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.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    First draft prepared by Dr L. Ivanova-Chemishanska,
    Institute of Hygiene and Occupational Health,
    Sofia, Bulgaria

    World Health Orgnization
    Geneva, 1993

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
    International Labour Organisation, and the World Health
    Organization. The main objective of the IPCS is to carry out and
    disseminate evaluations of the effects of chemicals on human health
    and the quality of the environment. Supporting activities include
    the development of epidemiological, experimental laboratory, and
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    comparable results, and the development of manpower in the field of
    toxicology. Other activities carried out by the IPCS include the
    development of know-how for coping with chemical accidents,
    coordination of laboratory testing and epidemiological studies, and
    promotion of research on the mechanisms of the biological action of

    WHO Library Cataloguing in Publication Data


        (Environmental health criteria ; 147)

        1.Acetanilides - adverse effects 2.Acetanilides - toxicity
        3.Environmental exposure 4.Herbicides - adverse effects
        5.Herbicides - toxicity     I.Series

        ISBN 92 4 157147 0        (NLM Classification: WA 249)
        ISSN 0250-863X

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    (c) World Health Organization 1993

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         The mention of specific companies or of certain manufacturers'
    products does not imply that they are endorsed or recommended by the
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    names of proprietary products are distinguished by initial capital




         1.1. Identity, use pattern, physical and chemical properties,
              analytical methods
         1.2. Environmental transport, distribution and transformation
         1.3. Environmental levels and human exposure
         1.4. Kinetics and metabolism
         1.5. Effects on laboratory animals and  in vitro test systems
         1.6. Effects on humans
         1.7. Effects on organisms in the environment


         2.1. Identity
         2.2. Physical and chemical properties
         2.3. Conversion factors
         2.4. Analytical methods


         3.1. Production and uses
         3.2. Methods and rates of application


         4.1. Transport and distribution between media
              4.1.1. Soil
             Abiotic factors
             Biotic factors
             Environmental conditions affecting
                              distribution and breakdown
              4.1.2. Water
              4.1.3. Plants
         4.2. Bioaccumulation and biomagnification


         5.1. Environmental levels
              5.1.1. Air
              5.1.2. Water
              5.1.3. Food
         5.2. Occupational exposure


         6.1. Absorption
         6.2. Metabolic transformation
         6.3. Elimination and excretion
         6.4. Metabolism in laying hens


         7.1. Single exposure
              7.1.1. Oral
              7.1.2. Dermal
              7.1.3. Inhalation
         7.2. Short-term exposure
              7.2.1. Oral
              7.2.2. Dermal
         7.3. Skin and eye irritation; sensitization
              7.3.1. Skin irritation
              7.3.2. Skin sensitization
              7.3.3. Eye irritation
         7.4. Reproduction, embryotoxicity and teratogenicity
              7.4.1. Reproduction
             Biochemical and histopathological studies
                              on gonads
             Reproduction studies
              7.4.2. Embryotoxicity and teratogenicity
         7.5. Mutagenicity and related end-points
              7.5.1. Bacterial test systems
              7.5.2. Yeast assays
              7.5.3. Plant assays
              7.5.4. Cultured mammalian cell CHO/HGPRT assay
              7.5.5.  In vitro unscheduled DNA synthesis in primary rat
                     hepatocyte cultures
              7.5.6.  In vitro test for induction of chromosomal
                     aberrations using Chinese hamster ovary cells
              7.5.7.  In vivo rat bone marrow cytogenetic assay
              7.5.8. Acute  in vivo mouse bone marrow cytogenicity assay
              7.5.9.  In vivo/in vitro hepatocyte DNA repair assay
         7.6. Long-term toxicity and oncogenicity studies
              7.6.1. Rat
              7.6.2. Mouse
              7.6.3. Dog
         7.7. Miscellaneous studies


         8.1. Occupational exposure
         8.2. General population exposure


         9.1. Microorganisms
              9.1.1. Soil
              9.1.2. Water
         9.2. Aquatic organisms
              9.2.1. Aquatic invertebrates
              9.2.2. Fish
         9.3. Terrestrial organisms
              9.3.1. Terrestrial invertebrates
              9.3.2. Birds


         10.1. Conclusions
         10.2. Recommendations for protection of human health







    Dr L.A. Albert, Consultores Ambientales Asociados, Xalapa, Veracruz,

    Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
         Experimental Station, Abbots Ripton, Huntingdon, Cambridgeshire,
         United Kingdom

    Dr L. Ivanova-Chemishanska, Institute of Hygiene and Occupational
         Health, Sofia, Bulgaria ( Joint Rapporteur)

    Dr J. Kangas, Kuopio Regional Institute of Occupational Health,
         Kuopio, Finland

    Dr S.K. Kashyap, National Institute of Occupational Health,
         Meghaninagar, Ahmedabad, India

    Professor A. Massoud, Department of Community, Environmental and
         Occupational Medicine, Faculty of Medicine, Ain Shams University,
         Cairo, Egypt ( Vice-Chairman)

    Professor Wai-on Phoon, Department of Occupational Health, University
         of Sydney, and Professional Education Program, National Institute
         of Occupational Health and Safety, Worksafe Australia, Sydney,
         Australia ( Chairman)

    Professor L. Rosival, Institute of Preventive and Clinical Medicine,
         Bratislava, Czechoslovakia

    Dr K.C. Swentzel, Health Effects Division, US Environmental Protection
         Agency, Washington, D.C., USA ( Joint Rapporteur)


    Dr M. Carroll, Monsanto Services International, Brussels, Belgium

    Dr B. Hammond, The Agricultural Group of Monsanto Company, St Louis,
         Missouri, USA


    Dr K.W. Jager, International Programme on Chemical Safety, World
         Health Organization, Geneva, Switzerland ( Secretary)


         Every effort has been made to present information in the criteria
    monographs as accurately as possible without unduly delaying their
    publication. In the interest of all users of the Environmental Health
    Criteria monographs, readers are kindly requested to communicate any
    errors that may have occurred to the Director of the International
    Programme on Chemical Safety, World Health Organization, Geneva,
    Switzerland, in order that they may be included in corrigenda.

                                    * * *

         A detailed data profile and a legal file can be obtained from the
    International Register of Potentially Toxic Chemicals, Palais des
    Nations, 1211 Geneva 10, Switzerland (Telephone No. 7988400 or

                                    * * *

         The proprietary information contained in this monograph cannot
    replace documentation for registration purposes, because the latter
    has to be closely linked to the source, the manufacturing route, and
    the purity/impurities of the substance to be registered. The data
    should be used in accordance with paragraph 82-84 and recommendations
    paragraph 90 of the Second FAO Government Consultation (FAO, 1982).


         A WHO Task Group on Environmental Health Criteria for Propachlor
    met at the World Health Organization, Geneva, from 4 to 8 November
    1991. Dr K.W. Jager, IPCS, welcomed the participants on behalf of Dr
    M. Mercier, Director of the IPCS, and the three IPCS cooperating
    organizations (UNEP/ILO/WHO). The Group reviewed and revised the draft
    and made an evaluation of the risks for human health and the
    environment from exposure to propachlor.

