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ACRYLIC ACID

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Acrylic acid is used as a monomer in the production of acrylic copolymers, as a binder for non-woven fabrics, and as a textile improver.

Specific Substances

    1) 2-Propenoic Acid
    2) Acroleic Acid
    3) Ethylenecarboxylic acid
    4) Propene acid
    5) Vinyl Formic Acid
    6) CAS 79-10-7
    7) A13-15717
    8) ACRYLIC ACID, INHIBITED
    1.2.1) MOLECULAR FORMULA
    1) C3-H4-O2

Available Forms Sources

    A) FORMS
    1) Acrylic acid is available in two grades in the US, technical and glacial. The glacial grade is, by weight, 98% to 99.5% acrylic acid (HSDB, 2002).
    2) Commercial acrylic acid is shipped with an inhibitor of polymerization (NIOSH , 2001).
    3) The inhibitor is usually monomethyl ether of hydroquinone at 180 - 200 ppm; technical grades are inhibited with phenothiazine at 1,000 ppm, or 0.1% hydroquinone, 0.5 to 1% methylene blue, or 0.05% N,N'-diphenyl-p-phenylenediamine (CHRIS , 2001).
    B) SOURCES
    1) Acrylic acid is produced by the hydrolysis of acrylonitrile or the air oxidation of acrolein. This occurs in a two stage process (ACGIH, 1991).
    2) NATURAL SOURCES - It has been reported to occur naturally in Clorophyceae, Rhodophyceae, and Phaeophyceae species of marine algae and in the rumen of sheep (HSDB , 2001).
    C) USES
    1) Acrylic acid is used in the following areas: Plastics manufacturing; molding powder; polymer solutions for coating applications; paint formulations; leather finishings; paper coatings; emulsion polymers; and in dentistry for dental plates, artificial teeth, and orthopedic cement (HSDB, 2002).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Acrylic acid is used in plastics manufacturing, molding powder, polymer solutions for coating applications, paint formulations, leather finishings, paper coatings, emulsion polymers, and in dentistry for dental plates, artificial teeth, and orthopedic cement.
    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: Exposure is rare. Acrylic acid is typically available for industrial purposes.
    D) WITH POISONING/EXPOSURE
    1) Acrylic acid exposure is unusual; limited data regarding specific human toxicity following acrylic acid exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    2) 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.
    3) 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.
    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.
    4) 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.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) 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.
    0.2.4) HEENT
    A) Vapors may cause eye irritation. The liquid may cause blindness if splashed into the eye. Vapors will also cause nasal irritation.
    0.2.6) RESPIRATORY
    A) Irritant effects may occur from acute inhalation.
    0.2.10) GENITOURINARY
    A) Rats given 700 mg/m(3) for 4 hours/day for 5 weeks developed reduced urine concentrating abilities. Another group of rats given four, 6-hour exposures to 1500 ppm were found to have kidney congestion upon histologic examination.
    0.2.13) HEMATOLOGIC
    A) Increased reticulocyte counts were seen in animals.
    0.2.14) DERMATOLOGIC
    A) Burns may be caused by splash contact.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no studies were found on the possible reproductive effects of acrylic acid in humans.
    B) Acrylic acid was neither embryotoxic nor teratogenic in rats by inhalation. Intraperitoneal doses in pregnant rats resulted in decreased birth weight, skeletal abnormalities, and resorptions.

Laboratory Monitoring

    A) No toxic levels of acrylic acid have been established.
    B) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    C) 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.
    D) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    E) 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.
    F) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) There is very little information available regarding the treatment of acrylic acid-induced injury; the following data is derived from experience with other acids.
    B) 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.
    C) 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.
    D) DILUTION
    1) Dilute with 4 to 8 ounces of water may be useful if it can be performed shortly after ingestion in patients who are able to swallow, with no vomiting or respiratory distress; then the patient should be NPO until assessed for the need for endoscopy. Neutralization, activated charcoal, and gastric lavage are all contraindicated.
    E) 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.
    F) 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 burns.
    G) BRONCHOSPASM
    1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids
    H) 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.
    I) 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.
    J) 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.
    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.
    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) 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).
    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%).
    C) ANIMALS: The no-ill-effect-level in rabbits is 0.025 mg/kg orally. Animals exposed by inhalation to 700 mg/m(3) of acrylic acid for 4 hours per day developed kidney damage.

