synthetic Organic ChemicalsUnited States Production and Sales, 1988. USITC Publication 1989. Washington, 

DC: United States International Trade Commission, 1989., p. 15-6] **PEER 

REVIEWED** 

(1990) 2.66 billion lb 

[Chem & Engineering News 70 (15): 17 (4/13/92)] **PEER REVIEWED** 

(1991) 2.73 billion lb 

[Chem & Engineering News 71 (15): 11 (4/12/93)] **PEER REVIEWED** 

(1992) 2.66 billion lb 

[Chem & Engineering News 72 (15): 13 (4/11/94)] **PEER REVIEWED** 

(1993) 2.83 billion lb 

[Chem & Engineering News 72 (15): 13 (4/11/94)] **PEER REVIEWED** 

Acetic acid ethenyl ester is listed as a High Production Volume (HPV) chemical (65FR81686). 

Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 

1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR 

part 710 subpart B; 51FR21438). 

[EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) 

Challenge Program. Available from the Database Query page at: 

http://www.epa.gov/hpv/pubs/general/opptsrch.htm on Acetic Acid Ethenyl Ester 

(108-05-4) as of February 24, 2009] **PEER REVIEWED** 

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. 

Year Production Range (pounds) 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

1986 greater than 1 billion 

1990 greater than 1 billion 

1994 greater than 1 billion 

1998 greater than 1 billion 

2002 greater than 1 billion 

[US EPA; Non-confidential Production Volume Information Submitted by 

Companies for Chemicals Under the 1986-2002 Inventory Update Rule (IUR). 

Acetic acid ethenyl ester (108-05-4). Available from, as of February 24, 

2009: http://www.epa.gov/oppt/iur/tools/data/2002-vol.html ] **PEER 

REVIEWED** 

PRODUCT PROFILE: Vinyl Acetate: Global vinyl acetate monomer capacity in 2001 

(thousand tonnes/year) 

Global VAM /vinyl acetate monomer/ capacity in 2001 (thousand tonnes/year)

Country 

Capacity 

Europe 

- Armenia 50 

- France 150 

- Germany 320 

- Lithuania 20 

- Romania 20 

- Russia 72 

- Spain 110 

- UK 365 

- Ukraine 30 

Americas 

- Brazil 80 

- Canada 85 

- Mexico 110 

- USA 1,560 

Asia/Middle East 

- China 352 

- India 50 

- Iran 30 

- Japan 566 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

- Singapore 190 

- South Korea 150 

- Taiwan 240 

[Burridge E; European Chemical News, 75 (1985): 16 (2001); 10-16 December 

2001] **PEER REVIEWED** 

PRODUCT PROFILE: Vinyl Acetate: European vinyl acetate monomer capacity in 2003 

(thousand tonnes/year) 

European vinyl acetate monomer capacity in 2003 (thousand tonnes/year)

Country 

Capacity 

Armenia 50 

France 185 

Germany 360 

Lithuania 20 

Poland 12 

Romania 20 

Russia 50 

Serbia 65 

Slovakia 15 

Spain 110 

UK 250 

Ukraine 30 

[Burridge E; European Chemical News, 79 (2069): 14 (2003); 22-28 September 

2003] **PEER REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global VAM production capacity in 

2003 

Global VAM capacity in 2003 (thousand tonnes/year)

Country 

Capacity 

North America 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

- Mexico 110 

- USA 1,538 

South America 

- Brazil 80 

Europe 

- France 150 

- Germany 345 

- Italy 155 

- Spain 135 

- UK 250 

MIdeast 

- Iran 180 

Asia 

- China 808 

- India 60 

- Japan 630 

- Korea 150 

- Singapore 210 

- Taiwan 240 

[Anonymous; Chemical Week, 165 (23): 31 (2003); 25 June 2003] **PEER 

REVIEWED** 

CHEMICAL PROFILE: Vinyl Acetate: Production and consumption in Western Europe this 

year is predicted ... at 800,000 tonnes and 893,000 tonnes, respectively. This compares to output 

of 761,000 tonnes and demand of 844,000 tonnes in 2004. East European production will be 

stable in 2005 at 55,000 tonnes with demand edging up 1000 tonnes to 53,000 tonnes. European 

operating rates have drifted down to 81.5% in 2005 from 85% in 2004. 

