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Ochratoxin A

PubChem CID
442530
Structure
Ochratoxin A_small.png
Ochratoxin A_3D_Structure.png
Molecular Formula
Synonyms
  • OCHRATOXIN A
  • 303-47-9
  • Phenylalanine - ochratoxin A
  • Antibiotic 9663
  • 3R14S-Ochratoxin A
Molecular Weight
403.8 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-06-24
  • Modify:
    2025-01-18
Description
Ochratoxin A can cause cancer according to The National Toxicology Program.
Ochratoxin a is a white crystalline powder. (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
Ochratoxin A is a phenylalanine derivative resulting from the formal condensation of the amino group of L-phenylalanine with the carboxy group of (3R)-5-chloro-8-hydroxy-3-methyl-1-oxo-3,4-dihydro-1H-2-benzopyran-7-carboxylic acid (ochratoxin alpha). It is among the most widely occurring food-contaminating mycotoxins, produced by Aspergillus ochraceus, Aspergillus carbonarius and Penicillium verrucosum. It has a role as a calcium channel blocker, a mycotoxin, a nephrotoxin, a carcinogenic agent, a teratogenic agent, an Aspergillus metabolite and a Penicillium metabolite. It is a phenylalanine derivative, an organochlorine compound, a member of isochromanes, a monocarboxylic acid amide and a N-acyl-L-phenylalanine. It is functionally related to an ochratoxin alpha. It is a conjugate acid of an ochratoxin A(1-).

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Ochratoxin A.png

1.2 3D Conformer

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

(2S)-2-[[(3R)-5-chloro-8-hydroxy-3-methyl-1-oxo-3,4-dihydroisochromene-7-carbonyl]amino]-3-phenylpropanoic acid
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=1S/C20H18ClNO6/c1-10-7-12-14(21)9-13(17(23)16(12)20(27)28-10)18(24)22-15(19(25)26)8-11-5-3-2-4-6-11/h2-6,9-10,15,23H,7-8H2,1H3,(H,22,24)(H,25,26)/t10-,15+/m1/s1
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

RWQKHEORZBHNRI-BMIGLBTASA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

C[C@@H]1CC2=C(C=C(C(=C2C(=O)O1)O)C(=O)N[C@@H](CC3=CC=CC=C3)C(=O)O)Cl
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C20H18ClNO6
Computed by PubChem 2.2 (PubChem release 2021.10.14)

2.3 Other Identifiers

2.3.1 CAS

303-47-9

2.3.2 European Community (EC) Number

2.3.3 UNII

2.3.4 UN Number

2.3.5 ChEBI ID

2.3.6 ChEMBL ID

2.3.7 DSSTox Substance ID

2.3.8 HMDB ID

2.3.9 KEGG ID

2.3.10 Metabolomics Workbench ID

2.3.11 NCI Thesaurus Code

2.3.12 Nikkaji Number

2.3.13 Wikidata

2.3.14 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

ochratoxin A

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
403.8 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3
Property Value
4.7
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
3
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Acceptor Count
Property Value
6
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Rotatable Bond Count
Property Value
5
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
403.0822650 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
403.0822650 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
113 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
28
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
608
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
2
Reference
Computed by PubChem
Property Name
Undefined Atom Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Undefined Bond Stereocenter Count
Property Value
0
Reference
Computed by PubChem
Property Name
Covalently-Bonded Unit Count
Property Value
1
Reference
Computed by PubChem
Property Name
Compound Is Canonicalized
Property Value
Yes
Reference
Computed by PubChem (release 2021.10.14)

3.2 Experimental Properties

3.2.1 Physical Description

Ochratoxin a is a white crystalline powder. (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
Solid with a green fluorescence; [Merck Index] Faintly yellow powder; [MSDSonline]
Solid

3.2.2 Color / Form

Crystals from xylene ... exhibits green fluorescence
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1254

3.2.3 Melting Point

336 °F (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
169 °C ... Also frequently reported as 90 °C from benzene (one mole of benzene of crystallization)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1254
169 °C

3.2.4 Solubility

less than 1 mg/mL at 66 °F (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
As acid, moderately soluble in organic solvents (eg. chloroform, ethanol, methanol, xylene)
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56: 489 (1993)
The sodium salt is soluble in water.
DHHS/NIEHS; Seventh Annual Rpt on Carcinogens Summary p. 310 (1994)

3.2.5 LogP

log Kow = 4.74
Sangster J; LOGKOW Database. A databank of evaluated octanol-water partition coefficients (Log P). Available from, as of Jun 24, 2013: https://logkow.cisti.nrc.ca/logkow/search.html
4.74

3.2.6 Stability / Shelf Life

Relatively unstable to light & air; fading and degradation upon brief exposure of chromatograms to light, especially at high humidity.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10 192 (1976)
Ethanol solutions are stable for more than a year if kept in dark and cold
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10 192 (1976)
Fairly stable in cereal products; up to 35% survives autoclaving for up to 3 hr
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10 192 (1976)

3.2.7 Optical Rotation

Specific optical rotation: -118 deg at 25 °C/D (concn = 1.1 in chloroform)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1254

3.2.8 Decomposition

When heated to decomposition it emits very toxic fumes of /hydrogen chloride/ and /nitric oxides/.
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 830

3.2.9 Collision Cross Section

194 Ų [M-H]- [CCS Type: TW; Method: calibrated with polyalanine]

193.27 Ų [M-H]-

188.74 Ų [M+H]+

S61 | UJICCSLIB | Collision Cross Section (CCS) Library from UJI | DOI:10.5281/zenodo.3549476

3.2.10 Other Experimental Properties

Fluorescent in UV light, emitting green and blue fluorescence in acid and alkaline solution
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56: 489 (1993)
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10: 192 (1976)
Partially degraded under normal cooking conditions ... Solutions of ochratoxin A are completely degraded by treatment with an excess of sodium hypochlorite solution ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56: 490 (1993)

3.3 Chemical Classes

Biological Agents -> Mycotoxins

3.3.1 Drugs

Pharmaceuticals -> Antibiotics
S6 | ITNANTIBIOTIC | Antibiotic List from the ITN MSCA ANSWER | DOI:10.5281/zenodo.2621956

3.3.2 Endocrine Disruptors

Potential endocrine disrupting compound
S109 | PARCEDC | List of 7074 potential endocrine disrupting compounds (EDCs) by PARC T4.2 | DOI:10.5281/zenodo.10944198

4 Spectral Information

4.1 1D NMR Spectra

1D NMR Spectra

4.2 Mass Spectrometry

4.2.1 GC-MS

NIST Number
53242
Library
Main library
Total Peaks
42
m/z Top Peak
239
m/z 2nd Highest
255
m/z 3rd Highest
241
Thumbnail
Thumbnail

4.2.2 LC-MS

1 of 13
View All
Authors
Justin B. Renaud, Mark W. Sumarah, Agriculture and Agri-Food Canada
Instrument
Q-Exactive Orbitrap Thermo Scientific
Instrument Type
LC-ESI-ITFT
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
10(NCE)
Fragmentation Mode
HCD
Column Name
Agilent RRHD Eclipse 50 x 2 mm, 1.8 uM
Retention Time
3.6
Precursor m/z
404.089
Precursor Adduct
[M+H]+
Top 5 Peaks

358.0841 999

404.0895 898

239.0106 192

257.0211 180

386.079 146

Thumbnail
Thumbnail
License
CC BY-SA
Reference
Renaud, J. B.; Sumarah, M. W. Data Independent Acquisition-Digital Archiving Mass Spectrometry: Application to Single Kernel Mycotoxin Analysis of Fusarium Graminearum Infected Maize. Analytical and Bioanalytical Chemistry 2016, 408 (12), 3083-91. DOI:10.1007/s00216-016-9391-5
2 of 13
View All
Authors
Justin B. Renaud, Mark W. Sumarah, Agriculture and Agri-Food Canada
Instrument
Q-Exactive Orbitrap Thermo Scientific
Instrument Type
LC-ESI-ITFT
MS Level
MS2
Ionization Mode
POSITIVE
Ionization
ESI
Collision Energy
20(NCE)
Fragmentation Mode
HCD
Column Name
Agilent RRHD Eclipse 50 x 2 mm, 1.8 uM
Retention Time
3.6
Precursor m/z
404.089
Precursor Adduct
[M+H]+
Top 5 Peaks

358.0841 999

257.0211 773

239.0106 735

341.0575 325

120.0808 155

Thumbnail
Thumbnail
License
CC BY-SA
Reference
Renaud, J. B.; Sumarah, M. W. Data Independent Acquisition-Digital Archiving Mass Spectrometry: Application to Single Kernel Mycotoxin Analysis of Fusarium Graminearum Infected Maize. Analytical and Bioanalytical Chemistry 2016, 408 (12), 3083-91. DOI:10.1007/s00216-016-9391-5

4.3 UV Spectra

UV max absorption (ethanol): 215, 333 nm (epsilon = 34000, 2400) ... Also frequently reported (benzene) ... UV max absorption: 213, 332 nm (epsilon = 36800, 6400)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1254

4.4 Other Spectra

UV max absorption: 215 nm (epsilon = 910, 1%, 1 cm), 333 nm (epsilon = 150, 1%, 1 cm) at pH 4; UV max absorption (ethanol): 333 nm (epsilon = 150, 1%, 1 cm), 380 nm (epsilon = 189, 1%, 1 cm). Above pH 9; in ethanol, fluorescence emission max 465 nm
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10: 191 (1976)

6 Chemical Vendors

7 Food Additives and Ingredients

7.1 Food Additive Classes

JECFA Functional Classes
Food Contaminant -> MYCOTOXIN;

7.2 Associated Foods

7.3 Evaluations of the Joint FAO / WHO Expert Committee on Food Additives - JECFA

Chemical Name
OCHRATOXIN A
Evaluation Year
2007
Comments
At its 37th meeting, the Committee established a PTWI of 112 ng/kg bw, based on deterioration of renal function in pigs, for which the LOEL was 8 μg/kg bw/d, and application of a safety factor of 500. None of the new studies on nephrotoxicity, developmental toxicity, neurotoxicity, or immunotoxicity published since the Committee’s last evaluation would impact the Committee’s previous selection of minimal renal changes in the pig, observed at a dose of 8 μg/kg bw per day (the LOEL), as a critical effect for risk assessment. The Committee therefore retained the previous PTWI of 112 ng/kg bw. The current estimate of overall dietary exposure to ochratoxin A is about 8–17 ng/kg bw/week, which is well below the PTWI. Owing to the very small number of samples contaminated above the highest proposed limit of 20 μg/kg for cereals, such an ML would have very limited impact compared with no ML. The Committee concluded that the use of an ML of 5 or 20 μg/kg would be unlikely to have an impact on dietary exposure to ochratoxin A.

8 Pharmacology and Biochemistry

8.1 MeSH Pharmacological Classification

Carcinogens
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. (See all compounds classified as Carcinogens.)
Calcium Channel Blockers
A class of drugs that act by selective inhibition of calcium influx through cellular membranes. (See all compounds classified as Calcium Channel Blockers.)

