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FORMIC ACID

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Formic acid is an organic acid. It is manufactured as a by-product of the liquid-phase oxidation of hydrocarbons to acetic acid. It has a pungent and penetrating odor and has irritant (skin and eyes) effects. Formic acid also has corrosive properties (Lewis, 2002; Bingham et al, 2001).

Specific Substances

    1) ADD-F
    2) Aminic acid
    3) A13-24237
    4) Bilorin
    5) Collo-didax
    6) Fema No 2487
    7) Formate
    8) Formira
    9) Formisoton
    10) Formylic acid
    11) Hydrogen Carboxylic Acid
    12) Methanoic acid
    13) Myrmic
    14) Chemical formula: HCOOH
    1.2.1) MOLECULAR FORMULA
    1) C-H2-O2 HCOOH

Available Forms Sources

    A) SOURCES
    1) Formic acid is a natural constituent of some fruits, nuts, and dairy products (Clayton & Clayton, 1994). Some wines may contain formic acid. Concentrations in the following produce: apples, pears, plums, and apricots ranged from 2.7 to 87 mg/L.
    B) USES
    1) SUMMARY - Formic acid is widely used in industry and agriculture.
    a) INDUSTRIAL - It has been used as a component of descaling and stain-removing agents, as a reducing agent in wool/textile dyeing, as a leather tanning, plumping and dehairing product for hides, as a catalyst in hydrocarbon-formaldehyde resins and phenolic resins, as a plasticizer for vinyl resins, and in coagulation of latex rubber and electroplating (Clayton & Clayton, 1994).
    1) Descaling agents can contain formic acid concentrations of 44 to 60% (Moore et al, 1994). Industrial workers (e.g. airplane glue makers, cellulose formate and tanning workers) can be exposed to up to 60% solutions of formic acid (Clayton & Clayton, 1994).
    b) AGRICULTURAL - It has also been used as an animal feed additive, food preservative, flavor enhancer, and brewing antiseptic (Clayton & Clayton, 1994). Formic acid has been used in Nordic countries as silage preservative. It also comes from fire ants.
    c) THERAPEUTIC - Additional uses for formic acid have included: removal of tattoos, as a component in some external preparations in the treatment of musculoskeletal and joint disorders (Liesivuori & Savolainen, 1991; Chan et al, 1995) Ellenhorn, 1997; Reynolds, 1999). It also has the ability to prevent the growth of Candida albicans (Clayton & Clayton, 1994).
    d) FOOD ADDITIVE - Formic acid has also been used as a food additive in small amounts (e.g., 0.1 to 6 ppm) in ice cream, ices, candy, and baked goods (Bingham et al, 2001).
    e) OTHER - Formic acid has also been examined as the toxic metabolite produced in methanol poisoning. This management refers only to the direct effects of formic acid toxicity.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Formic acid can be irritating or corrosive to the skin, eyes, and mucous membranes, depending on the concentration. It may cause severe caustic injury to the skin, eyes, or mucosal membranes.
    B) Symptoms of acute ingestion (50 grams or more) can initially include salivation, bloody vomiting, a burning sensation in the mouth and pharynx, diarrhea, severe pain. Circulatory collapse and death have occurred following exposure.
    C) In limited case reports, intentional oral ingestions of formic acid have resulted in life-threatening metabolic acidosis, profound hypotension, shock, ARDS, acute renal failure, and severe hemolysis. Systemic effects have also been reported following dermal exposure.
    D) Occupational exposure has caused nausea and albumin or blood in the urine. Formic acid is a sensitizer for some individuals; allergic contact dermatitis or possibly asthma could develop in these individuals.
    E) Combining formic and sulfuric acid produces carbon monoxide; severe carbon monoxide poisoning has resulted.
    0.2.5) CARDIOVASCULAR
    A) Profound hypotension and circulatory collapse resulting in death have been reported after ingestion.
    0.2.6) RESPIRATORY
    A) Dyspnea, pneumonitis, and ARDS have been reported following exposure.
    0.2.7) NEUROLOGIC
    A) Central nervous system depression can occur following exposure. Coma and muscle contractions may be present with severe intoxication.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting are frequently reported. Gastrointestinal bleeding and burns may develop after ingestion; potential complications include strictures, fistula formation, and perforation.
    0.2.11) ACID-BASE
    A) Profound metabolic acidosis may occur following oral or severe dermal exposure to formic acid.
    0.2.13) HEMATOLOGIC
    A) Hemolysis, coagulopathy, and disseminated intravascular coagulation have been reported following significant exposure.
    0.2.14) DERMATOLOGIC
    A) Anticipated dermal injuries can include: erythema, edema, superficial burns, and blistering of the skin. Superficial burns can progress to second or third degree burns. Infrequent reports of epidermal necrosis have also occurred.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for formic acid in humans.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of formic acid in humans.

