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ACETALDEHYDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Acetaldehyde is a reactive aldehyde which is used in production of acetic acid, plastics, synthetic rubber and resins, paraldehyde, aniline dyes, mirrors and disinfectants.
    B) It is used therapeutically as an inhalant in catarrh and ozena treatment (HSDB , 1989).

Specific Substances

    1) Acetic Aldehyde
    2) Ethanal
    3) Ethyl Aldehyde
    4) CAS 75-07-0
    5) ALDEHYDE (ACETALDEHYDE)
    1.2.1) MOLECULAR FORMULA
    1) C2-H4-O

Available Forms Sources

    A) FORMS
    1) It is colorless, irritating, flammable, and highly reactive. It is commonly in the liquid form but may also be a gas. At dilute concentrations it has a pleasant fruity odor. At high concentrations, the odor becomes pungent and suffocating. A technical grade of 99% is the most common form (AAR, 1998; ACGIH, 1996; (Ashford, 1994; Budavari, 1996; ILO, 1998; Lewis, 1996; Lewis, 1997; Lewis, 1998; NFPA, 1994; Verschueren, 1983).
    B) SOURCES
    1) Acetaldehyde is produced from ethylene by Wacker oxidation process; ethanol via catalytic dehydrogenation, ethanol oxidation; acetylene + water (vinylation); propane + butane (vapor-phase oxidation); and mixed Fischer-Tropsch oxygenates (fractionation, coproduced with several other compounds) (ACGIH, 1996; (Ashford, 1994; Lewis, 1997).
    2) Acetaldehyde can be produced by most hydrocarbon oxidations. It has been detected in wood smoke, tobacco smoke, marijuana smoke, diesel exhaust, and gasoline exhaust. It is also emitted from coffee-roasting and fat-rendering operations (HSDB , 1999; Sittig, 1991).
    3) Acetaldehyde is a normal intermediate product in the respiration of higher plants. It occurs in traces in all ripe fruits as well as in fresh leaf tobacco (Sittig, 1991).
    4) Acetaldehyde can be found in drinking water (Sittig, 1991).
    C) USES
    1) Acetaldehyde is used as a chemical intermediate in the manufacture of compounds such as acetic acid, acetic anhydride, butanol, paraldehyde, pentaerythritol, and pyridines, as well as various drugs. It is used in the production of perfumes, aniline dyes, polyester resins and dyes, plastics, synthetic rubber, silvering mirrors, and for hardening gelatin fibers. Acetaldehyde is also used as a food preservative and/or as a synthetic flavoring agent in foods and beverages (ACGIH, 1996; (Budavari, 1996; Hathaway et al, 1996; ILO, 1998; Lewis, 1997; Lewis, 1998).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) This agent is a skin and mucous membrane irritant which causes a burning sensation of the nose, throat, and eyes. Prolonged exposure to high concentrations may injure the corneal epithelium causing persistent lacrimation, photophobia, and foreign body sensation.
    B) Fatalities, following inhalation, are due to anesthesia when prompt and pulmonary edema when delayed. Very large exposures may cause death due to respiratory paralysis.
    C) Prolonged skin contact may cause dermal erythema and burns. Repeated exposures may cause dermatitis due to primary irritation or sensitization.
    D) Sympathomimetic effects of acetaldehyde include tachycardia, hypertension, and increased respiration. Bradycardia and hypotension occur at higher levels of acetaldehyde exposure.
    0.2.3) VITAL SIGNS
    A) Increased ventilation, hypertension, and tachycardia are sympathomimetic effects which may develop at low levels of exposure.
    B) Higher levels produce bradycardia and hypotension.
    0.2.4) HEENT
    A) Human eye irritation begins to occur at 50 ppm in the air and becomes excessive at 200 ppm. Splash contacts produce painful but superficial corneal injury. Changes in auditory sensitivity were noted in one foreign study of vapor exposures.
    0.2.5) CARDIOVASCULAR
    A) In humans, systemic poisoning can result in sympathomimetic effects of tachycardia and hypertension.
    B) Ventricular dysrhythmias have occurred in halothane anesthetized animals given acetaldehyde.
    0.2.6) RESPIRATORY
    A) Acetaldehyde is a pulmonary irritant and may cause bronchitis and pulmonary edema when inhaled. Very high concentrations may result in respiratory paralysis.
    0.2.7) NEUROLOGIC
    A) High serum concentrations have caused narcosis in animals.
    0.2.8) GASTROINTESTINAL
    A) Liquid acetaldehyde is an emetic.
    0.2.9) HEPATIC
    A) Acetaldehyde can impair mitochondrial respiration in the liver, similar to effects seen with ethanol.
    0.2.14) DERMATOLOGIC
    A) Prolonged contact causes erythema and burns. Repeated exposures may cause dermatitis.
    0.2.20) REPRODUCTIVE
    A) No human reproductive effects were found at the time of this review. Acetaldehyde was detected in 4 out of 8 samples of human breast milk. Embryotoxicity and malformations have been seen in animals.
    0.2.21) CARCINOGENICITY
    A) Acetaldehyde has been implicated as a cocarcinogen in the workplace. There was an increased incidence of total cancers in acetaldehyde production workers as compared with the general population, although this study failed to adjust for confounders.

