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TANNIC ACID

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Tannic acid is a tannin obtained from nutgall and species of oak, sumac and myrobalam. Tannins are widely distributed in the plant kingdom (Osol & Farrar, 1955; Peaslee & Einhellig, 1973).
    B) Tannic acid/tannins are complex compounds which are not uniform. They are divided into 2 groups, one which includes derivatives of flavonols (condensed tannins) and the other including hydrolyzable tannins which are esters of a sugar with one or more trihydroxybenzene- carboxylic acids (Budavari, 1996).

Specific Substances

    1) Acide gallotannique (French)
    2) Acide tannique (French)
    3) Acido galotanico (Spanish)
    4) Acido tanico (Spanish)
    5) Acido tannico (Italian)
    6) Acidum Gallotannicum
    7) Acidum Tannicum
    8) Digallic acid (Incorrectly)
    9) Gallotannic acid
    10) Gallusgerosaure (German)
    11) Gerbsaure (German)
    12) Glycerite
    13) Tanin officinal (French)
    14) Tannin
    15) Tannino (Italian)
    16) CAS 1401-55-4
    17) ACID, TANNIC
    18) D'ACIDE TANNIQUE (FRENCH)
    19) GALLOTANNIN

Available Forms Sources

    A) SOURCES
    1) Tannic acid is available medicinally as 5% tannic acid in a jelly base (Amertan - Lilly). Also known as Tannin, gallotannin and gallotannic acid, it is included in Universal Antidote, a preparation which should NOT be used. Acorns & beech nuts containing tannic acid may be dangerous when eaten in large quantities.
    2) Martinek & Wolman (1955) investigated the average amount of tannins in coffee, tea and cocoa. A summary of their data is below.
    ProductAverage % tannins
    Regular coffee1.0-1.1
    Instant coffee4.1-4.3
    Regular decaffeinated coffee1.2
    Instant decaffeinated coffee3.8-6.7
    Bulk tea10.5-11.8
    Tea bags9.1-13.1
    Instant tea14.7
    Bulk cocoa2.5-4

    3) ACORNS
    a) Contain various polyhydroxyphenolic compounds known as tannins. The primary chemicals involved are tannic acid, gallic acid, and pyrogallol (Sandusky et al, 1977; Dollahite et al, 1962).
    b) Concentration of total phenolics found in Arkansas plants of the following species (Basden & Dalvi, 1987):
     %Range
    Quercus alba1.090.41 to 2.54
    Quercus rubera4.103.72 to 4.47
    Quercus velutina4.513.29 to 6.13

    B) USES
    1) Tannic acid is used as a mordant in dyeing, as a coagulant in rubber manufacture, and as a boiler feedwater additive; used in manufacturing gallic acid, pyrogallol, and ink; used for sizing paper and silk and printing fabrics; used in tanning and photography; used to treat wastewater; used to clarify beer and wine (Budavari, 1996; HSDB , 2000).
    2) Suppositories have been used in the treatment of hemorrhoids (JEF Reynolds , 2000). Tannic acid was formerly used locally for sore throat and stomatitis and to harden nipples during nursing (Osol & Hoover, 1975). It was also formerly used in the treatment of extensive burns, orally as a antidiarrheal agent, and as an additive to barium sulfate enemas to improved radiological imaging of the colon (JEF Reynolds , 2000; HSDB , 2000).
    3) It has historically been used internally as an astringent, hemostatic, and heavy metal antidote in veterinary medicine (Budavari, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Acute ingestion of tannic acid may result in nausea, vomiting, abdominal pain, and hepatic necrosis if large amounts are absorbed. The minimal toxic or lethal dose is not well established in the literature. Severity of intoxication should be based on clinical findings.
    0.2.6) RESPIRATORY
    A) Respiratory failure has been reported with rapid demise of rats following large doses of tannic acid.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting, and abdominal pain may be develop if large amounts (greater than 1 gram) are ingested. Constipation may also occur.
    0.2.9) HEPATIC
    A) Hepatotoxicity may be noted following absorption of large amounts from the gastrointestinal tract. This is unlikely under normal circumstances.
    0.2.10) GENITOURINARY
    A) Nephritis due to gallic acid has been reported in rats given large doses of tannic acid.
    0.2.21) CARCINOGENICITY
    A) Except for epidemiologic evidences, there are no conclusive data available in humans and there is limited evidence of carcinogenicity in animals.