Laboratory Monitoring

    A) Monitor CBC, electrolytes, renal and hepatic function, urine output, and ABGs as needed.

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) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    D) METABOLIC ACIDOSIS - Monitor ABGs in all patients following a significant exposure. If pH less than 7.1 administer sodium bicarbonate at 1 to 2 mEq/kg every 1 to 2 hours. Repeat ABGs to evaluate response.
    E) ENDOSCOPY: Because acid ingestion may cause severe gastric burns with relatively few initial signs and symptoms, endoscopic evaluation is recommended within 24 hours in any patient with a definite history of ingesting a strong acid, even if asymptomatic. If burns are found, follow 10 to 20 days later with a barium swallow.
    F) PHARMACOLOGIC TREATMENT: The use of corticosteroids is controversial. Patients with first degree burns generally do well and rarely develop strictures. Corticosteroids are generally not beneficial in these patients. Some authors have advocated the use of corticosteroids for second degree, deep-partial thickness burns within 48 hours of ingestion in patients without gastrointestinal bleeding or evidence of perforation. However, no well-controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with second degree, superficial-partial thickness burns. Some authors have recommended steroids in patients with third degree burns. A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended. Antibiotics are indicated for suspected perforation or infection and in patients receiving corticosteroids.
    G) SURGICAL OPTIONS: Initially, if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed; if unsuccessful, either colonic intraposition or gastric tube placement may be performed. Consider early laparotomy in patients with severe esophageal and/or gastric burns.
    H) Maintain urine output using intravenous fluids and diuretics as needed. Administer folinic acid 1 mg/kg every 4 hours for 6 doses in patients with significant toxicity.
    I) Monitor for hemolysis and transfuse as needed.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) INHALATION: Administer oxygen. If respiratory symptoms develop obtain chest x-ray, monitor pulse oximetry and/or blood gases. Treat bronchospasm with inhaled beta2-adrenergic agonists. If acute lung injury develops, consider PEEP. Evaluate for esophageal, dermal and eye burns as indicated.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
    C) EYE ASSESSMENT: The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and 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) Refer to the oral treatment section as indicated to address systemic effects.

Range Of Toxicity

    A) Ingestions of less than 10 grams in children have resulted in oropharyngeal burns; no deaths were reported.
    B) Solutions of 10% or less are generally considered noncorrosive.
    C) Ingestions between 5 and 30 grams resulted in symptomatic burns of the gastrointestinal tract and hematemesis, but no deaths. Ingestions between 45 to 200 grams resulted in 87% of patients dying within the first 36 hours post ingestion.
    D) An adult survived an ingestion of 110 grams of formic acid.
    E) INHALATION - Textile workers complained of nausea from formic acid vapor concentrations around 15 ppm.

Clinical Effects

Summary Of Exposure

    A) Formic acid can be irritating or corrosive to the skin, eyes, and mucous membranes, depending on the concentration. It may cause severe caustic injury to the skin, eyes, or mucosal membranes.
    B) Symptoms of acute ingestion (50 grams or more) can initially include salivation, bloody vomiting, a burning sensation in the mouth and pharynx, diarrhea, severe pain. Circulatory collapse and death have occurred following exposure.
    C) In limited case reports, intentional oral ingestions of formic acid have resulted in life-threatening metabolic acidosis, profound hypotension, shock, ARDS, acute renal failure, and severe hemolysis. Systemic effects have also been reported following dermal exposure.
    D) Occupational exposure has caused nausea and albumin or blood in the urine. Formic acid is a sensitizer for some individuals; allergic contact dermatitis or possibly asthma could develop in these individuals.
    E) Combining formic and sulfuric acid produces carbon monoxide; severe carbon monoxide poisoning has resulted.