8.2 Absorption, Distribution and Excretion

Since there are pathomorphological similarities between porcine mycotoxic nephropathy caused by ochratoxin A and Balkan endemic nephropathy (BEN), it has been suggested that the same aetiological agent has a role in BEN. Based on the results from several field and experimental studies carried out on pigs, an appropriate analytical method of monitoring possible human exposure to ochratoxin A was developed. The toxicokinetic properties of the toxin were species specific, although in all the animal species studied (with the exception of fish), as well as in humans, two binding proteins were found in the plasma. The monkey had the longest elimination half-life of the toxin, 510 hr, in contrast to the fish whose elimination half-life was only 0.68 hr. The fish kidney displayed a specific pattern of distribution. In the laying quail the most prominent observation was the accumulation of labelled ochratoxin A in egg yolk. Generally, (14C)ochratoxin A was eliminated rapidly from the quail body, but had a long retention time in the circulating blood in the mouse. Although the elimination of ochratoxin A from the body depending on its binding to plasma constituents, the existence of enterohepatic circulation might have been partially responsible for its prolonged retention and elimination from the body of mammals. The toxicokinetic profile of ochratoxin A did not contradict the mycotoxic hypothesis in the aetiology of BEN.
Fuchs R, Hult K; Food Chem Toxicol 30 (3): 201-4 (1992)
... Ochratoxin A is rapidly absorbed throughout the entire gastrointestinal tract and distributes itself in the body as a two compartment open model and has a particular high affinity for serum albumin. Ochratoxin A is hydrolyzed by the intestinal microflora into nontoxic compounds (7-carboxy-5-chloro-8-hydroxy-3,4-dihydro-3R-methylisocoumarin (Ochratoxin alpha) and phenylalanine). It is excreted as either ochratoxin A, hydroxylated ochratoxin A or Ochratoxin alpha in both the urine and feces. Ochratoxin A appears to exert its toxic effect by promoting an increased level of lipid peroxidation by inhibition of an amino acylation reaction and possibly by conversion into metabolites that are capable of binding DNA. These in turn cause other secondary effects associated with ochratoxin A. It would appear that this compound presents a true potential hazard for humans as its occurrence is wide spread and it is highly carcinogenic.
Marquardt RR et al; Can J Physiol Pharmacol 68 (7): 991-9 (1990)
Rats intubated daily with 500 ug ochratoxin A or fed 250 ug daily in barley. There was little accumulation of cmpd in liver or kidneys. Avg total amount excreted daily in urine & feces was just over 10% of administered dose. Small amount of hydrolysis product also excreted.
VAN WALBEEK W ET AL; TOXICOL APPL PHARMACOL 20 (3): 439 (1971)
Rats given single ip injection of 1 mg ochratoxin A labelled with (14)C. Reached highest levels in serum (90%), liver (4.5%), & kidney (4.4%) 30 min later. Ochratoxin A was excreted primarily in urine as unchanged toxin or metabolites. Excretion in feces less significant.
CHANG FC, CHU FS; FOOD COSMET TOXICOL 15 (3): 199 (1977)
For more Absorption, Distribution and Excretion (Complete) data for OCHRATOXIN A (24 total), please visit the HSDB record page.

8.3 Metabolism / Metabolites

... Ochratoxin A is hydrolyzed by the intestinal microflora into nontoxic compounds (7-carboxy-5-chloro-8-hydroxy-3,4-dihydro-3R-methylisocoumarin (Ochratoxin alpha) and phenylalanine). It is excreted as either ochratoxin A, hydroxylated ochratoxin A or Ochratoxin alpha in both the urine and feces. ...
Marquardt RR et al; Can J Physiol Pharmacol 68 (7): 991-9 (1990)
Hydroxyochratoxin A was isolated & identified from urine of rats after injection with ochratoxin A. By incubating ochratoxin A with rat liver microsomes & NADPH, 1 major (90%) & 2 minor metabolites, more polar than ochratoxin A, were formed.
STORMER FC, PEDERSEN JI; APPL ENVIRON MICROBIOL 39 (5): 971 (1980)
Single oral or iv dose (2.5 mg/kg) ochratoxin A admin to healthy adult rats. Ochratoxin alpha only metabolite recovered from cecum & large intestine. Ochratoxin A excreted via urine & feces, both as free drug & ochratoxin alpha. Unidentified metabolites in urine.
GALTIER P ET AL; DRUG METAB DISPOS 7 (6): 429 (1979)
Ochratoxin A is cleaved into phenylalanine and a less toxic iso-coumarin derivative (ochratoxin alpha) by the microbial flora of the colon ... and by carboxypeptidase A and alpha-chymotrypsin ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 198 (1983)
For more Metabolism/Metabolites (Complete) data for OCHRATOXIN A (9 total), please visit the HSDB record page.
Ochratoxin A is cleaved into phenylalanine and a less toxic iso-coumarin derivative (ochratoxin alpha) by the microbial flora of the colon, and by carboxypeptidase A and alpha-chymotrypsim. This is is the major metabolic pathway. 4-Hydroxyochratoxin A is the main hepatic metabolite and its formation appears to be via a polymorphic-like debrisoquine 4-hydroxylation. Some cytochrome P-450 enzymes, such as CYP2C9, and known to metabolize ochratoxin A into more cytotoxic compounds. (T35, A2870, A3099)
A2870: Galtier P: Pharmacokinetics of ochratoxin A in animals. IARC Sci Publ. 1991;(115):187-200. PMID:1820333
A3099: Simarro Doorten AY, Bull S, van der Doelen MA, Fink-Gremmels J: Metabolism-mediated cytotoxicity of ochratoxin A. Toxicol In Vitro. 2004 Jun;18(3):271-7. PMID:15046773
T35: IARC (1983). Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-Present. (Multivolume work).

8.4 Biological Half-Life

Pregnant ICR mice were administered a single ip injection of 5 mg/kg ochratoxin A (OA) on day 11 or 13 of gestation. The half-life of OA in serum was calculated to be 28.7 hr on day 11 and 23.6 hr on day 13 of gestation.
Fukui Y et al; Fd Chem Toxic 25: 17-24 (1987)
In rats ... the plasma half-life of ochratoxin A is about 60 hr ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 198 (1983)
The apparent plasma elimination half-time of ochratoxin A after oral administration at 50 ug/kg bw varied from 0.68 hr in fish to 120 hr in rats and 510 hr in monkeys ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 499 (1993)
The fate of ochratoxin A has been studied in laboratory rodents and in breeding animals. In rats, orally administered ochratoxin A is readily absorbed, and considerable amounts of the toxin are detected in plasma, where maximal concentrations occur 2-4 hr after administration. Pharmacokinetic analysis of curves of plasma level versus time suggests its distribution in two distinct body compartments. The half-time of the toxin depends on both the dose and the animal species, varying from 0.7 hr in fish to 840 h in monkeys. In plasma, the toxin is bound to albumin, like many acidic compounds. This interaction is competitively inhibited by phenylbutazone, ethylbiscoumacetate and sulfamethoxy-pyridazine and is decreased in albumin-deficient rats.
Galtier P; IARC Sci Publ (115): 187-200 (1991)
The toxicokinetic properties of the toxin were species specific, although in all the animal species studied (with the exception of fish), as well as in humans, two binding proteins were found in the plasma. The monkey had the longest elimination half-life of the toxin, 510 hr, in contrast to the fish whose elimination half-life was only 0.68 hr. The fish kidney displayed a specific pattern of distribution. In the laying quail, the most prominent observation was the accumulation of labelled ochratoxin A in egg yolk. Generally, (14)C-ochratoxin A was eliminated rapidly from the quail body, but had a long retention time in the circulating blood in the mouse. Although the elimination of ochratoxin A from the body depending on its binding to plasma constituents, the existence of enterohepatic circulation might have been partially responsible for its prolonged retention and elimination from the body of mammals. The toxicokinetic profile of ochratoxin A did not contradict the mycotoxic hypothesis in the etiology of BEN.
Fuchs R, Hult K; Food Chem Toxicol 30 (3): 201-4 (1992)

8.5 Mechanism of Action

Ochratoxin A (OTA) is a widespread mycotoxin contaminating feed and food. Besides its potent nephrotoxicity, OTA also affects the immune system. /Investigators/ demonstrate here a role for Bcl-x(L) in OTA-induced apoptosis in human lymphocytes. In particular, human peripheral blood lymphocytes and the human lymphoid T cell line, Kit 225 cells, underwent apoptosis in a time- and dose-dependent manner. This apoptosis was inhibited by z-VAD.fmk, suggesting that caspases were responsible for the induction of apoptosis. Moreover, OTA triggered mitochondrial transmembrane potential (Deltachim) loss and caspase-9 and caspase-3 activation. Interestingly, Bcl-x(L) protein expression was decreased by OTA treatment, whereas Bcl-2 protein level was not affected. Down-regulation of bcl-x(L) mRNA was not observed in cells treated with OTA. Overexpression of Bcl-x(L) in Kit 225 cells protected them against mitochondrial perturbation and retarded the appearance of apoptotic cells. Taken together, /the/ data indicate that mitochondria are a central component in OTA-induced apoptosis and that the loss of Bcl-x(L) may participate in OTA-induced cell death.
Assaf H et al; Toxicol Sci 79 (2): 335-44 (2004)
Kidney samples of male Fischer 344 (F-344) rats fed a carcinogenic dose of OTA over 7 days, 21 days and 12 months were analyzed for various cell signaling proteins known to be potentially involved in chemical carcinogenicity. OTA was found to increase the phosphorylation of atypical-PKC. This was correlated with a selective downstream activation of the MAP-kinase extracellular regulated kinases isoforms 1 and 2 (ERK1/2) and of their substrates ELK1/2 and p90RSK. Moreover, analysis of effectors acting upstream of PKC indicated a possible mobilization of the insulin-like growth factor-1 receptor (lGFr) and phosphoinositide-dependent kinase-1 (PDK1) system. An increased histone deacetylase (HDAC) enzymatic activity associated with enhanced HDAC3 protein expression was also observed. These findings are potentially relevant with respect to the understanding of OTA nephrocarcinogenicity. HDAC-induced gene silencing has previously been shown to play a role in tumor development. Furthermore, PKC and the MEK-ERK MAP-kinase pathways are known to play important roles in cell proliferation, cell survival, anti-apoptotic activity and renal cancer development.
Marin-Kuan M et al; Toxicol Appl Pharmacol 224 (2):174-81 (2007)
Ochratoxin A (OTA) is a ubiquitous fungal metabolite with nephrotoxic, carcinogenic, and apoptotic potential. Although the toxic effects of OTA in various cell types are well characterized, it is not known whether OTA has an effect on stem cell differentiation. In this study, we demonstrate that OTA inhibits adipogenesis in human adipose tissue-derived mesenchymal stem cells, as indicated by decreased accumulation of intracellular lipid droplets. Further, OTA significantly reduces expression of adipocyte-specific markers, including peroxisome proliferator-activated receptor-gamma (PPAR-gamma), CCAAT enhancer binding protein-alpha (C/EBP-alpha), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein (aP2). At the molecular level, OTA phosphorylates PPAR-gamma2 through extracellular signal-related kinase activation and inhibits PPAR-gamma activity. /Investigators/ also found that treatment with the mitogen-activated protein kinase kinase inhibitor, PD98059, significantly blocked the OTA-induced inhibition of adipogenesis. /The/ results indicate that OTA suppresses adipogenesis in an extracellular signal-related kinase-dependent manner. Taken together, our results suggest a novel effect of OTA on adipocyte differentiation in human adipose tissue-derived mesenchymal stem cells and the possibility that OTA might affect the differentiation of other types of stem cells.
Lim S et al; Stem Cells Dev 20 (3): 415-26 (2011)
The mechanism of action (MOA) for OTA renal carcinogenicity is a controversial issue. In 2005, direct genotoxicity (covalent DNA adduct formation) was proposed as a MOA for OTA-mediated carcinogenicity. At that time, inconsistent results had been published on OTA genotoxicity/mutagenicity, and conclusive evidence for OTA-mediated DNA adduction had been lacking. In this update, published data from the past 6-7 years are presented that provide new hypotheses for the MOA of OTA-mediated carcinogenicity. While direct genotoxicity remains a controversial issue for OTA, new findings provide definitive results for the mutagenicity of OTA in the target tissue (outer medulla) of male rat kidney that rules out oxidative DNA damage. These findings, coupled with /the authors/ efforts /to/ provide new structural evidence for DNA adduction by OTA, has strengthened the argument for involvement of direct genotoxicity in OTA-mediated renal carcinogenesis. This MOA should be taken into consideration for OTA human risk assessment.
Pfohl-Leszkowicz A, Manderville RA; Chem Res Toxicol 25 (2): 252-62 (2012)
For more Mechanism of Action (Complete) data for OCHRATOXIN A (14 total), please visit the HSDB record page.