Laboratory Monitoring

    A) Plasma tannic acid levels are not clinically useful.
    B) Monitor liver function tests in symptomatic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) Monitor liver function tests in symptomatic patients.
    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) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The minimal toxic or lethal dose following acute ingestion in humans is unknown. Severity of intoxication should be based on clinical and laboratory findings. Hepatic necrosis is the most severe manifestation of tannic acid poisoning.
    B) Fatalities have been reported secondary to hepatic necrosis following the use of tannic acid in barium enemas and when applied to large surface burns.

Clinical Effects

Summary Of Exposure

    A) Acute ingestion of tannic acid may result in nausea, vomiting, abdominal pain, and hepatic necrosis if large amounts are absorbed. The minimal toxic or lethal dose is not well established in the literature. Severity of intoxication should be based on clinical findings.

Heent

    3.4.3) EYES
    A) CONJUNCTIVITIS - A 10% solution applied to intact conjunctiva caused a mild reaction; however, prolonged application produced discoloration (Grant & Schuman, 1993).
    B) Tannic acid's damage is virtually the same at pH 1.5 to 9 (Frienderwald et al, 1944). Grant & Schuman (1993) reported that several studies have suggested the possible use of tannic acid in emergent treatment of the eye contaminated with dyes, with no severe untoward effects.

Respiratory

    3.6.1) SUMMARY
    A) Respiratory failure has been reported with rapid demise of rats following large doses of tannic acid.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) RESPIRATORY FAILURE is the cause of rapid demise in rats given tannic acid at doses more than 2.3 g/kg (Gosselin et al, 1984).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) Coma was reported in the terminal phase of patients poisoned with tannic acid-containing enemas. Patients were thought to be in hepatic failure (McAlister et al, 1963).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting, and abdominal pain may be develop if large amounts (greater than 1 gram) are ingested. Constipation may also occur.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) If large amounts (greater than 1 g) are ingested, gastric irritation, nausea and vomiting may result (JEF Reynolds , 1990). These symptoms also occurred after administration of enemas containing tannic acid (Lucke et al, 1963).
    B) GASTROENTERITIS
    1) The ingestion of large doses can produce gastroenteritis with abdominal pain (Arena & Drew, 1986).
    C) CONSTIPATION
    1) Tannic acid also has a constipating effect which may lead to fecal impaction (Gilman et al, 1980).
    D) TANNIC ACID POISONING
    1) RECTAL ABSORPTION
    a) ENEMAS - Fatalities have resulted from using tannic acid enemas (Eshchar & Friedman, 1974; McAlister et al, 1963).

Hepatic

    3.9.1) SUMMARY
    A) Hepatotoxicity may be noted following absorption of large amounts from the gastrointestinal tract. This is unlikely under normal circumstances.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) SUMMARY - Tannic acid was formerly used as an application to burns and added to barium sulfate enemas to improve radiological imaging of the colon; these uses were sometimes associated with liver damage and fatalities in some cases (JEF Reynolds , 2000).
    2) The acute hepatotoxic effects usually present within 72 hours of exposure (Lucke et al, 1963) Wells et al, 1942; (Barnes & Rossiter, 1943).
    3) DERMAL - Tannic acid is absorbed when applied to skin burns (Robinson & Graessle, 1943). Fatal liver damage may occur through this route (Wells et al, 1942; (JEF Reynolds , 2000).
    4) INJECTION - Subcutaneous injection of tannic acid causes central necrosis in the liver (Wells et al, 1942; (Lee & Rhodes, 1944; Clark & Rossiter, 1943).
    5) ORAL - If large amounts are absorbed from the gastrointestinal tract (unlikely under normal circumstances), tannic acid is capable of producing hepatotoxicity culminating in hepatic necrosis.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Tannic acid does not normally injure the liver when given orally to rats (Handler & Baker, 1944), but may cause damage when taken in large amounts.

