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ACROLEIN

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Acrolein is a highly toxic, irritating, and reactive unsaturated aliphatic aldehyde compound used in the manufacture of various fuels, microbiocides, pharmaceuticals, herbicides, textiles, and synthetic rubbers (HSDB , 2000; Ghilarducci & Tjeerdema, 1995). Acrolein is the simplest member of the class of alpha, beta-unsaturated carbonyl compounds (2-alkenals) and it is the most toxic member of the 2-alkenals.
    B) Due to its molecular structure, acrolein is highly reactive; thus, any tissue exposed to acrolein is immediately irritated and can be seriously damaged.
    C) It is a photo-oxidation product of various hydrocarbon air pollutants such as 1,3-butadiene and a combustion by-product (HSDB , 2000; Ghilarducci & Tjeerdema, 1995).
    D) Commercial grade is 92 percent minimum purity in the US; 0.1 to 0.25 percent HYDROQUINONE may be present as an inhibitor of polymerization. Purity of up to 97 percent is available (HSDB , 2000).

Specific Substances

    1) ACROLEIN
    2) Acrylaldehyde
    3) Allyl aldehyde
    4) Aqualin
    5) Acraldehyde
    6) Acrylic aldehyde
    7) Ethylene aldehyde
    8) Propenal
    9) Pyran aldehyde
    10) 2-Formyl-3,4-dihydro-2H-pyran
    11) Molecular Formula: C3-H4-O
    12) CAS 107-02-8
    13) ACROLEIN, INHIBITED
    14) ACRYLALDEHYDE, INHIBITED
    15) ALDEHYDE ACRYLIGNE (FRENCH)
    16) SLIMCIDE
    1.2.1) MOLECULAR FORMULA
    1) C3-H4-O

Available Forms Sources

    A) FORMS
    1) Acrolein is a clear or yellow liquid with a disagreeable odor; it is a volatile, highly flammable liquid and vapor (Bingham et al, 2001).
    2) Commercial grade in the US is 92 percent minimum purity; 0.1 to 0.25 percent HYDROQUINONE may be present as an inhibitor of polymerization. Purity of up to 97 percent is available (HSDB , 2002).
    B) SOURCES
    1) Acrolein may be derived from the following reactions: oxidation of allyl alcohol or propylene; heating glycerol with magnesium sulfate; treating propylene with a bismuth-phosphorus-molybdenum catalyst (Ashford, 1994; Lewis, 2001).
    2) Acrolein is found in cigarette smoke, automobile exhaust, the fumes of overheated fat, sewage sludge, drinking water, and in many foods (Ballantyne et al, 1989; Harbison, 1998; ILO , 1998; HSDB , 2002; Ghilarducci & Tjeerdema, 1995; Hudgins & Karetzky, 1994). It is a toxic combustion by-product and firefighters may have significant exposure (Lee, 1995).
    3) Acrolein is a photooxidation product of various hydrocarbon air pollutants such as 1,3-butadiene (HSDB , 2002).
    4) Acrolein is a common air contaminant (Bingham et al, 2001; Ghilarducci & Tjeerdema, 1995). It is formed from the photochemical oxidation of hydrocarbons such as 1,3-butadiene and is thought to be one of the major sources of irritation from smog (HSDB , 2002).
    5) Acrolein is a constituent of the aroma volatiles of ripe arctic bramble berries (HSDB , 2002).
    6) Acrolein is a metabolite of the antineoplastic drug cyclophosphamide (McDiarmid et al, 1991).
    7) Acrolein is a toxic by-product of municipal solid waste incineration (Gochfeld, 1995).
    C) USES
    1) Acrolein is used as a liquid fuel, algicide, microbiocide, molluscicide, and slimicide (Ballantyne et al, 1989; HSDB , 2002; Ghilarducci & Tjeerdema, 1995).
    2) Acrolein is used in the manufacture of pharmaceuticals, perfumes, food supplements, resins, and herbicides (Hathaway et al, 1996). It is also used as a warning agent in methyl chloride refrigerating systems and as a fixative in histological work (Hathaway et al, 1996; HSDB , 2002).
    3) Acrolein is used in the manufacture of colloidal forms of metals and for making plastics. It has also been used in military poison gas mixtures (Budavari, 2000; HSDB , 2002).
    4) Acrolein is used as an herbicide: it is sold under the trade name of MAGNACIDE H containing 92 percent acrolein (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) Acrolein may be irritating to the eyes, skin, and mucous membranes. It is a severe pulmonary irritant and lacrimating agent.
    B) Skin and corneal burns may occur from direct contact with the liquid. Difficulty breathing, chest congestion, bronchospasm, as well as delayed onset of acute lung injury, and permanent lung damage may occur following acute exposure.
    1) Nausea and vomiting are common. CNS depression can occur from exposure to high concentrations. Ingestion may produce severe irritation of the mouth andagastrointestinal tract. Death may result from acute lung injury and/or respiratory failure.
    C) The strong irritant properties usually prevent more serious exposures, but fatalities have occurred.
    0.2.3) VITAL SIGNS
    A) Short-term exposure may cause increases in heart rate and blood pressure.
    0.2.4) HEENT
    A) Splash contact with the eyes may cause corneal injury. Exposure to the vapor at concentrations of 0.25 ppm or greater may cause eye irritation.
    0.2.5) CARDIOVASCULAR
    A) Hypertension and tachycardia may occur following inhalation exposure.
    0.2.6) RESPIRATORY
    A) Dyspnea, bronchospasm, acute lung injury, and permanent pulmonary damage may occur following acute exposure.
    0.2.7) NEUROLOGIC
    A) Serious poisoning may cause CNS depression.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and diarrhea have been reported. Irritation of the mouth and GI tract may occur following ingestion.
    0.2.14) DERMATOLOGIC
    A) Splash contact may cause irritation, erythema, and edema. Skin burns may occur.
    0.2.17) METABOLISM
    A) Microsomal oxidases were decreased in the lung and liver in exposed rats.
    0.2.20) REPRODUCTIVE
    A) Birth defects were produced by direct intra-amniotic injection in rats, but the offspring of rabbits treated by gavage did not have developmental toxicity.
    0.2.21) CARCINOGENICITY
    A) There is inadequate evidence of carcinogenicity in man.

