MOBILE VIEW  | 

PERACETIC ACID

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Peracetic acid is a strong oxidizing agent prepared in the presence of cobalt acetate from oxygen and acetaldehyde or by treating acetic anhydride with hydrogen peroxide in the presence of sulfuric acid (Budavari, 1989).

Specific Substances

    1) Acetyl Hydroperoxide
    2) Acide Peracetique (French)
    3) Ethaneperoxoic acid
    4) Hydroperoxide, acetyl
    5) Peracetic acid solution
    6) Peroxyacetic Acid
    7) CAS 79-21-0
    8) PEROXYACETIC ACID SOLUTION
    1.2.1) MOLECULAR FORMULA
    1) C2-H4-O3
    2) CH3CO-O-OH

Available Forms Sources

    A) FORMS
    1) Peracetic acid exists as a colorless liquid. Typical grades of purity are 40% peracetic acid, 40% acetic acid, 5% hydrogen peroxide, 13% water, 500 ppm stabilizer (CHRIS , 2000). "Not over 40% peracetic acid and not over 6% hydrogen peroxide (Lewis, 1996).
    2) Commercial preparations are available as 40 percent solutions (Gosselin et al, 1984), but cannot be obtained free from hydrogen peroxide (Coppinger et al, 1983).
    B) SOURCES
    1) Peracetic acid is produced from acetaldehyde (air oxidation, co-produced with acetic acid). It is also formed by mixing acetic acid and hydrogen peroxide (sulfuric acid process) (Ashford, 1994; Lewis, 1997). It is also formed by the reaction of acetaldehyde and oxygen in "the presence of cobalt acetate" (Budavari, 1996). "A 50% solution may be obtained from acetic anhydride, hydrogen peroxide, and sulfuric acid" (Budavari, 1996).
    2) "Commercially, ozone is used as a catalyst below 15 degrees C in the production of peracetic acid from acetaldehyde and ozone" (HSDB , 2000).
    C) USES
    1) Peracetic acid is used as a disinfectant for food and beverage equipment and as a biocide in paper production (Ashford, 1994). This compound is used as a polymerization initiator, curing agent, and cross-linking agent (Lewis, 1996). Peracetic acid has also been used as a cold-temperature sterilant because it is an effective bactericide, fungicide, and viricide. It has also been used as a pre-operative hand sterilant (Clayton & Clayton, 1993).
    2) Peracetic acid is used as a bleaching agent for textiles, papers, oils, waxes, and starches. It is also used as a polymerization catalyst; as a bactericide and fungicide (especially in food processing); in the epoxidation of fatty acid esters and epoxy resin precursors; as a reagent in making caprolactam and synthetic glycerine (ITI, 1995; Lewis, 1997). It is also used as an oxidant for preparing epoxy compounds and as a sterilizing agent (Sittig, 1991).
    3) Peracetic acid is used as a post-harvest spray for bananas, berries, other fruits, vegetables, and containers. It is also used as a wash for eggs and as a treatment for containers used in crop harvest (HSDB , 2000).
    4) A concentration of 0.1% peracetic acid in water is an effective disinfection for Schiotz tonometers (Grant, 1993).
    5) Peracetic acid and hydrogen peroxide acted synergistically as a sporicide. The minimal sporicidal concentration (MSC) was: peracetic acid 168 to 336 ppm (1 to 2 hours contact time), hydrogen peroxide 5625 to 11250 ppm (5 to 7 hours contact time). The combination of 21 ppm of peracetic acid and 2813 ppm of hydrogen peroxide gave total disinfection of hollow fibers in 2 to 3 h of contact (Alasri et al, 1993).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Peracetic acid as a vapor or liquid is corrosive to the eyes and skin, and to mucous membranes. Pain, irritation and ulceration of tissues may occur after contact. Contact with eyes may cause corrosive corneal burns and blindness. Significant absorption through the skin or by inhalation may be fatal.
    B) Ingestion may cause difficulty swallowing, nausea, vomiting, and oral, esophageal, and gastrointestinal tract burns, followed by circulatory collapse and shock.
    C) Animals that died from acute or subacute inhalation poisoning had lesions confined to the lungs.
    0.2.3) VITAL SIGNS
    A) An increase in blood pressure, respiratory rate and pulse has been noted in animal experiments.
    0.2.4) HEENT
    A) Peracetic acid can cause severe eye irritation.
    B) A 10 percent solution of peracetic acid applied to rabbit eyes caused corneal ulceration, perforation, and symblepharon formation.
    C) Irritation of nasal and throat mucosa is common with exposure to vapors.
    0.2.6) RESPIRATORY
    A) Mice exposed by inhalation developed signs of respiratory tract irritation.
    0.2.8) GASTROINTESTINAL
    A) Ingestion of peracetic acid may cause gastrointestinal tract irritation and possible oral and esophageal burns.
    0.2.9) HEPATIC
    A) Liver granulomas developed in exposed animals.
    0.2.13) HEMATOLOGIC
    A) A decrease in leukocyte counts was observed in animal studies.
    0.2.14) DERMATOLOGIC
    A) Peracetic acid is highly irritating and possibly corrosive to the skin.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) Peracetic acid is a potential animal carcinogen.