Vital Signs

    3.3.4) BLOOD PRESSURE
    A) Severe hypotension has been reported with significant formic acid toxicity (Rajan et al, 1985).
    B) Following formic acid intoxication, elevated blood pressure may be initially noted secondary to vasoconstriction (Malizia et al, 1977).

Heent

    3.4.3) EYES
    A) Topical exposure to formic acid can result in conjunctivitis and keratitis (Clayton & Clayton, 1994). Permanent scarring of cornea may occur.
    B) CORNEAL OPACIFICATION AND EPITHELIAL INJURY may occur with acid burns to the eyes (Saini & Sharma, 1993).
    1) CASE REPORT - Sudarsky (1965) reported transient opacification of the anterior half of the cornea in a 30-year-old male following a one drop splash to his eye containing concentrated formic acid (Sudarsky, 1965).

Cardiovascular

    3.5.1) SUMMARY
    A) Profound hypotension and circulatory collapse resulting in death have been reported after ingestion.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Profound hypotension and decreased cardiac output has been associated with significant oral exposure to formic acid (Malizia et al, 1977; Rajan et al, 1985).
    B) SHOCK
    1) WITH POISONING/EXPOSURE
    a) Shock and circulatory collapse may occur following ingestion (HSDB , 2000).
    C) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Brady- and tachyarrhythmias have occurred following exposure (Malizia et al, 1977; Rajan et al, 1985).
    D) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) Chest pain has been reported shortly after formic acid ingestion (Moore et al, 1994).

Respiratory

    3.6.1) SUMMARY
    A) Dyspnea, pneumonitis, and ARDS have been reported following exposure.
    3.6.2) CLINICAL EFFECTS
    A) CHRONIC RESPIRATORY CONDITION DUE TO FUMES AND/OR VAPORS
    1) WITH POISONING/EXPOSURE
    a) Farm workers who come in contact with storage silos can be exposed to 3 to 7 mg/m(3) of formic acid vapors which can lead to lacrimation, increased nasal discharge, rhinitis, coughing, throat irritation, bronchitis, and possible dyspnea (Clayton & Clayton, 1994).
    B) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 53-year-old male developed chemical pneumonitis following an inhalation exposure to a mixture of formic acid (98-100%) and sulfuric acid (95-98%). The patient's pulmonary status deteriorated on day 4 of admission with diffuse infiltrations evident on X-ray, and ARDS was suspected. Treatment with antibiotics, steroids, and N-acetylcysteine was successful, and the patient was weaned from the ventilator on day 8 (Yang et al, 2008).
    b) CASE SERIES - In a series of 53 cases of formic acid ingestion, 45 patients were diagnosed with inhalation pneumonitis with dyspnea, cough, and cyanosis (Rajan et al, 1985).
    C) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea has been reported following ingestion and dermal exposure to formic acid (Jefferys & Wiseman, 1980; Chan et al, 1995).
    D) RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) Acute respiratory distress syndrome and respiratory failure have been reported following severe formic acid exposures (Naik et al, 1980; Rajan et al, 1985; Verstraete et al, 1989).
    b) CASE REPORT - A 53-year-old male developed chemical pneumonitis following an inhalation exposure to a mixture of formic acid (98-100%) and sulfuric acid (95-98%). The patient's pulmonary status deteriorated on day 4 of admission with diffuse infiltrations evident on X-ray, and ARDS was suspected. Treatment with antibiotics, steroids, and N-acetylcysteine was successful, and the patient was weaned from the ventilator on day 8 (Yang et al, 2008).
    E) PHARYNGITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 53-year-old female developed a sore throat and pharyngitis after an inhalation exposure to a mixture of formic acid (98-100%) and sulfuric acid (95-98%). She was treated with 100% oxygen, and her clinical condition normalized on day 4 of admission (Yang et al, 2008).

Neurologic

    3.7.1) SUMMARY
    A) Central nervous system depression can occur following exposure. Coma and muscle contractions may be present with severe intoxication.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Depression, drowsiness, and asthenia can be observed (Malizia et al, 1977). Coma and muscle contractions are present in severe toxicity.