Laboratory Monitoring

    A) No toxic serum or blood levels have been established. Obtain a chest x-ray in patients with respiratory symptoms.
    B) Monitor pulse oximetry in patients with significant exposure. Obtain arterial blood gases in patients with the signs of hypoxia.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MUCOSAL DECONTAMINATION: 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. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
    B) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) Activated charcoal is of unproven benefit for attempting to decrease acrolein absorption following ingestion and can obscure endoscopic findings in patients with severe GI tract irritation or burns. Routine use is NOT recommended.
    E) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    F) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    0.4.3) INHALATION EXPOSURE
    A) The primary toxic effects involve irritation of the mucous membranes, eyes, and lungs. In severe cases, treatment of acute lung injury is of paramount importance. Acute lung injury may be delayed in onset by several hours.
    B) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Airborne levels as low as 10 to 150 ppm are potentially harmful to humans. An airborne concentration of 1 ppm produces marked eye, respiratory tract, and mucous membrane irritation in less than 5 minutes.
    B) Death due to massive delayed onset acute lung injury has been reported following a "soaking" splash contact with concentrated acrolein solution.
    C) Death occurred in an adult following a suspected ingestion of 250 mL of a pesticide containing 85% allyl alcohol, and is believed to be a result of cardiac arrest due to the presence of acrolein, the toxic metabolite of allyl alcohol.

Clinical Effects

Summary Of Exposure

    A) Acrolein may be irritating to the eyes, skin, and mucous membranes. It is a severe pulmonary irritant and lacrimating agent.
    B) Skin and corneal burns may occur from direct contact with the liquid. Difficulty breathing, chest congestion, bronchospasm, as well as delayed onset of acute lung injury, and permanent lung damage may occur following acute exposure.
    1) Nausea and vomiting are common. CNS depression can occur from exposure to high concentrations. Ingestion may produce severe irritation of the mouth andagastrointestinal tract. Death may result from acute lung injury and/or respiratory failure.
    C) The strong irritant properties usually prevent more serious exposures, but fatalities have occurred.

Vital Signs

    3.3.1) SUMMARY
    A) Short-term exposure may cause increases in heart rate and blood pressure.
    3.3.4) BLOOD PRESSURE
    A) Short-term exposure may cause increases in blood pressure and heart rate (Egle & Hudgins, 1974).