8.6 Human Metabolite Information

8.6.1 Cellular Locations

Membrane

9 Use and Manufacturing

9.1 Uses

Sources/Uses
Used as a research chemical; [HSDB] A toxic metabolite of Aspergillus ochraceus, Aspergillus sulphureus, Aspergillus melleus, and Penicillium viridicatum molds. Ochratoxins have been found as natural contaminants on corn, peanuts, storage grains, cottonseed, and other decaying vegetables; [Merck Index] Human exposure occurs primarily by ingestion of contaminated grain and pork products; [IARC] Produced by Penicillium verrucosum, a common contaminant of barley; [Reference #2]
Merck Index - O'Neil MJ, Heckelman PE, Dobbelaar PH, Roman KJ (eds). The Merck Index, An Encyclopedia of Chemicals, Drugs, and Biologicals, 15th Ed. Cambridge, UK: The Royal Society of Chemistry, 2013.
Experimentally as teratogen and carcinogen /Ochratoxins/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1166
Human exposure occurs mainly through consumption of improperly stored food products, particularly contaminated grain and pork products, as well as coffee, wine grapes and dried grapes. (L1939)
L1939: Wikipedia. Ochratoxin A. Last Updated 26 February 2010. http://en.wikipedia.org/wiki/Ochratoxin_A

9.1.1 Use Classification

Food Contaminant -> MYCOTOXIN; -> JECFA Functional Classes

9.2 Methods of Manufacturing

TOXIC METABOLITE FROM SPECIES OF ASPERGILLUS AND OTHER MOLDS
SRI
An efficient method for obtaining small amounts of ochratoxin A from fermented wheat has been reported ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31: 192 (1983)
Ochratoxin A is produced by inoculating strains of the fungi that produce this compound on autoclaved grains and oilseed.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56: 490 (1993)

9.3 U.S. Production

(1977) NOT PRODUCED COMMERCIALLY IN US
SRI
(1979) NOT PRODUCED COMMERCIALLY IN US
SRI

9.4 General Manufacturing Information

While ochratoxin A is not produced commercially, it is offered for sale in small quantities by one firm in Israel.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10: 191 (1976)
/Ochratoxin A is/ the major ochratoxin component /in Aspergillus sp./.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1166
Purity can be determined by visual exam of fluorescence on chromatograms under UV light; microgram quantities can be discerned under optimum conditions.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10: 192 (1976)
As these molds occur widely, some toxins have been found as natural contaminants on corn, peanuts, storage grains, cottonseed, and other decaying vegetation. /Ochratoxins/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 1166
In 1990, a WHO/FAO Joint Expert Committee on Food Additives reviewed the literature on ochratoxin A and recommended a provisional tolerable weekly intake of 112 ng/kg bw ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 494 (1993)

10 Identification

10.1 Analytic Laboratory Methods

A high pressure liquid chromatographic (HPLC) method has been developed for determining ochratoxin A ... in cereals. The sample is extracted with phosphoric acid and chloroform. The extract is cleaned by washing on a silica gel column with cyclohexane-ethylene dichloride-ethyl ether. ... Ochratoxin A is eluted with chloroform-formic acid. ... Ochratoxin A is purified by chromatography on aqueous sodium biarbonate-Celite. The ... /mycotoxin is/ determined by using a liquid chromatograph with 2 columns in series packed with Spherisorb ODS 10 micrometer and 5 micrometers, respectively. ... Detection limit ... /is/ 1-5 micrograms/kg for ochratoxin A.
Josefsson E, Moller T; J Assoc Off Anal Chem 62 (5): 1165 (1979)
Determination of ochratoxins in mixed feeds & other food products by thin layer chromatography.
GIMENO A; J ASSOC OFF ANAL CHEM 62 (3): 579 (1979)
Cereals: HPLC/UV (limit of detection 1-5 ug/kg); Cereals and coffee: TLC (12 ug/kg); Food and feedstuffs: HPLC/FL (5 ug/kg) or TLC (20 ug/kg); Feedstuffs: TLC (10 ug/kg) or HPLC/FL (1 ug/kg). /from table/
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 195 (1983)
Determination of ochratoxin A in pig's kidney using enzymic digestion, dialysis, and high-performance liquid chromatography with postcolumn derivatization.
Hunt DC et al; Analyst (London) 104 (1245): 1171 (1979)
For more Analytic Laboratory Methods (Complete) data for OCHRATOXIN A (14 total), please visit the HSDB record page.

10.2 Clinical Laboratory Methods

Methods ... have been reported for determining ochratoxins in blood, e.g., by fluorescence with HPLC confirmation. /Ochratoxins/
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 490 (1993)
This paper presents a simple method for the determination of ochratoxins A (OTA) and B (OTB) in pig blood serum. The method includes serum acidification (pH < 1.6) and precipitation of protein with 15% trichloroacetic acid, liquid partitioning with dichloromethane and fluorescence detection. The estimated detection limits were 0.1 ng OTA/mL and 0.2 ng OTB/mL. The mean recoveries from artificially contaminated samples (n = 6 replicates/mycotoxin) spiked at 0.3, 1 and 3 ng OTA and OTB/mL, respectively, were 86.8% (s.d. = 8.4) for OTA and 90.0% (s.d. = 9.8) for OTB. Forty-nine Romanian pig blood serum samples (94% of 52 analyzed) were found to be naturally contaminated with OTA in the range 0.1-13.4 ng/mL. No sample was found positive for OTB. The method is technically simple, specific, cost effective, suitable for large sample throughput and requires small amount of sample and reagents. It fulfills the criteria for a routine method and could be a suitable tool for surveying OTA in pig herds and in slaughtered pigs.
Curtui VG et al; Food Addit Contam 18 (7): 635-43 (2001)

11 Safety and Hazards

11.1 Hazards Identification

11.1.1 GHS Classification

Pictogram(s)
Acute Toxic
Irritant
Health Hazard
Signal
Danger
GHS Hazard Statements

H300 (90.9%): Fatal if swallowed [Danger Acute toxicity, oral]

H319 (36.4%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H330 (27.3%): Fatal if inhaled [Danger Acute toxicity, inhalation]

H351 (100%): Suspected of causing cancer [Warning Carcinogenicity]

H361 (36.4%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H413 (54.5%): May cause long lasting harmful effects to aquatic life [Hazardous to the aquatic environment, long-term hazard]

Precautionary Statement Codes

P203, P260, P264, P264+P265, P270, P271, P273, P280, P284, P301+P316, P304+P340, P305+P351+P338, P316, P318, P320, P321, P330, P337+P317, P403+P233, P405, and P501

(The corresponding statement to each P-code can be found at the GHS Classification page.)

ECHA C&L Notifications Summary

Aggregated GHS information provided per 11 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown.

11.1.2 Hazard Classes and Categories

Acute Tox. 2 (90.9%)

Eye Irrit. 2 (36.4%)

Acute Tox. 2 (27.3%)

Carc. 2 (100%)

Repr. 2 (36.4%)

Aquatic Chronic 4 (54.5%)

11.1.3 Health Hazards

SYMPTOMS: Symptoms of exposure to this compound may include irritation. It can also interfere with the carbohydrate metabolism of eye lenses.

ACUTE/CHRONIC HAZARDS: This compound is highly toxic orally. It may be fatal by ingestion or inhalation. When heated to decomposition it emits very toxic fumes of chlorine and nitrogen oxides. (NTP, 1992)

National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.1.4 Fire Hazards

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.1.5 Hazards Summary

May be fatal by ingestion or inhalation; [CAMEO] May cause irritation; Causes injury to the kidneys and liver in high-dose animal studies; [MSDSonline] Causes renal tubular injury and liver damage in high-dose animal studies; Oral LD50 = 0.2 mg/kg for dogs and 59 mg/kg for mice; High levels in the diet are associated with nephropathy in humans and swine in Balkan countries (Balkan nephropathy); [Hayes, p. 644] Factory workers handling contaminated coffee, cocoa beans, spices, and other foods have elevated ochratoxin serum levels; [Reference #1] MAC-2 (considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that it can make a significant contribution to cancer risk); [MAK]
Hayes - Hayes AW, Kruger CL (eds). Principles and Methods of Toxicology, 6th Ed. Boca Raton: CRC Press, 2014., p. 644

11.2 First Aid Measures

11.2.1 First Aid

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Generally, the induction of vomiting is NOT recommended outside of a physician's care due to the risk of aspirating the chemical into the victim's lungs. However, if the victim is conscious and not convulsing and if medical help is not readily available, consider the risk of inducing vomiting because of the high toxicity of the chemical ingested. Ipecac syrup or salt water may be used in such an emergency. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital.

OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.3 Fire Fighting

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.4 Accidental Release Measures

11.4.1 Isolation and Evacuation

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

11.4.2 Cleanup Methods

PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 15

11.4.3 Disposal Methods

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.
PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds & specific methods of chem destruction ... published have not been tested on all kinds of carcinogen-containing waste. ... summary of avail methods & recommendations ... /given/ must be treated as guide only. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 14
PRECAUTIONS FOR "CARCINOGENS": ... Incineration may be only feasible method for disposal of contaminated laboratory waste from biological expt. However, not all incinerators are suitable for this purpose. The most efficient type ... is probably the gas-fired type, in which a first-stage combustion with a less than stoichiometric air:fuel ratio is followed by a second stage with excess air. Some ... are designed to accept ... aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb soln onto suitable combustible material, such as sawdust. Alternatively, chem destruction may be used, esp when small quantities ... are to be destroyed in laboratory. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 15
PRECAUTIONS FOR "CARCINOGENS": HEPA (high-efficiency particulate arrestor) filters ... can be disposed of by incineration. For spent charcoal filters, the adsorbed material can be stripped off at high temp & carcinogenic wastes generated by this treatment conducted to & burned in an incinerator. ... LIQUID WASTE: ... Disposal should be carried out by incineration at temp that ... ensure complete combustion. SOLID WASTE: Carcasses of lab animals, cage litter & misc solid wastes ... should be disposed of by incineration at temp high enough to ensure destruction of chem carcinogens or their metabolites. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 15
For more Disposal Methods (Complete) data for OCHRATOXIN A (6 total), please visit the HSDB record page.

11.4.4 Preventive Measures

PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of food & beverage containers or utensils, & the application of cosmetics should be prohibited in any laboratory. All personnel should remove gloves, if worn, after completion of procedures in which carcinogens have been used. They should ... wash ... hands, preferably using dispensers of liq detergent, & rinse ... thoroughly. Consideration should be given to appropriate methods for cleaning the skin, depending on nature of the contaminant. No standard procedure can be recommended, but the use of organic solvents should be avoided. Safety pipettes should be used for all pipetting. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 8
PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their outdoor clothes & wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... Clothing should be changed daily but ... discarded immediately if obvious contamination occurs ... /also,/ workers should shower immediately. In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. If gowns are of distinctive color, this is a reminder that they should not be worn outside of lab. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 8
PRECAUTIONS FOR "CARCINOGENS": ... Operations connected with synth & purification ... should be carried out under well-ventilated hood. Analytical procedures ... should be carried out with care & vapors evolved during ... procedures should be removed. ... Expert advice should be obtained before existing fume cupboards are used ... & when new fume cupboards are installed. It is desirable that there be means for decreasing the rate of air extraction, so that carcinogenic powders can be handled without ... powder being blown around the hood. Glove boxes should be kept under negative air pressure. Air changes should be adequate, so that concn of vapors of volatile carcinogens will not occur. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 8
PRECAUTIONS FOR "CARCINOGENS": Vertical laminar-flow biological safety cabinets may be used for containment of in vitro procedures ... provided that the exhaust air flow is sufficient to provide an inward air flow at the face opening of the cabinet, & contaminated air plenums that are under positive pressure are leak-tight. Horizontal laminar-flow hoods or safety cabinets, where filtered air is blown across the working area towards the operator, should never be used ... Each cabinet or fume cupboard to be used ... should be tested before work is begun (eg, with fume bomb) & label fixed to it, giving date of test & avg air-flow measured. This test should be repeated periodically & after any structural changes. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 9
For more Preventive Measures (Complete) data for OCHRATOXIN A (9 total), please visit the HSDB record page.