[Burridge E; European Chemical News, 83 (2169): 38 (2005); 31 October-6 

November 2005] **PEER REVIEWED** 

CHEMICAL PROFILE: Vinyl Acetate: European vinyl acetate monomer capacity in 2005 

(thousand tonnes/year) 

European vinyl acetate monomer capacity in 2005 (thousand tonnes/year)

Country 

Capacity 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

France 165 

Germany 467 

Russia 62 

Spain 135 

UK 250 

Ukraine 12 

[Burridge E; European Chemical News, 83 (2169): 38 (2005); 31 October-6 

November 2005] **PEER REVIEWED**

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global VAM production capacity in 

2005 

Global VAM capacity in 2005 (thousand tonnes/year)

Country 

Capacity 

North America 

- Mexico 115 

- USA 1,544 

South America 

- Brazil 80 

Europe 

- France 150 

- Germany 350 

- Spain 135 

- UK 250 

Eastern and Central Europe 75 

MIdeast 

- Iran 30 

Asia 

- China 1,296 

- India 60 

- Japan 450 

- Korea 150 

- Singapore 190 

- Taiwan 240 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

[Anonymous; Chemical Week, 167 (23): 39 (2005); 13 July 2005] **PEER 

REVIEWED** 

PRODUCT FOCUS: Vinyl Acetate Monomer (VAM): Global VAM production capacity in 

2006 

Global VAM capacity in 2006 (thousand tonnes/year)

Country 

Capacity 

North America 

- Mexico 115 

- USA 1,553 

South America 

- Brazil 80 

Europe 

- France 150 

- Germany 370 

- Spain 135 

- UK 270 

Eastern Europe 125 

MIdeast/Africa 

- Iran 110 

Asia 

- China 1,221 

- India 60 

- Japan 701 

- Korea 150 

- Singapore 190 

- Taiwan 650 

[Anonymous; Chemical Week, 169 (20): 41 (2007); 13 June 2007] **PEER 

REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

CHEMICAL PROFILE: Vinyl Acetate: European and Americas vinyl acetate monomer 

capacity in 2008 (thousand tonnes/year) 

European and Americas vinyl acetate monomer capacity in 2008 (thousand 

tonnes/year)

Country 

Capacity 

Europe 

- France 165 

- Germany 485 

- Lithuania 20 

- Romania 20 

- Russia 60 

- Spain 200 

- UK 250 

- Ukraine 30 

Americas 

- Brazil 80 

- Mexico 115 

- USA 1,690 

[Burridge E; ICIS Chemical Business 273 (21): 50 (2008); 26 May-1 June 2008] 

**PEER REVIEWED** 

U. S. Imports:

(1972) NEGLIGIBLE 

[SRI] **PEER REVIEWED** 

(1975) 1.54X10+8 G 

[SRI] **PEER REVIEWED** 

(1984) 4.54X10+8 g (EST) 

[CHEMICAL PRODUCTS SYNOPSIS: VINYL ACETATE, 1984] **PEER REVIEWED** 

(1986) 1.16x10+7 lb 

[BUREAU OF THE CENSUS. US IMPORTS FOR CONSUMPTION AND GENERAL IMPORTS 1986 

P.1-529] **PEER REVIEWED** 

U. S. Exports:
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

(1972) NEGLIGIBLE 

[SRI] **PEER REVIEWED** 

(1975) 9.17X10+10 G 

[SRI] **PEER REVIEWED** 

(1981) Exceeded 2.5x10+11 g 

[Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New 

York, NY: John Wiley and Sons, 1978-1984., p. V23 825 (1983)] **PEER 

REVIEWED** 

(1984) 2.34X10+11 g 

[BUREAU OF THE CENSUS. U.S.A. EXPORTS 1984 p.2-79] **PEER REVIEWED** 

(1987) 7.83X10+7 

[BUREAU OF THE CENSUS. U.S.A. EXPORTS, SCHEDULE E, DECEMBER 1987 P.2-83] 

**PEER REVIEWED** 

Laboratory Methods:

Analytic Laboratory Methods:

NIOSH Method 278. Analyte: Vinyl acetate. Matrix: Air. Procedure: Gas chromatographyflame ionization detector. Method Evaluation: Method was validated over the range of 8.2 to 206 

mg/cu m using a 1.5 liter sample. Method detection limit: 0.5 ug. Precision (CVT): 8%. 