Heent

    3.4.1) SUMMARY
    A) Splash contact with the eyes may cause corneal injury. Exposure to the vapor at concentrations of 0.25 ppm or greater may cause eye irritation.
    3.4.3) EYES
    A) VAPORS - An airborne concentration of 0.25 ppm causes eye irritation; 1 ppm is noxious to workers if exposed for 5 minutes and causes profuse lacrimation (Hathaway et al, 1996).
    B) SPLASH CONTACT may cause corneal injury, palpebral edema, blepharoconjunctivitis, and a fibrinous or purulent discharge (Bingham et al, 2001; Hathaway et al, 1996; Grant & Schuman, 1993). Conjunctival suffusion was reported in an adult following a splash exposure with concentrated acrolein solution (Daly & Kosnett, 2000).
    C) Acrolein was found to be an eye irritant in humans using the Standard Draize test. It was a severe eye irritant in the rabbit using the Standard Draize test (RTECS , 2001).
    3.4.5) NOSE
    A) Following a "soaking" body splash from concentrated acrolein solution, immediate burning of the nose was reported (Daly & Kosnett, 2000).
    B) ANIMAL - In rat inhalational studies, histopathological changes and cell proliferation of the nasal epithelium are induced (Bingham et al, 2001).
    3.4.6) THROAT
    A) Acute bronchitis and laryngitis have been reported following exposure to a concentrated acrolein solution (Daly & Kosnett, 2000).
    B) Inhalation exposures are expected to result in injury to the lungs and bronchial airways. Burning of the throat, cough, and difficulty breathing may occur (Bingham et al, 2001).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypertension and tachycardia may occur following inhalation exposure.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOVASCULAR FINDING
    1) Increased heart rate and blood pressure occurred from inhalation of acrolein at concentrations comparable to those found in cigarette smoke (HSDB , 2000). It may have cardiovascular activity at levels less than those found in cigarette smoke (HSDB , 2000). Inhalation of high acrolein concentrations may result in hypertension (Bingham et al, 2001).

Dermatologic

    3.14.1) SUMMARY
    A) Splash contact may cause irritation, erythema, and edema. Skin burns may occur.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) SPLASH CONTACT - Severe irritation and redness, edema, pain and possible skin burns may occur following dermal contact. Prolonged contact may lead to sensitization dermatitis (Bingham et al, 2001; Hathaway et al, 1996).
    B) CHEMICAL BURN
    1) Skin burns may occur (Bingham et al, 2001; Hathaway et al, 1996).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) Acrolein was found to be a severe skin irritant in both the Standard Draize and the Open Draize test in rabbits (RTECS , 2001).
    2) LACK OF EFFECT
    a) Acrolein was not a skin sensitizer in guinea pigs (Susten & Breitenstein, 1990).

Reproductive

    3.20.1) SUMMARY
    A) Birth defects were produced by direct intra-amniotic injection in rats, but the offspring of rabbits treated by gavage did not have developmental toxicity.
    3.20.2) TERATOGENICITY
    A) HUMAN STUDIES
    1) Acrolein has been implicated as a possible reproductive hazard in firefighters (McDiarmid & Agnew, 1995).
    B) ANIMAL STUDIES
    1) Acrolein produced no birth defects when injected intra-amniotically into rat fetuses (HSDB , 2000), but the significance of this study for humans is not clear.
    2) It was embryotoxic but not teratogenic in rabbits injected IV at doses up to 6 mg/kg; malformations and increased resorptions occurred from direct injection into the yolk sac (HSDB , 2000).
    3) In rabbits, gavage doses of 0.01 to 2 mg/kg on days 9 through 19 of gestation did not cause developmental toxicity in the offspring (Parent et al, 1993), and acrolein is not a selective reproductive toxicant in rats (Parent et al, 1992a).
    4) Acrolein has been embryotoxic and teratogenic when given by injection to rats (RTECS; (Hales, 1982; Slott & Hales, 1985). It was also embryotoxic (Dankaanpaa, 1979) and teratogenic (Chhibber & Gilani, 1986) in chicks.
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMAN STUDIES
    1) Women working with acrolein and other substances had changes in the placenta, but it is not clear if these changes would have affected fertility or the unborn (Ferster, 1970).
    B) ANIMAL STUDIES
    1) An increase in post implantation mortality was observed in the rabbit following intravenous injection of acrolein (RTECS , 2001).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS107-02-8 (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: Acrolein
    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.
    3.21.2) SUMMARY/HUMAN
    A) There is inadequate evidence of carcinogenicity in man.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no studies were found on the possible carcinogenicity of acrolein in humans.
    B) ANIMAL STUDIES
    1) Acrolein did not produce local sarcomas in mice by injection, but complete pathology was not performed (HSDB , 2000).
    2) Acrolein did not induce respiratory tumors in hamsters by the inhalation route at 6 ppm for 52 weeks (HSDB , 2000).
    3) In one study, rats injected with acrolein for 6 weeks developed cancers of the urinary bladder (Cohen et al, 1992). However, acrolein administered by gavage for 2 years was not carcinogenic (Parent et al, 1992b).
    4) Acrolein has caused papillomas on the skin of mice and hamsters (IARC, 1979). Inhalation of 4 ppm for one year by hamsters caused nasal inflammation, but was not carcinogenic (Feron & Kruysse, 1977).