Laboratory Monitoring

    A) Baseline chest x-ray and arterial blood gases should be obtained in patients with significant inhalation exposure or respiratory tract irritation.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do not induce emesis or attempt to neutralize in any way.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) Passing a nasogastric tube is controversial, but may be beneficial if a large amount is ingested. Activated charcoal is of questionable value.
    D) Thoroughly irrigate all exposed areas with water.
    E) Evaluate for oral, esophageal, or gastrointestinal burns.
    F) Steroid administration is controversial.
    G) Surgical consultation should be obtained in severe cases where hemorrhage, necrosis, perforation, obstruction, or stricture formation is present or anticipated.
    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) Administer 100% supplemental humidified oxygen with assisted ventilation as required.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The minimum lethal and maximum tolerated human exposures have not been established. The upper tolerance limit for human skin is a 0.4% solution.

Summary Of Exposure

    A) Peracetic acid as a vapor or liquid is corrosive to the eyes and skin, and to mucous membranes. Pain, irritation and ulceration of tissues may occur after contact. Contact with eyes may cause corrosive corneal burns and blindness. Significant absorption through the skin or by inhalation may be fatal.
    B) Ingestion may cause difficulty swallowing, nausea, vomiting, and oral, esophageal, and gastrointestinal tract burns, followed by circulatory collapse and shock.
    C) Animals that died from acute or subacute inhalation poisoning had lesions confined to the lungs.

Vital Signs

    3.3.1) SUMMARY
    A) An increase in blood pressure, respiratory rate and pulse has been noted in animal experiments.
    3.3.2) RESPIRATIONS
    A) A peracetic acid disinfectant caused an increase in the respiratory rate of experimentally exposed dogs, but not rats (Heneghan & Gates, 1966).
    3.3.4) BLOOD PRESSURE
    A) A peracetic acid disinfectant caused an initial decrease followed by an increase in blood pressure in exposed dogs (Heneghan & Gates, 1966). This effect was not seen in experimentally exposed rats (Heneghan & Gates, 1966).
    3.3.5) PULSE
    A) An increased pulse was noted in experimentally exposed dogs and rats (Heneghan & Gates, 1966).

Heent

    3.4.1) SUMMARY
    A) Peracetic acid can cause severe eye irritation.
    B) A 10 percent solution of peracetic acid applied to rabbit eyes caused corneal ulceration, perforation, and symblepharon formation.
    C) Irritation of nasal and throat mucosa is common with exposure to vapors.
    3.4.3) EYES
    A) Peracetic acid can cause severe eye irritation (CHRIS , 1990; Sax & Lewis, 1989).
    B) When a 10% solution of peracetic acid was applied to rabbit eyes, there was corneal ulceration, perforation, and symblepharon formation despite prompt water irrigation after application (Grant, 1986).
    C) Peracetic acid induced severe eye irritation in the rabbit in the Standard Draize Test (RTECS , 1991).
    3.4.5) NOSE
    A) Peracetic acid is highly irritating to the mucosa of the nose (CHRIS , 1990; Sax & Lewis, 1989).
    3.4.6) THROAT
    A) Peracetic acid is highly irritating to the mucosa of the throat (CHRIS , 1990; Sax & Lewis, 1989).

