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Methyl Parathion

Publication Date: 5/94

TRADE OR OTHER NAMES

Alternate common names are parathion-methyl and and metafos (3). Trade names include Bladan M, Cekumethion, Dalf, Dimethyl Parathion, Devithion, E 601, Folidol-M, Fosferno M50, Gearphos, Kilex Parathion, Metacide, Metaphos, Metron, Nitrox 80, Partron M, Penncap-M, Tekwaisa.

REGULATORY STATUS

Some or all applications of methyl parathion may be classified as Restricted Use Pesticides (RUP) by EPA (3). RUPs may be purchased and used only by certified applicators. Products containing methyl parathion must bear the signal word "Danger" (3). No worker may enter a field treated with methyl parathion within 48 hours of treatment (EPA 1980).

INTRODUCTION

Methyl parathion is an insecticide and acaricide used to control boll weevils and many biting or sucking insect pests of agricultural crops (3). It kills insects by contact, stomach and respiratory action. Methyl parathion is available in dust, emulsifiable concentrate, ULV liquid, microencapsules and wettable powder formulations (3).

Methyl parathion is one of a class of insecticides referred to as organophosphates. These chemicals act by interfering with the activities of cholinesterase, an enzyme that is essential for the proper working of the nervous systems of humans, animals and insects. Please refer to the Toxicology Information Brief on cholinesterase-inhibition for a more detailed description of this topic.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Methyl parathion is highly toxic by inhalation and ingestion, and moderately toxic by dermal adsorption (9). As with all organophosphates, methyl parathion is readily absorbed through the skin. Skin which has come in contact with this material should be washed immediately with soap and water and all contaminated clothing should be removed. Accidental skin and inhalation exposure to methyl parathion have caused human fatalities. Methyl parathion may cause contact burns to the skin or eyes (13).

Because methyl parathion has a short half-life (1 hour on cotton) when applied to crops, the risk of exposure to agricultural workers is low. Factory workers who handle quantities of concentrated methyl parathion are at a higher risk (2). Exposure may occur during mixing, spraying or application of methyl parathion, during cleaning and repair of equipment or during early re-entry into fields (20). Persons with respiratory ailments, recent exposure to cholinesterase inhibitors, cholinesterase impairment, or liver malfunction are at increased risk from exposure to methyl parathion. High environmental temperatures or exposure of the chemical to visible or UV light may increase its toxicity (9).

The organophosphate insecticides are cholinesterase inhibitors. They are highly toxic by all routes of exposure. When inhaled, the first effects are usually respiratory and may include bloody or runny nose, coughing, chest discomfort, difficult or short breath, and wheezing due to constriction or excess fluid in the bronchial tubes. Skin contact with organophosphates may cause localized sweating and involuntary muscle contractions. Eye contact will cause pain, bleeding, tears, pupil constriction, and blurred vision. Following exposure by any route, other systemic effects may begin within a few minutes or be delayed for up to 12 hours. These may include pallor, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred vision, constriction or dilation of the eye pupils, tears, salivation, sweating, and confusion. Severe poisoning will affect the central nervous system, producing incoordination, slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle contractions, twitching, tremors of the tongue or eyelids, and eventually paralysis of the body extremities and the respiratory muscles. In severe cases there may also be involuntary defecation or urination, psychosis, irregular heart beats, unconsciousness, convulsions and coma. Death may be caused by respiratory failure or cardiac arrest (9).

Some organophosphates may cause delayed symptoms beginning 1 to 4 weeks after an acute exposure which may or may not have produced immediate symptoms. In such cases, numbness, tingling, weakness and cramping may appear in the lower limbs and progress to incoordination and paralysis. Improvement may occur over months or years, but some residual impairment will remain (9).

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for methyl parathion in rats is 18 to 50 mg/kg, in mice is 14.5 to 19.5 mg/kg, in rabbits is 420 mg/kg, in guinea pigs is 1270 mg/kg, and in dogs is 90 mg/kg (2, 3, 9). The dermal LD50 in rats is 63 to 491 mg/kg, in mice is 1200 mg/kg, and in rabbits is 300 mg/kg (3, 9)

The lethal concentration fifty, or LC50, is that concentration of a chemical in air or water that kills half of the experimental animals exposed to it for a set time period. The 4-hour inhalation LC50 for methyl parathion in rats is 34 mg/m3, and in mice is 120 mg/m3 (9).