11.5 Handling and Storage

11.5.1 Nonfire Spill Response

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with 60-70% ethanol and transfer the dampened material to a suitable container. Use absorbent paper dampened with 60-70% ethanol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

STORAGE PRECAUTIONS: You should store this material under freezer conditions. (NTP, 1992)

National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.5.2 Storage Conditions

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 13

11.6 Exposure Control and Personal Protection

11.6.1 Personal Protective Equipment (PPE)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). (NTP, 1992)
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.
PRECAUTIONS FOR "CARCINOGENS": ... Dispensers of liq detergent /should be available./ ... Safety pipettes should be used for all pipetting. ... In animal laboratory, personnel should ... wear protective suits (preferably disposable, one-piece & close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... In chemical laboratory, gloves & gowns should always be worn ... however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, & disposable plastic aprons might provide addnl protection. ... Gowns ... /should be/ of distinctive color, this is a reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 8

11.7 Stability and Reactivity

11.7.1 Air and Water Reactions

Insoluble in water.

11.7.2 Reactive Group

Acids, Carboxylic

Amides and Imides

Esters, Sulfate Esters, Phosphate Esters, Thiophosphate Esters, and Borate Esters

Phenols and Cresols

11.7.3 Reactivity Profile

OCHRATOXIN A is incompatible with strong oxidizing agents, strong acids and strong bases. (NTP, 1992). It is a carboxylic acid derivative. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt.
National Toxicology Program, Institute of Environmental Health Sciences, National Institutes of Health (NTP). 1992. National Toxicology Program Chemical Repository Database. Research Triangle Park, North Carolina.

11.7.4 Hazardous Reactivities and Incompatibilities

The lactone group is saponified by alkalis
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 192 (1983)

11.8 Transport Information

11.8.1 Shipment Methods and Regulations

PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top container that will not open when dropped & will resist attack from the carcinogen. Both bottle & the outside container should be appropriately labelled. ... National post offices, railway companies, road haulage companies & airlines have regulations governing transport of hazardous materials. These authorities should be consulted before ... material is shipped. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 13
PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container (primary container), which should be enclosed in a second, unbreakable, leakproof container that will withstand chem attack from the carcinogen (secondary container). The space between primary & secondary container should be filled with absorbent material, which would withstand chem attack from the carcinogen & is sufficient to absorb the entire contents of the primary container in the event of breakage or leakage. Each secondary container should then be enclosed in a strong outer box. The space between the secondary container & the outer box should be filled with an appropriate quantity of shock-absorbent material. Sender should use fastest & most secure form of transport & notify recipient of its departure. If parcel is not received when expected, carrier should be informed so that immediate effort can be made to find it. Traffic schedules should be consulted to avoid ... arrival on weekend or holiday ... /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 13

11.8.2 DOT Label

Poison

11.9 Regulatory Information

California Safe Cosmetics Program (CSCP) Reportable Ingredient

Hazard Traits - Carcinogenicity

Authoritative List - IARC Carcinogens - 2B; NTP RoC - reasonable; Prop 65

Report - regardless of intended function of ingredient in the product

11.10 Other Safety Information

11.10.1 History and Incidents

... A relation was first recognised between exposure to OTA in the Balkan geographical area and Balkan Endemic Nephropathy (BEN) with a high incidence (nearly 50 times higher than normal) of urinary tract tumours. Exposure rates of OTA are measurable in blood of humans and animals and are established in several countries including Scandinavia, Germany, France, Italy, Canada, Japan and Northern Africa mainly Tunisia and Egypt. The impact of OTA exposure in non- endemic areas in the world is not known, the rates of exposure being not correlated with the disease records, especially in developed countries, due to lack of well-designed epidemiological studies, genetic polymorphism and maybe to dietary contents of radical scavengers and antioxidants. However the incidence and mortality rates of renal cancer are increasing in European countries and Northern Africa which could be a global resultant of human exposure to natural compounds in food such as mycotoxins and especially ochratoxin A. ...
Creppy EE, et al; J Toxicol Sci 23 (2): 165-172 (1998)

11.10.2 Special Reports

HAYES AW; MYCO TOXINS A REVIEW OF BIOLOGICAL EFFECTS AND THEIR ROLE IN HUMAN DISEASES; CLIN TOXICOL 17(1) 45 (1980). A REVIEW OF BIOLOGICAL EFFECTS OF MYCOTOXINS.
DHHS/NTP; Toxicology & Carcinogenesis Studies of Ochratoxin A in F344/N Rats (Gavage Studies) Technical Report Series No. 358 (1989) NIH Publication No 89-2813
WHO; Environmental Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990)
U.S. Department of Health & Human Services/National Toxicology Program; Twelfth Report on Carcinogens (2011). The Report on Carcinogens is an informational scientific and public health document that identifies and discusses substances (including agents, mixtures, or exposure circumstances) that may pose a carcinogenic hazard to human health. Ochratoxin A (1402-68-2) is reasonably anticipated to be a human carcinogen. First listed in the Sixth Annual Report on Carcinogens (1991).[Available from, as of July 25, 2013: http://ntp.niehs.nih.gov/]

12 Toxicity

12.1 Toxicological Information

12.1.1 Toxicity Summary

Ochratoxin A has been shown to be weakly mutagenic, possibly by induction of oxidative DNA damage. The nephrotoxin ochratoxin A (OTA) causes a reduction of glomerular filtration rate (GFR) and of para-aminohippuric acid (PAH) clearance. It is a nephrotoxin which blocks plasma membrane anion conductance in Madin-Darby canine kidney (MDCK) cells. Some cytochrome P-450 enzymes, such as CYP2C9, are known to metabolize ochratoxin A into more cytotoxic compounds capable of forming DNA adducts. (A2869, A3099)
A2869: Gekle M, Silbernagl S: Mechanism of ochratoxin A-induced reduction of glomerular filtration rate in rats. J Pharmacol Exp Ther. 1993 Oct;267(1):316-21. PMID:8229758
A3099: Simarro Doorten AY, Bull S, van der Doelen MA, Fink-Gremmels J: Metabolism-mediated cytotoxicity of ochratoxin A. Toxicol In Vitro. 2004 Jun;18(3):271-7. PMID:15046773

12.1.2 Evidence for Carcinogenicity

Evaluation: There is inadequate evidence in humans for the carcinogenicity of ochratoxin A. There is sufficient evidence in experimental animals for the carcinogenicity of ochratoxin A. Overall evaluation: Ochratoxin A is possibly carcinogenic to humans (Group 2B).
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 509 (1993)
Ochratoxin A: reasonably anticipated to be a human carcinogen.
DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Ochratoxin A (303-47-9) (January 2005). Available from, as of July 31, 2009: https://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s140ochr.pdf

12.1.3 Carcinogen Classification

1 of 3
IARC Carcinogenic Agent
Ochratoxin A
IARC Carcinogenic Classes
Group 2B: Possibly carcinogenic to humans
IARC Monographs

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

Volume 56: (1993) Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins

2 of 3
Substance
NTP Technical Report
TR-358: Toxicology and Carcinogenesis Studies of Ochratoxin A (CASRN 303-47-9) in F344/N Rats (Gavage Studies) (1989 )
Peer Review Date
Conclusion for Male Rat
Clear Evidence Clear Evidence
Conclusion for Female Rat
Clear Evidence Clear Evidence
Conclusion for Male Mice
Chemical Not Tested in Species/Sex Chemical Not Tested in Species/Sex
Conclusion for Female Mice
Chemical Not Tested in Species/Sex Chemical Not Tested in Species/Sex
Summary

Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity of ochratoxin A for male F344/N rats as shown by substantially increased incidences of uncommon tubular cell adenomas and of tubular cell carcinomas of the kidney. There was clear evidence of carcinogenic activity for female F344/N rats shown by increased incidences of uncommon tubular cell adenomas and of tubular cell carcinomas of the kidney and by increased incidences and multiplicity of fibroadenomas of the mammary gland.

Ochratoxin A administration also caused nonneoplastic renal changes including tubular cell hyperplasia, tubular cell proliferation, cytoplasmic alteration, karyomegaly, and degeneration of the renal tubular epithelium.

3 of 3
Carcinogen Classification
2B, possibly carcinogenic to humans. (L135)

12.1.4 Health Effects

Ochratoxin exposure has been associated with acute tubular necrosis and Balkan endemic nephropathy. Ochratoxin A has been shown to be nephrotoxic and might delay sexual maturation. It can cause immunosuppression and immunotoxicity in animals. It's immunosuppressant activity in animals may include depressed antibody responses, reduced size of immune organs (such as the thymus, spleen, and lymph nodes), changes in immune cell number and function, and altered cytokine production. Immunotoxicity probably results from cell death following apoptosis and necrosis, in combination with slow replacement of affected immune cells due to inhibition of protein synthesis. (A704, L1939)
A704: Grond S, Sablotzki A: Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43(13):879-923. PMID:15509185
L1939: Wikipedia. Ochratoxin A. Last Updated 26 February 2010. http://en.wikipedia.org/wiki/Ochratoxin_A

12.1.5 Exposure Routes

Oral, dermal, inhalation, and parenteral (contaminated drugs). (A3101)
A3101: Peraica M, Domijan AM: Contamination of food with mycotoxins and human health. Arh Hig Rada Toksikol. 2001 Mar;52(1):23-35. PMID:11370295

12.1.6 Symptoms

Might cause respiratory irritation. (A704)
A704: Grond S, Sablotzki A: Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43(13):879-923. PMID:15509185

12.1.7 Adverse Effects

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

Nephrotoxin - The chemical is potentially toxic to the kidneys in the occupational setting.

IARC Carcinogen - Class 3: Chemicals are not classifiable by the International Agency for Research on Cancer.

NTP Carcinogen - Reasonably anticipated to be a human carcinogen.

12.1.8 Toxicity Data

LD50: 20 mg/kg (Oral, Rat) (A716) LD50: 12,600 ug/kg (Intraperitoneal, Rat) (A716) LD50: 12,750 ug/kg (Intravenous, Rat ) (A716) LD50: 46 mg/kg (Oral, Mouse) (A716)
A716: Begley JA, Colligan PD, Chu RC: Transcobalamin II mediated delivery of albumin-bound hydroxocobalamin to human liver cells. Proc Soc Exp Biol Med. 1993 Nov;204(2):206-10. PMID:8415778

12.1.9 Treatment

Care is symptomatic and supportive. (A704)
A704: Grond S, Sablotzki A: Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43(13):879-923. PMID:15509185

12.1.10 Interactions

... Ochratoxin A (OA) toxicity and the effect of supplemental ascorbic acid (AA) /was examined/ in laying hens housed under two environmental temperatures. /Two groups of/ ... 24 hens were randomly assigned to four dietary treatments in six replications. Treatments consisted of a control and three diets containing either 300 ppm AA, 3 ppm OA, or 300 ppm AA plus 3 ppm OA. Treatment diets were fed for 14 days following the feeding of the basal diet for 14 days. The test period temperature was 25 °C ... /for the first group/ and 33 °C in ... /the other group/. ... When laying hens were fed 3 ppm OA compared with those fed the control diet/, there were significant reductions in feed intake, body weight change, and egg production, and increased shell elasticity/. An analysis of plasma constituents showed that OA also increased Cl- concn and aspartate transaminase activity and decreased plasma calcium concentrations. Exposing hens to 33 °C (compared with 25 °C) appeared to aggravate the negative effects of OA. All the negative effects of OA, apart from body-weight changes, reductions in feed intake, and increases in egg shell elasticity at 33 °C were either moderated or significantly ... reversed by dietary AA supplementation. ... The results /indicate/ that the detrimental effects of OA in the diet of the laying hen can be counteracted by dietary /administration/ of AA.
Haazele FM et al; Can J Anim Sci 73 (1): 149-57 (1993)
Aldrin concentration increased in liver of neonatal rats during 1st 6 hr after oral administration then decreased over 72 hr to less than 0.1% dose. Aldrin and ochratoxin given together; aldrin increased 1st 6 hr then decreased to 0.4% dose over 18 hr.
FARB RM ET AL; PESTIC ENVIRON: CONTINUING CONTROVERSY, PAP INTER-AM CONF TOXICOL OCCUP MED, 8TH; 179 (1973)
Dieldrin, detected 2 hr after administration of aldrin to neonatal rats, increased to max 30% of initial aldrin by 18 hr. Aldrin & ochratoxin given together; dieldrin increased from 10% of aldrin dose at 2 hr to max 50% at 24 hr.
FARB RM ET AL; PESTIC ENVIRON: CONTINUING CONTROVERSY, PAP INTER-AM CONF TOXICOL OCCUP MED, 8TH; 179 (1973)
Rainbow trout fed a diet containing 20 ug ochratoxin A/kg of diet; together with sterculic acid, developed hepatomas (number unspecified).
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V10 193 (1976)
For more Interactions (Complete) data for OCHRATOXIN A (20 total), please visit the HSDB record page.