Respiratory

    3.6.1) SUMMARY
    A) Mice exposed by inhalation developed signs of respiratory tract irritation.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Mice exposed by inhalation developed signs of respiratory tract irritation and bronchopneumonia (Merka & Urban, 1976) Heinze & Natterman, 1984).
    2) PULMONARY CARCINOMA
    a) MICE - An increase in lung tumors was observed in mice exposed by inhalation (Heine Natterman, 1984).
    3) PNEUMONIA
    a) BRONCHOPNEUMONIA was observed in most of the mice and guinea pigs exposed to peracetic acid aerosol at doses of 186 or 280 mg/m(3) 30 minutes twice daily for 90 days (Heinze & Nattermann, 1984).
    b) Animals who died within 48 hours of inhalation had hemorrhagic exudative infiltrates of the parenchyma of all parts of the lungs, while those who died about the sixth day after inhalation had focal bronchopneumonia (Merka & Urban, 1976).

Gastrointestinal

    3.8.1) SUMMARY
    A) Ingestion of peracetic acid may cause gastrointestinal tract irritation and possible oral and esophageal burns.
    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL IRRITATION
    1) Ingestion of peracetic acid may cause gastrointestinal tract irritation including oral, esophageal, and gastrointestinal burns (CHRIS , 1990).

Hepatic

    3.9.1) SUMMARY
    A) Liver granulomas developed in exposed animals.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GRANULOMATOUS LESION
    a) Liver granulomas were observed in most of the mice and guinea pigs exposed to peracetic acid by inhalation (Heinze & Natterman, 1984).

Hematologic

    3.13.1) SUMMARY
    A) A decrease in leukocyte counts was observed in animal studies.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LEUKOPENIA
    a) Decreased leukocyte counts were observed in most of the mice and guinea pigs exposed to peracetic acid by inhalation (Heinze & Natterman, 1984).

Dermatologic

    3.14.1) SUMMARY
    A) Peracetic acid is highly irritating and possibly corrosive to the skin.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Peracetic acid is highly irritating to the skin (Bock et al, 1975; CHRIS , 1990; Sax & Lewis, 1989).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DERMATITIS CONTACT
    a) GUINEA PIGS - Dermatitis was observed on guinea pig skin as early as 2 hours after direct contact with a 3% solution (Bulnes, 1982).
    2) RASH
    a) RABBITS - Peracetic acid induced severe skin irritation in the rabbit in the Open Draize Test (RTECS , 1991).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) No data are available to assess the potential teratogenicity of peracetic acid or its possible effects during pregnancy and lactation.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS79-21-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Peracetic acid is a potential animal carcinogen.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Peracetic acid in water at a 1% or 3% (but not 0.3%) concentration was a skin tumor-promoting stimulus in Swiss mice exposed chronically by the dermal route (Bock et al, 1975). Peracetic acid in water at a 2% concentration was a weak, complete skin tumor carcinogen in Swiss mice chronically exposed by the dermal route (Bock et al, 1975).
    2) In MICE, peracetic acid was found to be an equivocal tumorigenic agent by RTECS criteria with skin and appendages tumors and tumors at the site of application (RTECS , 1991).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Baseline chest x-ray and arterial blood gases should be obtained in patients with significant inhalation exposure or respiratory tract irritation.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Baseline arterial blood gases are suggested in patients with significant inhalation exposure or respiratory tract irritation.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Baseline chest x-ray is suggested in patients with significant inhalation exposure or respiratory tract irritation.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with ingestion of large amounts of peracetic acid or signs of oral, esophageal, or gastrointestinal irritation or burns should be admitted.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Surgical consultation should be obtained in patients with signs of hemorrhage, necrosis, perforation, obstruction, or stricture formation.
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Patients with moderate to severe respiratory tract irritation should be admitted.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients with significant inhalation exposure but no signs of respiratory tract irritation should be observed in a controlled setting for several hours. Prior to discharge, patients should be warned to return immediately if symptoms of respiratory tract irritation develop later.