Laboratory Monitoring

    A) No toxic levels have been established. For significant exposures, base-line liver and kidney function tests may be indicated.
    B) Monitor vital signs and chest x-ray in all significant exposures.
    C) Monitor for signs of CNS depression following significant exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    D) 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.
    E) Acetaldehyde in high concentrations may result in narcosis; patients should be monitored for possible coma and respiratory depression.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) 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.
    C) Acetaldehyde in high concentrations may result in narcosis so patients should be monitored for possible coma and respiratory depression.
    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) 50 ppm for 15 minutes will cause eye irritation in the majority of subjects.
    B) Fatalities have occurred in animals exposed to levels of 16,000 ppm for four hours.

Clinical Effects

Summary Of Exposure

    A) This agent is a skin and mucous membrane irritant which causes a burning sensation of the nose, throat, and eyes. Prolonged exposure to high concentrations may injure the corneal epithelium causing persistent lacrimation, photophobia, and foreign body sensation.
    B) Fatalities, following inhalation, are due to anesthesia when prompt and pulmonary edema when delayed. Very large exposures may cause death due to respiratory paralysis.
    C) Prolonged skin contact may cause dermal erythema and burns. Repeated exposures may cause dermatitis due to primary irritation or sensitization.
    D) Sympathomimetic effects of acetaldehyde include tachycardia, hypertension, and increased respiration. Bradycardia and hypotension occur at higher levels of acetaldehyde exposure.

Vital Signs

    3.3.1) SUMMARY
    A) Increased ventilation, hypertension, and tachycardia are sympathomimetic effects which may develop at low levels of exposure.
    B) Higher levels produce bradycardia and hypotension.
    3.3.2) RESPIRATIONS
    A) INCREASED VENTILATION was observed after IV infusion of 5% acetaldehyde at 20.6 - 82.4 mg/min for up to 36 minutes in human volunteers (HSDB , 2001).
    3.3.4) BLOOD PRESSURE
    A) HYPERTENSION was noted when acetaldehyde was infused IV (HSDB , 2001).
    B) HYPOTENSION may occur with increasing levels of acetaldehyde (von Wartburg, 1987).
    3.3.5) PULSE
    A) TACHYCARDIA was observed after IV infusion of 5% acetaldehyde at 20.6 - 82.4 mg/min for up to 36 minutes in human volunteers (HSDB , 2001).
    B) BRADYCARDIA occurs at higher levels of acetaldehyde in the body (von Wartburg, 1987).