12.1.11 Antidote and Emergency Treatment

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160
/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St. Louis, MO 2005, p. 160-1

12.1.12 Medical Surveillance

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/
Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory: Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979., p. 23

12.1.13 Human Toxicity Excerpts

/HUMAN EXPOSURE STUDIES/ Mysterious deaths of archaeologists after opening Egyptian tombs have been suspected, but never proved, to be secondary to inhalation of mycotoxin. A case of acute renal failure (ARF) due to inhalation of ochratoxin A /was observed/. /It was/ produced by a mold of the species Aspergillus ochraceus. After working 8 hr in a granary closed for several months, a farmer and his wife suffered respiratory distress; the woman developed non-oliguric ARF and biopsy revealed tubulonecrosis. A strain of Aspergillus ochraceus producing ochratoxin was isolated from the wheat.
Di Paolo N et al; Nephrol Dialysis Transplant 9 (4): 116-20 (1994)
/EPIDEMIOLOGY STUDIES/ A study in Bulgaria of the association between BEN /Balkan endemic nephropathy/ and/or urinary system tumors and ochratoxin A content in blood samples taken from 187 subjects living in endemic villages and 125 individuals in non-endemic villages /was reported/. Among 61 patients with BEN and/or urinary system tumors, 14.8% had levels of 1-2 ng/mL and 11.5% had more than 2 ng/mL ochratoxin A in their blood. This proportion was significantly higher than that in a control group of 63 healthy individuals from unaffected families in the endemic villages (7.9 and 3.2%, respectively). The percentage of positive blood samples in the control group was similar to that measured among a random sample of healthy individuals from non-endemic villages (6.2 and 1.5% respectively). Intermediate proportions of positive blood samples were found among healthy individuals from families of patients with either endemic nephropathy and/or a urinary system tumor (9.5 and 6.3%, respectively). (The Working Group noted that no attempt was made by the authors to present separate results for the subgroup of urinary system tumors). Blood samples from 576 people living inside and outside the endemic areas in Bulgaria during 1984, 1986, 1989 and 1990 /were collected/. Overall, a significantly larger proportion of the blood samples from 105 patients with urinary tract tumors and/or BEN (26.7%) contained ochratoxin A than those from 116 healthy people living in villages in the endemic area (12.1%), or from 119 healthy people from non-affected villages in the endemic area (10.9%) or from 125 healthy people living in non-endemic areas of Bulgaria (7.2%); however, the proportion among the patients was not significantly higher than that among 111 healthy relatives of patients with urinary tract tumors and/or BEN living in affected villages (16.2%).
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 496 (1993)
/EPIDEMIOLOGY STUDIES/ ...Contamination by ochratoxin A of 65 samples of beans, maize or wheat flour from /Bulgarian/ households in an area endemic for BEN /Balkan endemic nephropathy/ and with a high incidence of urinary system tumors and in 65 samples from households in non-endemic areas. None of the samples was visibly moldy. Samples from high-risk areas were collected from families in which cases of BEN and/or urinary tract tumors had been diagnosed ('affected' households), while samples from nonendemic areas were taken at random. All samples of home-produced beans and maize were taken during February and March 1982 from the 1981 harvest; wheat flour samples were purchased from local shops, which were supplied from central state stocks. Although there was no significant difference between endemic and non-endemic areas in the mean values of ochratoxin A in contaminated samples of beans (range; 25-27 ug/kg in endemic area, 25-50 ug/kg in non-endemic area) and maize (25-35 and 10-25 ug/kg, respectively), a larger proportion of samples from the endemic area were contaminated: [16.7% of beans (95% CI, 4.8% -33.9%) and 27.3% of maize (11.2% -47.4%) in endemic areas, and 7.1% of beans and 9.0% of maize in non-endemic areas]. None of the samples of wheat flour analyzed contained measurable amounts of ochratoxin A. In an extension of this survey, ... 524 samples of home-produced, home-stored beans and maize /were collected/ from the harvests of 1984-86 and 1989-90. Of these, 298 were taken from 'affected' and 'non-affected' households in the endemic areas of Bulgaria and 226 from non-affected households in non-endemic areas. Overall, significantly more samples from endemic areas than from control areas were contaminated with ochratoxin A (54 versus 12%).
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 496 (1993)
/EPIDEMIOLOGY STUDIES/ ...Records of cases of urinary tract tumor collected over a period of 16 yr (1974-89) at the medical center of the County of Slavonski Brod in Croatia, /were used to study/ the distribution of these tumors in the areas of the County that were endemic for BEN (population, 10,094) and in the rest of the County (96,306). A total of 67 tumors were recorded in the endemic areas (estimated cumulative incidence, 0.664%) and 126 in the non-endemic area (0.131%). The difference in the recorded relative number of cases was highest for tumors of the renal pelvis (0.287% versus 0.021%) and ureter (0.089% versus 0.013%) and only moderate for bladder cancer (0.228 versus 0.089%). In general, more cases were seen among women that among men in the endemic area. Tumors of the renal parenchyma were not mentioned in this survey.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V56 495 (1993)
For more Human Toxicity Excerpts (Complete) data for OCHRATOXIN A (16 total), please visit the HSDB record page.

12.1.14 Non-Human Toxicity Excerpts

/LABORATORY ANIMALS: Acute Exposure/ Ochratoxin A administered to rats in single or multiple oral doses. Severe catarrhal or erosive enteritis of duodenum & jejunum within 4 hr of dosage. After several daily doses, massive acidophilic degeneration, necrosis & desquamation of epithelium in proximal tubules. Necrosis of cells in germinal centers of spleen & lymph nodes indicated sensitivity of lymphatic tissues. Hepatotoxicity limited to depletion of hepatic glycogen.
KANISAWA M ET AL; TOXICOL APPL PHARMACOL 42 (1): 55 (1977)
/LABORATORY ANIMALS: Acute Exposure/ In kidney cortex slices from rats fed ochratoxin A (2 mg/kg/day) for 2 days, gluconeogenesis from pyruvate was decr by 26%, & renal phosphoenolpyruvate carboxykinase activity lowered by approx 55%.
MEISNER H, SELANIK P; BIOCHEM J 180 (3): 681 (1979)
/LABORATORY ANIMALS: Acute Exposure/ .../It was/ observed that administration of a single high dose or multiple lower doses of ...ochratoxin A (OTA) to rats resulted in an incr of the renal cortex endoplasmic reticulum ATP-dependent calcium pump activity. The incr was very rapid, being evident within 10 min of OTA admin and remained elevated for at least 6 hr thereafter. The incr in calcium pump activity was inconsistent with previous observations that OTA enhances lipid peroxidation (ethane exhalation) in vivo, a condition known to inhibit the calcium pump. However, no evidence of enhanced lipid peroxidation was observed in the renal cortex, since levels of malondialdehyde and a variety of antioxidant enzymes including catalase, DT-diaphorase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione S-transferase were either unaltered or reduced. In in vitro studies addition of OTA to cortex microsomes during calcium uptake inhibited the uptake process although the effect was reversible. Preincubation of microsomes with NADPH had a profound inhibitory effect on calcium uptake but inclusion of OTA was able to reverse the inhibition. Changes in the rates of microsomal calcium uptake related with changes in the steady-state levels of the phosphorylated Mg2+/Ca(+2)-ATPase intermediate, suggesting that in vivo/in vitro conditions were affecting the rate of enzyme phosphorylation.
Chong X, Rahimtula AD; Biochem Pharmacol 44 (7): 1401-9 (1992)
/LABORATORY ANIMALS: Acute Exposure/ ...Treatment of male rats with OTA (up to 2 mg/24 hr exposure) did not increase the formation of biomarkers of oxidative damage such as the lipid peroxidation marker malondialdehyde in rat plasma, kidney, and liver, or the DNA damage marker 8-oxo-7,8-dihydro-2' deoxyguanosine in kidney DNA. However, OTA treatment (1 mg/kg) did result in a 22% decrease in alpha-tocopherol plasma levels and a 5-fold increase in the expression of the oxidative stress responsive protein haem oxygenase-1, specifically in the kidney. The selective alteration of these latter two markers indicates that OTA does evoke oxidative stress, which may contribute at least in part to OTA renal toxicity and carcinogenicity in rats during long-term exposure.
Gautier JC, et al; Free Radic Biol Med 30 (10): 1089-1098 (2001)
For more Non-Human Toxicity Excerpts (Complete) data for OCHRATOXIN A (78 total), please visit the HSDB record page.

12.1.15 Non-Human Toxicity Values

LD50 Mouse iv 30 mg/kg bw
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 197 (1983)
LD50 Mouse ip 40 mg/kg bw
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31 197 (1983)
LD50 Rat oral 20 mg/kg
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 830
LD50 Rat intraperitoneal 12,600 ug/kg
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 830
For more Non-Human Toxicity Values (Complete) data for OCHRATOXIN A (10 total), please visit the HSDB record page.

12.1.16 Ongoing Test Status

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of July 25, 2013: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=303-47-9]

12.1.17 National Toxicology Program Studies

... Toxicology and carcinogenesis studies were conducted by administering ochratoxin A (98% pure) in corn oil by gavage to groups of F344/N rats of each sex for ... 2 yr. Only rats were studied because ochratoxin A has been shown to be carcinogenic in mice. ... Groups of 80 rats per sex and dose group were administered 0, 21, 70 or 210 ug/kg ochratoxin in corn oil by gavage 5 days/wk for up to 2 yr. Conclusions: Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity of ochratoxin A for male F344/N rats as shown by substantially increased incidences of uncommon tubular cell adenomas and of tubular cell carcinomas of the kidney. There was clear evidence of carcinogenic activity for female F344/N rats shown by increased incidences of uncommon tubular cell adenomas and of tubular cell carcinomas of the kidney and by increased incidences and multiplicity of fibroadenomas of the mammary gland.
Toxicology & Carcinogenesis Studies of Ochratoxin A in F344/N Rats (Gavage Studies). Technical Report Series No. 358 (1989) NIH Publication No. 89-2813 U.S. Department of Health and Human Services, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709

12.2 Ecological Information

12.2.1 Ecotoxicity Excerpts

/BIRDS and MAMMALS/ During veterinary meat inspection porcine kidneys with macroscopic lesions indicating mycotoxic porcine nephropathy were /studied/. ... About 8 (12%) of the slaughtered pigs showed macroscopic changes in kidneys indicating the disease. Ochratoxin A was found in 35 (41%) kidneys with the highest concn 3.1 ng/g. Porcine blood samples (105) were collected at random and ochratoxin A was found in 63 (60%) samples with the highest concn being 122 ng/mL.
Kotowski K et al; Medycyna Weternary JNA; 49 (12): 554-56 (1993)
/BIRDS and MAMMALS/ The combined effect of ochratoxin A (at diet levels of 130, 305 and 790 ppb) and penicillic acid was studied in 100 broiler chicks. ...A statistically significant decr of the body weight and the relative weight of lymphoid organs as well as a significant incr of the relative weight of kidneys and liver were seen. The main degenerative changes were observed in the proximal convoluted tubules in kidneys and slight degenerative changes were found in the hepatocytes. Degenerative changes and depletion of lymphoid cells were observed in the bursa Fabricii, thymus, spleen and Peyer's patches of intestinal mucosa. Serum analyses revealed significant decreases of the total protein and cholesterol, and significant increases of the uric acid and glucose. Hematological analyses showed a slight anemia, leucocytosis and slightly decompensated metabolic acidosis. ...
Stoev SD, et al; Exp Toxicol Pathol 52 (1): 43-55 (2000)
/BIRDS and MAMMALS/ Sublethal doses of ochratoxin A given to 1-day-old babcock b-300 cockerels resulted in growth suppression proportional to dose. Visceral gout was major finding. Exam revealed acute nephritis, hepatic degeneration or focal necrosis, and enteritis.
Peckham JC et al; Appl Microbiol 21 (3): 492 (1971)
/BIRDS and MAMMALS/ Sublethal doses of ochratoxin A given to 1-day-old babcock b-300 cockerels produced suppression of hematopoiesis in bone marrow and depletion of lymphoid elements from spleen and bursa of fabricius.
Peckham JC et al; Appl Microbiol 21 (3): 492 (1971)
For more Ecotoxicity Excerpts (Complete) data for OCHRATOXIN A (7 total), please visit the HSDB record page.

