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T-2 Toxin

PubChem CID
5284461
Structure
T-2 Toxin_small.png
T-2 Toxin_3D_Structure.png
Molecular Formula
Synonyms
  • T-2 TOXIN
  • T2 Toxin
  • 21259-20-1
  • T2-Trichothecene
  • Mycotoxin T-2
Molecular Weight
466.5 g/mol
Computed by PubChem 2.2 (PubChem release 2024.11.20)
Dates
  • Create:
    2005-11-20
  • Modify:
    2025-01-11
Description
T-2 toxin is a trichothecene mycotoxin produced by fungi of the genus Fusarium. It is a common contaminant in food and feedstuffs of cereal origin and is known to cause a range of toxic effects in humans and animals. It has a role as a mycotoxin, a cardiotoxic agent, a neurotoxin, an environmental contaminant, an apoptosis inducer, a DNA synthesis inhibitor and a fungal metabolite. It is a trichothecene, an acetate ester and an organic heterotetracyclic compound. It is functionally related to a HT-2 toxin.
T2 Toxin has been reported in Fusarium heterosporum, Fusarium chlamydosporum, and other organisms with data available.
T-2 Toxin is a type A trichothecene mycotoxin produced by Fusarium langsethiae, Fusarium poae, and Fusarium sporotrichioides that interferes with the metabolism of membrane phospholipids by inhibiting protein synthesis and disrupting DNA and RNA synthesis. It is frequently responsible for the contamination of various grain crops and elicits a severe inflammatory reaction in animals.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
T-2 Toxin.png

1.2 3D Conformer

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

[(1S,2R,4S,7R,9R,10R,11S,12S)-11-acetyloxy-2-(acetyloxymethyl)-10-hydroxy-1,5-dimethylspiro[8-oxatricyclo[7.2.1.02,7]dodec-5-ene-12,2'-oxirane]-4-yl] 3-methylbutanoate
Computed by Lexichem TK 2.7.0 (PubChem release 2024.11.20)

2.1.2 InChI

InChI=1S/C24H34O9/c1-12(2)7-18(27)32-16-9-23(10-29-14(4)25)17(8-13(16)3)33-21-19(28)20(31-15(5)26)22(23,6)24(21)11-30-24/h8,12,16-17,19-21,28H,7,9-11H2,1-6H3/t16-,17+,19+,20+,21+,22+,23+,24-/m0/s1
Computed by InChI 1.07.0 (PubChem release 2024.11.20)

2.1.3 InChIKey

BXFOFFBJRFZBQZ-QYWOHJEZSA-N
Computed by InChI 1.07.0 (PubChem release 2024.11.20)

2.1.4 SMILES

CC1=C[C@@H]2[C@](C[C@@H]1OC(=O)CC(C)C)([C@]3([C@@H]([C@H]([C@H]([C@@]34CO4)O2)O)OC(=O)C)C)COC(=O)C
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C24H34O9
Computed by PubChem 2.2 (PubChem release 2024.11.20)

2.3 Other Identifiers

2.3.1 CAS

21259-20-1

2.3.2 Deprecated CAS

11051-21-1, 22916-10-5, 22916-18-3, 25152-34-5, 26400-47-5, 27640-92-2, 36653-66-4, 60119-99-5, 9061-58-9

2.3.3 European Community (EC) Number

2.3.4 UNII

2.3.5 ChEBI ID

2.3.6 ChEMBL ID

2.3.7 DSSTox Substance ID

2.3.8 Metabolomics Workbench ID

2.3.9 NCI Thesaurus Code

2.3.10 Nikkaji Number

2.3.11 Wikidata

2.3.12 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • Fusariotoxin
  • Fusaritoxin
  • T 2 Toxin
  • T-2 Toxin
  • T-2 Toxin, alpha,4 beta-Isomer
  • T2 Toxin
  • Toxin, T-2
  • Toxin, T2

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
466.5 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2024.11.20)
Property Name
XLogP3-AA
Property Value
0.9
Reference
Computed by XLogP3 3.0 (PubChem release 2024.11.20)
Property Name
Hydrogen Bond Donor Count
Property Value
1
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2024.11.20)
Property Name
Hydrogen Bond Acceptor Count
Property Value
9
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2024.11.20)
Property Name
Rotatable Bond Count
Property Value
9
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2024.11.20)
Property Name
Exact Mass
Property Value
466.22028266 Da
Reference
Computed by PubChem 2.2 (PubChem release 2024.11.20)
Property Name
Monoisotopic Mass
Property Value
466.22028266 Da
Reference
Computed by PubChem 2.2 (PubChem release 2024.11.20)
Property Name
Topological Polar Surface Area
Property Value
121 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2024.11.20)
Property Name
Heavy Atom Count
Property Value
33
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
881
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2024.11.20)
Property Name
Isotope Atom Count
Property Value
0
Reference
Computed by PubChem
Property Name
Defined Atom Stereocenter Count
Property Value
8
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

White solid; [HSDB] White powder; [MSDSonline]

3.2.2 Color / Form

White needles from benzene & Skellysolve B; acetate deriv: amorphous solid from ether & pentane
Cole, R. J. and R. H. Cox. Handbook of Toxic Fungal Metabolites. New York: Academic Press, Inc., 1981., p. 185
Crystals
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1817
White needles
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: 467 (1993)

3.2.3 Melting Point

151-152 °C
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1817

3.2.4 Solubility

Freely soluble in ethyl alcohol, ethyl acetate, chloroform, DMSO, and other organic solvents; slightly sol in petroleum ether; very slightly soluble in water.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1817

3.2.5 Stability / Shelf Life

Stable in the solid form
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 266 (1983)

3.2.6 Optical Rotation

Specific optical rotation: (c = 2.58 in ethanol): +15 °C at 26 °C/D
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1817
Specific optical rotation: -50 deg @ 24 °C/D (0.16 in cyclohexane)
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: 266 (1983)

3.2.7 Decomposition

Hazardous decomposition products formed under fire conditions. - Carbon oxides
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html

3.2.8 Collision Cross Section

214 Ų [M+NH4]+ [CCS Type: TW; Method: calibrated with polyalanine]
212.51 Ų [M+Na]+
S61 | UJICCSLIB | Collision Cross Section (CCS) Library from UJI | DOI:10.5281/zenodo.3549476

3.2.9 Other Experimental Properties

Ester groups are saponified by alkalis, and the epoxide is opened by strong mineral acids
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 266 (1983)
Colorless, mostly crystalline solids that have been well characterized by physical and spectroscopic techniques. ... require higher polarity solvents, such as aqueous methanol or aqueous acetonitrile. /Trichothecenes/
WHO; Environ Health Criteria 105: Selected Mycotoxins: ochratoxins, trichothecenes, ergot (1990). Available from, as of Oct 11, 2103: https://www.inchem.org/documents/ehc/ehc/ehc105.htm#SectionNumber:2.1
The trichothecenes are generally stable; for example, DON (deoxynivalenol) can be stored in organic solvents, such as ethyl acetate, for a long time without any significant deterioration ... They remain unaffected when refluxed with various organic solvents and also under mildly acidic conditions.
WHO; Environ Health Criteria 105: Selected Mycotoxins: ochratoxins, trichothecenes, ergot (1990). Available from, as of Oct 11, 2103: https://www.inchem.org/documents/ehc/ehc/ehc105.htm#SectionNumber:2.1

3.3 Chemical Classes

Biological Agents -> Mycotoxins

4 Spectral Information

4.1 Mass Spectrometry

4.1.1 GC-MS

MoNA ID
MS Category
Experimental
MS Type
GC-MS
MS Level
MS1
Instrument
HITACHI M-80
Instrument Type
EI-B
Ionization Mode
positive
Top 5 Peaks

43 99.99

57 38.67

121 37.97

85 25.63

105 22.70

Thumbnail
Thumbnail
License
CC BY-NC-SA

4.1.2 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
3.56
Precursor m/z
467.227
Precursor Adduct
[M+H]+
Top 5 Peaks