Genotoxicity

    A) Mutagenic in short-term tests.

Respiratory

    3.6.1) SUMMARY
    A) Dyspnea, bronchospasm, acute lung injury, and permanent pulmonary damage may occur following acute exposure.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Inhalation of acrolein can produce dyspnea or chest tightness (HSDB , 2000; Daly & Kosnett, 2000).
    B) BRONCHOSPASM
    1) Bronchospasm can occur following inhalation exposure (HSDB , 2000). Aggravation of pre-existing asthma is likely following inhalation exposures (Bingham et al, 2001).
    C) ACUTE LUNG INJURY
    1) Acute lung injury (ALI), delayed in onset for up to 24 to 48 hours, may occur after acute inhalational exposure (HSDB , 2000).
    2) CASE REPORT - Delayed fatal acute lung injury was reported in a 38-year-old male worker who was unintentionally high pressure-sprayed with a 95% concentrated acrolein solution. He reported to the ED a few hours later with chest discomfort and dyspnea. Initial respiratory rate was 24/min with a pO2 of 59 mmHg; chest radiograph and auscultation were normal. The patient was discharged with normal O2 saturation within 2.5 hours. He was found dead at home 20 hours later. Massive pulmonary congestion and edema were found on postmortem examination (Daly & Kosnett, 2000).
    D) SEQUELA
    1) Recovery from an acute inhalational exposure may be accompanied by permanent radiological and/or functional pulmonary impairment (HSDB , 2000).
    E) PULMONARY FUNCTION STUDIES ABNORMAL
    1) FIREFIGHTERS - Wildland firefighters working in visible smoke containing acrolein and other combustion by-products have been reported to have a persistent decrease in air flow rate during the fire season (Harrison et al, 1995). Only limited data are available about possible recovery at the end of the fire season.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DISORDER
    a) Acute inhalational toxicity studies in rats have found that most mortality is due to acute bronchopneumonia and occurred within the first 10 days of exposure. Concentration-dependent increases in submucosal lymphoid aggregates and rhinitis, and peribronchiolar and bronchiolar damage have been noted (Bingham et al, 2001).
    b) When rats were exposed to greater than 23.6 ppm (threshold effect) of acrolein for 6 hr/day, olfactory atrophy and squamous metaplasia in the larynx, trachea, and larger bronchi were noted. Squamous metaplasia in the anterior nasal passages was consistently observed. No biochemical or morphological findings suggestive of specific organ or tissue toxicity, with the exception of respiratory tract effects, were found (Ballantyne & Cawley, 2000).
    c) Tissue damage is reported in rats' respiratory tracts, particularly in nasal turbinates and lung tissues, with changes in the epithelial lining of the nasal cavity, such as necrotizing rhinitis following acrolein inhalation. Alveolitis, hemorrhage, airway epithelial sloughing, edema and Type II cell hyperplasia have been noted at an air concentration of 1.4 ppm (Bingham et al, 2001).
    d) Daily exposures of male Sprague Dawley rats for 6 hours to 0, 2, 6, or 20 ppm of formaldehyde or to 0, 0.2, or 0.6 ppm of acrolein caused proliferation of nasal and tracheal epithelial cells, and free lung cells (Roemer et al, 1993).
    e) Acrolein induced dose-dependent cytotoxicity in cultured human alveolar macrophages, as shown by apoptosis and necrosis. At sublethal doses, acrolein caused induction of heme oxygenase 1 protein, but not stress protein 72. Acrolein also inhibited release of IL-beta, TNF-alpha, and IL-2, in a dose-dependent manner (Li et al, 1997).
    f) The alveolar macrophage, in addition to the respiratory epithelium, is a likely target for acrolein-induced suppression of host defense against infection (Li & Holian, 1998).