Clinical Effects

Summary Of Exposure

    A) USES: Acrylic acid is used in plastics manufacturing, molding powder, polymer solutions for coating applications, paint formulations, leather finishings, paper coatings, emulsion polymers, and in dentistry for dental plates, artificial teeth, and orthopedic cement.
    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: Exposure is rare. Acrylic acid is typically available for industrial purposes.
    D) WITH POISONING/EXPOSURE
    1) Acrylic acid exposure is unusual; limited data regarding specific human toxicity following acrylic acid exposure is available. The following effects could be expected to occur, based on exposure data of other acids.
    2) 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.
    3) 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.
    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.
    4) 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.
    5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
    6) 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.

Heent

    3.4.1) SUMMARY
    A) Vapors may cause eye irritation. The liquid may cause blindness if splashed into the eye. Vapors will also cause nasal irritation.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Vapors may cause eye irritation. The liquid may cause corneal burns and irreversible changes if splashed into the eye (ACGIH, 1991; HSDB, 2002).
    2) Acrylic acid applied to the conjunctival sacs of rabbit eyes produced severe irritation (Bingham et al, 2001).
    3) Concentrated (glacial) acrylic acid applied to rabbit eyes caused grade 9 (scale of 1 to 10) corneal damage (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Vapors may cause nasal irritation (ACGIH, 1991).

Respiratory

    3.6.1) SUMMARY
    A) Irritant effects may occur from acute inhalation.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Mild irritation may occur from acute exposure (ACGIH, 1991).

Genitourinary

    3.10.1) SUMMARY
    A) Rats given 700 mg/m(3) for 4 hours/day for 5 weeks developed reduced urine concentrating abilities. Another group of rats given four, 6-hour exposures to 1500 ppm were found to have kidney congestion upon histologic examination.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL FUNCTION ABNORMAL
    a) Rats given 700 mg/m(3) for 4 hours/day for 5 weeks developed reduced urine concentrating abilities. Another group of rats given four, 6 hour exposures to 1500 ppm were found to have kidney congestion upon histologic examination (Clayton & Clayton, 1982).