Monitoring

    A) Baseline chest x-ray and arterial blood gases should be obtained in patients with significant inhalation exposure or respiratory tract irritation.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) Induction of emesis is not recommeded.
    B) DILUTION -
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    C) ACTIVATED CHARCOAL -
    1) Use of activated charcoal is of unknown value and not routinely recommended as it may induce vomiting and obscure endoscopy findings.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) Induction of emesis is not recommended.
    B) GASTRIC LAVAGE
    1) Penner (1980) argues that following a large ingestion of strong acids, a nasogastric tube should be passed and the stomach contents suctioned in an attempt to remove as much acid as possible. Many authorities oppose this procedure, fearing esophageal or gastric perforation.
    2) Soft nasogastric or orogastric tubes should probably only be passed within 30 minutes following a large ingestion of strong acid, as the probability of removing a significant amount of acid after that time is minimal.
    C) ACTIVATED CHARCOAL
    1) Activated charcoal is of unknown value and not routinely recommended as it may induce vomiting and obscure endoscopy findings.
    D) DILUTION
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    6) NEUTRALIZATION
    a) Neutralization with a base such as sodium bicarbonate is NOT recommended.
    6.5.3) TREATMENT
    A) IRRIGATION
    1) If age appropriate, irrigate the mouth with copious amounts of water. Immediate dilution with small amounts of milk or water may help decontaminate the oral mucosa or dislodge particles of granular acids from the esophageal mucosa.
    2) The amount of diluent recommended by the POISINDEX editorial board for caustic alkali ingestion varied, and may be useful in establishing guidelines for acid ingestion. Suggestions ranged from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum amount of 8 ounces in adults and 4 ounces in children (Consensus, 1988).
    3) Dilution of acid with water has been shown to be ineffective in altering the pH. The dilution of 50 milliliters of 9.5 percent HCl with 800 milliliters of water resulted in a pH change of 0.99 to 1.73 (Maull et al, 1985).
    4) Dilution with milk or water immediately or after 5 minutes reduced the extent of tissue injury induced by 0.5 N HCl in isolated rat esophagi (Homan et al, 1995).
    B) SUCRALFATE
    1) Sucralfate may be useful in relieving symptomatology from acid induced injury. Efficacy in accelerating healing or preventing complications has not been proven.
    2) CASE REPORT - Administration of sucralfate, 1 gram dissolved in 30 milliliters of water, four times a day, was used in a 25-year-old man with moderately severe gastric injury after ingestion of hydrochloric acid. No other therapy was given other than antibiotic. Within 48 hours, improvement in symptoms was noted, enabling progression to a liquid diet on the 3rd day. Strictures were not prevented, although nearly complete gastric mucosal healing occurred after 2 weeks. The patient received a gastrojejunostomy for pyloric stricture 6 weeks postingestion (Mittal et al, 1989).
    C) LEUCOVORIN CALCIUM
    1) Moore et al (1993) describe treatment of a case who had ingested 250 milliliters of a 44% solution of formic acid. Intravenously infused leucovorin (i.e, folinic acid) was used to enhance hepatic degradation of formate and furosemide was administered to prevent the renal absorption of formate. Hemofiltration was also instituted. The patient survived.
    D) INSERTION OF NASOGASTRIC TUBE
    1) Penner (1980) argues that following a large ingestion of strong acids, a nasogastric tube should be passed and suction performed in an attempt to remove as much acid as possible prior to cold water dilution which may result in an exothermic reaction and worsen the burn.
    2) Many authorities oppose this procedure fearing esophageal or gastric perforation. Soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.
    E) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    4) If hypotension is secondary to gastrointestinal bleeding, blood or blood products replacement therapy are the treatments of choice.
    F) BURN
    1) SUMMARY - Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. Early (within 24 hours) endoscopy should be performed to assess the severity of injury and guide future management.
    2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    3) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    6) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    G) DIETARY FINDING
    1) Depends on degree of damage as assessed by early endoscopy (Dilawari et al, 1984).
    1) mild (grade I): may have oral feedings first day
    2) moderate (grade II): may have liquids after 48 to 72 hours
    3) severe (grade III): jejunostomy tube feedings after 48 to 72 hours
    2) Observe for symptoms of gastric outlet obstruction, at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestions.
    H) FOLLOW-UP VISIT
    1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
    2) One 3-year-old child developed esophageal stricture 2 years after the acid ingestion in a prospective study of 41 patients. This child had a normal barium study at one year after ingestion (Zargar et al, 1989).
    I) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984a).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.
    J) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Administer 100 percent supplemental humidified oxygen with assisted ventilation as required.
    B) MONITORING OF PATIENT
    1) Monitor arterial blood gases and chest x-ray in patients with significant inhalation exposure or respiratory tract irritation.
    C) ANTIBIOTIC
    1) Antibiotics may be useful for infectious pulmonary complications.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