         The first draft was prepared by Dr L. Ivanova-Chemishanska of the
    Institute of Hygiene and Occupational Health, Sofia, Bulgaria, who
    also assisted in the preparation of the second draft, incorporating
    comments received following circulation of the first drafts to the
    IPCS Contact Points for Environmental Health Criteria monographs.

         Dr K.W. Jager of the IPCS Central Unit was responsible for the
    scientific content of the monograph, and Dr P.G. Jenkins for the
    technical editing.

         The fact that Monsanto Agrochemical Company, St Louis, USA, made
    available to the IPCS and the Task Group its proprietary toxicological
    information on their product is gratefully acknowledged. This allowed
    the Task Group to make its evaluation on a more complete data base.

         The effort of all who helped in the preparation and finalization
    of the monograph is gratefully acknowledged.


    a.i.           active ingredient
    AcP            acid phosphatase
    ATPase         adenosine triphosphatase
    CHO            Chinese hamster ovary
    DMSO           dimethyl sulfoxide
    GA             gibberillic acid
    GGPT = GGT     gamma-glutamyltransferase
    HGPRT          hypoxanthine-guanine phosphoribosyltransferase
    LAP            leucine aminopeptidase
    LDH            lactate dehydrogenase
    MAC            maximum allowable concentration
    MAP            mercapturic acid pathway
    mCi            millicurie
    MQL            minimum quantifiable limit
    NOAEL          no-observed-adverse-effect level
    NOEC           no-observed-effect concentration
    NOEL           no-observed-effect level
    OCT            ornithine carbamoyltransferase
    ppb            parts per billion
    ppm            parts per million
    SAP = AP       alkaline phosphatase
    SDH            succinate dehydroganase
    SGOT = AST     aspartate aminotransferase
    SGPT = ALT     alanine aminotransferase
    UDS            unscheduled DNA synthesis
    uv             ultraviolet
    WP             wettable powder


    1.1  Identity, use pattern, physical and chemical properties,
         analytical methods

         Propachlor is a pre-emergence and early post-emergence herbicide
    derived from acetanilide, and has been in use since 1965. The major
    formulations are as wettable powder, liquid flowable (suspension
    concentrate) and as granules. Its uses in agriculture include the
    control of annual grasses and some broad-leaved weeds in several crops
    including corn, sorghum, pumpkins, flax and flowers.

         Propachlor is slightly soluble in water and readily soluble in
    most organic solvents. It has a low volatility, is non-flammable and
    is stable to ultraviolet radiation. The most practical method for
    analysis is gas chromatography with electron capture detection after
    suitable extraction and clean-up procedures.

    1.2  Environmental transport, distribution and transformation

         Propachlor is not known to photodegrade on soil surfaces.
    Volatilization of the compound occurs under windy conditions while the
    soil surface is still moist.

         The adsorption of the compound to soil particles and organic
    matter is only moderate. This leads to the potential for leaching
    through the soil profile and into ground water. However, all studies
    show that this potential is unlikely to be realised in practice. Very
    high rainfall is required to move residues 30 cm down the soil
    profile. Most authors report that the great majority of residues
    remain within the upper 4 cm of soil. The characteristics of the soil
    greatly influence movement of the compound. Most leaching occurs in
    sandy soil with little organic matter.

         Run-off of propachlor has been studied in both the laboratory and
    field. The organic matter in the soil reduced run-off from 7% to 1% of
    the applied herbicide in one study. Incorporation of propachlor into
    the soil also reduced loss through run-off (from 3% to 0.8% in one

         By far the most significant factor in reducing propachlor levels
    in soil and water is degradation by microorganisms. Both bacteria and
    fungi have been shown to be involved in breakdown of the compound. Few
    bacteria appear to be able to use propachlor as the sole carbon
    source. Bacteria capable of utilizing soil metabolites of propachlor
    have also been isolated.

         The predominant metabolites formed in soil are water-soluble
    oxanilic and sulfonic acids. A large number of other metabolites can
    be formed, but these represent a small proportion of the total.

         Propachlor disappears rapidly from soil, half-lives of up to 3
    weeks having been reported. Most studies report almost complete
    degradation within less than 6 months. Environmental conditions affect
    the rate of degradation, which is favoured by high temperature and
    soil moisture content. Those studies reporting longer persistence of
    propachlor in soil were conducted under conditions of low temperature
    or dry soil. Adequate nutrient levels in soil are also necessary for

         The conjugated  N-isopropylaniline metabolite is much more
    persistent than the parent compound. Residues of this metabolite have
    been found up to 2 years after the application of propachlor
    experimentally at higher rates than would normally be used in

         Under normal conditions of use, propachlor is not expected to
    leach through soil to ground water and will not persist in soil.
    Exceptional conditions of low temperature or dryness will lead to
    greater persistence of propachlor and its metabolites.

         Under normal conditions, propachlor does not photodegrade
    significantly in water. In the presence of photosensitizers,
    photodegradation may take place. Propachlor is hydrolytically stable.
    Volatilization from water is unlikely because of the high water
    solubility and low vapour pressure of the compound.

         As in soil, the major route of loss of propachlor from water is
    biotic degradation. The rate of loss of propachlor from water is,
    therefore, dependent on the microbial population. A study in water
    with few bacteria present yielded a half-life of about 5 months. Ring
    cleavage did not occur within six weeks in another study. Laboratory
    model ecosystem studies showed almost complete degradation of
    propachlor within 33 days.

         In several studies on different plant species, propachlor was
    shown to be rapidly metabolized in both intact plants and excized
    plant tissues. The metabolic pathways were similar in all plants
    studied, at least for the first 6 to 24 h, producing water-soluble
    metabolites. No metabolic breakdown of the  N-isopropylaniline moiety
    was observed. Only a very small proportion (< 1% in one study) of the
    metabolites was found in the fruit of the plants; the great majority
    was in the roots and foliage. The major metabolites produced in plants
    are identical with those produced in soil. Uptake of these metabolites
    from soil is known to take place and it is uncertain in some studies
    whether measured metabolites derive from the plant or the soil.

         Although the octanol/water partition coefficient suggests a
    moderate potential for bioaccumulation, studies show that propachlor
    neither bioconcentrates nor biomagnifies in organisms.

    1.3  Environmental levels and human exposure

         Reported measurements of air concentrations of propachlor during
    application are few and inadequate.

         Concentrations in surface and ground water in the USA were
    consistently low, the maxima being at 10 µg/litre in surface and 0.12
    µg/litre in ground water. The highest water concentration recorded in
    a run-off study was 46 µg/litre.

         Propachlor residues in food are usually below the detection limit
    of the analytical method (0.005 mg/kg). Experimental studies have
    identified residues in the order of 0.05 mg/kg in tomatoes, peppers,
    onions and cabbage.

         Measurements of propachlor in the air of the working zone of
    tractor drivers applying the compound ranged between 0.1 and 3.7

    1.4  Kinetics and metabolism

         Propachlor can be absorbed into mammals through the respiratory
    and gastrointestinal tract as well as through the skin. It does not
    accumulate in the body. After 48 h it is not detectable in the

         Most animal species (rats, pigs, chickens) metabolize propachlor
    through the mercapturic acid pathway (MAP). Cysteine conjugates are
    formed by glutathione conjugation and this conjugate has been proposed
    as an intermediate in the metabolic formation of mercapturic acids.
    Bacterial C-S lyase participates in the further metabolism of the
    cysteine conjugate of propachlor and in the formation of the final
    methylsulfonyl-containing metabolites, which are mainly excreted in
    the urine (68% of the dose of propachlor), and insoluble residues,
    which are excreted in the faeces (19%). The propachlor C-S lyase is
    not active in germ-free rats.

