National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• 2-Amino-4,6-dinitrophenol
• PHENOL, 2-AMINO-4,6-DINITRO- (8CI)(9CI)

Human Toxicity Excerpts

• TOXIC SYMPTOMS /OF 2-AMINO-4,6-DINITROPHENOL ARE/ SIMILAR TO 2,4-DINITROPHENOL ...PRODUCES MARKED INCR IN METABOLISM & TEMPERATURE, PROFUSE SWEATING, COLLAPSE, DEATH. MAY CAUSE DERMATITIS, CATARACTS, WT LOSS, GRANULOCYTOPENIA, POLYNEUROPATHY, EXFOLIATIVE DERMATITIS. /2,4-DINITROPHENOL/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976., p. 964]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: 1. MARKED FATIGUE, TREMENDOUS THIRST, PROFUSE SWEATING, FLUSHING OF FACE. 2. NAUSEA, VOMITING, ABDOMINAL PAIN, & OCCASIONALLY DIARRHEA. 3. RESTLESSNESS, ANXIETY, EXCITEMENT, OCCASIONALLY LEADING TO CONVULSIONS. /DINITROPHENOL/ [Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. III-135]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: 4. RISE IN BODY TEMP...ROUGHLY PROPORTIONAL TO TOXIC DOSE, MAY CULMINATE IN SEVERE HYPERPYREXIA... 5. TACHYCARDIA, HYPERPNEA, DYSPNEA, CYANOSIS, &...MUSCLE CRAMPS. 6. LOSS OF CONSCIOUSNESS, CESSATION OF BREATHING, & DEATH. /DINITROPHENOL/ [Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. III-135]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: 7. LATE COMPLICATIONS: A. DECR URINE OUTPUT WITH ALBUMINURIA, CASTS, PIGMENTS, SOMETIMES BLOOD CELLS, DUE TO TOXIC NEPHRITIS. B. JAUNDICE & TENDERNESS IN LIVER REGION DUE TO TOXIC HEPATITIS. /DINITROPHENOL/ [Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. III-135]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: 8. OCCASIONAL HYPERSENSITIVITY REACTIONS AFTER REPEATED EXPOSURES (OR IN CHRONIC POISONING) INCLUDE AGRANULOCYTIC ANGINA, SKIN RASHES, PERIPHERAL NEURITIS, & LATE CATARACT FORMATION. /DINITROPHENOL/ [Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. III-135]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• OTHER COMPD WHICH HAVE BEEN FOUND TO PRODUCE ACUTE TRANSIENT TYPE OF CATARACT IN DUCKLINGS OR CHICKENS ARE 2,4-DINITRO-6-AMINOPHENOL ... . [Grant, W. M. Toxicology of the Eye. 2nd ed. Springfield, Illinois: Charles C. Thomas, 1974., p. 414]**PEER REVIEWED**
  
• 5-53 MG/KG OF PICRAMIC ACID INTRAVENOUSLY INCREASED BILE FLOW MODERATELY WITHOUT AFFECTING TEMPERATURE OF DOGS. FOR THIS TYPE OF EFFECT ON BILE SECRETION, IT IS NECESSARY TO HAVE NITRO GROUPS IN POSITIONS 2 & 4 OF BENZENE RING & FREE OR POTENTIAL HYDROXYL GROUP. [PUGH PM, STONE SL; J PHYSIOL (LONDON) 198(1) 39 (1968)]**PEER REVIEWED**
  
• PICRAMIC ACID (1 MUG/PLATE) INDUCED BOTH BASE PAIR SUBSTITUTION & FRAME SHIFT-TYPE MUTATIONS IN HISTIDINE-REQUIRING STRAINS OF SALMONELLA TYPHIMURIUM WITHOUT ACTIVATION BY RAT LIVER PREPARATION. [WYMAN ET AL; APPL ENVIRON MICROBIOL 37(2) 222 (1979)]**PEER REVIEWED**
  
