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Fenitrothion

Publication Date: 9/95

TRADE OR OTHER NAMES

The active ingredient fenitrothion is found in a variety of commercial insecticides. Trade names for products containing fenitrothion include Accothion, Agrothion, Bay 41831, Cyfen, Cytel, Dicofen, Fenstan, Folithion, Kaleit, Mep, Metathion, Micromite, Novathion, Nuvanol, Pestroy, Sumanone, Sumithion, and Verthion (4, 5, 7, 9, 10).

The common name methylnitrophos is used in Eastern Europe (16).

REGULATORY STATUS

Fenitrothion is a general use pesticide. Check with specific state regulations for local restrictions which may apply. Products containing fenitrothion must bear the Signal Word "Caution" on their label (4).

Novathion 500-E with malathion is not marketed in the U.S. (4, 25).

INTRODUCTION

Fenitrothion is a contact insecticide and selective acaricide of low ovicidal properties (14). It belongs to the organophosphate family of insecticides (4, 9). It is considered a cholinesterase inhibitor (1). Fenitrothion is effective against a wide range of pests, i.e. penetrating, chewing and sucking insect pests (coffee leafminers, locusts, rice stem borers, wheat bugs, flour beetles, grain beetles, grain weevils) on cereals, cotton, orchard fruits, rice, vegetables, and forests. It may also be used as a fly, mosquito, and cockroach residual contact spray for farms and public health programs (2, 4, 5). Fenitrothion is also effective against household insects and all of the nuisance insects listed by the World Health Organization. Its effectiveness as a vector control agent for malaria is confirmed by the World Health Organization (2, 9). Fenitrothion is non- systemic, and non-persistent (3, 8, 14).

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).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

The acute toxicity of fenitrothion to mammals is considered to be low (14, 16, 18). Typical symptoms of acute poisoning are observed in rats at doses considerably higher than those applied for parathion-methyl, a structural analogue of this substance (22). The acute oral LD50 for rats ranges between 250-800 mg/kg; 715-870 mg/kg for mice; and 500 mg/kg for guinea pigs. The acute dermal LD50 for rats is >890 mg/kg and >3,000 mg/kg for mice. The acute inhalation LC50 in rats was reported to be 5.0 mg/l (1, 2, 4, 6, 9, 10, 24).

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).

CHRONIC TOXICITY

Chronic symptoms in humans include: general malaise, fatigue, headache, loss of memory and ability to concentrate, anorexia, nausea, thirst, loss of weight, cramps, muscular weakness and tremors. Fenitrothion at sufficient dosage produces typical cholinergic poisoning (16, 18).

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).

Reproductive Effects

Damage to the nuclear membrane, decreases in staining capacity of cells, and an increase in anomalous mitoses were reported in monolayer cultures of fibroblasts taken from rats that received 0.1 or 0.2 of the LD50 level of fenitrothion daily during the first 15 days of pregnancy. However, the results were not dosage related, nor was there any change in rate of proliferation or mitotic phase distribution from that of the controls (16, 18). Behavioral deficits have been noted in newborn mammals (8).

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).

Teratogenic Effects

No teratogenic effects were observed in albino rabbits dosed with 0, 0.3 or 1 mg fenitrothion/kg/day in gelatine capsules on gestation days 6 through 18 (25, 27).

Mutagenic Effects

No mutagenic effects were seen in Drosophila melanogaster or mice (16, 18).

Carcinogenic Effects

In a two-year feeding study in rats (50 males and 50 females), no dose- related increase in tumor incidence was found upon histopathological examinations of all groups (25, 27, 28).

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).

Organ Toxicity

One of the contaminants of fenitrothion, O,O,S-trimethyl phosphorothioate, has a distinct cytotoxic effect on the lungs of rats and is known to modulate immune responses in mice (16, 18). Fenitrothion is an immunotoxin (8).

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).

Fate in Humans and Animals

Fenitrothion is oxidized by mono-oxygenases in animals, insects and plants and is thereby changed to derivatives containing the P=O group, which are more powerful inhibitors of cholinesterase than was the original thiophosphate. After that, further degradation occurs by rupture of a P-O-CH3 linkage which is more quickly metabolized in the liver than the P-O phenyl linkage rupture occurring with parathion, which could contribute to fenitrothion's low mammalian toxicity (13).

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).

ECOLOGICAL EFFECTS

Effects on Birds

Negative results were observed in studies on delayed neurotoxicity in hens (6, 24). The oral LD50 for chickens was reported as 28 mg/kg (10).