Neurologic

    3.7.1) SUMMARY
    A) Serious poisoning may cause CNS depression.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) CNS depression may occur in patients with significant exposure (ACGIH, 1991).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and diarrhea have been reported. Irritation of the mouth and GI tract may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Nausea, vomiting, and diarrhea have been reported following inhalational exposures (Bingham et al, 2001; Plunkett, 1976). Severe irritation of the mouth and gastrointestinal tract may occur following ingestion.
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GASTRIC ULCER
    a) RATS/RABBITS - Endogastrically administered acrolein solution induces gastric ulceration and sloughing of gastric mucosa in rats and rabbits (Bingham et al, 2001).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic serum or blood levels have been established. Obtain a chest x-ray in patients with respiratory symptoms.
    B) Monitor pulse oximetry in patients with significant exposure. Obtain arterial blood gases in patients with the signs of hypoxia.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) No toxic blood or serum levels have been established.
    B) OTHER
    1) Monitor arterial blood gases or pulse oximetry in patients with significant exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest x-ray may be helpful in patients with severe pulmonary irritation.

Methods

    A) OTHER
    1) Acrolein can be determined in biological tissues (kidney and liver) by HPLC of its 2,4-dinitrophenylhydrazine adduct with UV detection at 356 nm or by fluorescence spectroscopy (HSDB , 1989; HSDB , 1999).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Consider prolonged (24 hours) observation for late-onset airway compromise, including acute lung injury, following acrolein exposures (Daly & Kosnett, 2000).
    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Exposed patients with initial pulmonary symptoms should be observed for 24 hours due to the possibility of delayed acute lung injury (Daly & Kosnett, 2000).

Monitoring

    A) No toxic serum or blood levels have been established. Obtain a chest x-ray in patients with respiratory symptoms.
    B) Monitor pulse oximetry in patients with significant exposure. Obtain arterial blood gases in patients with the signs of hypoxia.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Emesis is not recommended because of the potential for CNS depression and mucosal irritation.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is of unproven benefit for attempting to decrease acrolein absorption following ingestion and can obscure endoscopic findings in patients with severe GI tract irritation or burns. Routine use is NOT recommended. However, in the case of life-threatening exposure, charcoal may have theoretical benefit.
    C) DILUTION
    1) Irrigate the mouth with copious amounts of water. Immediate dilution with small amounts of milk or water may help decontaminate the oral mucosa.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Activated charcoal is of unproven benefit for attempting to decrease acrolein absorption following ingestion and can obscure endoscopic findings in patients with severe GI tract irritation or burns. Routine use is NOT recommended. However, in the case of life-threatening exposure, charcoal may have theoretical benefit.
    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, 1985; 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) NASOGASTRIC ASPIRATION
    1) INDICATIONS: Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after large, recent ingestion of caustics. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric emptying.
    b) AIRWAY PROTECTION: Alert patients - place in Trendelenburg and left lateral decubitus position, with suction available. Obtunded or unconscious patients - cuffed endotracheal intubation. COMPLICATIONS:
    1) Complications of gastric aspiration may include: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach (Vale, 1997). Combative patients may be at greater risk for complications.
    6.5.3) TREATMENT
    A) IRRIGATION
    1) Irrigate the mouth with copious amounts of water. Immediate dilution with small amounts of milk or water may help decontaminate the oral and esophageal mucosa.
    B) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    C) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; 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)
    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.
    7) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
    8) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).
    D) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

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) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    C) EXPERIMENTAL THERAPY
    1) N-acetylcysteine protected against the cytotoxicity of acrolein in isolated rat hepatocytes by acting as a source of SH- groups (HSDB , 2000). However, the value of N-acetylcysteine in the human clinical setting has not been proven.
    2) Atropine, aminophylline, isoproterenol, and epinephrine partially or completely reversed the increased pulmonary resistance caused by acrolein in guinea pigs (HSDB , 2000). However, the value of these therapeutic agents in the human clinical setting has not been proven.
    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).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Airborne levels as low as 10 to 150 ppm are potentially harmful to humans. An airborne concentration of 1 ppm produces marked eye, respiratory tract, and mucous membrane irritation in less than 5 minutes.
    B) Death due to massive delayed onset acute lung injury has been reported following a "soaking" splash contact with concentrated acrolein solution.
    C) Death occurred in an adult following a suspected ingestion of 250 mL of a pesticide containing 85% allyl alcohol, and is believed to be a result of cardiac arrest due to the presence of acrolein, the toxic metabolite of allyl alcohol.