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting are frequently reported. Gastrointestinal bleeding and burns may develop after ingestion; potential complications include strictures, fistula formation, and perforation.
    3.8.2) CLINICAL EFFECTS
    A) BURN OF GASTROINTESTINAL TRACT
    1) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and intense thirst are common findings following oral and dermal exposure, which has resulted from systemic absorption (HSDB , 2000). Formic acid increases gastric secretions and intestinal peristalsis (Malizia et al, 1977).
    b) Corrosion of mucous membranes following ingestion can occur in the mouth, throat, and esophagus with pain and dysphagia (HSDB , 2000).
    c) CASE REPORT - One patient died from refractory hypotension following a 50 to 100 mL ingestion of a kitchen descaling agent containing 55% formic acid; postmortem exam revealed extensive erosion of the esophagus, stomach, and duodenum (Naik et al, 1980).
    B) BLEEDING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Frank hematemesis and hemoptysis occurred after a 250 mL ingestion of 44% (110 grams) formic acid in an adult (Moore et al, 1994).
    b) CASE REPORTS - Five deaths were reported secondary to gastrointestinal bleeding following formic acid ingestions (Rajan et al, 1985).
    C) STRICTURE OF ESOPHAGUS
    1) WITH POISONING/EXPOSURE
    a) Esophageal stricture has been reported in several intentional formic acid ingestions (Rajan et al, 1985; Moore et al, 1994), and in one case, necessitated ongoing intermittent esophageal dilatation (Moore et al, 1994).
    b) CASE SERIES - In a series of 53 cases of formic acid ingestion, 16 patients developed esophageal stricture (Rajan et al, 1985).
    D) PYLORIC STENOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - A 21-year-old male worker accidentally drank a cup of formic acid and developed inflammatory changes immediately following ingestion, which progressed to antral obstruction which was corrected surgically (Lambeth & Somasundaram, 1970).
    E) PERFORATION OF INTESTINE
    1) WITH POISONING/EXPOSURE
    a) In a review of 45 patients who had ingested formic acid, painful deaths occurred in 14 of 16 patients who ingested between 45 to 200 grams of formic acid. The majority died from corrosive perforation of the abdominal viscera within the first 36 hours of exposure (Jefferys & Wiseman, 1980).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) DIURESIS
    1) WITH POISONING/EXPOSURE
    a) Diuresis may be present secondary to vasodilatation or an osmotic effect (Malizia et al, 1977).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Renal failure may occur following formic acid ingestion (Mozingo et al, 1988). Onset may be delayed up to a week after exposure (Moore et al, 1994). Its been suggested that progressive hemoglobinuria, hypoperfusion, and direct formate toxicity may contribute to acute renal failure (Chan et al, 1995).
    b) CASE SERIES - Of 53 cases of formic acid ingestions, 20 patients developed acute renal failure with 4 deaths reported (Rajan et al, 1985).
    C) HEMOGLOBINURIA
    1) WITH POISONING/EXPOSURE
    a) Hemoglobinuria may develop secondary to hemolysis after formic acid ingestion (Greif & Kaplan, 1986; Jefferys & Wiseman, 1980).
    b) CASE REPORT - A 3-year-old girl developed hemoglobinuria, which was not associated with renal failure after dermal exposure to 90% formic acid. Second and third degree burns were reported which resulted in significant systemic absorption; initial serum formate level was 400 mcg/mL (Chan et al, 1995).

Acid-Base

    3.11.1) SUMMARY
    A) Profound metabolic acidosis may occur following oral or severe dermal exposure to formic acid.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis has been reported in several case reports following oral ingestion and severe dermal exposure resulting in systemic absorption (Moore et al, 1994; Chan et al, 1995).
    b) CASE REPORT - A 3-year-old girl developed systemic symptoms of metabolic acidosis after dermal exposure to 90% formic acid resulting in second and third degree burns over 35% of her body (Chan et al, 1995).
    c) CASE REPORT - A 36-year-old female with a history of depression ingested a 250 mL solution containing 44% formic acid and developed anion gap metabolic acidosis, approximately 13 hours after exposure. Acidosis normalized 72 hours after admission following supportive therapy (Moore et al, 1994).

