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PARA-AMINOBENZOIC ACID (PABA)

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) PABA and its compounds are used primarily in sunscreening products. PABA has also been used as treatment for various rickettsial diseases. PABA esters are also used for sunscreens, but are less effective. Examples of these are:
    1) Glyceryl PABA (Escalol 102)
    2) Amyldimethyl PABA (Escalol 506)
    3) Octyldimethyl PABA (Escalol 507)

Specific Substances

    A) PARA-AMINOBENZOIC ACID
    1) 1-Amino-4-carboxy benzene
    2) 4-aminobenzoic acid
    3) 4-carboxyaniline
    4) Acidum paraminobenzoicum
    5) Anti-canitic vitamin
    6) Anti-chromotrichia factor
    7) Anti-grayhair factor
    8) Bacterial vitamin H1
    9) Molecular Formula: C7-H7-N-O2
    10) Chromotrichia factor
    11) gamma-aminobenzoic acid
    12) NIOSH/RTECS DG 1400000
    13) PAB
    14) PABA
    15) p-aminobenzoic acid
    16) p-carboxyphenylamine
    17) Trichochromogenic factor
    18) Vitamin Bx
    19) Vitamin H
    20) CAS 150-13-0
    GLYCERYL-p-AMINO BENZOATE
    1) Molecular Formula: C10-H13-N-O4
    2) Glycerol-1-p-aminobenzoate
    3) Glyceryl aminobenzoate
    4) Glyceryl PABA
    5) Monoglycerol-p-aminobenzoate
    6) NIOSH/RTECS TZ 9900000
    7) p-Aminobenzoic acid monoglyceryl ester
    8) CAS 136-44-7
    AMYL-p-DIMETHYLAMINOBENZOATE
    1) Amyl dimethyl PABA
    2) NIOSH/RTECS DG 8958000
    3) CAS 14779-78-3
    4) Molecular Formula: C14-H21-N-O2
    AMYL DIMETHYL-p-AMINOBENZOIC ACID
    1) p-dimethylaminobenzoic acid, pentyl ester
    2) p-dimethylaminobenzoic acid, octyl ester
    3) Octyl-dimethyl-p-aminobenzoic acid
    4) NIOSH/RTECS DG 8957000
    5) CAS 58817-05-3
    6) Molecular Formula: C17-H27-N-O2
    OCTYL DIMETHYL PARAAMINOBENZOIC ACID
    1) Octyl Dimethyl PABA
    2) Padimate O
    3) 2-Ethylhexyl 4(dimethylamino)benzoate
    4) Molecular Formula: C17-H27-N-O2
    5) CAS 21245-02-3
    POTASSIUM PARA-AMINOBENZOATE
    1) Potassium p-aminobenzoate
    2) p-Aminobenzoic acid potassium salt
    3) Potaba
    4) CAS 138-84-1
    5) Molecular Formula: C7-H6-K-N-O2
    GENERAL TERMS
    1) PABACIDUM
    2) ANTI-GRAY HAIR FACTOR
    3) AMBEN