Heent

    3.4.1) SUMMARY
    A) Human eye irritation begins to occur at 50 ppm in the air and becomes excessive at 200 ppm. Splash contacts produce painful but superficial corneal injury. Changes in auditory sensitivity were noted in one foreign study of vapor exposures.
    3.4.3) EYES
    A) At sufficient concentrations, acetaldehyde is a mucous membrane irritant (Proctor & Hughes, 1978). Conjunctivitis is reported following repeated exposures to vapors (HSDB , 2001).
    B) Human eye irritation occurs at acetaldehyde concentrations of 50 ppm in air and becomes excessive under industrial exposures at 200 ppm. The higher percentages and/or extended exposures may damage corneal epithelium, and produce photophobia, foreign body sensitization and persistent lacrimation (HSDB , 2001; Baselt, 2000).
    C) SPLASH CONTACTS in the eye may result in painful but superficial corneal injury that rapidly heals (Grant & Schuman, 1993). Concentrations of 0.012 mg/m(3) of air has been noted to cause changes in light sensitivity of the eye (HSDB , 2001; Grant & Schuman, 1993).
    3.4.4) EARS
    A) HEARING - Changes in auditory sensitivity were noted in one study at levels of approximately 0.05 mg/m(3) (HSDB , 2001; Grant & Schuman, 1993).
    3.4.5) NOSE
    A) Nasal irritation may occur following inhalation of acetaldehyde vapors (Bingham et al, 2001).
    3.4.6) THROAT
    A) Throat irritation may occur following inhalation of acetaldehyde vapors (Bingham et al, 2001).

Cardiovascular

    3.5.1) SUMMARY
    A) In humans, systemic poisoning can result in sympathomimetic effects of tachycardia and hypertension.
    B) Ventricular dysrhythmias have occurred in halothane anesthetized animals given acetaldehyde.
    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) Acetaldehyde, when given intravenously or perhaps when ingested, may result in sympathomimetic responses of tachycardia and hypertension. This is due to a release of norepinephrine from adrenergic nerve endings (HSDB , 2001).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSRHYTHMIA VENTRICULAR
    a) Ventricular dysrhythmias were induced in halothane-anesthetized cats by intravenously administered acetaldehyde (Condouris & Havelin, 1987). It is not clear if this could occur in humans.

Respiratory

    3.6.1) SUMMARY
    A) Acetaldehyde is a pulmonary irritant and may cause bronchitis and pulmonary edema when inhaled. Very high concentrations may result in respiratory paralysis.
    3.6.2) CLINICAL EFFECTS
    A) INJURY OF UPPER RESPIRATORY TRACT
    1) 134 ppm for 30 minutes led to upper airway irritation (Proctor & Hughes, 1978). Low to moderate air concentrations (50-200 ppm) have been reported to cause upper respiratory irritation (Baselt, 2000). Following inhalation of 100 to 200 ppm, ciliastatic effects on the upper respiratory tract which may enhance uptake of other vapor-phase chemicals may occur (Bingham et al, 2001; HSDB , 2001). This agent may also cause bronchitis. Acetaldehyde has been shown to depress pulmonary macrophage numbers (Clayton & Clayton, 1982).
    B) ACUTE LUNG INJURY
    1) Acetaldehyde may cause pulmonary edema because of its irritant effects (ITI, 1975). Delayed pulmonary edema is a concentration-dependent reaction from inhalation or dermal exposure to acetaldehyde vapors (Bingham et al, 2001). Pulmonary edema may be the cause of death following large exposures (HSDB , 2001).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) At very high acetaldehyde concentrations, paralysis of the central respiratory system leading to death can occur. Increased ventilation and pulse rates, with decreases in alveolar CO2, has been reported in volunteers given intravenous acetaldehyde (Bingham et al, 2001).

Neurologic

    3.7.1) SUMMARY
    A) High serum concentrations have caused narcosis in animals.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Irritation usually prevents the patient from being exposed to concentrations high enough to cause narcosis. Concentration-dependent moderate narcosis and CNS depression may occur following inhalation or dermal exposures. Human industrial exposures are typically limited because acetaldehyde is explosive and is usually handled in a hood (Bingham et al, 2001) Clayton & Clayton, 1982).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) Acetaldehyde in high concentrations has caused narcosis in animals (ITI, 1985) Proctor & Hughes, 1978).

Gastrointestinal

    3.8.1) SUMMARY
    A) Liquid acetaldehyde is an emetic.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) While ingestion of the liquid would be rare, acetaldehyde does have emetic properties (OHM/TADS , 1989).