         Studies showed some differences in metabolism between the rat and
    pig. The bile is the major route of elimination of MAP metabolites in
    the rat, but it is has been proved that an extrabiliary route of
    metabolism exists in the pig.

         Metabolic studies on calves showed that they may be unable to
    form mercapturic acids from glutathione conjugates, which may make
    them more susceptible to poisoning.

    1.5  Effects on laboratory animals and in vitro test systems

         Propachlor is slightly toxic in acute oral exposure (the LD50
    in rats ranges from 950 to 2176 mg/kg body weight). Signs of acute
    intoxication are predominantly central nervous system effects
    (excitement and convulsion followed by depression). The acute

    inhalation toxicity in rodents is low (LC50 = 1.0 mg/litre).
    Propachlor caused severe irritation effects on eyes and skin.

         Propachlor has been tested in short- and long-term exposure
    studies on rats, mice and dogs. The liver and kidneys are the target
    organs. In dogs, the no-observed-adverse-effect level (NOAEL) was 45
    mg/kg body weight in a 3-month dietary exposure study. In a one-year
    study on dogs, the NOAEL was 9 mg/kg body weight (250 ppm in diet).
    The no-observed-effect level (NOEL) in a 24-month dietary exposure
    study on rats was 50 mg/kg diet (2.6 mg/kg body weight). In an
    18-month dietary study in mice, the NOEL was 1.6 mg/kg body weight (10

         Propachlor was not found to be carcinogenic in mice and rats. It
    showed a negative mutagenic response in most of the mammalian test
    systems and positive results in a few assays. The experimental data
    available provide insufficient evidence of the mutagenic potential.

         When tested as a single dose (675 mg/kg) in rats and mice,
    propachlor showed positive evidence of embryotoxicity. Embrytoxic
    effects were also observed in repeated dose regimens (35.7-270 mg/kg).
    However, in another rat study using a dose range of 20-200 mg/kg, no
    embryotoxicity was observed.

         At levels of 12 and 60 mg/kg body weight, propachlor (wettable
    powder) resulted in a decrease in protein content and an increase in
    ATPase and 5-nucleotidase activity in rat testis homogenate and
    degenerative changes in the testes. In a two-generation reproduction
    study there was no definite evidence of adverse effects.

    1.6  Effects on humans

         A few cases of contact and allergic dermatitis of farmers and
    production workers exposed to propachlor (Ramrod and Satecid) have
    been reported. Patch tests were carried out among some of them,
    revealing a positive patch test reaction, irritation reaction or mono-
    and bi-valent hypersensitivity.

         There have been no reports of symptoms or diseases either among
    occupationally exposed humans or the general population other than the
    few reports of its effects on the skin of occupationally exposed

    1.7  Effects on organisms in the environment

         In studies on soil microorganisms, nitrifying bacteria were the
    most sensitive group to the inhibitory effects of propachlor, their
    numbers being reduced by a factor of 3 to 4 after the application of
    8 to 10 kg propachlor/ha. Cellulose-decomposing bacteria were the
    least sensitive. High adsorption to clay particles in soil and high
    temperature both reduce the inhibitory effects.

         A 96-h EC50 of 0.02 mg/litre for growth and a no-observed-
    effect concentration (NOEC) of 0.01 mg/litre have been reported for
    the alga  Selenastrum capricornutum. A second study using a
    formulation and conducted over 72 h suggested substantially less
    hazard for the same organism.

         LC50 values of 7.8 and 6.9 mg/litre have been reported for the
    water flea  Daphnia magna and a NOEC of < 5.6 mg/litre. The NOEC for
    reproduction was 0.097 mg/litre. LC50 values of 0.79 and 1.8
    mg/litre have been reported for two species of midge larvae.

         The 96-h LC50 for rainbow trout is 0.17 mg/litre and the NOEC
    in a 21-day study was 0.019 mg/litre.

         Propachlor is considered to be moderately to highly toxic to
    aquatic organisms.

         Propachlor is not toxic to earthworms at exposure concentrations
    in soil expected from normal use (the NOEC is 100 mg/kg soil). The
    contact LD50 for honey bees (311 µg/bee) shows that propachlor will
    not pose a hazard to these insects. Some beneficial parasitic insects
    have been reported to be adversely affected by propachlor in
    laboratory and field studies.

         Propachlor is more toxic to birds when administered via the
    stomach than when fed in the diet. Acute LD50 values range between
    137 and 735 mg/kg body weight for different bird species. The LC50
    values from dietary exposure exceed 5620 mg/kg diet in birds.

         Propachlor does not pose a hazard to birds in the field, even
    with the granular formulation.


    2.1  Identity

    Common name:        Propachlor

    Chemical structure


    Chemical formula:   C11H14ClNO

    Common synonyms
    and trade names:    Ramrod, Acylide, Bexton (discontinued by Dow
                        Chemical Company), Niticid, Satecid

    CAS chemical name:  2-chloro- N-(1-methylethyl)- N-phenyl acetamide

    IUPAC name:         2-chloro- N-isopropylacetanilide (formerly
                        alpha-chloro- N-isopropylacetanilide)

    CAS registry
    number:             1918-16-7

    RTECS registry
    number:             AE1575000

         Propachlor is available as a technical material containing 93%
    active ingredient for formulation of propachlor end-use products. It
    is available in the form of granules (200 g active ingredient/kg),
    wettable powder (WP, 650 g active ingredient/kg) and as a liquid
    flowable formulation (suspension concentrate), among others. Mixtures
    with other herbicides, e.g., atrazine and propazine are also used.

    2.2  Physical and chemical properties

         Some of the physical and chemical properties of propachlor are
    given in Table 1.

    Table 1.  Some physical and chemical properties of propachlor
    Physical state                   solid
    Colour                           tan

    Relative molecular mass          211.7

    Melting point (°C)               77

    Boiling point (°C) at 0.03 mmHg  110

    Decomposition (°C)               > 170

    Vapour pressure (25 °C)          103 mPa

    Solubility in water (20 °C)      580 mg/litre
                        (25 °C)      613 mg/litre

    Solubility in organic solvents   readily soluble in most organic
                                     solvents except aliphatic
                        acetone      448 g/kg
                        benzene      737 g/kg
                        chloroform   602 g/kg
                        ethanol      408 g/kg
                        xylene       239 g/kg

    Log Kow                          1.62-2.30

         It is non-flammable and stable to ultraviolet radiation.

    2.3  Conversion factors

         At 25 °C       1 mg/m3 = 8.802 ppm
                        1 ppm = 0.1136 mg/m3

    2.4  Analytical methods

         The analytical methods described in the literature, which are
    based on different types of determination of propachlor in different
    media, are given in Table 2.