Available Forms Sources

    A) USES
    1) SUNSCREEN PRODUCTS: PABA and its esters are common ingredients in sunblocking or sunscreening products. The percentages range from 1 to 5%.
    2) PABA has been used in the treatment of Peyronie's disease (Borum et al, 1991).
    3) The aminoalkyl esters of PABA are local anesthetics such as benzocaine and butesin (Sandmeyer & Kirwin, 1981).
    4) PABA may be bought as vitamin Bx in some health food stores.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Para-aminobenzoic acid (PABA) and its esters are ingredients in sunscreens (refer to "Sunscreens" document for more information). PABA is available in some health food stores, but it is not considered an essential nutrient. PABA has also been used in the treatment of Peyronie's disease and various rickettsial diseases. The aminoalkyl esters of PABA are local anesthetics such as benzocaine and butesin.
    B) PHARMACOLOGY: PABA is absorbed cutaneously and diffuses into the horny layer, which then acts as a sunscreen reservoir. PABA absorbs ultraviolet B light from 290 to 320 nm when used as a 0.1 mg/mL solution in ethanol and up to 360 nm when the concentration is increased to 50 mg/mL (5%). PABA may accumulate with continued use and protect even after bathing, swimming or sweating.
    C) EPIDEMIOLOGY: Use in sunscreens was once common, but it is rarely used now.
    D) WITH POISONING/EXPOSURE
    1) Human overdose data with PABA or its esters are rare. Most toxicology data derives from animal studies or chronic, large dose therapeutic use. Allergic, eczematous dermatitis with superimposed photo allergic reaction to PABA has been reported. Since some PABA sunscreens contain 50% or more ethanol, ethanol toxicity may be the greater risk for those products. Nausea, vomiting, abdominal cramps, metallic taste, hypoglycemia, glycosuria, and nephritis have been reported with ingestion. Hepatitis and jaundice may be noted, and have occurred with PABA doses of 3 to 20 g/day. Leukopenia has been reported with doses of 48 g/day. Drug fever has been observed with doses ranging from 4 to 12 g/day for 8 to 28 days.

Laboratory Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Toxic serum levels have not been established, but levels in excess of 60 mg/dL have been associated with significant side effects.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Monitor CBC with differential and liver enzymes in symptomatic patients.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF TOXICITY
    1) Treatment is symptomatic and supportive. Maintain adequate hydration if vomiting or diarrhea becomes extensive. Refer to "Sunscreens" document for further information.
    B) DECONTAMINATION
    1) PREHOSPITAL: INGESTION: Gastrointestinal decontamination is generally unnecessary.
    2) HOSPITAL: Gastrointestinal decontamination is generally unnecessary. Consider activated charcoal only if coingestants with significant toxicity are involved.
    C) ANTIDOTE
    1) None.
    D) ENHANCED ELIMINATION
    1) Hemodialysis, hemoperfusion, and peritoneal dialysis are not necessary in these cases.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with deliberate/self harm ingestions should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    F) PITFALLS
    1) Missing an ingestion of another chemical or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    G) DIFFERENTIAL DIAGNOSIS
    1) Other chemicals or drugs that cause gastrointestinal distress.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Ingestion of more than 10 g/day for days has been necessary to induce effects other than local gastrointestinal irritation. Hepatitis and jaundice have occurred with PABA doses of 3 to 20 g/day. Leukopenia has been reported with doses of 48 g/day. Drug fever has been observed with doses ranging from 4 to 12 g/day for 8 to 28 days. Sunscreens usually contain approximately 5% PABA or its derivatives. Ingestion of 100 mL would only result in a 5 g exposure. When used as an antirickettsial, PABA was dosed at 1 to 2 grams every 3 to 4 hours. PABA has a short half-life of elimination, and dosing was done every 3 to 4 hours to maintain significant blood levels. Therapeutic blood concentrations were 30 to 60 mg/dL, and levels greater than this were associated with significant side effects.

Clinical Effects

Summary Of Exposure

    A) USES: Para-aminobenzoic acid (PABA) and its esters are ingredients in sunscreens (refer to "Sunscreens" document for more information). PABA is available in some health food stores, but it is not considered an essential nutrient. PABA has also been used in the treatment of Peyronie's disease and various rickettsial diseases. The aminoalkyl esters of PABA are local anesthetics such as benzocaine and butesin.
    B) PHARMACOLOGY: PABA is absorbed cutaneously and diffuses into the horny layer, which then acts as a sunscreen reservoir. PABA absorbs ultraviolet B light from 290 to 320 nm when used as a 0.1 mg/mL solution in ethanol and up to 360 nm when the concentration is increased to 50 mg/mL (5%). PABA may accumulate with continued use and protect even after bathing, swimming or sweating.
    C) EPIDEMIOLOGY: Use in sunscreens was once common, but it is rarely used now.
    D) WITH POISONING/EXPOSURE
    1) Human overdose data with PABA or its esters are rare. Most toxicology data derives from animal studies or chronic, large dose therapeutic use. Allergic, eczematous dermatitis with superimposed photo allergic reaction to PABA has been reported. Since some PABA sunscreens contain 50% or more ethanol, ethanol toxicity may be the greater risk for those products. Nausea, vomiting, abdominal cramps, metallic taste, hypoglycemia, glycosuria, and nephritis have been reported with ingestion. Hepatitis and jaundice may be noted, and have occurred with PABA doses of 3 to 20 g/day. Leukopenia has been reported with doses of 48 g/day. Drug fever has been observed with doses ranging from 4 to 12 g/day for 8 to 28 days.

