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Fenitrothion |
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A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Michigan State University, Oregon State University, and University of California at Davis. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.
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The common name methylnitrophos is used in Eastern Europe (16).
Novathion 500-E with malathion is not marketed in the U.S. (4, 25).
Fenitrothion was introduced in 1959 by both Sumitomo Chemical Company and Bayer Leverkusen and later by American Cyanamid Company (9, 16, 18). Fenitrothion is far less toxic than parathion with a range of insecticidal activity that is very similar and is similar enough in structure to be produced in the same factories. The difference in precursor chemicals might make it somewhat more expensive, but it is heavily used in other countries, including Japan, where parathion has been banned (21).
Fenitrothion comes in dust, emulsifiable concentrate, flowable, fogging concentrate, granules, ULV, oil-based liquid spray, and wettable powder formultaions (1, 2, 4, 5). It is available as a 95% concentrate, 50% emulsifiable concentrate, 40% and 50% wettable powder and 2%, 2.5%, 3% and 5% dusts (16, 18). It is compatible with other neutral insecticides (1).
Other lethal dose values for rats were given as: 378 mg/m3/4-hour inhalation LC50; 950 mg/kg intratracheal LD50; 33 mg/kg intravenous LD50; 300 mg/kg intraperitoneal LD50 (6). Another source reported the dermal LDlo for rats to be 300 mg/kg (10).
Mice had acute toxicity values of 2500 mg/kg dermal LD50; 229 mg/kg oral LD50; 1,000 mg/kg subcutaneous LD50; 280 mg/kg intraperitoneal LD50; and 1,000 mg/kg intracerebral LD50 (6).
Guinea pigs were reported to have acute toxicity values of 500 mg/kg oral LD50; and 112 mg/kg intravenous LD50 (6). The oral acute toxicity for cats was 142 mg/kg (6).
Studies reported primary dermal irritation; mild dermal irritation was reported in a rabbit study. Primary eye irritation was also reported; mild irritation was seen after a single application of 0.1 ml of fenitrothion into unwashed eyes of albino rabbits (24).
The acute oral toxicity reported for a human female was a TDlo of 800 mg/kg (6).
In a study with rats, a dietary level of 500 ppm for 90 days was tolerated. They grew normally, and cholinesterase in plasma, red cells and tissues was decreased. A dietary level of 30 ppm for six months decreased the red cell and brain cholinesterase of female but not male rats; neither sex showed any sign of toxicity. A dietary level of 5 ppm for 92 weeks was a no- effect-level (NEL) (16, 18).
Mice that received fenitrothion at a dietary level of 1000 ppm 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. Monkeys are more susceptible than dogs. A dosage of 2 mg/kg/day produced no effect on serum or erythrocyte cholinesterase in dogs but after 2 months of administration, did cause a reduction of erythrocyt enzyme activity in monkeys. A dietary concentration of 5 ppm was found to be a NEL in calves (16, 18).
Adverse effects and death were observed in rats given a diet containing 400 ppm for 63 weeks. Some of the animals survived, although at this level there was a 100% drop in erythrocyte cholinesterase. In 1.77-year feeding trials, the NEL for rats was 5 mg/kg diet (2). In dogs, doses of 0, 2, 9 and 40 mg/kg body weight/day of fenitrothion were administered for 98 days; at 40 mg/kg/day signs of poisoning and cholinergic stimulation were observed (22).
Rats receiving a diet containing 10 ppm showed a slight drop in erythrocyte cholinesterase activity after 5 weeks of treatment; activity returned to normal 2 weeks after treatment stopped; with a 20 ppm level dose there was a reduction inerythrocyte and brain cholinesterase activity. No significant effect on cholinesterase activity was observed in plasma or erythrocytes at a dietary level of 20 ppm, and it was only with 100 ppm or more that effects were observed; enzyme activity returned to normal 30-40 days after the end of treatment (22).
Rats fed on a diet containing 400 ppm for two years showed a 100% drop in erythrocyte cholinesterase activity. At 100 ppm, 10-30% depression of brain and 30-65% depression of erythrocyte and plasma cholinesterase activity occurred (22).