    Table 2.  Analytical methods for the determination of propachlor and metabolites
    Sample type        Method of detection               Extraction and clean-up                   Detection limit        Reference
    Soil and plants    thin-layer chromatography         2-h extraction with                       0.02-0.04 mg/kg        Kofman &
                                                         chloroform                                                       Nishko

    Soil and plants    gas chromatography with           extraction with benzene; clean-up         0.004-0.005 mg/kg      Balinova
                       electron-capture detection        by partition with hexane-acetonitrile                            (1981)
                                                         followed by column chromatography

    Soil               gas chromatography with           acetone extraction followed by alkane     0.01 mg/kg; re-        Caverly &
                       electron-capture detection        hydrolysis, steam distillation and        coveries at residual   Denney
                                                         concentration of anilines in toluene      levels are generally   (1978)
                                                                                                   better than 80%

    Soil               gas liquid chromatography         extraction with isopropanol and benzene;  < 0.05 mg/kg           Markus &
                       with flame-ionization detection   column chromatography (Florisil)                                 Puma (1973)

    Immature plants    gas-liquid chromatography         extraction with isopropanol; column       < 0.05 mg/kg           Markus &
                       with flame-ionization detection   chromatography (Florisil)                                        Puma (1973)

    Mature grain       gas-liquid chromatography         extraction with acetonitrile; column      < 0.05 mg/kg           Markus &
                       with flame-ionization detection   chromatography (Florisil)                                        Puma (1973)

    Cabbage            gas chromatography with NP        extraction with acetone followed by       0.06 mg/kg (fresh      Warholic et
                       detection                         alkaline hydrolysis to                    weight)                al. (1983)
                                                          N-isopropylaniline; steam
                                                         distillation and extraction with

    Table 2 (contd).
    Sample type        Method of detection               Extraction and clean-up                   Detection limit        Reference
    Industrial and     gas chromatography with           extraction with methylene chloride;       1 ng/litre             Pressley &
    municipal waste    electron-capture detection        clean-up on a Florisil column                                    Longbottom
    water                                                                                                                 (1982)

    Urine metabolites  gas or liquid chromatography      fractionation with lipophilic ion         not given              Sjovall et
    of propachlor      and mass spectrometry             exchangers (Lipidex 1000, Lipidex DEAP                           al. (1983)
    (glutathione                                         SP-LH-20 and Sep pack C18)
         High-pressure liquid chromatography with radioactive detection or
    liquid scintillation has been used to purify the metabolites from
    14C-labelled propachlor in several biological media, including egg
    yolk, egg white, edible tissues and excreta of laying hens, after
    extraction with organic solvents. The metabolites were characterized
    by gas chromatography with radioactive detection mass spectrometry
    (Bleeke et al., 1987). With liquid scintillation detection, the
    minimum quantifiable limit (MQL) was 0.01 to 0005 ppm.


    3.1  Production and uses

         Propachlor was developed by the Monsanto Chemical Company and
    commercially introduced in 1965. Technical propachlor is produced in
    the USA by Monsanto and in Germany by BASF. There are other
    manufacturers of technical propachlor.

         Propachlor is prepared by the reaction of chloracetyl chloride
    and  N-isopropylaniline.

         It is a pre-emergence, pre-planting (incorporated) or early
    post-emergence herbicide effective against annual grasses and some
    broad-leaved weeds (Worthing & Hance, 1991). It is used on field corn,
    hybrid seed corn, silage corn, grain sorghum (milo), green peas,
    soybeans, flax, pumpkins and flowers. In 1971, 10 000 tonnes were
    produced (US EPA, 1984a), but a more recent estimate of annual use in
    the USA is 1800 tonnes.

    3.2  Methods and rates of application

         Application rates range from 4 to 6 kg active ingredient in
    150-300 litres of water per ha (6-9 kg wettable powder formulation/ha)
    in pre-emergence use. Some tests indicate that early post-emergence
    applications are equally effective for weed control. The best response
    occurred when broad-leaved weeds were between the cotyledonous stage
    and the 2´-leaf stage and when grassy weeds were up to the one-leaf

         Irrigation following application improves activity, particularly
    under dry soil conditions. The duration of weed control ranges from 4
    to 6 weeks, depending on the soil structure and organic content
    (Humburg et al., 1989).


    4.1  Transport and distribution between media

    4.1.1  Soil

         The fate and transport of propachlor in soil has been well
    studied. The principal aim has been to determine the rate and products
    of degradation, persistence, environmental factors and organisms
    participating in the biodegradation, and the conditions under which
    degradation takes place.  Abiotic factors

         Beestman & Deming (1974) found that leaching did not contribute
    to dissipation since no residues were found below the upper 4-cm
    layer. The weak leaching ability was related to the high adsorption of
    propachlor by soil. The ultraviolet absorption spectrum of propachlor
    reveals no absorption at wavelengths longer than 280 nm. On the basis
    of these data it was suggested that photodecomposition of soil-applied
    propachlor would not be significant. Rapid herbicide volatilization
    occurred under windy conditions during the period that exposed soil
    surfaces remain moist.

         In a study by Nesterova et al. (1980), propachlor was applied,
    under dry weather conditions, at a rate of 7 kg/ha for 4 consecutive
    years. The residues of propachlor in the soil were measured up to 4
    weeks following the application. On the 5th day, residues were found
    in the upper layers (0-10 cm), and on the 15th day, after abundant
    rain (74 mm), they had reached 0-30 cm. There was rapid
    biodegradation, mainly in the first 5 days, followed by reduced
    degradation over the next 10 days. Between the 15th and 30th day, no
    residues were detected.

         The mobility of 14C-propachlor in the soil was investigated by
    Brightwell et al. (1981) by determining its leaching as well as its
    adsorption coefficient and desorption behaviour. Results were very
    variable and depended on soil type. With a sandy loam, 89.5% of the
    14C activity applied leached through laboratory soil columns,
    whereas only 5.4% leached through silty clay loam. A high organic
    matter content reduced the leachability of propachlor. Most of the
    radioactivity represented the parent compound. Propachlor was adsorbed
    only moderately, although the equivalent of 50 cm of rain was needed

    to desorb 40 to 70% of the activity previously bound to soil to a
    depth of 30 cm in the profile.

         The mobility of propachlor in soil was the object of a study
    carried out by Ritter et al. (1973). The diffusion coefficient of
    propachlor in a silt loam soil was determined and was compared with
    the coefficients of two other pesticides, atrazine and diazinone. It
    was found that propachlor had the highest solubility and the largest
    diffusion coefficient, which allowed it to move rapidly in the soil.
    The movement increased with the temperature and moisture contents.

         The run-off losses of propachlor have been studied by Baker &
    Laflen (1979), Baker (1980) and Baker et al. (1982). Rainfall
    simulation was used by Baker et al. (1982) to determine the effects of
    corn residue on herbicide run-off losses from the soil. Propachlor was
    applied to plots with 0, 375, 750 and 1500 kg corn residue per ha, and
    a 2-h rainfall of 127 mm was simulated. For plots with no corn
    residue, the average time to run-off was 11 min; run-off was 63 mm,
    soil loss 11 tonnes/ha, and herbicide loss 7% of the amount applied.
    Increased corn residue amounts increased time to run-off and decreased
    run-off, erosion and herbicide losses. Time to run-off for the largest
    corn residue amount was 30 min, run-off 18 mm, soil loss 1 tonne/ha,
    and herbicide loss 1%. At least 84% of the herbicide losses were in
    the dissolved phase. Herbicide placement had little or no effect on
    the concentrations of herbicide in run-off water and sediment.
    Herbicide concentrations in water and sediment were negatively
    correlated with time to run-off.

