Health and Safety Guide No. 75






    This is a companion volume to Environmental Health Criteria
    145: Methyl Parathion

    Published by the World Health Organization for the International
    Programme on Chemical Safety (a collaborative programme of the
    United Nations Environment Programme, the International Labour
    Organisation, and the World Health Organization)

    This report contains the collective views of an international group
    of experts and does not necessarily represent the decisions or the
    stated policy of the United Nations Environment Programme, the
    International Labour Organisation, or the World Health Organization

    WHO Library Cataloguing in Publication Data

    Methyl parathion : health and safety guide.

    (Health and safety guide ; no. 75)

    1.Methyl parathion - poisoning 2.Methyl parathion - standards
    3.Methyl parathion - toxicity 4.Environmental exposure

    ISBN 92 4 151075 7          (NLM Classification: WA 240)
    ISSN 0259-7268

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         1.1. Identity
         1.2. Physical and chemical properties
         1.3. Analytical methods
         1.4. Production and uses

         2.1. Environmental exposure
         2.2. Uptake, metabolism, and excretion
         2.3. Effects on organisms in the environment
         2.4. Effects on experimental animals and  in vitro
              test systems
         2.5. Effects on human beings

         3.1. Conclusions
         3.2. Recommendations

         4.1. Human health hazards, prevention and protection,
              first aid
              4.1.1. Advice to physicians
                 Symptoms of poisoning
                 Medical treatment
                 Health surveillance advice
         4.2. Explosion and fire hazards
         4.3. Storage
         4.4. Transport
         4.5. Spillage and disposal
              4.5.1. Spillage
              4.5.2. Disposal


         6.1. Previous evaluations by international bodies
         6.2. Exposure limit values
         6.3. Specific restrictions
         6.4. Labelling, packaging, and transport
         6.5. Waste disposal
         6.6. Other measures


    ANNEX 1


    The Environmental Health Criteria (EHC) documents produced by the
    International Programme on Chemical Safety include an assessment of
    the effects on the environment and on human health from exposure to
    a chemical or combinations of chemicals, or physical or biological
    agents. They also provide guidelines for setting exposure limits.

    The purpose of a Health and Safety Guide is to facilitate the
    application of these guidelines in national chemical safety
    programmes. The first three sections of a Health and Safety Guide
    highlight the relevant technical information in the corresponding
    EHC. Section 4 includes advice on preventive and protective measures
    and emergency action; health workers should be thoroughly familiar
    with the medical information to ensure that they can act efficiently
    in an emergency. The section on regulatory information has been
    extracted from the legal file of the International Register of
    Potentially Toxic Chemicals (IRPTC) and from other United Nations

    The target readership includes occupational health services, those
    in ministries, governmental agencies, industry, and trade unions who
    are involved in the safe use of chemicals and the avoidance of
    environmental health hazards, and those wanting more information on
    this topic. An attempt has been made to use only terms that will be
    familiar to the intended user. However, sections 1 and 2 inevitably
    contain some technical terms. A bibliography has been included for
    readers who require further background information.

    Revision of the information in this Guide will take place in due
    course, and the eventual aim is to use standardized terminology.
    Comments on any difficulties encountered in using the Guide would be
    very helpful and should be addressed to:

    The Director
    International Programme on Chemical Safety
    World Health Organization
    1211 Geneva 27


    1.1  Identity

    Chemical structure:


    Common names:            parathion-methyl, methyl parathion,
                             metaphos (USSR)

    Molecular formula:       C8H10NO5PS

    IUPAC name:               O,O-dimethyl  O-4-nitrophenyl

    CAS name:                 O,O-dimethyl  O-(4-nitrophenyl)
                             phosphorothioate (9CI)

    CAS registry number:     298-00-0

    OMS number:              213

    RTECS registry number:   TG0175000

    1.2  Physical and chemical properties

    Pure methyl parathion is crystalline and white. It is relatively
    insoluble in water, poorly soluble in petroleum ether and mineral
    oils, and readily soluble in most organic solvents. Methyl parathion
    is stable at pH 1-7, but undergoes rapid decomposition in alkaline
    media at pH 8-9. On heating, methyl parathion readily isomerizes to
    the  O,S-dimethyl analogue.

    Technical methyl parathion, which is at least 90% pure, is a light
    to dark tan liquid.

    Some physical properties of methyl parathion are given in Table 1. 

    Table 1. Physical properties

    Relative molecular mass            263.2
    Melting point (C)                 35-38
    Boiling point (C)                 143

    Density d 25                       1.358
    Vapour pressure (20 C)            1.3 mPa
    Water solubility (25 C)           55-60 mg/litre 
    Partition coefficient (log Pow)    1.81-3.43 (reported range)

    Conversion factors            1 ppm = 10.76 mg/m3
    (25 C, 1066 mbar):           1 mg/m3 = 0.0929 ppm.

    1.3  Analytical methods

    The active ingredient of the formulated product is determined using
    gas chromatography, high pressure liquid chromatography, or
    hydrolysis to 4-nitrophenol followed by colorimetric determination.
    Similar methods and thin-layer chromatography are available for
    residue analysis. FAO/WHO recommended methods for the analysis of
    methyl parathion residues are given in FAO/WHO (1989).

    1.4  Production and uses

    Methyl parathion is produced throughout the world and has been
    registered for use on many crops. It is a non-systemic insecticide
    that controls numerous insects by contact and stomach action. It is
    generally applied as a spray, mainly from the emulsifiable
    concentrate formulation. It is recommended for application after
    mixing at 15-25 g active ingredient (a.i.) per 100 litres. In some
    countries, the dust and dispersible powder formulations are also
    available. On a global basis, the available emulsifiable
    concentrates contain 400, 480, and 600 g a.i./litre. The wettable
    powder contains 40% a.i., while the dust formulations contain 1.5,
    2, and 3% a.i.


    2.1  Environmental exposure

    The distribution of methyl parathion in air, water, soil, and in
    organisms in the environment is influenced by several physical,
    chemical, and biological factors.

