ホスホロチオ酸O,O-ジメチルO-(3-メチル-4-ニトロフェニル)

log Kow = 3.30

3.30

3.27

1.32 at 77 °F (EPA, 1998) - Denser than water; will sink

1.3227 g/cu cm at 25 °C

Relative density (water = 1): 1.3

Yellow-brown liquid

Yellow oily liquid

In water, 38.0 mg/L at 25 °C

Readily soluble in alcohols, esters, ketones, aromatic hydrocarbons and chlorinated hydrocarbons. In hexane 24 g/L, isopropanol 138 g/L (20 °C)

Readily soluble in dichloromethane, 2-propanol, toluene, hardly sol in n-hexane.

Low solubility in aliphatic hydrocarbons; soluble in most organic solvents

0.038 mg/mL at 25 °C

Solubility in water at 20 °C: none

> 100.00 °C (> 212.00 °F)

157 °C

244 °F at 0.05 mmHg (EPA, 1998)

BP: 118 °C at 0.05 mm Hg

0.3 °C

3.4 °C

0.3 °C

6e-06 mmHg at 68 °F (EPA, 1998)

0.000054 [mmHg]

5.40X10-5 mm Hg at 20 °C

Vapor pressure, Pa at 20 °C: 0.018

Warning

H302: Harmful if swallowed [Warning Acute toxicity, oral]；H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]；H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P264, P270, P273, P301+P317, P330, P391, and P501 (click each P-code to see the statement)

Warning

Hazard Traits - Developmental Toxicity; Neurotoxicity；Authoritative List - CECBP - Priority Chemicals；Report - if used as a fragrance or flavor ingredient

Commission Regulation (EC) No 451/2000

Fenitrothion is listed in the dataset of EPA Human Health Benchmarks for Pesticides under the Safe Drinking Water Act (40 eCFR 141)

2007/379

Status: Active Update: 22-02-2019 https://echa.europa.eu/registration-dossier/-/registered-dossier/27782

Fenitrothion: Does not have an individual approval but may be used under an appropriate group standard

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)

Combustible. Liquid formulations containing organic solvents may be flammable. Gives off irritating or toxic fumes (or gases) in a fire.

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]

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).

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.

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.

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.

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 cau

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.

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.

(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)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Refer immediately for medical attention.

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.

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]

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

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

/Storage temperature should be less than 40 °C on account of the tendency/ to isomerize.

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.

(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)

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.

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.

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.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

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.

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).

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.

... 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.

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.

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.

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.

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: cholinergi

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%/

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%/

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%/

LC50; Species: Colinus virginianus (Northern Bobwhite Quail) juvenile age 2-3 wk; food 157 ppm for 8 days (95% confidence interval: 135-183 ppm)

For more Ecotoxicity Values (Complete) data for Fenitrothion (120 total), please visit the HSDB record page.

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).

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.

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.

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%.

For more Environmental Fate (Complete) data for Fenitrothion (6 total), please visit the HSDB record page.

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).

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).

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

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.

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).

/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.

/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.

/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.

/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.

For more Ecotoxicity Excerpts (Complete) data for Fenitrothion (41 total), please visit the HSDB record page.

Hazard Traits - Developmental Toxicity; Neurotoxicity；Authoritative List - CECBP - Priority Chemicals；Report - if used as a fragrance or flavor ingredient

Commission Regulation (EC) No 451/2000

Fenitrothion is listed in the dataset of EPA Human Health Benchmarks for Pesticides under the Safe Drinking Water Act (40 eCFR 141)

2007/379

Status: Active Update: 22-02-2019 https://echa.europa.eu/registration-dossier/-/registered-dossier/27782

Fenitrothion: Does not have an individual approval but may be used under an appropriate group standard

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.

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.

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.

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 cau

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.

Cholinesterase inhibitor.

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.

... /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.

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.

.... 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 ...

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.

After exposure of rats and guinea pigs to sumithion, desmethyl analog, dimethyl phosphorothioate, dimethyl phosphate, and 4 unidentified compounds were found.

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.

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.

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.

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.

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.

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.

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.

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.

... Rapid absorption through skin.

For more Absorption, Distribution and Excretion (Complete) data for Fenitrothion (17 total), please visit the HSDB record page.

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]

Banned in the EU for use as pesticide for plant protection; [eChemPortal: ESIS]

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./

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.

Insecticide (acaricide).

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%.

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/

Preparation: Belgium patent 594669 (1960 to Sumitomo); Belgium patent 596091 (1960 to Bayer).

PRODUCED BY REACTION OF O,O-DIMETHYL PHOSPHOROCHLORIDOTHIOATE WITH ALKALI METAL SALT OF 3-METHYL-4-NITROPHENOL.

Sumithion Technical (Sumitomo Chemical America, Inc): Active ingredient: Fenitrothion 94.2%.

Dust, emulsifiable concentrate, flowable, fogging concentrate, granules, oil-based liquid spray, ULV, wettable powder.

Premix Partners: Cypermethrin; Esfenvalerate; Fenobucarb; Fenpropathrin; Fenvalerate; Methabenzithiazuron; d-Tetramethrin; Trichlorfon.

Environmental transformation -> Pesticides (parent, predecessor)

INSECTICIDES