An official website of the United States government

Fenitrothion

PubChem CID
31200
Structure
Fenitrothion_small.png
Fenitrothion_3D_Structure.png
Molecular Formula
Synonyms
  • FENITROTHION
  • 122-14-5
  • Phenitrothion
  • Methylnitrophos
  • Sumithion
Molecular Weight
277.24 g/mol
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Dates
  • Create:
    2005-03-27
  • Modify:
    2025-01-18
Description
Fenitrothion is a brownish-yellow oil. Used as a selective acaricide and a contact and stomach insecticide against chewing and sucking insects on rice, orchard fruits, vegetables, cereals, cotton and forest. Also used against flies, mosquitoes, and cockroaches. (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
Fenitrothion is an organic thiophosphate that is O,O-dimethyl O-phenyl phosphorothioate substituted by a methyl group at position 3 and a nitro group at position 4. It has a role as an EC 3.1.1.7 (acetylcholinesterase) inhibitor, an agrochemical, an acaricide, an EC 3.1.1.8 (cholinesterase) inhibitor and an insecticide. It is an organic thiophosphate and a C-nitro compound. It is functionally related to a 4-nitro-m-cresol.
Fenitrothion is a synthetic organophosphate acetylcholinesterase inhibitor and endocrine disrupter that is used as a pesticide. It is characterized as a volatile yellow brown oily liquid, and exposure occurs by inhalation, ingestion, or contact.

1 Structures

1.1 2D Structure

Chemical Structure Depiction
Fenitrothion.png

1.2 3D Conformer

2 Names and Identifiers

2.1 Computed Descriptors

2.1.1 IUPAC Name

dimethoxy-(3-methyl-4-nitrophenoxy)-sulfanylidene-λ5-phosphane
Computed by Lexichem TK 2.7.0 (PubChem release 2021.10.14)

2.1.2 InChI

InChI=1S/C9H12NO5PS/c1-7-6-8(4-5-9(7)10(11)12)15-16(17,13-2)14-3/h4-6H,1-3H3
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.3 InChIKey

ZNOLGFHPUIJIMJ-UHFFFAOYSA-N
Computed by InChI 1.0.6 (PubChem release 2021.10.14)

2.1.4 SMILES

CC1=C(C=CC(=C1)OP(=S)(OC)OC)[N+](=O)[O-]
Computed by OEChem 2.3.0 (PubChem release 2024.12.12)

2.2 Molecular Formula

C9H12NO5PS
Computed by PubChem 2.2 (PubChem release 2021.10.14)
C9H12NO5PS

2.3 Other Identifiers

2.3.1 CAS

122-14-5

2.3.2 Deprecated CAS

12764-87-3, 54182-70-6, 94650-98-3
54182-70-6, 94650-98-3

2.3.3 European Community (EC) Number

2.3.4 UNII

2.3.5 UN Number

2.3.6 ChEBI ID

2.3.7 ChEMBL ID

2.3.8 DSSTox Substance ID

2.3.9 HMDB ID

2.3.10 ICSC Number

2.3.11 KEGG ID

2.3.12 Metabolomics Workbench ID

2.3.13 NCI Thesaurus Code

2.3.14 Nikkaji Number

2.3.15 Wikidata

2.3.16 Wikipedia

2.4 Synonyms

2.4.1 MeSH Entry Terms

  • Agria 1050
  • Fenitrothion
  • Folithion
  • Metathion
  • Methylnitrophos
  • Nitrophos
  • Sumithion
  • Sumithione

2.4.2 Depositor-Supplied Synonyms

3 Chemical and Physical Properties

3.1 Computed Properties

Property Name
Molecular Weight
Property Value
277.24 g/mol
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
XLogP3
Property Value
3.3
Reference
Computed by XLogP3 3.0 (PubChem release 2021.10.14)
Property Name
Hydrogen Bond Donor Count
Property Value
0
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
4
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Exact Mass
Property Value
277.01738065 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Monoisotopic Mass
Property Value
277.01738065 Da
Reference
Computed by PubChem 2.2 (PubChem release 2021.10.14)
Property Name
Topological Polar Surface Area
Property Value
106 Ų
Reference
Computed by Cactvs 3.4.8.18 (PubChem release 2021.10.14)
Property Name
Heavy Atom Count
Property Value
17
Reference
Computed by PubChem
Property Name
Formal Charge
Property Value
0
Reference
Computed by PubChem
Property Name
Complexity
Property Value
313
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
0
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

Fenitrothion is a brownish-yellow oil. Used as a selective acaricide and a contact and stomach insecticide against chewing and sucking insects on rice, orchard fruits, vegetables, cereals, cotton and forest. Also used against flies, mosquitoes, and cockroaches. (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
Yellow liquid; [Merck Index] Brown to yellow liquid; mp = 0.3 deg C; [ICSC] Yellow or yellowish-brown liquid; mp = 3.4 deg C; [HSDB] Brown-yellow liquid; mp = 3.4 deg C; [MSDSonline]
Liquid
BROWN-TO-YELLOW LIQUID WITH CHARACTERISTIC ODOUR.

3.2.2 Color / Form

Yellow-brown liquid
MacBean C, ed; e-Pesticide Manual. 15th ed., ver. 5.1, Alton, UK: British Crop Protection Council. Fenitrothion (122-14-5) (2008-2010)
Yellow oily liquid
Larranaga, M.D., Lewis, R.J. Sr., Lewis, R.A.; Hawley's Condensed Chemical Dictionary 16th Edition. John Wiley & Sons, Inc. Hoboken, NJ 2016., p. 610

3.2.3 Odor

Faint characteristic odor
MacBean C, ed; e-Pesticide Manual. 15th ed., ver. 5.1, Alton, UK: British Crop Protection Council. Fenitrothion (122-14-5) (2008-2010)

3.2.4 Boiling Point

244 °F at 0.05 mmHg (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
BP: 118 °C at 0.05 mm Hg
Haynes, W.M. (ed.). CRC Handbook of Chemistry and Physics. 95th Edition. CRC Press LLC, Boca Raton: FL 2014-2015, p. 3-272

3.2.5 Melting Point

0.3 °C
MacBean C, ed; e-Pesticide Manual. 15th ed., ver. 5.1, Alton, UK: British Crop Protection Council. Fenitrothion (122-14-5) (2008-2010)
3.4 °C

3.2.6 Flash Point

> 100.00 °C (> 212.00 °F)
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
157 °C

3.2.7 Solubility

In water, 38.0 mg/L at 25 °C
Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187 (1990)
Readily soluble in alcohols, esters, ketones, aromatic hydrocarbons and chlorinated hydrocarbons. In hexane 24 g/L, isopropanol 138 g/L (20 °C)
MacBean C, ed; e-Pesticide Manual. 15th ed., ver. 5.1, Alton, UK: British Crop Protection Council. Fenitrothion (122-14-5) (2008-2010)
Readily soluble in dichloromethane, 2-propanol, toluene, hardly sol in n-hexane.
Farm Chemicals Handbook 1999. Willoughby, OH: Meister Publishing Co., 1999., p. C 177
Low solubility in aliphatic hydrocarbons; soluble in most organic solvents
Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 675
0.038 mg/mL at 25 °C
Solubility in water at 20 °C: none

3.2.8 Density

1.32 at 77 °F (EPA, 1998) - Denser than water; will sink
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
1.3227 g/cu cm at 25 °C
Haynes, W.M. (ed.). CRC Handbook of Chemistry and Physics. 95th Edition. CRC Press LLC, Boca Raton: FL 2014-2015, p. 3-272
Relative density (water = 1): 1.3

3.2.9 Vapor Pressure

6e-06 mmHg at 68 °F (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
0.000054 [mmHg]
5.40X10-5 mm Hg at 20 °C
Mackay D, Shiu WY; J Phys Chem Ref Data 19: 1175-99 (1981)
Vapor pressure, Pa at 20 °C: 0.018

3.2.10 LogP

log Kow = 3.30
Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - Hydrophobic, Electronic, and Steric Constants. Washington, DC: American Chemical Society., 1995., p. 60
3.30
3.27

3.2.11 Henry's Law Constant

Henry's Law constant= 9.30X10-7 atm-cu m/mol at 25 °C
Metcalfe CD et al; Chemosphere 9: 151-5 (1980)

3.2.12 Stability / Shelf Life

Stable under recommended storage conditions.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

3.2.13 Decomposition

140-145 °C

3.2.14 Refractive Index

Index of refraction: 1.5528 at 25 °C
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 730

3.2.15 Collision Cross Section

156.22 Ų [M+H]+
S61 | UJICCSLIB | Collision Cross Section (CCS) Library from UJI | DOI:10.5281/zenodo.3549476

3.2.16 Kovats Retention Index

Standard non-polar
1885 , 1908 , 1913 , 1904 , 1922 , 1944 , 1913.5 , 1905 , 1912.2 , 1924.7 , 1875 , 1958 , 1912.3 , 1905.4 , 1900 , 1905 , 1904.6 , 1930 , 1907.8 , 1916.2
Semi-standard non-polar
1941 , 1946 , 1949 , 1921.9 , 1941 , 1931.9 , 1933.8 , 1928.7 , 1928.3 , 1927.1 , 1933.3 , 1924.2 , 1914.2 , 1944.3 , 1970 , 1931.5 , 1931.6 , 1929.8 , 1923.9 , 1954 , 1921.5 , 1934.6 , 1920.4 , 1920.8 , 1924.4 , 1946.1

3.2.17 Other Experimental Properties

Thermal decomp at 100-140 °C produces mixture of organophosphorus polymers
Menzie, C.M. Metabolism of Pesticides. U.S. Department of the Interior, Bureau of Sport Fisheries and Wildlife, Publication 127. Washington, DC: U.S. Government Printing Office, 1969., p. 292
Hydroxyl radical reaction rate constant = 6.21X10-11 cu cm/mole-sec at 25 °C
Atkinson R; Environ Toxicol Chem 7: 435-42 (1988)

3.3 Chemical Classes

3.3.1 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

3.3.2 Pesticides

Acaricides, Insecticides
Active substance -> EU Pesticides database: Not approved
Pesticides -> Organophosphate Insecticides
Environmental transformation -> Pesticides (parent, predecessor)
S60 | SWISSPEST19 | Swiss Pesticides and Metabolites from Kiefer et al 2019 | DOI:10.5281/zenodo.3544759
Pesticide (Fenitrothion) -> USDA PDB

4 Spectral Information

4.1 1D NMR Spectra

4.1.1 1H NMR Spectra

Instrument Name
Varian A-60
Source of Sample
I. Pastorek, Research Institute of Agrochemical Technology, Bratislava, Czechoslovakia
Copyright
Copyright © 2009-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.1.2 31P NMR Spectra

1 of 2
Copyright
Copyright © 2016-2024 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights Reserved.
Thumbnail
Thumbnail
2 of 2
Copyright
Copyright © 2016-2024 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights Reserved.
Thumbnail
Thumbnail

4.2 Mass Spectrometry

4.2.1 GC-MS

1 of 13
View All
Spectra ID
Instrument Type
EI-B
Ionization Mode
positive
Top 5 Peaks

260.0 99.99

79.0 88.10

93.0 59.70

47.0 47.90

125.0 22.60

Thumbnail
Thumbnail
Notes
instrument=JEOL JMS-01-SG
2 of 13
View All
Spectra ID
Instrument Type
EI-B
Ionization Mode
positive
Top 5 Peaks

277.0 99.99

109.0 75.79

125.0 71.75

260.0 34.62

278.0 11.20

Thumbnail
Thumbnail
Notes
instrument=HITACHI M-80

4.2.2 Other MS

1 of 2
Authors
KOGA M, UNIV. OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH
Instrument
JEOL JMS-01-SG
Instrument Type
EI-B
MS Level
MS
Ionization Mode
POSITIVE
Ionization
ENERGY 70 eV
Top 5 Peaks

260 999

79 881

93 597

47 479

125 226

Thumbnail
Thumbnail
License
CC BY-NC-SA
2 of 2
Authors
HASHIMOTO K, KYOTO COLLEGE OF PHARMACY
Instrument
HITACHI M-80
Instrument Type
EI-B
MS Level
MS
Ionization Mode
POSITIVE
Ionization
ENERGY 20 eV
Top 5 Peaks

277 999

109 758

125 718

260 346

278 112

Thumbnail
Thumbnail
License
CC BY-NC-SA

4.3 UV Spectra

UV Max absorption: 269.5 nm (e = 6756)
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 730

4.3.1 UV-VIS Spectra

Copyright
Copyright © 2008-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.4 IR Spectra

4.4.1 FTIR Spectra

Technique
CAPILLARY CELL: NEAT
Source of Sample
I. Pastorek, Research Institute of Agrochemical Technology, Bratislava, Czechoslovakia
Copyright
Copyright © 1980, 1981-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.4.2 Vapor Phase IR Spectra

Instrument Name
DIGILAB FTS-14
Technique
Vapor Phase
Copyright
Copyright © 1980, 1981-2024 John Wiley & Sons, Inc. All Rights Reserved.
Thumbnail
Thumbnail

4.5 Other Spectra

Intense mass spectral peaks: 109 m/z (100%), 125 m/z (97%), 277 m/z (67%), 260 m/z (42%)
Hites, R.A. Handbook of Mass Spectra of Environmental Contaminants. Boca Raton, FL: CRC Press Inc., 1985., p. 297

6 Chemical Vendors

7 Drug and Medication Information

7.1 Reported Fatal Dose

Probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon and 1 oz for 70 kg person (150 lb).
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-295

8 Agrochemical Information

8.1 Agrochemical Category

Insecticide
Pesticide active substances -> Acaricides, Insecticides

8.2 Agrochemical Transformations

Fenitrothion has known environmental transformation products that include FNO, FA-FNT, AM-FNT, DM-FNO, NMA, DM-FNT, and NMC.
S60 | SWISSPEST19 | Swiss Pesticides and Metabolites from Kiefer et al 2019 | DOI:10.5281/zenodo.3544759
Fenitrothion has known environmental transformation products that include 3-methyl-4-nitrophenol.
S78 | SLUPESTTPS | Pesticides and TPs from SLU, Sweden | DOI:10.5281/zenodo.4687924

8.3 EU Pesticides Data

Active Substance
fenitrothion
Status
Not approved [Reg. (EC) No 1107/2009]
Legislation
2007/379
ADI
0.005 mg/kg bw/day [EFSA 06]
ARfD
0.013 mg/kg bw [EFSA 06]

8.4 USDA Pesticide Data Program

9 Pharmacology and Biochemistry

9.1 MeSH Pharmacological Classification

Insecticides
Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. (See all compounds classified as Insecticides.)
Cholinesterase Inhibitors
Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system. (See all compounds classified as Cholinesterase Inhibitors.)