    Studies using model ecosystems and mathematical modelling indicate
    that methyl parathion partitions mainly to air and soil in the
    environment, with lesser amounts in plants and animals. There is
    virtually no movement through soil and neither the parent compound
    nor its breakdown products will reach ground water. Methyl parathion
    in air is mainly derived from spraying of the compound, though some
    volatilization occurs with the evaporation of water from leaves and
    the soil surface. Background atmospheric levels of methyl parathion
    in agricultural areas range from not detectable to about 70 ng/m3.
    Air concentrations after spraying declined rapidly over 3 days and
    returned to background levels after about 9 days. Levels in river
    water (in laboratory studies) declined to 80% of the initial
    concentration after 1 h and 10% after 1 week. Methyl parathion is
    retained longer in soil than in air or water, though retention is
    greatly influenced by soil type; sandy soil can lose residues of the
    compound more rapidly than loams. Residues on plant surfaces and
    within leaves decline rapidly with half-lives of the order of a few
    hours; complete loss of the methyl parathion occurs within about 6-7

    Animals can degrade methyl parathion and excrete the degradation
    products within a very short time. However, this occurs more slowly
    in lower vertebrates and invertebrates than in mammals and birds.
    Bioconcentration factors are low and the accumulated methyl
    parathion levels transitory.

    By far the most important route for the environmental degradation of
    methyl parathion is microbial degradation. Loss of the compound in
    the field and in model ecosystems is more rapid than predicted from
    laboratory studies. This is because of the presence of a variety of
    microorganisms capable of degrading the compound in different
    habitats and circumstances. When sediment or plant surfaces are
    present, the microbial populations increase with a resulting
    increase in the rate of breakdown of methyl parathion.
    Methyl parathion can undergo oxidative degradation, to the less
    stable methylparaoxon, in the presence of ultraviolet radiation
    (UVR) or sunlight; sprayed films degrade under UVR with a half-life
    of about 40 h. However, the contribution of photolysis to total loss
    in an aquatic system was estimated to be only 4%. Hydrolysis of
    methyl parathion also occurs and is more rapid under alkaline
    conditions. High salinity also favours hydrolysis of the compound.
    Half-lives of a few minutes were recorded in strongly reducing
    sediments though methyl parathion is more stable when sorbed on
    other sediments. 

    In towns in the centre of agricultural areas of the USA, methyl
    parathion concentrations in air varied with season and peaked in
    August or September; maximum levels in surveys were mainly in the
    range of 100-800 ng/m3, during the growing season. Concentrations
    in natural waters of agricultural areas in the USA ranged up to
    0.46 g/litre, with highest levels in summer. There is only a small
    number of published reports on the residues of methyl parathion in
    food throughout the world. In the USA, residues of methyl parathion
    in food have generally been reported at very low levels with few
    individual samples exceeding maximum residue limits (MRLs). Only
    trace residue levels of methyl parathion have been detected in the
    total dietary studies reported. Methyl parathion residues were
    highest in leafy (up to 2 mg/kg) and root vegetables (up to 1 mg/kg)
    in market basket surveys in the USA between 1966 and 1969. Food
    preparation, cooking, and storage all cause decomposition of methyl
    parathion residues further reducing human exposure. Raw vegetables
    and fruits may contain higher residues after misuse.

    The production, formulation, handling, and use of methyl parathion
    as an insecticide are the main potential sources of human exposure.
    Skin contact and, to a lesser degree, inhalation are the main routes
    of exposure of workers. In a study of farm spray-men (with
    unprotected workers and ULV hand-spray) an intake of 0.4-13 mg
    methyl parathion (per 24 h) was calculated from the  p-nitrophenol
    excreted in the urine.

    Early re-entry into treated crops is a further source of exposure.
    The general population may be exposed to air-, water- and food-borne
    residues of methyl parathion as a consequence of agricultural or
    forestry practices, and the misuse of the agent resulting in
    contamination of fields, crops, water, and air through off-target

    2.2  Uptake, metabolism, and excretion

    Methyl parathion is readily absorbed via all routes of exposure
    (oral, dermal, and inhalation) and is rapidly distributed to the
    tissues of the body. Maximum concentrations in various organs were
    detected 1-2 h after treatment. Conversion of methyl parathion to
    methylparaoxon occurs within minutes following administration. In
    dogs, a mean terminal half-life of 7.2 h was determined following
    i.v. administration of methyl parathion. The liver is the primary
    organ of metabolism and detoxification. Methyl parathion or
    methylparaoxon are mainly detoxified in the liver by oxidation,
    hydrolysis, and demethylation or dearylation with reduced
    glutathione (GSH). The reaction products are
     O-methyl- O-p-nitrophenyl phosphorothioate or dimethyl
    phosphorothioic or dimethylphosphoric acids and  p-nitrophenol.
    Therefore, it is possible to estimate the exposure by measuring the
    urinary excretion of  p-nitrophenol. The urinary excretion of
     p-nitrophenol was 60% within 4 h and approximately 100% within

    24 h. The metabolism of methyl parathion is important for species
    selective toxicity, and the development of resistance. The
    elimination of methyl parathion and metabolic products occurs
    primarily via the urine. Studies conducted with radiolabelled
    32P-methyl parathion revealed, after 72 h, 75% of radioactivity in
    the urine and up to 10% radioactivity in the faeces.

    2.3  Effects on organisms in the environment

    Microorganisms can use methyl parathion as a carbon source and
    studies on a natural community showed that concentrations of up to
    5 mg/litre increased biomass and reproductive activity. Bacteria and
    actinomycetes showed a positive effect of methyl parathion while
    fungi and yeasts were less able to utilize the compound. A 50%
    inhibition of growth of a diatom occurred at about 5 mg/litre. Cell
    growth of unicellular green algae was reduced by between 25 and
    80 g methyl parathion/litre. Populations of algae became tolerant
    after exposure for several weeks.

    Methyl parathion is highly toxic for aquatic invertebrates, most
    LC50s ranging from <1 g to about 40 g/litre. A few arthropod
    species are less susceptible. The no-observed-effect level for the
    water flea  (Daphnia magna) is 1.2 g/litre. Molluscs are much less
    susceptible with LC50s ranging between 12 and 25 mg/litre.

    Most fish species in both fresh and sea water have LC50s between 6
    and 25 mg/litre, a few species being substantially more or less
    sensitive to methyl parathion. The acute toxicity of amphibians is
    similar to that of fish.