CHRONIC TOXICITY

Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking and drowsiness or insomnia. An influenza-like condition with headache, nausea, weakness, loss of appetite, and malaise has also been reported (9).

Studies with human volunteers have found that 1 to 22 mg/person/day have no effect on cholinesterase activity. In a 4-week study of volunteers given 22, 24, 26, 28 or 30 mg/person/day, mild cholinesterase inhibition appeared in some individuals in the 24, 26 and 28 mg dosage groups. In the 30 mg/person/day (about 0.43 mg/kg/day) group, red blood cholinesterase activity was depressed by 37%. When methyl parathion was fed to dogs for 12 weeks, a dietary level of 1.25 mg/kg soon caused a significant depression of red blood cell and plasma cholinesterase. A dietary level of 0.125 mg/kg produced no effects (2).

The EPA has established a Lifetime Health Advisory (LHA) level of 60 micrograms per liter (ug/l) for 4-nitrophenol, a breakdown product of methyl parathion, in drinking water. This means that EPA believes that water containing 4-nitrophenol at or below this level is acceptable for drinking every day over the course of one's lifetime, and does not pose any health concerns. However, consumption of 4-nitrophenol at high levels well above the LHA level over a long period of time has been shown to cause adverse health effects, including damage to the liver, respiratory stress, and inflammation of the stomach in animal studies (11).

Reproductive Effects

In a 3-generation study with rats fed dietary levels of 0, 0.5, or 1.5 mg/kg/day, there was reduced weanling survival, reduced weanling weights, and an increase in the number of stillbirths at the 1.5 mg/kg. Some of these effects also occurred at the 0.5 mg/kg dosage level. In rats and mice, a single injection of LD50 rates during pregnancy caused suppression of fetal growth and bone formation in the offspring that survived. These injections also caused high fetal mortality. The rats had been injected with 25 mg/kg on day 12 of pregnancy, and the mice were injected with 60 mg/kg on day 10. In another study, there were no adverse effects observed in the offspring of rats given oral doses of 4 or 6 mg/kg on day 9 or 15 of pregnancy (2). Once in the bloodstream, methyl parathion may cross the placenta (9). Large doses of methyl parathion injected into pregnant rats and mice reduced litter size and survival of offspring (6).

Teratogenic Effects

Methyl parathion is a possible human teratogen (14).

Mutagenic Effects

No signs of mutagenicity were seen in mice given dosages of 5 to 100 mg/kg, nor in mice fed methyl parathion for 7 weeks (2). No mutagenic changes were seen when cell cultures were grown from factory workers who had been exposed to low levels of methyl parathion for very long periods of time (15, Mut. Res. 103 (1):71-76. 1982). Other research has shown mutations to occur in cells exposed to methyl parathion (Mut. Res. 102 (1):89-102. 1982).

Carcinogenic Effects

Methyl parathion is not a suspected carcinogen (20, 21).

Organ Toxicity

Methyl parathion primarily affects the nervous system through inhibition of cholinesterase, an enzyme required for proper nerve functioning (9).

Consumption of 4-nitrophenol, a breakdown product of methyl parathion, at high levels well above the Lifetime Health Advisory level of 60 ug/l over a long period of time has been shown to cause adverse health effects, including damage to the liver, respiratory stress, and inflammation of the stomach in animal studies (11).

Fate in Humans and Animals

Methyl parathion is rapidly absorbed into the bloodstream through all normal routes of exposure. Following administration of a single oral dose, the highest concentration of methyl parathion in body tissues occurred within 1 to 2 hours (2). Metabolism occurs in the liver, eventually to phenols which can be detected in the urine(14). Methyl parathion does not accumulate in the body. It is almost completely excreted through the kidneys (urine) within 24 hours (8).