12.2.2 Environmental Fate / Exposure Summary

Ochratoxin A's limited production and use experimentally as a teratogen and carcinogen may result in its release to the environment through various waste streams. Ochratoxin A is a naturally occurring carcinogenic mycotoxin which is a toxic metabolite from Aspergillus ochraceus, A. sulphureus, A. melleus and Penicillium viridicatum. If released to air, an estimated vapor pressure of 3.1X10-14 mm Hg at 25 °C indicates ochratoxin A will exist solely in the particulate phase in the atmosphere. Particulate-phase ochratoxin A will be removed from the atmosphere by wet and dry deposition. Ochratoxin A absorbs UV light at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. If released to soil, the neutral species of ochratoxin A is expected to have slight mobility based upon an estimated Koc of 3800. The estimated pKa values of ochratoxin A are 2.6 and 8.2, indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts. Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Ochratoxin A is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation half-lives in soil of 0.2-1 days suggest that biodegradation may be an important environmental fate process in soil or water. If released into water, the neutral species of ochratoxin A is expected to adsorb to suspended solids and sediment based upon the estimated Koc. The estimated pKa values indicate ochratoxin A will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process. An estimated BCF of 1200 suggests the potential for bioconcentration in aquatic organisms is very high. Ochratoxin A may undergo hydrolysis in the environment as it contains a cyclic ester functionality and a labile substituted amino acid moiety. Occupational exposure to ochratoxin A may occur potentially through inhalation of dusts and dermal contact at workplaces where handling of grains, nuts, corn, cereals, and animal feeds occurs. Monitoring data indicate that the general population is exposed to ochratoxin A predominately via ingestion of and dermal contact with grains, beans, rice, maize, and pork products contaminated with this compound. (SRC)

12.2.3 Natural Pollution Sources

Ochratoxin A is a naturally occurring carcinogenic mycotoxin which has been detected in foods(1). Ochratoxins are toxic metabolites from Aspergillus ochraceus Wilh:, A. sulphureus, A. melleus, Penicillium viridicatum Westling(2), and P. verrucosum(3). While ochratoxin A occurs in many commodities world-wide, it has been found primarily in north-temperate barley- and wheat-growing regions(4).
(1) Austwick P, Matocks R; Chem Ind 1979: 76-83 (1979)
(2) O'Neil MJ, ed; The Merck Index. 14th ed., Whitehouse Station, NJ: Merck and Co., Inc., p. 1166 (2006)
(3) Mortensen GK et al; Chemosphere 62: 1673-1680 (2006)
(4) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 495 (1993)
Ochratoxin A is a naturally occurring mycotoxin ... a natural contaminant on corn, peanuts, storage grains, cottonseed, and decaying vegetation ... .
DHHS/NIEHS; Seventh Annual Rpt on Carcinogens Summary p. 310 (1994)
... Ochratoxin A is a mycotoxin produced by fungi occurring frequently on cereals. Their growth, and the associated toxin production, are closely correlated to the degree of moisture to which they are exposed, which itself is dependent upon weather conditions. ...
Frank HK; IARC Sci Publ 115: 321-5 (1991)
Ochratoxin A is a toxin produced by fungi which can be found in many food stuffs, particularly cereals and pork products.
International Labour Office. Encyclopaedia of Occupational Health and Safety. 4th edition, Volumes 1-4 1998. Geneva, Switzerland: International Labour Office, 1998., p. 8.11
Ochratoxin A is primarily produced by Aspergillus ochraceous, A. carbonarius, and Penicillium verrucosum. Contaminated commodities: grains, peanuts, grapes, and green coffee.
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 7th ed. New York, NY: McGraw-Hill, 2008., p. 1220

12.2.4 Artificial Pollution Sources

Ochratoxin A's limited production and use experimentally as a teratogen and carcinogen(1) may result in its release to the environment through various waste streams(SRC).
(1) O'Neil MJ, ed; The Merck Index. 14th ed., Whitehouse Station, NJ: Merck and Co., Inc., p. 1166 (2006)

12.2.5 Environmental Fate

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 3800(SRC), determined from a log Kow of 4.74(2) and a regression-derived equation(3), indicates that the neutral species of ochratoxin A is expected to have slight mobility in soil(SRC). The estimated pKa values of ochratoxin A are 2.6 and 8.2(4), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Ochratoxin A is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.1X10-14 mm Hg at 25 °C(SRC), determined from a fragment constant method(3). Biodegradation half-lives in soil of 0.2-1 days(6) suggest that biodegradation may be an important environmental fate process in soil(SRC).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) Sangster J; LOGKOW Database. A databank of evaluated octanol-water partition coefficients (Log P). Available from, as of Jun 24, 2013: https://logkow.cisti.nrc.ca/logkow/search.html
(3) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(4) ACE Organic; Public access ACE pages. ACE acidity and basicity calculator., Grossman RB, Finkel R., Univ KY, Dept Chem. 2006. Available from, as of Jun 24, 2012: https://aceorganic.pearsoncmg.com/epoch-plugin/public/pKa.jsp
(5) Doucette WJ; pp. 141-188 in Handbook of Property Estimation Methods for Chemicals. Boethling RS, Mackay D, eds. Boca Raton, FL: Lewis Publ (2000)
(6) Mortensen GK et al; Chemosphere 62: 1673-1680 (2006)
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 3800(SRC), determined from a log Kow of 4.74(2) and a regression-derived equation(3), indicates that the neutral species of ochratoxin A is expected to adsorb to suspended solids and sediment(SRC). Estimated pKa values of 2.6 and 8.2(4) indicate ochratoxin A will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(5), an estimated BCF of 1200(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). Ochratoxin A may undergo hydrolysis as it contains a cyclic ester functionality and a labile substituted amino acid moiety(6). Biodegradation half-lives in soil of 0.2-1 days(7) suggest that biodegradation may be an important environmental fate process in water(SRC).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) Sangster J; LOGKOW Database. A databank of evaluated octanol-water partition coefficients (Log P). Available from, as of Jun 24, 2013: https://logkow.cisti.nrc.ca/logkow/search.html
(3) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(4) ACE Organic; Public access ACE pages. ACE acidity and basicity calculator., Grossman RB, Finkel R., Univ KY, Dept Chem. 2006. Available from, as of Jun 24, 2012: https://aceorganic.pearsoncmg.com/epoch-plugin/public/pKa.jsp
(5) Franke C et al; Chemosphere 29: 1501-14 (1994)
(6) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 7-4, 7-5 (1990)
(7) Mortensen GK et al; Chemosphere 62: 1673-1680 (2006)
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ochratoxin A, which has an estimated vapor pressure of 3.1X10-14 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase ochratoxin A may be removed from the air by wet and dry deposition(SRC). Ochratoxin A absorbs UV light at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).
(1) Bidleman TF; Environ Sci Technol 22: 361-367 (1988)
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) O'Neil MJ, ed; The Merck Index. 14th ed., Whitehouse Station, NJ: Merck and Co., Inc., p. 1166 (2006)

12.2.6 Environmental Biodegradation

AEROBIC: Ochratoxin A, present at 24.3, 25.3 and 16.0 ug/kg, was not detected after 225 days using three agricultural topsoils from Danish experimental farms: a sandy soil (Jundevad, 3.9% clay, 4.1% silt, 89.0% sand), a sandy clay soil (Askov, 10.6% clay, 11.8% silt, 74.6% sand) and a gyttja soil with a high content of silt (Lammefjorden, 4.4% clay, 12.1% silt, 80.6% sand), respectively. Degradation proceeded fast initially followed by a slower transformation step. The first-order degradation rates were 0.73, 1.56 and 2.91/day, respectively, corresponding to a half-lives of 0.2-1 days. Degradation was faster in experimental pots planted with barley. The ochratoxin A employed was produced by Penicillium verrucosum(1).
(1) Mortensen GK et al; Chemosphere 62: 1673-1680 (2006)

12.2.7 Environmental Abiotic Degradation

Ochratoxin A may undergo hydrolysis in the environment as it contains a cyclic ester functionality and a labile substituted amino acid moiety(1). A base-catalyzed second-order hydrolysis rate constant of 4.4X10-12 L/mole-sec(SRC) was estimated using a structure estimation method(2); this corresponds to half-lives of 5 years and 183 days at pH values of 7 and 8, respectively(2). Ochratoxin A absorbs UV light at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).
(1) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 7-4, 7-5 (1990)
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 25, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) O'Neil MJ, ed; The Merck Index. 14th ed., Whitehouse Station, NJ: Merck and Co., Inc., p. 1166 (2006)
It has previously been shown that the biosynthesis of the mycotoxins ochratoxin A and B and of citrinin by Penicillium is regulated by light. However, not only the biosynthesis of these mycotoxins, but also the molecules themselves are strongly affected by light of certain wavelengths. The white light and blue light of 470 and 455 nm are especially able to degrade ochratoxin A, ochratoxin B and citrinin after exposure for a certain time. After the same treatment of the secondary metabolites with red (627 nm), yellow (590 nm) or green (530 nm) light or in the dark, almost no degradation occurred during that time indicating the blue light as the responsible part of the spectrum. The two derivatives of ochratoxin (A and B) are degraded to certain definitive degradation products which were characterized by HPLC-FLD-FTMS /high perfromance liquid chromatography-postcolumn fluorescence derivatization-Fourier transform mass spectrometry/. The degradation products of ochratoxin A and B no longer contained phenylalanine; however, the products were still chlorinated in the case of ochratoxin A. Citrinin is completely degraded by blue light. A fluorescent band was no longer visible after detection by TLC suggesting a higher sensitivity and apparently greater absorbance of energy by citrinin. The fact that especially blue light degrades the three secondary metabolites is apparently attributed to the absorption spectra of the metabolites which all have an optimum in the short wave length range. The absorption range of citrinin is, in particular, broader and includes the wave length of blue light. In wheat, which was contaminated with an ochratoxin A producing culture of Penicillium verrucosum and treated with blue light after a pre-incubation by the fungus, the concentration of the preformed ochratoxin A reduced by roughly 50% compared to the control and differed by > 90% compared to the sample incubated further in the dark. This indicates that the light degrading effect is also exerted in vivo, e.g., on food surfaces. The biological consequences of the light instability of the toxins are discussed.
(1) Schmidt-Heydt M et al; Toxins 4(12): 1525-51 (2012)