Applicability: Under the conditions of sample size (300 mg) the useful range is 0.5 ug. 

Interferences: None identified. 

[U.S. Department of Health, Education Welfare, Public Health Service. Center 

for Disease Control, National Institute for Occupational Safety Health. NIOSH 

Manual of Analytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. 

Government Printing Office, 1977-present., p. 278-1] **PEER REVIEWED** 

Air samples of vinyl acetate were collected & desorbed with carbon disulfide with a mean 

efficiency of 83.0%. The analytical column was packed with 10% free fatty acid phase on acidwashed Chromosorb-P. Gas chromatography identification was also conducted on another 

column packed with 0.4% Carbowax-1500 on Carbopack A. Analysis was performed on a 

chromatograph equipped with a flame ionization detector. The precision was 4.0%. Based on a 

10 liter air sample, the limit of detection was 0.1 ppm. 

[Sidhu KS; J Appl Toxicol 1 (6): 300-2 (1981)] **PEER REVIEWED** PubMed 

Abstract

Determination of vinyl acetate in the air using calorimetric method. Absorption is measured at 

510 nm wavelength. 

[Suwalska D, Lipi'nska Z; Med Pr 35 (5): 379-82 (1984)] **PEER REVIEWED** 

PubMed Abstract

Air samples containing vinyl acetate were adsorbed on charcoal & desorbed by solvent 

extraction (carbon disulfide with 2% acetone). Analysis was by gas chromatography/flame 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

ionization. Limit of detection was 1.3 mg/cu m. /From table/ 

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 120 (1986)] **PEER REVIEWED** 

Vinyl acetate was determined in polyvinyl acetate balloon paste by gas chromatography-mass 

fragmentography. 

[Iwaida M et al; Bunseki Kagaku 31 (10): T86-90 (1982)] **PEER REVIEWED** 

EPA Method 5030. Purge and Trap extraction procedure for the analysis of volatile organics. 

Such cmpds include low-molecular weight halogenated hydrocarbons, aromatics, ketones, 

nitriles, acetates, acrylates, ethers and sulfides. An inert gas is bubbled through the solution at 

ambient temperature, and the volatile components are efficiently transferred from the aqueous 

phase to the vapor phase. After purging is complete, the sorbent column is heated and 

backflushed with inert gas to desorb the components onto a GC column. Water samples can be 

analyzed directly, while preparation is necessary for water-miscible liquids, solids, wastes and 

soil/sediments. 

[USEPA/Office of Solid Waste (OSW); Test Methods for Evaluating Solid Waste, 

Physical/Chemical Methods SW846 Methods (1986)] **PEER REVIEWED** 

EPA Method 5040. Protocol for Analysis of Sorbent Cartridges from Volatile Organic Sampling 

Train. This method covers the determination of volatile principal organic hazardous constituents 

collected on Tenax and Tenax/charcoal sorbent cartridges using a volatile organic sampling train, 

from wet stack gas effluents from hazardous waste incinerators. The contents of the sorbent 

cartidges are thermally desorbed, bubbled, and trapped on an analytical adsorbent trap. The 

desired target detection limit of the analytical method is 0.1 ng/l. Interferences include phthalate 

esters, detectable levels of volatile principal hazardous constituents in blanks, and soap residue 

on the glassware. 

[USEPA/Office of Solid Waste (OSW); Test Methods for Evaluating Solid Waste, 

Physical/Chemical Methods SW846 Methods (1986)] **PEER REVIEWED** 

EPA Method 8240. Gas Chromatography/Mass Spectrometry for the determination of volatile 

organics. This method can be used to quantify most volatile organic compounds including vinyl 

chloride that have boiling points below 200 deg C and are insoluble or slightly soluble in water. 