In dogs, a slight depression in blood plasma and erythrocyte cholinesterase activity was observed after 60 days with a dosage level of 9 mg/kg/day. Moderated depression occurred with 40 mg/kg/day for 29 days (22).
Daily feeding of 100 mg/kg body weight/day over 60-90 days to dairy cows and sheep does not result in its excretion in milk (1).
Other studies indicated that there is a significant inhibition of growth and various cholenergic signs for 2 to 3 weeks following administration of 500 ppm fenitrothion in rats (14). The no-observable-effect-level (NOEL) for brain and red blood cell cholinesterase is 10 ppm, while the systemic NOEL for plasma inhibition in dogs is 5 ppm (24).
Sumithion 50EC (a product containing fenitrothion) has been shown to cause delayed neurotoxicity in adult rats, as well as humans (11).
Results from a study where pregnant rats were treated with 0, 5, 10 and 15 mg/kg of the product Sumithion 50EC daily through gestation days 7 to 15, showed the following results:
There were no significant differences in number of pups born per litter, weight per litter or day of eye and ear opening. There was a significant difference in mortality up to day 16 postpartum: at the 15 mg/kg dose, 17.5% of the pups died; at the 10 and 5 mg/kg dose, 16.0% of the pups died; at the 0 mg/kg dose, 5% of the pups died. One pup in the 15 mg/kg group was anophthalmic and one developed tremor and ataxia on day 16, and thus both were excluded from the study. The remaining pups gained weight normally and showed no overt signs of intoxication.
No significant behavioral effects could be measured at the lowest dose of 5 mg/kg/day. At the 10 and 15 mg/kg/day doses, while several of the behavioral outcomes were significantly different from controls, there seemed to be a difference between the "simple" behavioral measures such as motor activity and motor coordination and the more "complex" measures such as conditioned escape and social interactions.
Behavioral measures showed significant alterations as long as 104 days following birth, indicating that prenatal intoxication with Sumithion had persistent effects that showed the offspring to be different from untreated animals.
The lack of effect at the 5 mg/kg/day dose indicates that this chemical has a steep dose-response function and that exposure of agricultural workers should be carefully monitored (11).
Fenitrothion was administered in the diet to groups of 50 male and 50 female ICR Swiss mice at dose levels of 0, 30, 100 and 200 ppm for 78 weeks. There was no evidence of compound-related effects on appearance and behavior, body weight or mortality. Gross necropsies revealed no consistent compound- related changes in any organs or tissues. The histopathological examinations revealed no consistent treatment-related increase in tumor incidences (25, 28).
In patients who died of pesticide poisoning, 240 ppm fenitrothion were found in the liver (13).
Fenitrothion is considered a suspect viral enhancer, implicated in Reye's syndrome (8).
Studies in the mouse, rat and guinea pig have shown that fenitrothion is rapidly absorbed from the mammalian gastrointestinal tract. The presence of the oxygen analogue has been demonstrated in all tissues examined and this oxygen analogue has been detected in blood one minute after an intravenous injection of fenitrothion (22).
Daily fenitrothion doses of 2.5 and 5 mg/man/day for 5 days were excreted within a 12 hour period and there was no indication of accumulation. Fenitrothion applied to the skin of rats disappeared most rapidly in the first hour, suggesting an absorption rate of slightly over 1%. After 31 hours, the highest concentration, other than on the skin, was found in the cartilaginous part of the bones (6, 16, 18).
When volunteers were given single oral doses ranging from 2.5 to 20 mg/person, the maximal concentration of p-nitro-m-cresol in the urine was reached within 12 hours, and nearly the entire amount discharged was eliminated during the first 24 hours. Although the amount recovered was directly dosage-related, the proportion recovered was inversely dosage- related. With one exception, cholinesterase activity remained normal following these doses (16, 18).