Hematologic

    3.13.1) SUMMARY
    A) Increased reticulocyte counts were seen in animals.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MYELOPROLIFERATIVE DISORDER
    a) Increased reticulocyte counts were seen in animals (Clayton & Clayton, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Burns may be caused by splash contact.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Splash contact may cause burns (Sittig, 1991). Alpha, beta-diacryloxypropionic acid has been identified as a sensitizing impurity in commercial grade acrylic acid (Proctor et al, 1988).
    B) URTICARIA
    1) WITH POISONING/EXPOSURE
    a) Hypersensitivity reactions and urticaria have been reported (Bingham et al, 2001).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Application of acrylic acid to uncovered rabbit skin produced a severe irritation (Bingham et al, 2001). The standard test for skin sensitization potential showed low to moderate activity in three of five animals tested.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no studies were found on the possible reproductive effects of acrylic acid in humans.
    B) Acrylic acid was neither embryotoxic nor teratogenic in rats by inhalation. Intraperitoneal doses in pregnant rats resulted in decreased birth weight, skeletal abnormalities, and resorptions.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) No human reproductive effects have been observed. Teratogenicity in animals was seen only at high doses. There appears to be no risk with occupational exposure within the TLV limit (AMA, 1985).
    B) ANIMAL STUDIES
    1) RATS - A single 14 mg/kg dose given to pregnant rats (IP) was teratogenic. As little as 2 mg/kg resulted in decreased fetal birth weight, gross and skeletal abnormalities and resorptions (Bingham et al, 2001; Clayton & Clayton, 1982).
    a) When injected intra-amniotically at 1000 mcg/fetus, acrylic acid was embryotoxic.
    b) The significance of these animal studies to man is not known because of the high doses and routes of administration (Proctor et al, 1988).
    2) Effects on testes, epididymis, and sperm ducts have been noted in rats (RTECS , 2002).
    3) Acrylic acid is an animal teratogen at high doses. It induced skeletal abnormalities in fetal rats when given intraperitoneally at 7 or 8 mg/kg on days 5, 10, and 15 of gestation (Singh et al, 1972) 1972a).
    4) Dose-related signs of toxicity were seen in F1 and F2 rat pups fed 2,500 or 5,500 ppm (in drinking water), in the form of retarded growth and some delay in the eye/auditory canal opening in the F2 pups (Hellwig et al, 1997).
    5) Reduced weights, but no teratogenicity, were seen in rats exposed to acrylic acid at levels up to 5000 ppm in the drinking water for 3 generations; this was attributed to reduced water and food intake in pregnant females (IRIS, 1995).
    6) No embryotoxicity or teratogenicity was seen in rats exposed to 40 to 360 ppm on days 6 to 15 of gestation (Hathaway et al, 1996). Acrylic acid was not teratogenic at doses up to 1000 mcg, when injected into the amniotic fluid of pregnant rats on day 13 of gestation (Slott & Hales, 1985).
    7) Acrylic acid did not produce developmental abnormalities in rats by the inhalation exposure route at concentrations up to 360 ppm for 6 hours per day on days 6 to 15 of gestation. Maternal toxicity was evident (Klimisch & Hellwig, 1991).
    8) Marine fish and invertebrates were studied for potential toxic effects of acrylic acid. The chronic MATC for acrylic acid with Daphnia Magna was 27 mg/L based on length and young produced per adult reproduction day (Staples, 2000).
    9) No embryotoxicity or teratogenicity was observed when pregnant rats were exposed to 15-60 ppm by inhalation on days 6-15 of gestation. Some maternal toxicity was seen at the highest dose (Proctor et al, 1988).
    10) It was not teratogenic in rabbits at concentrations up to 250 ppm on days 20 to 23 of gestation (Chun et al, 1993; Chun et al, 1993).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Reduced body weight was seen in fetal rats exposed to 300 ppm for 6 hours/day on days 6-20 of gestation (Saillenfait et al, 1999).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS79-10-7 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Acrylic acid
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Acrylic acid was carcinogenic at 37 gm/kg/78 weeks when applied to the skin of mice; leukemia was induced (RTECS , 2002).
    2) It was an equivocal tumor agent when administered SC to mice at a dose of 2.9 gm/kg/52 weeks; tumors were formed at the site of application (RTECS , 2002).
    3) It was an equivocal tumor agent in a skinpainting study in mice at a dose of 37 gm/kg/78 weeks (RTECS , 2002).
    4) Squamous cell carcinomas were observed in mice after topical application 3 times/week for 1.5 years (ACGIH, 1991).
    5) It induced tumors at the application site when administered by the subcutaneous route in female mice (20 mcmoles injected once weekly for 52 weeks). Two of 30 mice developed sarcomas. Acrylic acid may be a weak carcinogen in mice (Segal et al, 1987).
    6) No skin tumors were seen in male mice treated with 25 mcL of a 1% acrylic acid solution on the back (3 applications per week) with a mean survival time of 515 days (DePass et al, 1984).
    7) Acrylic acid was not carcinogenic in rats when given in the drinking water at concentrations up to 5000 ppm for 12 months, or at 1200 ppm for 26 or 28 months (Hellwig et al, 1993).
    8) Acrylic acid did not act as a carcinogenic promoter for 7,12-dimethylbenz(a)anthracene in mice (ACGIH, 1991).