The detection limit is not given. Precision and method accuracy were found to be directly related 

to the concentration of the analyte and essentially independent of the sample matrix. 

[USEPA/Office of Solid Waste (OSW); Test Methods for Evaluating Solid Waste, 

Physical/Chemical Methods SW846 Methods (1986)] **PEER REVIEWED** 

Gas chromatography/mass spectrometric analysis of volatiles including vinyl acetate. The 

Contract Required Quantitation Limit is 10 ug/kg in solids at low level and 1000 ug kg in water 

as used in EPA Contract Laboratory Program. 

[USEPA/OST; List of Lists: A Catalog of Analytes and Methods p.529 (1991) OST 

Pub 21W-4005] **PEER REVIEWED** 

Gas chromatography/mass spectrometric analysis of volatiles including vinyl acetate in solids at 

medium level . The Contract Required Quantitation Limit is 1000 ug/kg as used in EPA Contract 

Laboratory Program. 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

[USEPA/OST; List of Lists: A Catalog of Analytes and Methods p.529 (1991) OST 

Pub 21W-4005] **PEER REVIEWED** 

EPA Method 1624. Isotope Dilution Purge and Trap Gas Chromatography/Mass Spectrometry. 

This method is applicable for the determination of volatile organic compounds in municipal and 

industrial discharges. By adding a known amount of an isotopically labeled compound to every 

sample prior to purging, a correction of recovery of the pollutant can be made. If isotopically 

labeled compounds are not available, an internal standard method is used. Under the prescribed 

conditions, vinyl chloride has a minimum detection level of 50 ug/l in solids at high level and 50 

ug/l in water with no interferences present as defined by EPA. 

[USEPA/OST; List of Lists: A Catalog of Analytes and Methods p.529 (1991) OST 

Pub 21W-4005] **PEER REVIEWED** 

OSW Method 8240B. Determination of Volatile Organics Compounds by Gas 

Chromatography/Mass Spectrometry (GC/MS). Applicable to various type of samples, 

regardless of water content, including ground water, aqueous sludge, caustic liquors, acid 

liquors, waste solvents, and oily waste. Estimated quantitation limit=50 ug/Ll 

[USEPA/Office of Solid Waste (OSW); Test Methods for Evaluating Solid Waste, 

Physical/ Chemical Methods, SW-846, 3rd Edition, Final Update II, September 

(1994)] **PEER REVIEWED** 

Method: EPA-OSW 8260B; Procedure: gas chromatography/mass spectrometry (GC/MS); 

Analyte: vinyl acetate; Matrix: various; Detection Limit: not provided. 

[National Environmental Methods Index; Analytical, Test and Sampling Methods. 

Available from http://www.nemi.gov on Vinyl Acetate (108-05-4) as of February 

25, 2009] **PEER REVIEWED** 

Method: NIOSH 1453, Issue 2; Procedure: gas chromatography with flame ionization detector; 

Analyte: vinyl acetate; Matrix: air; Detection Limit: 1 ug per sample. 

[CDC; NIOSH Manual of Analytical Methods, 4th ed. Available from: 

http://www.cdc.gov/niosh/nmam/ on Vinyl Acetate (108-05-4) as of February 25, 

2009] **PEER REVIEWED** 

Method: OSHA 51; Procedure: gas chromatography with flame ionization detection; Analyte: 

vinyl acetate; Matrix: air; Detection Limit: 0.04 mg/cu m (0.01 ppm). 

[U.S. Department of Labor/Occupational Safety and Health Administration's 

Index of Sampling and Analytical Methods. Available from: 

http://www.osha.gov/dts/sltc/methods/toc.html on Vinyl Acetate (108-05-4) as 

of February 25, 2009] **PEER REVIEWED** 

Sampling Procedures:

A solid sorbent tube employing inhibited carbon preceded by a drying agent permits collection of 

environmental air samples up to 90 liters at flow rates up to 1 liter/min. Samples could be stored 

up to 10 days without loss of the vinyl acetate monomer. 

[Kimble HJ et al; Am Ind Hyg Assoc J 43 (3): 137-44 (1982)] **PEER REVIEWED** 

NIOSH Method 278. Analyte: Vinyl acetate. Matrix: Air. Procedure: Adsorption on chromosorb 

107, thermal desorption. Flow Rate: 0.1 liter/min. Sample Size: 3 liters. 