ECOLOGICAL EFFECTS

Effects on Birds

A number of studies indicate that birds are highly tolerant of the effects of methyl parathion (NRC Drinking Water and Health 1977).

Effects on Aquatic Organisms

Methyl parathion is toxic to fish and to animals which eat fish (8). Other studies, however, indicate that fish kills may be caused by the following series of events. Methyl parathion kills insects and crustaceans (i.e. crayfish) which feed on algae. When these organisms are killed , algal populations rapidly "bloom," consuming all available oxygen in the pond water. It may be the lack of oxygen which kills fish (Ecotoxicol. Environ. Safety 8 (5):482-495. 1984).

Effects on Other Animals (Nontarget species)

Methyl parathion is moderately toxic to mammals such as rats, dogs and rabbits (8).

ENVIRONMENTAL FATE

Methyl parathion is rapidly metabolized by both plants and animals and it is not expected to persist or bioconcentrate (7).

Breakdown of Chemical in Soil and Groundwater

In most situations, methyl parathion adsorbs to soil particles and degrades rapidly. It is therefore unlikely to contaminate groundwater (3, 4, 7) and has rarely been detected in groundwater outside of areas where it is used on farms. It has been detected in the groundwater of Mississippi at 8 ppb (12). When it is applied as an insecticide, methyl parathion breaks down within several months, primarily by photolysis and biodegradation. The rate of degradation increases with temperature and with exposure to sunlight. Its biodegradation half-life in soil is 10 days to 2 months. Degradation was faster in flooded soils than in non-flooded soils. Mineralization may occur, especially in moist soils. Some volatilization of applied methyl parathion may occur. When large concentrations of methyl parathion reach the soil, as in an accidental spill, degradation will occur only after many years, with photolysis being the dominant route (7). It is unlikely that methyl parathion will run-off into surface waters (J. Environ. Qual. 9:665-672. 1980). 4-Nitrophenol is an insecticide and a break down product of methyl parathion. It may have been detected at very low levels by EPA during a national survey of drinking water wells. EPA is uncertain and cannot quantify the amount or frequency of 4-nitrophenol in drinking water wells, because the tests used to detect the presence of 4-nitrophenol are not reliable for measuring concentrations of this material in water. However, 4-nitrophenol does not adsorb to soil particles and may contaminate groundwater (11).

Breakdown of Chemical in Water

Methyl parathion degrades rapidly in seawater, lake, and river waters, with 100% degradation occurring within 2 weeks to 1 month or more. Degradation is faster in the presence of sediments, and is faster in fresh water than in salt water. Mineralization occurs at a rate of 5 to 11% in 4 days in rivers, and more slowly in marine waters. In water, methyl parathion is subject to photolysis, with a half-life of 8 days during the summer and 38 days in winter (7).

Breakdown of Chemical in Vegetation

Uptake and metabolism of methyl parathion in plants is fairly rapid. Four days after applying methyl parathion to the leaves of corn, it was almost completely metabolized (7).

PHYSICAL PROPERTIES AND GUIDELINES

Pure methyl parathion is a white crystalline solid with a characteristic odor of rotten eggs or garlic. Technical product is light to dark tan with about 80% purity (2). Methyl parathion is hydrolyzed by, and therefore not compatible with, alkaline materials. It may react with strong oxidizers. Methyl parathion should not be heated above 55 degrees C. It decomposes rapidly above 100 degrees C, creating an explosion hazard. Thermal decomposition may release toxic fumes of dimethyl sulfide, sulfur dioxide, carbon monoxide, carbon dioxide, phosphorus pentoxide, and nitrogen oxides (3, 9).

The National Fire Protection Agency ratings for methyl parathion include:

A. health: 4 = a few whiffs of the fumes could prove fatal; normal fire fighting gear is inadequate to protect against any exposure to the skin.

B. flammability: 1 = solids which must be preheated to burn; 3 = liquids which when burning can not be extinguished with water (in fact water may be dangerous to use). Dusts may create flash fires.

C. reactivity: 2 = normally unstable materials which will react violently (with water). Are potentially explosive when mixed with water (18).