Vital Signs

    3.3.3) TEMPERATURE
    A) FEVER: Drug fever has been reported with therapeutic use of doses ranging from 4 to 12 g/day for 8 to 28 days (Borum et al, 1991; Yeomans et al, 1944). There appears to be some allergic component to these reactions since it is possible to desensitize patients (Zarafonetis et al, 1948).

Heent

    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) METALLIC TASTE is often reported with ingestion (Sones & Israel, 1961).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HEART FAILURE
    1) Cardiac failure has not been a consistently reported symptom with overdose or therapeutic use. However, in a human fatality and in animal experiments, cardiac failure and fatty changes of the myocardium have been noted (Cruickshank & Mitchell, 1951).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea, vomiting, and abdominal cramps often occur with oral therapy and should be expected in significant oral overdose (Zarafonetis & Horrax, 1959).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) GASTROENTERITIS
    a) Gastroenteritis and hemorrhage of the small intestine has been reported in experimental animal overdoses (Scott & Robins, 1942).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) TOXIC HEPATITIS
    1) SUMMARY: Jaundice, fatty liver changes, and hepatitis have been noted in several cases of therapeutically administered PABA in doses of 3 to 20 g/day. The reactions were thought to be of the hypersensitivity type (Davies & Cavanagh, 1967).
    2) CASE REPORT: A 4-year-old given 1 g every 3 hours developed toxic hepatitis 14 days after treatment was initiated. This fatal reaction may have been an idiosyncratic drug reaction (Zarafonetis et al, 1948).
    3) Fatty changes of the liver in a human case and animal experiments have been reported (Cruickshank & Mitchell, 1951).
    4) Acute hepatic reactions to potassium para-aminobenzoate are uncommon (Zarafonetis et al, 1986), but do occur (Kantor & Ratz, 1985).
    5) CASE REPORT: A 51-year-old man taking PABA 3 grams 4 times/day for 4 weeks developed myalgias, weakness, fever, increased hepatic enzyme levels (peak Alk Phos 270 U/L; ALT 4275 U/L; AST 2341 U/L; Bili 5.5 mg/dL; GGT 202 U/L). Liver enzymes continued to rise while the patient was taking PABA. All symptoms resolved when PABA was discontinued and liver enzymes normalized within 10 days (Borum et al, 1991).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATIC NECROSIS
    a) Acute necrosis of the liver has been reported in fatally poisoned dogs (Scott & Robins, 1942).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) WITH POISONING/EXPOSURE
    a) Data on PABA's kidney toxicity is inconsistent. Several reports (Tierney, 1946; Zarafonetis et al, 1948) do not report renal changes. Others report fatty infiltrates in the kidney in both a human fatality and animal experiments (Cruickshank & Mitchell, 1951).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOPENIA
    1) Oral doses of 48 g/day resulted in reductions of white blood cells to under 4000 in 30% of the patients where it was used (Yeomans et al, 1944; Tierney, 1946).
    B) METHEMOGLOBINEMIA
    1) Methemoglobinemia has been seen as a rare side effect in both animals and man (Spicer, 1949).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) PHOTOSENSITIVITY
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Although generally rare with PABA and its derivatives, it is most often reported with glyceryl PABA (Algra & Knox, 1978).
    b) CROSS REACTIONS in patients with allergic contact dermatitis to glyceryl PABA does not occur with other PABA esters, but may with PABA, benzocaine, paraphenylenediamine, aniline, and sulfa drugs (Algra & Knox, 1978).
    c) Octyl dimethyl para-aminobenzoate and amyl dimethyl para-aminobenzoate were reported as frequent sunscreen allergens in one clinic (English et al, 1987).
    d) Allergic, eczematous dermatitis with superimposed photo allergic reaction to PABA has been reported (Fisher, 1988).
    B) DRY SKIN
    1) WITH POISONING/EXPOSURE
    a) Stinging and dryness are common dermatologic effects with PABA solutions, most likely due to the ethanol content (Roelandts et al, 1983).
    C) ITCHING OF SKIN
    1) WITH POISONING/EXPOSURE
    a) Pruritus may occur only a few minutes after ingestion, even with therapeutic oral doses of approximately 2 g (Zarafonetis et al, 1948).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) PABA has been shown to decrease blood sugar in rats, and this effect has also been shown in humans taking therapeutic doses (Altrom, 1957; Seltzer, 1979; Zarafonetis & Horrax, 1959).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) DRUG-INDUCED LUPUS ERYTHEMATOSUS
    1) CASE REPORT: Systemic lupus erythematosus was seen in a patient receiving 48 g/day for 6 days, and another receiving 8 g/day for 7 months (Worobec & LaChine, 1984).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Toxic serum levels have not been established, but levels in excess of 60 mg/dL have been associated with significant side effects.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Monitor CBC with differential and liver enzymes in symptomatic patients.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Therapeutic blood concentrations are 30 to 60 mg/dL. Amounts in excess of this were associated with significant side effects when the drug was taken chronically (Cruickshank & Mitchell, 1951; Tierney, 1946).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, and electrolyte abnormalities.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with deliberate/self harm ingestions should be referred to a healthcare facility.