[U.S. Department of Health, Education Welfare, Public Health Service. Center 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

for Disease Control, National Institute for Occupational Safety Health. NIOSH 

Manual of Analytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. 

Government Printing Office, 1977-present., p. 278-1] **PEER REVIEWED** 

Special References:

Special Reports:

Holmberg B; Prog Clin Biol Res 141: 99-112 (1984). This is a review of the toxicology of 

monomers of the polyvinyl plastic series incl vinyl acetate.

NIOSH; Criteria Document: Vinyl Acetate (1978) DHEW Pub. NIOSH 78-205

DHHS/ATSDR; Toxicological Profile for Vinyl Acetate (1992) ATSDR/TP-91/30

European Commission, ESIS; IUCLID Dataset, Vinyl acetate (108-05-4) (2000 CD-ROM 

edition). Available from the Database Query page at: http://ecb.jrc.ec.europa.eu/esis/ as of 

March, 3 2009. 

Synonyms and Identifiers:

Synonyms:

ACETATE DE VINYLE (FRENCH) 

**PEER REVIEWED** 

ACETIC ACID, ETHYLENE ETHER 

**PEER REVIEWED** 

ACETIC ACID, ETHENYL ESTER 

**PEER REVIEWED** 

ACETIC ACID VINYL ESTER 

**PEER REVIEWED** 

1-ACETOXYETHYLENE 

**PEER REVIEWED** 

ETHANOIC ACID, ETHENYL ESTER 

**PEER REVIEWED** 

ETHENYL ACETATE 

**PEER REVIEWED** 

Ethenyl ethanoate 

**PEER REVIEWED** 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

OCTAN WINYLU (POLISH) 

**PEER REVIEWED** 

VAC 

**PEER REVIEWED** 

VAM 

**PEER REVIEWED** 

VINILE (ACETATO DI) (ITALIAN) 

**PEER REVIEWED** 

VINYLACETAAT (DUTCH) 

**PEER REVIEWED** 

VINYL ACETATE HQ 

**PEER REVIEWED** 

Vinyl acetate monomer 

**PEER REVIEWED** 

VINYLACETAT (GERMAN) 

**PEER REVIEWED** 

VINYLE (ACETATE DE) (FRENCH) 

**PEER REVIEWED** 

VINYL A MONOMER 

**PEER REVIEWED** 

VINYLESTER KYSELINY OCTOVE 

**PEER REVIEWED** 

VINYL ETHANOATE 

**PEER REVIEWED** 

VYAC 

**PEER REVIEWED** 

ZESET T 

**PEER REVIEWED** 

Formulations/Preparations:

Various commercial grades of vinyl acetate are available in USA, which differ only in the amt 

of inhibitor added: 3-5 mg/L (ppm) hydroquinone are present when use is expected within 2 mo 

of delivery; 14-17 mg/L (ppm) hydroquinone for up to 4 mo of storage; & 200-300 mg/L (ppm) 

diphenylamine when indefinite storage is anticipated. 
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~qF1sHh:1 July 1, 2010

[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to 

Man. Geneva: World Health Organization, International Agency for Research on 

Cancer, 1972-PRESENT. (Multivolume work). Available at: 

http://monographs.iarc.fr/index.php p. V39 114 (1986)] **PEER REVIEWED** 

GRADES OR PURITY: GRADE A (DIPHENYLAMINE-INHIBITED): 99.8%; GRADE H 

(HYDROQUINONE-INHIBITED): 99.8% 

[U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical 

Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.] 

**PEER REVIEWED** 

Shipping Name/ Number DOT/UN/NA/IMO:

UN 1301; Vinyl acetate, stabilized 

IMO 3.2; Vinyl acetate, stabilized 

Standard Transportation Number:

49 072 70; Vinyl acetate, flammable liquid, polymerizable

Administrative Information:

Hazardous Substances Databank Number: 190

Last Revision Date: 20090820 

Last Review Date: Reviewed by SRP on 5/7/2009