Genitourinary

    3.10.1) SUMMARY
    A) Nephritis due to gallic acid has been reported in rats given large doses of tannic acid.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHRITIS
    a) Kidney damage may result due to the formation of gallic acid if large doses (>1 g) are administered orally (JEF Reynolds , 1990). Doses of 2,000 mg/kg of gallic acid produced renal damage in rats (Harris et al, 1966).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) Two adults developed exacerbation of eczema symptoms (increased inflammation) following application of a topical ointment containing tannin (van Ketel & Bruynzeel, 1991). Patch testing was positive in both cases. The authors concluded that tannin may act as a weak sensitizer in some individuals.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1401-55-4 (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: Tannic acid and tannins
    b) Carcinogen Rating: 3
    1) The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    3.21.2) SUMMARY/HUMAN
    A) Except for epidemiologic evidences, there are no conclusive data available in humans and there is limited evidence of carcinogenicity in animals.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) ESOPHAGEAL CANCER - Unusually high incidence of esophageal cancer have been noted in certain areas of Transkei, South Africa where there is consumption of high-tannin sorghum (Mardon, 1970).
    3.21.4) ANIMAL STUDIES
    A) HEPATIC CARCINOMA
    1) Tannic acid has been shown to be a hepatocarcinogen in animals (Korpassy, 1959; Hirono, 1981; Rashid et al, 1985).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma tannic acid levels are not clinically useful.
    B) Monitor liver function tests in symptomatic patients.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Baseline hepatic function test should be obtained.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Plasma tannic acid levels are not clinically useful.
    B) Monitor liver function tests in symptomatic patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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) 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) SUPPORT
    1) Evaluate for toxic effects to mucous membranes caused by the astringent action, although very unlikely.
    B) MONITORING OF PATIENT
    1) Baseline hepatic function studies should be obtained following a significant overdose. Keep in mind that hepatic necrosis is the usual mechanism of death in humans suffering from large overdoses.

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) IRRITATION SYMPTOM
    1) Many chemicals cause irritation of the eyes, skin, and respiratory tract. In severe cases respiratory tract irritation can progress to ARDS/acute lung injury, which may be delayed in onset for up to 24 to 72 hours in some cases.
    2) Irritation or burns of the esophagus or gastrointestinal tract are also possible if caustic or irritant chemicals are ingested.
    B) MONITORING OF PATIENT
    1) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    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) The minimal toxic or lethal dose following acute ingestion in humans is unknown. Severity of intoxication should be based on clinical and laboratory findings. Hepatic necrosis is the most severe manifestation of tannic acid poisoning.
    B) Fatalities have been reported secondary to hepatic necrosis following the use of tannic acid in barium enemas and when applied to large surface burns.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) Human dosage recommended for the treatment of diarrhea has been 0.2 to 1.3 gram/day and apparently was tolerated with no significant effects (Osol & Farrar, 1955).
    2) When used locally, irrigation solutions ranged from 1 to 20 percent (Osol & Farrar, 1955).