Hematologic

    3.13.1) SUMMARY
    A) Hemolysis, coagulopathy, and disseminated intravascular coagulation have been reported following significant exposure.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Gross hemolysis (hemoglobin 15.1 g/dL) occurred in a 36-year-old female after ingesting 110 grams of formic acid. The patient recovered following a complicated intensive care course (Moore et al, 1994).
    b) In vitro hemolytic activity of formic acid in a phosphate buffered saline are reported below (Verstraete et al, 1989):
    ACID PARTIAL HEMOLYSIS COMPLETE HEMOLYSIS
     Conc (mcg/mL)pHConc (mcg/mL)pH
    Formic Acid2504.025003.43

    B) BLOOD COAGULATION DISORDER
    1) WITH POISONING/EXPOSURE
    a) Coagulopathy and disseminated intravascular coagulation have been reported after ingestion of formic acid (Naik et al, 1980; Verstraete et al, 1989; Moore et al, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Anticipated dermal injuries can include: erythema, edema, superficial burns, and blistering of the skin. Superficial burns can progress to second or third degree burns. Infrequent reports of epidermal necrosis have also occurred.
    3.14.2) CLINICAL EFFECTS
    A) SKIN NECROSIS
    1) WITH POISONING/EXPOSURE
    a) Although infrequently reported, epidermal necrosis has developed following dermal contact (Malizia et al, 1977).
    B) BURN
    1) WITH POISONING/EXPOSURE
    a) Second and third degree burns may also occur depending on the strength and the amount of solution that comes in contact with the skin (Chan et al, 1995).
    b) CASE REPORT - A 3-year-old girl had second and third degree burns over 35% of her body after an accidental spill with a solution containing 90% formic acid. The injuries resulted in significant systemic absorption, with an initial serum formate level of 400 mcg/mL (Chan et al, 1995).
    c) CASE REPORT - A 53-year-old male sustained partial thickness chemical burns to his right thigh after inhalation and dermal exposure to a mixture of formic acid (98-100%) and sulfuric acid (95-98%). The patient also developed severe carbon monoxide poisoning (carboxyhemoglobin concentration 45.8%, coma, myocardial ischemia), pneumonitis and acute lung injury, but made a successful recovery (Yang et al, 2008).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for formic acid in humans.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Formic acid was not teratogenic in chickens (MALORNY, 1969). In a multi-generation study of calcium formate in the drinking water at levels of 0.2 or 0.4%, formate had no effect on reproduction in rats for at least 5 generations (MALORNY, 1969).
    2) Formic acid produced growth retardation and anomalies in mouse and rat embryo culture (Andrews et al, 1995). However, this system is non-physiologic, and results may reflect pH alteration.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS64-18-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of formic acid in humans.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor CBC, electrolytes, renal and hepatic function, urine output, and ABGs as needed.
    4.1.2) SERUM/BLOOD
    A) Obtain CBC, electrolytes, and ABGs as indicated following ingestion or severe dermal exposure.