9.2 Absorption, Distribution and Excretion

We aimed to evaluate prognostic factors and toxicokinetics in acute fenitrothion self-poisoning. We reviewed 12 patients with fenitrothion self-poisoning admitted to the intensive care unit between 2003 and 2006. We compared the characteristics, initial vital signs, physiological scores, corrected QT interval on electrocardiogram and laboratory data (serum fenitrothion concentration and cholinesterase activity) of non-survivors and survivors. Furthermore, we evaluated the correlation between the prognostic factors and severity of poisoning (lengths of intensive care unit and hospital stays), and the toxicokinetics of the patients. In the 2 non-survivors, the estimated fenitrothion ingestion dose and the serum fenitrothion concentration at the emergency department and at 24 hr after ingestion were significantly higher than those in the 10 survivors. (p=0.008, 0.003, and 0.04, respectively). In the 10 survivors, the serum fenitrothion concentration at 24 hr after ingestion was significantly correlated with the lengths of intensive care unit and hospital stays (p=0.004 and 0.04, respectively); however, the initial vital signs, physiological scores, corrected QT interval on electrocardiogram at the emergency department, and serum cholinesterase activity did not show any correlation. In five patients successfully fitted to a two-compartment model, the distribution and elimination half-lives were 2.5 and 49.8 hr, respectively, which is compatible with the slow and prolonged clinical course of fenitrothion poisoning. Estimated fenitrothion ingestion dose and serum fenitrothion concentration at the emergency department and at 24 hr after ingestion may be useful prognostic factors in acute fenitrothion self-poisoning. Furthermore, we should take care for the patients whose serum fenitrothion concentration is high.
Inoue S et al; Clin Toxicol (Phila) 46 (6): 528-33 (2008)
An unblinded crossover study of fenitrothion 0.18 mg/kg/day [36 times the acceptable daily intake (ADI)] and 0.36 mg/kg/day (72 X ADI) administered as two daily divided doses for 4 days in 12 human volunteers was designed and undertaken after results from a pilot study. On days 1 and 4, blood and urine samples were collected for analysis of fenitrothion and its major metabolites, as well as plasma and red blood cell cholinesterase activities, and biochemistry and hematology examination. Pharmacokinetic parameters could only be determined at the higher dosage, as there were insufficient measurable fenitrothion blood levels at the lower dosage and the fenitrooxone metabolite could not be measured. There was a wide range of interindividual variability in blood levels, with peak levels achieved between 1 and 4 hr and a half-life for fenitrothion of 0.8-4.5 hr. Although based on the half-life, steady-state levels should have been achieved; the area under the curve (AUC)(0-12 hr) to AUC(0-(infinity) )ratio of 1:3 suggested accumulation of fenitrothion. There was no significant change in plasma or red blood cell cholinesterase activity with repeated dosing at either dosage level of fenitrothion, and there were no significant abnormalities detected on biochemical or hematologic monitoring.
Meaklim J et al; Environ Health Perspect 111 (3): 305-8 (2003)
The purpose of this study was to characterize tissue esterase activity and blood fenitrothion concentrations in the rat dam and fetus following in-utero exposure to the organophosphate insecticide fenitrothion. Time-mated, 8-week-old rats were gavaged on gestation day 19 with 0, 5, or 25 mg fenitrothion/kg. Fenitrothion was absorbed rapidly from the gastrointestinal tract, with peak maternal and fetal blood levels observed 0.5-1.0 hr after dosing. Fenitrothion concentrations in maternal and fetal blood were virtually identical and demonstrated a non-linear dose-response relationship. Acetylcholinesterase and carboxylesterase activities in maternal liver and blood and in fetal liver and brain decreased within 30-60 min of fenitrothion exposure. Esterase inhibition occurred at a fenitrothion dose (5 mg/kg) that has not been previously associated with reproductive toxicity, suggesting that esterase inhibition should be considered as the critical effect in risk assessments for this pesticide.
Sochaski MA et al; Xenobiotica 37 (1): 19-29
... Rapid absorption through skin.
Hartley, D. and H. Kidd (eds.). The Agrochemicals Handbook. 2nd ed. Lechworth, Herts, England: The Royal Society of Chemistry, 1987., p. A199/AUG 87
For more Absorption, Distribution and Excretion (Complete) data for Fenitrothion (17 total), please visit the HSDB record page.

9.3 Metabolism / Metabolites

Fenitrothion is metabolized unremarkably in the goat. The metabolites result from one or more of the following pathways: reduction of the nitro-group to an amine followed by conjugation with sulfate or acetate; formation of oxon; O-demethylation.
The Royal Society of Chemistry. Foreign Compound Metabolism in Mammals. Volume 6: A Review of the Literature Published during 1978 and 1979. London: The Royal Society of Chemistry, 1981., p. 303
After exposure of rats and guinea pigs to sumithion, desmethyl analog, dimethyl phosphorothioate, dimethyl phosphate, and 4 unidentified compounds were found.
Menzie, C.M. Metabolism of Pesticides. U.S. Department of the Interior, Bureau of Sport Fisheries and Wildlife, Publication 127. Washington, DC: U.S. Government Printing Office, 1969., p. 291
In comparative study of biotransformations in mice of sumithion ... and methyl parathion ... similar urinary metabolites resulted. They included methyl phosphorothioates, ... dimethyl phosphates ... and methyl phosphates ... and together with dimethyl phosphorothionate, dimethylphosphate, methyl phosphate and phosphate.
The Chemical Society. Foreign Compound Metabolism in Mammals. Volume 1: A Review of the Literature Published Between 1960 and 1969. London: The Chemical Society, 1970., p. 285
After the beetle Tribolium castaneum was topically treated with fenitrothion, main hydrolytic metabolite was o-demethyl analog. Dimethyl thiophosphate and dimethyl phosphate were also found. Fenitroxon and ... phenol were observed. Application of formic, acetic or n-propionic acid to tribolium castaneum inhibited formation of oxon and desmethyl analogs.
Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 3
For more Metabolism/Metabolites (Complete) data for Fenitrothion (14 total), please visit the HSDB record page.
Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure.

9.4 Biological Half-Life

Following administration of 10 or 3 mg fenitrothion/kg body weight per day to male native Japanese rabbits for 6 months, blood, skeletal muscle, and abdominal fat were analyzed by gas chromatography for fenitrothion and fenitrooxon. In most cases, blood and muscle did not contain any detectable amounts of either compound (detection limit for fenitrothion 0.005 or 0.002 mg/kg, and that of fenitrooxon, 0.01 mg/kg). Averages of 0.131 mg fenitrothion/kg (0.243 mg/kg maximum) and of 0.045 mg/kg were measured in the fat of rabbits dosed at 10 and 3 mg/kg body weight per day, respectively, while muscle contained a maximum of 0.006 mg fenitrothion/kg. No fenitrooxon was detected.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.67 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html
.... We reviewed 12 patients with fenitrothion self-poisoning admitted to the intensive care unit between 2003 and 2006 ... In five patients successfully fitted to a two-compartment model, the distribution and elimination half-lives were 2.5 and 49.8 hr, respectively, which is compatible with the slow and prolonged clinical course of fenitrothion poisoning ...
Inoue S et al; Clin Toxicol (Phila) 46 (6): 528-33 (2008)

9.5 Mechanism of Action

Cholinesterase inhibitor.
Hartley, D. and H. Kidd (eds.). The Agrochemicals Handbook. 2nd ed. Lechworth, Herts, England: The Royal Society of Chemistry, 1987., p. A199/AUG 87
Fenitrothion is not a strong inhibitor of AChE in vitro, but is much more so in vivo. The compound converted in the animal body to the active esterase inhibitor, fenitrooxon (O,O-dimethyl O-(3-methyl-4-nitrophenyl)phosphate), by the action of microsomal mixed function monooxygenase in liver and other tissues.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.95 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html
... /Authors/ concluded that dealkylation was an important factor among the many that contribute to the lower mammalian toxicity of fenitrothion compared with that of methylparathion. For example, the cholinesterase inhibition of fenitrooxon is less, the activation by conversion of P=S to P=O, slower, the translocation of fenitrothion more rapid, and the detoxification rate of fenitrothion, higher. Comparison of metabolites, at equitoxic doses in white mice (i.e., 17 mg methylparathion/kg and 850 mg fenitrothion/kg) showed that demethylation is the major detoxification path for fenitrothion at high doses (200-850 mg/kg), but not for methylparathion. However, inherently, demethylation of both compounds proceeds in a similar way and both fenitrothion and methylparathion are metabolized at a similar rate in vivo. ... /It was/ concluded that the relatively poorer penetration of fenitrooxon into the brain explained the selectively lower toxicity of fenitrothion rather than the dealkylation detoxification mechanism.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.95 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html

9.6 Human Metabolite Information

9.6.1 Cellular Locations

Membrane

9.7 Transformations

10 Use and Manufacturing

10.1 Uses

Sources/Uses
Used as insecticide and acaricide for cereals, cotton, orchard fruits, rice, vegetables, forestry, turf, greenhouses, animal houses, public health, and stored products; [HSDB] Used in Australia on stored wheat; Only registered in the US for use in ant and roach bait containers; [Reference #1]
Restricted Notes
Banned in the EU for use as pesticide for plant protection; [eChemPortal: ESIS]
Industrial Processes with risk of exposure
Farming (Pesticides) [Category: Industry]
For fenitrothion (USEPA/OPP Pesticide Code: 105901) ACTIVE products with label matches. /SRP: Registered for use in the USA but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
National Pesticide Information Retrieval System's Database on Database on Fenitrothion (122-14-5). Available from, as of December 15, 2016: https://npirspublic.ceris.purdue.edu/ppis/
There are no registered food uses in the U.S. Fenitrothion is used in Australia on stored wheat and there is a U.S. tolerance for imported wheat gluten. Residential: The only registered use in the U.S. is for containerized ant and roach baits in child resistant packaging.
USEPA/Office of Prevention, Pesticides and Toxic Substances; Report on FQPA Tolerance Reassessment Progress and Interim Risk management Decision for Fenitrothion p.4 EPA 738-R-00-012 (October 2000). Available from, as of January 31, 2017: https://www.epa.gov/pesticides/reregistration/status.htm
Insecticide (acaricide).
United States Environmental Protection Agency/ Prevention, Pesticides and Toxic Substances; Status of Pesticides in Registration, Reregistration, and Special Review. (1998) EPA 738-R-98-002, p. 119
For use on cereals, cotton, forests, fruit, rice, and vegetables. Fly and mosquito sprays for farms. ... for locust and grasshopper. /Not registered for food use in the USA/
Crop Protection Handbook Volume 100, Meister Media Worldwide, Willoughby, OH 2014, p. 294
This is a man-made compound that is used as a pesticide.

10.1.1 Use Classification

Environmental transformation -> Pesticides (parent, predecessor)
S60 | SWISSPEST19 | Swiss Pesticides and Metabolites from Kiefer et al 2019 | DOI:10.5281/zenodo.3544759
INSECTICIDES

10.2 Methods of Manufacturing

Preparation: Belgium patent 594669 (1960 to Sumitomo); Belgium patent 596091 (1960 to Bayer).
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 730
PRODUCED BY REACTION OF O,O-DIMETHYL PHOSPHOROCHLORIDOTHIOATE WITH ALKALI METAL SALT OF 3-METHYL-4-NITROPHENOL.
Spencer, E. Y. Guide to the Chemicals Used in Crop Protection. 7th ed. Publication 1093. Research Institute, Agriculture Canada, Ottawa, Canada: Information Canada, 1982., p. 289

10.3 Impurities

Technical grade fenitrothion contains the S-methyl tautomer, which is formed from fenitrothion in varying amounts in presence of heat. This compound, which is much more toxic than the O-methyl compound, occurs in fenitrothion in concentrations ranging from 0.4 to 4%.
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-295
The analysis of technical organophosphorus insecticides by (31)Phosphorous nuclear magnetic resonance showed the major known toxic contaminants to be simple trialkyl phosphorothio- and -dithioic acid esters and the S-alkyl insecticide isomers. Small amt of the bis derivatives & the dithiopyrophosphate were also detected. These contaminants included both byproducts from the synthesis as well as degradation products. This procedure was used to analyze the following technical grade products: ronnel, sulfotepp, methyl parathion, dimethoate, malathion, methidathion, ethion, phosalone, & fenitrothion. /Organophosphorous insecticides/
Greenhalgh R et al; J Agric Food Chem 31 (4): 710-3 (1983)

10.4 Formulations / Preparations

Sumithion Technical (Sumitomo Chemical America, Inc): Active ingredient: Fenitrothion 94.2%.
National Pesticide Information Retrieval System's Database on Fenitrothion (122-14-5). Available from, as of December 15, 2016: https://npirspublic.ceris.purdue.edu/ppis/
Dust, emulsifiable concentrate, flowable, fogging concentrate, granules, oil-based liquid spray, ULV, wettable powder.
Crop Protection Handbook Volume 100, Meister Media Worldwide, Willoughby, OH 2014, p. 294
Premix Partners: Cypermethrin; Esfenvalerate; Fenobucarb; Fenpropathrin; Fenvalerate; Methabenzithiazuron; d-Tetramethrin; Trichlorfon.
Crop Protection Handbook Volume 100, Meister Media Worldwide, Willoughby, OH 2014, p. 294

10.5 General Manufacturing Information

The WHO Recommended Classification of Pesticides by Hazard identifies Fenitrothion (technical grade) as Class II: moderately hazardous; Main Use: insecticide.
WHO International Programme on Chemical Safety; The WHO Recommended Classification of Pesticides by Hazard and Guidelines to Classification 2009 p.27 (2010)

11 Identification

11.1 Analytic Laboratory Methods

Method: EPA-OW/OST 1699; Procedure: high resolution gas chromatography with high resolution mass spectrometry; Analyte: fenitrothion; Matrix: water, soil, sediment, biosolids; Detection Limit: 24 pg/L.
National Environmental Methods Index; Analytical, Test and Sampling Methods. Fenitrothion (122-14-5). Available from, as of December 22, 2016: https://www.nemi.gov
Method: EPA-RCA 8141B (GC-FPD); Procedure: gas chromatography with flame photometric detector; Analyte: fenitrothion; Matrix: water, soil, waste samples; Detection Limit: not provided.
National Environmental Methods Index; Analytical, Test and Sampling Methods. Fenitrothion (122-14-5). Available from, as of December 22, 2016: https://www.nemi.gov
Method: EPA-RCA 8141B (GC-NPD); Procedure: gas chromatography with a nitrogen-phosphorus detector (NPD); Analyte: fenitrothion; Matrix: water, soil, waste samples; Detection Limit: not provided.
National Environmental Methods Index; Analytical, Test and Sampling Methods. Fenitrothion (122-14-5). Available from, as of December 22, 2016: https://www.nemi.gov
GC determination in stored barley.
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 730
For more Analytic Laboratory Methods (Complete) data for Fenitrothion (17 total), please visit the HSDB record page.