Monitoring

    A) No specific laboratory tests are necessary unless otherwise clinically indicated.
    B) Toxic serum levels have not been established, but levels in excess of 60 mg/dL have been associated with significant side effects.
    C) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    D) Monitor CBC with differential and liver enzymes in symptomatic patients.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) INGESTION: Gastrointestinal decontamination is generally unnecessary. Consider activated charcoal only if coingestants with significant toxicity are involved.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Gastrointestinal decontamination is generally unnecessary. Consider activated charcoal only if coingestants with significant toxicity are involved.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF TOXICITY
    a) Treatment is symptomatic and supportive. Maintain adequate hydration if vomiting or diarrhea becomes extensive. Refer to "Sunscreens" document for further information.
    B) MONITORING OF PATIENT
    1) No specific laboratory tests are necessary unless otherwise clinically indicated.
    2) Toxic serum levels have not been established, but levels in excess of 60 mg/dL have been associated with significant side effects.
    3) Monitor serum electrolytes in patients with significant vomiting and/or diarrhea.
    4) Monitor CBC with differential and liver enzymes in symptomatic patients.

Eye Exposure

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

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) TOXICITY: Ingestion of more than 10 g/day for days has been necessary to induce effects other than local gastrointestinal irritation. Hepatitis and jaundice have occurred with PABA doses of 3 to 20 g/day. Leukopenia has been reported with doses of 48 g/day. Drug fever has been observed with doses ranging from 4 to 12 g/day for 8 to 28 days. Sunscreens usually contain approximately 5% PABA or its derivatives. Ingestion of 100 mL would only result in a 5 g exposure. When used as an antirickettsial, PABA was dosed at 1 to 2 grams every 3 to 4 hours. PABA has a short half-life of elimination, and dosing was done every 3 to 4 hours to maintain significant blood levels. Therapeutic blood concentrations were 30 to 60 mg/dL, and levels greater than this were associated with significant side effects.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) When used as an anti-rickettsial, PABA has been dosed at 1 to 2 grams every 3 to 4 hours. PABA has a short half-life of elimination, and dosing must be done every 3 to 4 hours to maintain significant blood levels (Zarafonetis et al, 1948).