Radiographic Studies

    A) Obtain a chest x-ray as indicated or if aspiration occurs.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor CBC, electrolytes, renal and hepatic function, urine output, and ABGs as needed.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) DILUTION -
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    B) EMESIS/NOT RECOMMENDED -
    1) Do not induce vomiting.
    C) ACTIVATED CHARCOAL
    1) Activated charcoal is of no value, may induce vomiting and may obscure endoscopy findings. It is NOT recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) Emesis/NOT RECOMMENDED
    1) Do not induce vomiting.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is of no value.
    C) NASOGASTRIC SUCTION
    1) Consider insertion of a soft, flexible nasogastric tube for aspiration of gastric contents after large, recent ingestions (Penner, 1980). Potential benefit must be weighed against possibility of further injuring burned mucosa.
    D) DILUTION
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    6.5.3) TREATMENT
    A) CONTRAINDICATED TREATMENT
    1) Do NOT induce vomiting or give bicarbonate to neutralize. Addition of buffer to strong acid causes an exothermic reaction and an immediate rise in solution temperature (Maull et al, 1985).
    2) A report concerning emergency surgical resection of the alimentary tract following caustic ingestions has indicated that 5 out of 6 patients sustained injuries beyond the pylorus as a result of gastric lavage (Wu & Lai, 1993).
    B) DILUTION
    1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans.
    3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).
    C) LEUCOVORIN CALCIUM
    1) Moore et al (1994) described treatment of a case who had ingested 250 mL of a 44% solution of formic acid. Intravenously infused leucovorin (ie, folinic acid) was used to enhance hepatic degradation of formate and furosemide was administered to prevent the renal absorption of formate. Hemofiltration was also instituted. The patient survived.
    D) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    4) If hypotension is secondary to gastrointestinal bleeding, blood or blood products replacement therapy is the treatment of choice.
    E) METABOLIC ACIDOSIS
    1) Monitor ABGs in all patients following a significant oral exposure or large dermal exposure resulting in systemic effects.
    2) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    F) BURN
    1) SUMMARY - Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. Early (within 24 hours) endoscopy should be performed to assess the severity of injury and guide future management.
    G) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    H) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    I) SUCRALFATE
    1) Sucralfate may be useful in relieving symptomatology from acid induced injury. Efficacy in accelerating healing or preventing complications has not been proven.
    2) CASE REPORT: Administration of sucralfate, 1 gram dissolved in 30 mL of water, four times a day, was used in a 25-year-old man with moderately severe gastric injury after ingestion of hydrochloric acid. No other therapy was given other than antibiotic. Within 48 hours, improvement in symptoms was noted, enabling progression to a liquid diet on the 3rd day. Strictures were not prevented, although nearly complete gastric mucosal healing occurred after 2 weeks. The patient received a gastrojejunostomy for pyloric stricture 6 weeks postingestion (Mittal et al, 1989).
    J) DIETARY FINDING
    1) Depends on degree of damage as assessed by early endoscopy (Dilawari, 1984).
    1) mild (grade I): may have oral feedings first day
    2) moderate (grade II): may have liquids after 48 to 72 hours
    3) severe (grade III): jejunostomy tube feedings after 48 to 72 hours
    2) Observe for symptoms of gastric outlet obstruction, at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestions.
    K) FOLLOW-UP VISIT
    1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
    2) One 3-year-old child developed esophageal stricture 2 years after the acid ingestion in a prospective study of 41 patients. This child had a normal barium study at one year after ingestion (Zargar et al, 1989).
    L) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993a). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) OXYGEN
    1) With severe dyspnea or hypoxemia, administer humidified oxygen until symptoms subside.
    B) BURN
    1) Evaluate for nasopharyngeal burns. Patients with upper airway burns may develop edema abruptly; early intubation is advised.
    C) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    D) 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).
    E) 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).
    B) The pH of the conjunctival sac should be tested after irrigation and irrigation continued until it is no longer acidic.
    6.8.2) TREATMENT
    A) INJURY OF GLOBE OF EYE
    1) EVALUATION
    a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000).
    b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000; Singh et al, 2013):
    1) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
    2) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
    3) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
    4) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.
    c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):
    1) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
    2) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
    3) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
    4) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
    5) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
    6) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.
    2) MEDICAL FACILITY IRRIGATION
    a) Begin irrigation immediately with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available. Lactated Ringer's solution may also be effective. Once irrigation has begun, instill a drop of local anesthetic (eg, 0.5% proparacaine) for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Singh et al, 2013; Spector & Fernandez, 2008; Ernst et al, 1998; Grant & Schuman, 1993). In one study, isotonic saline, lactated Ringer's solution, normal saline with bicarbonate, and balanced saline plus (BSS Plus) were compared and no difference in normalization of pH were found; however, BSS Plus was better tolerated and more comfortable (Fish & Davidson, 2010).
    1) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000a). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
    2) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993).
    3) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).
    3) MINOR INJURY
    a) SUMMARY
    1) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) TOPICAL CYCLOPLEGIC
    1) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000b; Grant & Schuman, 1993). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    d) TOPICAL ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008).
    e) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    4) SEVERE INJURY
    a) SUMMARY
    1) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.
    b) ARTIFICIAL TEARS
    1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    c) PAIN CONTROL
    1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).
    d) CARBONIC ANHYDRASE INHIBITOR
    1) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    e) TOPICAL STEROIDS
    1) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993a).
    2) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
    3) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    f) ASCORBATE
    1) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
    3) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993a). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    g) CITRATE
    1) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
    2) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
    3) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993a). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000a).
    a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000a).
    h) COLLAGENASE INHIBITORS
    1) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
    2) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
    3) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).
    i) ANTIBIOTICS
    1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).
    j) TOPICAL CYCLOPLEGIC
    1) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).
    k) SOFT CONTACT LENSES
    1) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.
    5) SURGICAL THERAPY
    a) SURGICAL THERAPY CAUSTIC EYE INJURY
    1) Early insertion of methylmethacrylate ring or suturing saran wrap over palpebral and cul-de-sac conjunctiva may prevent fibrinosis adhesions and reduce fibrotic contracture of conjunctiva, but the advantage of such treatments is not clear.
    2) Limbal stem cell transplantation has been used successfully in both the acute stage of injury and the chronically scarred healing phase in patients with persistent epithelial defects after chemical burns (Azuara-Blanco et al, 1999; Morgan & Murray, 1996; Ronk et al, 1994).
    3) In some patients, amniotic membrane transplantation (AMT) has been successful in improving corneal healing and visual acuity in patients with persistent epithelial defects after chemical burns. It can restore the conjunctival surface and decrease limbal stromal inflammation (Fish & Davidson, 2010; Sridhar et al, 2000; Su & Lin, 2000; Meller et al, 2000; Azuara-Blanco et al, 1999).
    4) Control glaucoma. Remove any cataracts formed (Fish & Davidson, 2010; Tuft & Shortt, 2009).
    5) In patients with severe injury, tenonplasty can be performed to promote epithelialization and prevent melting (Tuft & Shortt, 2009).
    6) A keratoprosthesis placement has also been indicated in severe cases (Fish & Davidson, 2010). Penetrating keratoplasty is usually delayed as long as possible as results appear to be better with a greater lag time between injury and keratoplasty (Grant & Schuman, 1993).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN INJURY
    1) Once irrigation is completed standard burn therapy should be instituted including tetanus prophylaxis, dressings and careful follow up to observe for complications and infection.
    2) GRAFTS - Skin grafts are often required for severe burns (Sigurdsson et al, 1983).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) A 3-year-old girl developed severe metabolic acidosis (arterial pH 6.85, serum bicarbonate 6 mEq/L) after dermal exposure to 90% formic acid which resulted in 35% body surface area second and third degree burns (Chan et al, 1995). She was treated with 2.5 hours of hemodialysis with resolution of her acidosis. Pre-dialysis serum formate level was 400 mcg/mL. Post-dialysis it had fallen to 50 mcg/mL.
    B) HEMOFILTRATION
    1) Moore et al (1994) describe treatment of a case who had ingested 250 mL of a 44% solution of formic acid. Intravenously infused folinic acid was used to enhance hepatic degradation of formate and furosemide was administered to prevent the renal absorption of formate. Hemofiltration was also instituted. The patient survived.