The half-life of fenitrothion was noticeably longer after 10 doses of 30 mg/kg/day than after a single dose of 300 mg/kg. It was concluded that this effect was caused by suppression of the metabolism of the compound during its repeated administration and was associated with inhibition of demethylation and hydrolysis by microsomal enzymes (16, 18).
Fenitrothion is decomposed rapidly in tissues to desmethylsumition, dimethyl-phosphorothioic acid and phosphorothionic acid (14). The oxygen derivative of fenitrothion is formed in the microsomal fraction of the cell, the main metabolizing organs being the liver and kidneys. The major excretion product is 3-methyl-4-nitrophenol, which can be further oxidized to 3-carboxy- 4-nitrophenol. Another metabolite is the desmethyl-derivative (22).
Eighteen people were subjected to clinical examination while spraying fenitrothion. The level of blood plasma cholinesterase was determined at regular intervals but no abnormalities were found. Blood cholinesterase was analysed in a large number of inhabitants of Nigeria where fenitrothion had been sprayed. After spraying for one week, a 50% reduction in blood cholinesterase in 20 spraymen was recorded. Rapid return to normal levels subsequently took place (22).
Single oral doses of between 2.5 and 20 mg fenitrothion (approximately 0.042 to 0.33 mg/kg body weight) were administered orally to 24 human subjects. The urinary excretion of the metabolite 3-methyl-4-nitrophenol was almost complete in 24 hours, the excretion peak occurring after 12 hours. The plasma cholinesterase level did not decline, except in one of the subjects who had received 0.33 mg/kg fenitrothion (22).
Fenitrothion was found to be highly toxic to upland gamebirds and slightly toxic to waterfowl (acute oral toxicity value to bobwhite quail and mallards was determined to be 23.6 mg/kg and 1,190 mg/kg, respectively) (4, 24). The LC50 for pheasants was 450 to 500 ppm in diets of 2-week-old birds when fed fenitrothion-treated feed for 5 days, followed by untreated feed for 3 days (19).
Fenitrothion is considered somewhat toxic to fish (5). The 96-hour LC50 was 1.7 ppm for brook trout and 3.8 ppm for bluegill sunfish; moderately toxic to both warmwater and coldwater fish (4, 24). The 96-hour LC50 to various species of North American freshwater fish has also been reported as 2-12 micrograms/l. The chronic toxicity of fenitrothion to fish is considered low (20). The 48-hour LC50 values for carp ranged between 2.0 mg/l and 4.1 mg/l (1, 2, 9). One source stated that aerial spraying of fenitrothion at 2 or 3 oz/acre, on New Brunswick forests has been reported to have no deleterious effect on fish in streams in the treated area (17).
In a study on the acute toxicity of fenitrothion to rainbow trout, embryos were found to be the least sensitive, the sacfry stage was intermediate, and fingerlings and adults were the most sensitive. The toxicity of fenitrothion to rainbow trout increased with increasing temperature. The sublethal effects of fenitrothion exposure on fish include:
The compound is considered very toxic to crustaceans and aquatic insects and has a medium toxicity to aquatic worms (8). A freshwater invertebrate toxicity (48-hour or 96-hour EC50) reported fenitrothion to be very highly toxic to aquatic invertebrates (3 ppb for Gammarus fasciatus ) (24).
There is sufficient information to characterize fenitrothion as highly toxic to honeybees (acute toxicity value = 0.383 micrograms/bee) when bees are exposed to direct treatment or to dried residues on foliage (1, 5, 23). Fenitrothion is considered toxic to spider mites with long residual action (14).
Fenitrothion, applied to host eggs at field rates in the laboratory were found to be highly toxic to Trichogramma orasiliensis released on the eggs, causing 84-100% mortality in 24 hours (15).
The long-term effects of fenitrothion and phosphamidon were evaluated on predaceous carabid beetles and lycosid spiders one year after treatment of Northwestern Ontario forests at 6 oz/A and 4 oz/A, respectively. The populations of these predators were clearly suppressed in the treated area. The results "did not imply a one year persistence of the insecticides, but rather a persistent disturbance of the ecosystem" (19).