11.2 Clinical Laboratory Methods

The measurement of blood cholinesterase (ChE) activities is adopted worldwide for biological monitoring of exposure to organophosphorus insecticides (OPs). Recent development of analytical chemistry has made sensitive quantification possible of non-specific OP metabolites, dialkylphosphates, in urine as a biomarker of low-level OP exposure. In this study, we established a method for quantification of urinary 3-methyl-4-nitrophenol (MNP), a specific metabolite of fenitrothion (FNT), and a parathion metabolite p-nitrophenol (PNP), using gas chromatography-mass spectrometry. The limits of detection of MNP and PNP were 0.3 and 0.5 ug/L, respectively. The method enabled the quantification of both free and conjugated metabolites. This method was actually applied to monitor human urine in summer and winter in FNT sprayers (n=29 and 9, respectively) and control workers (n=17 and 29, respectively). Geometric mean total MNP concentrations (ug/gcreatinine) in the FNT sprayers (28.8 in summer and 8.6 in winter) were significantly higher than those of the controls (3.1 in summer and 2.3 in winter) in both seasons. Among the sprayers, total MNP concentrations in summer were significantly higher than in winter. In contrast, no significant difference in total PNP concentrations was observed between FNT sprayers (geometric mean 3.4 in summer and 3.0 in winter) and controls (3.6 in summer and 2.1 in winter). No seasonal difference was observed in each group. In conclusion, the present new method is sensitive enough for biological monitoring of FNT and parathion metabolites even in a non-spraying population.
Okamura A et al; Toxicol Lett 210 (2): 220-4 (2012)
Method: EPA-OW/OST 1699; Procedure: high resolution gas chromatography with high resolution mass spectrometry; Analyte: fenitrothion; Matrix: tissue; Detection Limit: 24 pg/L.
National Environmental Methods Index; Analytical, Test and Sampling Methods. Fenitrothion (122-14-5). Available from, as of December 22, 2016: https://www.nemi.gov

12 Safety and Hazards

12.1 Hazards Identification

12.1.1 GHS Classification

1 of 6
View All
Pictogram(s)
Irritant
Environmental Hazard
Signal
Warning
GHS Hazard Statements

H302 (50.4%): Harmful if swallowed [Warning Acute toxicity, oral]

H312 (49.6%): Harmful in contact with skin [Warning Acute toxicity, dermal]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (55.6%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

Precautionary Statement Codes

P264, P270, P273, P280, P301+P317, P302+P352, P317, P321, P330, P362+P364, P391, 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 117 reports by companies from 5 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.

12.1.2 Hazard Classes and Categories

Acute Tox. 4 (50.4%)

Acute Tox. 4 (49.6%)

Aquatic Acute 1 (100%)

Aquatic Chronic 1 (55.6%)

Acute toxicity - category 4

Hazardous to the aquatic environment (acute) - category 1

Hazardous to the aquatic environment (chronic) - category 1

12.1.3 Health Hazards

This compound is an organophosphate insecticide. It is a highly toxic cholinesterase inhibitor, that acts on the nervous system. Does not cause delayed neurotoxicity and contact produces little irritation. (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.

12.1.4 Fire Hazards

When heated to decomposition, it emits very toxic fumes of oxides of nitrogen, phosphorus and sulfur. Decomposition at 212-284F produces a mixture of organophosphorus polymers. Unstable in alkaline media. Stable for 2 years if stored at 68-77F. Do not store above 104F. (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
Combustible. Liquid formulations containing organic solvents may be flammable. Gives off irritating or toxic fumes (or gases) in a fire.

12.1.5 Hazards Summary

A skin and eye irritant; Can be absorbed through skin; A cholinesterase inhibitor that may affect the nervous system causing convulsions, respiratory failure, and death; [ICSC] Some evidence of contact dermatitis following exposure; No evidence of delayed neurotoxicity; [HSDB] A very toxic cholinesterase inhibitor that does not cause delayed neurotoxicity; [CAMEO] The average of two baseline respective cholinesterase activity determinations three days apart, with no exposures to enzyme inhibiting pesticides for at least 30 days, is recommended for each worker prior to exposure to cholinesterase inhibitors because of large inter-individual differences in published baseline values. To be established at least once a year. Removal from workplace exposures is recommended until the cholinesterase activity returns to within 20% of baseline. [TLVs and BEIs]
TLVs and BEIs - _Threshold Limit Values for Chemical Substances and Physical Agents & Biological Exposure Indices. _Cincinnati: ACGIH, 2020.

12.2 First Aid Measures

Inhalation First Aid
Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer immediately for medical attention.
Skin First Aid
Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .
Eye First Aid
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Ingestion First Aid
Rinse mouth. Refer immediately for medical attention.

12.2.1 First Aid

Warning: Effects may be delayed up to 12 hours. Caution is advised.

Note: Fenitrothion is a cholinesterase inhibitor.

Signs and Symptoms of Fenitrothion Exposure: Acute exposure to fenitrothion may produce the following signs and symptoms: sweating, pinpoint pupils, blurred vision, headache, dizziness, profound weakness, muscle spasms, seizures, and coma. Mental confusion and psychosis may occur. Excessive salivation, nausea, vomiting, anorexia, diarrhea, and abdominal pain may also occur. The heart rate may decrease following oral exposure or increase following dermal exposure. Chest pain may be noted. Hypotension (low blood pressure) may be observed, although hypertension (high blood pressure) is not uncommon. Respiratory symptoms include dyspnea (shortness of breath), pulmonary edema, respiratory depression, and respiratory paralysis.

Emergency Life-Support Procedures: Acute exposure to fenitrothion exposure may require decontamination and life support for the victims. Emergency personnel should wear protective clothing appropriate to the type and degree of contamination. Air-purifying or supplied-air respiratory equipment should also be worn, as necessary. Rescue vehicles should carry supplies such as plastic sheeting and disposable plastic bags to assist in preventing spread of contamination.

Inhalation Exposure:

1. Move victims to fresh air. Emergency personnel should avoid self-exposure to fenitrothion.

2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

3. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

4. Transport to a health care facility.

Dermal/Eye Exposure:

1. Remove victims from exposure. Emergency personnel should avoid self-exposure to fenitrothion.

2. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

3. Remove contaminated clothing as soon as possible.

4. If eye exposure has occurred, eyes must be flushed with lukewarm water for at least 15 minutes.

5. Wash exposed skin areas three times with soap and water.

6. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

7. Transport to a health care facility.

Ingestion Exposure:

1. Evaluate vital signs including pulse and respiratory rate, and note any trauma. If no pulse is detected, provide CPR. If not breathing, provide artificial respiration. If breathing is labored, administer oxygen or other respiratory support.

2. Obtain authorization and/or further instructions from the local hospital for administration of an antidote or performance of other invasive procedures.

3. Vomiting may be induced with syrup of Ipecac. If elapsed time since ingestion of fenitrothion is unknown or suspected to be greater than 30 minutes, do not induce vomiting and proceed to Step

4. Ipecac should not be administered to children under 6 months of age.Warning: Ingestion of fenitrothion may result in sudden onset of seizures or loss of consciousness. Syrup of Ipecac should be administered only if victims are alert, have an active gag-reflex, and show no signs of impending seizure or coma. If ANY uncertainty exists, proceed to Step

4.The following dosages of Ipecac are recommended: children up to 1 year old, 10 mL (1/3 oz); children 1 to 12 years old, 15 mL (1/2 oz); adults, 30 mL (1 oz). Ambulate (walk) the victims and give large quantities of water. If vomiting has not occurred after 15 minutes, Ipecac may be readministered. Continue to ambulate and give water to the victims. If vomiting has not occurred within 15 minutes after second administration of Ipecac, administer activated charcoal.

4. Activated charcoal may be administered if victims are conscious and alert. Use 15 to 30 g (1/2 to 1 oz) for children, 50 to 100 g (1-3/4 to 3-1/2 oz) for adults, with 125 to 250 mL (1/2 to 1 cup) of water.

5. Promote excretion by administering a saline cathartic or sorbitol to conscious and alert victims. Children require 15 to 30 g (1/2 to 1 oz) of cathartic; 50 to 100 g (1-3/4 to 3- 1/2 oz) is recommended for adults.

6. Transport to a health care facility. (EPA, 1998)

U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.

12.3 Fire Fighting

(Non-Specific -- Organophosphate Pesticide n.o.s.) Move containers from fire area if you can do so without risk. Fight fire from maximum distance. Dike fire control water for later disposal; do not scatter the material. Wear positive pressure breathing apparatus and special protective clothing.

This compound is an organophosphate insecticide.

Small fires: dry chemical, carbon dioxide, water spray, or foam. Large fires: water spray, fog or foam. (EPA, 1998)

U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
Use water spray, powder, foam, carbon dioxide.

12.3.1 Fire Fighting Procedures

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.4 Accidental Release Measures

12.4.1 Isolation and Evacuation

Excerpt from ERG Guide 131 [Flammable Liquids - Toxic]:

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

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)

12.4.2 Spillage Disposal

Personal protection: chemical protection suit including self-contained breathing apparatus. Absorb remaining liquid in sand or inert absorbent. Collect leaking liquid in covered containers. Then store and dispose of according to local regulations. Do NOT wash away into sewer. Do NOT let this chemical enter the environment.

12.4.3 Cleanup Methods

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.4.4 Disposal Methods

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.
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; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.4.5 Preventive Measures

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
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; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.5 Handling and Storage

12.5.1 Nonfire Spill Response

(Non-Specific -- Organophosphate Pesticide n.o.s.) Keep unnecessary people away; isolate hazard area and deny entry. Stay upwind; keep out of low areas. Ventilate closed spaces before entering them. Remove and isolate contaminated clothing at the site. Do not touch spilled material; stop leak if you can do so without risk. Use water spray to reduce vapors.

Small spills: absorb with sand or other noncombustible absorbent material and place into containers for later disposal.

Large spills: dike far ahead of spill for later disposal. (EPA, 1998)

U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.

12.5.2 Safe Storage

Provision to contain effluent from fire extinguishing. Separated from food and feedstuffs. Keep in a well-ventilated room.

12.5.3 Storage Conditions

Conditions for safe storage, including any incompatibilities: Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Recommended storage temperature 2-8 °C Storage class (TRGS 510): Non-combustible, acute toxic Cat. 1 and 2 / very toxic hazardous materials
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
/Storage temperature should be less than 40 °C on account of the tendency/ to isomerize.
Hartley, D. and H. Kidd (eds.). The Agrochemicals Handbook. 2nd ed. Lechworth, Herts, England: The Royal Society of Chemistry, 1987., p. A199/Aug 87

12.6 Exposure Control and Personal Protection

Exposure Summary
Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]
ACGIH - Documentation of the TLVs and BEIs, 7th Ed. Cincinnati: ACGIH Worldwide, 2020.
TLVs and BEIs - _Threshold Limit Values for Chemical Substances and Physical Agents & Biological Exposure Indices. _Cincinnati: ACGIH, 2020.

12.6.1 Inhalation Risk

No indication can be given about the rate at which a harmful concentration of this substance in the air is reached on evaporation at 20 °C.

12.6.2 Effects of Short Term Exposure

The substance is irritating to the eyes and skin. The substance may cause effects on the nervous system. This may result in convulsions, respiratory failure and death. Cholinesterase inhibition. The effects may be delayed. Medical observation is indicated.

12.6.3 Effects of Long Term Exposure

Cholinesterase inhibition. Cumulative effects are possible. See Acute Hazards/Symptoms.

12.6.4 Acceptable Daily Intakes

Acceptable Daily Intake: 0-0.001 mg/kg body-wt.
Nat'l Research Council Canada; Fenitrothion: The Effects of its Use on Environmental Quality and its Chemistry p.129 (1975) NRCC No. 14104
FAO/WHO ADI: 0.005 mg/kg
FAO/WHO; Pesticide Residues in Food - 1989. Evaluations Part 1 - Residues p.351 Plant & Prod Protect Paper 100 (1989)

12.6.5 Allowable Tolerances

Tolerances are established for residues of the insecticide fenitrothion, O,O-dimethyl O-(4-nitro-m-tolyl) phosphorothioate, from the postharvest application of the insecticide to stored wheat in Australia, in or on the following food commodity: wheat, gluten 3.0 ppm. There are no USA registrations on food commodities since 1987.
40 CFR 180.540 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of December 5, 2016: https://www.ecfr.gov

12.6.6 Personal Protective Equipment (PPE)

For emergency situations, wear a positive pressure, pressure-demand, full facepiece self-contained breathing apparatus (SCBA) or pressure- demand supplied air respirator with escape SCBA and a fully-encapsulating, chemical resistant suit. (EPA, 1998)
U.S. Environmental Protection Agency. 1998. Extremely Hazardous Substances (EHS) Chemical Profiles and Emergency First Aid Guides. Washington, D.C.: U.S. Government Printing Office.
Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
Skin protection: Handle with gloves.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: 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; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) 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; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html
While handling, wear protective gloves & goggles or full face shield.
Farm Chemicals Handbook 1984. Willoughby, Ohio: Meister Publishing Co., 1984., p. C-101

12.6.7 Preventions

Fire Prevention
NO open flames.
Exposure Prevention
PREVENT GENERATION OF MISTS! AVOID EXPOSURE OF ADOLESCENTS AND CHILDREN! IN ALL CASES CONSULT A DOCTOR!
Inhalation Prevention
Use ventilation, local exhaust or breathing protection.
Skin Prevention
Protective gloves. Protective clothing.
Eye Prevention
Wear face shield or eye protection in combination with breathing protection.
Ingestion Prevention
Do not eat, drink, or smoke during work. Wash hands before eating.

12.7 Stability and Reactivity

12.7.1 Air and Water Reactions

No rapid reaction with air. No rapid reaction with water.

12.7.2 Reactive Group

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

Nitro, Nitroso, Nitrate, and Nitrite Compounds, Organic

12.7.3 Reactivity Profile

Organophosphates, such as FENITROTHION, are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.

12.7.4 Hazardous Reactivities and Incompatibilities

Incompatible materials: Strong oxidizing agents.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.8 Transport Information

12.8.1 DOT Emergency Guidelines

/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
U.S. Department of Transportation. 2016 Emergency Response Guidebook. Washington, D.C. 2016
/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
U.S. Department of Transportation. 2016 Emergency Response Guidebook. Washington, D.C. 2016
/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Public Safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind, uphill and/or upstream. Ventilate closed spaces before entering. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
U.S. Department of Transportation. 2016 Emergency Response Guidebook. Washington, D.C. 2016
/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
U.S. Department of Transportation. 2016 Emergency Response Guidebook. Washington, D.C. 2016
For more DOT Emergency Guidelines (Complete) data for Fenitrothion (16 total), please visit the HSDB record page.

12.8.2 Shipping Name / Number DOT/UN/NA/IMO

UN 2784; Organophosphorus pesticides, liquid, flammable, toxic, flash point less than 23 °C
UN 2783; Organophosphorus pesticides, solid, toxic
UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, flash point not less than 23 °C
UN 3018; Organophosphorus pesticides, liquid, toxic
For more Shipping Name/ Number DOT/UN/NA/IMO (Complete) data for Fenitrothion (8 total), please visit the HSDB record page.

12.8.3 Shipment Methods and Regulations

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
49 CFR 171.2 (USDOT); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of December 13, 2016: https://www.ecfr.gov
The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, toxic, flammable; and Organophosphorus pesticide, liquid, toxic are included on the dangerous goods list. /Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, toxic, flammable; and Organophosphorus pesticide, liquid, toxic/
International Air Transport Association. Dangerous Goods Regulations. 57th Edition. Montreal, Quebec Canada. 2016., p. 292
The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. /Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic, flashpoint less than 23 °C; Organophosphorus pesticide, liquid, toxic, flammable, flashpoint not less than 23 °C; and Organophosphorus pesticide, liquid, toxic are included on the dangerous goods list. /Organophosphorus pesticide, liquid, flammable, toxic, flashpoint less than 23 °C; Organophosphorus pesticide, liquid, toxic, flammable, flashpoint not less than 23 °C; and Organophosphorus pesticide, liquid, toxic/
International Maritime Organization. IMDG Code. International Maritime Dangerous Goods Code Volume 2 2014, p. 135, 149

12.8.4 DOT Label

Poison Flammable Liquid

12.8.5 Packaging and Labelling

Do not transport with food and feedstuffs. Severe marine pollutant.