Genotoxicity

    A) Acrylic acid induced mutations and chromosome aberrations in mouse cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic levels of acrylic acid have been established.
    B) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    C) 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.
    D) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    E) 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.
    F) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    2) Monitor renal function tests and liver enzymes in patients with signs and symptoms suggestive of severe burns, perforation or bleeding.
    B) COAGULATION STUDIES
    1) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood.
    4.1.3) URINE
    A) OTHER
    1) Monitor urine output and urinalysis in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain an upright chest x-ray to evaluate for pneumomediastinum or free air under the diaphragm to evaluate for pneumomediastinum or free air under the diaphragm.
    a) The absence of these findings DOES NOT rule out the possibility of necrosis or perforation of the esophagus or stomach.
    2) Obtain a chest radiograph in patients with pulmonary signs or symptoms.

Methods

    A) CHROMATOGRAPHY
    1) Acrylic acid can be determined by gas-liquid chromatography.
    B) OTHER
    1) Acrylic acid can also be determined by tests for determination of unsaturation such as bromination, addition of mercaptan, sodium bisulfite, morpholine, or mercuric acetate (HSDB , 2001). Note, however, that the methods for detecting unsaturation would not be specific for acrylic acid.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) 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.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) 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.

Monitoring

    A) No toxic levels of acrylic acid have been established.
    B) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
    C) 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.
    D) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
    E) 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.
    F) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade II or III burns, to evaluate for strictures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL/NOT RECOMMENDED
    1) Activated charcoal is NOT recommended as it has not been shown to reduce corrosive gastrointestinal injury and may obscure endoscopy findings.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Activated charcoal should NOT be used. It may cause vomiting which can worsen caustic gastrointestinal injury, and may obscure endoscopy findings.
    6.5.3) TREATMENT
    A) CONTRAINDICATED TREATMENT
    1) Do not induce vomiting or give bicarbonate to neutralize. Addition of buffer to strong acid causes an exothermic reaction and an immediate rise in solution temperature (Maull et al, 1985; Penner, 1980).
    2) A report concerning emergency surgical resection of the alimentary tract following caustic ingestions has indicated that 5 out of 6 patients sustained injuries beyond the pylorus as a result of gastric lavage (Wu & Lai, 1993).
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) INSERTION OF NASOGASTRIC TUBE
    1) It has been suggested 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 (Penner, 1980).
    2) Many authorities oppose this procedure fearing esophageal or gastric perforation. A soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.
    D) BURN
    1) 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.
    E) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) 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.
    3) 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)
    4) 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).
    5) 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.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    F) ULTRASONOGRAPHY
    1) A small study suggests that esophageal ultrasonography may be useful in predicting the likelihood of strictures after corrosive ingestion (Kamijo et al, 2004).
    a) Miniprobe ultrasonography was performed endosopically at the site of the most severe lesion in 11 patients with corrosive esophageal injury. Grading was as follows: grade 0 distinct muscular layers without thickening (5 patients); grade I distinct muscular layers with thickening (4 patients): grade II obscured muscular layers with indistinct margins 1 patient); and grade III muscular layers that could not be differentiated (1 patient). Lesions were also classified as to whether the area of worst damage involved part of the circumference (type a) or the entire circumference (type b).
    b) Strictures did not develop in patients with grade 0 or 1 lesions. A transient stricture developed in the patient with a grade IIa lesion. A stricture that required repeated dilatation developed in the patient with a grade IIIb lesion.
    G) 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, 1989a; 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).
    H) 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, 1993a). 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.
    I) 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.
    J) 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) A 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).

Inhalation Exposure

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

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) Skin burns have been reported after splash contact from acrylic acid; the patient should be observed closely for skin burns.
    2) Once irrigation is completed, standard burn therapy should be instituted including tetanus prophylaxis, dressings and careful follow-up to observe for complications and infection.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    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).
    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%).
    C) ANIMALS: The no-ill-effect-level in rabbits is 0.025 mg/kg orally. Animals exposed by inhalation to 700 mg/m(3) of acrylic acid for 4 hours per day developed kidney damage.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.
    B) The lowest published lethal concentration for rats, following inhalation, is 4,000 ppm/4 hours (RTECS , 2002).