467.2276 999

305.1384 610

245.1172 455

215.1067 303

365.1595 286

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
3.56
Precursor m/z
467.227
Precursor Adduct
[M+H]+
Top 5 Peaks

245.1172 999

215.1067 706

85.0648 633

227.1067 604

305.1384 592

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

4.1.3 Other MS

Authors
YAMAMOTO M, DEP. CHEMISTRY, FAC. SCIENCE, NARA WOMEN'S UNIV.
Instrument
HITACHI M-80
Instrument Type
EI-B
MS Level
MS
Ionization Mode
POSITIVE
Ionization
ENERGY 70 eV
Top 5 Peaks

43 999

57 387

121 380

85 256

105 227

Thumbnail
Thumbnail
License
CC BY-NC-SA

6 Chemical Vendors

7 Pharmacology and Biochemistry

7.1 Absorption, Distribution and Excretion

T2-Trichothecene is readily absorbed through skin & the gut in pigs & rats.
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 271 (1983)
T-2 toxin is transmitted in the milk in lactating cattle & pigs.
Humphreys, D.J. Veterinary Toxicology. 3rd ed. London, England: Bailliere Tindell, 1988., p. 301
Estimated that the eggs from chickens treated orally with 1 mg T-2 toxin/kg body weight daily for 8 consecutive days, which is equivalent to 1.6 mg/kg dietary T-2, contain 0.9 ug of this material.
Humphreys, D.J. Veterinary Toxicology. 3rd ed. London, England: Bailliere Tindell, 1988., p. 302
The radioactivity of orally admin (3)H-T2-trichothecene (1 mg/kg body wt) to mice & rats was recovered in feces (55%) & urine (15%) within 72 hr. It was distributed in the liver, kidneys & other organs, without specific accumulation.
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 272 (1983)
(3)H-T-2 Toxin given orally to mice and rats was distributed rapidly to tissues and eliminated in feces and urine. Maximal levels of radiolabel were found after 30 min in plasma of mice after oral administration ... and of guinea pigs after intramuscular injection ... . In chicks administered (3)H-T-2 toxin in the diet, maximal levels were reached by 4 hr in blood, plasma, abdominal fat, heart, kidneys, gizzard, liver and the remainder of the carcass and by 12 hr in muscle, skin, bile and gall bladder ... . The distribution of T-2 toxin in tissues of swine was similar to that in chickens ... .
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 472 (1993)

7.2 Metabolism / Metabolites

Two major metabolites were obtained from the urine of a lactating cow given 180 mg of T-2 toxin orally. They were 3'-hydroxy-HT 2 toxin & 3'-hydroxy T 2 toxin.
YOSHIZAWA T ET AL; AGRIC BIOL CHEM 46 (10): 2613-15 (1982)
Human liver enzymes deacetylate T2-trichothecene to HT2-trichothecene in vitro.
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 273 (1983)
The radioactivity of orally admin (3)H-T2-trichothecene (1 mg/kg body wt) to mice & rats was recovered in feces (55%) & urine (15%) within 72 hr. ... Analysis of the radioactivity recovered in feces of rats revealed that 2.7% of the dose was excreted as unchanged T2-trichothecene & 7.5% as 4-O-deacetylated T2-trichothecene (HT2-trichothecene)...the remaining fecal excretion products were not identified. In urine, HT2-trichothecene, representing 1.4% of the total dose & 8-hydroxydiacetoxyscirpenol (1.8%) were identified; 3 unidentified metabolites...were also isolated. The epoxide moeity...seems to be essential for its toxicological activity; the liver detoxifies T2-trichothecene, probably through epoxide hydrolase. In vitro, rat liver homogenate metabolizes T2-trichothecene to HT2-trichothecene, T2-trichothecene tetraol, 4-deacetylneosolaniol...& neosolaniol... The same metabolites were obtained from HT2-trichothecene, indicating that T2-trichothecene was preferentially hydrolyzed at the C-4 position to give NT2-trichothecene.
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 272 (1983)
Trichothecenes are sesquiterpenoid toxins produced by Fusarium species. Since these mycotoxins are very stable, there is interest in microbial transformations that can remove toxins from contaminated grain or cereal products. Twenty-three yeast species assigned to the Trichomonascus clade (Saccharomycotina, Ascomycota), including four Trichomonascus species and 19 anamorphic species presently classified in Blastobotrys, were tested for their ability to convert the trichothecene T-2 toxin to less-toxic products. These species gave three types of biotransformations: acetylation to 3-acetyl T-2 toxin, glycosylation to T-2 toxin 3-glucoside, and removal of the isovaleryl group to form neosolaniol. Some species gave more than one type of biotransformation. Three Blastobotrys species converted T-2 toxin into T-2 toxin 3-glucoside, a compound that has been identified as a masked mycotoxin in Fusarium-infected grain. This is the first report of a microbial whole-cell method for producing trichothecene glycosides, and the potential large-scale availability of T-2 toxin 3-glucoside will facilitate toxicity testing and development of methods for detection of this compound in agricultural and other products.
McCormick SP et al; Appl Environ Microbiol 78 (24): 8694-702 (2012)
For more Metabolism/Metabolites (Complete) data for T-2 TOXIN (6 total), please visit the HSDB record page.

7.3 Biological Half-Life

The plasma half-life for T-2 toxin is less than 20 minutes.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
T-2 toxin was converted to 3'-hydroxy-HT 2 when incubated with 9000 g supernatants of human or bovine liver homogenates for 75 min at 37 °C. The metabolism of T-2 toxin was more rapid in human (20 min half-life) than in bovine (40 min half-life). The metabolite was as toxic & produced emesis almost as rapidly as T-2 toxin.
ELLISON RA, KOTSONIS FN; APPL MICROBIOL 27 (2): 423-4 (1974)

7.4 Mechanism of Action

Studies with whole cells, cell-free protein synthetic system, & acid-insol cell fractions of Tetrahymena pyriformis indicated that T-2 toxin inhibited protein synthesis by impairing the 60 S ribosome subunit & inhibited RNA & dna synthesis by disturbing the cell membrane function.
IWAHASHI T ET AL; MAIKOTOKISHIN (TOKYO) 15: 31-3 (1982)
T2-trichothecene binds in vitro to active SH groups of creatine phosphokinase, lactate dehydrogenase & alcohol dehydrogenase, inhibiting their catalytic activity.
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 271
The high affinity of T2-trichothecene & higher trichothecenes to SH compounds provides a molecular basis for an interaction with the spindle fiber mechanism. ...
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 272 (1983)
T-2 toxin could inhibit synthesis of DNA and RNA both in vivo (0.75 mg/kg bw single or multiple doses) and in vitro (> 0.1-1 ng/mL).
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
For more Mechanism of Action (Complete) data for T-2 TOXIN (14 total), please visit the HSDB record page.