12.8.6 EC Classification

Symbol: Xn, N; R: 22-50/53; S: (2)-60-61

12.8.7 UN Classification

UN Hazard Class: 6.1; UN Pack Group: III

12.9 Regulatory Information

California Safe Cosmetics Program (CSCP) Reportable Ingredient

Hazard Traits - Developmental Toxicity; Neurotoxicity

Authoritative List - CECBP - Priority Chemicals

Report - if used as a fragrance or flavor ingredient

Status Regulation (EC)
2007/379
REACH Registered Substance
New Zealand EPA Inventory of Chemical Status
Fenitrothion: Does not have an individual approval but may be used under an appropriate group standard

12.9.1 FIFRA Requirements

Tolerances are established for residues of the insecticide fenitrothion, O,O-dimethyl O-(4-nitro-m-tolyl) phosphorothioate, from the postharvest application of the insecticide to stored wheat in Australia, in or on the following food commodity: wheat, gluten. There are no USA registrations on food commodities since 1987.
40 CFR 180.540 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of December 5, 2016: https://www.ecfr.gov
EPA has concluded, after completing its assessment of the cumulative risks associated with exposures to all of the OPs /including fenitrothion/, that: (1) the pesticides covered by the IREDs that were pending the results of the OP cumulative assessment (listed in Attachment A) are indeed eligible for reregistration; and (2) the pesticide tolerances covered by the IREDs and TREDs that were pending the results of the OP cumulative assessment (listed in Attachment A) meet the safety standard under Section 408(b)(2) of the FFDCA. Thus, with regard to the OPs, EPA has fulfilled its obligations as to FFDCA tolerance reassessment and FIFRA reregistration, other than product-specific reregistration.
USEPA/Office of Prevention, Pesticides and Toxic Substances; Reregistration Eligibility Decision (RED) for Fenitrothion p.1 (July 2006). Available from, as of January 31, 2017: https://www.epa.gov/pesticides/reregistration/status.htm
The Agency has completed its assessment of the dietary risk of fenitrothion but has not considered the cumulative effects of organophosphates as a class. Based on review of the generic and other data, EPA has sufficient information on the human health effects of fenitrothion to make an interim decision as part of the tolerance reassessment process under FQPA. Although the Agency has not yet completed its cumulative risk assessment for the organophosphates, the Agency has completed its assessment of risk from dietary exposure to fenitrothion alone in order to determine whether any risk reduction measures are necessary to allow the continued importation of wheat gluten containing fenitrothion, pending completion of the cumulative assessment. As a result of its assessment, EPA has determined that dietary risk from exposure to fenitrothion does not exceed the Agency's level of concern. Therefore, no mitigation is necessary and no further actions are warranted at this time. The Agency may determine that further action is necessary after assessing the cumulative risk of the organophosphate class. At that time, the Agency will also address any other outstanding risk concerns that may arise. ... Because the Agency has not yet completed the cumulative risk assessment for the organophosphates, this interim decision does not specifically address the reassessment of the existing fenitrothion food residue import tolerance as called for by the FQPA. When the Agency has completed the cumulative assessment, the fenitrothion tolerance will be reassessed in that light. At that time, the Agency will reassess fenitrothion along with the other organophosphate pesticides to complete the FQPA requirements.
USEPA/Office of Prevention, Pesticides and Toxic Substances; Report on FQPA Tolerance Reassessment Progress and Interim Risk management Decision for Fenitrothion p.8 EPA 738-R-00-012 (October 2000). Available from, as of January 31, 2017: https://www.epa.gov/pesticides/reregistration/status.htm
The Agency has determined that fenitrothion uses as currently registered pose adverse effects to humans, aquatic organisms and wildlife. The technical registrant, Sumitomo Chemical Company, has submitted a draft label for Sumithion 8E significantly reducing fenitrothion use on ornamentals. These proposed label changes have mitigated human health and ecological impact concerns making the high-pressure handwand treatment of ornamentals use eligible for reregistration. This eligibility determination for reregistration is contingent upon all ornamental end-use product labels (there are three products registered for use on ornamentals) being revised as proposed. On February 28, 1995 the registrant requested voluntary cancellation of the mosquito (malaria) control uses of fenitrothion. The Agency defers making a regulatory decision on both the low-pressure handwand and knapsack/backpack methods of application until chemical-specific worker exposure studies are submitted. Uncertainties in the existing worker exposure database do not allow the Agency to determine, with confidence, the appropriate MOEs for these exposure scenarios. However, the Agency believes it is in the public's best interest to implement the human health and ecological effect exposure/risk mitigation measures negotiated with the registrant at this time. Therefore, the Agency has decided not to delay issuing the fenitrothion RED until these studies are submitted and reviewed. The Agency is requiring the registrant to submit the worker exposure studies on an accelerated schedule, i.e., one year from issuance of this document. Details concerning the required label changes can be found in Section V, Actions Required by Registrants. When the chemical specific exposure data required by this RED are received, the Agency will make a regulatory decision regarding the reregistration eligibility of the low-pressure handwand and knapsack/backpack methods of application. Fenitrothion has significant potential for causing adverse effects in aquatic organisms, wildlife and the environment. Sumitomo Chemical Co. has proposed eliminating the highest risk uses, and reducing the maximum application rate for all other uses. The proposed label changes and the fact that this insecticide is not widely used (<1% of U.S. nursery acreage are treated annually) were given consideration in making the reregistration decision for this insecticide. The high-pressure handwand treatment of ornamentals and the two bait formulations are eligible for reregistration.
USEPA/Office of Prevention, Pesticides and Toxic Substances; Reregistration Eligibility Decision Document for Fenitrothion p.44 EPA 738-R-95-018 (July 1995). Available from, as of January 31, 2017: https://www.epa.gov/pesticides/reregistration/status.htm
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer safety standards, such as those described in the Food Quality Protection Act of 1996. Fenitrothion is found on List A, which contains most pesticides that are used on foods and, hence, have a high potential for human exposure. List A consists of the 194 chemical cases (or 350 individual active ingredients) for which EPA issued registration standards prior to FIFRA '88. Case No: 0445; Pesticide type: insecticide (acaricide); Registration Standard Date: 07/01/87; Case Status: RED Approved 03/95; OPP has made a decision that some/all uses of the pesticide are eligible for reregistration, as reflected in a Reregistration Eligibility Decision (RED) document.; Active ingredient (AI): Fenitrothion; Data Call-in (DCI) Date(s): 06/28/91, 07/25/95; AI Status: OPP has completed a Reregistration Eligibility Decision (RED) document for the case/AI.
United States Environmental Protection Agency/ Prevention, Pesticides and Toxic Substances; Status of Pesticides in Registration, Reregistration, and Special Review. (1998) EPA 738-R-98-002, p. 119

12.10 Other Safety Information

Chemical Assessment

IMAP assessments - Phosphorothioic acid, O,O-dimethyl O-(3-methyl-4-nitrophenyl) ester: Environment tier I assessment

IMAP assessments - Phosphorothioic acid, O,O-dimethyl O-(3-methyl-4-nitrophenyl) ester: Human health tier I assessment

12.10.1 Toxic Combustion Products

Special hazards arising from the substance or mixture: Carbon oxides, nitrogen oxides (NOx), sulfur oxides, oxides of phosphorus.
Sigma-Aldrich; Safety Data Sheet for Fenitrothion. Product Number: 45487, Version 5.4 (Revision Date 03/11/2015). Available from, as of February 2, 2017: https://www.sigmaaldrich.com/safety-center.html

12.10.2 Special Reports

USEPA/Office of Prevention, Pesticides and Toxic Substances; Reregistration Eligibility Decision Document - Fenitrothion EPA 738-R-95-018 (July 1995). The RED summarizes the risk assessment conclusions and outlines any risk reduction measures necessary for the pesticide to continue to be registered in the USA.[Available from, as of January 31, 2017: http://www.epa.gov/pesticides/reregistration/status.htm]
USEPA/Office of Prevention, Pesticides and Toxic Substances; Report on FQPA Tolerance Reassessment Progress and Interim Risk management Decision for Fenitrothion EPA 738-R-00-012 (October 2000). EPA issues a TRED for a pesticide that requires tolerance reassessment decisions, but does not require a reregistration eligibility decision at present because: the pesticide was initially registered after November 1, 1984, and by law is not included within the scope of the reregistration program; EPA completed a RED for the pesticide before FQPA was enacted on August 3, 1996; or the pesticide is not registered for use in the USA but tolerances are established that allow crops treated with the pesticide to be imported from other countries.[Available from, as of January 31, 2017: http://www.epa.gov/pesticides/reregistration/status.htm]
Toxicology data sheets on chemicals-fenitrothion; Industrial Toxicology Research Centre, Mahatma Gandhi Marg, Lucknow-226001, India, July 1982, Contents of this data sheet: properties; uses; production; metabolism; toxicity studies; aquatic toxicity; residual toxicity; phytotoxicity; case reports and epidemiological studies; environmental fate; residues; sampling and analysis; legal status (incl occupational health standards).
USEPA; Pesticide Fact sheet No. 142: Fenitrothion EPA/540/FS-88/045 (1988).

13 Toxicity

13.1 Toxicological Information

13.1.1 Toxicity Summary

IDENTIFICATION AND USE: Fenitrothion is a yellow-brown liquid. It is used as an insecticide (acaricide). HUMAN EXPOSURE AND TOXICITY: The signs and symptoms of poisoning in humans were those of parasympathetic stimulations. It has been suggested that the slow release of the insecticide from adipose tissue can give rise to a protracted clinical course or late symptoms of intoxication. In some cases, contact dermatitis has been attributed to exposure to this insecticide. There is no evidence of delayed neurotoxicity or of an association with Reye's syndrome. Moderate poisoning of 25 workers was reported, where a formulation containing 50% fenitrothion was applied by aircraft during a strong wind. Onset of poisoning developed 2.5-6 hr after inhalation and the symptoms were typical. Whole blood ChE activity was decreased by 48%. Recovery required 3 days of treatment with atropine. In another study, Cholinesterase activity was significantly reduced at the end of the working week in 3 out of 28 fenitrothion workers in Haiti. ANIMAL STUDIES: In experimental animals, fenitrothion causes cholinesterase activity depression in plasma, red blood cells, and brain and liver tissues. It is metabolized to fenitrooxon, which is more acutely toxic. Its toxicity may be potentiated by some other organophosphate compounds. Fenitrothion is only minimally irritating to the eyes and is nonirritating to the skin. A single oral dose of 250 mg fenitrothion/kg resulted in a slight decrease in a number of biochemical indices of liver function in rats, including mitochondrial ATPase activity, cytochrome P450 content, aniline hydroxylase activity, and aminopyrine N-demethylase activity. A dose of 25 mg/kg also had a slight effect on P450 content and xenobiotic metabolism, while 5 mg/kg did not have any significant effects. The magnitude of the effects was greater in females than in males. Mice that received fenitrothion at dietary level of 1000 ppm (about 12.8 mg/kg/day) developed symptoms within a week and at the end of a 20 day feeding period had cholinesterase activity in brain, red cells, and plasma reduced to 45, 26, and 5% of normal, respectively; body weight and liver weight were not affected. Prenatal administration in rats at 5, 10 and 15 mg/kg from days 7 to 15 of gestation, resulted in dose related decrease in open field activity and motor coordination in the offspring treated with the two higher doses. Long lasting alterations in the acquisition and extinction of a conditioned escape response, as well as increased social interactions were observed in the adult offspring. No embryotoxic or teratogenic effects were observed in mice or rats. Fenitrothion was found to be non-mutagenic in Salmonella typhimurium strains of TA98, TA1535 and TA1537 and in Escherichia coli WP2uvrA both with and without S9 mix, while weak mutagenicity was observed only in Salmonella typhimurium TA100 and enhanced by the addition of S9 mix. ECOTOXICITY STUDIES: The unexpectedly high sensitivity of Australian marsupials to fenitrothion was described. Signs of intoxication in mallards and pheasants from acute oral administration: regurgitation (in mallards), ataxia, high carriage, wing-drop, wing shivers, falling, salivation, tremors, loss of righting reflex, tetanic seizures, dyspnea, miosis, lacrimation, and wing-beat convulsions. Short term fenitrothion treatment in bluerock pigeons (Columba livia Gmelin) resulted in a reduction of total count of peripheral erythrocytes, hemoglobin content, hematocrit and total spleen cell count, but an increase in total peripheral leukocyte count, with marked heterophilia along with lymphopenia and monocytopenia. Also, there was consistent prolongation of both bleeding and clotting time in the experimental birds. Fenitrothion appears to have anti-androgenic effects on both the physiology and behavior of the male stickleback. Fenitrothion was highly toxic to crayfish, a nontarget organism that can be used for monitoring of environmental effects. Prawns exposed to fenitrothion showed alterations in enzymes involved in the production of energy (LDH and IDH) possibly in an attempt to cope with additional energetic demands. Pregnant female guppies were exposed to 10 mg fenitrothion/liter for 4 hr, 5, 10, or 15 days before the next parturition. Half of the females gave premature birth when exposed 5 or 10 days before parturition, and only 32 or 63%, respectively, of the eggs were delivered alive. The females exposed to the fenitrothion 15 days before parturition had normal births and only 9.4% of the offspring were stillborn. The body lengths of the young produced by the females after exposure were significantly shorter than those produced before exposure in all the studies.
Fenitrothion is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

13.1.2 RAIS Toxicity Values

Oral Acute Reference Dose (RfDoa)(mg/kg-day)
0.00025
Oral Acute Reference Dose Reference
OPP
Oral Chronic Reference Dose (RfDoc) (mg/kg-day)
0.000125
Oral Chronic Reference Dose Reference
OPP

13.1.3 EPA Human Health Benchmarks for Pesticides

Chemical Substance
Acute or One Day PAD (RfD) [mg/kg/day]
0.00025
Acute or One Day HHBPs [ppb]
1.7
Acute HHBP Sensitive Lifestage/Population
Children
Chronic or One Day PAD (RfD) [mg/kg/day]
0.00013
Chronic or One Day HHBPs [ppb]
0.77
Chronic HHBP Sensitive Lifestage/Population
General Population

13.1.4 Evidence for Carcinogenicity

Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans
USEPA Office of Pesticide Programs, Health Effects Division, Science Information Management Branch: "Chemicals Evaluated for Carcinogenic Potential" (April 2006)

13.1.5 Carcinogen Classification

Carcinogen Classification
No indication of carcinogenicity to humans (not listed by IARC).

13.1.6 Health Effects

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

13.1.7 Exposure Routes

The substance can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion.