Maximum Tolerated Exposure

    A) The maximum tolerated human exposure to this agent has not been delineated.
    B) Reports of acute human exposures of unspecified concentrations include moderate and severe skin burns, moderate eye burns, and mild inhalation effects. While acrylic acid is acutely irritating at contact sites, it causes little systemic toxicity (Hathaway, 1996).
    C) ANIMAL DATA
    1) No-ill-effect-level in rabbits was 0.025 mg/kg orally. Rats exposed to 80 ppm for 6 hours/day for 20 days developed no adverse effects (ACGIH, 1980).
    2) Animals exposed to 700 mg/m(3) for 4 hours/day for 5 weeks did develop reduced urine concentrating abilities, nasal discharge, and increased reticulocyte count.
    3) Rats exposed to 25 ppm for 6 hours/day, 5 days per week for 13 weeks showed no apparent gross effects other than reduced weight gain. Exposure of rats to 75 ppm and of mice to 5, 25, or 75 ppm produced histopathologic lesions in the nasal mucosa. These effects were interpreted to be due to irritation by the acrylic acid vapors (Miller et al, 1981).

Workplace Standards

    A) ACGIH TLV Values for CAS79-10-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Acrylic acid
    a) TLV:
    1) TLV-TWA: 2 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT irr
    d) Molecular Weight: 72.06
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS79-10-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Acrylic acid
    2) REL:
    a) TWA: 2 ppm (6 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS79-10-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Acrylic acid
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Acrylic acid
    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): 3 ; Listed as: Acrylic acid
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Acrylic acid
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS79-10-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Clayton & Clayton, 1994 HSDB, 2002 ITI, 1995 Lewis, 2000 OHM/TADS, 2000 RTECS, 2002
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 144 mg/kg
    b) 0.016 mL/kg (Clayton & Clayton, 1994)
    2) LD50- (ORAL)MOUSE:
    a) 830 mg/kg (OHM/TADS, 2000)
    b) 2400 mg/kg -- active as anti-cancer agent
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 1590 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 22 mg/kg
    b) 22-24 mg/kg (Clayton & Clayton, 1994)
    c) 24 mg/kg (HSDB, 2002)
    5) LD50- (ORAL)RAT:
    a) 1250 mg/kg (OHM/TADS, 2000)
    b) 2590 mg/kg (OHM/TADS, 2000)
    c) 33,500 mcg/kg
    d) 340-3200 mg/kg (Clayton & Clayton, 1994)
    e) 340 mg/kg (ITI, 1995)
    f) 193 mg/kg (HSDB, 2002)
    g) 2.5 g/kg (HSDB, 2002)
    6) TCLo- (INHALATION)MOUSE:
    a) 223 ppm for 6H/2W- intermittent -- changes in sense organs, weight loss, decreased weight gain
    b) 25 ppm for 6H/13W- intermittent -- changes in sense organs, weight loss, decreased weight gain
    c) 225 ppm for 6H/10D- intermittent -- changes in sense organs, muscle contraction or spasticity, weight loss, decreased weight gain
    7) TCLo- (INHALATION)RAT:
    a) 75 ppm for 6H/13W-intermittent -- changes in sense organs
    b) 223 ppm for 6H/2W-intermittent -- changes in sense organs, weight loss, decreased weight gain
    c) 225 ppm for 6H/10D - intermittent -- changes in sense organs, changes in respiration, weight loss or decreased weight gain

Pharmacology Toxicology

Toxicologic Mechanism

    A) IRRITANT - Acrylic acid appears to exert its local and systemic effects via irritation.
    B) PREDISPOSING MEDICAL CONDITIONS - Persons with poor uncorrected vision or chronic lung disease should avoid exposure (HSDB , 1989).

Physicochemical

Physical Characteristics

    A) Acrylic acid is a colorless and corrosive liquid. It has an acrid odor (HSDB, 2002).
    B) Acrylic acid is a colorless solid below 55 degrees F (HSDB, 2002).

Ph

    A) Acrylic acid forms acidic solutions in water (OHM/TADS , 2001).

Molecular Weight

    A) 72.06

Other

    A) ODOR THRESHOLD
    1) Currently not available (CHRIS , 2002)

References

General Bibliography

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