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HSDB Env. Health & Toxicology TOXNET HSDB
ACETIC ACID
CASRN: 64-19-7
For more information, search the NLM HSDB database.
Human Health Effects:
Toxicity Summary:
IDENTIFICATION AND USE: Acetic acid is a colorless liquid or solid, having a pungent characteristic odor, and when diluted in water an
acidic taste. Glacial acetic acid is a 99% active chemical. It is used as an acidifier, flavoring agent, for the prevention of rope in baking, and as
a solvent. Acetic acid is used as a laboratory reagent in chemical and biochemical analysis, in field testing of lead fumes, vinyl chloride
determination, uric acid in urine, aniline vapors, and separation of gases. In addition, acetic acid is used in pesticide formulations as a
herbicide to controls weeds on fruits, vegetables, ornamentals and turf. It is also a component of the hydraulic fracturing fluids preventing
precipitation of metal oxides (iron control). Registered for use in the U.S., but approved pesticide uses may change periodically, so federal,
state and local authorities must be consulted for currently approved uses. Three to 5% acetic acid is commonly used in the field of
gynecology for colposcopic examinations of the cervix. It gives an 'acetowhite' effect that may assist clinicians in identifying neoplastic areas.
HUMAN EXPOSURE AND TOXICITY: Acetic acid is absorbed from the gastrointestinal tract and through the lungs and almost completely
oxidized by tissues. The metabolic pathways are reasonably well known and involve the formation of ketone bodies. As little as 1.0 mL of
glacial acetic acid has resulted in perforation of the esophagus. During acetic acid dialysis, patients showed a frequent onset of sudden
hypotension and arrhythmia with concomitant symptoms of the so-called disequilibrium syndrome. Extreme eye and nasal irritation has
occurred at concentrations in excess of 25 ppm and conjunctivitis from concentrations below 10 ppm has been reported. Glacial acetic acid
has caused permanent corneal opacification. Ingestion of 200 mL of an 80% solution of acetic acid caused repeated shock due to myocardial
infarction and massive intestinal bleeding led to an organic brain psychosyndrome. The patient survived the intoxication by use of
hemodialysis and intensive care therapy. An excess of prostate cancer was observed among former chemical plant workers, some of whom
had been exposed to both acetic acid and acetic anhydride. ANIMAL STUDIES: Toxic effects of acetic acid are due to irritant properties as
well as its effect on the central nervous system and kidneys. Large oral doses cause CNS depression and death in rats and mice. Inhalation
of 16,000 ppm killed 1 of 6 exposed rats. Groups of 3-6 rats were given acetic acid in drinking water for periods from 9-15 weeks. Fluid
uptake was the same in all treatment groups, at the high dose group there was a progressive reduction in body weight gain, loss of appetite
and fall in food consumption. Four groups of two young pigs were fed daily diets for successive 30 day periods for a total of 150 days. There
were differences in growth rate, weight gain, early morning urinary ammonia and terminal blood pH between controls and test groups. Acetic
acid had no effects on implantation or on maternal or fetal survival in rats, mice or rabbits dosed via gavage during gestation days 6-19 at
doses up to 1600 mg/kg/day. The number of abnormalities seen in either soft or skeletal tissues of the test groups did not differ from the
number occurring in the controls. Acetic acid has shown no evidence of mutagenic activity with or without metabolic activation using several
strains of Salmonella typhimurium. Acetic acid did not show clastogenicity on cultured Chinese hamster ovary K1 cells at neutral pH, but it
was clastogenic at pH 5.2 to 6.0 with or without metabolic activation. ECOTOXITY STUDIES: Acetic acid was harmful to aquatic life. High
concentrations produced pH levels toxic to oxidizing bacteria, inhibiting oxygen demand. It was lethal to Mosquito fish: at 320 ppm and higher
all fish were dead at 24 hours.
**PEER REVIEWED**
Human Toxicity Excerpts:
/HUMAN EXPOSURE STUDIES/ Six patients with frequent episodes of symptomatic hypotension during acetate dialysis were treated with
bicarbonate dialysis. ... During acetate dialysis, the patients showed a frequent onset of sudden hypotension and arrhythmia with concomitant
symptoms of the so-called disequilibrium syndrome. None of these symptoms were seen during bicarbonate dialysis. /Acetate/
[Hampl H et al; Artif Organs 6 (4): 410-6 (1982)] **PEER REVIEWED** PubMed Abstract
/HUMAN EXPOSURE STUDIES/ Acetic acid is used in plastics, chemical and pharmaceutical industries. ...The aim of this study was to
evaluate acute irritation during controlled exposure to vapors of acetic acid. Six female and six male healthy volunteers were exposed to 0
ppm (control exposure), 5 and 10 ppm acetic acid vapor for 2 hr at rest in a balanced order. Subjective ratings of nasal irritation and smell
increased significantly with exposure level. Except for smell, all average ratings at 10 ppm were at the lower end of the 0-100mm visual
analogue scale, and did not exceed the verbal expression "somewhat" (26 mm). No effects on pulmonary function, nasal swelling, nasal
airway resistance or plasma inflammatory markers (C-reactive protein, and interleukin-6), measured before and after exposure, were seen.
There was a non-significant tendency to increased blinking frequency, as measured continuously during exposure, after exposure to 10 ppm
acetic acid. In conclusion, our study suggests a mild irritative effect at 10 ppm acetic acid.
[Ernstgard L et al; Toxicol Lett. 165(1):22-30 (2006).] **PEER REVIEWED** PubMed Abstract
/SIGNS AND SYMPTOMS/ ...A splash of vinegar (4 to 10% acetic acid solution) in the human eye causes immediate pain and conjunctival
hyperemia, sometimes with injury of the corneal epithelium.
[Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH)
Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 2] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Repeated or prolonged contact with skin may cause dermatitis. The substance may have effects on the
gastrointestinal tract , resulting in digestive disorders including pyrosis and constipation.
[IPCS,CEC; International Chemical Safety Card on Acetic acid (October 1997). Available from, as of February 9, 2004:
http://www.inchem.org/documents/icsc/icsc/eics0466.htm **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Long-term exposure can lead to darkening of the skin, erosion of tooth enamel and chronic inflammation of the
respiratory tract.
[Anon; Canadian Centre for Occupational Health and Safety L8N 1H6 14p (1984)] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Workers exposed for a number of years to concentration of up to 200 ppm have been found to suffer from
palpebral edema with hypertrophy of the lymph nodes, conjunctival hyperaemia, chronic pharyngitis, chronic catarrhal bronchitis and in some
cases asthmatic bronchitis and traces of erosion on the vestibular surface of teeth (incisors and canines). Following repeated exposures,
workers may complain of digestive disorders with pyrosis and constipation. Skin on palms of hands... become dry, cracked and
hyperkeratotic.
[International Labour Office. Encyclopaedia of Occupational Health and Safety. 4th edition, Volumes 1-4 1998. Geneva, Switzerland: International Labour
Office, 1998., p. 104.13] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ ...Unacclimatized humans experience extreme eye and nasal irritation at concentrations in excess of 25 ppm;
conjunctivitis from concentrations below 10 ppm has been reported. ...Glacial (100%) acetic acid... has caused permanent corneal
opacification.
Publication No. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981., p. 1-2] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Local effects of acetic acid vapor include irritation and damage of the eyes, nose, throat, and lungs.
Bronchopneumonia, pulmonary edema, and reactive airway dysfunction syndrome may follow acute inhalation overexposure. Contact with
concentrated acetic acid may lead to severe skin and eye damage sufficient to cause loss of sight. Repeated or prolonged exposure to acetic
acid may cause skin darkening, erosion of the exposed front teeth, and chronic inflammation of nose throat and bronchi.
[Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1298] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ Bronchopneumonia and pulmonary edema may develop following acute overexposure. Chronic exposure may
result in pharyngitis and catarrhal bronchitis. Ingestion, though not likely to occur in industry, may result in penetration of the esophagus,
bloody vomiting, diarrhea, shock, hemolysis, and hemoglobinuria... followed by anuria.
[Sittig M; Handbook of Toxic and Hazardous Chemicals p.20-21 (1981)] **PEER REVIEWED**
/SIGNS AND SYMPTOMS/ After ingestion or skin contact: Corrosion of mucous membranes of mouth, throat, and esophagus, with
immediate pain and dysphagia. The necrotic areas are at first grayish white but soon acquire a blackish discoloration and sometimes a
shrunken or wrinkled texture; the process is described as a "coagulation necrosis." Epigastric pain, which may be associated with nausea and
the vomiting of mucoid and "coffee-ground" material. At times, gastric hemorrhage may be intense, and the vomitus then contains fresh
blood. Profound thirst. Ulceration of all membranes and tissues with which the acid comes in contact... . Circulatory collapse with clammy
skin, weak and rapid pulse, shallow respirations, and scanty urine. Circulatory shock is often the immediate cause of death. Asphyxial death
due to glottic edema. Late esophageal, gastric and pyloric strictures and stenoses, which may require major surgical repair, should be
anticipated. Signs of obstruction commonly appear within a few weeks but may be delayed for months and even years. Permanent scars may
also appear in the cornea, skin and oropharynx. Uncorrected circulatory collapse of several hours' duration may lead to renal failure and
ischemic lesions in the liver and heart.
[Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-102] **PEER
REVIEWED**
/SIGNS AND SYMPTOMS/ ...An excess of prostate cancer (SMR=330.4; 95% confidence interval= 121.3-719.1) was observed among
former chemical plant workers, some of whom had been exposed to both acetic acid and acetic anhydride.
[Whorton MD et al; Am J Ind Med 33 (3): 293-6 (1998)] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ ... Workers exposed for 7 to 12 yrs at concentrations of 60 ppm, plus 1 hr daily at 100-200 ppm, /were reported to have/
had no injury except slight irritation of the respiratory tract ... and skin. However, ... /a different report/ found conjunctivitis, bronchitis,
pharangitis, and erosion of exposed teeth, apparently in the same workers.
[American Conference of Governmental Industrial Hygienists. Documentation of the TLVs and BEIs with Other World Wide Occupational Exposure Values.
7th Ed. CD-ROM Cincinnati, OH 45240-1634 2013., p. 3] **PEER REVIEWED**