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).

Effects on Aquatic Organisms

The time for achieving the highest levels of uptake and the extent of retention of organophosphate residues by fish was directly related to the extent of persistence of a compound in water. Motsugo fish exposed to 0.6-1.2 mg/l of fenitrothion attained the highest body concentrations (162 mg/kg) after 3 days. Fenitrothion (4.9 mg/kg) persisted longer than 4 weeks in fish (17).

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:

Morpho Anatomical Changes:

Swelling of the abdomen of fathead minnows occured. Young Atlantic salmon exposed to 1 mg/l swam with distended fins.

Behavioral Changes:

There was a pronounced decline in various agonistic behaviors (chasing, vacating, nipping, etc.) within 2 hours of exposure to several concentrations of fenitrothion. Comfort behaviors (flicks, thrusts, etc.) increased with increasing concentration of toxicant, but declined at higher concentration. Altered station selection occured. At higher concentrations, some fish were unable to maintain position and were swept downstream. After a 5-hour exposure, fish swam near the surface with bloated stomachs and heads pointing downward. Movement was slowed so much that Atlantic salmon did not attempt to avoid capture with a dipnet. Salmon parr exposed to 1 mg/l fenitrothion were more vulnerable to predation by brook trout.

Biochemical Changes:

Acetylcholinesterase activity was inhibited 13% to 25% after various sublethal concentrations of fenitrothion. Cholinesterase activity in the erythrocytes, gills, heart, and serum of rainbow trout was reduced within 1 hour after exposure to fenitrothion.

Respiratory Effects:

Oxygen consumption of Labeo rohita exposed to fenitrothion progressively decreased with increasing concentrations of insecticide. Exposure caused increased ventilation rate and buccal amplitude at concentrations slightly higher than the 48-hour LC50.

Effect on Growth:

Orally administrated fenitrothion had no effect on the growth of rainbow trout (20).

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).

Effects on Other Animals (Nontarget species)

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).

ENVIRONMENTAL FATE

In studies of lesser date moth control, fenitrothion was added to a 1:1 mixture of wheat flour and pollen grains. This mixture was dusted on female clusters of date palms at the time of pollination. Not only did it prove to be effective, but this method of application was less environmentally polluting than the use of high-pressure sprays (3).

Breakdown of Chemical in Soil and Groundwater

Preliminary data indicates fenitrothion degrades fairly rapidly in soil with a half-life of less than one week in non-sterile muck, sandy loam soils. The compound is intermediately mobile in a variety of soils ranging from sandy loam to clay (4, 24).

Breakdown of Chemical in Surface Water

Surface foam on lakes acts as a scavenger and a trap for organic pollutants. Following aerial spraying of fenitrothion, 701 micrograms/l of fenitrothion was recorded in a surface slick formed by wind actions, compared to 9.5 micrograms/l in the subsurface water (17).

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).

Breakdown of Chemical in Vegetation

Damage to cabbage and fruit is possible only if the application dose is exceeded. Fenitrothion has been know to be phytotoxic to cotton, Brassica crops, and certain fruit crops when high rates were applied. Certain apple varieties may be russeted (1, 5).

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).

Breakdown of Chemical in Air

An experiment was carried out in a vacant dormitory building in order to establish the airborne residue of concentrations of seven pesticides used for cockroach control. Airborne concentrations of fenitrothion on the day of application were 3 micrograms/cubic meter. All were below 0.7 micrograms/cubic meter by the third day after application. The airborne concentrations correlated well with the vapor pressures of the various pesticides (13).

PHYSICAL PROPERTIES AND GUIDELINES

Exposure Guidelines:

ADI: temporary for man 0.003 mg/kg (until 1986) (9). 0.005 (22)

Physical Properties:

Fenitrothion is completely stable for two years if stored at temperatures between 20 and 25 degrees C. Storage temperature should not exceed 40 degrees C. It is unstable in alkaline media (16, 18). The thermal stability of this compound is low, and when it is heated above 100 degrees C it undergoes Pishchemuka isomerization and may decompose explosively. It must be stored in enameled, aluminum or glass containers. Iron promotes decomposition of fenitrothion (12).
Appearance: pure material forms a yellowish brown liquid with an unpleasant odor (16, 18)
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)

BASIC MANUFACTURERS

CHEMINOVA Agro A/S
P.O. Box 9
Lemvig, Dk-7620 Denmark
Telephone: 45-97-83-4100
Emergency: 45-97-83-4100