The acute oral toxicity of fenitrothion to mule deer was reported to be 727 mg/kg (19).
Another study indicated the half-life for the disappearance of fenitrothion at 23 degrees C and pH 7.5 in buffered lake water and natural lake water in the dark (10 ppm sol.) was 21.6 and 49.5 days, respectively. In a field experiment (pH 7.0-7.5, 19-23 degrees C), the half-life of fenitrothion was 1.5-2 days upon spraying of a 10% fenitrothion EC-formulation at a rate of 4 oz/A to a model water system (25).
In a study conducted by FAO/WHO, about 50% of 32P-labelled fenitrothion sprayed on rice plants penetrated into the tissues in 24 hours. At the end of this period only 10% was left, indicating rapid decomposition. Some fenitrooxon was formed but it disappeared from the tissues more rapidly than fenitrothion. Rice grains harvested 46 days after treatment contained 0.0007 ppm fenitrothion and less than 1 ppm of p-nitrocresol and dimethyl phosphorothioic acid (25).
Although the oxon may form in plants, it occurs only during the first few days after treatment and in proportions (ca 1%) smaller than those in animals. Desmethyl compounds occur only in minor amounts in plants.
The half-life of fenitrothion in green plants ranges between the values established for Parathion and Parathion-Methyl, i.e. between one and two days; the half-life of the oxon is estimated to be only a few hours (FAO/WHO) (25).
| ADI: | temporary for man 0.003 mg/kg (until 1986) (9). 0.005 (22) |
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| Appearance: | pure material forms a yellowish brown liquid with an unpleasant odor (16, 18) |
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| CAS No.: | 122-14-5 (1, 6) |
| Chemical name: | O,O-dimethyl O-4-nitro-m-tolyl phosphorothioate (IUPAC), O,O-dimethyl O-(3-methyl-4-nitrophenyl) phosphorothioate (CA), O,O-dimethyl O-(3-methyl-4-nitrophenyl) thiophosphate (1) |
| Molecular weight: | 277.25 (10, 16, 18) |
| Molecular formula: | C9H12NO5PS (10, 16, 18) |
| Chemical Class/Use: | organophosphate/contact insecticide; selective acaricide (4) |
| Specific gravity: | 1.3227 (6); 1.32-1.34 (14, 24); 1.3084 at 20 degrees C (12, 16, 18) |
| Solubility in water: | In water at 20 degrees C, 30 mg/l (1, 12, 25); at 30 degrees C, 14 mg/l water (2); nearly insoluble in water (3, 4); insoluble in water (16) |
| Solubility in other solvents: | Readily soluble in common organic solvents, e.g. acetone, alcohol, benzene and chlorinated hydrocarbons (1).
dichloromethane, 2-propanol, toluene (4). Hardly soluble in n-hexane (4). Soluble in ethers, methanol, xylene, ketones, esters, and aromatic hydrocarbons. Low solubility in alaphatic hydrocarbons (6, 16). At 20 -25 degrees C, > 1 kg/kg dichloromethane, methanol and xylene, 42 g/kg haxane, 0.1 - 1.0 kg/kg propan-2-ol. It is hydrolyzed by alkali; at 30 degrees C, 50% loss occurs in 4.5 hours in 10M sodium hydroxide (9) |
| Melting point: | 0.3 degrees C (24) |
| Boiling point: | 109 degrees C at 0.13 mbar; 164 degrees C at 1.3 mbar (1). 140-145 degrees C/0.1 mmHg (2, 9, 16, 18, 25). 244 degrees F (118 degrees C) at 0.05 mmHg (6). 118 degrees C at 0.01 mmHg (24) |
| Flashpoint: | 166 degrees C (closed cup) (25) |
| Vapor pressure: | 7 x 10 to the minus 5 mbar at 20 degrees C (1); 18 mPa at 20 degrees C (2) |
| Volatility: | 0.09 mg/m3 (12) |
| Kow: | 2380 (25) |
Sumitomo Chemical America, Inc.
345 Park Avenue
New York, NY 10154
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