/CASE REPORTS/ Acetic acid may cause allergic reactions in humans. ...A patient with bronchial asthma who reacted to acetic acid
challenge /is reported/. ...Some researchers consider acetic acid capable of causing a syndrome known as "reactive airways dysfunction," or
RADs. ...This syndrome resembles bronchial asthma but differs in that exposure to small doses does not cause a reaction a few weeks after
onset. Symptoms include dyspnea, wheezing, and cough.
[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V5 703] **PEER
REVIEWED**
/CASE REPORTS/ Two patients admitted after ingestion of 80% acetic acid are described. Only the first patient developed hemolysis, slight
intravascular coagulation and oliguric kidney insufficiency. They were treated with a nasogastric tube and total parenteral feeding. During the
first week after admission urinary excretion of beta 2-microglobulin, alanine-aminopeptidase and N-acetyl-glucosaminidase was significantly
increased. The patients remained hemodynamically stable and did not develop fever. The above-mentioned elevated excretions returned to
normal levels. Both patients showed similar patterns of tubular proteinuria. The observations in the second patient suggest a direct toxic
effect of acetic acid on the proximal tubule of the kidney.
[Schardijn GH et al; Ned Tijdschr Geneeskd 133 (11): 556-59 (1989)] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ In two patients, accidental application of acetic acid to the eyes followed very quickly by irrigation with water resulted in
immediate corneal opacification. The corneas cleared sufficiently in a few days to reveal severe iritis and small pupils fixed by posterior
synechiae. Regeneration of the epithelium took many months, but corneal anesthesia and opacity were permanent.
REVIEWED**
/CASE REPORTS/ /Investigators/ report a case of rapidly progressive severe upper airway obstruction in a small child caused by accidental
ingestion of 80% acetic acid. Emergency cricothyrotomy was necessary after both endotracheal intubation and bag-valve-mask ventilation
were not possible. Although intubation was eventually achieved, a tracheostomy was necessary. Toxin spilled over the anterior chest and
abdomen caused third degree skin burns which required grafting. Mild liver dysfunction was observed. Complete recovery occurred.
[Tibballs J et al; Anaesth Intensive Care. 34(3):379-81 (2006).] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ 3 to 5% acetic acid is commonly used in the field of gynecology for colposcopic examinations of the cervix. It gives an
'acetowhite' effect that may assist clinicians in identifying neoplastic areas. CASE: A perimenopausal woman was treated with acetic acid for
abnormal Pap smear report (cervical intraepithelial neoplasia 1). During application, the patient complained of burning sensation of vagina
and vulva. The vagina was saline-irrigated after realizing that the acetic acid had not been diluted. Following this incident, the patient was
seen weekly and treated with conjugated vaginal estrogen cream. The patient recovered and the vaginal mucosa healed within two weeks.
CONCLUSION: Acetic acid is corrosive and may cause vaginal bleeding. Estrogen cream can be used in an attempt to minimize the adverse
reaction and speed the healing process.
[Ou KY et al; Aust N Z J Obstet Gynaecol. 47(4):345-6 (2007).] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ A 37 year old man who worked as a maintenance fitter developed both reversible airways obstruction and steroid
responsive interstitial pneumonitis after accidental exposure to glacial acetic acid. He was exposed to a blow back of the acid in a
petrochemical works, and suffered first degree burns on the face and arms. He developed progressive exertional dyspnea, limiting him to
quiet walking on flat areas. Physical examination revealed burns to the face and arms and inspiratory basal crackles. Chest radiograph
indicated patchy bilateral reticulonodular infiltration dominantly of the bases. Even after 3 months, there was no improvement in his condition.
Bronchoscopy showed widespread bronchial inflammatory changes. A doubling of macrophages and a ten fold increase in lymphocytes were
noted which amounted to 34% of the total inflammatory cells. A diffuse, moderate, mainly mononuclear, interstitial pneumonitis was noted on
transbronchial biopsy. He was treated with high dose nebulized bronchodilators and corticosteroids. A prompt and sustained improvement
was noted in spirometry and clearing of his chest radiograph. Progress was maintained for at least 18 months.
[Rajan KG, Davies BH; Br J Ind Med 46 (1): 67-68 (1989)] **PEER REVIEWED** PubMed Abstract Full text: PMC1009727
/CASE REPORTS/ ... Glacial acetic acid is widely used as a substitute for chemical peeling because it is readily ... available and affordable.
However, its use can result in a number of serious complications. A 28-year-old female patient was admitted to /the/ hospital with deep
second-degree chemical burns on her face caused by the application of a mixture of glacial acetic acid and flour for chemical peeling. During
a 6-month follow-up, hypertrophic scarring developed on the both nasolabial folds despite scar management. Glacial acetic acid is a
concentrated form of the organic acid, which gives vinegar its sour taste and pungent smell, and it is also an important reagent during the
production of organic compounds. Unfortunately, misleading information regarding the use of glacial acetic acid for chemical peeling is
causing serious chemical burns. Furthermore, there is high possibility of a poor prognosis, which includes inflammation, hypertrophic scar
formation and pigmentation associated with its misuse. ...
[Yoo JH et al; . J Plast Reconstr Aesthet Surg. 63(12):e829-31 (2010).] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ A 22 year old woman developed anaphylactic reations to pure ethyl alcohol (ethanol) and an immediate type allergy to
acetic acid. Prick tests with ethyl alcohol, wine, and beer were negative, whereas vinegar and acetic acid (9.6 and 0.96%) gave +++
reactions. Control tests with acetic acid in 10 patients yielded negative or (+) reactions to the 9.6% concentration and negative reactions to
the 0.96% concentration. Oral provocation tests led to severe anaphylaxis with urticaria, facial flushing, itching of the mucous membranes,
hoarseness, dyspnea, tachycardia, and painful uterine cramps after the ingestion of one ml of ethyl alcohol or 50 mL of beer. The severe
anaphylactic reation after ingestion of as little as one ml of ethyl alcohol associated with a +++ prick test reaction to acetic acid in a definitely
non-irritating concentration strongly suggests that the patient's anaphylactic reactions are based on an immediate type allergy to acetic acid,
the main metabolite of ethyl alcohol.
[Przybilla B, Ring J; Lancet 1 (Feb 26): 483 (1983)] **PEER REVIEWED**
/CASE REPORTS/ A case study is reported where an individual ingested 200 mL of an 80% solution of acetic acid. The patient survived the
intoxication by use of hemodialysis and intensive care therapy. Repeated shock due to myocardial infarction and massive intestinal bleeding
led to an organic brain psychosyndrome.
[Hakenbeck H et al; Z Urol Nephrol 77 (5): 311-4 (1984)] **PEER REVIEWED** PubMed Abstract
/CASE REPORTS/ A patient with bronchial asthma who developed a late asthmatic response to inhalation challenge with glacial acetic acid
is presented. This is believed to be the first description of a reaction to this allergen in an asthmatic patient.
[Kivity S et al; Thorax 49 (7): 727-8 (1994)] **PEER REVIEWED** PubMed Abstract Full text: PMC475071
/CASE REPORTS/ The enhanced toxicity of acid instilled directly into the rectum, without benefit of dilution and neutralization in the upper
intestine, is evident in a case of acetic acid intoxication by accidental rectal administration of 50 mL of 9% acetic acid to a 5-yr-old boy. The
complications included necrosis of the colon, acute renal failure, acute liver dysfunction, disseminated intravascular coagulopathy (DIC) and
sepsis.
[Kawamata M et al; J Toxicol Clin Toxicol 32 (3): 333-36 (1994)] **PEER REVIEWED** PubMed Abstract
/SURVEILLANCE/ Acetic acid is a widely used organic acid with corrosive properties that depend on its concentration. If acetic acid is
ingested in concentrations above 30 % it may severely damage the upper gastrointestinal tract and cause intravascular hemolysis, which can
result in severe kidney and liver disorders and disseminated intravascular coagulation. ...this retrospective study ...analyzed acetic acid
ingestion data collected at the University Clinic for Toxicology of Skopje, Macedonia from 1 January 2002 to 31 December 2011. The analysis
included systemic complications, kidney damage, and the outcomes in particular. Over the ten years, 84 patients were reported at the Clinic
to have ingested highly concentrated acetic acid. Twenty-eight developed kidney disorders, while the remaining 56 had no complications.
Fatal outcome was reported for 11 patients, seven of whom had systemic complications and four severe gastrointestinal complications.
[Chibishev A et al; Arh Hig Rada Toksikol. 64(1):153-8 (2013).] **PEER REVIEWED** PubMed Abstract
/SURVEILLANCE/ Respiratory function was assessed in a follow-up study of workers exposed to acetic acid in a food processing occupation.
Forty nine of an original 152 female workers in a Croatian vegetable pickling factory were exposed to heated acetic acid (4-10%) during the
work day at average concentrations of 19 to 40 mg/cu m. No progression or worsening was found but were still present 2 years following the
original survey in which symptoms of occupational asthma were recorded, including hoarseness and rhinitis, as well as decreases in lung
function, including forced expiratory volume and forced vital capacity.
REVIEWED**
/ALTERNATIVE and IN VITRO TESTS/ The antiseptic... 0.25% acetic acid was directly applied to cultured human fibroblasts to quantitatively
assess its cytotoxicity. It was cytotoxic and adversely affected wound healing in an animal model. Comparison of bactericidal and cytotoxic
effects of serial dilutions indicated that cellular toxicity exceeded its bacterial potency. ...This experiment provides evidence that 0.25% acetic
acid is unsuitable for use in wound care.
[Lineaweaver W, et al; Arch Surg 120 (3): 267-70 (1985)] **PEER REVIEWED** PubMed Abstract
/OTHER TOXICITY INFORMATION/ ... Thirty-five patients with histologically confirmed high-grade squamous intraepithelial lesions of the
cervix entered the study. ...Telomerase activity was detectable in 27 of 35 (77.1%) fresh tissue samples, 15 of 35 (42.9%) tissue samples
swabbed with 5% acetic acid, and 0 of 10 (0%) normal cervical tissue samples, respectively. Twelve samples became telomerase negative
after 5% acetic acid applied. Among the 15 telomerase-positive tissue samples swabbed with 5% acetic acid, 12 had relative weak
telomerase activity compared to corresponding fresh tissue samples, the other 3 remained the same.
[ChangChien CC, et al; Gynecol Oncol 71 (1): 99-103 (1998)] **PEER REVIEWED** PubMed Abstract
Skin, Eye and Respiratory Irritations:

The vapor of acetic acid is irritating to the eyes and nose, causing lacrimation and hyperemia.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 40] **PEER REVIEWED**
Irritating concn: 25 mg/cu m.

[Ruth JH; Am Ind Hyg J 47: A142-51 (1986)] **PEER REVIEWED**
... Eye irritation has been noted at a concentration below 10 ppm.

Vapors strongly irritating to eyes and respiratory tract.

[OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGraw-Hill, New York, NY 2012, p. 585] **PEER REVIEWED**
Drug Warnings:
... Glacial acetic acid is widely used as a substitute for chemical peeling because it is readily ... available and affordable. However, its use can
result in a number of serious complications. A 28-year-old female patient was admitted to /the/ hospital with deep second-degree chemical
burns on her face caused by the application of a mixture of glacial acetic acid and flour for chemical peeling. During a 6-month follow-up,
hypertrophic scarring developed on the both nasolabial folds despite scar management. Glacial acetic acid is a concentrated form of the
organic acid, which gives vinegar its sour taste and pungent smell, and it is also an important reagent during the production of organic
compounds. Unfortunately, misleading information regarding the use of glacial acetic acid for chemical peeling is causing serious chemical
burns. Furthermore, there is high possibility of a poor prognosis, which includes inflammation, hypertrophic scar formation and pigmentation
associated with its misuse. ...
[Yoo JH et al; . J Plast Reconstr Aesthet Surg. 63(12):e829-31 (2010).] **PEER REVIEWED** PubMed Abstract
The enhanced toxicity of acid instilled directly into the rectum, without benefit of dilution and neutralization in the upper intestine, is evident in
a case of acetic acid intoxication by accidental rectal administration of 50 mL of 9% acetic acid to a 5-yr-old boy. The complications included
necrosis of the colon, acute renal failure, acute liver dysfunction, disseminated intravascular coagulopathy (DIC) and sepsis.
[Kawamata M et al; J Toxicol Clin Toxicol 32 (3): 333-36 (1994)] **PEER REVIEWED** PubMed Abstract
In two patients, accidental application of acetic acid to the eyes followed very quickly by irrigation with water resulted in immediate corneal
opacification. ... Regeneration of the epithelium took many months, but corneal anesthesia and opacity were permanent.
REVIEWED**
Medical Surveillance:
Employees should be screened for history of ... /chronic respiratory, skin and, eye diseases/ ... which might place the employee at an
increased risk from acetic acid exposure.
Probable Routes of Human Exposure:

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial
manufacturing, processing, and use of acetic acid is 1000 or greater; the data may be greatly underestimated(1).
[(1) US EPA; Inventory Update Reporting (IUR). Non-confidential 2006 IUR Records by Chemical, including Manufacturing, Processing and Use Information.
Washington, DC: U.S. Environmental Protection Agency. Available from, as of May 27, 2014: http://cfpub.epa.gov/iursearch/index.cfm **PEER REVIEWED**
NIOSH (NOES Survey 1981-1983) has statistically estimated that 907,205 workers (322,123 of these are female) are potentially exposed to
acetic acid in the US(1). Occupational exposure to acetic acid may occur through inhalation and dermal contact with this compound at
workplaces where acetic acid is produced or used(SRC). Acetic acid occurs ubiquitously and is a normal metabolite in animals; therefore, the
general population is continually exposed to the compound(SRC). Monitoring data indicate that the general population may be exposed to
acetic acid via inhalation of ambient air, ingestion of food, and dermal contact with consumer products containing acetic acid(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 from, as of May 27, 2014: http://www.cdc.gov/noes/ **PEER REVIEWED**
Body Burden:
Acetic acid was qualitatively detected in 2 of 12 human milk samples collected from volunteers in four US cities(1). Acetic acid at 19.9 mg/day
was measured from non-specified human emissions(2). Humans exude <90mg/day of volatile fatty acids in exhaled breath and perspiration,
80% of which is acetic acid(3); in a confined environment, as much as 15-20 mg/cu m can accumulate and such concentrations can become
serious in submarines or space capsules(3).
[(1) Pellizzari ED et al; Bull Environ Contam Toxicol 28: 322-8 (1982) (2) Otson R, Fellin P; in Gas Pollut: Charactization and Cycling. Nriagu JO, ed, New
York, NY: John Wiley & Sons, Inc (1989) (3) Wagner FS; Acetic Acid. Kirk-Othmer Encyclopedia of Chemical Technology. (1999-2014). New York, NY: John
Wiley & Sons. Online Posting Date: Apr 29, 2014] **PEER REVIEWED**
Emergency Medical Treatment:
Emergency Medical Treatment:

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The following Overview, *** ACIDS ***, 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) USES: Household uses include toilet, metal and drain
cleaners, rust remover, in batteries, and as a primer
for artificial nails. Used in clandestine
methamphetamine labs (ie, hydrochloric and sulfuric
acid). Industrial uses include: metal refining,
plumbing, bleaching, engraving, plating, photography,
disinfection, munitions, fertilizer manufacture, metal
cleaning, and rust removal.
B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen
ions desiccate epithelial cells, causing edema,
erythema, tissue sloughing and necrosis, with formation
of ulcers and eschars.
C) EPIDEMIOLOGY: Inadvertent ingestions occur with
moderate frequency in children, and are less common
than alkaline exposures. Serious exposures are rare in
the developed world (generally only seen with
deliberate ingestions), largely because only low
concentration acids are available in the home. Serious
effects are more common in developing countries.
D) WITH POISONING/EXPOSURE
1) MILD TO MODERATE ORAL TOXICITY: Patients with mild
ingestions may only develop irritation or Grade I
(superficial hyperemia and edema) burns of the
oropharynx, esophagus or stomach; acute or chronic
complications are unlikely. Patients with moderate
toxicity may develop Grade II burns (superficial
blisters, erosions and ulcerations) are at risk for
subsequent stricture formation, particularly gastric
outlet and esophageal. Some patients (particularly
young children) may develop upper airway edema.
2) SEVERE ORAL TOXICITY: May develop deep burns and
necrosis of the gastrointestinal mucosa. Complications
often include perforation (esophageal, gastric, rarely
duodenal), fistula formation (tracheoesophageal,
aortoesophageal), and gastrointestinal bleeding. Upper
airway edema is common and often life threatening.
Hypotension, tachycardia, tachypnea and, rarely, fever
may develop. Other rare complications include
metabolic acidosis, hemolysis, renal failure,
disseminated intravascular coagulation, elevated liver
enzymes, and cardiovascular collapse. Stricture
formation (primarily gastric outlet and esophageal,
less often oral) is likely to develop long term.
Esophageal carcinoma is another long term
complication. Severe toxicity is generally limited to
deliberate ingestions in adults in the US, because
acidic products available in the home are generally of
low concentration.
a) PREDICTIVE: The grade of mucosal injury at endoscopy
is the strongest predictive factor for the occurrence
of systemic and GI complications and mortality.
Initial signs and symptoms may not reliably predict
the extent of GI burns.
3) INHALATION EXPOSURE: Mild exposure may cause dyspnea,
pleuritic chest pain, cough and bronchospasm. Severe
inhalation may cause upper airway edema and burns,
hypoxia, stridor, pneumonitis, tracheobronchitis, and
rarely acute lung injury or persistent pulmonary
function abnormalities. Pulmonary dysfunction similar
to asthma has been reported.
4) OCULAR EXPOSURE: Ocular exposure can produce severe
conjunctival irritation and chemosis, corneal
epithelial defects, limbal ischemia, permanent vision
loss and in severe cases perforation.
5) DERMAL EXPOSURE: A minor exposure can cause irritation
and partial thickness burns. More prolonged or a high
concentration exposure can cause full thickness burns.
Complications may include cellulitis, sepsis,
contractures, osteomyelitis, and systemic toxicity.
0.2.3 VITAL SIGNS
0.2.20 REPRODUCTIVE HAZARDS
A) Single doses of dibromoacetic acid has resulted in
reductions of sperm and serum testosterone in
experimental animals. Repeated or single oral
administration of monobromoacetic acid did not produce
effects on male rat reproductive organs or sperm.
Laboratory:
A) Obtain a complete blood count and electrolytes in all
patients with significant burns after acid ingestion.
B) In patients with signs and symptoms suggesting severe
burns, perforation, or bleeding (or adults with
deliberate, high volume or high concentration
ingestions), obtain renal function tests, liver enzymes,
serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation
products, type and crossmatch for blood, and monitor
urine output and urinalysis. Serum lactate and base
deficit may also be useful in these patients.
C) Monitor pulse oximetry or arterial blood gases in
patients with signs and symptoms suggestive of upper
airway edema or burns.
D) Obtain an upright chest x-ray in patients with signs and
symptoms suggesting severe burns, perforation, or
bleeding (or adults with deliberate, high volume or high
concentration ingestions) to evaluate for
pneumomediastinum or free air under the diaphragm. The
absence of these findings DOES NOT rule out the
possibility of necrosis or perforation of the esophagus
or stomach. Obtain a chest radiograph in patients with
pulmonary signs or symptoms.
E) Several weeks after ingestion, barium contrast
radiographs of the upper GI tract are useful in patients
who sustained grade 2 or 3 burns, to evaluate for
strictures.
Treatment Overview:
0.4.2 ORAL EXPOSURE
A) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY
1) Within the first 12 hours of exposure, if burns are
absent or grade I severity, patient may be discharged
when able to tolerate liquids and soft foods by mouth.
If mild grade II burns, admit for intravenous fluids,
slowly advance diet as tolerated. Perform barium
swallow or repeat endoscopy several weeks after
ingestion (sooner if difficulty swallowing) to evaluate
for stricture formation.
B) MANAGEMENT OF SEVERE ORAL TOXICITY
1) Resuscitate with 0.9% saline; blood products may be
necessary. Early airway management in patients with
upper airway edema or respiratory distress. Early
(within 12 hours) gastrointestinal endoscopy to
evaluate for burns. Early bronchoscopy in patients with
respiratory distress or upper airway edema. Early
surgical consultation for patients with severe grade II
or grade III burns, large deliberate ingestions, or
signs, symptoms or laboratory findings concerning for
tissue necrosis or perforation.
C) DECONTAMINATION
1) INGESTION: In patients without vomiting or respiratory
distress who are able to swallow, dilute with 4-8
ounces milk/water if possible shortly after ingestion;
then NPO until after endoscopy. Neutralization, gastric
lavage, and activated charcoal are all contraindicated.
OCULAR: Copious irrigation until pH neutral. DERMAL:
Remove contaminated clothes, brush off particulate
corrosives, follow with copious irrigation. INHALATION:
Humidified oxygen.
D) AIRWAY MANAGEMENT
1) Aggressive airway management in patients with
deliberate ingestions or any indication of upper airway
injury. Severe edema may make intubation difficult; be
prepared for surgical airway management
(cricothyroidotomy) in patients with severe upper
airway edema.
E) ENDOSCOPY
1) Should be performed as soon as possible (preferably
within 12 hours, not more than 24 hours) in any patient
with acid ingestion. The grade of mucosal injury at
endoscopy is the strongest predictive factor for the
occurrence of systemic and GI complications and
mortality. The absence of visible oral burns does NOT
reliably exclude the presence of esophageal or gastric
burns.
F) BRONCHOSPASM
1) Treat with oxygen, inhaled beta agonists and consider
systemic corticosteroids.
G) CORTICOSTEROIDS
1) The use of corticosteroids to prevent stricture
formation is controversial. Corticosteroids should not
be used in patients with grade I or grade III injury,
as there is no evidence that it is effective. Evidence
for grade II burns is conflicting, and the risk of
perforation and infection is increased with steroid
use, so routine use is not recommended.
H) STRICTURE
1) A barium swallow or repeat endoscopy should be
performed several weeks after ingestion in any patient
with grade II or III burns or with difficulty
swallowing to evaluate for stricture formation.
Recurrent dilation may be required. Some authors
advocate early stent placement in these patients to
prevent stricture formation.
I) SURGICAL MANAGEMENT
1) Immediate surgical consultation should be obtained on
any patient with grade III or severe grade II burns on
endoscopy, significant abdominal pain, metabolic
acidosis, hypotension, coagulopathy, or a history of
large ingestion. Early laparotomy can identify tissue
necrosis and impending or unrecognized perforation,
early resection and repair in these patients is
associated with improved outcome.
J) EYE INJURY
1) Copious irrigation until pH neutral; perform slit lamp
exam. Ophthalmology consult. Antibiotics and mydriatics
may be indicated.
K) PATIENT DISPOSITION
1) OBSERVATION CRITERIA: Patients with an acid ingestion
should be sent to a health care facility for
evaluation. Patients with an endoscopic evaluation that
demonstrates no burns or only minor grade I burns and
who can tolerate oral intake can be discharged to home.
2) ADMISSION CRITERIA: Symptomatic patients, and those
with endoscopically demonstrated grade II or higher
burns should be admitted. Patients with respiratory
distress, grade III burns, or extensive grade II burns,
acidosis, hemodynamic instability, gastrointestinal
bleeding, or large ingestions should be admitted to an
intensive care setting.
L) PITFALLS
1) The absence of oral burns does NOT reliably exclude the
possibility of significant esophageal burns.
2) Patients may have severe tissue necrosis and impending
perforation requiring early surgical intervention
without having severe hypotension, rigid abdomen, or
radiographic evidence of intraperitoneal air.
3) Patients with any evidence of upper airway involvement
require early airway management before airway edema
progresses.
4) The extent of eye injury (degree of corneal
opacification and perilimbal whitening) may not be
apparent for 48 to 72 hours after the burn. All
patients with acidic eye injury should be evaluated by
an ophthalmologist.
M) DIFFERENTIAL DIAGNOSIS
1) Alkaline corrosive ingestion, gastrointestinal
hemorrhage, or perforated viscus.
0.4.3 INHALATION EXPOSURE
A) INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and assist
ventilation as required. Treat bronchospasm with an
inhaled beta2-adrenergic agonist. Consider systemic
corticosteroids in patients with significant
bronchospasm.
B) INHALATION: Administer oxygen. If respiratory symptoms
develop obtain chest x-ray, monitor pulse oximetry
and/or blood gases. Treat bronchospasm with inhaled
beta2-adrenergic agonists. If acute lung injury
develops, consider PEEP. Evaluate for esophageal, dermal
and eye burns as indicated.
0.4.4 EYE EXPOSURE
A) DECONTAMINATION: Remove contact lenses and irrigate
exposed eyes with copious amounts of room temperature
0.9% saline or water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist after 15 minutes of irrigation, the patient
should be seen in a healthcare facility.
B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each
affected eye with copious amounts of water or sterile
0.9% saline for about 30 minutes. Irrigating volumes up
to 20 L or more have been used to neutralize the pH.
After this initial period of irrigation, the corneal pH
may be checked with litmus paper and a brief external
eye exam performed. Continue direct copious irrigation
with sterile 0.9% saline until the conjunctival fornices
are free of particulate matter and returned to pH
neutrality (pH 7.4). Once irrigation is complete, a full
eye exam should be performed with careful attention to
the possibility of perforation.
C) EYE ASSESSMENT: The extent of eye injury (degree of
corneal opacification and perilimbal whitening) may not
be apparent for 48 to 72 hours after the burn.
0.4.5 DERMAL EXPOSURE
A) OVERVIEW
1) DECONTAMINATION: Remove contaminated clothing and
jewelry and irrigate exposed areas with copious amounts
of water. A physician may need to examine the area if
irritation or pain persists.
Range of Toxicity:
A) TOXICITY: Serious burns are less likely if the pH >3.
Injury is usually greater with either a large ingestion
(usually deliberate), or a high concentration acid
(usually not a household product). With highly
concentrated liquids (eg, 20N), severe burns may occur in
up to 100% of all patients.
B) In a case series of unintentional caustic ingestions
(mixed liquid and solid, acids and bases) among children,
the incidence of significant esophageal or gastric burns
was 5% to 35%. However, adults with deliberate acid
ingestions are more likely to develop significant
esophageal and/or gastric burns (40% to 95%).
[Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO, 2017; CCIS Volume 172, edition expires May, 2017. Hall AH & Rumack
BH (Eds): TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2017; CCIS Volume 172, edition expires May, 2017.] **PEER REVIEWED**
Antidote and Emergency Treatment:

Garlic contains many sulfhydryl compounds that act as antioxidants. However, the role of nitric oxide (NO) in inflammation is controversial.
The aim of the present study is to investigate the possible protective effect of garlic against acetic acid-induced ulcerative colitis in rats, as
well as the probable modulatory effect of L-arginine (NO precursor) on garlic activity. Intra-rectal inoculation of rats with 4% acetic acid for 3
consecutive days caused a significant increase in the colon weight and marked decrease in the colon length. In addition, acetic acid induced
a significant increase in serum levels of nitrate as well as colonic tissue content of malondialdehyde (MDA). Moreover, colonic tissue contents
of glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were markedly reduced. On the other hand, pre-treatment of rats with
garlic (0.25 g/kgbwt, orally) for 4 consecutive weeks and 3 days during induction of colitis significantly reduced the increase in the colon
weight induced by acetic acid and ameliorated alterations in oxidant and antioxidant parameters. Interestingly, oral co-administration of garlic
(0.25 g/kgbwt) and L-arginine (625 mg/kgbwt) for the same period of garlic administration mitigated the changes in both colon weight and
length induced by acetic acid and increased garlic effect on colon tissue contents of MDA and GSH. In conclusion, L-arginine can augment
the protective effect of garlic against ulcerative colitis; an effect that might be mainly attributed to its NO donating property resulting in
enhancement of garlic antioxidant effect...
[Harisa GE et al; Pak J Pharm Sci. 22(4):373-80 (2009).] **PEER REVIEWED** PubMed Abstract
The "cholinergic anti-inflammatory pathway" provides neurological modulation of cytokine synthesis to limit the magnitude of the immune
response. This study aimed to evaluate the impact of the cholinergic anti-inflammatory pathway on the extent of tissue integrity, oxidant-
antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Colitis was induced by
intrarectal administration of 5% acetic acid (1mL) to Sprague-Dawley rats (200-250g; n=7-8 per group). Control group received an equal
volume of saline intrarectally. The rats were treated with either nicotine (1mg/kg/day) or huperzine A (0.1mg/kg/day) intraperitoneally for 3
days. After decapitation, the distal colon was scored macroscopically and microscopically. Tissue samples were used for the measurement of
malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Formation of reactive oxygen species was
monitored by using chemiluminescence (CL). Nuclear factor (NF)-kappaB expression was evaluated in colonic samples via
immunohistochemical analysis. Trunk blood was collected for the assessment of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-
10, resistin and visfatin levels. Both nicotine and huperzine A reduced the extent of colonic lesions, increased colonic MDA level, high MPO
activity and NF-kappaB expression in the colitis group. Elevation of serum IL-1beta level due to colitis was also attenuated by both
treatments. Additionally, huperzine A was effective to reverse colitis-induced high lucigenin-enhanced CL values and serum TNF-alpha levels.
Colitis group revealed decreased serum visfatin levels compared to control group which was completely reversed by nicotine. In conclusion,
modulation of the cholinergic system either by nicotine or ACh esterase inhibition improved acetic acid-induced colonic inflammation as
confirmed by macroscopic and microscopic examination and biochemical assays.
[Kolgazi M et al; Chem Biol Interact. 205(1):72-80 (2013).] **PEER REVIEWED** PubMed Abstract
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-valve-mask 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. /Organic acids and related compounds/
[Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3rd revised edition, Elsevier Mosby, St. Louis, MO
2007, p. 176] **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 respirations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for
pulmonary edema and treat if necessary ... . Monitor for shock 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. Activated
charcoal is not effective ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after
decontamination ... . /Organic acids and related compounds/
2007, p. 176-7] **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. Early intubation, at the first sign of upper airway obstruction, may be necessary.
Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... .
Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as
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 ... .
/Organic acids and related compounds/
2007, p. 177] **PEER REVIEWED**
3 to 5% acetic acid is commonly used in the field of gynecology for colposcopic examinations of the cervix. It gives an 'acetowhite' effect that
may assist clinicians in identifying neoplastic areas. CASE: A perimenopausal woman was treated with acetic acid for abnormal Pap smear
report (cervical intraepithelial neoplasia 1). During application, the patient complained of burning sensation of vagina and vulva. The vagina
was saline-irrigated after realizing that the acetic acid had not been diluted. Following this incident, the patient was seen weekly and treated
with conjugated vaginal estrogen cream. The patient recovered and the vaginal mucosa healed within two weeks. CONCLUSION: Acetic acid
is corrosive and may cause vaginal bleeding. Estrogen cream can be used in an attempt to minimize the adverse reaction and speed the
healing process.
[Ou KY et al; Aust N Z J Obstet Gynaecol. 47(4):345-6 (2007).] **PEER REVIEWED** PubMed Abstract
Animal Toxicity Studies:
Toxicity Summary:
IDENTIFICATION AND USE: Acetic acid is a colorless liquid or solid, having a pungent characteristic odor, and when diluted in water an
acidic taste. Glacial acetic acid is a 99% active chemical. It is used as an acidifier, flavoring agent, for the prevention of rope in baking, and as
a solvent. Acetic acid is used as a laboratory reagent in chemical and biochemical analysis, in field testing of lead fumes, vinyl chloride
determination, uric acid in urine, aniline vapors, and separation of gases. In addition, acetic acid is used in pesticide formulations as a
herbicide to controls weeds on fruits, vegetables, ornamentals and turf. It is also a component of the hydraulic fracturing fluids preventing
precipitation of metal oxides (iron control). Registered for use in the U.S., but approved pesticide uses may change periodically, so federal,
state and local authorities must be consulted for currently approved uses. Three to 5% acetic acid is commonly used in the field of
gynecology for colposcopic examinations of the cervix. It gives an 'acetowhite' effect that may assist clinicians in identifying neoplastic areas.
HUMAN EXPOSURE AND TOXICITY: Acetic acid is absorbed from the gastrointestinal tract and through the lungs and almost completely
oxidized by tissues. The metabolic pathways are reasonably well known and involve the formation of ketone bodies. As little as 1.0 mL of
glacial acetic acid has resulted in perforation of the esophagus. During acetic acid dialysis, patients showed a frequent onset of sudden
hypotension and arrhythmia with concomitant symptoms of the so-called disequilibrium syndrome. Extreme eye and nasal irritation has
occurred at concentrations in excess of 25 ppm and conjunctivitis from concentrations below 10 ppm has been reported. Glacial acetic acid
has caused permanent corneal opacification. Ingestion of 200 mL of an 80% solution of acetic acid caused repeated shock due to myocardial
infarction and massive intestinal bleeding led to an organic brain psychosyndrome. The patient survived the intoxication by use of
hemodialysis and intensive care therapy. An excess of prostate cancer was observed among former chemical plant workers, some of whom
had been exposed to both acetic acid and acetic anhydride. ANIMAL STUDIES: Toxic effects of acetic acid are due to irritant properties as
well as its effect on the central nervous system and kidneys. Large oral doses cause CNS depression and death in rats and mice. Inhalation
of 16,000 ppm killed 1 of 6 exposed rats. Groups of 3-6 rats were given acetic acid in drinking water for periods from 9-15 weeks. Fluid
uptake was the same in all treatment groups, at the high dose group there was a progressive reduction in body weight gain, loss of appetite
and fall in food consumption. Four groups of two young pigs were fed daily diets for successive 30 day periods for a total of 150 days. There
were differences in growth rate, weight gain, early morning urinary ammonia and terminal blood pH between controls and test groups. Acetic
acid had no effects on implantation or on maternal or fetal survival in rats, mice or rabbits dosed via gavage during gestation days 6-19 at
doses up to 1600 mg/kg/day. The number of abnormalities seen in either soft or skeletal tissues of the test groups did not differ from the
number occurring in the controls. Acetic acid has shown no evidence of mutagenic activity with or without metabolic activation using several
strains of Salmonella typhimurium. Acetic acid did not show clastogenicity on cultured Chinese hamster ovary K1 cells at neutral pH, but it
was clastogenic at pH 5.2 to 6.0 with or without metabolic activation. ECOTOXITY STUDIES: Acetic acid was harmful to aquatic life. High
concentrations produced pH levels toxic to oxidizing bacteria, inhibiting oxygen demand. It was lethal to Mosquito fish: at 320 ppm and higher
all fish were dead at 24 hours.
**PEER REVIEWED**
Non-Human Toxicity Excerpts:

/LABORATORY ANIMALS: Acute Exposure/ ...No effect /was found/ in guinea pigs or rabbits after /application/ of 10% acetic acid solution to
intact or abraded skin patches. Concentrations from 80% to glacial produced severe burns to guinea pig skin, concentrations form 50-80%
produced moderate to severe burns, and below 50% there was relatively mild injury.
REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ Liquid glacial acetic acid causes devastating injury when applied to the eyes of rabbits.
[Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 39] **PEER REVIEWED**
/LABORATORY ANIMALS: Acute Exposure/ ...Acetic acid exposure resulted in a significant (P<0.02) increase in lung resistance (by 80%)
and lung elastance (by 67%), lasting <10 minutes postexposure, but no significant change in methacholine responsiveness at one day and
seven days postexposure.
[Ariel AP et al; Can Respir J 5 (5): 349-54 (1998)] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Acute Exposure/ ... Minor changes in respiration in guinea pigs inhaling 5 ppm acetic acid, with more pronounced
effects at 100 ppm.
/LABORATORY ANIMALS: Acute Exposure/ ... Inhalation of 16,000 ppm killed one of six exposed rats.
/LABORATORY ANIMALS: Acute Exposure/ A classical feature of visceral pain is its referring to somatic locations. Gastric ulcer is a source
of visceral pain. In the present study /researchers/ investigated whether gastric ulcers may trigger the changes in somatic nociception. For
this aim somatic pain sensitivity was estimated under conditions of gastric ulcer development and healing. Gastric ulcers were induced by
luminal application of 60% acetic acid under surgical conditions. Control rats were subjected to the same surgical procedure, but with the
application of saline instead of the acid. Somatic pain sensitivity (tail flick latency), plasma corticosterone level, adrenal and thymus weight
were investigated under conditions of the formation and the healing of gastric ulcers. The application of the acid resulted in the formation of
kissing gastric ulcers, the increase of somatic pain sensitivity (the decrease of tail flick latency) as well as the appearance of typical signs of
chronic stress: long-lasting increase of plasma corticosterone level, adrenal gland hypertrophy and thymus gland involution. Natural healing
of gastric ulcers was accompanied by restoration of pain sensitivity as well as attenuation of the signs of chronic stress. Delay of ulcer healing
by the daily indomethacin administration (2 mg/kg, s.c.) prevented the restoration of somatic pain sensitivity. The results suggest that chronic
gastric ulcers may trigger somatic hypersensitivity.
[Yarushkina N et al; Auton Neurosci. 126-127:100-5 (2006).] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Acute Exposure/ The ototoxicity of an otic drop preparation containing 2% acetic acid and 3% propylene glycol ...
was investigated according to measurements of endocochlear potential and inner ear fluid pH. /Twenty healthy chinchillas weighing 450 to
550 g were anesthetized by an intramuscular injection of ketamine hydrochloride (40 mg/kg). Artificial ventilation was provided by a respirator
through a tracheal cannula, and an intramuscular injection of gallamine triethiodine (6 mg/kg) was administered as a muscle relaxant. The
tympanic bulla was then opened./ The application of this preparation to the round window membrane for 30 minutes caused a depression in
endocochlear potential from 80.5 +/- 2.5 mV (mean +/- SD; n= 6) to 11.7 +/- 7.7 mV, and lowered inner ear fluid pH from 7.55 +/- 0.09 to 5.06
+/- 0.19 (n= 6) in perilymph and from 7.52 +/- 0.07 to 5.88 +/- 0.63 (n= 6) in endolymph. Two percent acetic acid produced similar changes
after 30 minutes: endocochlear potential was reduced from 83.0 +/- 2.2 mV to 34.0 +/- 2.9 mV and endolymphatic pH from 7.49 +/- 0.04 to
6.83 +/- 0.21 (n= 4). However, the application of artificial perilymph of pH 4 titrated with hydrochloric acid induced no significant changes in
either endocochlear potential or endolymphatic pH.
[Ideda K, Morizono T; Am J Otolaryngol 10 (6): 382-85 (1989)] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Acute Exposure/ ...As little as 1.0 mL of glacial acetic acid has resulted in perforation of the esophagus.
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Laboratory animals (unspecified species) that inhaled acetic acid vapors (27
to 86 mg/cu m) for 3 to 35 days showed changes in treadmill run duration, open field activity, and ethylene, acetaldehyde, and acetone
concentrations in their exhaled air.
REVIEWED**
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Four groups of 2 young pigs were fed daily diets containing 0, 240, 720, 960
and 1200 mg/kg body-weight/day for successive 30-day periods to a total of 150 days. There were no significant differences in growth rate,
weight gain, early morning urinary ammonia and terminal blood pH between controls and test groups.
[WHO Food Additive Series 64: Acetic acid (1967). Available from, as of February 9, 2004: http://www.inchem.org/documents/jecfa/jecmono/40abcj37.htm
**PEER REVIEWED**
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ /The study/ investigated the effect of acetic acid (AcOH) on the prevention of
obesity in high-fat-fed mice. The mice were intragastrically administrated with water or 0.3 or 1.5% AcOH for 6 weeks. AcOH administration
inhibited the accumulation of body fat and hepatic lipids without changing food consumption or skeletal muscle weight. Significant increases
were observed in the expressions of genes for peroxisome-proliferator-activated receptor alpha (PPARalpha) and for fatty-acid-oxidation- and
thermogenesis-related proteins: acetyl-CoA oxidase (ACO), carnitine palmitoyl transferase-1 (CPT-1), and uncoupling protein-2 (UCP-2), in
the liver of the AcOH-treatment groups. PPARalpha, ACO, CPT-1, and UCP-2 gene expressions were increased in vitro by acetate addition to
HepG2 cells. However, the effects were not observed in cells depleted of alpha2 5'-AMP-activated protein kinase (AMPK) by siRNA. In
conclusion, AcOH suppresses accumulation of body fat and liver lipids by upregulation of genes for PPARalpha and fatty-acid-oxidation-
related proteins by alpha2 AMPK mediation in the liver.
[Kondo T et al ; J Agric Food Chem. 57(13):5982-6 (2009).] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ To investigate the efficacy of the intake of vinegar for prevention of
hyperlipidemia, /the study/ examined the effect of dietary acetic acid, the main component of vinegar, on serum lipid values in rats fed a diet
containing 1 % (w/w) cholesterol. Animals were allowed free access to a diet containing no cholesterol, a diet containing 1 % cholesterol
without acetic acid, or a diet containing 1 % cholesterol with 0.3 % (w/w) acetic acid for 19 days. Then, they were killed after food deprivation
for 7 hrs. Cholesterol feeding increased serum total cholesterol and triacylglycerol levels. Compared with the cholesterol-fed group, the
cholesterol and acetic acid-fed group had significantly lower values for serum total cholesterol and triacylglycerols, liver ATP citrate lyase
(ATP-CL) activity, and liver 3-hydroxy-3-methylglutaryl-CoA content as well as liver mRNA levels of sterol regulatory element binding protein-
1, ATP-CL and fatty acid synthase (P<0.05). Further, the serum secretin level, liver acyl-CoA oxidase expression, and fecal bile acid content
were significantly higher in the cholesterol and acetic acid-fed group than in the cholesterol-fed group (P<0.05). However, acetic acid feeding
affected neither the mRNA level nor activity of cholesterol 7alpha-hydroxylase. In conclusion, dietary acetic acid reduced serum total
cholesterol and triacylglycerol: first due to the inhibition of lipogenesis in liver; second due to the increment in fecal bile acid excretion in rats
fed a diet containing cholesterol.
[Fushimi T et al; Br J Nutr. 95(5):916-24 (2006).] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Intragastric intubation of 3 mL of 10 percent solution acetic acid to rats for 90
days produced a drop in hemoglobin concentration and erythrocyte count.
**PEER REVIEWED**
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Methyltriacetoxysilane undergoes rapid hydrolysis in moist/aqueous
environments (t1/2 is less than 12 seconds) to acetic acid and the corresponding trisilanols, thus observed toxicity is likely due primarily to
acetic acid... Methyltriacetoxysilane is severely irritating and corrosive to the skin, and corrosive to the eyes of animals and is likely to be a
respiratory irritant based on production of acetic acid following hydrolysis. In a 7-day oral range-finding study (gavage) rats were treated with
0, 17 (males), 23 (females), 100, 500 and 1000 mg/kg/d). Ethyltriacetoxysilane rapidly hydrolyzes (in seconds) to acetic acid and a trisilanol
(3:1). The silanol generated is insignificant in both quantity and toxicity relative to the production of acetic acid and its associated toxicity.
Animals from the 17 (males), 23 (females) and 100 mg/kg/day dose groups survived to day 7. Animals from the 500 and 1000 mg/kg/day
dose groups were sacrificed after the third dose as a consequence of two deaths (one from each group), marked body weight loss, and
severity of lesions (ulceration and erosion of stomach and esophagus) observed in necropsied animals. The stomach lesions observed
resembled irritation from acetic acid production. This 7-day range-finder study indicated that a maximum dose level of less than 17 (males)
and 23 (females) mg/kg/day would be required for a longer duration repeated dose study in order to avoid death or obvious suffering due to
the corrosivity of the hydrolysis product, acetic acid. NOAELs following repeated exposure to acetic acid and its salts range from 210 mg/kg
bw/day (2-4 month acetic acid drinking water study; systemic toxicity) to 3600 mg/kg bw/day (acetic acid, sodium salt, 4 week dietary study;
no effects reported). Signs of irritation/corrosion at the site of contact as well as systemic toxicity have been reported. Prolonged inhalation
exposure to acetic acid results in muscle imbalance, increase in blood cholinesterase activity, decreases in albumins and decreased growth
at concentrations greater than 0.01 mg/cu m/day...
[SIDS. Screening Information Data Set for High Production Volume Chemicals. P140. (2006)] **PEER REVIEWED**
/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Ethanol and acetic acid are common end products from silages. The main
objective of this study was to determine whether high concentrations of ethanol or acetic acid in total mixed ration would affect performance in
dairy cows. Thirty mid-lactation Holstein cows were grouped in 10 blocks and fed one of the following diets for 7 wk: (1) control (33%
Bermuda hay + 67% concentrates), (2) ethanol [control diet + 5% ethanol, dry matter (DM) basis], or (3) acetic acid (control diet + 5% acetic
acid, DM basis). Ethanol and acetic acid were diluted in water (1:2) and sprayed onto total mixed rations twice daily before feeding. An equal
amount of water was mixed with the control ration. To adapt animals to these treatments, cows were fed only half of the treatment dose
during the first week of study. Cows fed ethanol yielded more milk (37.9 kg/d) than those fed the control (35.8 kg/d) or acetic acid (35.3 kg/d)
diets, mainly due to the higher DM intake (DMI; 23.7, 22.2, and 21.6 kg/d, respectively). The significant diet x week interaction for DMI, mainly
during wk 2 and 3 (when acetic acid reached the full dose), was related to the decrease in DMI observed for the acetic acid treatment. There
was a diet x week interaction in excretion of milk energy per DMI during wk 2 and 3, due to cows fed acetic acid sustained milk yield despite
lower DMI. Energy efficiency was similar across diets. Blood metabolites (glucose, insulin, nonesterified fatty acids, ethanol, and gamma-
glutamyl transferase activity) and sensory characteristics of milk were not affected by these treatments. Animal performance suggested
similar energy value for the diet containing ethanol compared with other diets. Rumen conversion of ethanol to acetate and a concomitant
increase in methane production might be a plausible explanation for the deviation of the predicted energy value based on the heat of
combustion. Therefore, the loss of volatile compounds during the drying process in the laboratory should be considered when calculating
energy content of fermented feedstuffs.
[Daniel JL et al; J Dairy Sci. 96(1):398-406 (2013)] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Long-term treatment /of unspecified animals/ with 3% acetic acid
administered intragastrically for 6 months resulted in chronic inflammation of the esophageal mucosa.
REVIEWED**
/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The potency of acetic-acid in the tumor progression phase of the mouse
skin model of chemical carcinogenesis and the role of cytotoxicity in carcinogenesis was discussed. ...Mice treated with acetic-acid had a
greater carcinoma incidence than mice treated with acetone alone, 80 versus 47%, respectively. The total number of papillomas that
progressed to carcinomas was 55% greater in the acetic-acid treatment group. Papilloma regression was not significantly altered in the
acetic-acid group, compared to the acetone group. Histological examination revealed no significant differences in the cancers formed.
[Rotstein JB et al; Cancer Lett 42 (1-2): 87-90 (1988)] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ...Acetic acid had no effects on implantation or on maternal or fetal
survival in rats, mice or rabbits dosed via gavage during gestation days 6-19 at doses up to 1600 mg/kg/day. The number of abnormalities
seen in either soft or skeletal tissues of the test groups did not differ from the number occurring in the controls...
[SIDS. Screening Information Data Set for High Production Volume Chemicals. P140. (2006)] **PEER REVIEWED**
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ A major class of disinfection by-products found in drinking water are the
haloacetic acids. Haloacetic acids can be formed by a variety of processes, e.g. chloroacetic acids can be formed during chlorination and