13.1.8 Symptoms

Inhalation Exposure
Pupillary constriction. Excessive salivation. Lacrimation. Urination. Diarrhoea. Shortness of breath. Muscle cramps. Unconsciousness.
Skin Exposure
MAY BE ABSORBED! Redness. Pain. Further see Inhalation.
Eye Exposure
Redness. Pain. Further see Inhalation.
Ingestion Exposure
Abdominal cramps. Confusion. Vomiting. Weakness. Further see Inhalation.
Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

13.1.10 Adverse Effects

Other Poison - Organophosphate

13.1.11 Acute Effects

13.1.12 Toxicity Data

LC50 (rat) > 2,200 mg/m3/4h

13.1.13 Treatment

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

13.1.14 Interactions

... The present study was carried out to evaluate the effects of palm oil tocotrienol-rich fraction (TRF) in reducing the detrimental effects occurring in spermatozoa of FNT-treated rats. Adult male Sprague-Dawley rats were divided into four equal groups: a control group and groups of rats treated orally with palm oil TRF (200 mg/kg), FNT (20 mg/kg) and palm oil TRF (200 mg/kg) combined with FNT (20 mg/kg). The sperm characteristics, DNA damage, superoxide dismutase (SOD) activity, and levels of reduced glutathione (GSH), malondialdehyde (MDA), and protein carbonyl (PC) were evaluated. Supplementation with TRF attenuated the detrimental effects of FNT by significantly increasing the sperm counts, motility, and viability and decreased the abnormal sperm morphology. The SOD activity and GSH level were significantly increased, whereas the MDA and PC levels were significantly decreased in the TRF+FNT group compared with the rats receiving FNT alone. TRF significantly decreased the DNA damage in the sperm of FNT-treated rats. A significant correlation between abnormal sperm morphology and DNA damage was found in all groups. TRF showed the potential to reduce the detrimental effects occurring in spermatozoa of FNT-treated rats.
Taib IS et al; Exp Anim 63 (4): 383-93 (2014)
The effects of pesticide mixtures on cholinesterase activity in aggregate cultures of neural cells were investigated; it was also determined whether exogenous rat-liver microsomal fraction (S-9) might be used in conjunction with the cultures to mimic the in vivo activation of pesticides such as malathion. Studies of the effects of pesticide mixtures on the cholinesterase activity of cultures demonstrated that a hepatic microsomal fraction (S-9) played a major role in the nature of the interaction between combinations of malathion and fenitrothion or carbofuran. In the absence of S-9, malathion potentiated the anticholinesterase effect of fenitrothion, while neither synergistic nor antagonistic interactions occurred with mixtures of carbofuran and malathion. When S-9 was added to cultures with the pesticide mixtures, malathion's interaction with fenitrothion was antagonistic, and a synergistic response was observed for the mixtures of malathion and carbofuran. The antagonistic interaction of mixtures of fenitrothion and carbofuran was demonstrated to be independent of exogenously added S-9. Neither antagonistic nor synergistic interactions were observed for mixtures of triallate and fenitrothion or carbofuran. The data indicate that the addition of exogenous S-9 may be used to mimic certain aspects of the in vivo biotransformation of pesticides in aggregate cultures of neural cells from rat brain. Furthermore, the effects on cholinesterase activity of several of the pesticide mixtures tested were dependent upon the presence of exogenous S-9.
Segal LM, Fedoroff S; Toxicol In Vitro 3 (2): 123-8 (1989)
Depletion of hepatic glutathione in the mouse by pretreatment with diethyl maleate is known to potentiate the acute toxicities of many dimethyl substituted organothiophosphate insecticides. However, certain studies have raised doubts regarding the participation of glutathione in the detoxification of methyl parathion in the mouse, and hence the putative mechanism of action of diethyl maleate induced potentiation of this insecticide. The present study evaluates the hypothesis that diethyl maleate potentiates the acute toxicities of methyl parathion, methyl paraoxon, and fenitrothion by a mechanism other than glutathione depletion. One hour following pretreatment of mice with diethyl maleate (0.75 ml/kg ip) glutathione was markedly depleted and the acute toxicities of methyl parathion, methyl paroxon and fenitrothion were potentiated. Administration of glutathione monoethyl ester (20 mmol/kg po) to diethyl maleate pretreated mice attenuated diethyl maleate depletion of hepatic glutathione, or maintaining glutathine at or above control levels. However, glutathione monoethyl ester did not alter the diethyl maleate induced potentiation of the lethality of these insecticides. Furthermore, administration of glutathione monoethyl ester to naive mice increased hepatic glutathione levels, but did not affect the percentage of animals succumbing to a challenge dose of methyl parathion, methyl paraoxon, or fenitrothion. These data indicate that diethyl maleate potentiates the toxicity of methyl parathion, methyl paraoxon or fenitrothion by a mechanism unrelated to hepatic glutathione content.
Sultatos LG et al; Toxicol Lett 55 (1): 77-84 (1991)
The effects of a combination of fenitrothion with malathion in male rats were more than additive. The potentiation was most pronounced (half of the expected LD50) with a combination rate of 1:1. No potentiation was observed with other tested organophosphates, ie bromophos, amidithion, and trichlorfon.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.96 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html

13.1.15 Antidote and Emergency Treatment

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. /Organophosphates and related compounds/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3rd revised edition, Elsevier Mosby, St. Louis, MO 2007, p. 294
Basic Treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway if needed). Suction if necessary. Aggressive airway control may be needed. Watch for signs of respiratory insufficiency and assist ventilations if necessary. 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. Administer activated charcoal ... . /Organophosphates and related compounds/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3rd revised edition, Elsevier Mosby, St. Louis, MO 2007, p. 294
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. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/ Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously and consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Administer atropine. Correct hypoxia before giving atropine ... . Administer pralidoxime chloride (2-PAM). UNDER DIRECT PHYSICIANS ORDER ... . Treat seizures with adequate atropinization and correction of hypoxia. In rare cases diazepam (Valium) or lorazepam (Ativan) may be necessary ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organophosphates and related compounds/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3rd revised edition, Elsevier Mosby, St. Louis, MO 2007, p. 294
Ensure that a clear airway exists. Intubate the patient and aspirate the secretions with a large bore suction device if necessary. Administer oxygen by mechanically assisted pulmonary ventilation if respiration is depressed and keep patient on a high FiO2. In severe poisonings, patients should be treated in an intensive care unit setting. /Organophosphate pesticides/
U.S. Environmental Protection Agency/Office of Prevention, Pesticides, and Toxic Substances. Roberts, J.R., Reigart, J.R. Recognition and Management of Pesticide Poisonings. 6th ed. 2013. EPA Document No. EPA 735K13001, and available in electronic format at: https://www2.epa.gov/pesticide-worker-safety, p. 47
For more Antidote and Emergency Treatment (Complete) data for Fenitrothion (18 total), please visit the HSDB record page.

13.1.16 Medical Surveillance

Workers handling & applying pesticides must undergo an annual medical examination at the beginning of each agricultural season. /SRP: Protect from exposure those individuals with/ organic diseases of the central nervous system, mental disorders & epilepsy, pronounced endocrine & vegetative disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory diseases, cardiovascular diseases & circulatory disorders, gastrointestinal diseases (peptic ulcer), gastroenterocolitis, diseases of liver & kidneys, eye diseases (chronic conjunctivitis & keratitis). The blood cholinesterase activity must be determined before work starts. In the event of prolonged work periods, this activity should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be transferred to other work where they are not exposed to organophosphorus pesticides until this activity is completely restored. Persons with initial signs of indisposition should cease work with pesticides. /Organophosphorus pesticides/
International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983., p. 1646

13.1.17 Human Toxicity Excerpts

/HUMAN EXPOSURE STUDIES/ An unblinded crossover study of fenitrothion 0.18 mg/kg/day [36 times the acceptable daily intake (ADI)] and 0.36 mg/kg/day (72 X ADI) administered as two daily divided doses for 4 days in 12 human volunteers was designed and undertaken after results from a pilot study. On days 1 and 4, blood and urine samples were collected for analysis of fenitrothion and its major metabolites, as well as plasma and red blood cell cholinesterase activities, and biochemistry and hematology examination. Pharmacokinetic parameters could only be determined at the higher dosage, as there were insufficient measurable fenitrothion blood levels at the lower dosage and the fenitrooxone metabolite could not be measured. There was a wide range of interindividual variability in blood levels, with peak levels achieved between 1 and 4 hr and a half-life for fenitrothion of 0.8-4.5 hr. Although based on the half-life, steady-state levels should have been achieved; the area under the curve (AUC)(0-12 hr) to AUC(0-(infinity) )ratio of 1:3 suggested accumulation of fenitrothion. There was no significant change in plasma or red blood cell cholinesterase activity with repeated dosing at either dosage level of fenitrothion, and there were no significant abnormalities detected on biochemical or hematologic monitoring.
Meaklim J et al; Environ Health Perspect 111 (3): 305-8 (2003)
/HUMAN EXPOSURE STUDIES/ Fenitrothion was given to a total of 24 human volunteers in single oral doses of 0.042-0.33 mg/kg body weight or 2.5-2.0 mg per person. The excretion of a metabolite, 3-methyl-4-nitrophenol, in the urine was almost complete within 24 hr, and ranged from about 70% of the dose (0.042 mg/kg) to about 50% (0.33 mg/kg). Neither plasma nor erythrocyte cholinesterase (ChE) activities were depressed below normal, except in one person given 0.33 mg/kg, whose plasma ChE activity was about 65% of the pretest level after 6 and 24 hr. When repeated doses of 0.04-0.08 mg/kg were given to 5 individuals, 4 times at 24 hr intervals, most of the metabolites appeared in the urine within 12 hr of administration. After receiving the third and fourth doses, there was a trend towards a rise in erythrocyte ChE activity.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.99 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html
/CASE REPORTS/ Three young men who had worked as pest control operators for 3 months and who had recently applied fenitrothion for periods varying from 2 to 8 hours complained of general malaise, fatigue, headache, loss of memory and of ability to concentrate, anorexia, nausea, thirst, and loss of weight. With the exception of proteinuria in one case, all laboratory tests, including serum cholinesterase and EEG, were normal.
Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 1023
/CASE REPORTS/ A 56-year-old male attempted suicide by the ingestion of about 60 mL of 50% fenitrothion emulsion. Five hours later, combined hemoperfusion and hemodialysis (HP-HD) treatment was performed for 60 min and, subsequently, the symptoms gradually improved. Four days after ingestion, cholinergic symptoms recurred. Immediate HP-HD treatment was of no use and the patient died 6 days after ingestion of fenitrothion. Analysis of the organ and tissue distribution of fenitrothion revealed that the highest concentration of fenitrothion was found in fat (59.0 mg/kg wet weight, more than 10 times the concentrations in other organs). It was suggested that a slow release of the pesticide from adipose tissue can give rise to a protracted clinical course or late symptoms of intoxication.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.99 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html
For more Human Toxicity Excerpts (Complete) data for Fenitrothion (12 total), please visit the HSDB record page.

13.1.18 Non-Human Toxicity Excerpts

/LABORATORY ANIMALS: Acute Exposure/ Rats were exposed by a "nose-only" apparatus for 1 hr to 2 or 500 mg/cu m of aerosolized fenitrothion (15%) mixed with solvent Cyclosol 63 (35%) and diluent oil 585 (50%). Rat lungs were examined under light and electron microscopy at 3, 7, 21, and 60 days after exposure. It is concluded that a single exposure to this fenitrothion mixture at 500 mg/cu m presents no serious hazard of pulmonary toxicity.
LeBouffant L; Toxicol Appl Pharmacol 76 (2): 349-55 (1984)
/LABORATORY ANIMALS: Acute Exposure/ The pulmonary toxicity of fenitrothion was studied in male Wistar rats administered 0 or 30 mg/kg fenitrothion intratracheally. Animals were killed 0, 1, 4, 7, 14, 21, or 30 days after treatment and the lungs were removed, weighed, and lavaged. The lavage fluid was assayed for lactate dehydrogenase, protein, sialic acid, phospholipids, and ascorbic acid. The mitochondrial fraction was isolated and the extent of lipid peroxidation was determined by measuring the amount of malondialdehyde formed. Lavage fluid lactate dehydrogenase activity was increased at all time points by fenitrothion, the maximum increase 636% of the control value occurring at 4 days. Protein and sialic acid concentrations were significantly increased at all times. The maximum increase in protein concentration, 135%, occurred on day 1 and the maximum increase in sialic acid, 332%, occurred after 4 days. Lavage fluid ascorbic acid concentration was decreased by fenitrothion during the first 7 days and increased thereafter. The maximum increase, 38%, occurred on day 14. The phospholipid concentration showed a transient decrease followed by an increase. The maximum increase, 124%, occurred on day 14. Lung weights were significantly increased by fenitrothion on days 4 and 14. Significant lipid peroxidation was induced by fenitrothion at all times except on day 30. It was concluded that acute exposure to fenitrothion induces significant pulmonary biochemical changes in rats. The time pattern of the changes could reflect an initial injury to lung tissue followed by a period of defensive adaptation.
Khan MF et al; Bull Environ Contam Toxicol 45 (4): 598-603 (1990)
/LABORATORY ANIMALS: Acute Exposure/ A significant increase in plasma corticosterone levels and depletion of ascorbic acid content in adrenal glands occurred in rats between 1 and 5 hr after a single dose (50% LD50) of fenitrothion, returning to normal levels within 12 hr; brain AChE activity decreased to about 59-43% and a significant inhibition of the enzyme was observed for up to 24 hr after intoxication. Repeated dosing with fenitrothion (2.5% LD50) for 14 days caused insignificant elevation of plasma corticosterone levels, while brain AChE activity was inhibited to about 19% of control values and uptake of 4-(14)Carbon-corticosterone in tissue was significantly diminished.
Osicka-Koprowska A et al; Arch Toxicol 61 (1): 76-8 (1987)
/LABORATORY ANIMALS: Acute Exposure/ One tenth mL of fenitrothion (technical) was applied to one eye of 9 male, New Zealand White rabbits. The untreated eye served as a control. The treated eyes of 6 animals remained unwashed. The treated eyes of the other 3 animals were flushed for 1 minute with about 300 mL lukewarm water, 30 sec after application. Slight hyperemia in the conjunctiva was observed 1 hr after application in the unwashed eyes. This change had disappeared 48 hr after application. No irritating reactions were induced in any washed eyes. The irritating potency of fenitrothion in eyes was judged to be minimal for the unwashed group, and negative for the washed group.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 133, Fenitrothion p.72 (1992). Available from, as of February 2, 2017: https://www.inchem.org/pages/ehc.html
For more Non-Human Toxicity Excerpts (Complete) data for Fenitrothion (43 total), please visit the HSDB record page.

13.1.19 Human Toxicity Values

Probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon and 1 oz for 70 kg person (150 lb).
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-295

13.1.20 Non-Human Toxicity Values

LD50 Rat (female) acute oral 800 mg/kg
Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 373
LD50 Rat (male) acute dermal 890 mg/kg
Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 373
LD50 Rat (female) acute dermal 1200 mg/kg
Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 373
LD50 Rat oral 500 mg/kg
Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V13 440 (1981)
For more Non-Human Toxicity Values (Complete) data for Fenitrothion (12 total), please visit the HSDB record page.