12.2.8 Environmental Bioconcentration

An estimated BCF of 1200 was calculated in fish for ochratoxin A(SRC), using a log Kow of 4.74(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC). However, it has been demonstrated that ochratoxin A is toxic in marine water-reared sea bass (Dicentrarchus labrax L.); exposure via contaminated feed(4).
(1) Sangster J; LOGKOW Database. A databank of evaluated octanol-water partition coefficients (Log P). Available from, as of Jun 24, 2013: https://logkow.cisti.nrc.ca/logkow/search.html
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm/
(3) Franke C et al; Chemosphere 29: 1501-14 (1994)
(4) El-Sayed YS et al; Chemosphere 75: 878-82 (2009)

12.2.9 Soil Adsorption / Mobility

The Koc of the neutral species of ochratoxin A is estimated as 3800(SRC), using a log Kow of 4.74(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that ochratoxin A is expected to have slight mobility in soil. The estimated pKa values of ochratoxin A are 2.6 and 8.2, indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).
(1) Sangster J; LOGKOW Database. A databank of evaluated octanol-water partition coefficients (Log P). Available from, as of Jun 24, 2013: https://logkow.cisti.nrc.ca/logkow/search.html
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) Swann RL et al; Res Rev 85: 17-28 (1983)
(4) Doucette WJ; pp. 141-188 in Handbook of Property Estimation Methods for Chemicals. Boethling RS, Mackay D, eds. Boca Raton, FL: Lewis Publ (2000)

12.2.10 Volatilization from Water / Soil

The estimated pKa values of 2.6 and 8.2(1) indicate ochratoxin A will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process. Ochratoxin A is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.1X10-14 mm Hg(SRC), determined from a fragment constant method(2).
(1) ACE Organic; Public access ACE pages. ACE acidity and basicity calculator., Grossman RB, Finkel R., Univ KY, Dept Chem. 2006. Available from, as of Jun 24, 2012: https://aceorganic.pearsoncmg.com/epoch-plugin/public/pKa.jsp
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Jun 24, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm

12.2.11 Food Survey Values

Kidneys from 385 slaughtered pigs were collected in 6 slaughter-houses in various districts of northern Belgium from February to June 1987. 6.3% of kidneys had ochratoxin A present at concentrations from 0.2-0.99 ng/g, 9.1% had ochratoxin A present at concentrations from 1-4.99 ng/g, 1.0% had ochratoxin A present at concentrations from 5-9.99 ng/g, 1.3% had ochratoxin A present at concentrations above 10 ng/g(1). In Denmark, 35% of analyzed porcine kidneys contained ochratoxin A from 2-68 ng/g; Sweden 25% of kidneys from 2-10 ng/g; W.Germany 21% of kidneys from 0.1-1.8 ng/g; Poland 45% of kidneys from 2-23 ng/g; Hungary 39% of kidneys from 5-100 ng/g; Belgium 17.7% of kidneys from 0.2-12 ng/g(1). A maximum level of 67 ppb has been reported in meat(2).
(1) Rousseau DM, Van Peteghem CH; Bull Environ Contam Toxicol 42: 181-6 (1989)
(2) Austwick P, Matocks R; Chem Ind 1979: 76-83 (1979)
Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from <0.2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (<60 ppb) were found in suspect feed from two episodes. ... Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. ... The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2(1).
(1) Hamilton PB et al; Poultry Sci 61: 1832-41 (1982). Available from, as of Jun 26, 2013: https://ps.fass.org/content/61/9/1832.abstract
Ochratoxin A was detected in dried black beans (n=5, 113-136 ug/kg beans), dried white corn (32 ug/kg), cassava flour (32-65 ug/kg), dried Carioquinha beans (94 ug/kg), and dried Rosinha beans (160 ug/kg) from Brazil(1). In the US, ochratoxin A was detected in maize (3 of 293 samples, 80-170 ug/kg), wheat (11 of 577 samples, 10-29 ug/kg), and barley (41 of 309 samples, 10-40 ug/kg)(3). In Canada, ochratoxin A was detected in wheat/hay (7 of 95 samples, 30-6000 ug/kg), grain/forage (5 of 474 samples, 30-4000 ug/kg), cereals (11 of 755 samples, 3-50 ug/kg), and peas/beans (1 of 84 samples, 20 ug/kg)(2). Although ochratoxin A occurs in many commodities all over the world, it has been found primarily in north-temperate barley- and wheat-growing areas(2).
(1) Valente Soares LM, Rodriguez-Amaya DB; J Assoc Off Anal Chem 72: 22-6 (1989)
(2) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 494 (1993)
Ochratoxin A concentrations of <limit of quantitation to 2 ug/kg were reported in peanut cake samples; the limit of quantitation is 0.3 ug/kg in peanut cake obtained from markets in the Republic of Benin, West Africa(1). A maximum level of 60 ppb (with an exceptional level of 27,500 ppb) was reported in cereals(2).
(1) Njumbe Ediage E et al; J Agric Food Chem 59: 5173-5180 (2011)
(2) Austwick P, Matocks R; Chem Ind 1979: 76-83 (1979)
For more Food Survey Values (Complete) data for OCHRATOXIN A (10 total), please visit the HSDB record page.

12.2.12 Plant Concentrations

Ochratoxin A has been detected at contamination levels in cereals ranging from 0.03 ppm to 27.5 ppm(1).
(1) DHHS/NIEHS; Report on Carcinogens. Twelfth Edition p. 335 (2011). Washington, DC: US Dept Health Human Services., Public Health Service., Natl Toxicol Program. Available from, as of Aug 2, 2013: https://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf
Although the carryover from barley into beer is possible, one survey of all 130 US breweries did not detect ochratoxin A (up to 10 ug/kg) in beer or malted barley. In moderately contaminated barley, the malting process completely degrades ochratoxin A; however, 2-7% of the toxin remained in the final product from heavily contaminated barley(1).
(1) DHHS/NIEHS; Report on Carcinogens. Twelfth Edition p. 335 (2011). Washington, DC: US Dept Health Human Services., Public Health Service., Natl Toxicol Program. Available from, as of Aug 2, 2013: https://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf
Natural occurrence of ochratoxin A in plant products was reported as follows: maize, up to 2.6% of samples analyzed contaminated at concentration up to 200 ug/kg; wheat, up to 2.8% contaminated at up to 115 ug/kg; barley, up to 12.6% contaminated at up to 3800 ug/kg; coffee beans, up to 7.1% contaminated at up to 360 ug/kg; bread, up to 2% contaminated at up to 210 ug/kg; flour, up to 28.5% contaminated at up to 2900 ug/kg; rice, contaminated at up to 430 ug/kg; beans, up to 8.5% contaminated at up to 442 ug/kg; peas, up to 2.8% contaminated at up to 10 ug/kg. In commodities from Yugoslavia (an area of endemic human nephropathy), up to 8.3% of maize samples were contaminated at concentrations up to 140 ug/kg; 8.5% of wheat contaminated at up to >100 ug/kg; and 12.5% of barley contaminated at up to 26 ug/kg. In feed (including barley, wheat, oats, rye, maize, hay) from various countries, up to 57.6% of the samples were contaminated at concentrations up to 27,500 ug/kg(1).
(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 494 (1993)

12.2.13 Animal Concentrations

Residues of ochratoxin A have been detected in samples of meat from pigs slaughtered immediately after consuming contaminated feed. It has been detected at levels of 10-920 ug/kg in sausage, ham, and bacon samples(1).
(1) DHHS/NIEHS; Report on Carcinogens. Twelfth Edition p. 335 (2011). Washington, DC: US Dept Health Human Services., Public Health Service., Natl Toxicol Program. Available from, as of Aug 2, 2013: https://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf
In an area of Balkan endemic nephropathy, ochratoxin A was found in 28.9% of ham samples at levels of 40-70 ug/kg, 18.9% of bacon samples at levels of 37-200 ug/kg, 13.3% of kulen (specially prepared sausage) samples at levels of 10-460 ug/kg and 12% of sausage samples at levels of 10-920 ug/kg ... .
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V31: 195 (1983)

12.2.14 Milk Concentrations

ENVIRONMENTAL: Ochratoxin A was detected in 4 of 36 human milk samples collected in Germany at concentrations of 0.017 to 0.03 ng/mL. 9 of 50 human milk samples collected in Italy between 1989 and 1990 contained ochratoxin A at concentrations of 1.7 to 6.6 ng/mL(1)
(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 494 (1993)
EXPERIMENTAL: ... /Ochratoxin A/ diffusion into the milk of female rabbits is seen after intravenous administration but in cows given 50 mg of the mycotoxin, barely detectable amounts of ochratoxin alpha were recovered in milk.
Galtier P; IARC Sci Pub 115: 187-200 (1991)
... The aim of this study was to assess the exposure of infants to OTA by analysing breast milk samples from 2 German areas. Breast milk samples were obtained from 90 mothers who had signed an informed consent sheet. The previously validated analytical method (LOD=10 ng/L, LOQ=30 ng/L) involves liquid-liquid extraction and analysis by HPLC with tandem mass spectrometric detection. A preliminary risk assessment was done using the TDI approach. More than 50% of the collected 90 milk samples contained detectable OTA levels. Overall, the average concentration in milk from -Dortmund (24.4 +/- 21.1 ng/L (n=30), range:<10-100 ng/L) were significant higher than those measured in the Hannover cohort (14.4 +/-1 5.1 ng/L (n=60), range: <10-78 ng/L). The OTA levels of 13 samples were measured with concentrations >/= LOQ. The burden of breast milk in different lactation stages, differentiated by colostrum, transitional milk and mature milk, did not differ in the 2 samples collectives Dortmund and Hannover. The infants' exposure was assessed by calculating their OTA intake via human milk. These results were then compared to the recently re-evaluated Tolerable Daily Intake (TDI) of 3 ng/kg body weight/day. In 29% of the cases (with 26 milk samples), the TDI of 3 ng/kg body weight/day was exceeded.In summary, infant exposure to OTA with human milk in Germany is usually low compared to several other countries. ...
Munoz K et al; Gesundheitswesen 75 (4): 194-7 (2013)
The transfer of ochratoxin A from the blood to the milk of lactating rabbit does and subsequently the exposure of their sucklings to the mycotoxin were investigated. An effective transfer of ochratoxin A from blood to milk was shown in lactating rabbit does fed a naturally-contaminated diet (10-20 g/kg of body weight/day) throughout a lactation period of 19 days. The ochratoxin A concentrations in plasma and in milk did not significantly change throughout the lactation period with a mean milk/plasma concentration ratio of 0.015. These variables were however significantly correlated (p < 0.05), as were the ingested amounts and milk concentrations. At slaughter, the highest concentration of ochratoxin A accumulated in the body of the rabbit does were found in kidney (1.2 g/kg) followed by liver (158 ng/kg), mammary gland (105 ng/kg) and muscle (38 ng/kg). A linear relationship was found between the ochratoxin A concentrations in milk and in the plasma of the sucklings, indicating an effective transfer of the toxin to the sucklings. If the same is true in humans, the exposure of the breast-fed infant to the toxin, which has been largely reported in the literature, should be a major matter of concern for human health.
Ferrufino-Guardia EV, et al; Food Addit Contam 17 (2): 167-175 (2000)

12.2.15 Probable Routes of Human Exposure

Occupational exposure to ochratoxin A may occur potentially through inhalation of dusts and dermal contact at workplaces where handling of grains, nuts, corn, cereals, and animal feeds occurs. Monitoring data indicate that the general population is exposed to ochratoxin A predominately via ingestion of and dermal contact with grains, beans, rice, maize, and pork products contaminated with this compound. (SRC)
The widespread occurrence of ochratoxin A in food and animal feed probably results human exposure ... Potential worker exposure exists for all personnel handling and storing grains, nuts, corn, cereals, and animal feeds.
DHHS/NIEHS; Seventh Annual Rpt on Carcinogens Summary p. 310 (1994)