• PICRAMIC ACID WAS MUTAGENIC IN SALMONELLA TYPHIMURIUM TA98 STRAIN IN THE PRESENCE OF S9 MIXTURE. [YOSHIKAWA K, UCHINO H, KURATA H; EISEI SHIKENSHO HOKOKU 94: 28 (1976)]**PEER REVIEWED**
  
• Juvenile rainbow trout (S. gairdneri) and American oyster spat (C. virginica) were exposed to sublethal concentrations of picric acid (2,4,6-trinitrophenol) and picramic acid (2-amino-4,6-dinitrophenol) for 42 days. No significant inhibition of growth was observed for rainbow trout exposed to 0.45 and 0.05 mg/l picric acid or 0.23 and 0.02 mg/l picramic acid; trout exposed to both compounds developed petechial hemorrhages along the abdomen with > 80% possessing lesions by the end of 42 days. American oysters exposed to 0.45 and 0.05 mg/l picric acid, and 0.24 and 0.02 mg/l picramic acid showed significant inhibition of shell deposition during the 42 days of exposure. Discoloration of the nacre layer of the shell and body mass was observed in oysters exposed to both compounds by the end of the 42 days. Concentrations < 0.001 of the 96 hr LC50 for rainbow trout and 144 hr LC50 of oysters continuously exposed to picric or picramic acids cause sublethal effects. The consequences of the hemorrhages to rainbow trout were not clear; the inhibition of growth in American oysters could have had a significant impact on an oyster fishery because of delays in reaching marketable size. [Goodfellow W L JR et al; Chemosphere 12 (9-10): 1259-68 (1983)]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• None found

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Absorption, Distribution and Excretion

• The bioconcentration of metabolism of picric acid and picramic acid were determined for rainbow trout. The bioconcentration factor (BCF) in the epaxial muscle at 42 days for both of these compounds was < 1; the skin had a bioconcentration factor value of 1 and 9, respectively. The half-life elimination for the high and low dose of picric acid was 12.0 and 12.5 days, respectively; and for picramic acid was 9.0 and 9.5 days, respectively. In separate experiments, (14C)picric acid was metabolized to picramic acid, glucuronide conjugates and an unidentified group of compounds, and 42% of the (14C)picric acid was metabolized to picric acid, glucuronide conjugates and an unidentified group of compounds. The low bioconcentration in the trout muscle may be due to the trout's ability to excrete the parent compound and metabolites. The higher radioactivity observed on the skin may be due to the water route of exposure and the binding of the parent compounds to protein. [Cooper KR et al; J Toxicol Environ Health 14 (5-6): 731-48 (1984)]**PEER REVIEWED**
  

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Metabolism/Metabolites

• A STRAIN OF P AERUGINOSA REDUCED 2,4,6-TRINITROPHENOL (PICRIC ACID) TO PICRAMIC ACID UNDER ANAEROBIC CONDITIONS. [WYMAN ET AL; APPL ENVIRON MICROBIOL 37 (2): 222 (1979)]**PEER REVIEWED**
  
• Picric acid (2,4,6-trinitrophenol) is widely used ... The acute toxicity, distribution, and metabolism of picric acid were investigated using Fischer 344 rats. The LD50 for picric acid following oral dosing of male and female rats was established as 290 and 200 mg/kg, respectively. Blood gas analysis indicated severe acidosis during acute intoxication. Metabolism of picric acid was limited to reduction of nitro groups to amines. Metabolites isolated from urine included N-acetylisopicramic acid (14.8%), picramic acid (18.5%), N-acetylpicramic acid (4.7%), and unidentified components (2.4%). Approximately 60% of the parent picric acid was excreted unchanged. ... [Wyman JF et al; J Toxicol Environ Health 37 (2): 313-27 (1992)]**PEER REVIEWED**
  

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TSCA Test Submissions

• None found

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.