         The effects of incorporation and surface application on run-off
    losses of propachlor were determined by measuring losses in water and
    sediment from small plots during 122 mm of simulated rainfall (Baker
    & Laflen, 1979). Losses of propachlor that was surface-applied to
    plots were 3%, whereas losses from plots where the herbicide was
    incorporated by disking were only 0.8%. Incorporation of herbicide has
    the potential to decrease run-off losses and may be considered the
    best application method.

         In a laboratory study, propachlor was applied at rates of 0.4 and
    1.8 kg/ha to corn ( Zea mays) residue, which in turn was subjected to
    simulated rainfall (Martin et al., 1978). Initial concentrations in
    wash-off water were high (9 mg/litre for the high application rate),
    but this decreased rapidly with time. The mass balance showed that
    most of the applied dose was washed off and little was retained by the

    corn residue. Unexplained losses indicated the possibility of
    volatilization occurring between application of herbicide and
    application of wash-off water about 12 h later.

         Gustafson (1989) described a method combining persistence and
    mobility parameters to assess the potential for leaching and
    contamination of ground water by propachlor. The author concluded that
    propachlor was unlikely to leach through the soil into subsoil water
    and ground water.  Biotic factors

         Beestman & Deming (1974) carried out a large study to determine
    the dissipation rate under laboratory and field conditions from Ray
    silt and Wabash silty clay soils and to quantify the contributions of
    microbial decomposition, chemical breakdown, volatilization and
    leaching. Dissipation followed first-order kinetics with half-lives
    ranging from 2 to 14 days. In moist Ray silt the half-life of
    propachlor was 4.5 days. The important role of microbial degradation
    was clearly established. Dissipation from sterilized soil was 50 times
    slower (T´ = 141-151 days) than from unsterilized soil under
    identical conditions.

         Rankov & Velev (1977) conducted a model study over 120 days with
    10 microscopic fungi from the genera  Penicillium, Aspergillus,
     Fusarium and  Trichoderma concerning the degradation and
    detoxication of propachlor in alluvial meadow soil at 28 °C and 65%
    soil humidity. The results confirmed the important role of microscopic
    fungi in increasing the rate of propachlor degradation and

         Villarreal et al. (1991) enriched microbial cultures from a
    pesticide disposal site to identify the range of metabolic capacity
    for propachlor and its metabolites and the species involved in
    breakdown of the compound. A single strain, corresponding most closely
    to the genus  Moraxella, could grow on propachlor as its sole carbon
    source releasing a metabolite (2-chloro- N-isopropyl-acetamide) into
    the medium. A second strain, corresponding to the genus  Xanthobacter
    grew on the metabolite. The  Moraxella strain appears to use the
    aromatic carbon atoms of the propachlor for growth since there was
    induction of catechol 2,3-oxygenase activity in the cells and the
    growth rate was sustainable only from this source.

         Novick et al. (1986) showed that suspensions of soil treated in
    the field with propachlor could mineralize 16-61% and 0.6-63% of

    ring-labelled propachlor in 30 days at propachlor concentrations of
    0.025 and 10 mg/litre, respectively. A mixture of two bacteria
    mineralized 57.6% of propachlor within 52.5 h, producing
     N-isopropylaniline as a metabolite.  Metabolites

          N-isopropylaniline,  N-isopropylacetanilide,
     N-(1-hydroxyiso-propyl)-acetanilide and  N-isopropyl-2-
    acetoxyacetanilide are formed as metabolites of propachlor in soil
    (Lee et al., 1982). Frank et al. (1977) demonstrated the existence of
    a longer-lasting conjugated degradation product of propachlor in
    onions and in organic soils following soil application. This was
    conjugated  N-isopropylaniline, which could be found in soil up to 2
    years after application.

         An extensive study on the environmental and metabolic fate of
    propachlor was conducted by Brightwell et al. (1981). A variety of
    soil metabolites was identified, the most significant resulting from
    the modification of the C-2 carbon to yield water-soluble oxanilic and
    sulfonic acids. The soil metabolism studies demonstrated the
    predominant proportion of the water-soluble metabolites, i.e.
    [(1-methylethyl) phenylamino] oxoacetic acid (IV), 2-[(1-methylethyl)
    phenylamino]-2-oxoethanesulfonic acid (V) and {{[(methylethyl)
    phenylamino] acetyl}sulfinyl}acetic acid (VI). These metabolites
    accounted for 25, 17, and 6% of the applied 14C activity,
    respectively, at different sampling points during the studies. There
    was a decline in the level of these metabolites with time (Fig. 1).

         In addition, several organic soluble metabolites were isolated
    and identified; these included  N-(1-methylethyl)-2-(methyl-
    sulfinyl)- N-phenylacetamide (VII),  N-(1-methylethyl)-2(methyl
    sulfonyl)- N-phenylacetamide and 2-hydroxy- N-(1-methyl-ethyl)-
     N-phenylacetamide (II). These accounted for no more than 6% of the
    applied activity. The degradation products observed in the anaerobic
    soil metabolism study were comparable to those observed under aerobic
    conditions, but the rate of degradation in aerobic conditions was

         Lamoureux & Rusness (1989) studied the metabolism of propachlor
    and the cysteine conjugate of propachlor in sandy loam soil. Both
    compounds were metabolized at similar rates to three major products:
     N-isopropyloxanilic acid, 2-sulfo- N-isopropyl-acetanilide and
    2-(sulfinylmethylenecarboxy)- N-isopropyl-acetanilide.

    FIGURE 1

    I.   R = CH2Cl
         2-chloro- N-(1-methylethyl)- N-phenylacetamide = propachlor

    II.  R = CH2OH
         2-hydroxy- N-(1-methylethyl)- N-phenylacetamide

    III. R = CH3
          N-(1-methylethyl)- N-phenylacetamide

    IV.  R = COH
         [(1-methylethyl)phenylamino]oxoacetic acid

    V.   R - CH2SO3H
         2-[(1-methylethyl)phenylamino]-2-oxoethanesulfonic acid

                O   O
                "   "
    VI.  R = CH2SCH2COH
         {{[(methylethyl)phenylamino]acetyl}sulfinyl}-acetic acid

    VII. R = CH2SCH3
          N-(1-methylethyl)-2-(methylsulfinyl)- N-phenylacetamide

    Fig. 1.  Structures of propachlor degradation products.  Persistence

         Fletcher & Kirkwood (1982) reported a half-life of 2-3 weeks for
    propachlor. Free propachlor disappeared rapidly in soil treated by
    Ritter et al. (1973); in 21-28 days residues of free propachlor
    declined 72-80%. In earlier laboratory studies and field bioassays
    carried out by Menges & Tamez (1973), the soil persistence (> 90%
    degradation) was found to be less than 6 months. According to Melnikov
    et al. (1985) and Zhukova & Shirko (1979), the period of propachlor
    degradation in soil to non-toxic products is about 2 months. The
    presence of an alkyl group attached to the nitrogen atom in its
    molecule prevents its decomposition to aniline or to azobenzolic

    residues, which could later be transferred into tetrachlorazobenzene
    (Panshina, 1985). Propachlor applied at 4-8 kg/ha was detoxified in
    peat soil within 59-63 days (Vasilev, 1982). When it was applied at
    6.5, 9 and 11 kg/ha, it was still detectable after 113 days in two
    types of soil in the Voronezh and Krasnodar regions of the former USSR
    (Kolesnikov et al., 1980). The longer persistence determined in this
    study might be connected with the climatic conditions, particularly
    the low temperatures. Roberts et al. (1978) and Balinova (1981)
    confirmed that propachlor is rapidly decomposed in soil.