Range Of Toxicity

Summary

    A) Ingestions of less than 10 grams in children have resulted in oropharyngeal burns; no deaths were reported.
    B) Solutions of 10% or less are generally considered noncorrosive.
    C) Ingestions between 5 and 30 grams resulted in symptomatic burns of the gastrointestinal tract and hematemesis, but no deaths. Ingestions between 45 to 200 grams resulted in 87% of patients dying within the first 36 hours post ingestion.
    D) An adult survived an ingestion of 110 grams of formic acid.
    E) INHALATION - Textile workers complained of nausea from formic acid vapor concentrations around 15 ppm.

Minimum Lethal Exposure

    A) INGESTION
    1) The lowest published lethal dose of formic acid for a woman via ingestion is 2,440 mcg/kg (RTECS , 2000).
    2) Accidental or intentional overdoses (50 grams or more) are reported to produce salivation, vomiting (which may be bloody), a burning sensation in the mouth and pharynx, diarrhea, and severe pain. Circulatory collapse may follow, causing death (Clayton & Clayton, 1994).
    3) CASE REPORT - A 56-year-old male died of cardiac arrest and multiple organ system failure 10 days after ingesting an unknown amount of a descaling agent which contained 55% formic acid, 1.6% phosphoric acid, and 4% quinoline (Jacques, 1982).
    4) CASE REPORT - A 27-year-old male died approximately 26 hours after intentional ingestion of a decalcifying agent. The patient developed immediate vomiting and was transported to a hospital. Signs and symptoms of massive acidosis, excessive hemolysis, bleeding complications and eventually hepatic and renal failure occurred. It was estimated that the patient had ingested at least 30 to 60 grams (44 to 88 mL) of a solution containing 60% formic acid (Westphal et al, 2001).
    5) CASE SERIES - Jefferys & Wiseman (1980) found that in a review of 45 patients who had ingested formic acid, painful deaths occurred in 14 of 16 patients who ingested between 45 to 200 grams of formic acid. The majority died from corrosive perforation of the abdominal viscera within the first 36 hours of exposure (Jefferys & Wiseman, 1980).
    6) CASE SERIES - Three fatalities were reported following ingestion of household descaling agents which contained between 40% to 55% formic acid. One patient died of refractory hypotension, and postmortem exam revealed extensive erosion of the esophagus, stomach, and duodenum following a 50 to 100 mL ingestion of a kitchen descaling agent containing 55% formic acid (Naik et al, 1980).
    B) DERMAL
    1) CASE REPORT - A worker who had suffered splashes of hot formic acid to his face developed marked dyspnea with difficulty in swallowing and inability to speak; death occurred 6 hours later (ACGIH, 1991).