    Population effects have been seen in communities of aquatic
    invertebrates in experimental ponds treated with methyl parathion.
    The concentrations needed to cause these effects would occur only
    with overspraying of water bodies and, even then, would last for
    only a short time. Population effects are, therefore, unlikely to be
    seen in the field. Kills of aquatic invertebrates would be unlikely
    to lead to lasting effects.

    Care should be taken to avoid the overspraying of ponds, rivers, and
    lakes, when using methyl parathion. The compound should never be
    sprayed in windy conditions.

    Methyl parathion is a non-selective insecticide that kills
    beneficial species as readily as pests. Kills of bees have been
    reported following the spraying of methyl parathion. Effects on bees
    in methyl parathion incidents were more severe than those of other
    insecticides. Africanized honey bees are more tolerant of methyl
    parathion than European strains.

    Methyl parathion was moderately toxic for birds in laboratory
    studies, acute oral LD50s ranging between 3 and 8 mg/kg body
    weight. Dietary LC50s ranged from 70 to 680 mg/kg diet. There is
    no indication that birds would be adversely affected from the
    recommended usage of methyl parathion in the field.

    Extreme care must be taken to time methyl parathion spraying to
    avoid adverse effects on honey bees.

    2.4  Effects on experimental animals and  in vitro test systems

    Oral LD50 values of methyl parathion in rodents range from 3 to
    35 mg/kg body weight, and dermal LD50 values from 44 to 67 mg/kg
    body weight.

    Methyl parathion poisoning causes the usual organophosphate
    cholinergic signs attributed to accumulation of acetylcholine at
    nerve endings. Methyl parathion becomes toxic when it is metabolized
    to methylparaoxon. This conversion is very rapid. No indications of
    organophosphorus-induced delayed neuropathy (OPIDN) have been

    Technical methyl parathion was found not to have any primary eye or
    skin irritating potential.

    In short-term toxicity studies using various routes of
    administration on the rat, dog, and rabbit, inhibition of plasma,
    red blood cells, and brain ChE and related cholinergic signs were
    observed. In a 12-week feeding study on dogs, the
    no-observed-adverse-effect level (NOAEL) was 5 mg/kg diet
    (equivalent to 0.1 mg/kg body weight per day). In a 3-week dermal
    toxicity study on rabbits, the no-observed-effect level (NOEL) was
    10 mg/kg body weight per day. Inhalation exposure for 3weeks
    indicated a NOEL of 0.9 mg/m3 air. At 2.6 mg/m3, only slight
    inhibition of plasma ChE was observed.

    Long-term toxicity/carcinogenicity studies were carried out on mice
    and rats. The NOEL in rats was 0.1 mg/kg body weight per day, based
    on ChE inhibition. There is no evidence of carcinogenicity in mice
    and rats, following long-term exposure. In another 2-year study on
    rats, however, there was evidence of a peripheral neurotoxic effect
    at a dose of 50 mg/kg diet.

    Methyl parathion has been reported to have DNA alkylating properties
     in vitro.

    Most of the results of  in vitro genotoxicity studies on both
    bacterial and mammalian cells were positive, while 6  in vivo
    studies using 3 different test systems produced equivocal results.

    In reproduction studies, at toxic dose levels (ChE inhibition),
    there were no consistent effects on litter sizes, number of litters,
    survival rates of pups, and lactation performance. No primary
    teratogenic or embryotoxic effects were noted.

    2.5  Effects on human beings

    Several cases of acute methyl parathion poisoning have been
    reported. Signs and symptoms are those characteristic of systemic
    poisoning by cholinesterase-inhibiting organophosphorus compounds.
    They include peripheral and central cholinergic nervous system
    manifestations appearing as rapidly as a few minutes after exposure.
    In case of dermal exposure, symptoms may increase in severity for
    more than one day and may last for several days.

    The results of studies on volunteers, following repeated long-term
    exposures, suggest that there is a decrease in blood cholinesterase
    activity without clinical manifestations.

    No cases of organophosphorus-induced delayed peripheral neuropathy
    (OPIDN) have been reported. Neuropsychiatric sequelae have been
    reported in cases of multiple exposures to pesticides including
    methyl parathion.

    An increase in chromosomal aberrations has been reported in cases of
    acute intoxication.

    No human data were available to evaluate the teratogenic and
    reproductive effects of methyl parathion.

    The available epidemiological studies deal with multiple exposures
    to pesticides and it has not been possible to evaluate the effects
    of long-term exposure to methyl parathion.


    3.1  Conclusions

    Methyl parathion is a highly toxic organophosphorus ester
    insecticide. Overexposure from handling during manufacture or use,
    and/or accidental or intentional ingestion may cause severe or fatal
    poisoning. Methyl parathion formulations may, or may not, be
    irritating to the eyes or the skin, but they are readily absorbed.
    As a consequence, hazardous exposures may occur without warning.

    Methyl parathion is not persistent in the environment. It is not
    bioconcentrated and is not transferred through food-chains and is
    degraded rapidly by many microorganisms and other forms of wildlife.
    It is only likely to cause damage to ecosystems in instances of
    heavy overexposure resulting from misuse or accidental spills.
    However, pollinators and other beneficial insects are at risk from
    spraying with methyl parathion.

    Exposure of the general population to methyl parathion residues
    occurs predominantly via food. If good agricultural practice is
    followed, the Acceptable Daily Intake (0-0.02 mg/kg body weight)
    established by FAO/WHO will not be exceeded. Dermal exposure may
    occur through accidental contact with foliar residues in sprayed
    fields or in areas adjacent to spraying operations as a consequence
    of off-target spraying of the chemical.

    With good work practices, hygienic measures and safety precautions,
    methyl parathion is unlikely to present a hazard for those
    occupationally exposed.

    3.2  Recommendations

    *    For the health and welfare of workers and the general
         population, the handling and application of methyl parathion
         should be entrusted only to competently supervised and
         well-trained applicators, who must follow adequate safety
         measures and use the chemical according to good application

    *    The manufacture, formulation, agricultural use, and disposal of
         methyl parathion should be carefully managed to minimize
         contamination of the environment.

    *    Regularly exposed workers should undergo appropriate monitoring
         and health evaluations.

    *    To minimize risks for all individuals, a 48-h interval between
         spraying and re-entry into any sprayed area is recommended.

    *    Pre-harvest intervals should be established and enforced by
         national authorities.

    *    In view of its high toxicity, methyl parathion should not be
         considered for use in hand-applied, ultra-low-volume (ULV)
         spraying practices.