Hepatic

    3.9.1) SUMMARY
    A) Acetaldehyde can impair mitochondrial respiration in the liver, similar to effects seen with ethanol.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) Acetaldehyde has been implicated as the active agent in ethanol-induced liver disease by damaging mitochondrial respiration (HSDB , 2001; von Wartburg, 1987; Barry & McGivan, 1985).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER FATTY
    a) Animal studies indicate liver fatty degeneration (ACGIH, 1980).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ALBUMINURIA
    a) Albuminuria is mentioned as an effect seen in animals (ACGIH, 1980).

Dermatologic

    3.14.1) SUMMARY
    A) Prolonged contact causes erythema and burns. Repeated exposures may cause dermatitis.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Prolonged contact causes erythema and burns. Repeated exposures may cause dermatitis due to primary irritation or sensitization (HSDB , 2001) Proctor & Hughes, 1978). Contact with liquid acetaldehyde can cause painful but not serious burns (Bingham et al, 2001).

Reproductive

    3.20.1) SUMMARY
    A) No human reproductive effects were found at the time of this review. Acetaldehyde was detected in 4 out of 8 samples of human breast milk. Embryotoxicity and malformations have been seen in animals.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) While acetaldehyde is a metabolite of ethanol and the latter is a known human teratogen, metabolic studies suggest that acetaldehyde is not responsible for the teratogenicity (EPA, 1983). No human reproductive effects have been reported.
    B) ANIMAL STUDIES
    1) Acetaldehyde was embryotoxic (increased resorptions) and induced neural tube defects and musculoskeletal defects in mice (HSDB , 2001; RTECS , 2001).
    2) It induced delayed ossification, wavy ribs, eye/ear defects, and craniofacial abnormalities in fetal rats (HSDB , 2001; RTECS , 2001).
    3) Neural tube defects were found in mice treated acutely with 0.1 mL of 2% acetaldehyde intravenously (O'Shea & Kaufman, 1981).
    4) A slight increase in fetal defects was seen in the offspring of mice administered 4 percent acetaldehyde intraperitoneally as a single dose on days 7 through 10 of gestation (Webster et al, 1983).
    5) Acetaldehyde was 100 percent embryolethal to explanted rat embryos when added to the culture medium at a concentration of 20 mcg/dL and caused growth retardation and teratogenic effects at a concentration of 10 mcg/dL (Giavini et al, 1991) 1992).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) Since chronic maternal ethanol consumption produces high acetaldehyde concentrations, a fetal alcohol syndrome is theoretically possible.
    B) OCCUPATIONAL EXPOSURE
    1) Occupational exposure is thought to present no risk when PEL guidelines are followed and no maternal toxicity exists (AMA, 1985).
    C) ANIMAL STUDIES
    1) Pregnant rats administered 240 mg/kg of acetaldehyde throughout gestation produced offspring with lower body weights and immature and hemorrhagic viscera (Imai & Omato, 1992; (HSDB , 2001).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Acetaldehyde was detected in 4 out of 8 samples of human breast milk (HSDB , 2001).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-07-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) IARC Classification
    a) Listed as: Acetaldehyde
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) Acetaldehyde has been implicated as a cocarcinogen in the workplace. There was an increased incidence of total cancers in acetaldehyde production workers as compared with the general population, although this study failed to adjust for confounders.
    3.21.3) HUMAN STUDIES
    A) OCCUPATIONAL EXPOSURE
    1) NIOSH regards acetaldehyde as a potential occupational carcinogen (Chemsoft(R) , 1996).
    2) Acetaldehyde has been implicated as a cocarcinogen in an occupational study of persons exposed to it as well as aldol and other aldehydes (EPA, 1983).
    3) There was an increased incidence of total cancers in acetaldehyde production workers as compared to the general population (Bittersohl, 1974). This study had several major limitations, however, including failure to adjust for age, gender, cigarette smoking, and other important confounders (IRIS, 1997).
    3.21.4) ANIMAL STUDIES
    A) CARCINOGENICITY RISK
    1) IARC has concluded that there is sufficient evidence to classify acetaldehyde as an animal carcinogen (Lewis, 1996).
    2) Acetaldehyde has been carcinogenic in rats and hamsters for squamous cell carcinomas and adenocarcinomas at 735 ppm or higher (Proctor et al, 1988; RTECS , 2001).
    3) Acetaldehyde has produced respiratory tract tumors in rats and hamsters, including nasal mucosa adenocarcinomas and squamous cell carcinomas (Hathaway et al, 1991; ACGIH, 1991; HSDB , 2001; RTECS , 2001).