Minimum Lethal Exposure

    A) ROUTE OF EXPOSURE
    1) SUMMARY - Tannic acid was formerly used in the treatment of large burns and added to barium sulfate enemas (to improve radiological imaging) (JEF Reynolds , 2000).
    2) Tannic acid has also been included in barium enemas in concentrations of 0.25 to 3 percent; however, there have been human deaths (5 children, 3 adults) reported from its therapeutic use in barium enemas. Death was due to hepatic necrosis (Arena, 1974).
    3) This procedure (tannic acid in barium enema) is NOT recommended and absolutely should not be used in children or adults with hepatic disease.
    B) ACUTE
    1) ESTIMATED ACUTE LETHAL DOSE - For humans is 0.5 to 5 grams/kilogram (Arena & Drew, 1986).
    C) ANIMAL DATA
    1) LDLo (ORAL) RAT - 200 mg/kg (Lewis, 1996)
    2) LDLo (Subcutaneous) RAT - 200 mg/kg (RTECS, 2000)
    3) LDLo (PARENTERAL) RAT - 1400 mg/kg (RTECS, 2000)
    4) LDLo (ORAL) MOUSE - 2,000 mg/kg (RTECS, 2000)
    5) LDLo (Subcutaneous) MOUSE - 75 mg/kg (RTECS, 2000)
    6) LDLo (IV) MOUSE - 10 mg/kg (RTECS, 2000)
    7) LDLo (IV) GUINEA PIG - 40 mg/kg (RTECS, 2000)

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Humans may ingest up to 1 gram/day in foods and drinks (Gosselin et al, 1984).
    2) Very little is known about the concentration or orally administered amount of tannic acid needed to cause liver cell death (Janower et al, 1965).
    B) ANIMAL DATA
    1) Dogs who were given toxic doses of tannic acid developed liver toxicity with levels of 14.2 milligrams percent tannic acid (Lucke et al, 1963).

Workplace Standards

    A) ACGIH TLV Values for CAS1401-55-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS1401-55-4 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS1401-55-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Tannic acid and tannins
    a) 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    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 CAS1401-55-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAMUSCULAR)MOUSE:
    1) 350 mg/kg (RTECS, 2000)
    B) LD50- (INTRAPERITONEAL)MOUSE:
    1) 120 mg/kg (RTECS, 2000)
    C) LD50- (ORAL)RAT:
    1) 2260 mg/kg (RTECS, 2000)

Pharmacology Toxicology

Toxicologic Mechanism

    A) Tannic acid is an astringent which acts locally by precipitating proteins. Usually only the surface of the cell is affected, consequently, the membrane permeability of the cell is greatly reduced but the cell itself remains viable (Osol & Farrar, 1955; Budavari, 1996).
    B) Tannic acid has little effect (except for possible discoloration) on the intact skin; however, it coagulates protein and precipitates abraded skin and at one time found wide application in the treatment of burns (Osol & Farrar, 1955; Budavari, 1996).
    C) Tannic acid exerts an astringent action on the mucous membranes of the gastrointestinal tract, but it is erratically absorbed (Gosselin et al, 1984; Gilman et al, 1985; HSDB , 2000).
    D) Tannic acid also forms insoluble precipitates with many heavy metal ions, alkaloids and glycosides (Sollmann, 1957).
    E) Tannic acid has been classified among the cytotoxic agents that interfere with essential metabolic pathways thus causing necrosis and/or cholestatic injury (Ellenhorn & Barceloux, 1988).
    F) The hepatocarcinogenicity of tannic acid has been attributed to its capacity to disaggregate polyribosomes and degranulate microsomal membranes in vivo and in vitro (Gupta & Dani, 1987; Reddy et al, 1970).
    G) As a local antidote (in the form of strong tea) in the management of poisoning, it is of limited or no value since tannic acid does not precipitate the alkaloids cocaine, nicotine, physostigmine, atropine and morphine; nor does it complex the heavy metals arsenic, antimony or mercury (Osol & Farrar, 1955; Sollmann, 1957).
    H) MEDICINAL USES - Tannic acid has been shown to have anti-ulcerogenic and anti-secretory effects (Herz & Kaplan, 1968; Duncan et al, 1970; Radcliffe et al, 1971; Kimura et al, 1983). It has also been shown to inhibit enzyme gastric H+,K+ ATPase (Murakami et al, 1992).