    *    Do not overspray water bodies. Choose spraying time to avoid
         killing pollinating insects.

    *    Information on the health status of workers exposed only to
         methyl parathion (i.e., in its manufacture and formulation)
         should be published, in order to assist in a better evaluation
         of the risks of this chemical for human health.

    *    More definitive studies should be conducted on the residues of
         methyl parathion in fresh foods.

    *    A more definitive genotoxic assessment of methyl parathion
         should be conducted.


    4.1  Human health hazards, prevention and protection, first aid

    The acute oral and dermal toxicities of methyl parathion are high
    and it is hazardous for human beings if incorrectly handled. With
    excessive exposure, typical signs and symptoms of organophosphorus
    poisoning may occur rapidly. The human health hazards associated
    with certain types of exposure to methyl parathion, together with
    preventive and protective measures and first aid, are listed in the
    Table 2.

    4.1.1  Advice to physicians

    For a more complete treatise on the effects of organophosphorus
    insecticides, especially their short- and long-term effects on the
    nervous system, please refer to EHC 63:  Organophosphorus
     insecticides - a general introduction (WHO, 1986).

    Methyl parathion is an indirect cholinesterase inhibitor in that the
    active cholinesterase inhibitor, methyl paraoxon, is formed in the
    liver. Signs and symptoms of toxicity appear rapidly.  Symptoms of poisoning

    Signs and symptoms may include a feeling of exhaustion, headache,
    blurred vision, weakness, and confusion. Vomiting, abdominal pain,
    excessive sweating, and salivating may develop. The pupils may also
    be constricted. Difficulty in breathing may be experienced, due to
    congestion of the lungs and weakness of the respiratory muscles.
    Arrhythmias and cardiac failure have been reported. On severe
    poisoning, there will be muscle spasms, unconsciousness, and
    convulsions. Breathing may stop, followed by death.

        Table 2. Human health hazards, preventive and protective measures, first aid

    HAZARDS/SYMPTOMS                              PREVENTION AND PROTECTION                FIRST AID

    GENERAL: Cholinesterase                       Avoid exposure

    SKIN: Contamination may cause                 Wear PVC or neoprene gloves,             Wash contaminated skin with soap and 
    organophosphate poisoning: weakness,          apron and rubber boots                   water; remove contaminated clothing
    headache, vomiting, excessive sweating                                                 and launder before reuse; obtain
    and salivation, pin-point pupils; in                                                   medical attention immediately
    severe cases: convulsions,
    unconsciousness and death due to
    respiratory paralysis may occur

    EYES: Irritation, redness                     Wear face shield or goggles              Flush immediately with clean water
                                                                                           for at least 15 min; if irritation persists,
                                                                                           obtain medical attention immediately;
                                                                                           launder contaminated clothing

    INHALATION: Inhalation may                    Avoid breathing mist or dust; use        In case of signs of symptoms, remove
    cause poisoning (see skin)                    proper (exhaust) ventilation or          from contaminated area and obtain
                                                  suitable respiratory protection          medical attention immediately

    INGESTION: Unlikely to be a                   Wash hands before eating, drinking,
    significant occupational hazard               using the toilet, and after work;
                                                  do not keep food in areas with
                                                  potential exposure

    Accidental or deliberate ingestion                                                     Obtain medical attention immediately;
    may rapidly lead to severe poisoning                                                   induce vomiting, if subject is conscious,
    (see skin)                                                                             except in the case of an emulsifiable 
                                                                                           concentrate; if breathing has stopped
                                                                                           apply artificial respiration
  Medical treatment

    If ingested and the formulation does not contain petroleum
    distillates, induce vomiting, or preferably perform gastric lavage
    using 5% sodium bicarbonate. In the case of ingestion of liquid
    formulations containing hydrocarbon solvents, vomiting involves a
    risk of aspiration pneumonia. Instead, the stomach should be emptied
    as soon as possible by careful gastric lavage (using a cuffed
    endotracheal tube). If possible, identify the solvents present in
    the formulation and observe the victim for additional toxic effects.
    As early as possible, administer 2 mg atropine sulfate intravenously
    (i.v.) and 1000-2000 mg of pralidoxime chloride or 250 mg of
    obidoxime chloride (adult dose) i.v., to patients suffering from
    severe respiratory difficulties, convulsions, and unconsciousness.
    Repeated doses of 2 mg of atropine sulfate should be given, as
    required, based on the respiration, blood pressure, pulse frequency,
    salivation, and convulsion conditions. Diazepam should be given in
    all but the mildest cases in doses of 10 mg s.c. or i.v., repeated
    as required.

    For children, the doses are 0.04-0.08 mg atropine/kg body weight,
    250 mg pralidoxime chloride per child, or 4-8 mg obidoxime chloride
    per kg body weight.

    Artificial respiration should be applied, if required.

    Note: Contraindications: morphine, barbiturates,
    phenothiazine derivatives, tranquillizers, and all
    kinds of central stimulants

    The diagnosis of intoxication should be confirmed as soon as
    possible by determination of the cholinesterase activity in venous

    For more information on the treatment of organophosphorus
    insecticides see EHC 63:  Organophosphorus insecticides - a general
     introduction (WHO, 1986). The section from this publication on
    therapy is attached as Annex 1 of this guide.  Health surveillance advice

    In human beings exposed to methyl parathion, the cholinesterase
    activity of the blood should be monitored regularly. Measurement of
    whole blood AChE is the most widely adopted method. Because
    physiological variations of blood ChE levels occur in a healthy
    person and amongst populations, results should preferably be
    compared with pre-exposure ChE levels.

    Depressions of AChE or ChE of 20-25% are considered diagnostic of
    exposure, but not necessarily indicative of hazard. Depressions of
    30-50% or more are considered indicators for removal of an exposed
    individual from further contact with pesticides until levels return

    to normal. Work procedures and hygiene should also be checked.
    Exposure can also be monitored by measuring the urinary excretion of

    4.2  Explosion and fire hazards

    Liquid formulations may be flammable. With sufficient burning or
    external heat, methyl parathion will decompose, emitting toxic
    fumes. Fire-fighters must wear protective clothing and
    self-contained breathing apparatus. Extinguish fires with alcohol
    resistant foam or powder. Confine the use of water spray to the
    cooling of unaffected stock, thus avoiding polluted run-off from the

    4.3  Storage

    Technical methyl parathion and its formulations should be stored in
    the original labelled containers in locked, well-ventilated storage
    areas, preferably dedicated to insecticides. Do not expose to direct
    sunlight. Keep products out of reach of children and unauthorized
    personnel. Do not store near food or animal feed.