13.1.21 Ongoing Test Status

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of December 8, 2016: http://actor.epa.gov/dashboard/]

13.2 Ecological Information

13.2.1 EPA Ecotoxicity

Pesticide Ecotoxicity Data from EPA

13.2.2 Ecotoxicity Values

LD50; Species: /Colinus virginianus/ (Bobwhite quail) 2-3 month old males; oral 27.4 mg/kg (95% confidence limit 19.0-39.5 mg/kg) /sample purity 95%/
U.S. Department of the Interior, Fish and Wildlife Service. Handbook of Toxicity of Pesticides to Wildlife. Resource Publication 153. Washington, DC: U.S. Government Printing Office, 1984., p. 42
LD50; Species: /Colinus virginianus/ (Bobwhite quail) 5 month old males; oral 32 mg/kg (95% confidence limit: 17.4-59.0 mg/kg) /sample purity 95%/
U.S. Department of the Interior, Fish and Wildlife Service. Handbook of Toxicity of Pesticides to Wildlife. Resource Publication 153. Washington, DC: U.S. Government Printing Office, 1984., p. 42
LD50; Species: /Colinus virginianus/ (Bobwhite quail) 5 month old females; oral 23.6 mg/kg (95% confidence limit 12.6-43.5 mg/kg) /sample purity 95%/
U.S. Department of the Interior, Fish and Wildlife Service. Handbook of Toxicity of Pesticides to Wildlife. Resource Publication 153. Washington, DC: U.S. Government Printing Office, 1984., p. 42
LC50; Species: Colinus virginianus (Northern Bobwhite Quail) juvenile age 2-3 wk; food 157 ppm for 8 days (95% confidence interval: 135-183 ppm)
Heath RG et al; USDOI/FWS; Special Sci Rept-Wildlife 152: 57 (1972) as cited in the ECOTOX database. Available from, as of April 4, 2017
For more Ecotoxicity Values (Complete) data for Fenitrothion (120 total), please visit the HSDB record page.

13.2.3 Ecotoxicity Excerpts

/BIRDS and MAMMALS/ The effect of fenitrothion exposure on birds was examined by measuring aerobic metabolism, blood hemoglobin content, plasma cholinesterases, and body weight for up to 21 d postdose. Peak metabolic rate was measured in a flight chamber in three-dose groups of house sparrows (Passer domesticus; 100 mg/kg = high, 60 mg/kg = medium, 30 mg/kg = low) and one-dose groups of zebra finches (Taeniopygia guttata; 3 mg/kg) and king quails (Coturnix chinensis; 26 mg/kg). Aerobic metabolism was measured during 1 hr of exposure to subfreezing thermal conditions in low-dose house sparrows and king quails (26 mg/kg). Fenitrothion had no effect on metabolic rate during cold exposure or on blood hemoglobin at any time. By contrast, aerobic performance during exercise in sparrows was reduced by 58% (high), 18% (medium), and 20% (low), respectively, 2 d postdose. House sparrows (high) had the longest recovery period for peak metabolic rate (21 d) and plasma cholinesterase activity (14 d). House sparrows (high) and treated king quails had significantly lower myoglobin at 48 hr postdose, whereas myoglobin was invariant in zebra finches and house sparrows (medium and low). Cholinesterase was maximally inhibited at 6 hr postdose, and had recovered within 24 hr, in house sparrows (low), king quails, and zebra finches. Exercise peak metabolic rate in zebra finches and king quails was reduced by 23% at 2 d and 3 d, respectively, despite these birds being asymptomatic in both behavior and plasma cholinesterase activities.
Fildes K et al; Environ Toxicol Chem 28 (2): 388-94 (2009)
/BIRDS and MAMMALS/ Huge aggregations of flightless locust nymphs pose a serious threat to agriculture when they reach plague proportions but provide a very visible and nutritious resource for native birds. Locust outbreaks occur in spring and summer months in semiarid regions of Australia. Fenitrothion, an organophosphate pesticide, is sprayed aerially to control locust plagues. To evaluate fenitrothion exposure in birds attending locust outbreaks, we measured total plasma cholinesterase (ChE), butrylcholinesterase (BChE), and acetylcholinesterase (AChE) activities in four avian species captured pre- and post-fenitrothion application and ChE reactivation in birds caught postspray only. Eleven of 21 plasma samples from four species had ChE activity below the diagnostic threshold (two standard deviations below the mean ChE activity of prespray samples). Granivorous zebra finches (Taeniopygia guttata) and insectivorous white-winged trillers (Lalage sueurii) had significantly lower mean plasma total ChE, BChE, and AChE activity postspray, while other insectivores, white-browed (Artamus superciliosus) and masked woodswallows (Artamus personatus), did not. Cholinesterase was reactivated in 19 of the 73 plasma samples and in one of three brain samples. We conclude that native bird species are exposed to fenitrothion during locust control operations. This exposure could have detrimental impacts, as both locust outbreaks and avian reproductive events are stimulated by heavy summer rainfall, leading to co-occurrence of locust control and avian breeding activities.
Fildes K et al; Environ Toxicol Chem 25 (11): 2964-70 (2006)
/BIRDS and MAMMALS/ We measured aerobic metabolism during cold exposure and exercise performance (run duration and oxygen consumption while running at 1 m/s) in the fat-tailed dunnart Sminthopsis crassicaudata, a dasyurid marsupial, before and after ingestion of 30 mg/kg of fenitrothion, an organophosphate (OP) pesticide. Running endurance of OP-exposed animals was less than half that of control animals over the first 3 days after dosing and 55% of control animal endurance on day 5 post-dose. Despite these declines, peak metabolic rate at this running speed (9.3 times basal metabolic rate; BMR) was unaffected by OP exposure. Peak metabolic rate (PMR) and cumulative oxygen consumption during a 1-hr exposure to conditions equivalent to -20 °C did not differ between OP-treated and control dunnarts, with PMR averaging 11 times BMR. We conclude that fenitrothion-induced exercise fatigue is not due to limitations in oxygen or substrate delivery to muscle or in their uptake per se, but more likely relates to decreased ability to sustain high-frequency neuromuscular function. The persistence of locomotor impairment following OP exposure in otherwise asymptomatic animals emphasizes the importance of using performance-based measures when characterizing sublethal effects of pesticide exposure in an ecological context.
Buttemer WA et al; Chemosphere 72 (9): 1315-20 (2008)
/BIRDS and MAMMALS/ ... The concern that endemically old and unique Australian vertebrate fauna might display high sensitivity to pesticides used for locust control provoked examination of the acute oral toxicity of the organophosphorus pesticide fenitrothion for the fat-tailed dunnart, Sminthopsis crassicaudata (Gould 1844), and the stripe-faced dunnart, S. macroura (Gould 1845). By using the up-and-down method for determining acute oral toxicity, S. crassicaudata and S. macroura were found to have estimated median lethal doses (LD50s) of 129 mg/kg (95% confidence interval [CI]= 74.2-159.0) and 97 mg/kg (95% CI = 88.3-120.0), respectively. These values are 10 to 14 times lower than the reported LD50 values for a similar-sized eutherian mammal, Mus musculus (L. 1758; LD50 = 1,100-1,400 mg/kg) and lower than all other reported mammalian LD50 values. Such wide interspecific variation in sensitivity to fenitrothion may be a consequence of underlying differences in the metabolic pathway for fenitrothion detoxification in mammals and a possible explanation for the increased toxicity of fenitrothion to dunnarts, compared with other mammals, is proposed. The unexpectedly high sensitivity of these Australian marsupials to fenitrothion emphasises the importance of adequately evaluating the risks of pesticides to endemic Australian fauna.
Story P et al; Environ Toxicol Chem 30 (5): 1163-9 (2011)
For more Ecotoxicity Excerpts (Complete) data for Fenitrothion (41 total), please visit the HSDB record page.

13.2.4 ICSC Environmental Data

The substance is very toxic to aquatic organisms. The substance may cause long-term effects in the aquatic environment. Bioaccumulation of this chemical may occur in fish. This substance may be hazardous to the environment. Special attention should be given to crustacea and bees. This substance does enter the environment under normal use. Great care, however, should be taken to avoid any additional release, for example through inappropriate disposal.

13.2.5 Environmental Fate / Exposure Summary

Fenitrothion's production may result in its release to the environment through various waste streams; its use as an indoor/outdoor ant and roach insecticide will result in minimal release to the environment. It's use outside the US as an agricultural insecticide will result in its direct release to the environment. If released to air, a vapor pressure of 5.40X10-5 mm Hg at 20 °C indicates fenitrothion will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase fenitrothion will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 6.4 hours. Particulate-phase fenitrothion will be removed from the atmosphere by wet and dry deposition. Fenitrothion contains chromophores that absorb at wavelengths >290 nm and, therefore, may be susceptible to direct photolysis by sunlight. The reported photolysis half-life of fenitrothion is 61 minutes. If released to soil, fenitrothion is expected to have moderate to low mobility based upon Koc values ranging from 254 to 1,531. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 9.30X10-7 atm-cu m/mole. Fenitrothion is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Fenitrothion has aerobic degradation half-lives ranging from 4.4 to 153.7 days in soils under various conditions, indicating that biodegradation is an important fate process under certain conditions in soils. If released into water, fenitrothion may adsorb to suspended solids and sediment based upon the Koc range. Fenitrothion exhibited 82% degradation after 4-7 days in pond water indicating that biodegradation is an important fate process in water. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. BCF values of 1.5 to 650 suggest bioconcentration in aquatic organisms is low to high. Hydrolysis is expected to be a variable environmental fate process based upon hydrolysis half-lives ranging between 247.5 to 4.3 days in buffered solutions at 20-23 °C and pH 5-9. Photolysis in sea and river water occurred in 0.9 and 1.1 days, respectively, compared to a dark half-life of 32 days. Occupational exposure to fenitrothion may occur through inhalation and dermal contact with this compound at workplaces where fenitrothion is produced or used. Use data indicate that minimal exposure will occur for the general US population due to its use in container baits for pest control. Limited monitoring data indicate that the general population may be exposed to fenitrothion via ingestion of imported crops containing fenitrothion residues. Exposure is expected to be low or non-existent since fenitrothion is no longer used in agriculture on food or feed crops in the US, subsequent to the 1995 EPA RED. (SRC)

13.2.6 Artificial Pollution Sources

Fenitrothion's production may result in its release to the environment through various waste streams; its use as an indoor/outdoor ant and roach insecticide(1) will result in minimal release to the environment(SRC). It's former use as an agricultural insecticide(2) resulted in its direct release to the environment(SRC).
(1) USEPA/OPPTS; Fenitrothion Summary Document. Reregistration Review: Initial Docket. March 2009. USEPA-HQ-OPP-2009-0172. Washington, DC: US EPA, Off Pollut Prev Toxics. Available from, as of Mar 3, 2017: https://java.epa.gov/oppt_chemical_search/
(2) USEPA/OPPTS; Reregistration Eligibility Decision (RED) Fenitrothion. July 1995. EPA 738-R-895-018. Available from, as of Mar 3, 2017: https://java.epa.gov/oppt_chemical_search/

13.2.7 Environmental Fate

TERRESTRIAL FATE: Based on a classification scheme(1), measured Koc values ranging from 254 to 1,531(2,3) indicate that fenitrothion is expected to have moderate to low mobility in soil(SRC). Volatilization of fenitrothion from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 9.0X10-7 atm-cu m/mole(4). Fenitrothion is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 5.40X10-5 mm Hg at 20 °C(5). Fenitrothion's half-life under sunlight illumination in two soils was 1 day compared to a half-life of 12 days in the dark(6). Fenitrothion has aerobic degradation half-lives ranging from 4.4 to 153.7 days in soils under various conditions(6-8), indicating that biodegradation is an important environmental fate process in soils under certain conditions(SRC).
(1) Swann RL et al; Res Rev 85: 17-28 (1983)
(2) Kanazawa J; Environ Toxicol Chem 8: 477-84 (1989)
(3) Singh N et al; J Environ Sci Health B25: 713-28 (1990)
(4) Metcalfe CD et al; Chemos 9: 151-5 (1980)
(5) Mackay D, Shiu WY; J Phys Chem Ref Data 19: 1175-99 (1981)
(6) Mikami N et al; J Pesticide Sci 10: 263-72 (1985)
(7) Adhya TK et al; Biol Fertil Soils 4: 36-40 (1987)
(8) Liu D et al; Environ Sci Technol 15: 788-93 (1981)
FIELD: Sumithion has been used over a period of years for spruce budworm control. Some studies have shown that, although 70-85% of the initial dose deposited on trees was lost within 2 wk ... about 10% persists for @ least 10 mo. In view of these findings a survey was made to check residue accumulations in areas of nb, canada which had been treated for up to 5 consecutive yr. No measurable amt of sumithion or known breakdown products were found in any tested soils.
Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2. Washington, DC: U.S. Government Printing Office, 1978., p. 255
FIELD: After treatment of coastal bermudagrass & corn with accothion ... the parent compd disappeared rapidly. Residues of oxygen analog were low & none were detected 21 days posttreatment. Residues of the nitrocresol were highest from 1-7 days posttreatment. In the forest environment, about half the initial accothion deposit was lost by foliage within 4 days & 70-85% within about 2 wk after spraying. Loss from spruce was at a faster rate than from fir. The remainder was more stable than anticipated. Only traces of the oxon & nitrocresol were found at any stage.
Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 3
FIELD: In a Piedmont site, New Hope Forest near Research Triangle Park, North Carolina, an aqueous solution of 2% fenitrothion was sprayed uniformly to the soil and litter of a loblolly pine forest. Trees were not sprayed. Less than 2% of the fenitrothion applied was found in the soil at day 1, and by day 107, this had decreased to 0.3%.
Hastings FL et al; Environ Entomol 18 (2): 245-50 (1989)
For more Environmental Fate (Complete) data for Fenitrothion (6 total), please visit the HSDB record page.