Maximum Tolerated Exposure

    A) INGESTION
    1) CASE REPORT - A 36-year-old female ingested 110 grams of formic acid and developed acute renal failure, requiring intensive supportive care. Recovery was complete with the exception of intermittent dilation needed for persistent esophageal stricture (Moore et al, 1994).
    2) CASE SERIES - In retrospective review of 45 cases of formic acid poisoning, 34 were found to be deliberate ingestions. Of those cases, 23 ingested between 5 and 30 grams of formic acid, and no deaths occurred. Serious toxicity was reported following ingestions between 30 to 45 grams (Jefferys & Wiseman, 1980).
    B) INHALATION
    1) The lowest published toxic concentration of formic acid for a man via inhalation is 7,300 mcg/m(3)/8 hours (RTECS , 1995).
    2) Workers exposed to a mixture of formic and acetic acids at an average concentration of 15 ppm each complained of nausea (Hathaway et al, 1991).
    C) OCULAR
    1) CASE REPORT - transient opacification of the anterior half of the cornea was reported in a 30-year-old male following a one drop splash of concentrated formic acid in the eye (Sudarsky, 1965).
    D) ANIMAL DATA
    1) In studies of rats repeatedly exposed to oral doses (up to 360 mg/kg) of formic acid in drinking water, no adverse effects were reported with the exception of weight loss and decreased appetite. Likewise, Swiss mice exposed to formic acid (8% solution in water) painted on the ears did not develop any adverse effects (Clayton & Clayton, 1994).

Workplace Standards

    A) ACGIH TLV Values for CAS64-18-6 (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) Formic acid
    a) TLV:
    1) TLV-TWA: 5 ppm
    2) TLV-STEL: 10 ppm
    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): URT, eye, and skin irr
    d) Molecular Weight: 46.02
    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 CAS64-18-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Formic acid
    2) REL:
    a) TWA: 5 ppm (9 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 30 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS64-18-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Formic acid
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Formic acid
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Formic acid
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS64-18-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Formic acid
    2) Table Z-1 for Formic acid:
    a) 8-hour TWA:
    1) ppm: 5
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 9
    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: Clayton & Clayton, 1982 RTECS, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 940 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 700 mg/kg
    3) LD50- (ORAL)RAT:
    a) 1100 mg/kg
    4) TCLo- (INHALATION)HUMAN:
    a) 7300 mcg/m(3) for 8H

Pharmacology Toxicology

Toxicologic Mechanism

    A) Formic acid is both an irritant and a corrosive. Once absorbed it can also cause severe metabolic acidosis along with subsequent respiratory acidosis (Malizia et al, 1977). Reports of hemolysis are probably a direct effect of formic acid on the red blood cell (Jefferys & Wiseman, 1980). The toxic effects, unrelated to direct cutaneous or mucosal injury, are due to its inhibitory action on aerobic glycolysis, with consequent diminution of ATP synthesis.

Physicochemical

Physical Characteristics

    A) Formic acid is a colorless, fuming liquid with a pungent, penetrating odor, and sour taste (Lewis, 1996; Budavari, 1996; HSDB , 2000).

Ph

    A) In an aqeous solution (pKa= 3.76, compared with 4.76 for acetic acid) (HSDB , 2000).

Molecular Weight

    A) 46.03 (Budavari, 1996)

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