         Field studies evaluating the degradation of propachlor in soil
    showed that 70 days after application, propachlor was detectable in
    insignificant quantities (0.04 mg/kg, i.e. 2% of the dose applied).
    Degradation was slower in dry than humid weather (Zhukova & Shirko,
    1979) (Table 3). The conclusions of the authors were that degradation
    in soil is rapid and there is no possibility of propachlor
    accumulation in crops.
    Table 3.  Dynamics of dissipation of propachlor in soil (average data
              for 1974-1976)a
    Dose application    After 10th day  On 30th day     On 50th day     On 70th day
    (kg propachlor/ha)  mg/kg   %b      mg/kg   %b      mg/kg   %b      mg/kg   %b
        6               1.73    86.4    0.95    42.8    0.10    5.2     0.04    2

        8               2.44    92.6    1.55    58.3    0.20    7.8     0.04    2

       10               3.14    94.2    2.53    76.0    0.40    12.0    0.04    2

    a  From: Zhukova & Shirko (1979)
    b  Percentage of dose applied
             In a study by Frank et al. (1977), soil with high organic matter
    content was treated with 19 kg propachlor/ha. The treatment times and
    rates are given in Table 4. Soil samples were collected to a depth of
    20 cm and analysed. Residues of the conjugated metabolite
     N-isopropylaniline of up to 3.7 mg/kg soil were detected 2 years
    after the application. They were released from soil by hydrolysis,
    indicating the presence of active bonding sites for the metabolite in
    the soil. The authors concluded that using propachlor in successive
    years led to accumulation of long-lasting conjugated
     N-isopropylaniline. Applications made once every 3 years, however,
    did not lead to such accumulation and they recommended this type of

    Table 4.  Residues of conjugated  N-isopropylaniline in organic soil
              treated with propachlor in 1971, 1972 and 1975a.
    Year  Time of application  Rate of application    N-isopropylaniline
                               (kg/ha)b              residues in
                                                     oven-dried soil
    1971  May and June         9 + 10                not analysed

    1972  untreated            none                  3.67
          May, July, August    6.7 + 3.4 + 3.4       7.70
          May, July, August    6.7 + 6.7 + 6.7       9.47

    1975  May and June         6.7 + 6.7             3.16

    a From: Frank et al. (1977)
    b Soil samples were collected in May 1973 and April 1976 and analysed
      in January and April 1976, respectively.

         US EPA (1984b) re-evaluated the existing data concerning some
    environmental aspects of propachlor. It was concluded that microbes
    were the primary factor in its breakdown in soil and that its loss
    from photodecomposition and/or volatilization was low. Although this
    earlier assessment suggested a potential for propachlor to contaminate
    ground water, a later assessment (US EPA, 1988) concluded that "the
    rapid degradation of low levels of propachlor in soil is expected to
    result in a low potential for groundwater contamination by
    propachlor".  Environmental conditions affecting distribution and breakdown

         Walker & Brown (1982, 1985) carried out laboratory studies and
    field trials in parallel. They found first-order kinetics dissipation
    of propachlor and confirmed the results of Beestman & Deming (1974).
    They also described a clear temperature dependence: an increase in
    temperature of 10 °C reduced the half-life by a factor of between 1.9
    and 2.5. Soil moisture also influenced degradation: slower rates of
    loss were found in drier soil. The half-life in soil with a moisture
    content of 6% was about twice as long as at 15% (Table 5). In general,
    the time of persistence in the field was comparable to that measured
    in laboratory studies. The half-life of propachlor varied from 4 to 22
    days (Table 5).

    Table 5.  Half-life for propachlor degradation (days)a

    Temperature (°C)    25       25       25       25       15        5

    Moisture (%)         6        9       12       15       12       12

    Propachlor           7.7      4.6      4.2      3.7      9.2     21.7

    a From: Walker & Brown (1985)

         The persistence of propachlor in soil as a result of all
    microbial, chemical and physical processes has been studied by Zimdahl
    & Clark (1982). They measured the half-life of propachlor in clay loam
    and sandy loam soils in the laboratory, using different temperature
    and moisture conditions (Table 6). An increase in temperature (from 10
    to 30 °C) and moisture content (from 20 to 80%) shortened the

         Vasilev (1982) confirmed the importance of meterological
    conditions, type of soil, and rate and period of application on the
    degradation in soil. In dry weather, degradation took longer than in
    humid conditions. Based on field experiments where soil was treated
    with propachlor and carrots were then planted, the author reported the
    following residues (measured at the moment of harvest in the soil
    layer 0-20 cm) in soil: at an application rate of 4 kg/ha the
    propachlor residues were 0.05 mg/kg; at 6 kg/ha they were 0.15 mg/kg;
    and at 8 kg/ha they were 0.2 mg/kg.

    Table 6.  Half-lives of propachlor in clay loam and sandy loam as
              determined by bioassaya
               Storage conditions                 Half-life (days)

         Temperature       Soil moisture     Sandy loam        Clay loam
            (°C)                (%)
             10                 50               16.7              14.3

             20                 50                3.3               5.3

             30                 50                1.9               1

             20                 20               23.1              21.5

             20                 50                3.3               5.3

             20                 80                3.3               4.1

    a From: Zimdahl & Clark (1982)

         Shirko & Belova (1982) found that residues of propachlor in soil
    and plants depended on the nitrogen and potassium content of the soil.
    At the moment of harvesting, no residues of propachlor were detected
    in soil after application at a rate of 4.5-6.5 kg/ha. According to the
    authors, a better supply of plants with nutrients (in this case,
    nitrogen and potassium fertilizers) leads to more intense
    detoxification and degradation of the herbicide and, conversely, an
    insufficiency delays the detoxification processes and leads to the
    accumulation of residues.

    4.1.2  Water

         Photodegradation of propachlor in aqueous media was studied by
    Tanaka et al. (1981) under laboratory conditions. They used a 10-ml
    sample with propachlor concentrations ranging up to 100 mg/litre, and
    the sample was irradiated for 135 min with a 300-nm sunlight lamp.
    Very weak photolysis was registered; by the end of the study only 1%
    of herbicide had been lost. Addition of a commercial surfactant (2%
    heterogeneous non-ionic Tergitol TMN, acting as photosensitizer)
    allowed 37% of propachlor to be photodegraded. It is difficult to make
    conclusions on this study because of certain deficiencies. The use of
    a commercial formulation in such studies should be avoided since some
    of the constituents may cause indirect photochemical reactions. No
    mention was made in the report of the purity of the compound studied.
    The test should preferably be carried out at constant temperature. The
    lack of data concerning the intensity of the irradiation source (US
    EPA, 1984a) does not allow any extrapolation of these data to the

         Rejtö et al. (1984) investigated the effects of ultraviolet
    irradiation of propachlor solutions and found that 5 h of irradiation
    led to 80% decomposition. The three photodecomposition products
    identified were:  N-isopropyloxindole,  N-isopropyl-3-
    hydroxyoxindole and a spiro compound. Irradiation of a solution of
    propachlor with visible light for 12 h led to almost complete
    decomposition in the presence of riboflavin as a photosensitizer. The
    photodecomposition products after visible light irradiation were found
    to be non-phytotoxic.

