Fenitrothion

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)

H302 (50%): Harmful if swallowed [Warning Acute toxicity, oral]

H312 (50%): 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 (55.9%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P264, P270, P273, P280, P301+P317, P302+P352, P317, P321, P330, P362+P364, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 118 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H312: Harmful in contact with skin [Warning Acute toxicity, dermal]

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

H320: Causes eye irritation [Warning Serious eye damage/eye irritation]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

P203, P260, P261, P264, P264+P265, P270, P272, P273, P280, P301+P317, P302+P352, P305+P351+P338, P308+P316, P317, P318, P319, P321, P330, P333+P317, P337+P317, P362+P364, P391, P405, and P501 (click each P-code to see the statement)

P260, P264, P270, P280, P301+P317, P302+P352, P308+P316, P317, P319, P321, P330, P362+P364, P405, and P501 (click each P-code to see the statement)

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H330: Fatal if inhaled [Danger Acute toxicity, inhalation]

P260, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P317, P320, P321, P330, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

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.

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)

(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.

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.

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)

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. 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.

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.

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.

(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)

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

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.

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]

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.

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.

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

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.

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)

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).

Skin protection: Handle with gloves.

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.

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).

While handling, wear protective gloves & goggles or full face shield.

NO open flames.

PREVENT GENERATION OF MISTS! AVOID EXPOSURE OF ADOLESCENTS AND CHILDREN! IN ALL CASES CONSULT A DOCTOR!

Use ventilation, local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear face shield or eye protection in combination with breathing protection.

Do not eat, drink, or smoke during work. Wash hands before eating.

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)

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]

BROWN-TO-YELLOW LIQUID WITH CHARACTERISTIC ODOUR.

Yellow-brown liquid

Yellow oily liquid

Faint characteristic odor

244 °F at 0.05 mmHg (EPA, 1998)

BP: 118 °C at 0.05 mm Hg

> 100.00 °C (> 212.00 °F)

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

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

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

log Kow = 3.30

Henry's Law constant= 9.30X10-7 atm-cu m/mol at 25 °C

Stable under recommended storage conditions.

140-145 °C

Index of refraction: 1.5528 at 25 °C

163.2 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: ESI+; Dataset: Pesticides]

156.22 Ų [M+H]+

156.09 Ų [M+H]+ [CCS Type: TW; Buffer gas: N2; Ionization: GC-APCI+]

153.74 Ų [M]+ [CCS Type: TW; Buffer gas: N2; Ionization: GC-APCI+]

Thermal decomp at 100-140 °C produces mixture of organophosphorus polymers

Hydroxyl radical reaction rate constant = 6.21X10-11 cu cm/mole-sec at 25 °C

Potential endocrine disrupting compound

Pesticides

Acaricides, Insecticides

Active substance -> EU Pesticides database: Not approved

Pesticides -> Organophosphate Insecticides

Environmental transformation -> Pesticides (parent, predecessor)

Pesticide (Fenitrothion) -> USDA PDB

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

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

Nitro, Nitroso, Nitrate, and Nitrite Compounds, Organic

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.

Incompatible materials: Strong oxidizing agents.

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.

Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans

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

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.

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

Pupillary constriction. Excessive salivation. Lacrimation. Urination. Diarrhoea. Shortness of breath. Muscle cramps. Unconsciousness.

MAY BE ABSORBED! Redness. Pain. Further see Inhalation.

Redness. Pain. Further see Inhalation.

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.

Chemical: FENITROTHION

Other Poison - Organophosphate

Acceptable Daily Intake: 0-0.001 mg/kg body-wt.

FAO/WHO ADI: 0.005 mg/kg

Fenitrothion

Children

General Population

Human Health Benchmarks for Pesticides - 2021 Update

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

Probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon and 1 oz for 70 kg person (150 lb).

LD50 Rat (female) acute oral 800 mg/kg

LD50 Rat (male) acute dermal 890 mg/kg

LD50 Rat (female) acute dermal 1200 mg/kg

LD50 Rat oral 500 mg/kg

For more Non-Human Toxicity Values (Complete) data for Fenitrothion (12 total), please visit the HSDB record page.

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.

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/

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/

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/

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/

For more Antidote and Emergency Treatment (Complete) data for Fenitrothion (18 total), please visit the HSDB record page.

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/

/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.

/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.

/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.

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.

/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.

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.

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)

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).

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.

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).

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).[Table#3280]

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).

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).

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).

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.

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).

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).

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).

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).

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).

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).

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).

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).

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).

It was reported that fenitrothion persisted in leaf tissues and may act as a micro sink for the pesticide(1).

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).

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).

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).

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).

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).

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.

/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/

/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/

/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/

/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/

For more DOT Emergency Guidelines (Complete) data for Fenitrothion (16 total), please visit the HSDB record page.

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.

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)./

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/

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/

Poison Flammable Liquid

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

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

UN Hazard Class: 6.1; UN Pack Group: III