13.2.8 Environmental Biodegradation

AEROBIC: Fenitrothion, present at 100 mg/L, reached 0% of its theoretical BOD in 2 weeks using an activated sludge inoculum at 30 mg/L(1). Fenitrothion exhibited 75% degradation after 90 days in alluvial soil from the Northern plains of India; three unknown metabolites were reported(2). In another experiment with five alluvial Indian rice soils, biodegradation half-lives ranged from 4.4 to 153.7 days under non-flooded conditions, where degradation was due to microbially-mediated hydrolysis producing 3-methyl-4-nitrophenol(3). Biodegradation half-lives of fenitrothion using activated sludge, soil, and sediments were 5.5 days with co-metabolites and 73 days in the absence of co-metabolites (glucose and peptone were added as carbon source of co-metabolites)(4). Fenitrothion biodegradation rate in Ara-ike, Makinoga-ike and Tatsuga-ike ponds in Nagoya City, Japan, in 4 and 7 days ranged from 1-35 and 13-55%, 10-26 and 12-82%, and 3-39 and 18-50%, respectively(5). Fenitrothion sprayed on a pond fell below detectable levels in 2 days and the only metabolite detected in water was 3-methyl-4-nitrophenol possibly due to microbial-mediated hydrolysis(7). In the sediment, aminofenitrothion was detected possibly due to reduction of the nitro group and the aminofenitrothion persisted in the sediment for less than 4 days(7). Fenitrothion was degraded more extensively by estuarine water microorganisms than by lake water and distilled water microorganisms(7,8). Desmethyl fenitrothion and 3-methyl-4-nitrophenol were the major degradation products(7,8). Fenitrothion applied to Balsam fir and spruce foliage resulted in 75 to 80% degradation within 2 weeks; major metabolites include 3-methyl-4-nitrophenol, the oxygen analogue and decomposition products desmethylfenitrothion, dimethylphosphorothionic acid and phosphorothionic acid(9).
(1) NITE; Chemical Risk Information Platform (CHRIP). Biodegradation and Bioconcentration. Tokyo, Japan: Natl Inst Tech Eval. Available from, as of Feb 28, 2017: https://www.safe.nite.go.jp/english/db.html
(2) Roy S et al; Biomed Chromat 10: 60-4 (1996)
(3) Adhya TK et al; Biol Fertil Soils 4: 36-40 (1987)
(4) Liu D et al; Environ Sci Technol 15: 788-93 (1981)
(5) Hashizume K et al; Jpn J Toxicol Environ Health 40: 78-90 (1994)
(6) Maguire RJ, Hale EJ; J Agric Food Chem 28: 372-8 (1980)
(7) Weinberger P et al; Bull Environ Contam Toxicol 28: 484-9 (1982)
(8) MacRae IC; Rev Environ Contam Toxicol 109: 1-87 (1989)
(9) MacBean C, ed; e-Pesticide Manual. 15th ed., ver. 5.1, Alton, UK: British Crop Protection Council. Fenitrothion (122-14-5) (2008-2010)
AEROBIC: Degradation of fenitrothion in sterile and non-sterile soils at various pH and moisture content was examined resulting in half-lives ranging from 13 to over 5,000 days. Overall the loss of fenitrothion in soil was attributed to both biotic and abiotic processes and was generally faster in non-sterile soil than sterile soil. The rate of degradation was dependant on pH, soil type, organic amendment, soil moisture content and fenitrothion concentration(1).
Half-life (days)
13
Concn (ppm)
100
pH
10
Moisture content (%)
50
Soil
non-sterile clay loam
Half-life (days)
44
Concn (ppm)
100
pH
10
Moisture content (%)
50
Soil
non-sterile sandy loam
Half-life (days)
65
Concn (ppm)
100
pH
7.3
Moisture content (%)
50
Soil
non-sterile clay loam
Half-life (days)
81
Concn (ppm)
100
pH
7.3
Moisture content (%)
50
Soil
sterile clay loam
Half-life (days)
138
Concn (ppm)
100
pH
7.2
Moisture content (%)
50
Soil
non-sterile sandy loam
Half-life (days)
144
Concn (ppm)
100
pH
7.2
Moisture content (%)
50
Soil
sterile sandy loam
Half-life (days)
1,249
Concn (ppm)
1000
pH
7.3
Moisture content (%)
50
Soil
sterile clay loam
Half-life (days)
1,348
Concn (ppm)
1000
pH
7.2
Moisture content (%)
50
Soil
sterile sandy loam
Half-life (days)
1,608
Concn (ppm)
1000
pH
7.2
Moisture content (%)
50
Soil
non-sterile sandy loam
Half-life (days)
1,883
Concn (ppm)
1000
pH
7.3
Moisture content (%)
50
Soil
non-sterile clay loam
Half-life (days)
2,068
Concn (ppm)
1000
pH
4.0
Moisture content (%)
50
Soil
non-sterile clay loam
Half-life (days)
5,873
Concn (ppm)
1000
pH
7.2
Moisture content (%)
50
Soil
sterile sandy loam
(1) Schoen SR, Winterlin WL; J Environ Sci Health B22: 347-7 (1987)
ANAEROBIC: In an experiment with five alluvial Indian rice soils, biodegradation half-lives ranged from 3.9-10.9 days under flooded conditions, where the nitro group was reduced to form aminofenitrothion(1). The biodegradation half-lives of fenitrothion in cyclone fermentors with a mixture of microorganisms from activated sludge, soil and sediments were 1 day with cometabolites (glucose and peptone were added as carbon source of cometabolites) and anaerobic conditions, and 9.8 days in the absence of cometabolites and anaerobic conditions(2).
(1) Adhya TK et al; Biol Fertil Soils 4: 36-40 (1987)
(2) Liu D et al; Environ Sci Technol 15: 788-93 (1981)

13.2.9 Environmental Abiotic Degradation

The rate constant for the vapor-phase reaction of fenitrothion with photochemically-produced hydroxyl radicals has been reported as 6.21X10-11 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 6.4 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(SRC). In estuarine waters, fenitrothion degradation occurred via photolysis which produced fenitrooxon and the S-methyl isomer of fenitrothion, both of which are then converted to 3-methyl-4-nitrophenol via hydrolysis(2). The hydrolysis half-lives of fenitrothion were 247.5, 86.1 and 4.3 days, at pH 5, 7 and 9, respectively, in buffered solutions at 20 °C(3). At pH 5 and 7, a de-alkylated product and methanol were formed; at pH 9, dimethyl phosphoric acid and 3-methyl-4-nitrophenol were formed(3). Fenitrothion has hydrolysis half-lives of 83.7, 72.6, 51.6 and 25.2 days at pH of 5,7,8 and 9, respectively, in buffered solutions at 23 °C(4). Aqueous photolysis half-lives for fenitrothion of 1.1 and 0.9 days in river water at pH 7.4 and sea water at a pH of 7.8, respectively were faster when compared to a dark half-life of greater than 32 days(5). The half-life of fenitrothion in two soils, using soil thin layer plates at a pH range 5.2-6.4, was 1 day under sunlight illumination conditions compared to a half-life of greater than 12 days in the absence of light(5). Depending on the pH of the solution, a number of photo degradation products were formed including oxidation of P=S to P=O (oxon), oxidation of aryl methyl group to carboxyl group, reduction of nitro group to amino group and coupling of the amino group with the carboxyl group leading to the formation of dimeric products(5). Photo-reaction was indicated to be important fate process of fenitrothion present in vapor, solution and on soil surfaces(6,7). 3-Methyl-4-nitrophenol was found to be the major photodegradation product(6). The photolysis half-life of fenitrothion vapor due to irradiation with a Xenon arc lamp of up to 2 watts of UV output was 61 minutes(8). Introduction of 0.45 ppm of ozone reduced the half-life to 24 minutes(8). After 8 hours of irradiation with a xenon arc lamp, fenitrothion applied to leaf wax and fruit wax of tomatoes resulted in 9.1 and 12.3% photodegradation, respectively(9).
(1) Atkinson R; Environ Toxicol Chem 7: 435-42 (1988)
(2) Lacorte S, Barcelo D; Environ Sci Technol 28: 1159-63 (1994)
(3) Aly AO, Badawy MI; Environ Int 7: 373-7 (1982)
(4) Greenhalgh R et al; J Agric Food Chem 28: 102-5 (1980)
(5) Mikami N et al; J Pesticide Sci 10: 263-72 (1985)
(6) Brewer DG et al; Chemosphere 3: 91-5 (1974)
(7) Gan J et al; Chemosphere 21: 589-96 (1990)
(8) Addison JB; Bull Environ Contam Toxicol 27: 250-5 (1981)
(9) Fukushima M & Katagi T; J Agr Food Chem 54: 474-479 (2006)

13.2.10 Environmental Bioconcentration

BCF values of 8.0 to 53.6 and 1.5 to 101.7 were calculated in fish for fenitrothion(SRC), using carp (Cyprinus carpio) which were exposed over an 8-week period at concentrations of 20 and 2 ppb, respectively(1). Measured BCF values of 246 in topmouth gudgeon(2), 225-650 in lake trout(3), and 129 in mussels(4) have also been reported. An experiment using the European eel measured BCFs of 2.6-24.8(5). Average BCFs of 71.1, 141, 37.5, 24.6, and 30.8 were measured in the female guppy, male guppy, killifish, goldfish and white cloud mountain fish, respectively(6). Bioconcentration factors for fenitrothion in whole body freshwater fish ranged from 158.0 (+/-29.3) at 6 hr to 364 (+/-97.8) at 168 hr using willow shiner (Gnathopogon caerulescens) which were exposed to 25 ug/L (+/-3.5) in continuous flow-through tanks for up to 168 hours(7). Following an EPA guideline study, a whole body BCF of 130 was reported for fenitrothion in bluegill fish (Lepomic macrochirus) exposed for 28 days(8). According to a classification scheme(9), BCF values of less than 30 are low and values from 100 to 1000 are considered high(SRC).
(1) NITE; Chemical Risk Information Platform (CHRIP). Biodegradation and Bioconcentration. Tokyo, Japan: Natl Inst Tech Eval. Available from, as of Feb 28, 2017: https://www.safe.nite.go.jp/english/db.html
(2) Kanazawa J; Pestic Sci 12: 417-24 (1981)
(3) Holmes SB et al; Bull Environ Contam Toxicol 33: 468-75 (1984)
(4) Hawker DW, Connell DW; Ecotoxicol Environ Safety 11: 184-97 (1986)
(5) Sancho E et al; Bull Environ Contam Toxicol 60: 809-815 (1998)
(6) Tsuda T et al; Comp Biochem Physiol 116C: 213-18 (1997)
(7) Tsuda T et al; Toxicol Environ Chem 24: 185-90 (1989)
(8) Jackson SH et al; J Agric Food Chem 57: 958-67 (2009)
(9) Franke C et al; Chemosphere 29: 1501-14 (1994)

13.2.11 Soil Adsorption / Mobility

Measured fenitrothion Koc values of 593 and 254 in Tsukuba and Kanuma soils(1) and 1531, 1201, 833, and 1061 in 4 rice soils(2) have been determined. A study conducted on organic and silty clay loam soil, from the Boreal Forest in Ontario, Canada, indicate a maximum adsorption rate of 92 ug/g and 81 ug/g, respectively, in 30 hrs when fenitrothion-acetone is added to the soils(3). In the same experiment, studies with a buffer solution showed 38 and 48% desorption rate after 50 hrs extraction time(3). According to a classification scheme(4), these Koc values suggests that fenitrothion is expected to have low to moderate mobility in soil(SRC). The soil sorption coefficients ((ug pesticide/g soil)/(ug pesticide/g water)) for fenitrothion were 25.1 in clay loam and 3.5 in high clay soil. The soil sorption constants were 593 and 254 respectively, with a mean of 424.
(1) Kanazawa J; Environ Toxicol Chem 8: 477-84 (1989)
(2) Singh N et al; J Environ Sci Health B25: 713-28 (1990)
(3) Sundaram KMS et al; J Environ Sci Health B32: 1-24 (1997)
(4) Swann RL et al; Res Rev 85: 17-28 (1983)

13.2.12 Volatilization from Water / Soil

The Henry's Law constant for fenitrothion is 9.3X10-7 atm-cu m/mole(1). This Henry's Law constant indicates that fenitrothion is expected to be essentially nonvolatile from water surfaces(2). However, volatilization half-life of fenitrothion from a 5 mg/L distilled water solution at a temperature 20 °C was determined to be 65 days(4). Addition of fulvic acid at a concentration 5 mg/L increased the volatilization half-life to more than 180 days(4). However, the volatilization half-life from surface slicks after spraying fenitrothion formulation over a pond water was only 18 minutes at 20 °C(4). Fenitrothion's Henry's Law constant(1) indicates that volatilization from moist soil surfaces would occur slowly(SRC). Fenitrothion is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 5.4X10-5 mm Hg at 20 °C(3).
(1) Metcalfe CD et al; Chemosphere 9: 151-5 (1980)
(2) Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990)
(3) Mackay D, Shiu WY; J Phys Chem Ref Data 19: 1175-99 (1981)
(4) Maguire RJ, Hale EJ; J Agric Food Chem 28: 372-78 (1980)

13.2.13 Environmental Water Concentrations

DRINKING WATER: Water quality data compiled from the Retrieval (STORET) Data Warehouse report 2010 monitoring data from the Shoaltwater Bay Tribe Quality Assurance Project Plan (Washington) indicating that fenitrothion was not detected in water samples; monitoring data from 2010 through 2016 from California State Water Resources Control Board indicate that concentrations of fenitrothion were below detection limits (0.04 -0.05 ug/L)(1). In a study published in 1979, fenitrothion was not detected in tap water from Ottawa, Canada(detection limit of 1 ng/L)(2).
(1) National Water Quality Monitoring Council. Water Quality Data. Organics, Pesticides. Fenitrothion. USGS/EPA/ACWI. Available from as of Mar 2, 2017: https://www.waterqualitydata.us/portal
(2) LeBel GL et al; J Assoc Off Anal Chem 62: 241-9 (1979). Available from, as of Mar 3, 2017: https://www.ncbi.nlm.nih.gov/pubmed/447594?dopt=Abstract
SURFACE WATER: In June and July of 1985-1987, fenitrothion was detected in 1 of 58 Swedish stream water samples and 1 of 56 water samples at maximum concentrations of 0.1 ug/L(2). The concentration of fenitrothion in a Spanish Lake water ranged from less than 0.05-2.02 ug/L during 1983-1985(1). During the summer of 1974, no fenitrothion was detected in water from the upper Great Lakes at a detection limit of 0.005 ug/L(3). Concentration of fenitrothion ranged from 0.01-1.48 ug/L in unsprayed stream and pond water located approx. 200 m from a conifer forest sprayed with this chemical in New Brunswick, Canada(4). The concentration range in samples from the same waters were less than 0.01-0.07 ug/L a year later, suggesting low persistence of fenitrothion in water systems(4). Following an accidental pesticide storehouse fire in Switzerland, the estimated concentration of fenitrothion in Rhine River water at Village Neuf was 15-65 ug/L(5). Fenitrothion was not detected in the waters of the River Elbe near Hamburg, Germany in 1992-1993(6). In 2007, fenitrothion was detected in waters from the southern and northen basins of Lake Biwa in Japan at concentrations less than 0.02 ug/L(7).
(1) Carrasco JM et al; J Assoc Off Anal Chem 70: 752-3 (1987)
(2) Kreuger J, Brink N; Vaextskyddsrapp Jordbruk 49: 50-61 (1988)
(3) Glooschenko WA et al; Pestic Monit J 10: 61-7 (1976)
(4) Sundaram KMS; J Environ Sci Health B22: 413-38 (1987)
(5) Capel PD et al; Environ Sci Technol 22: 992-7 (1988)
(6) Gotz R et al; Chemosphere 36: 2103-118 (1998)
(7) Tsuda T et al; Bull Env Cont Tox 82: 683-689 (2009)
RAIN/SNOW/FOG: Fenitrothion was detected at a concentration of 32.9 ng/L in an ice core collected in 1998 from the summit of Austofonna and at concentrations ranging from not detected to 320 ng/L in ice samples taken from several sites in Russia(1). Fenitrothion was detected at a concentration range of less than 0.01 to 0.86 ug/L in rain water collected in New Brunswick, Canada in 1978( 2).
(1) Hermanson MH, et al; Env Sci Tech 39: 8163-8169 (2005)
(2) Pearce PA et al; Bull Environ Contam Toxicol 23: 503-8 (1979). Available from, as of Mar 3, 2017: https://www.ncbi.nlm.nih.gov/pubmed/497457?dopt=Abstract

13.2.14 Effluent Concentrations

Following an accidental pesticide storehouse fire in Switzerland on November 1, 1986, the estimated concentration of fenitrothion in Rhine River water at Village Neuf was 15-65 ug/L(1).
(1) Capel PD et al; Environ Sci Technol 22: 992-7 (1988)

13.2.15 Sediment / Soil Concentrations

SEDIMENT: Following the spraying of a stream in New Brunswick, Canada at a peak water concentration of 15.2 ug/L, the max concentration of fenitrothion in a bottom sediment was 0.9 ug/g (ppm)(1). The concentration of fenitrothion in sediments generally decreased as the distance downstream from the treated area increased(1). During the summer of 1974, no fenitrothion was detected in sediment from the upper Great Lakes at a detection limit of 0.02 ug/g(2). Concentration of fenitrothion ranged from less than 0.01 to 0.21 ug/g in unsprayed stream and pond sediments located approx. 200 m from a conifer forest in New Brunswick, Canada which was sprayed with fenitrothion(3). No fenitrothion was detected in these sediments (detection limit 0.01 ppm) a year later suggesting that fenitrothion is not persistent in sediments(3). The concentration of fenitrothion in an unsprayed soil within 200 m of a spraying zone ranged 0.01-0.20 ppm, but the concentration dropped below the detection limit (0.01 ppm) a year later(3). In 2007, fenitrothion was detected in sediments from the southern and northen basins of Lake Biwa in Japan at concentrations of less than 1 ug/kg(4).
(1) Eidt DC et al; Arch Environ Contam Toxicol 13: 43-52 (1984)
(2) Glooschenko WA et al; Pestic Monit J 10: 61-7 (1976)
(3) Sundaram KMS; J Environ Sci Health B22: 413-38 (1987)
(4) Tsuda T et al; Bull Env Cont Tox 82: 683-689 (2009)