Genotoxicity

    A) Acetaldehyde has been active in short-term assays for DNA damage and repair, mutagenicity, chromosome aberrations, sister chromatid exchanges, micronucleus test, and oncogenic transformation (HSDB , 2001; RTECS , 2001).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic levels have been established. For significant exposures, base-line liver and kidney function tests may be indicated.
    B) Monitor vital signs and chest x-ray in all significant exposures.
    C) Monitor for signs of CNS depression following significant exposures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No toxic levels have been established. For significant exposures base-line liver and kidney function tests may be indicated.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor for CNS depression, including respiratory depression, following significant exposures. Monitor vital signs for hypertension and tachycardia.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor chest X-ray in symptomatic patients for signs of delayed-onset of pulmonary edema following inhalation of vapors.

Methods

    A) CHROMATOGRAPHY
    1) In NIOSH Analytical Method 3507 acetaldehyde can be measured in ambient air by collecting on an impinger or fretted bubbler, followed by derivatization with Grignard T reagent and high pressure liquid chromatography; the range of detection is 170 - 670 mg/m(3) (HSDB , 2001).
    2) It can be quantitated by gas chromatography/mass spectrometry with detection limits of <10 ppb (HSDB , 2001). Ultraviolet spectrophotometry has been used for analysis of blood or urine acetaldehyde (Baselt, 2000).
    3) Acetaldehyde can be measured in human blood by high-pressure liquid chromatography or gas chromatography (HSDB , 2001; Baselt, 2000).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic levels have been established. For significant exposures, base-line liver and kidney function tests may be indicated.
    B) Monitor vital signs and chest x-ray in all significant exposures.
    C) Monitor for signs of CNS depression following significant exposures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/ NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) 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).
    B) MONITORING OF PATIENT
    1) No toxic concentrations have been established. For significant exposures, base-line liver and kidney function tests may be indicated. Treatment is symptomatic and supportive.
    2) Since acetaldehyde in high concentrations may result in narcosis, patients should be monitored for possible coma and respiratory depression.

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) 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).
    B) MONITORING OF PATIENT
    1) Monitor liver and kidney functions.
    2) Since acetaldehyde in high concentrations may result in narcosis, patients should be monitored for possible coma and respiratory depression.
    C) 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).

Range Of Toxicity

Summary

    A) 50 ppm for 15 minutes will cause eye irritation in the majority of subjects.
    B) Fatalities have occurred in animals exposed to levels of 16,000 ppm for four hours.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) Acetaldehyde is primarily an inhalation hazard. The irritating properties of acetaldehyde vapor are prominent at concentrations low enough to warn workers of exposure. Low to moderate air concentrations (50-200 ppm) cause eye irritation and upper respiratory discomfort. Higher concentrations and prolonged exposure may cause dyspnea, narcosis, CNS depression, and injury to the corneal epithelium resulting in persistent lacrimation, photophobia, and foreign body sensation. Nausea, loss of consciousness, and pulmonary edema have been reported with heavy exposure. However, no chronic effects associated with long-term occupational exposure to acetaldehyde have been reported (Baselt, 2000; Harbison, 1998) ACGIH, 1996; (Hathaway et al, 1996; Grant & Schuman, 1993).
    a) Mild eye irritation was reported by subjects exposed to 50 ppm acetaldehyde for 15 minutes; mild upper respiratory irritation was reported after exposure to 134 ppm for 30 minutes. At 200 ppm, all subjects had red eyes and transient conjunctivitis, and the majority also reported nose and throat irritation (ACGIH, 1996; (Clayton & Clayton, 1993; Hathaway et al, 1996).
    2) Dermal contact with liquid acetaldehyde may result in erythema and burns if the acetaldehyde is not washed away promptly. Sensitization and subsequent dermatitis is possible for some individuals. When splashed into the eyes, liquid acetaldehyde causes a painful burning sensation, lacrimation, blurred vision, and corneal injury. However, liquid acetaldehyde evaporates so quickly at body temperature that contact is usually brief and self-limited, and healing is rapid (Bingham et al, 2001; Harbison, 1998) ACGIH, 1996; (Hathaway et al, 1996; Grant & Schuman, 1993).