8 Use and Manufacturing

8.1 Uses

Sources/Uses
Trichothecene mycotoxin found in Fusarium tricinctum; Thought to be used in the past as a chemical warfare agent in Southeast Asia; [Merck Index] Produced by various Fusarium fungi; Human exposure has occurred from consumption of contaminated cereals; [HSDB] Produced mainly by Fusarium sporotrichioides; Occasionally found on cereals like wheat and maize; Caused mass human poisonings in Siberia in the last century; [IARC]
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.
Implicated as a chemical warfare agent in Southeast Asia with Nivalenol.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1817

8.2 Methods of Manufacturing

T2-trichothecene was first isolated ... from a culture of the fungus Fusarium tricinctum, strain T-2, by ethyl acetate extraction of the whole blended and lyophilized culture. The yield of toxin was 0.5%, based on dry weight of the lyophilized culture. There is no evidence that T2-trichothecene is produced commercially, but it can be readily prepared in gram quantities by culturing of Fusarium tricinctum on corn.
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 266 (1983)
This toxin is readily produced in liquid fermentations at yields approaching 1 g/L. It can also be produced in large quantities in solid fermentations. ... T-2 toxin is produced by Fusarium sporotrichioides, F. poae, F. equiseti and F. acuminatum.
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 468 (1993)

8.3 General Manufacturing Information

Type A Trichothecene
WHO; Environ Health Criteria 105: Selected Mycotoxins: ochratoxins, trichothecenes, ergot (1990). Available from, as of Oct 11, 2103: https://www.inchem.org/documents/ehc/ehc/ehc105.htm#SectionNumber:2.1

9 Identification

9.1 Analytic Laboratory Methods

Method: EPA-OW T2 Myco; Procedure: liquid chromatography/atmospheric-pressure chemical ionization - mass spectrometry; Analyte: T-2 mycotoxins; Matrix: foodstuffs; Detection Limit: 0.1 ng/g.
National Environmental Methods Index; Analytical, Test and Sampling Methods. T-2 Mycotoxins (21259-20-1). Available from, as of November 22, 2013: https://www.nemi.gov
The best technique to date for quantitating trichothecenes is gas liquid chromatography with electron capture or mass spectrometric detection.
SCOTT PM; J ASSOC OFF ANAL CHEM 65 (4): 876-83 (1982)
A microtest plate enzyme immunoassay was developed for detection of T-2 toxin in food. The lower detection limit was 2 pg/assay.
PETERS H ET AL; HOPPE-SEYLER'S Z PHYSIOL CHEM 363 (12): 1437-42 (1982)
T-2 toxin is eluted with methanol & methylene chloride from a treated ground sample, solvents removed, & residue silylated. O-trimethylsilyl deriv of T-2 toxin is detected by gas chromatography-mass spectrometry.
CHAYTOR JP, SAXBY MJ; J CHROMATOGR 237 (1): 107-13 (1982)
For more Analytic Laboratory Methods (Complete) data for T-2 TOXIN (8 total), please visit the HSDB record page.

9.2 Clinical Laboratory Methods

T-2 toxin in serum, urine, & saline was determined by a modified radioimmunoassay in which the specimens were added directly to the assay tubes without extraction. Reaction between antibody & ligands was optimal at 1 hr.
FONTELO PA ET; APPL ENVIRON MICROBIOL 45 (2): 640-3 (1983)
Methods for the analysis of T2-trichothecene
Sample Matrix
Feces, urine, tissues
Sample Preparation
Extract (acetonitrile); clean-up (XAD-2. Florisil, Sep-Pak C18); TLC (silica gel); spray (20% sulphuric acid); scrape; denitrate (bis-trimethylsilyl or trifluoroacetic anhydride)
Assay Procedure
Gas chromatography with flame-ionization determination
Limit of Detection
100 ug/kg
Sample Matrix
Feces, urine, tissues
Sample Preparation
Extract (acetonitrile); clean-up (XAD-2. Florisil, Sep-Pak C18); TLC (silica gel); spray (20% sulphuric acid); scrape; denitrate (bis-trimethylsilyl or trifluoroacetic anhydride)
Assay Procedure
Gas chromatography with mass spectrometry
Limit of Detection
1-5 ug/kg
Sample Matrix
Serum, urine
Sample Preparation
Extract (ethyl acetate); wash (water); concentrate; dissolve (methanol); dilute (water); purify (Sep-Pak C18 column)
Assay Procedure
Radioimmunoassay
Limit of Detection
0.5 ug.kg (serum); 2.5 ug/kg (urine)
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 269 (1983)

10 Safety and Hazards

10.1 Hazards Identification

10.1.1 GHS Classification

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

H300 (97.6%): Fatal if swallowed [Danger Acute toxicity, oral]

H310 (97.6%): Fatal in contact with skin [Danger Acute toxicity, dermal]

H315 (97.6%): Causes skin irritation [Warning Skin corrosion/irritation]

H330 (97.6%): Fatal if inhaled [Danger Acute toxicity, inhalation]

Precautionary Statement Codes

P260, P262, P264, P270, P271, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P332+P317, P361+P364, P362+P364, 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 41 reports by companies from 2 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.

10.1.2 Hazard Classes and Categories

Acute Tox. 1 (97.6%)

Acute Tox. 1 (97.6%)

Skin Irrit. 2 (97.6%)

Acute Tox. 1 (97.6%)

10.1.3 Hazards Summary

May cause severe irritation and tissue necrosis to skin and mucous membranes; Topical application has caused systemic toxicicity and death in animal studies; [Merck Index] A strong skin irritant; May cause blistering and necrosis to skin; Trichothecene mycotoxins causes bone marrow suppression, leukopenia, immunosuppression, and secondary sepsis; [HSDB] Within minutes, the effects of T-2 mycotoxin include irritation of the skin and injury to the GI and respiratory tracts. In severe cases patients have skin necrosis, fever, ataxia, epistaxis, chest pain, wheezing, hemoptysis, bone marrow depression, hemorrhagic diathesis, and shock. [Weinstein, p. 104]
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.

10.1.4 Fire Potential

Not flammable or combustible.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Fire: Toxins are not volatile but may be spread by efforts to extinguish the fire. Toxins may be decomposed by heat to produce other toxic gases. /Toxins - Dermally Hazardous/
Ellison, D.H., Emergency Action for Chemical and Biological Warfare Agents. CRC Press, Boca Raton, FL 1999., p. 114

10.1.5 Skin, Eye, and Respiratory Irritations

T-2 toxin produces edema, intradermal hemorrhage and necrosis of the skin.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf

10.2 Fire Fighting

10.2.1 Fire Fighting Procedures

Wear self contained breathing apparatus for fire fighting if necessary.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html

10.3 Accidental Release Measures

10.3.1 Cleanup Methods

Protection: Evacuation: Immediately isolate an area around any liquid or solid contamination for at least 200 feet in all directions. If possible, identify the agent and develop a downwind hazard diagram ... Adjust the initial isolation distance as appropriate. Based on the type of release, amount of material aerosolized, persistence of the agent and local conditions (e.g., weather, population density, time of day), shelter-in-place until the initial cloud passes may be the most appropriate course of action since timely evacuation of the threatened downwind population may not be possible. Depending on the persistence of the agent and the potential for condensation of agent from the cloud, evacuation of the threatened population after passage of the initial cloud may be appropriate. /Toxins - Dermally Hazardous/
Ellison, D.H., Emergency Action for Chemical and Biological Warfare Agents. CRC Press, Boca Raton, FL 1999., p. 114

10.3.2 Disposal Methods

SRP: At the time of review, 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.
Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html

10.3.3 Preventive Measures

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Decontamination: Casualties/personnel: Remove potentially contaminated clothing. Wash skin with soap and water. Small Areas: Wash all surfaces with undiluted household bleach insuring a minimum contact time of 10 minutes. Wash the area with soap and water followed by rinsing with copious amounts of water. Extreme care must be exercised when dealing with dry or powdered agents as Toxins may adhere to the skin or clothing and present an inhalation hazard later. /Toxins -Dermally Hazardous/
Ellison, D.H., Emergency Action for Chemical and Biological Warfare Agents. CRC Press, Boca Raton, FL 1999., p. 115

10.4 Handling and Storage

10.4.1 Storage Conditions

Keep container tightly closed in a dry and well-ventilated place. Recommended storage temperature: -20 °C Keep in a dry place.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html

10.5 Exposure Control and Personal Protection

10.5.1 Other Standards Regulations and Guidelines

An official tolerance level of 0.1 mg/kg was established to T-2 toxin in grains in the USSR in 1984.
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 470 (1993)

10.5.2 Personal Protective Equipment (PPE)

Skin protection: Handle with gloves.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Body Protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Respiratory protection Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html
Personal Protective Requirements: These Toxins pose both a severe respiratory and severe contact hazard. Toxins are generally dispersed as aerosols. Although Toxins are nonvolatile and do not pose an inhalation hazard once the aerosol has settled, residue from aerosols of Dermally Hazardous Toxins can still pose a contact threat. Wear appropriate fully encapsulating protective gear with positive pressure self-contained breathing apparatus (SCUBA). There is a significant hazard posed by contact of contaminated material with abraded skin or injection of toxins through contact with debris. Appropriate protection to avoid any potential abrasion, laceration or puncture of the skin is essential. /Toxins - Dermally Hazardous/
Ellison, D.H., Emergency Action for Chemical and Biological Warfare Agents. CRC Press, Boca Raton, FL 1999., p. 115