    4.4  Transport

    Comply with any local regulations regarding movement of hazardous
    goods. Do not transport with food or animal feed. Food and feed
    should not be transported in vehicles that have been used for the
    transport of pesticides. Make sure that containers are in good
    condition and the labels are undamaged before dispatch.

    4.5  Spillage and Disposal

    4.5.1  Spillage

    Avoid skin contamination and inhalation of vapour. Absorb spilled
    liquid and cover contaminated areas with a 1:3 mixture of sodium
    carbonate crystals and damp sawdust, lime, sand, or earth. Sweep up
    and place it in an impervious container. Ensure that the container
    is tightly closed and labelled before transfer to a safe place for

    Prevent liquid from spreading and contaminating other cargo,
    vegetation, or waterways by using a barrier of the most suitable and
    readily available material, e.g., earth or sand.

    Empty any of the product remaining in the damaged/leaking container
    into a clean empty container, which should then be tightly closed
    and suitably labelled. Decontaminate emptied leaking containers with
    a 10% sodium carbonate (washing soda) solution, added at a rate of
    at least 1 litre/20-litre drum. Swirl round to rinse walls, empty,
    and add rinsings to sawdust. Do not reuse containers for any other
    purpose. Puncture and crush the container to prevent reuse.

    4.5.2  Disposal

    Large amounts should be incinerated at high temperature in a unit
    with effluent gas scrubbing or should be adsorbed on vermiculite and
    disposed of in a landfill, if incineration is impossible. When no
    incinerator is available, bury in an approved dump, or in an area
    where there is no risk of contamination of surface or ground water.
    Before burying, mix liberally with sodium carbonate (washing soda)
    crystals to help neutralize the product and with soil rich in
    organic matter. Comply with any local legislation.


    Methyl parathion is readily degraded and non-persistent in the
    environment. It is highly toxic for aquatic invertebrates, birds,
    bees, and wild mammals. It is moderately toxic for fish and
    non-toxic for soil microorganisms.

    Do not overspray water; time spraying to avoid killing of

    Avoid contamination of soil, water, and the atmosphere by proper
    methods of use, storage, transport, handling, and waste disposal. In
    case of spillage, use the methods advised in section 4.5.1.


    The information given in this section has been extracted from the
    International Register of Potentially Toxic Chemicals (IRPTC) legal
    file and other United Nations sources. A full reference to the
    original national document from which the information was extracted
    can be obtained from IRPTC.

    The reader should be aware that regulatory decisions about chemicals
    taken in a certain country can only be fully understood in the
    framework of the legislation of that country. Furthermore, the
    regulations and guidelines of all countries are subject to change
    and should always be verified with the appropriate regulatory
    authorities before application.

    6.1  Previous evaluations by international bodies

    The Joint FAO/WHO Meeting on Pesticide Residues (JMPR) evaluated
    methyl parathion in 1968, 1972, 1975, 1979, 1980, and 1984 (FAO/WHO,
    1969, 1973, 1976, 1980, 1981, and 1985). The acceptable daily intake
    for humans (ADI) was estimated at 0-0.02 mg/kg body weight in 1984.
    This was based on the following levels causing no toxicological

         - 2 mg/kg diet, equivalent to 0.1 mg/kg body weight in the rat;

         - 0.3 mg/kg body weight per day in man.

    The FAO/WHO Codex Alimentarius Commission (FAO/WHO, 1986)
    recommended Maximum Residue Limits (MRLs) in several food
    commodities, ranging from 0.05 to 0.2 mg/kg, including: 

    Commodity MRL (mg/kg)            Commodity MRL (mg/kg)

    cantaloupes            0.2       hops (dry cones)           0.05a
    cole crops             0.2       melons                     0.2
    cottonseed oil         0.05      sugar beets                0.05a
    cucumbers              0.2       tea (fermented and dried)  0.2
    fruit, other           0.2       tomatoes                   0.2


    a Levels at or about the limit of determination.

    The International Agency for Research on Cancer (IARC) classified
    methyl parathion in Group 3 in 1982 and in 1987 (IARC, 1983, vol.
    30, 1987, suppl. 7), and concluded that the available data do not
    provide evidence that methyl parathion is carcinogenic to
    experimental animals. No data on humans were available. The
    available data provide no evidence that methyl parathion is likely
    to present a carcinogenic risk to humans.

    WHO (1990) classified technical methyl parathion as "extremely
    hazardous" in normal use, on the basis of the oral LD50 in the rat
    of 14 mg/kg. WHO/FAO (1975) issued a data sheet on methyl parathion
    (No. 7).

    6.2  Exposure limit values

    Some exposure limit values are given on pp. 28-29


    Pre-harvest intervals (the time between the last application of
    methyl parathion and the harvest of the treated plants) have been
    set in many countries. These intervals vary from 1 to 60 days (most
    of them between 14 and 21 days), depending on the crop, the
    harvesting technique, and the country, and can be verified with the
    competent national authority.

    6.3  Specific restrictions

    In many countries where methyl parathion is approved as a pesticide,
    specific uses, restrictions, and precautions are listed in national
    regulatory documents, e.g., no liquid methyl parathion formulations
    have been approved for registration in Finland because of their high
    acute toxicity. In the USSR, the agricultural use of methyl
    parathion has been restricted. In Hungary, it may only be applied in
    agriculture by properly trained staff, using protective equipment.

    Methyl parathion has either not been registered or has been banned
    in: Bangladesh, Belgium, Bulgaria, Canada, China, Ecuador, Egypt,
    Hong Kong, Ireland, Japan, Sri Lanka, and the United Kingdom.

    In Japan and the USA, methyl parathion and its preparations may only
    be handled by certified operators. In Germany, it may not be handled
    by adolescents or pregnant and nursing women.

    6.4  Labelling, packaging, and transport

    The United Nations Committee of Experts on the Transportation of
    Dangerous Goods classifies methyl parathion in:

         -    Hazard Class 6.1: poisonous substance;

         -    Packing Group 2: substances and preparations presenting a
              serious risk of poisoning, for formulations containing
              12-100% methyl parathion.