Minimum Lethal Exposure

    A) ADULT
    1) INHALATION - Exposures to concentrations of 10 ppm may be fatal in a short time (Bingham et al, 2001; HSDB , 2002).
    2) Human fatalities have been reported after exposure to 150 ppm for 10 minutes. Exposures to 10 ppm have also been fatal (ACGIH, 1991; Bingham et al, 2001; Hathaway et al, 1996).
    3) (The following values are from RTECS, 2002:)
    1) LCLo - (INHL) HUMAN: 5500 ppb
    2) LCLo - (INHL) HUMAN: 153 ppm for 10M
    4) DERMAL/INHALATION - A "soaking" splash contact with concentrated 95% acrolein solution resulted in delayed onset (up to 20 hours) massive acute lung injury and death in an adult (Daly & Kosnett, 2000).
    5) CASE REPORT - A 55-year-old man died following a suspected ingestion of 250 mL of a pesticide containing 85% allyl alcohol. Autopsy revealed bloody, reddish fluid in the mouth, larynx, esophagus, and trachea, reddening of the trachea, stomach, and duodenum, a pungent green-black fluid within the stomach and duodenum, and an enlarged heart. Externally, all of the other internal organs appeared normal. It is believed that the patient died of cardiac arrest due to the presence of acrolein, the toxic metabolite of allyl alcohol (Toennes et al, 2002). Postmortem toxicologic analysis of the patient's blood, bile, and urine indicated acrolein concentrations of 7.2 mg/L, 13.8 mg/L, and 5.4 mg/L, respectively.

Maximum Tolerated Exposure

    A) ADULT
    1) Concentrations of 5.5 ppm acrolein are intolerable to humans within the first minute. Exposure to 1 ppm becomes intolerable in four to five minutes (Grant & Schuman, 1993).
    B) GENERAL/SUMMARY
    1) Acrolein is acutely irritating to the eyes, skin, and upper respiratory tract. The primary route of exposure is inhalation, and acute exposure may result in lacrimation, tracheobronchitis, pneumonia, and acute lung injury (at 20 ppm) (ACGIH, 1991; Harbison, 1998; Hathaway et al, 1996; Lewis, 1998).
    2) The low irritation threshold (0.25-0.5 ppm) and acutely irritating effects of acrolein usually prevent chronic toxicity, although, as a highly reactive aldehyde, it can produce long-term respiratory effects by significantly reducing ciliary action in the upper airways and causing tissue damage throughout the lungs manifested as emphysema. Prolonged or repeated contact may result in skin irritation, burns, and sensitization. Splashes to the eye may result in blepharoconjunctivitis, lid edema, fibrinous or purulent discharge, and deep or long-lasting corneal injury (ACGIH, 1991; Bingham et al, 2001; Grant & Schuman, 1993; Harbison, 1998; Hathaway et al, 1996; Lewis, 1998; Morgan, 1993).
    3) Bingham et al (2001) estimates the TLV for human exposure to be 0.02 ppm (0.05 mg/m(3)).
    C) ANIMAL DATA
    1) INHALATION - When rats were exposed to greater than 23.6 parts per million (threshold effect) of acrolein for 6 hours/day, olfactory atrophy and squamous metaplasia in the larynx, trachea, and larger bronchi were noted. Squamous metaplasia in the anterior nasal passages was consistently noted. No biochemical or morphological findings suggestive of specific organ or tissue toxicity, with the exception of respiratory tract effects, were found (Ballantyne & Cawley, 2000).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) Postmortem acrolein concentration in the body fluids of a 55-year-old man, who died following a suspected ingestion of 250 mL of a pesticide containing 85% allyl alcohol, were as follows (Toennes et al, 2002):
    Specimen Acrolein concentration (mg/L)
    Blood 7.2
    Bile 13.8
    Urine 5.4

    a) It is believed that the patient died of cardiac arrest due to the presence of acrolein, the toxic metabolite of allyl alcohol.