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) DOGS: One gram/kilogram or more was fatal for dogs. Liver necrosis was seen in dogs at 2 grams/kilogram (Scott & Robins, 1942). No acute exposure overdose data are available.
    2) RATS: An oral dose of 10,000 mg/kg in rats caused death in 90% of the juvenile animals and 45% of the adult animals (Robin et al, 1947).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) No adverse effects were reported following administration of a single 6.2 gram dose of sodium para-aminobenzoate in an adult (Tabor et al, 1951).
    2) Oral doses of 48 g/day resulted in reductions of white blood cells to under 4000 in 30% of the patients where it was used (Yeomans et al, 1944; Tierney, 1946).
    3) Jaundice, fatty liver changes, and hepatitis have been noted in several cases of therapeutically administered PABA in doses of 3 to 20 g/day. The reactions were thought to be of the hypersensitivity type (Davies & Cavanagh, 1967).
    4) Drug fever has been reported with doses ranging from 4 to 12 g/day for 8 to 28 days (Borum et al, 1991; Yeomans et al, 1944).
    5) When used as an anti-rickettsial, PABA was dosed at 1 to 2 grams every 3 to 4 hours. PABA has a short half-life of elimination, and dosing was done every 3 to 4 hours to maintain significant blood levels (Zarafonetis et al, 1948).
    6) Therapeutic blood concentrations are 30 to 60 mg/dL. Amounts in excess of this were associated with significant side effects when the drug was taken chronically (Cruickshank & Mitchell, 1951).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) Therapeutic blood concentrations are 30 to 60 milligrams/deciliter. Amounts in excess of 60 milligrams/deciliter has been associated with significant side effects when the drug has been taken chronically (Cruickshank & Mitchell, 1951).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (ORAL)MOUSE:
    a) 2850 mg/kg (RTECS , 2001)
    2) LD50- (ORAL)RAT:
    a) >6,000 mg/kg (RTECS , 2001)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) SUNSCREEN -
    1) PABA absorbs ultraviolet light from 290 to 320 nm when used as a 0.1 mg/mL solution in ethanol and up to 360 nm when the concentration is increased to 50 mg/ml (5%).
    2) PABA can penetrate the outer layer of the skin and with continued use, may accumulate and protect even after bathing, swimming or sweating (Algra & Knox, 1978).
    B) USE AS A VITAMIN - Although PABA is an essential vitamin in bacteria, necessary for the production of folic acid, humans cannot use PABA and must obtain pre-formed folic acid.

Physicochemical

Physical Characteristics

    A) PABA: White to yellow almost odorless crystals (JEF Reynolds , 1988)
    B) GLYCERYL PABA: Aromatic odor, semi-solid (Sax & Lewis, 1989)
    C) POTASSIUM AMINOBENZOATE: Crystalline power with taste of saline (JEF Reynolds , 1988)

Ph

    A) POTASSIUM AMINOBENZOATE (1% solution): 7 (JEF Reynolds , 1988)

Molecular Weight

    A) PABA: 137.13
    B) GLYCERYL PABA: 211.24 (Sax & Lewis, 1988)

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Algra RJ & Knox JM: Topical photoprotective agents. Int J Dermatol 1978; 17:628-634.
    3) Altrom I: Effect of para-aminobenzoic acid on the blood sugar level and the liver glycogen content of white rats. Acta Med Scand 1957; 157:327-331.
    4) Borum M, Nsien E, & Zimmerman H: Hepatotoxicity from paraaminobenzoic acid. Digestive Diseases Sci 1991; 36:1793.
    5) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    6) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    7) Cruickshank AH & Mitchell GW Jr: Myocardial, hepatic and renal damage resulting from para-aminobenzoic acid therapy. Bull John Hopkins Hosp 1951; 88:211-229.
    8) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    9) Davies DM & Cavanagh J: Jaundice from potassium p-aminobenzoate (letter). Lancet 1967; 1:896.
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