10.6 Stability and Reactivity

10.6.1 Hazardous Reactivities and Incompatibilities

Strong oxidizing agents.
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: hhttps://www.sigmaaldrich.com/safety-center.html
Reactivity: Varies depending on the specific Toxin but generally toxins selected for warfare purposes are not exceptionally reactive to common materials. /Toxins - Dermally Hazardous/
Ellison, D.H., Emergency Action for Chemical and Biological Warfare Agents. CRC Press, Boca Raton, FL 1999., p. 114

10.7 Other Safety Information

10.7.1 Toxic Combustion Products

Hazardous decomposition products formed under fire conditions. - Carbon oxides
Sigma-Aldrich; Material Safety Data Sheet for T-2 Toxin, Product Number: T4887, Version 4.1 (Revision Date 4/2/2014). Available from, as of April 24, 2014: https://www.sigmaaldrich.com/safety-center.html

10.7.2 History and Incidents

The potent acute toxicity and chemical stability of T-2 toxin.../and some other trichothecene mycotoxins/ make them candidates for bioterrorism. Mycotoxins may already have been used for weapons based on toxicity syndromes, typical for exposure to trichothothene mycotoxins, associated with"yellow rain" in southeast Asia and Afghanistan.
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
The Soviet Union was alleged to have provided mycotoxins to the armies of Vietnam and Laos for use against resistance forces in Laos and Cambodia and to have used mycotoxins in combat operations in Afghanistan. Confirmation of this use of mycotoxins has been difficult and controversial. T-2 toxin, nivalenol, and dexynivalenol were identified in vegetation at affected sites and both T-2 toxin and HT-2 toxin, a metabolite of T-2 toxin, were found in urine and blood samples from victims of alleged attacks. T-2 toxin was also reportedly found in high concentrations in spots found on rocks and gas masks. While mycotoxins are considered impractical as a tactical weapons, crude preparations could be readily produced and used by terrorist organizations to contaminate food or water supplies, or be released as an aerosol in small crowded areas.
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
Alimentary toxic aleukia (ATA) that occurred in the USSR in the period 1941-47 was suggested to be related to the presence of Fisarium species in mouldy over-wintered grain. An association to F. poae and F. sporotrichioides, which in later fungal cultures have been found to produce several trichothecenes including T-2 - and HT-2 toxin, was established. Extractions of the suspected wheat were also tested on the skin of animals, and showed toxic dermal effects. The most severe outbreak of the disease was in 1944, but outbreaks have also been reported in 1952, 1953, and 1955 particularly in people consuming over-wintered wheat. Clinical symptoms include vomiting, abdominal pain and diarrhea followed by leukopenia, bleeding from the nose and throat, depletion of the bone marrow and fever. Depending on severity necrotic lesions in the oral cavity, esophagus and stomach may occur and the lethality may be high. ATA in the second stage is characterised by leukopenia, hemorrhagic diathesis, granulopenia, bone marrow aplasia and sepsis. Although the symptoms characterising ATA resemble symptoms seen in cats and rodents exposed to crude extracts of infected wheat or T-2 toxin, no epidemiological studies have been reported to link trichothecenes to ATA.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
In an outbreak of toxicosis in a Chinese county 165 subjects consumed rice infected with F. heterosporum and F. Graminearum. About 50 % of the persons consuming the rice fell ill with symptoms consisting of nausea, dizziness, vomiting, abdominal distension and pain, chills and diarrhea. Samples of the suspected rice were analysed for T-2 toxin using an ELISA assay and a level of 180 - 420 mg/kg was found. Analysis for other toxins was not reported. It has to be noted that these Fusarium species are not known to produce T-2 toxin, but are known to produce several other trichothecenes such as DON, nivalenol and acetyl-DON.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
Other outbreaks of trichothecene-related disease have also been reported, one in China 1984/85 and one in India in 1987. Each involved several hundred cases. Typical symptoms were throat irritation, nausea, vomiting, abdominal pain diarrhoea and some with blood in stools. In the first case DON and zearalenon were detected, but not T-2 toxin. In the outbreak in India DON, acetyl-DON, nivalenol and T-2 toxin were detected. No information on blood cells were reported and no fatalities occurred.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf

10.7.3 Special Reports

Toxicology Review- Nutrition Reviews 31 (6): 169 (1973).
WHO; Environmental Health Criteria 105: Selected Mycotoxins: Ochratoxins, Trichothecenes, Ergot (1990)
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)

11 Toxicity

11.1 Toxicological Information

11.1.1 Evidence for Carcinogenicity

Evaluation: No data were available on the carcinogenicity to humans of toxins derived from Fusarium sporotrichioides. There is limited evidence in experimental animals for the carcinogenicity of T-2 toxin. Overall evaluation: Toxins derived from Fusarium sporotrichiodes are not classifiable as to their carcinogenicity to humans (Group 3).
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. 56 482 (1993)

11.1.2 Carcinogen Classification

IARC Carcinogenic Agent
T2-Trichothecene
IARC Carcinogenic Classes
Group 3: Not classifiable as to its carcinogenicity to humans
IARC Monographs

Volume 31: (1983) Some Food Additives, Feed Additives and Naturally Occurring Substances

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)

11.1.3 Adverse Effects

Dermatotoxin - Skin burns.

Toxic Pneumonitis - Inflammation of the lungs induced by inhalation of metal fumes or toxic gases and vapors.