12.2.16 Body Burden

Ochratoxin A was detected in 4 of 36 human milk samples collected in Germany at concentrations of 0.017 to 0.03 ng/mL. 9 of 50 human milk samples collected in Italy between 1989 and 1990 contained ochratoxin A at concentrations of 1.7 to 6.6 ng/mL(1).
(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 494 (1993)
Ochratoxin A levels in human blood(1).
Country
Bulgaria
Year
1984-90
No. Pos/Total No.
82/576
Content (ng/mL)
1-35
Country
Canada
Year
1988
No. Pos/Total No.
63/159
Content (ng/mL)
0.27-35.3
Country
Denmark
Year
1986-88
No. Pos/Total No.
78/144
Content (ng/mL)
0.1-13.2
Country
France
Year
NR
No. Pos/Total No.
approx 18%
Content (ng/mL)
0.1-6
Country
Germany
Year
1977-85
No. Pos/Total No.
173/306
Content (ng/mL)
0.1-14.4
Country
Germany
Year
NR
No. Pos/Total No.
4/36
Content (ng/mL)
0.017-0.03
Country
Italy
Year
1989-90
No. Pos/Total No.
9/50
Content (ng/mL)
1.7-6.6
Country
Poland
No. Pos/Total No.
9/216
Content (ng/mL)
1.3-4.8
Country
Poland
Year
1983-84
No. Pos/Total No.
77/1065
Content (ng/mL)
Mean 0.10
Country
Sweden
Year
1989
No. Pos/Total No.
38/297
Content (ng/mL)
0.3-6.7
Country
Yugoslavia
Year
1980
No. Pos/Total No.
42/639
Content (ng/mL)
1-40
Country
Yugoslavia
Year
1981-89
No. Pos/Total No.
240/17175
Content (ng/mL)
5-100
(1) IARC; Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins 56: 494 (1993)
Ochratoxin A was determined in human serum samples, collected in the south of Italy in November 1992, using ion-pair liquid chromatography and fluorescence detection. The samples were collected from healthy people (65 subjects) as well as from people with different kidney disorders. Five different kinds of kidney disorders were represented: transplanted subjects (13), chronic glomerulonephritis (8), renal calculus or cyst (6), chronic renal failure (13), and subjects treated by dialysis (28). The mean and median concentration of ochratoxin A in the healthy group was 0.53 and 0.44 ng/mL serum, respectively. The highest mean concentration was found in the group of patients treated by dialysis, 1.4 ng/mL serum. A higher incidence of samples containing > 0.44 ng ochratoxin A/mL serum was found in the dialysis group, compared to the other groups. Comparing the mean concentration by Student's t-test, a significant difference was found between the mean concentration of the healthy group and of the group of patients treated by dialysis (p < 0.01). No other significant differences were found when comparing the groups two at a time.
Breitholtz-Emanuelsson A et al; Nat Toxins 2 (6): 366-70 (1994)
... Analyses of serum samples in European countries revealed that blood from healthy humans was contaminated with ochratoxin A at concentration 0.1-14.4 ug/L. The frequency of contamination of human sera indicates continuous widespread exposure. ...
Hald B; IARC Sci Publ 115: 159-64 (1991)
For more Body Burden (Complete) data for OCHRATOXIN A (14 total), please visit the HSDB record page.

13 Associated Disorders and Diseases

14 Literature

14.1 Consolidated References

14.2 NLM Curated PubMed Citations

14.3 Springer Nature References

14.4 Thieme References

14.5 Chemical Co-Occurrences in Literature

14.6 Chemical-Gene Co-Occurrences in Literature

14.7 Chemical-Disease Co-Occurrences in Literature

15 Patents

15.1 Depositor-Supplied Patent Identifiers

15.2 WIPO PATENTSCOPE

15.3 Chemical Co-Occurrences in Patents

15.4 Chemical-Disease Co-Occurrences in Patents

15.5 Chemical-Gene Co-Occurrences in Patents

16 Interactions and Pathways

16.1 Protein Bound 3D Structures

16.1.1 Ligands from Protein Bound 3D Structures

PDBe Ligand Code
PDBe Structure Code
PDBe Conformer

16.2 Chemical-Target Interactions

17 Biological Test Results

17.1 BioAssay Results

18 Taxonomy

The LOTUS Initiative for Open Natural Products Research: frozen dataset union wikidata (with metadata) | DOI:10.5281/zenodo.5794106

19 Classification

19.1 MeSH Tree

19.2 NCI Thesaurus Tree

19.3 ChEBI Ontology

19.4 KEGG: Natural Toxins

19.5 CAMEO Chemicals

19.6 ChEMBL Target Tree

19.7 UN GHS Classification

19.8 NORMAN Suspect List Exchange Classification

19.9 CCSBase Classification

19.10 EPA DSSTox Classification

19.11 International Agency for Research on Cancer (IARC) Classification

19.12 The Natural Products Atlas Classification

19.13 LOTUS Tree

19.14 MolGenie Organic Chemistry Ontology

20 Information Sources

  1. California Office of Environmental Health Hazard Assessment (OEHHA)
  2. CAMEO Chemicals
    LICENSE
    CAMEO Chemicals and all other CAMEO products are available at no charge to those organizations and individuals (recipients) responsible for the safe handling of chemicals. However, some of the chemical data itself is subject to the copyright restrictions of the companies or organizations that provided the data.
    https://cameochemicals.noaa.gov/help/reference/terms_and_conditions.htm?d_f=false
    CAMEO Chemical Reactivity Classification
    https://cameochemicals.noaa.gov/browse/react
  3. ChEBI
  4. LOTUS - the natural products occurrence database
    LICENSE
    The code for LOTUS is released under the GNU General Public License v3.0.
    https://lotus.nprod.net/
  5. NCI Thesaurus (NCIt)
    LICENSE
    Unless otherwise indicated, all text within NCI products is free of copyright and may be reused without our permission. Credit the National Cancer Institute as the source.
    https://www.cancer.gov/policies/copyright-reuse
  6. Toxin and Toxin Target Database (T3DB)
    LICENSE
    T3DB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (T3DB) and the original publication.
    http://www.t3db.ca/downloads
  7. California Safe Cosmetics Program (CSCP) Product Database
  8. CAS Common Chemistry
    LICENSE
    The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc/4.0/
  9. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  10. European Chemicals Agency (ECHA)
    LICENSE
    Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page.
    https://echa.europa.eu/web/guest/legal-notice
    (R)-N-((5-chloro-3,4-dihydro-8-hydroxy-3-methyl-1-oxo-1H-benzo[c]pyran-7-yl)carbonyl)-3-phenylalanine
    https://echa.europa.eu/substance-information/-/substanceinfo/100.005.586
    (R)-N-((5-chloro-3,4-dihydro-8-hydroxy-3-methyl-1-oxo-1H-benzo[c]pyran-7-yl)carbonyl)-3-phenylalanine (EC: 206-143-7)
    https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/37780
  11. FDA Global Substance Registration System (GSRS)
    LICENSE
    Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required.
    https://www.fda.gov/about-fda/about-website/website-policies#linking
  12. Hazardous Substances Data Bank (HSDB)
  13. Human Metabolome Database (HMDB)
    LICENSE
    HMDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (HMDB) and the original publication (see the HMDB citing page). We ask that users who download significant portions of the database cite the HMDB paper in any resulting publications.
    http://www.hmdb.ca/citing
  14. Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
    LICENSE
    Copyright (c) 2022 Haz-Map(R). All rights reserved. Unless otherwise indicated, all materials from Haz-Map are copyrighted by Haz-Map(R). No part of these materials, either text or image may be used for any purpose other than for personal use. Therefore, reproduction, modification, storage in a retrieval system or retransmission, in any form or by any means, electronic, mechanical or otherwise, for reasons other than personal use, is strictly prohibited without prior written permission.
    https://haz-map.com/About
  15. CCSbase
    CCSbase Classification
    https://ccsbase.net/
  16. NORMAN Suspect List Exchange
    LICENSE
    Data: CC-BY 4.0; Code (hosted by ECI, LCSB): Artistic-2.0
    https://creativecommons.org/licenses/by/4.0/
    Ochratoxin A
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  17. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  18. Comparative Toxicogenomics Database (CTD)
    LICENSE
    It is to be used only for research and educational purposes. Any reproduction or use for commercial purpose is prohibited without the prior express written permission of NC State University.
    http://ctdbase.org/about/legal.jsp
  19. Therapeutic Target Database (TTD)
  20. FooDB
    LICENSE
    FooDB is offered to the public as a freely available resource. Use and re-distribution of the data, in whole or in part, for commercial purposes requires explicit permission of the authors and explicit acknowledgment of the source material (FooDB) and the original publication.
    https://foodb.ca/about
  21. International Agency for Research on Cancer (IARC)
    LICENSE
    Materials made available by IARC/WHO enjoy copyright protection under the Berne Convention for the Protection of Literature and Artistic Works, under other international conventions, and under national laws on copyright and neighbouring rights. IARC exercises copyright over its Materials to make sure that they are used in accordance with the Agency's principles. All rights are reserved.
    https://publications.iarc.fr/Terms-Of-Use
    IARC Classification
    https://www.iarc.fr/
  22. NTP Technical Reports
  23. Japan Chemical Substance Dictionary (Nikkaji)
  24. Joint FAO/WHO Expert Committee on Food Additives (JECFA)
    LICENSE
    Permission from WHO is not required for the use of WHO materials issued under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Intergovernmental Organization (CC BY-NC-SA 3.0 IGO) licence.
    https://www.who.int/about/policies/publishing/copyright
  25. KEGG
    LICENSE
    Academic users may freely use the KEGG website. Non-academic use of KEGG generally requires a commercial license
    https://www.kegg.jp/kegg/legal.html
  26. The Natural Products Atlas
    LICENSE
    The Natural Products Atlas is licensed under a Creative Commons Attribution 4.0 International License.
    https://www.npatlas.org/terms
    The Natural Products Atlas Classification
    https://www.npatlas.org/
  27. MassBank Europe
  28. MassBank of North America (MoNA)
    LICENSE
    The content of the MoNA database is licensed under CC BY 4.0.
    https://mona.fiehnlab.ucdavis.edu/documentation/license
    NCGC00162403-05_C20H18ClNO6_L-Phenylalanine, N-[[(3R)-5-chloro-3,4-dihydro-8-hydroxy-3-methyl-1-oxo-1H-2-benzopyran-7-yl]carbonyl]-
    https://mona.fiehnlab.ucdavis.edu/spectra/browse?query=exists(compound.metaData.name:%27InChIKey%27%20and%20compound.metaData.value:%27RWQKHEORZBHNRI-BMIGLBTASA-N%27)
  29. Metabolomics Workbench
  30. NIST Mass Spectrometry Data Center
    LICENSE
    Data covered by the Standard Reference Data Act of 1968 as amended.
    https://www.nist.gov/srd/public-law
  31. NMRShiftDB
  32. Protein Data Bank in Europe (PDBe)
  33. RCSB Protein Data Bank (RCSB PDB)
    LICENSE
    Data files contained in the PDB archive (ftp://ftp.wwpdb.org) are free of all copyright restrictions and made fully and freely available for both non-commercial and commercial use. Users of the data should attribute the original authors of that structural data.
    https://www.rcsb.org/pages/policies
  34. Springer Nature
  35. Thieme Chemistry
    LICENSE
    The Thieme Chemistry contribution within PubChem is provided under a CC-BY-NC-ND 4.0 license, unless otherwise stated.
    https://creativecommons.org/licenses/by-nc-nd/4.0/
  36. Wikidata
  37. Wikipedia
  38. PubChem
  39. Medical Subject Headings (MeSH)
    LICENSE
    Works produced by the U.S. government are not subject to copyright protection in the United States. Any such works found on National Library of Medicine (NLM) Web sites may be freely used or reproduced without permission in the U.S.
    https://www.nlm.nih.gov/copyright.html
  40. GHS Classification (UNECE)
  41. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  42. PATENTSCOPE (WIPO)
  43. NCBI
CONTENTS