bromoacetic acids can be by-products of ozonation. Both dichloro- and trichloroacetic acids have been reported to be teratogenic. There is
little information regarding the developmental toxicity of bromoacetates and no structure-activity analysis of haloacetates. Therefore, 3-6
somite CD-1 mouse embryos were exposed to acetic acid (AA), or mono (M), di (D), and tri (T) substituted chloro (C) or bromo (B)-acetic
acids (A) (e.g. DCA= dichloroacetic acid) in whole embryo culture and the morphological effects were evaluated. Conceptuses exposed to
these agents for 24 hours exhibited malformations. Neural tube defects ranged from prosencephalic hypoplasia to non-closure throughout the
cranial region. Other craniofacial defects included optic, otic and pharyngeal arch dysmorphogenesis. Benchmark concentrations (BC) for a
5% increase in NTDs for the studied chemicals in order of increasing potency are dichloroacetic acid (2452 uM) <acetic acid (1888 uM)
<tribromoacetic acid (1403 uM) <trichloroacetic acid (1336 uM) <dibromoacetic acid (162 uM) <monochloroacetic acid (91.5 uM)
<monobromoacetic acid (2.68 uM). Quantitative structure-activity relationships were derived from these data and other (iodo(I) and fluoro (F))
haloacetic acid data not presented (monoiodoacetic acid, monofluoroacetic acid, difluoroacetic acid, trifluoroacetic acid). The best regression
was derived by excluding acetic acid (n=10) and relating log (1/BC) to Elumo and pKa with r=0.96, adj.r2 =0.90. These studies indicate that
all of the haloacetates can directly alter development and there is a wide range of concentration that produce dysmorphogenesis.
[Rogers EH et al; Teratology 51 (3): 195 (1995)] **PEER REVIEWED**
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Following mating, adult female albino CD-1 mice were dosed daily by
oral intubation beginning on day 6 of gestation at concentrations of 0 (control), 16, 74, 345, and 1600 mg/kg bw/day. Animals were observed
daily and body weights recorded for 10 days. On day 17, Caesarian sections were performed on all dams and the numbers of implantation
sites, resorption sites, and live and dead fetuses was recorded. General external and internal examinations were also made of the dams. No
effects on nidation or on maternal or fetal survival were observed at doses up to 1600 mg/kg bw/day. The number of abnormalities seen in
either soft or skeletal tissues of the test groups did not differ from the number occurring in the controls.
[EPA/Office of Pollution Prevention and Toxics; High production Volume (HPV) Challenge Program's Robust summaries and Test Plans. Acetic acid and Salts
(April 2003). Available from, as of February 9, 2004: http://www.epa.gov/hpv/pubs/hpvrstp.htm **PEER REVIEWED**
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Suckling rats were exposed to one of three soln, 2.6X10-3 M lead
acetate, 5X10-3 M acetic acid or water, from parturition until the pups were 18 days old. Male offspring from dams on acetic acid
demonstrated above normal preweaning body weights and were significantly less active than normals in the open field by day 44.
[Barrett J, Livesey PJ; Neurobehav Toxicol Teratol 4 (1): 105-8 (1982)] **PEER REVIEWED** PubMed Abstract
/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Ethanol and its metabolites acetaldehyde and acetic acid were injected
into the eggs during incubation, and the course of the egg development was observed during 21 days covering 3 stages (early, middle, and
terminal). Lethal eggs occurred mainly in the early stage. The toxicity was the highest for acetaldehyde, followed by ethanol and acetic acid in
decreasing order. Chickens with some deformities were hatched from treated eggs. A strong resemblance was shown between the
deformities in the chickens during the early stage of development and the fetal alcohol syndrome in man at the 3rd month of gestation.
[Kawamoto K; Nichidai Igaku Zasshi 40 (3): 249-59 (1981)] **PEER REVIEWED**
/GENOTOXICITY/ Acetic acid (sodium salt) elicited no mutagenic response in the Ames Salmonella typhimurium assay or in Saccharomyces
cerevisiae with or without liver preparations from mouse, rat, or monkey.
REVIEWED**
/GENOTOXICITY/ ...The clastogenicity of acetic acid on cultured Chinese hamster ovary K1 cells /was studied. It was/... concluded that
acetic acid was not clastogenic at concentrations close to those that showed cytotoxicity up to 16 mM). Although chromosomal aberrations
could be induced at these high concentrations, they were shown to be artifacts due to acidification of the culture medium and could be
eliminated by neutralizing the medium or enhancing its buffering ability.
REVIEWED**
/GENOTOXICITY/ Acetic acid (64-19-7) has shown no evidence of mutagenic activity with or without metabolic activation using Ames
Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 97 and TA 1537 at concentrations of 100, 333,0 1000, 3333, 6666, and 10000
microg/plate.
/GENOTOXICITY/ ...Concentrations of up to 16 millimolar (mM) formic-acid, acetic-acid, and lactic-acid were incubated with Chinese-
hamster-ovary-K1 cells with or without metabolic activation from liver S9 mix from phenobarbital and 5,6-benzoflavone induced rats. ...All
three acids induced chromosome aberrations at concentrations of 12 to 14mM and initial pHs of 5.2 to 6.1 in the presence or absence of S9
mix. ...The acids induced chromosome aberrations at pH 5.8 or 6.0, but their clastogenicity disappeared when the medium was neutralized.
[Morita T et al; Mutat Res 240 (3): 195-202 (1990)] **PEER REVIEWED** PubMed Abstract
/ALTERNATIVE and IN VITRO TESTS/ The direct effects of ethanol and its metabolites on the guinea pig lung mast cell /were studied./ High
concentrations of ethanol (100 mg/mL), acetaldehyde (0.3-3 mg/mL) and acetic acid (3 mg/mL) induced histamine release that was not
inhibited by sodium cyanide (0.3 mM). Lower concentration of ethanol (10 mg/mL) and acetic acid (0.3 mg/mL), but not acetaldehyde,
inhibited the histamine release induced by antigen and ionophore A23187. The histamine release induced by phorbol 12-miristate 13-acetate
(1 microM) was also inhibited by ethanol (10 mg/mL). Changes in the levels of calcium, glucose and phosphatidic acid did not influence the
effect of ethanol.
[Martinez Ruiz C et al; Alcohol 20 (2): 133-138 (2000)] **PEER REVIEWED** PubMed Abstract
/VETERINARY CASE REPORTS/ ...Death of 2 out of six horses dosed by their owner for the treatment of Oxyuris infection with 15 L of a
2.5% solution of acetic acid; two other horses were seriously affected and all showed symptoms of enteritis. ...Dullness, loss of appetite, red
and jaundiced appearance of the visible mucous membranes and rapid pulse and respiration. Post mortem findings included hemorrhages in
the small intestine and its mesentery, hyperemia of the mesenteric lymph nodes, diphtheritic inflammation of the small colon with subserous
hemorrhages and edema of the rectum.
[Humphreys, D.J. Veterinary Toxicology. 3rd ed. London, England: Bailliere Tindell, 1988., p. 183] **PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ Toxic effects of acetic acid are due to its irritant properties as well as its effect on the central nervous
system and kidneys. Large oral doses causes ... CNS depression and death in rats and mice.
**PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ ...Long-term administration of vinegar or the acetic acid to /spontaneously hypertensive rats/ was
examined. As a result, it was observed that acetic acid itself ...significantly reduced both blood pressure (p<0.05) and renin activity (p<0.01)
compared to controls... .
[Kondo S et al; Biosci Biotechnol Biochem 65 (12): 2690-94 (2001) ] **PEER REVIEWED**
/OTHER TOXICITY INFORMATION/ Although acetic acid has been shown to induce apoptosis in yeast, the exact apoptotic mechanisms
remain unknown. Here, /the study examined/ the effects of acetic acid treatment on yeast cells by 2-DE, revealing alterations in the levels of
proteins directly or indirectly linked with the target of rapamycin (TOR) pathway: amino-acid biosynthesis, transcription/translation machinery,
carbohydrate metabolism, nucleotide biosynthesis, stress response, protein turnover and cell cycle. The increased levels of proteins involved
in amino-acid biosynthesis presented a counteracting response to a severe intracellular amino-acid starvation induced by acetic acid.
Deletion of GCN4 and GCN2 encoding key players of general amino-acid control (GAAC) system caused a higher resistance to acetic acid
indicating an involvement of Gcn4p/Gcn2p in the apoptotic signaling. Involvement of the TOR pathway in acetic acid-induced apoptosis was
also reflected by the higher survival rates associated to a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-
negative phenotype and lower reactive oxygen species levels of Deltator1 cells. In addition, deletion mutants for several downstream
mediators of the TOR pathway revealed that apoptotic signaling involves the phosphatases Pph21p and Pph22p but not Sit4p. Altogether,
/these/ results indicate that GAAC and TOR pathways (Tor1p) are involved in the signaling of acetic acid-induced apoptosis.
[Almeida B et al; Proteomics. 9(3):720-32 (2009).] **PEER REVIEWED** PubMed Abstract
/OTHER TOXICITY INFORMATION/ The acetic acid and phenyl-p-benzoquinone are easy and fast screening models to access the activity of
novel candidates as analgesic drugs and their mechanisms. These models induce a characteristic and quantifiable overt pain-like behavior
described as writhing response or abdominal contortions. The knowledge of the mechanisms involved in the chosen model is a crucial step
forward demonstrating the mechanisms that the candidate drug would inhibit because the mechanisms triggered in that model will be
addressed. Herein, it was investigated the role of spinal mitogen-activated protein (MAP) kinases ERK (extracellular signal-regulated kinase),
JNK (Jun N-terminal Kinase) and p38, PI(3)K (phosphatidylinositol 3-kinase) and microglia in the writhing response induced by acetic acid
and phenyl-p-benzoquinone, and flinch induced by formalin in mice. Acetic acid and phenyl-p-benzoquinone induced significant writhing
response over 20 min. The nociceptive response in these models were significantly and in a dose-dependent manner reduced by intrathecal
pre-treatment with ERK (PD98059), JNK (SB600125), p38 (SB202190) or PI(3)K (wortmannin) inhibitors. Furthermore, the co-treatment with
MAP kinase and PI(3)K inhibitors, at doses that were ineffective as single treatment, significantly inhibited acetic acid- and phenyl-p-
benzoquinone-induced nociception. The treatment with microglia inhibitors minocycline and fluorocitrate also diminished the nociceptive
response. Similar results were obtained in the formalin test. Concluding, MAP kinases and PI(3)K are important spinal signaling kinases in
acetic acid and phenyl-p-benzoquinone models of overt pain-like behavior and there is also activation of spinal microglia indicating that it is
also important to determine whether drugs tested in these models also modulate such spinal mechanisms.
[Pavao-de-Souza GF et al; Pharmacol Biochem Behav. 101(3):320-8 (2012).] **PEER REVIEWED** PubMed Abstract
/OTHER TOXICITY INFORMATION/ Animal models that closely resemble the pathophysiology of human overactive bladder are important for
evaluating novel therapeutics to treat the disorder. /The authors/ established a non-invasive hyperactive bladder model that is sensitive to
anti-muscarinic drugs and without bladder inflammation. Acetic acid solution was infused into the bladder for 5 min via the urethral orifice
without any surgical procedures under isoflurane anesthesia. After washing the bladder with saline, voiding frequency (VF) and total urine
volume were determined for 9 hr under conscious conditions. Infusion of a 0.5% acetic acid solution caused a significant increase in VF,
without influencing total urine volume or inducing significant histopathological inflammatory alterations in the bladder urothelium. Oral
administration of oxybutynin (3 and 10 mg/kg) significantly ameliorated increases in VF induced by 0.5% acetic acid. Infusion of 0.75% acetic
acid induced intensive urinary inflammation and a decrease in total urine volume as well as an increase in VF. Oral treatment with oxybutynin
(10 mg/kg) did not significantly improve the increased VF due to 0.75% acetic acid. Acetic acid (0.5%) infusion evoked bladder hyper-
responsiveness whether applied at night or during the day. However, VF was increased more by the nighttime application of acetic acid, while
there were no significant differences in basal levels of VF between daytime and nighttime. In this study, the non-invasive rat urinary
hyperactive bladder model indicated minimizes the secondary effects of experimental procedures such as surgical operations and anesthesia
on bladder function and is sensitive to oxybutynin. Thus, the model may be useful for investigating novel therapeutics for OAB treatment.
[Mitobe M et al; J Pharmacol Toxicol Methods. 57(3):188-93 (2008).] **PEER REVIEWED** PubMed Abstract
Ecotoxicity Excerpts:
/AQUATIC SPECIES/ Acetic acid is harmful to aquatic life. High concentrations will produce pH levels toxic to oxidizing bacteria, inhibiting
oxygen demand.
[Environment Canada; Tech Info for Problem Spills: Acetic acid (Draft) p.1 (1981)] **PEER REVIEWED**
/AQUATIC SPECIES/ Ten Mosquito fish were exposed to test concentrations for a period of 96 hours. The concentrations used for the first
experiment were 10, 18, 32, 56 and 100 ppm. When deaths did not occur at these concentrations within 96 hours the same series was run
between 100 and 1,000 ppm. The temperature, turbidity, and pH of the experimental water were measured after the test substance was
added and daily throughout the experiment. Survivor observations were made at 24, 48, 72 and 96 hours. Test water was maintained at pH
6.9 -8.7 and 16-25 deg C. Fish transferred to concentrations between 100 and 1,000 ppm swam frantically and at 100 and 180 ppm returned
to normal in 24 hours. At 320 ppm and higher all fish were dead at 24 hours.
Non-Human Toxicity Values:

LD50 Rat oral 3.53 g/kg
[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 11]
**PEER REVIEWED**
LD50 Mouse iv 525 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. 16]
**PEER REVIEWED**
LD50 Rabbit dermal 1060 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. 16]
**PEER REVIEWED**
LD50 Mouse oral 4960 mg/kg

**PEER REVIEWED**
LD50 Rabbit sc 1200 mg/kg

**PEER REVIEWED**
LD50 Rabbit oral 1200 mg/kg

**PEER REVIEWED**
LD50 Rat oral 3.31 g/kg

**PEER REVIEWED**
LC50 Rat inhalation 11.4 mg/L /4 hr

LC50 Mouse inhalation 5,620 ppm/1 hr

Ecotoxicity Values:
EC50; Species: Chlorococcales (Green Algae Order); Conditions: freshwater, static; Concentration: 156000 ug/L for 24 hr; Effect: physiology,
assimilation efficiency /formulation/
[Krebs F; Dtsch Gewaesserkd Mitt 35 (5-6): 161-170 (1991) as cited in the ECOTOX database. Available from, as of June 21, 2014:
http://cfpub.epa.gov/ecotox/quick_query.htm **PEER REVIEWED**
LC50; Species: Crangon septemspinosa (Bay Shrimp, Sand Shrimp) weight 0.003 g; Conditions: saltwater, renewal, 15 deg C, pH 3.64-8.07;
Concentration: 116000 ug/L for 14 days (95% confidence interval: 85900-157000 ug/L) /99.7% purity/
[Locke A et al; Aquat Invasions 4 (1): 221-236 (2009) as cited in the ECOTOX database. Available from, as of June 21, 2014:
LC50; Species: Crangon septemspinosa (Bay Shrimp, Sand Shrimp) weight 0.003 g; Conditions: saltwater, static, 15 deg C, pH 2.26-7.96;
Concentration: 158000 ug/L for 96 hr (95% confidence interval: 50000-500000 ug/L) /99.7% purity/
[Locke A et al; Aquat Invasions 4 (1): 221-236 (2009) as cited in the ECOTOX database. Available from, as of June 21, 2014:
EC50; Species: Daphnia magna (Water flea); Conditions: static bioassay, neutralized to pH 8.0 and 20 deg C; Concentration: 6,000 mg/L for
24 hr; Effect: immobilization
LC50; Species: Daphnia magna (Water flea); Conditions: freshwater, static, 21-25 deg C; Concentration: 47000 ug/L for 24 hr /formulation/
[Dowden BF, Bennett HJ; J Water Pollut Control Fed 37 (9): 1308-1316 (1965) as cited in the ECOTOX database. Available from, as of June 21, 2014:
LC50; Species: Daphnia magna (Water flea); Conditions: freshwater, static, 21-25 deg C; Concentration: 426000 ug/L for 100 hr
[Dowden BF, Bennett HJ; J Water Pollut Control Fed 37 (9): 1308-1316 (1965) as cited in the ECOTOX database. Available from, as of June 21, 2014:
LC50; Species: Oreochromis mossambicus (Mozambique Tilapia) adult male/female, weight 11.83 g; Conditions: freshwater, renewal, pH
7.21; Concentration: 272870 ug/L for 96 hr (95% confidence interval: 268990-276750 ug/L) /99% purity/
[Saha NC et al; Hum Ecol Risk Assess 12 (1): 192-202 (2006) as cited in the ECOTOX database. Available from, as of June 21, 2014:
LC50; Species: Pimephales promelas (Fathead minnow); Conditions: static bioassay in Lake Superior water at 18-22 deg C; Concentration:
>315 mg/L for 1 hr
[Verschueren, K. Handbook of Environmental Data on Organic Chemicals. Volumes 1-2. 4th ed. John Wiley & Sons. New York, NY. 2001, p. 104] **PEER
REVIEWED**
122 mg/L for 24 hr
REVIEWED**
92 mg/L for 48 hr
REVIEWED**
88 mg/L for 72 hr
REVIEWED**
88 mg/L for 96 hr
REVIEWED**
LC50; Species: Pimephales promelas (Fathead minnow); Conditions: static bioassay in reconstituted water at 18-22 deg C, pH</= 5.9;
Concentration: 175 mg/L for 1 hr
REVIEWED**
LC50; Species: Pimephales promelas (Fathead minnow); Conditions: static bioassay in reconstituted water at 18-22 deg C, pH</= 5.9;

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HSDB Env. Health & Toxicology TOXNET HSDB

For more information, search the NLM HSDB database.

Human Health Effects:

Skin, Eye and Respiratory Irritations:

Irritating concn: 25 mg/cu m.

... Eye irritation has been noted at a concentration below 10 ppm.

Vapors strongly irritating to eyes and respiratory tract.

Probable Routes of Human Exposure:

Emergency Medical Treatment:

Emergency Medical Treatment:

Antidote and Emergency Treatment:

Animal Toxicity Studies:

Non-Human Toxicity Excerpts:

Non-Human Toxicity Values:

LD50 Mouse iv 525 mg/kg

LD50 Rabbit dermal 1060 mg/kg

LD50 Mouse oral 4960 mg/kg

LD50 Rabbit sc 1200 mg/kg

LD50 Rabbit oral 1200 mg/kg

LD50 Rat oral 3.31 g/kg

LC50 Rat inhalation 11.4 mg/L /4 hr

LC50 Mouse inhalation 5,620 ppm/1 hr

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