11.1.4 Acute Effects

11.1.5 Toxicity Data

LC50 (rat) = 20 mg/m3/10min

11.1.6 Interactions

Experiments were conducted to determine the effect of dietary fibers on T-2 toxicosis in rats. Weanling rats were fed varying levels of cellulose, hemicellulose, lignin and pectin with and without T-2 toxin (3 ug/g feed) for 2 weeks. Only lignin showed promise of overcoming feed refusal and growth depression in animals fed T-2 toxin. Further experiments feeding alfalfa meal (0, 5, 10, 15, 20 or 25%) with and without T-2 toxin indicated that this lignin-rich feedstuff could largely overcome feed refusal and growth depression caused by the toxin. There was no effect of diet, however, on the activity of hepatic esterase, the enzyme believed to catabolize T-2 toxin. Rats were fed diets containing 0, 5, 12.5 or 20% alfalfa for 2 weeks and then dosed orally with [(3)H]T-2 toxin. Dietary alfalfa increased fecal excretion of 3H, whereas urinary excretion was unaffected. Residual (3)H in kidney and muscle was reduced with alfalfa feeding when [(3)H]T-2 toxin was administered orally. Residual (3)H in the digesta in the intestinal lumen increased. Alfalfa feeding was found to reduce intestinal transit time. It was concluded that the feeding of alfalfa reduced T-2 toxicosis in rats by binding the toxin in the intestinal lumen thereby promoting fecal excretion.
CARSON MS, SMITH TK; J NUTR 113 (2): 304-13 (1983)
Active oxygen species are reported to cause organ damage. This study was therefore designed to determine whether oxidative stress contributed to the initiation or progression of hepatic DNA damage produced by T-2 toxin. The aim of the study was also to investigate the behavior of the antioxidants coenzyme Q10 (CoQ10), and alpha-tocopherol (vitamin E) against DNA damage in the livers of mice fed T-2 toxin. Treatment of fasted mice with a single dose of T-2 toxin (1.8 or 2.8 mg/kg body weight) by oral gavage led to 76% hepatic DNA fragmentation. T-2 toxin also decreased hepatic glutathione (GSH) levels markedly. Pretreatment with CoQ10 (6 mg/kg) together with alpha tocopherol (6 mg/kg) decreased DNA damage. The CoQ10 and vitamin E showed some protection against toxic cell death and glutathione depletion caused by T-2 toxin. Oxidative damage caused by T-2 toxin may be one of the underlying mechanisms for T-2 toxin-induced cell injury and DNA damage, which eventually lead to tumourigenesis.
Atroshi F et al; Mol Aspects Med 18: PS255-8 (1997)
The objective of this study was to determine whether two antioxidant vitamins, vitamins E and C, were able to counteract the production of lipid peroxides and the corresponding toxic signs of two important but diverse mycotoxins, T-2 toxin and ochratoxin A (OA). Experiment 1 was designed in a 3 x 3 factorial arrangement using three doses of vitamin E (dl-alpha-tocopheryl acetate) in the diet of Leghorn cockerels (required level according to NRC, 10x, and 100x requirements) and three toxin treatment [no toxin (Diets 1, 2, and 3), 4 mg T-2/kg of diet (Diets 4, 5, and 6), and 2.5 mg OA/kg of diet (Diets 7, 8, and 9)]. The experimental design for Experiment 2 was the same as for Experiment 1 except that Vitamin C (0, 200, and 1,000 mg/kg of diet) was used in place of vitamin E and the concentration of T-2 in Diets 4, 5, and 6 was increased to 5 mg/kg of diet. Six replicates were used per treatment with four birds per replicate. In both experiments, OA and T-2 decreased the performance of the chicks significantly. The concentration of uric acid in the plasma increased (P < 0.001) when OA was added to the diet, whereas the supplementation of the diet with vitamin E (100x the requirement) partially counteracted this effect (P = 0.07). The presence of T-2, and especially OA, in the diet decreased the concentration of alpha-tocopherol in the liver (P < 0.001). Consistent with these findings were increased values of malondialdehyde (MDA) in the liver due to OA. In Experiment 1, vitamin E supplementation partially ameliorated the prooxidative effects of OA by decreasing the concentrations of MDA (P < 0.05). These data suggest that lipid peroxides are formed in vivo by T-2 and especially by OA and that these effects can be partially counteracted by an antioxidant such as vitamin E but not by vitamin C.
Hoehler D, Marquardt RR et al; Poult Sci 75 (12): 1508-15 (1996)
The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. /These/ results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.
Guan F et al; Rheumatol Int 33 (1): 157-66 (2013)
For more Interactions (Complete) data for T-2 TOXIN (22 total), please visit the HSDB record page.

11.1.7 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
Emergency and supportive measures. 1. Provide aggressive supportive care. Treat hypotension with IV fluids and vasopressors and respiratory failure with assisted ventilation. 2. Isolate patients with suspected plague, smallpox, or viral hemorrhagic fevers, who may be highly contagious. Patient isolation is not needed for suspected anthrax, botulism, or tularemia because person-to-person transmission is not likely. However, health care workers should always use universal precautions. /Warfare agents-biological/
OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGraw-Hill, New York, NY 2012, p. 402
Decontamination. NOTE: The clothing and skin of exposed individuals may be contaminated with spores, toxin, or bacteria. rescuers and health care providers should take precautions to avoid secondary contamination. 1. Remove all potentially contaminated clothing and wash the patient thoroughly with soap and water. 2. Dilute bleach (0.5%) and ammonia are effective for cleaning surfaces possibly contaminated with viruses and bacteria. 3. All clothing should be cleaned with hot water and bleach. /Warfare agents-biological/
OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGraw-Hill, New York, NY 2012, p. 403

11.1.8 Human Toxicity Excerpts

/SIGNS AND SYMPTOMS/ The general toxicity, hematotoxicity and immunotoxicity of T-2 toxin are considered to be the critical effects.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
/CASE REPORTS/ Accidental contact of laboratory workers with crude extracts containing T2-trichothecene (approx 100 mg/L) caused severe irritation, loss of sensitivity & desquamation of skin of the hands. A soln of crude toxin caused dermatitis of the hands & face of laboratory workers.
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 273 (1983)
/CASE REPORTS/ Alimentary toxic aleukia (ATA) that occurred in the USSR in the period 1941-47 was suggested to be related to the presence of Fusarium species in moldy over-wintered grain. An association to F. poae and F. sporotrichioides, which in later fungal cultures have been found to produce several trichothecenes including T-2 - and HT-2 toxin, was established. Extractions of the suspected wheat were also tested on the skin of animals, and showed toxic dermal effects. The most severe outbreak of the disease was in 1944, but outbreaks have also been reported in 1952, 1953, and 1955 particularly in people consuming over-wintered wheat. Clinical symptoms include vomiting, abdominal pain and diarrhea followed by leukopenia, bleeding from the nose and throat, depletion of the bone marrow and fever. Depending on severity necrotic lesions in the oral cavity, esophagus and stomach may occur and the lethality may be high. ATA in the second stage is characterized by leukopenia, hemorrhagic diathesis, granulopenia, bone marrow aplasia and sepsis. Although the symptoms characterizing ATA resemble symptoms seen in cats and rodents exposed to crude extracts of infected wheat or T-2 toxin, no epidemiological studies have been reported to link trichothecenes to ATA.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
/CASE REPORTS/ In an outbreak of toxicosis in a Chinese county 165 subjects consumed rice infected with F. heterosporum and F. Graminearum. About 50% of the persons consuming the rice fell ill with symptoms consisting of nausea, dizziness, vomiting, abdominal distension and pain, chills and diarrhea. Samples of the suspected rice were analyzed for T-2 toxin using an ELISA assay and a level of 180-420 mg/kg was found. Analysis for other toxins was not reported. It has to be noted that these Fusarium species are not known to produce T-2 toxin, but are known to produce several other trichothecenes such as /Deoxynivalenol/ DON, nivalenol and acetyl-DON.
EUROPEAN COMMISSION; Opinion of the Scientific Commitee on Food on Fisarium toxins part 5: T-2 toxin and HT-2 toxin, adopted on 30 May 2001; Available from, as of October 29, 2013: https://ec.europa.eu/food/fs/sc/scf/out88_en.pdf
For more Human Toxicity Excerpts (Complete) data for T-2 TOXIN (31 total), please visit the HSDB record page.