         Monsanto (1987) demonstrated that propachlor is hydrolytically

         Volatilization of propachlor from aqueous media is of limited
    significance because of the high solubility in water and relatively
    low vapour pressure of the compound. In agreement with Henry's
    constant, the loss of propachlor by sorption and sedimentation in
    water bodies does not appear to be very significant (US EPA, 1984a).

         The role of microbial biodegradation appears to be of major
    significance in water as well as in soil. Novick & Alexander (1985)
    studied the metabolism of low concentrations (10 µg/litre) of
    propachlor in sewage and lake water. They found that under aerobic

    conditions microbial populations from sewage and lake waters were not
    able to mineralize the carbon ring of propachlor in six weeks.
    However, propachlor was extensively metabolized, the products obtained
    were organic, and they were found to accumulate in the environment. In
    a parallel study, it was found that aniline was readily cleaved under
    similar conditions, indicating rapid mineralization of this compound.
    It was concluded that structural characteristics of propachlor, other
    than the ring, account for the mineralization of the compound. The
    presence of the three substituents on the nitrogen atom in propachlor
    may be the reason for its persistence. Steen & Collette (1989)
    determined microbial transformation rate constants for seven amides in
    natural pond water. A second order mathematical rate expression served
    to describe propachlor degradation, and a value of 1.1 x 10-9
    litres/organism per h was calculated. Brightwell et al. (1981)
    presented data showing slow degradation of propachlor in lake water
    under aerobic conditions. After 30 days, 84.5% of the propachlor
    remained unchanged; under these conditions a half-life of about 5
    months would be expected. The low rate of metabolism was due to a low
    level of microorganisms. Yu et al. (1975) studied the degradation of
    propachlor in water using a model ecosystem. An aquarium with
    7-day-old sorghum plants was used with the addition of 50 µCi of 14C
    ring-labelled propachlor. By the end of the 33-day experimental
    period, 7 degradation products in water were determined by thin-layer
    chromatography but were not identified. At that time only 0.4% of the
    radioactivity of the dose applied remained in the water.

    4.1.3  Plants

         The metabolism of propachlor in corn seedlings and in excized
    leaves of corn, sorghum, sugar cane and barley was studied by
    Lamoureux et al. (1971). Metabolism was rapid and similar in all
    mentioned plant species during the first 6-24 h following treatment.
    At least 3 water-soluble metabolites were produced in each species
    during this period. Two of these metabolites were isolated; the first
    one was identified as the glutathione conjugate of propachlor
    (compound I) and the second one appeared to be the gamma-
    glutamylcysteine conjugate (compound II). The primary mode of
    metabolism is a nucleophilic displacement of the alpha-chloro group of
    propachlor by the sulfhydryl group of a peptide. The metabolic
    reactions of propachlor proceed non-enzymatically  in vitro, and the
     in vivo reaction may be enzymatic and/or non-enzymatic. The high
    percentage of propachlor converted to compounds I and II in corn
    seedlings during the first 18 h following treatment indicates that the
    reaction of propachlor with glutathione and/or gamma-glutamylcysteine
    is quite specific. This would be expected if the reaction is
    enzymatic. Some glutathione and gamma-glutamylcysteine conjugates in
    plants may be end-products, but, in the case of propachlor, these
    metabolites are transient intermediates. Further studies are needed to
    establish the final steps (Lamoureux et al., 1971).

         Pantano & Anderson (1987) studied the metabolism of propachlor in
    sorghum (milo). Sorghum seeds were planted in soil treated with 14C

    ring-labelled propachlor at a rate of 3.3 kg/ha and grown to maturity
    in a greenhouse. Following senescence, plants were separated into
    various anatomical parts, freeze-dried and analysed for activity. The
    uptake of 14C in the foliage and grain was 9.5 and 0.5 mg/kg dry
    weight, respectively. Four metabolites were identified in the foliage
    extract; these represented 66.5% of the metabolites in foliage. The
    four metabolites were [( N-iso-propyl) phenylamino]oxoacetic acid,
    {{[( N-isopropyl)-phenyl-amino]acetyl}sulfinyl}lactic acid,
    {{[( N-isopropyl)phenylamino] acetyl}sulfinyl}acetic acid and
    2-[( N-isopropyl)phenylamino]-2-oxoethanesulfonic acid. In addition,
    other metabolites found at low levels in the foliage extract were
    characterized. Freeze-dried sorghum grain contained only 0.5 mg/kg of
    14C activity and only one metabolite was identified (the first
    compound mentioned above). This metabolite constituted at least 24.9%
    of the activity in grain. In all of the major metabolites identified
    in this study, no modification of the  N-isopropylaniline moiety was
    observed. On the basis of metabolites identified in this study and
    known pathways for the metabolic transformations of related
    chloroacetamides, a scheme for the metabolic fate of propachlor in
    sorghum plants was postulated by the authors. The biotrans-formations
    include: 1) displacement of the chlorine by an oxygen-containing
    nucleophile followed by oxidation, and 2) conjugation with glutathione
    followed by further metabolic modification of this conjugate.

         Lamoureux & Rusness (1989) studied the metabolism of propachlor
    in soybean and found that it was rapidly metabolized to
    homoglutathione conjugate in roots and foliage. This conjugate was
    rapidly metabolized to the cysteine conjugate and then slowly
    converted to a variety of other metabolites; four of these were
    present up to 72 days after application of propachlor. These four were
    malonylcysteine, malonylcysteine  S-oxide, 3-sulfinyllactic acid and
     O-malonyl glucoside conjugates of propachlor. Less than 1% of
    metabolites was isolated from beans or pods, the great majority being
    in roots and foliage. The major metabolites found in plants were the
    same as those produced in soil. The authors suggested that it is
    difficult to differentiate between metabolites formed in the plant and
    those taken up from soil as to the relative importance of the two
    sites of metabolic degradation.

    4.2  Bioaccumulation and biomagnification

         The two published values for the log octanol/water partition
    coefficient (log Kow) of propachlor, i.e. 1.62 and 2.3 (US EPA,
    1984b, 1988), indicate a moderate potential for bioaccumulation.

         Barrows & Macek (1974) used bluegill sunfish exposed to
    14C-labelled propachlor in a continuous-flow experiment in order to
    assess the potential for the compound to bioconcentrate in aquatic
    organisms. The fish were exposed for 35 days to a mean
    14C-propachlor concentration of either 0.54 mg/litre (high level) or
    0.012 mg/litre (low level) in the water. Analysis of the fish tissues
    indicated bioconcentration factors (BCFs) in the edible tissue of 34

    and 22 for the high and low levels, respectively, and in the
    non-edible tissue of 22 and 20. When the fish were placed in clean
    water the activity was rapidly eliminated from the non-edible portion
    of the fish and at a somewhat slower rate from the edible tissue.
    Because of the polar, water-soluble nature of the soil metabolites
    (section 4.1.1), they would be less likely to bioconcentrate in
    aquatic organisms. The results of a static study on catfish by Malik
    (1982) showed that BCFs for both edible and non-edible tissues were
    0.23 and that the low level of accumulated activity was eliminated
    rapidly when the fish were placed in clean water.