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received: December, 1994

Sumitomo Chemical America, Inc.
345 Park Avenue
New York, NY 10154

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received:

REFERENCES

  1. The Agrochemicals Handbook. 1983. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Worthing, C. R. (ed.) The Pesticide Manual: A World Compendium. 1983. Seventh Edition. Published by The British Crop Protection Council.
  3. Hassall, K. A. 1990. The Biochemistry and Uses of Pesticides: Structure, Metabolism, Mode of Action and Uses in Crop Protection. 2nd edition. VCH Publishers, NY.
  4. Meister, R. T. 1994. Farm Chemicals Handbook.. Meister Publishing Co. Willoughby, OH.
  5. Thomson, W. T. 1989. Agricultural Chemicals. Book I: Insecticides. Thomson Publications, Fresno, CA.
  6. Occupational Health Services, Inc. 1993 (August). OHS Database. MSDS for Fenitrothion. OHS Inc., Secaucus, NJ.
  7. Thomson, W. T. 1992. Agricultural Chemicals Book I: Insecticides. Thomson Publications, Fresno, CA.
  8. Briggs, S. A. 1992. Basic Guide to Pesticides: Their Characteristics and Hazards. Hemisphere Publishing Corp., Washington, Philadelphia, London.
  9. Worthing, C. R. (ed.) 1987. The Pesticide Manual: A World Compendium. Eighth edition. Published by The British Crop Protection Council.
  10. Fairchild, E. J. (ed.) 1977. Agricultural Chemicals and Pesticides: A Subfile of the Registry of Toxic Effects of Chemical Substances. U. S. Department of Health, Education, and Welfare, Cincinnati, OH.
  11. Lehotsky, Kornelia, M. Judit Szeberenyi and Anna Kiss. 1989. Behavioral Consequences of Prenatal Exposure to the Organophosphate Insecticide Sumithion. Neurotoxicology and Teratology, 11:321-324.
  12. Melnikov, N. N. 1971. Chemistry of Pesticides. Springer-Verlag. New York, Heidelberg, Berlin.
  13. Hayes, W. J. and E. R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, General Principles, Vol. 2. Academic Press, Inc., NY.
  14. Spencer, E. Y. 1981. Guide to the Chemicals Used in Crop Protection. 7th edition. Publication 1093. Research Branch. Agriculture Canada.
  15. Elzen, G. W. 1989. Sublethal Effects of Pesticides on Beneficial Parasitoids. In: Pesticides and Non-target Invertebrates. Ed. by Paul C. Jepson. Intercept Ltd. Dorset, England. pp 129-150.
  16. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Classes of Pesticides, Vol. 2. Academic Press, Inc., NY.
  17. Murty, A. S. 1986. Toxicity of Pesticides to Fish. Vol. I. CRC Press, Boca Raton, FL.
  18. Hayes, W. J., Jr. 1982. Pesticides Studied in Man. Williams and Wilkins. Baltimore, London.
  19. Pimentel, David. 1971. Ecological Effects of Pesticides on Non-Target Species. Cornell University, Ithaca, NY.
  20. Murty, A. S. 1986. Toxicity of Pesticides to Fish. Vol. II. CRC Press, Boca Raton, FL.
  21. Francis, B. M. 1994. Toxic Substances in the Environment. John Wiley and Sons, NY.
  22. Organophosphorus Pesticides: Criteria (Dose/Effect relationships) for Organophophorus Pesticides. 1977. Published for the Commission of the European Communities by Pergamon Press.
  23. U.S. Environmental Protection Agency. July, 1987. Guidance for the Reregistration of Pesticide Products Containing Fenitrothion. US EPA, Office of Pesticide Programs, Registration Div., Washington, DC. 132 pp.
  24. U.S. Environmental Protection Agency. July 30, 1987. Pesticide Fact Sheet Number 142. US EPA, Office of Pesticide Programs, Registration Div., Washington, DC.
  25. Data Manual: Novathion Technical. March 1987. Cheminova Agro A/S. Lemvig, Denmark.
  26. FAO/WHO. 1970. 1969 Evaluations of some pesticide residues in food. The Monographs. WHO. Rome, Italy.
  27. FAO/WHO. 1975. 1974 Evuations of some pesticide residues in food. The Monographs. WHO: Pesticide Residues Series, No. 4. Rome, Italy.
  28. National Research Council. 1975. Proceedings of a symposium on fenitrothion: the long-term effects of its use in forest ecosystems. Ottawa, Canada. p. 307-319.