Workplace Standards

    A) ACGIH TLV Values for CAS107-02-8 (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) Acrolein
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.1 ppm
    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): Eye and URT irr; pulm edema; pulm emphysema
    d) Molecular Weight: 56.06
    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 CAS107-02-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Acrolein
    2) REL:
    a) TWA: 0.1 ppm (0.25 mg/m(3))
    b) STEL: 0.3 ppm (0.8 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix C (Aldehydes)
    3) IDLH:
    a) IDLH: 2 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS107-02-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Acrolein
    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 applicable. This substance was not assessed using the EPA's 1986 cancer guidelines. ; Listed as: Acrolein
    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: Acrolein
    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: Acrolein
    5) MAK (DFG, 2002): Category 3B ; Listed as: Acrolein
    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 CAS107-02-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Acrolein
    2) Table Z-1 for Acrolein:
    a) 8-hour TWA:
    1) ppm: 0.1
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.25
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: HSDB, 2002 Lewis, 2000 RTECS, 2002
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 9008 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 13,900 mcg/kg -- somnolence/ depressed activity, affected hair, weight loss or decreased weight gain
    b) 40 mg/kg (Lewis, 2000)
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 30 mg/kg -- general anesthetic effect, fatty liver degeneration
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 4 mg/kg
    5) LD50- (ORAL)RAT:
    a) 26 mg/kg
    b) 46 mg/kg (HSDB, 2002; Lewis, 2000)
    c) 46 mg/kg
    6) LD50- (SKIN)RAT:
    a) 562 mg/kg (HSDB, 2002)
    7) LD50- (SUBCUTANEOUS)RAT:
    a) 50 mg/kg -- general anesthetic effect, fatty liver degeneration
    8) TCLo- (INHALATION)HUMAN:
    a) Male, 1 ppm -- lacrimation
    b) Child, 300 ppb for 2H -- respiratory obstruction, other respiratory changes
    9) TCLo- (INHALATION)RAT:
    a) 510 mcg/m(3) for 24H/9W- continuous -- changes in urine composition, changes in leukocyte count, weight loss or decreased weight gain
    b) 3 ppm for 6H/3W intermittent -- changes in sense organs and spleen weight
    c) 4 ppm for 6H/62D intermittent -- lung, thorax, or respiratory changes; weight loss or decreased weight gain; death
    d) 4900 ppb for 6H/13W intermittent -- changes in sense organs and adrenal weight; death

Pharmacology Toxicology

Toxicologic Mechanism

    A) Due to its molecular structure, acrolein is highly reactive and can cause serious damage to any exposed tissue. It has a corrosive effect on contact, and causes severe irritation to eyes, skin, oral and gastric mucosa, and especially the respiratory tract. Many biochemical and toxic effects are due to reaction with critical sulfhydryl groups (Bingham et al, 2001; HSDB , 2000).
    B) Acrolein appears to act on glyceraldehyde-3-phosphate dehydrogenase to suppress glycolysis (Plunkett, 1976).
    C) Its bronchoconstrictive effect appears to be mediated via reflex cholinergic stimulation (HSDB , 2000).
    D) In 3-day rat inhalation studies, acrolein induces histopathological changes and cell proliferation of nasal epithelium; it reduces activities of glutathione s-transferase and glutathione reductase; it increases intracellular activity of glutathione peroxidase (Bingham et al, 2001).
    E) In rat and rabbit studies, when acrolein liquid is instilled endogastrically, gastric ulceration and sloughing of gastric mucosa occurs (Bingham et al, 2001).
    F) The cardiovascular effects of hypertension and tachycardia may be due to release of catecholamines from sympathetic nerve endings and from the adrenal medulla in rats (HSDB , 2000).
    G) In vitro exposures of human isolated bronchi to aqueous acrolein solutions have shown the mechanism of action of acrolein to include inactivation of airway neutral endopeptidase in addition to alterations in the pharmacomechanical, but not electromechanical, coupling of human bronchial smooth muscle (Ben-Jebria et al, 1994).

Physicochemical

Physical Characteristics

    A) Acrolein is a colorless to yellow, volatile liquid at room temperature; its odor has been described as pungent or disagreeable and choking. It is lighter than water. Acrolein readily polymerizes unless inhibited with hydroquinone (or other polymerization inhibitors). Its stability depends upon the pH (AAR, 2000; Ashford, 1994; Bingham et al, 2001; Harbison, 1998) IARC, 1987; (ILO , 1998).

Ph

    A) 6.0 (max) (for a 10% aqueous solution at 25 degrees C) (HSDB , 2002)

Molecular Weight

    A) 56.06

References

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