TOXICOLOGICAL PROFILE FOR
PICRIC ACID
Criteria and Standards Division
Office of Drinking Water
U.S. Environmental Protection Agency
Washington, DC 20460
June, 1989
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TOXICOLOGICAL PROFILE
FOR
PICRIC ACID
June 1989
Criteria and Standards Division
Office of Drinking Water
U.S. Environmental Protection Agency
Washington, DC 20460
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PICRIC ACID
A. GENERAL
1. CAS Number; 88-89-1
2. RTECS Number; TJ7877000
3. General Name/Svnonvms: Ammonium pi crate
Carbazotic acid
Picronitric acid
2,4,6-Trinitrophenol
4. Molecular Formula; C6H3N307
5. Molecular Weight; 229.11
6. Structure:
B. PHYSICAL AND CHEMICAL PROPERTIES
1. State: Pale yellow, odorless, intensely
bitter crystals
Windholz et al. (1983)
2. Vapor Pressure: <1 mmHg at 20°C
NIOSH/OSHA (1978)
3. Melting Point: 122-123°C
Windholz et al. (1983)
4. Boiling Point: Explodes above 300°C
Windholz et al. (1983)
5. Specific Gravity; 1.763
Windholz et al. (1983)
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6. Solubility: 1 g dissolves in 78 ml water; Windholz et al. (1983)
15 ml boiling water, 12 ml
alcohol 10 ml benzene; 35 ml
chloroform; and 65 ml ether
7. Loq_KoW: No information was found.
8. UV Absorption: No information was found.
C. PHYSICAL/CHEMICAL EQUILIBRIUM FACTORS
1. Bioconcentration Factors (BCF): For the American oysters (Crassostrea
viroinica). the 42-day BCF was 65.5 for exposure to 0.45 mg/L picric
acid and 16.5 for exposure to 0.05 mg/L picric acid (Burton et al.,
1983). Cooper et al. (1984) found that the BCF was less than 1 in the
epaxial muscle of rainbow trout (Salmo aairdneri) exposed to picric
acid for 42-days in a continuous-flow system.
2. Kwa: No information was found.
3. KOC: No information was found.
D. ENVIRONMENTAL FATE
1. Photolysis: No information was found.
2. Leaching: No information was found.
3. Route of Water Contamination: No information was found.
4. Hydrolysis: No information was found.
5. Plant Uptake: No information was found.
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6. Microbial Degradation; In vitro studies showed that the concentration
of picric acid was reduced by 22% (from 240 to 187 ^g/mL) during 30
days of incubation with Pseudomonas aeruginosa (Wyman et al., 1979).
Approximately 2% was converted to picramic acid; the remaining 20%
loss of picric acid was attributed to adsorption onto bacterial
surfaces, uptake and accumulation by bacteria, and the formation of
unidentified degradation products. In contrast, picric acid (as a
0.1% aqueous solution) was not degraded when incubated for 3 months
under aerobic or anaerobic conditions with mixed cultures obtained
from soil, compost, activated sewage sludge, and estuarine sediment
(Wyman et al., 1979).
7. Persistence in Soil/Water: No information was found.
8. Byproducts: No information was found.
9. Vaporization: No information was found. A
E. ACUTE TOXICITY IN MAMMALS
No information was found.
F. SKIN AND EYE IRRITATION AND SENSITIZATION IN MAMMALS
No information was found.
G. SUBCHRONIC TOXICITY IN MAMMALS
No information was found.
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H. REPRODUCTION AND TERATOGENICITY IN MAMMALS
No information was found.
I. MUTAGENICITY/GENOTOXICITY
Data are presented in tabular form on page 6.
J. CHRONIC TOXICITY/CARCINOGENICITY STUDIES IN MAMMALS
Data are presented in tabular form on page 6.
K. PHARMACOKINETICS IN MAMMALS
No information was found.
L. HUMAN HEALTH EFFECTS
Gleason et al. (1969) rated picric acid as an extremely toxic compound
with a probable oral lethal dose of 5 to 50 mg/kg in humans. Ingestion of 1
to 2 g causes severe poisoning accompanied by headache, progressive stupor,
coma, and death. Other effects may include severe gastroenteritis,
intravascular hemolysis, hemorrhagic nephritis, and occasionally hepatitis.
Arena and Drew (1986) reported that the local irritant properties of
picric acid can cause severe conjunctivitis, palpebral edema, keratitis, and
yellow vision. Contact with skin may cause intense pruritic dermatitis with
vesicles and weeping lesions. Ingestion can cause acute gastroenteritis with
severe abdominal pain, nausea, vomiting, and diarrhea; the vomitus is yellow.