13.2.16 Atmospheric Concentrations

URBAN/SUBURBAN: The concentration of fenitrothion in air samples within 200 m from a neighboring spraying area in New Brunswick, Canada ranged from 48 to 82 ng/cu m, the concentration dropped below the detection limit (10 ng/cu m) a year later (1982-1983)(1).
(1) Sundaram KMS; J Environ Sci Health B22: 413-38 (1987)
INDOOR: The concentrations of fenitrothion in room air following application of fenitrothion for pest control at the recommended rate inside a dormitory room were 3.3 ug/cu m on day 0, 1.1 ug/cu m on day 1, 0.8 ug/cu m on day 2 and 0.5 ug/cu m on day 3 after application(1).
(1) Wright CG et al; Bull Environ Contam Toxicol 26: 548-53 (1981)

13.2.17 Food Survey Values

Fenitrothion was detected in US processed fruits and vegetables during 1970-1976(1). It was also detected in infant and toddler food composite samples collected from 10 U.S. cities during 1977-1978(2). Fenitrothion was found as residues in U.S. foods during regulatory monitoring in fiscal years 1978-1986(3,4). Fenitrothion was detected in several domestic and imported Danish fruits and vegetables at a maximum concentration of 0.43 ppm(5). Potato and citrus fruits, analyzed from Egyptian local markets in 1991-1992, found fenitrothion levels ranging from 0.668-3.815 and 0.023-0.681, respectively(6).
(1) Duggan RE et al; Pesticide Residue Levels in Foods in the United States from July 1, 1969 to June 30, 1976. Washington, DC: Food and Drug Admin, Div Chem Tech (1983)
(2) Podrebarac DS; J Assoc Off Anal Chem 67: 166-75 (1984)
(3) Yess NJ et al; J Assoc Off Anal Chem 74: 265-72 (1991)
(4) Yess NJ et al; J Assoc Off Anal Chem 74: 273-80 (1991)
(5) Andersen KS; Pesticide Residues in Danish Foods (1978-79), Statens Levnedsmiddelinst 54: 1-75 (1981)
(6) Dogheim SM et al; J AOAC Intern 79: 949-52 (1996)
Fenitrothion residues were detected at an average concentration of 28.0 ppb with a detection frequency of 50% in unprocessed vegetable samples and at an average concentration of 6.0 ppb with a detection frequency of 22.2% in processed vegetable samples collected in 1997-1998 from Alexandria City in Egypt(1). Results from an agricultural product monitoring effort in the Hyogo Prefecture, Japan during April 1995 through March 2000 reported fenitrothion detections in 4 out of 106 samples of mandarin oranges at concentrations between less than 0.01 and less than 0.05 ug/g(2). Fenitrothion was not detected in seven tomato plant samples at an LOD of 0.0018 mg/g, nor in 2 onion samples at an LOD of 0.0004 mg/g, collected July and Aug 2006 in a survey of agricultural areas in Belgrade, Serbia(3). In a study published in 2007, fenitrothion was detected in 1 out of 173 agricultural product samples from a local market in Japan at concentration of 26.6 ng/g(4). Fenitrothion residues were not detected in six cucumber, one apricot, one zucchini, and 8 cabbage samples collected June to Oct 2009 in a survey of 50 random agricultural areas in Belgrade, Serbia(5).
(1) Abbassy MS; Bull Env Cont Tox 67: 225-232 (2001)
(2) Akiyama Y et al; J AOAC Int 85: 692-703 (2002)
(3) Markovic M, et al; Arch Env Cont Tox 58: 341-351 (2010)
(4) Okihashi M, et al; Journal of AOAC International. 90(4): 1165-1178 (2007)
(5) Dordevic T & Durovic R; Bull Env Cont Tox 88: 385-390 (2012)

13.2.18 Plant Concentrations

It was reported that fenitrothion persisted in leaf tissues and may act as a micro sink for the pesticide(1).
(1) Sundaram KMS; J Environ Health B22: 413-38 (1987)

13.2.19 Fish / Seafood Concentrations

In study published in 1987, fenitrothion was not detected in fish collected from neighboring unsprayed streams following application of the pesticide in a nearby forest(1). It was not detected in fish analyzed from Egyptian local markets in 1991-1992(2).
(1) Sundaram KMS; J Environ Sci Health B22: 413-38 (1987)
(2) Dogheim SM et al; J AOAC Intern 79: 949-52 (1996)

13.2.20 Other Environmental Concentrations

In studies conducted in the 1980's and 90's, fenitrothion was detected in water-cress, moss and several aquatic organisms following application on forest and streams(1,2). Following spray applications in Canadian forest, fenitrothion was detected in Poplar (Populus tremuloides), green birch (Betula populifolia), fir (Abies balsamea) and other foilages(2-4). In a Piedmont site, New Hope Forest near Research Triangle Park, North Carolina, an aqueous solution of 2% fenitrothion was sprayed uniformly to the soil and litter of a loblolly pine forest. Trees were not sprayed. Less than 2% of the fenitrothion applied was found in the soil at day 1, and by day 107, this had decreased to 0.3%(5).
(1) Eidt DC et al; Arch Environ Contam Toxicol 13: 43-52 (1984)
(2) Sundaram KMS; J Environ Health B22: 413-38 (1987)
(3) LaPierre LE; Bull Environ Contam Toxicol 35: 471-5 (1985)
(4) Sundaram KMS; J Environ Sci Health B25: 643-63 (1990)
(5) Hastings FL et al; Environ Entomol 18 (2): 245-50 (1989)

13.2.21 Probable Routes of Human Exposure

Occupational exposure to fenitrothion may occur through inhalation and dermal contact with this compound at workplaces where fenitrothion is produced or used(SRC). Use data indicate that minimal exposure will occur for the general population due to its limited use in container baits for pest control. Limited monitoring data indicate that the general population may be exposed to fenitrothion via ingestion of imported crops containing fenitrothion residues(SRC). Exposure is expected to be low or non-existent since fenitrothion is no longer used in agriculture on food or feed crops in the US, subsequent to the 1995 EPA RED(1).
(1) USEPA/OPPTS; Reregistration Eligibility Decisions (REDs) Database on Fenitrothion (122-14-5). USEPA DOC NO EPA-HQ-OPP-2006-0618. Available from, as of February 28, 2017: https://iaspub.epa.gov/apex/pesticides/f?p=chemicalsearch:1
In a 1998 occupational monitoring study of 5 females aged 20 to 49 yrs, inhalation was found to be the most likely route of exposure to fenitrothion as a result of manual operations in greenhouses(1).
(1) Aprea C et al; Arch Env Contam Tox 36: 490-497 (1999)

13.2.22 Average Daily Intake

The daily dietary intakes of fenitrothion per unit body weight to different U.S. subgroups of populations during 1982-1984 were as follows (in ng/kg body wt/day): 6-11 months, 0.2; 2 yr, 0.8; 14-16 yr female, 0.3, 14-16 yr. male, 0.4; 25-30 yr female, 0.3; 25-30 yr male, 0.3(1). The daily dietary intakes of fenitrothion to different subgroups of U.S. populations during 1988 were as follows (in ng/kg body wt/day): 6-11 months, 1.4; 14-16 yr male, 2.3; 60-65 yr female, 1.7(2).
(1) Gunderson EL; J Assoc Off Anal Chem 71: 1200-9 (1988)
(2) FDA; Residues in Foods-1988, Food & Drug Administration, Washington, DC (1989)

13.2.23 Body Burden

The rate of exposure to fenitrothion on different body parts of Chinese pesticide applicators in tea plantations were as follows (ug/sq cm): face, 5.92-15.1; chest, 5.86-10.5; abdomen, 9.97-51.4; thigh, 33.4-204; and ankle, 23.9-288(1). The total dermal exposure of applicators to fenitrothion was estimated to be 1152 mg/kg excluding hands; exposure on hands was estimated to be 115 mg/kg(1).
(1) Wan H; Bull Environ Contam Toxicol 45: 459-62 (1990)

14 Associated Disorders and Diseases

Associated Occupational Diseases with Exposure to the Compound

15 Literature

15.1 Consolidated References

15.2 NLM Curated PubMed Citations

15.3 Springer Nature References

15.4 Thieme References

15.5 Wiley References

15.6 Chemical Co-Occurrences in Literature

15.7 Chemical-Gene Co-Occurrences in Literature

15.8 Chemical-Disease Co-Occurrences in Literature

16 Patents

16.1 Depositor-Supplied Patent Identifiers

16.2 WIPO PATENTSCOPE

16.3 Chemical Co-Occurrences in Patents

16.4 Chemical-Disease Co-Occurrences in Patents

16.5 Chemical-Gene Co-Occurrences in Patents

17 Interactions and Pathways

17.1 Chemical-Target Interactions

18 Biological Test Results

18.1 BioAssay Results

19 Classification

19.1 MeSH Tree

19.2 NCI Thesaurus Tree

19.3 ChEBI Ontology

19.4 KEGG: Pesticides

19.5 KEGG: Risk Category of Japanese OTC Drugs

19.6 KEGG: OTC drugs

19.7 KEGG: Animal Drugs

19.8 ChemIDplus

19.9 CAMEO Chemicals

19.10 ChEMBL Target Tree

19.11 UN GHS Classification

19.12 NORMAN Suspect List Exchange Classification

19.13 EPA DSSTox Classification

19.14 EPA Substance Registry Services Tree

19.15 MolGenie Organic Chemistry Ontology

20 Information Sources

  1. Australian Industrial Chemicals Introduction Scheme (AICIS)
    Phosphorothioic acid, O,O-dimethyl O-(3-methyl-4-nitrophenyl) ester
    https://services.industrialchemicals.gov.au/search-assessments/
  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. 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/
  4. ChemIDplus
    ChemIDplus Chemical Information Classification
    https://pubchem.ncbi.nlm.nih.gov/source/ChemIDplus
  5. EPA DSSTox
    CompTox Chemicals Dashboard Chemical Lists
    https://comptox.epa.gov/dashboard/chemical-lists/
  6. EPA Safe Drinking Water Act (SDWA)
  7. 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
  8. 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
  9. Hazardous Substances Data Bank (HSDB)
  10. 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
  11. ILO-WHO International Chemical Safety Cards (ICSCs)
  12. New Zealand Environmental Protection Authority (EPA)
    LICENSE
    This work is licensed under the Creative Commons Attribution-ShareAlike 4.0 International licence.
    https://www.epa.govt.nz/about-this-site/general-copyright-statement/
  13. Risk Assessment Information System (RAIS)
    LICENSE
    This work has been sponsored by the U.S. Department of Energy (DOE), Office of Environmental Management, Oak Ridge Operations (ORO) Office through a joint collaboration between United Cleanup Oak Ridge LLC (UCOR), Oak Ridge National Laboratory (ORNL), and The University of Tennessee, Ecology and Evolutionary Biology, The Institute for Environmental Modeling (TIEM). All rights reserved.
    https://rais.ornl.gov/
  14. California Safe Cosmetics Program (CSCP) Product Database
  15. EU Pesticides Database
  16. 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
  17. ChEBI
  18. 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
  19. 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
  20. 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
  21. 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
  22. Drug Gene Interaction database (DGIdb)
    LICENSE
    The data used in DGIdb is all open access and where possible made available as raw data dumps in the downloads section.
    http://www.dgidb.org/downloads
  23. EPA Pesticide Ecotoxicity Database
  24. 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/
    fenitrothion
    NORMAN Suspect List Exchange Classification
    https://www.norman-network.com/nds/SLE/
  25. USDA Pesticide Data Program
  26. Hazardous Chemical Information System (HCIS), Safe Work Australia
  27. NITE-CMC
    Fenitrothion - FY2006 (New/original classication)
    https://www.chem-info.nite.go.jp/chem/english/ghs/06-imcg-0151e.html
    O,O-Dimethyl-O-(3-methyl-4-nitrophenyl) thiophosphate [Fenitrothion] - FY2017 (Revised classification)
    https://www.chem-info.nite.go.jp/chem/english/ghs/17-mhlw-2076e.html
  28. Regulation (EC) No 1272/2008 of the European Parliament and of the Council
    LICENSE
    The copyright for the editorial content of this source, the summaries of EU legislation and the consolidated texts, which is owned by the EU, is licensed under the Creative Commons Attribution 4.0 International licence.
    https://eur-lex.europa.eu/content/legal-notice/legal-notice.html
    fenitrothion (ISO); O,O-dimethyl O-4-nitro-m-tolyl phosphorothioate
    https://eur-lex.europa.eu/eli/reg/2008/1272/oj
  29. 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
  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. SpectraBase
    phosphorothioic acid, O,O-dimethyl O-4-nitro-m-tolyl ester
    https://spectrabase.com/spectrum/3to2Jji5cLk
    FENITROTHION;O,O-DIEMTHYL-O-(3-METHYL-4-NITROPHENYL)-PHOSPHOROTHIOATE
    https://spectrabase.com/spectrum/JBgzOXAqJWI
    FENITROTHION;O,O-DIEMTHYL-O-(3-METHYL-4-NITROPHENYL)-PHOSPHOROTHIOATE
    https://spectrabase.com/spectrum/6fUhtM0nmjy
    PHOSPHOROTHIOIC ACID, O,O-DIMETHYL O-4-NITRO-M-TOLYL ESTER
    https://spectrabase.com/spectrum/3t1741guSkm
    phosphorothioic acid, O,O-dimethyl O-4-nitro-m-tolyl ester
    https://spectrabase.com/spectrum/FdqP5K9HYHF
    PHOSPHOROTHIOIC ACID, O,O-DIMETHYL O-4-NITRO-M-TOLYL ESTER
    https://spectrabase.com/spectrum/7SaiMtDxOCh
  32. Japan Chemical Substance Dictionary (Nikkaji)
  33. 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
    Risk category of Japanese OTC drugs
    http://www.genome.jp/kegg-bin/get_htext?br08312.keg
    Classification of Japanese OTC drugs
    http://www.genome.jp/kegg-bin/get_htext?br08313.keg
  34. MassBank Europe
    O,O-DIMETHYL O-(3-METHYL-4-NITROPHENYL) PHOSPHOROTHIOATE
    https://massbank.eu/MassBank/Result.jsp?inchikey=ZNOLGFHPUIJIMJ-UHFFFAOYSA-N
  35. Metabolomics Workbench
  36. USGS Columbia Environmental Research Center
  37. Springer Nature
  38. 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/
  39. Wikidata
  40. Wikipedia
  41. Wiley
  42. 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
  43. PubChem
  44. GHS Classification (UNECE)
  45. EPA Substance Registry Services
  46. MolGenie
    MolGenie Organic Chemistry Ontology
    https://github.com/MolGenie/ontology/
  47. PATENTSCOPE (WIPO)
CONTENTS