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)

(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.

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.

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.

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: 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.

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 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.

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.

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 causing adverse effects in aquatic organisms, wildlife and the environment. Sumitomo Chemical Co. has proposed eliminating the highest risk uses, and reducing the maximum application rate for all other uses. The proposed label changes and the fact that this insecticide is not widely used (<1% of U.S. nursery acreage are treated annually) were given consideration in making the reregistration decision for this insecticide. The high-pressure handwand treatment of ornamentals and the two bait formulations are eligible for reregistration.

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.

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