The target organ of toxicity is the kidney, and the renal involvement may in
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part be due to the hemolytic action of picric acid on red blood corpuscles;
acute nephritis is not uncommon when kidneys are affected. In severe acute
poisoning, nervous system symptoms are prominent and consist of headache,
progressive depression, and finally coma and death.
M. EXISTING STANDARDS/CRITERIA
Type Standards/Criteria Proponent Reference
TLV-TWA*
STEL"
PELe
IDLH"
0.1 mg/m3
0.3 mg/m3 (skin)
0.1 mg/m3
100 mg/m3
ACGIH
ACGIH
OSHA
NIOSH/OSHA
ACGIH (1986)
ACGIH (1988)
CFR (1988)
NIOSH/OSHA (1978)
•Threshold Limit Value-Time Weighted Average.
"Short-Term Exposure Limit.
Permissible Exposure Limit.
"Immediately Dangerous to Life or Health.
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I. MUTAGENICITY/GENOTOXICITY
I
CTs
I
Test
Ames
(reverse mutation)
Ames
Sex- 1 inked
recessive
lethal nutations
and reciprocal
trans location
Strain Activation Dose/concentration
Salmonella + S9 10 jig/plate
typhimurium (rat liver)
TA98, TA100
Salmonella None 10 /tL/plate
tvphimuriura
TA 98, TA 100
Orosophila NA Injected: 400 ppm
melanogaster Feeding: 450 ppn
Toxic effects
Positive only
with activation
Negative
Positive for sex- 1 inked
recessive lethal
mutations; negative for
reciprocal translocation
Reference
Uyman et al. (1979)
Chiu et al. (1978)
Woodruff et al. (1985)
J. CHRONIC/CARCINOGENICITY STUDIES IN MAMMALS
Animal/strain/sex
Route
Dose
Duration
Effects
Reference
Rat/Uistar/M,F
Oral
(dietary)
500 ppm
Up to 2.5 years
None
Van Esch et al. (1957,
as cited in PHS, 1969)
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N. REFERENCES
ACGIH. 1986. American Conference of Governmental Industrial Hygienists.
Documentation of the Threshold Limit Values and Biological Exposure Indices.
Cincinnati, OH: ACGIH, p. 490.
Arena JM, Drew RH. 1986. Poisoning. Toxicology, Symptoms and Treatments.
5th ed. Springfield, IL: Charles C. Thomas Publisher, p. 617-618.
Burton DT, Goodfellow WL, Cooper KR. 1983. Bioconcentration, Elimination and
Metabolism of Picric and Picramic Acid in Freshwater Fish and Estuarine
Bivalves. Final report. Fort Detrick, Frederick, MD: U.S. Army Medical
Research and Development Command, Available from DTIC, Alexandria, VA. AD
A129212.
CFR. Code of Federal Regulations. 1910.1000, table 2.1 1988.
Chiu CW, Lee LH, Wang CY, Bryan GT. 1978. Mutagenicity of some commercially
available nitro compounds for Salmonella tvphimurium. Mutat. Res. 58:11-22.
Cooper KR, Burton DT, Goodfellow WL, Rosenblatt DH. 1984. Bioconcentration
and metabolism of picric acid (2,4,6-trinitrophenol) and picramic acid (2-
amino-4,6-dinitrophenol) in rainbow trout Sal mo oairdneri. J. Toxicol.
Environ. Health. 14:731-747.
Gleason MN, Gosselin RE, Hodge HC, Smith RP. 1969. Clinical Toxicology of
Commercial Products. Acute Poisoning. 3rd Ed. Baltimore, MD: William &
Wilkins Co., pp. 1-2, 11-114.
NIOSH/OSHA. 1978. National Institute for Occupational Safety and
Health/Occupational Safety and Health Administration. Pocket Guide to
Chemical Hazards. Washington, DC: U.S. Department of Health and Human
Services, Public Health Service, Centers for Disease Control/U.S. Department
of Labor. September.
Van Esch et al. 1957. Cited in survey of compounds tested for carcinogenic
activity. U.S. Public Health Service. 1969. Suppl.2. p. 169.
Windholz M, Budavasri S, Blumetti RF, Otterbein ES. Eds. 1983. The Merck
Index -- An Encyclopedia of Chemicals, Drugs, and Biologicals. 10th Ed.
Rahway, NJ: Merck & Co. Inc., p. 1068.
Woodruff RC, Mason JM, Valencia R, Zimmering S. 1985. Chemical mutagenesis
testing in Drosophila. V. Results of 53 coded compounds tested for the
National Toxicology Program. Environ. Mutagen. 7:677-702.
Wyman JF, Guard HE, Won WD, Quay JH. 1979. Conversion of 2,4,6-
trinitrophenol to a mutagen by Pseudomonas aeruqinosa. Appl. Environ.
Microbiol. 37:222-226.
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