         -    Packing Group 3: harmful substances and preparations
              presenting a serious risk of poisoning, for solid
              formulations containing 3-12% active material, and liquid
              formulations containing 1.2-12% active material.

        Exposure limit values

    Medium     Specification     Country/          Exposure limit description                 Value           Effective
                                 organization                                                                 date

    AIR        Workplace         Argentina         Maximum permissible concentration
                                                   - Time-weighted average (TWA) a            0.2 mg/m3       1984
                                                   - Short-term exposure limit (STEL)         0.6 mg/m3

                                 Finland           Maximum permissible concentration
                                                   - Time-weighted average (TWA)              0.2 mg/m3       1987
                                                   - Short-term exposure limit                0.6 mg/m3

                                 United Kingdom    Occupational exposure standard (TWA) a     0.2 mg/m3       1989
                                                   - Short-term exposure limit (STEL)         0.6 mg/m3

                                 USA (ACGIH)       Threshold limit value (TLV)
                                                   - Time-weighted average (TWA)              0.2 mg/m3 b     1986
                                                   - Short-term exposure limit                deleted
                                                   (STEL = 10 minutes)

                                 USSR              Maximum allowable concentration (MAC)
                                                   - Ceiling value (vapour + aerosol)         0.1 mg/m3       1977

    AIR        Ambient           USSR              Maximum allowable concentration (MAC)      0.008 mg/m3     1984
                                                   (once per day)

    FOOD       Uptake from       FAO/WHO           Acceptable daily intake (ADI)              0-0.02 mg/kg    1984
                                                                                              body weight

               Residues          FAO/WHO           Maximum residue limit (MRL)                0.05-0.2 mg/kg  1986
                                                   (in specified products)

    Exposure limit values (continued)

    Medium     Specification     Country/          Exposure limit description                 Value           Effective
                                 organization                                                                 date

    WATER      Ambient           Japan             Environmental water quality standard       not detectable  1981

               Surface           USSR              Maximum acceptable concentration           0.02 mg/litre   1983

               Effluent          Japan             Emission of total organophosphorus         1 mg/litre      1981

    SOIL                         USSR              Maximum acceptable concentration           0.1 mg/kg       1981


    a TWA usually 8 h.
    b Skin absorption possible.

    The label should be as follows:

    Packaging Group I and II:

    FIGURE 1

    Packaging Group III:

    FIGURE 2

    In the International Maritime Dangerous Goods (IMDG) Code, methyl
    parathion is classified as a marine pollutant with a severe
    pollution potential. It should bear the following mark on the label:

    FIGURE 3

    For flammable formulations, the following subsidiary label is
    required, when the flashpoint of the solution is below, or equal to,
    61 C (closed cup):

    FIGURE 4

    There is no WHO specification on methyl parathion as the material is
    not used in public health. However, specifications for technical
    material and some formulations have been agreed upon between FAO and
    the manufacturers.

    All packages should bear, durably and legibly marked on the
    container, the following:

         -    Manufacturer's name
         -    Technical parathion to specification
         -    Batch or reference number, and date of test
         -    Net weight of contents
         -    Date of manufacture

    and, in the case of the formulated products:

         -    Manufacturer's name
         -    Methyl parathion to specification
         -    Methyl parathion ... g/kg
         -    Batch or reference number, and date of test
         -    Net weight of contents
         -    Instructions for dilution
         -    Date of formulation

    and the following minimum cautionary notice:

          Methyl parathion is an organophosphorus compound that inhibits
          cholinesterase. It is poisonous if swallowed or inhaled. It
          may be absorbed through the skin. Avoid skin contact; wear
          protective gloves, clean protective clothing and a respirator
          when handling the material. Wash thoroughly with soap and
          water after using.

          Keep the material out of the reach of children and well away
          from foodstuffs and animal feed and their containers.

          If poisoning occurs, call a physician. Atropine and
          pralidoxime are specific antidotes, and artificial respiration
          may be needed.

    The methyl parathion content should be declared (minimum 90% for the
    technical product) and should not differ from the declared
    percentage by more than 2% for the technical product and 5-10% for
    its formulations.

    Containers should be suitable, clean, dry, and as specified in the
    order, and should not adversely affect, or be affected by, the
    product, but should adequately protect it from external conditions.
    They should comply with pertinent national and international
    transport and safety regulations.

    Specifications for storage stability are given.

    The European Economic Community legislation requires labelling as
    dangerous substance using the symbol:

    FIGURE 5

    The label must read:

          Very toxic by inhalation, in contact with skin and if
          swallowed; keep locked up; keep away from food, drink and
          animal feeding stuffs; after contact with skin, wash
          immediately with plenty of ____ - (to be specified by the
          manufacturer); in case of accident or if you feel unwell, seek
          medical advice immediately (show the label where possible)

    The European Economic Community legislation on labelling of
    pesticide preparations classifies pesticide preparations that
    contain methyl parathion in Class 1A, as toxic at concentrations
    > 1% and as harmful at > 0.05-1%. Member States should ensure that
    pesticides cannot be placed on the market unless their packaging,
    fastenings, and labels comply with the requirements laid down.

    6.5  Waste disposal

    In the USA, any non-domestic waste containing methyl parathion is
    considered a hazardous waste and the competent authority should be
    notified. Permits are required for its handling, transport,
    treatment, storage, or disposal. Waste incinerators must achieve
    99.99% destruction and removal of this substance.

    6.6  Other measures

    The European Economic Community legislation has listed methyl
    parathion as a dangerous substance at quantities >100 kg in the
    directive on the major accident hazards of certain industrial
    activities. Any person in charge of an industrial activity
    involving, or possibly involving, one or more dangerous substances
    is obliged to take all the measures necessary to prevent major
    accidents, to limit their consequences for man and the environment,
    and to notify the competent authority about the industrial activity.


    CEC (1987) Legislation on dangerous substances - classification and
    labelling in the European Communities. Vol. 1 & 2. Commission of the
    European Communities, London, Graham & Trotman, Ltd.

    FAO (1971) Parathion-methyl - FAO specifications for plant
    protection products. Rome, Food and Agriculture Organization of the
    United Nations, pp 22.