Physicochemical

Physical Characteristics

    A) An amorphous, yellowish-white to brown powder or flakes with faint characteristic odor and astringent taste (Budavari, 1996; HSDB , 2000).
    B) Tannic acid of commerce usually contains about 10% water (Budavari, 1996).

Molecular Weight

    A) 1500-2000 (Gosselin et al, 1984)
    B) 1701.28 (RTECS , 2000)

Other

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

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Marzo et al (1990) found that the addition of 25 to 30 grams tannic acid/kg diet impaired the immune function of growing chickens. Total IgM and IgG levels were depressed, and lymphoid organ weights were decreased compared with controls.
    1) The growth of the tannic-acid fed birds was also significantly decreased when compared with controls. It is uncertain whether immune system impairment was a direct effect of tannic acid or of poor body condition.
    11.1.2) BOVINE/CATTLE
    A) Cows died following ingestion of 50 grams tannic acid for 16 days (Clarke & Clarke, 1975).
    B) No toxic symptoms were observed in cows given 25 grams tannic acid daily for 28 days (Clarke & Clarke, 1975).
    C) OAK LEAF POISONING - There was a 70% mortality rate in cattle who ate immature Quercus incana leaves. Symptoms included anorexia, constipation, and brisket edema. Feces were hard and covered with blood and mucous. BUN and creatinine levels were increased. There was extensive kidney and liver toxicity seen (Garg et al, 1992).
    1) Oak leaf poisoning in the United States is primarily due to Quercus havardii, Quercus breviloba, and Quercus gambelii. There are 6 different Quercus species in China which have been shown to be toxic (Shi et al, 1989) and 4 in the Northwest Himalayan region (Makkar et al, 1986).
    11.1.5) EQUINE/HORSE
    A) Horses given 50 to 300 grams of tannic acid per stomach tube had colic, jaundice, hemolytic anemia, gastric mucosal necrosis, heart muscle degeneration, nephritis, and hepatic changes (Clarke & Clarke, 1975).
    11.1.12) RODENT
    A) RAT -
    1) No tumors were noted in 11 surviving white rats painted daily with fresh 5% aqueous solution of tannic acid (IARC, 1985).
    2) No liver damage was observed in rats fed with 60 mg tannic acid/kg body weight for 152 days (IARC, 1985).
    3) Hepatic centrilobular necrosis was reported with a single subcutaneous dose of 250 mg tannic acid/kg body weight (IARC, 1985).
    4) Tannic acid plant extracts injected subcutaneously weekly for 12 weeks caused local sarcomas in 2 of 10 rats after 1 year (IARC, 1975).
    5) Of 28 rats which received subcutaneous tannic acid every 5th day for 290 days, 5 had hepatomas and 6 had cholangiomas (IARC, 1985).
    6) Death by respiratory failure occurred rapidly in rats given high-dose tannic acid (Gosselin et al, 1984).
    B) MOUSE -
    1) No tumors were found in young mice injected with 0.75 mg tannic acid/kg body weight for 12 months (IARC, 1985).
    2) A year after weekly subcutaneous injection of tannic acid for 12 weeks, local sarcomas and liver tumors were noted in stock mice (IARC, 1985).
    3) Depressed growth and increased pituitary activity were observed in mice given 5 to 10% tannic acid in diet (Peaslee & Einhellig, 1973).
    11.1.13) OTHER
    A) OTHER
    1) CHICK -
    a) Growth rate depression were observed in chicks fed with 0.5% tannic acid (Clarke & Clarke, 1975).
    b) A 70% mortality rate was reported in chicks fed with 5% tannic acid (Clarke & Clarke, 1975).
    2) RABBIT -
    a) Corneal injury was incurred following application of tannic acid to rabbit eyes (Grant, 1986).
    b) Hemorrhagic gastritis was observed in rabbits fed with tannic acid (Clarke & Clarke, 1975).

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