11.1.9 Non-Human Toxicity Excerpts

/LABORATORY ANIMALS: Acute Exposure/ Single iv admin of T-2 toxin to rabbits at dosages of 0.5 mg/kg produced alteration in several blood coagulation parameters. Activities of factors, x, vii, viii, ix, & xi were decreased by approx 40%, 6 hr after admin of T-2 toxin. T-2 toxin does not function as a vitamin K antagonist.
GENTRY PA; CAN J COMP MED 46 (4): 414-19 (1982)
/LABORATORY ANIMALS: Acute Exposure/ By histopathologic, electron microscopic, and immunochemical observation, the mechanism of cellular death was investigated in thymus, spleen, and liver of mice given intraperitoneally sublethal doses of T-2 toxin, a trichothecene mycotoxin. In the thymus and spleen of mice given 5.0 mg/kg body weight of T-2 toxin and killed 12 hours later, a massive cellular destruction characterized by chromatin condensation was evident, and electron microscopy analysis revealed the presence of apoptotic bodies. In the liver of mice given 2.5 mg/kg of T-2 toxin and killed 2 hours later, the induction of apoptotic cellular lesions was observed by electron microscopy, and Kupffer cells phagocytosed the apoptotic bodies. Such lesions were not observed in the mice killed 12 hours after receiving the toxin. In situ nick translation analysis (Tunel method) revealed DNA fragmentation in thymus, spleen, and liver shortly after administration of T-2 toxin. As previously observed in vitro, these findings indicated that T-2 toxin is a potent inducer of apoptotic cell death in thymus, spleen, and liver in vivo; especially in liver, apoptosis is induced rapidly as compared with the other tissues observed, and Kupffer cells play an important role for clearance of apoptosis.
Ihara T et al; Nat Toxins 5 (4): 141-5 (1997)
/LABORATORY ANIMALS: Acute Exposure/ T-2 toxin belongs to group of mycotoxins and is found as a natural contaminant in cereals, feed and vegetables. In the present study /investigators/ evaluated acute toxicity of dermal and subcutaneous exposure of T-2 toxin on brain oxidative stress in mice. Mice were exposed to 1 LD50 of T-2 toxin either by dermal (5.94 mg/kg) or subcutaneous (1.54 mg/kg body weight) route and sacrificed at 1, 3 and 7 days post-exposure. T-2 toxin treated animals showed time dependent increase in reactive oxygen species generation, glutathione depletion, lipid peroxidation and protein carbonyl content in brain in both the routes of exposure. Gene expression profile of antioxidant enzymes showed significant increase in superoxide dismutase and catalase in percutaneous route and glutathione reductase and glutathione peroxidase in subcutaneous route. Immunoblot analysis of antioxidant enzymes correlated with gene expression profile. T-2 toxin exposure resulted in down regulation of transcription factor Nrf2 and its downstream target genes of phase II detoxifying enzymes NQO1, Gclc, Gclm and hemeoxygenase-1. Results of /this/ study show that percutaneously and subcutaneously applied T-2 toxin can cause brain oxidative damage possibly after crossing blood-brain barrier by altering its permeability.
Chaudhary M, Rao PV; Food Chem Toxicol 48 (12): 3436-42 (2010)
/LABORATORY ANIMALS: Acute Exposure/ T-2 toxin is one of the most potent trichothecenes, and on exposure causes severe human and animal diseases. /Researchers/ investigated the dose- and time-dependent effect of T-2 toxin on certain biochemical variables, oxidative damage in terms of antioxidant enzyme activity, and gene expression profile in mice. Mice treated intraperitoneally with either 1 LD50 or 2 LD50 dose (5.61 and 11.22 mg/kg body weight, respectively) of T-2 toxin showed significant alterations in hepatic alanine amino transferase, aspartate amino transferase, and lactate dehydrogenase. Significant changes in hepatic lipid peroxidation, depletion of glutathione (GSH), and expression of heat shock protein-70 indicated oxidative damage. /Researchers/ also evaluated the activity of antioxidant enzymes and compared the gene expression profile by quantitative real-time reverse transcriptase-polymerase chain reaction. Except for glutathione reductase (GR), there was a significant increase in activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase at 1 LD50 dose. At 2 LD50 dose, SOD showed decrease in activity, whereas GST, GPx, and catalase showed significant increase. In contrast, gene expression profile showed downregulation in GR, GPx, GST, and catalase at 1 LD50 dose. At 2 LD50 dose except GSH synthetase, all other genes were downregulated. The results clearly show oxidative stress as one of the mechanisms of T-2 toxin-mediated toxicity.
Chaudhari M et al; J Biochem Mol Toxicol 23 (3): 212-21 (2009)
For more Non-Human Toxicity Excerpts (Complete) data for T-2 TOXIN (77 total), please visit the HSDB record page.

11.1.10 Non-Human Toxicity Values

LC50 Pig inhalation 1.5-3.0 mg/kg (18 hr)
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
LD50 Pig i.v. 1.21 mg/kg
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
LD50 Mice inhalation 0.16 mg/kg (24 hr)
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
LD50 Mice i.v. or i.p. 3.0-5.3 mg/kg
Hascheh WM and Beasley VR; p. 353-369 in Handbook of Toxicology of Chemical Warfare Agents; Gupta RC, ed (2009)
For more Non-Human Toxicity Values (Complete) data for T-2 TOXIN (11 total), please visit the HSDB record page.

11.2 Ecological Information

11.2.1 Ecotoxicity Values

LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 35 °C; Concentration: 160 ug/L for 16 hr /formulated product/
Eppley RM; J Assoc Off Anal Chem 57 (3): 618-20 (1974) as cited in the ECOTOX database. Available from, as of November 13, 2013
LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 30 °C; Concentration: 180 ug/L for 16 hr /formulated product/
Eppley RM; J Assoc Off Anal Chem 57 (3): 618-20 (1974) as cited in the ECOTOX database. Available from, as of November 13, 2013
LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 35 °C; Concentration: 160 ug/L for 24 hr /formulated product/
Eppley RM; J Assoc Off Anal Chem 57 (3): 618-20 (1974) as cited in the ECOTOX database. Available from, as of November 13, 2013
LC50; Species: Artemia salina (Brine Shrimp) larva; Conditions: saltwater, static, 30 °C; Concentration: 60 ug/L for 24 hr /formulated product/
Eppley RM; J Assoc Off Anal Chem 57 (3): 618-20 (1974) as cited in the ECOTOX database. Available from, as of November 13, 2013
For more Ecotoxicity Values (Complete) data for T-2 TOXIN (8 total), please visit the HSDB record page.

11.2.2 Ecotoxicity Excerpts

/BIRDS and MAMMALS/ Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.
Grizzle JM et al; Avian Dis 48 (2): 392-9 (2004)
/AQUATIC SPECIES/ Chemical induction of apoptosis in cells is believed to contribute to toxicity. Techniques for measuring apoptosis have increased in both sensitivity and number and in many cases can be readily extended to nontraditional research species. A comparison of established assays for measuring apoptosis of lymphoid cells has thus far not been performed in the fish and thus would be efficacious in assessing immunotoxicity. The present study evaluated chemical-induced immune cell apoptosis in fish (tilapia, Oreochromis niloticus) exposed to two known immunotoxic chemicals, azathioprine and T-2 toxin. Cytocentrifugation and light microscopy of leukocyte-enriched cell samples from the pronephros (i.e., the fish primary hematopoietic compartment) demonstrated chemical-related increases in apoptotic bodies. This observation was examined further with the ApoAlert Annexin V Apoptosis kit and two DNA-binding dyes employed for detecting apoptosis, 7-aminoactinomycin D (7-AAD) and propidium iodide (PI). The apoptotic probes confirmed the microscopic observations of increased apoptosis in the chemical-exposed fish. The ApoAlerttrade mark annexin V and 7-AAD assays, which discriminate early and late apoptosis/necrosis, compared well in identifying apoptotic populations. PI staining in Vindelov's solution was unable to detect early apoptosis. The present data suggest that apoptotic immune cells may be a useful marker for certain immunotoxicant exposures in fish. These findings agree with those of previous reports that fish may respond immunologically in a manner similar to mammals after immunotoxicant challenge.
Gogal RM Jr et al; Cytometry 39 (4): 310-8 (2000)
/PLANTS/ ... T-2 toxin-treated seedlings exhibited dwarfism with aberrant morphological changes (e.g. petiole shortening, curled dark-green leaves, and reduced cell size). These results imply that the phytotoxic action of trichothecenes differed among their molecular species. Cycloheximide (CHX)-treated seedlings displayed neither feature, although it is known that trichothecenes inhibit translation in eukaryotic ribosomes. Microarray analyses suggested that T-2 toxin caused a defence response, the inactivation of brassinosteroid (BR), and the generation of reactive oxygen species in Arabidopsis. This observation is in agreement with our previous reports in which trichothecenes such as T-2 toxin have an elicitor-like activity when infiltrated into the leaves of Arabidopsis.
Masuda D et al; J Exp Bot 58 (7): 1617-26 (2007)

11.2.3 Environmental Fate / Exposure Summary

T-2 Toxin is a trichothecene mycotoxin produced by fungi from the genus Fusarium growing on barley, corn, oats, rye, or wheat. Its artificial production may result in its release to the environment through various waste streams; its potential use as a biological agent will result in its direct release to the environment. If released to air, an estimated vapor pressure of 3.1X10-11 mm Hg at 25 °C indicates T-2 Toxin will exist solely in the particulate phase in the atmosphere. Particulate-phase T-2 Toxin will be removed from the atmosphere by wet and dry deposition. Trichothecenes, such as T-2 Toxin, are stable to UV light and, therefore, may not be susceptible to direct photolysis by sunlight. If released to soil, T-2 Toxin is expected to have low mobility based upon an estimated Koc of 910. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 5.6X10-19 atm-cu m/mole. T-2 Toxin is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data in soil or water were not available. If released into water, T-2 Toxin is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 14 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is expected to be an environmental fate process since this compound contains functional groups that hydrolyze under environmental conditions (pH 5 to 9). Occupational exposure to T-2 Toxin may occur through inhalation and dermal contact with this compound at workplaces where grain is handled or processed. Monitoring data indicate that the general population may be exposed to T-2 Toxin via ingestion of contaminated food and dermal contact with consumer products containing T2-toxin. (SRC)