    FAO (1985a) Guidelines for the packaging and storage of pesticides.
    Rome. Food and Agriculture Organization of the United Nations.

    FAO (1985b) Guidelines for the disposal of waste pesticides and
    pesticide containers on the farm. Rome, Food and Agriculture
    Organization of the United Nations.

    FAO (1985c) Guidelines on good labelling practice for pesticides.
    Rome, Food and Agriculture Organization of the United Nations.

    FAO (1986) International code of conduct on the distribution and use
    of pesticides. Rome, Food and Agriculture Organization of the United

    FAO/WHO (1964-present) Evaluations of pesticide residues in food,
    Rome. Food and Agriculture Organization of the United Nations.

    FAO/WHO (1986) Codex Maximum Limits for pesticide residues. 3rd ed.
    Rome, Codex Alimentarius Commission, Food and Agriculture
    Organization of the United Nations (CAC/Vol XIII).

    FAO/WHO (1986) Codex Maximum Limits for pesticide residues. Codex
    Alimentarius Commission CAC/Vol. XIII. 3rd ed. Rome, Food and
    Agriculture Organization of the United Nations.

    FAO/WHO (1989) Guide to Codex recommendations concerning pesticide
    residues. Part 8. Recommendations for methods of analysis of
    pesticide residues. 4th ed. Rome, Codex Committee on Pesticide

    GIFAP (1982) Guidelines for the safe handling of pesticides during
    their formulation, packing, storage and transport. Brussels,
    Groupement International des Associations Nationales des Fabricants
    de Produits Agrochimiques.

    GIFAP (1983) Guidelines for the safe and effective use of
    pesticides. Brussels, Groupement International des Associations
    Nationales des Fabricants de Produits Agrochimiques.

    GIFAP (1984) Guidelines for emergency measures in cases of pesticide
    poisoning. Brussels, Groupement International des Associations
    Nationales des Fabricants de Produits Agrochimiques.

    GIFAP (1987) Guidelines for the safe transport of pesticides.
    Brussels, Groupement International des Associations Nationales des
    Fabricants de Produits Agrochimiques.

    Hayes WJJ Jr & Laws ER Jr (1991) Handbook of pesticide toxicology. 3
    Vol. New York, Academic Press.

    IARC (1972-present) IARC Monographs on the evaluation of
    carcinogenic risk of chemicals to man. Lyon, International Agency
    for Research on Cancer.

    IARC (1983) IARC monographs on the evaluation of carcinogenic risk
    of chemicals to man. Vol. 30. Miscellaneous chemicals. Lyon,
    International Agency for Research on Cancer.

    ILO (1991) Safety and health in the use of agro-chemicals - a guide.
    Geneva, International Labour Office.

    IRPTC (1985) IRPTC file on treatment and disposal methods for waste
    chemicals. Geneva, International Register of Potentially Toxic
    Chemicals, United Nations Environment Programme.

    IRPTC (1987) IRPTC legal file 1986. Geneva, International Register
    of Potentially Toxic Chemicals, United Nations Environment

    Plestina R (1984) Prevention, diagnosis, and treatment of
    insecticide poisoning. Geneva, World Health Organization
    (Unpublished document No. VBC/84.889).

    Sax NI (1984) Dangerous properties of industrial materials. New
    York, Van Nostrand Reinhold Company, Inc.

    UNEP/IEO (1990) Storage of hazardous materials: a technical guide
    for safe warehousing of hazardous materials. Paris, United Nations
    Environment Programme, Industry and Environment Office, 80 pp.

    UNITED NATIONS (1989a) Consolidated list of products whose
    consumption and/or sale have been banned, withdrawn, severely
    restricted or not approved by governments. 2nd ed. New York, United

    UNITED NATIONS (1989b) Recommendations on the transport of dangerous
    goods. 6th ed. New York, United Nations.

    US NIOSH/OSHA (1981) Occupational health guidelines for chemical
    hazards. 3 Vol. Washington DC, US Department of Health and Human
    Services, US Department of Labor (Publication No. DHHS(NIOSH)

    WHO (1986) EHC 63: Organophosphorus insecticides - a general
    introduction. Geneva, World Health Organization, 181 pp.

    WHO (1992) The WHO recommended classification of pesticides by
    hazard and guidelines to classification, 1992-93. Geneva, World
    Health Organization, 66 pp. (Unpublished document, WHO/PCS/92.14).

    WHO/FAO (1975-87) Methyl parathion: Data sheets on pesticides, No.
    7. Geneva, World Health Organization (Unpublished documents).

    WHO (in preparation) EHC: 145 Methyl parathion. Geneva, World Health

    Worthing CR & Hance RJ (1991) The pesticide manual. 9th ed. Unwin
    Brothers Ltd., Surrey, United Kingdom, British Crop Protection


    All cases of organophosphorus poisoning should be dealt with as an
    emergency and the patient sent to hospital as quickly as possible.
    Although symptoms may develop rapidly, delay in onset or a steady
    increase in severity may be seen up to 48 h after ingestion of some
    formulated organophosphorus insecticides.

    Extensive descriptions of treatment of poisoning by organophosphorus
    insecticides are given in several major references (Kagan, 1977;
    Taylor, 1980; UK DHSS, 1983; Plestina, 1984) and will also be
    included in the IPCS Health and Safety Guides to be prepared for
    selected organophosphorus insecticides.

    The treatment is based on:

    (a)  minimizing the absorption;

    (b)  general supportive treatment; and

    (c)  specific pharmacological treatment.

    I.1  Minimizing the absorption

    When dermal exposure occurs, decontamination procedures include
    removal of contaminated clothes and washing of the skin with
    alkaline soap or with a sodium bicarbonate solution. Particular care
    should be taken in cleaning the skin area where venepuncture is
    performed. Blood might be contaminated with direct-acting
    organophosphorus esters and, therefore, inaccurate measures of ChE
    inhibition might result. Extensive eye irrigation with water or
    saline should also be performed. In the case of ingestion, vomiting
    might be induced, if the patient is conscious, by the administration
    of ipecacuanha syrup (10-30 ml) followed by 200 ml water. This
    treatment is, however, contraindicated in the case of pesticides
    dissolved in hydrocarbon solvents. Gastric lavage (with addition of
    bicarbonate solution or activated charcoal) can also be performed,
    particularly in unconscious patients, taking care to prevent
    aspiration of fluids into the lungs (i.e., only after a tracheal
    tube has been put into place).