Methyl parathion will react violently with oxidizing agents (16). It may explode upon heating. The temperature around containers of methyl parathion should not exceed 25-30 degrees C (75-85 degrees F) (1).

Contaminated clothing is best thrown away. It takes many washings to bring the level of methyl parathion down to non-hazardous levels (Bull. Envir. Contam. Tox. 27:518-523; 29:461-468. 1982).

Exposure Guidelines:

0.2 mg/m3 OSHA TWA (skin) (9)
0.2 mg/m3 ACGIH TWA (skin) (9)
0.2 mg/m3 NIOSH Recommended TWA (skin) (9)

Physical Properties:

CAS #: 298-00-0
Specific gravity: 1.20 - 1.36 at 20 degrees C (2, 3)
H20 solubility: 55 - 60 mg/l at 20 degrees C (3)
Solubility in other solvents: Soluble in dichloromethane, 2-propanol, toluene, and most organic solvents.
Slightly soluble in aliphatic hydrocarbons, and in light petroleum and mineral oils.Nearly insoluble in n-hexane (2, 3, 9).
Melting point: 35 - 36 degrees C (97 degrees F) (3, 9)
Boiling point: 143 degrees C (7); 228 degrees F (109 degrees C) at 0.05 mm Hg (9)
Decomposition temperature: 100 degrees C (9)
Flashpoint: 42 degrees C (3)
Vapor pressure: 0.97 x 10 to the minus 5 mm Hg at 20 degrees C (2)
Koc: 5100 g/ml (4)
Chemical Class/Use: Organophosphate insecticide

BASIC MANUFACTURER

Cheminova Agro A/S
P.O. Box 9
DK-7620 Lemvig Denmark
Telephone: 45-9-783-4100

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: January, 1994

REFERENCES

  1. Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby, OH: Meister Publishing Co.
  2. Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  3. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  4. U.S. Department of Agriculture, Soil Conservation Service. 1990 (Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0 (Summary). USDA - Soil Conservation Service, Syracuse, NY.
  5. Worthing, C.R. (ed.). 1987. The pesticide manual: A world compendium. 8th Ed. The British Crop Protection Council. Croydon, England.
  6. Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore, MD: Williams & Wilkins.
  7. Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis Publishers, Chelsea, MI.
  8. Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  9. Occupational Health Services, Inc. 1991 (Feb. 25). MSDS for Methyl Parathion. OHS Inc., Secaucus, NJ.
  10. Witt, J. M., ed. 1985. Chemistry, biochemistry, and toxicology of pesticides. Proceedings of an Extension Service Short Course at Oregon State University. Pest control education program. Eugene, OR.
  11. US Environmental Protection Agency. 1990 (Fall). National Pesticide Survey: 4-Nitrophenol. Office of Water, Office of Pesticides and Toxic Substances, US EPA, Washington, DC.
  12. Agency for Toxic Substances and Disease Registry. 1990 (Oct.). Toxicological Profile for Methyl Parathion. Public Health Service, US Dept. of Health and Human Services, Washington, DC.
  13. Department of Transportation. 1984. Emergency Response Guidebook: Guidebook for hazardous materials incidents. Washington, DC: U.S. DOT.
  14. Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and human health. New York: Springer-Verlag.
  15. TOXNET. 1985. National library of medicine's toxicology data network. Hazardous Substances Databank. Public Health Service. National Institute of Healtyh. U.S. Department of Health and Human Services. Bethesda, MD: NLM.
  16. Sax, N.I. 1975. Dangerous properties of industrial materials. 4th Ed. New York: Van Nostrand Reinhold Co.
  17. Gosselin, R.E. 1984. Clinical toxicology of commercial products. 5th Ed. Baltimore, MD: Williams & Wilkins.
  18. National Fire Protection Association (NFPA). 1978. Fire Protection Guide. Hazardous Materials.
  19. Review by Cheminova Agro A/S. January 12, 1994.
  20. Environmental Health Criteria 145. Methyl parathion. World Health Organization, Geneva. 1993.
  21. IARC Monographs on the Carcinogenic Risk of Chemicals to Humans, Vol. 30, 1983. Supplement 7. 1987.