11.2.4 Natural Pollution Sources

Fungi from the genus Fusarium, growing on barley, corn, oats, rye, or wheat, produce dozens of derivatives of tetracyclic sesquiterpenes are called trichothecenes. The best known of these mycotoxins are nivalenol, deoxynivalenol, diacetoxyscirpenol, and T-2 Toxin. /Trichothecenes/
(1) Langford RE; Introduction to Weapons of Mass Destruction. New York, NY: Wiley-Interscience p. 180 (2004)
Fungal source: Fusarium tricinctum; Fusarium culmorum (F roseum); Fusarium solani; Fusarium poae; Fusarium sporotrichioides; Trichoderma lignorum
Cole, R. J. and R. H. Cox. Handbook of Toxic Fungal Metabolites. New York: Academic Press, Inc., 1981., p. 185
A strain of Fusarium tricinctum isolated from infected corn
Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. V2: 1840
T-2 Toxin is a potent mycotoxin produced in feedstuffs by several species of the genus Fusarium(1,2) and Trichoderma lignorum(1).
(1) Wishart DS et al; HMDB: the Human Metabolome Database. ver 3.5. Showing metabocard for T2 Toxin (HMDB36600). Univ Alberta, Canada. Available from, as of Jan 31 2014: https://www.hmdb.ca/metabolites/HMDB36600
(2) NIH; PubChem. T-2 Toxin Compound Summary. Available from, as of Jan 31, 2014: https://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=442400
.../Trichothecene/ compounds are produced primarily by moulds belonging to the genus Fusarium, though other genera, including Trichoderma, Trichothecium, Myrothecium, and Stachybotrys, are also known to produce metabolites now characterized as trichothecenes. Only a few of the known trichothecenes have been found to contaminate food or animal feed ... (1). /Trichothecenes/
Trichothecene
Type A: T-2 Toxin; HT-2; Diacetoxyscirpemol; NS
Fungal species
Fusarium tricinctum, F. sprotrichioides, F. poae, F. acuminatum
Trichothecene
Type A: Diacetoxyscirpenol
Fungal species
F. equiseti, F. semitectum
Trichothecene
Type B: Deoxynivalenol, 3-Acetyl-deoxynivalenol; Nivalenol; Fusarenon
Fungal species
F. graminearum, Gibberella zeae (anamorph)
Trichothecene
Tyep B: Deoxynivalenol; 3-Acetyl-deoxynivalenol
Fungal species
F. culmorum
Trichothecene
Type B: Trichotecin
Fungal species
Trichothecium rosem
Trichothecene
Type C: Baccharin
Fungal species
Baccharis megapotamica (higher plant)
Trichothecene
Type D: Roridin A, D, E
Fungal species
Mycothecium roridum
Trichothecene
Type D: Verrucarin J
Fungal species
M. verrucaria
Trichothecene
Type D: Stratoxin G, H
Fungal species
Stachybotrys atra
(1) WHO; Environ Health Criteria 105: Selected Mycotoxins: ochratoxins, trichothecenes, ergot (1990). Available from, as of Oct 22, 2013: https://www.inchem.org/documents/ehc/ehc/ehc105.htm

11.2.5 Artificial Pollution Sources

T-2 Toxin's use as a biological agent(1) will result in its direct release to the environment(SRC).
(1) Langford RE; Introduction to Weapons of Mass Destruction. New York, NY: Wiley-Interscience p. 180 (2004)

11.2.6 Environmental Fate

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 910(SRC), determined from a structure estimation method(2), indicates that T-2 Toxin is expected to have low mobility in soil(SRC). Volatilization of T-2 Toxin from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.4X10-19 atm-cu m/mole(SRC), using a fragment constant estimation method(3). T-2 Toxin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.1X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2013).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 910(SRC), determined from a structure estimation method(2), indicates that T-2 Toxin is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 5.6X10-19 atm-cu m/mole(SRC), developed using a fragment constant estimation method(3). According to a classification scheme(4), an estimated BCF of 14(SRC), from an estimated log Kow of 2.27(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2013).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
(4) Franke C et al; Chemosphere 29: 1501-14 (1994)
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), T-2 Toxin, which has an estimated vapor pressure of 3.1X10-11 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 T-2 Toxin may be removed from the air by wet and dry deposition(SRC). Trichothecenes, such as T-2 Toxin, are stable to UV light(3) and, therefore, may not 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 Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(3) Langford RE; Introduction to Weapons of Mass Destruction. New York, NY: Wiley-Interscience p. 180 (2004)

11.2.7 Environmental Abiotic Degradation

A base-catalyzed second-order hydrolysis rate constant of 1.4X10-1 L/mole-sec(SRC) was estimated for T-2 Toxin using a structure estimation method(1); this corresponds to half-lives of 1.6 years and 59 days at pH values of 7 and 8, respectively(1). An estimated acid-catalyzed hydrolysis half-life for the epoxide moiety of 121 years at pH 7 was calculated(1). Trichothecenes, such as T-2 Toxin, are stable to UV light(2) and, therefore, may not be susceptible to direct photolysis by sunlight(SRC).
(1) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 11, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(2) Langford RE; Introduction to Weapons of Mass Destruction. New York, NY: Wiley-Interscience p. 180 (2004)
Stable in the solid state; ester groups are saponified by alkalis, and the epoxide is opened by strong mineral acids.
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: 467 (1993)

11.2.8 Environmental Bioconcentration

An estimated BCF of 14 was calculated in fish for T-2 Toxin(SRC), using an estimated log Kow of WWW(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).
(1) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm/
(2) Franke C et al; Chemosphere 29: 1501-14 (1994)

11.2.9 Soil Adsorption / Mobility

Using a structure estimation method based on molecular connectivity indices(1), the Koc of T-2 Toxin can be estimated to be 910(SRC). According to a classification scheme(2), this estimated Koc value suggests that T-2 Toxin is expected to have low mobility in soil.
(1) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm
(2) Swann RL et al; Res Rev 85: 17-28 (1983)

11.2.10 Volatilization from Water / Soil

The Henry's Law constant for T-2 Toxin is estimated as 5.5X10-18 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that T-2 Toxin is expected to be essentially nonvolatile from water and moist soil surfaces(2). T-2 Toxin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.1X10-11 mm Hg(SRC), determined from a fragment constant method(3).
(1) Meylan WM, Howard PH; Environ Toxicol Chem 10: 1283-93 (1991)
(2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990)
(3) US EPA; Estimation Program Interface (EPI) Suite. Ver. 4.1. Nov, 2012. Available from, as of Oct 15, 2013: https://www.epa.gov/oppt/exposure/pubs/episuitedl.htm

11.2.11 Food Survey Values

T-Toxin levels were measured in 189 naturally contaminated cereal crop samples from Aba area in Sichuan Province of China. Sampling was conducted in September, 2010. The incidence of T-toxin in was 11.64% and the average level was 0.565 ug/kg; a maximum of 3.332 ug/kg was detected. The limit of detection was 0.20 ug/kg(1).