Serum Plasma Blood Concentrations

    7.5.1) THERAPEUTIC CONCENTRATIONS
    A) THERAPEUTIC CONCENTRATION LEVELS
    1) ADULT
    a) Normal endogenous acetaldehyde blood levels generally do not exceed 0.2 milligrams/liter (Baselt, 2000).

Workplace Standards

    A) ACGIH TLV Values for CAS75-07-0 (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) Acetaldehyde
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 25 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: Not Listed
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    c) TLV Basis - Critical Effect(s): Eye and URT irr
    d) Molecular Weight: 44.05
    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) Under Study
    1) Acetaldehyde
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    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 CAS75-07-0 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Acetaldehyde
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A; See Appendix C (Aldehydes)
    3) IDLH:
    a) IDLH: 2000 ppm
    b) Note(s): Ca
    1) Ca: NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A).

    C) Carcinogenicity Ratings for CAS75-07-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Acetaldehyde
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Acetaldehyde
    3) EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Acetaldehyde
    a) B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.
    4) 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): 2B ; Listed as: Acetaldehyde
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Acetaldehyde
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    6) MAK (DFG, 2002): Category 3B ; Listed as: Acetaldehyde
    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.)
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-07-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Acetaldehyde
    2) Table Z-1 for Acetaldehyde:
    a) 8-hour TWA:
    1) ppm: 200
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 360
    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: Lewis, 1996 RTECS, 2001
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 500 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 900 mg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 560 mg/kg
    4) LD50- (ORAL)RAT:
    a) 661 mg/kg
    5) LD50- (SUBCUTANEOUS)RAT:
    a) 640 mg/kg
    6) TCLo- (INHALATION)HUMAN:
    a) 134 ppm for 30M
    7) TCLo- (INHALATION)RAT:
    a) 735 ppm for 6H/2Y-I

Pharmacology Toxicology

Toxicologic Mechanism

    A) The sympathomimetic effects of acetaldehyde, including tachycardia, hypertension, and increased respiratory ventilation, are due to release of norepinephrine from adrenergic nerve endings (HSDB , 2001). Catecholamines are released from tissue stores (Condouris & Havelin, 1987).
    B) Acetaldehyde inhibited mitochondrial oxygen consumption and energy production in rat liver in vitro (HSDB , 2001).
    C) Acetaldehyde can deplete cellular stores of glutathione and lead to lipid peroxidation (von Wartburg, 1987).
    D) Acetaldehyde exerts its genotoxic effects by virtue of its electrophilic activity to react with proteins and nucleic acids (von Wartburg, 1987).

Physicochemical

Physical Characteristics

    A) Acetaldehyde is colorless, irritating, flammable, and highly reactive. It is commonly in the form of a liquid but can also be a gas. At dilute concentrations, it has a pleasant fruity odor and a leafy green taste. At high concentrations, the odor becomes pungent and suffocating (HSDB , 2001) AAR, 1998; ACGIH, 1996; (Ashford, 1994; Budavari, 1996; ILO, 1998; Lewis, 1996; Lewis, 1997; Lewis, 1998; NFPA, 1994; Verschueren, 1983).
    B) 30% to 60% mixtures of acetaldehyde vapor in air ignite at temperatures above 100 degrees centigrade. Acetaldehyde is highly soluble in water and in most common organic solvents, such as alcohol (Bingham et al, 2001).

Molecular Weight

    A) 44.05 (HSDB , 2001)

Other

    A) ODOR THRESHOLD
    1) 0.21 ppm (Sittig, 1991)

References

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