    The volume of fluid introduced into the stomach should be recorded
    and samples of gastric lavage frozen and stored for subsequent
    chemical analysis. If the formulation of the pesticide involved is
    available, it should also be stored for further analysis (i.e.,
    detection of toxicologically relevant impurities). A purgative can
    be administered to remove the ingested compound.


    a  From EHC 63: Organophosphorus insecticides - a general
       introduction. Geneva, World Health Organization, 1986.

    I.2  General supportive treatment

    Artificial respiration (via a tracheal tube) should be started at
    the first sign of respiratory failure and maintained for as long as

    Cautious administration of fluids is advised, as well as general
    supportive and symptomatic pharmacological treatment and absolute

    I.3  Specific pharmacological treatment

    I.3.1  Atropine

    Atropine should be given, beginning with 2 mg iv and given at
    15-30-min intervals. The dose and the frequency of atropine
    treatment varies from case to case, but should maintain the patient
    fully atropinized (dilated pupils, dry mouth, skin flushing, etc.).
    Continuous infusion of atropine may be necessary in extreme cases
    and total daily doses up to several hundred mg may be necessary
    during the first few days of treatment.

    I.3.2  Oxime reactivators

    Cholinesterase reactivators (e.g., pralidoxime, obidoxime)
    specifically restore AChE activity inhibited by organophosphates.
    This is not the case with enzymes inhibited by carbamates. The
    treatment should begin as soon as possible, because oximes are not
    effective on "aged" phosphorylated ChEs. However, if absorption,
    distribution, and metabolism are thought to be delayed for any
    reasons, oximes can be administered for several days after
    intoxication. Effective treatment with oximes reduces the required
    dose of atropine. Pralidoxime is the most widely available oxime. A
    dose of 1 g pralidoxime can be given either im or iv and repeated
    2-3 times per day or, in extreme cases, more often. If possible,
    blood samples should be taken for AChE determinations before and
    during treatment. Skin should be carefully cleansed before sampling.
    Results of the assays should influence the decision whether to
    continue oxime therapy after the first 2 days.

    There are indications that oxime therapy may possibly have
    beneficial effects on CNS-derived symptoms.

    I.3.3  Diazepam

    Diazepam should be included in the therapy of all but the mildest
    cases. Besides relieving anxiety, it appears to counteract some
    aspects of CNS-derived symptoms that are not affected by atropine.
    Doses of 10 mg sc or iv are appropriate and may be repeated as
    required (Vale & Scott, 1974). Other centrally acting drugs and
    drugs that may depress respiration are not recommended in the
    absence of artificial respiration procedures.

    I.3.4  Notes on the recommended treatment

    I.3.4.1  Effects of atropine and oxime

    The combined effect far exceeds the benefit of either drug singly.

    I.3.4.2  Response to atropine

    The response of the eye pupil may be unreliable in cases of
    organophosphorus poisoning. A flushed skin and drying of secretions
    are the best guide to the effectiveness of atropinization. Although
    repeated dosing may well be necessary, excessive doses at any one
    time may cause toxic side-effects. Pulse-rate should not exceed

    I.3.4.3  Persistence of treatment

    Some organophosphorus pesticides are very lipophilic and may be
    taken into, and then released from, fat depots over a period of many
    days. It is therefore quite incorrect to abandon oxime treatment
    after 1-2 days on the supposition that all inhibited enzyme will be
    aged. Ecobichon et al. (1977) noted prompt improvement in both
    condition and blood-ChEs in response to pralidoxime given on the
    11th-15th days after major symptoms of poisoning appeared due to
    extended exposure to fenitrothion (a dimethyl phosphate with a short
    half-life for aging of inhibited AChE).

    I.3.4.4  Dosage of atropine and oxime

    The recommended doses above pertain to exposures, usually for an
    occupational setting, but, in the case of very severe exposure or
    massive ingestion (accidental or deliberate), the therapeutic doses
    may be extended considerably. Warriner et al. (1977) reported the
    case of a patient who drank a large quantity of dicrotophos, in
    error, while drunk. Therapeutic dosages were progressively increased
    up to 6 mg atropine iv every 15 min together with continuous iv
    infusion of pralidoxime chloride at 0.5 g/h for 72 h, from days 3 to
    6 after intoxication. After considerable improvement, the patient
    relapsed and further aggressive therapy was given at a declining
    rate from days 10 to 16 (atropine) and to day 23 (oxime),
    respectively. In total, 92 g of pralidoxime chloride and 3912 mg of
    atropine were given and the patient was discharged on the
    thirty-third day with no apparent sequelae.

    References to Annex 1

    Ecobichon DJ, Ozere RL, Reid E, & Crocker JFS (1977) Acute
    fenitrothion poisoning. Can Med Assoc J, 116: 377-379.

    Kagan Ju S (1977) [Toxicology of organophosphorus pesticides],
    Moscow, Meditsina, pp. 111-121, 219-233, 260-269 (in Russian).

    Plestina R (1984) Prevention, diagnosis, and treatment of
    insecticide poisoning, Geneva, World Health Organization
    (Unpublished document VBC/84.889).

    Taylor P (1980) Anticholinesterase agents. In: Goodman LS & Gilman
    A, ed. The pharmacological basis of therapeutics, 6th ed., New York,
    Macmillan Publishing Company, pp. 100-119.

    UK DHSS (1983) Pesticide poisoning: notes for the guidance of
    medical practitioners, London, United Kingdom Department of Health
    and Social Security, pp. 41-47.

    Vale JA & Scott GW (1974) Organophosphorus poisoning. Guy's Hosp
    Rep, 123: 13-25.

    Warriner RA III, Nies AS, & Hayes WJ Jr (1977) Severe
    organophosphate poisoning complicated by alcohol and turpentine
    ingestion. Arch environ Health, 32: 203-205.

    See Also:
       Toxicological Abbreviations
       Methyl parathion (EHC 145, 1992)
       Methyl parathion (ICSC)
       Methyl Parathion (FAO Meeting Report PL/1965/10/1)
       Methyl Parathion  (IARC Summary & Evaluation, Supplement7, 1987)
       Methyl Parathion (IARC Summary & Evaluation, Volume 30, 1983)