Table: No. of samples/No. >Limit of detection

Region/total samples
Zangtang Co/98
Highland barley
44/3
Rice
26/8
Flour
28/0
Broad bean
0/0
Region/total samples
Aba Co/67
Highland barley
36/0
Rice
16/3
Flour
15/0
Broad bean
0/0
Region/total samples
Maerkang Co/24
Highland barley
5/2
Rice
4/2
Flour
9/0
Broad bean
6/3

(1) Wang X et al; Bull Environ Contam Toxicol 88: 396-400 (2012)
In the present study, the occurrence of eighteen mycotoxins, nine trichothecenes (deoxynivalenol, 3-acetyl-deoxynivalenol, 15-acetyl-deoxynivalenol, nivalenol, neosolaniol, diacetoxyscirpenol, fusarenon-X, T-2 toxin and HT-2 toxin), three zearalenones (zearalenone, alpha-zearalenol and beta-zearalenol), and six emergent mycotoxins, beauvericin and five enniatins (A, A1, B, B1 and B4), was monitored in different Italian organic cereals and cereal products by using a liquid chromatography coupled to triple quadrupole mass spectrometry method. A total of 93 organic cereal samples (wheat, barley, rye and oat) were collected from Italy. Limits of quantification ranged from 5 to 15 ug/kg. 80% of analyzed samples contained mycotoxins. The occurrence was 33%, 6.5%, 2%, 27%, 7%, 10% and 43% for deoxynivalenol, HT-2, T-2, nivalenol, zearalenone, beauvericin and enniatins, respectively. The major mycotoxin found was enniatin B4; it was detected in 40% of all analyzed samples and its levels ranged from 5.7 to 284.2 ug/kg. Risk assessment was evaluated by EDI calculations which were lower than TDI for all legislated Fusarium mycotoxins.
Juan C et al; Food Chem 141(3): 1747-55 (2013)
One of the first trichothecenes to be implicated in an episode of moldy corn toxicosis was T-2 Toxin; in 1972, it was reported that T-2 Toxin at the level of 2 mg/kg was present in moldy corn involved in lethal toxicosis in dairy cattle .... This event, along with increasing information regarding the acute toxicity of T-2 Toxin, prompted considerable efforts to develop methods of analysis for T-2 Toxin and the analysis of a wide range of agricultural commodities .... Only occasional samples were found to contain T-2 Toxin (incidence well below 10% in most cases), most frequently at levels <0.1 mg/kg. Usually, other trichothecenes were also found .... On the other hand, there have been isolated reports of the finding of rather high levels of T-2 Toxin, e.g., the finding of 25 mg T-2 Toxin/kg in barley ..., and 38.9 mg T-2 Toxin/kg in peanuts .... These findings, as well as reports from India of the presence of T-2 Toxin in safflower seed and sweet corn ..., and sorghum ..., and from Italy of its presence in barley, corn feed, oats, rice, and wheat ... need to be further investigated(1).
(1) WHO; Environ Health Criteria 105: Selected Mycotoxins: ochratoxins, trichothecenes, ergot (1990). Available from, as of Oct 11, 2103: https://www.inchem.org/documents/ehc/ehc/ehc105.htm#SectionNumber:2.1

11.2.12 Milk Concentrations

T-2 toxin is transmitted in the milk in lactating cattle & pigs.
Humphreys, D.J. Veterinary Toxicology. 3rd ed. London, England: Bailliere Tindell, 1988., p. 301

11.2.13 Probable Routes of Human Exposure

Occupational exposure to T-2 Toxin may occur through inhalation and dermal contact with this compound at workplaces where grain is handled or processed. Monitoring data indicate that the general population may be exposed to T-2 Toxin via ingestion of contaminated food and dermal contact with consumer products containing T2-toxin. (SRC)
Trichothecenes are useful as a warfare agent because they can enter the body through the skin, by inhalation and ingestion(1). /Trichothecenes/
(1) Langford RE; Introduction to Weapons of Mass Destruction. New York, NY: Wiley-Interscience p. 180 (2004)
There is exposure to this toxin from the consumption of cereals contaminated with T2-trichothecene.
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 274 (1983)

11.2.14 Average Daily Intake

Mycotoxins are harmful substances produced by fungi in several commodities with a widespread presence in foodstuffs. Human exposure to mycotoxins occurs mainly by contaminated food. The quantitation of mycotoxins in cereal-based food, highly consumed by different age population, is of concern. In this survey, 159 cereal-based samples classified as wheat, maize and rice-based, have been evaluated for the occurrence of patulin, deoxynivalenol, 3-acetyl-deoxynivalenol, fusarenon-X, diacetoxyscirpenol, nivalenol, neosolaniol, HT-2, T-2 and zearalenone by gas chromatography-tandem mass spectrometry. Intakes were calculated for average consumers among adults, children and infants and compared with the tolerable daily intakes (TDI). Data obtained were used to estimate the potential exposure levels. 65.4% of the samples were contaminated with at least one mycotoxin and 15.7% of the analyzed samples showed co-occurrence of mycotoxin. The dietary exposure to HT-2 and T-2 toxins was estimated as 0.010 and 0.086 ugkg-1bwd-1, amounting to 10% and 86% of the TDI, for adults and infants respectively. These results back up the necessity to take a vigilant attitude in order to minimize human intake of mycotoxins.
(1) Rodriguez-Carrasco Y et al; Chemosphere (2013)

12 Associated Disorders and Diseases

13 Literature

13.1 Consolidated References

13.2 NLM Curated PubMed Citations

13.3 Chemical Co-Occurrences in Literature

13.4 Chemical-Gene Co-Occurrences in Literature

13.5 Chemical-Disease Co-Occurrences in Literature

14 Patents

14.1 Depositor-Supplied Patent Identifiers

14.2 WIPO PATENTSCOPE

14.3 Chemical Co-Occurrences in Patents

14.4 Chemical-Disease Co-Occurrences in Patents

14.5 Chemical-Gene Co-Occurrences in Patents

15 Interactions and Pathways

15.1 Protein Bound 3D Structures

15.2 Chemical-Target Interactions

16 Biological Test Results

16.1 BioAssay Results

17 Taxonomy

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

18 Classification

18.1 MeSH Tree

18.2 ChEBI Ontology

18.3 ChemIDplus

18.4 UN GHS Classification

18.5 NORMAN Suspect List Exchange Classification

18.6 CCSBase Classification

18.7 EPA DSSTox Classification

18.8 International Agency for Research on Cancer (IARC) Classification

18.9 LOTUS Tree

18.10 EPA Substance Registry Services Tree

18.11 MolGenie Organic Chemistry Ontology

19 Information Sources

  1. CCSbase
    CCSbase Classification
    https://ccsbase.net/
  2. 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/
    T2 toxin
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  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
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    http://www.ebi.ac.uk/Information/termsofuse.html
  7. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  8. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  9. European Chemicals Agency (ECHA)
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    https://echa.europa.eu/web/guest/legal-notice
    (3α,4β,8α)-12,13-epoxytrichothec-9-ene-3,4,8,15-tetrol 4,15-diacetate 8-(3-methylbutyrate)
    https://echa.europa.eu/substance-information/-/substanceinfo/100.040.255
    (3α,4β,8α)-12,13-epoxytrichothec-9-ene-3,4,8,15-tetrol 4,15-diacetate 8-(3-methylbutyrate) (EC: 244-297-7)
    https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/90632
  10. FDA Global Substance Registration System (GSRS)
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    https://www.fda.gov/about-fda/about-website/website-policies#linking
  11. Hazardous Substances Data Bank (HSDB)
  12. Comparative Toxicogenomics Database (CTD)
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    http://ctdbase.org/about/legal.jsp
  13. Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
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    https://publications.iarc.fr/Terms-Of-Use
    IARC Classification
    https://www.iarc.fr/
  15. Japan Chemical Substance Dictionary (Nikkaji)
  16. Natural Product Activity and Species Source (NPASS)
  17. MassBank Europe
  18. MassBank of North America (MoNA)
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    https://mona.fiehnlab.ucdavis.edu/documentation/license
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  20. Wikidata
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  23. PubChem
  24. GHS Classification (UNECE)
  25. EPA Substance Registry Services
  26. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  27. PATENTSCOPE (WIPO)
  28. NCBI
CONTENTS