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

Enhanced Elimination

    A) SUMMARY
    1) Extracorporeal elimination techniques such as hemodialysis or hemoperfusion are of no value in peracetic acid poisoning.

Summary

    A) The minimum lethal and maximum tolerated human exposures have not been established. The upper tolerance limit for human skin is a 0.4% solution.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) At the time of this review, the minimum lethal human exposure has not been established. But is felt to be in the range of 50-500 mg/kg (Sittig, 1991).
    2) The upper tolerance limit for human skin is a 0.4% solution (Merka & Urban, 1976).
    B) ANIMAL DATA
    1) A solution of 2 percent peracetic acid in acetone killed all mice early in a chronic dermal application study, while solutions of 1 percent peracetic acid in acetone or 3 percent peracetic acid in water were well tolerated (Bock et al, 1975).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The upper tolerance limit for human skin is a 0.4 percent concentration (Merka & Urban, 1976).
    B) ANIMAL DATA
    1) RABBIT - 500 milligrams applied to open rabbit skin caused severe irritative effects, while 1 milligram applied to rabbit eyes had similarly severe irritative effects (Sax, 1984).
    2) RABBIT - A 0.1 percent solution in water was not irritating to rabbit eyes, while a 10 percent solution caused ulceration, corneal perforation, and symblepharon formation despite prompt water irrigation following the application (Grant, 1986).
    3) MICE - Temporary lung lesions and a negative effect on weight gain was noted in mice with subacute inhalation exposure to 70 milligrams/cubic meter (Merka & Urban, 1976).

Workplace Standards

    A) ACGIH TLV Values for CAS79-21-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS79-21-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS79-21-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Category 3B ; Listed as: Peracetic acid
    a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS79-21-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Clayton & Clayton, 1993 Lewis, 1996 ) RTECS, 2000
    1) LD50- (ORAL)MOUSE:
    a) 210 mg/kg
    2) LD50- (ORAL)RAT:
    a) 1540 mcL/kg
    b) 1540 mg/kg (Clayton & Clayton, 1993; Lewis, 1996)
    c) 1540 mg/kg; 100% peracetic acid
    d) 1230 mg/kg; 40% in acetic acid (Clayton & Clayton, 1993)
    3) LD50- (SKIN)RAT:
    a) 1410 mg/kg; 100% peracetic acid (Clayton & Clayton, 1993)
    b) 0.71 mL/kg; 40% in acetic acid (Clayton & Clayton, 1993)

Toxicologic Mechanism

    A) Peracetic acid is a direct irritant of eyes, skin, and mucous membranes (CHRIS , 1990; Grant, 1986; Bock et al, 1975).

Physical Characteristics

    A) Colorless liquid with a strong, acrid odor (CHRIS, 2005; Ashford, 1994) . It is stable in a dilute aqueous solution (Budavari, 1996). Does not react with water (CHRIS, 2005). Peracetic acid is a strong oxidizing agent (Budavari, 1996).

Molecular Weight

    A) 76.06

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