         Yu et al. (1975) studied 14C-propachlor in a model ecosystem
    containing seven species. There was no indication of either
    bioconcentration or biomagnification; total radioactivity declined
    from 0.21 to 0.015 mg propachlor/kg through the seven stages of the
    food chain.


    5.1  Environmental levels

         The application of propachlor as a herbicide in plant protection
    results in its presence in air, soil and water. It is taken up from
    the soil into plants through the root system.

    5.1.1  Air

         Propachlor application resulted in its presence in the ambient
    air 300 m away from the treated field at concentrations ranging from
    0.02-0.6 mg/m3 (Panshina, 1976). No details on the analytical method
    or quantity of propachlor sprayed were given in this report.

    5.1.2  Water

         Propachlor was found in 34 of 1690 surface water samples analysed
    in the USA (US EPA, 1988). Samples of surface water were collected at
    475 locations and groundwater samples at 94 locations. The compound
    was detected in eight different states. The maximum concentration
    found was 10 µg/litre in surface water and 0.12 µg/litre in
    groundwater (the 85th percentile for all non-zero samples was 2
    µg/litre in surface water and 0.12 µg/litre in ground water). Spalding
    & Snow (1989) detected propachlor at a maximum concentration of 46
    µg/litre in stream water receiving its flow from agricultural land
    planted principally with corn. The monitoring was carried out during
    a spring period of high water flow and run-off.

    5.1.3  Food

         The residues of propachlor in potato tubers and tomatoes were
    lower than 0.005 mg/kg (the limit of detection) approximately 60-70
    days after application of the recommended dose of 4-6 kg/ha (Balinova,
    1981). Warholic et al. (1983) could not detect propachlor (detection
    limit, 0.06 mg/kg fresh weight) in cabbages grown on soil treated with
    propachlor at 0.6 kg a.i./ha (wettable powder).

         Frank et al. (1977) reported the results of a study on the fate
    of propachlor applied to onions. Planted in May, the onions were
    harvested in September and analysed in January the following year.
    Conjugated  N-isopropylaniline was present in onion tissue after
    harvest and after a normal storage period for the crop before sale.
    Bearing in mind the reports of other authors (Lamoureux et al., 1971),
    Frank et al. (1977) suggested that 2-chloro- N-isopro-pylacetanilide
    could be hydrolysed to 2-hydroxy- N-isopropyl-acetanilide and bonded
    to glutathione. It is probable that alkaline hydrolysis cleaved the

    weaker  N-carbonyl C linkage to given  N-isopropylaniline rather
    than the stronger C-S bond which would have resulted in 2-hydroxy- N-
    isopropylaniline. Tissue residues of  N-isopropylaniline increased as
    the rate of application of propachlor was increased, and the later the
    application was made the higher the tissue residues (see Table 7).
        Table 7.  Residues of conjugated  N-isopropylanilinea
    Year  Time of application             Rate of propachlor    N-isopropylaniline
                                          application (kg/ha)  residues (mg/kg)
    1974  untreated                       0                    0.03
          pre-emergence                   7.2                  0.05
                                          12.0                 0.09

          pre-emergence and early post-
          emergence (21 May and 13 June,  7.2 + 7.2            0.17
          respectively)                   12.0 + 12.0          0.15

          pre-emergence and late post-
          emergence (21 May and 9 July,   7.2 + 7.2            0.28
          respectively)                   12.0 + 12            0.40

    a From: Frank et al. (1977). Onions were planted 6 May 1974 and harvested
      4 September 1974. Analyses were performed in January 1975.
             Propachlor has been used for soil treatment (6 kg/ha) before
    planting tomatoes and peppers. Sampling was performed at 15-day
    intervals and the samples were analysed by gas chromatography
    (detection limits, 0.005 mg/kg). Small quantities of propachlor (of
    the order of 0.04 mg/kg) were found in tomatoes on the 70th and 85th
    days after soil treatment. On the 73rd day, 0.07 mg/kg was found in
    peppers, and on the 88th and 108th days the residues had decreased to
    0.05 and 0.04 mg/kg, respectively. No herbicide residues were found in
    the following years (Balinova & Konstantinov, 1975).

         In a study where soil was treated (8 kg/ha) before the seedlings
    were planted, samples of cabbages contained propachlor residues
    0.6-0.8, 0.3-0.4 and 0.1-0.16 mg/kg after one, two and three months,
    respectively (Medved, 1977). No residues were detected in cabbages 96
    days after the application of propachlor, at harvesting (Kolesnikov et
    al., 1979). A decrease in dose and application by conveyor belt
    perceptibly reduced the residues (Table 8).

        Table 8.  Residues (mg/kg) of propachlor in cabbages (type Amager 611)
    Propachlor                      Date of         Sampling time (no. of days after application)
    application rate                application
                                                    13           33           64           96
    8 kg/ha (before setting out)    31 May          0.6          0.3          0.1          No

    8 kg/ha (after prior            31 May          0.8          0.4          0.16         No
      application of 5 kg/ha)

    4 kg/ha (conveyor-belt          7 June          0.4          0.2          0.03         No
      application after setting
         In a study by Nesterova et al. (1980), a dry soil area planted
    with cabbages was treated with propachlor (7 kg/ha) each year. In the
    second year no residues were detectable two months after application.
    In the third year, when the moisture content of the soil had
    increased, propachlor degradation was more rapid and no residues were
    detectable 15 days after the application. The soil was dry in the
    fourth year, and residues were detectable in cabbages up to two months
    after application.

         Lottman & Cowell (1986) reported propachlor residues in sorghum
    grains of between < 0.02 and 0.24 mg/kg after treatment of soil at
    4.4 kg/ha. Lottman & Cowell (1987) found residues in corn grain of <
    0.02 to 0.04 mg/kg after soil treatment with propachlor at 4.4 kg/ha
    and of < 0.02 to 0.19 mg/kg after treatment at 6.6 kg/ha.

    5.2  Occupational exposure

         Only limited data are available on occupational exposure to
    propachlor. Its application by a tractor-mounted sprayer to cabbages
    resulted in its presence in the breathing zone of the tractor drivers
    at levels of 0.8 to 2.1 mg/m3 (Panshina, 1977) and 0.1 to 3.7
    mg/m3 (Panshina, 1976).


    6.1  Absorption

         Propachlor may be absorbed through the respiratory and
    gastrointestinal tracts as well as through the skin. Following a
    single oral administration in mammals, it is rapidly taken up into the
    blood and internal organs, reaching its maximum blood concentration in
    1 h. After 48 h it is no longer detectable in the organs (Panshina,
    1985). An estimated 68% of a single 10 mg dose of ring-labelled
    14C-propachlor administered to 12 rats was recovered in urine 56 h
    later (Malik, 1986). These results are supported by those of other
    studies in which 54-64% (Lamoureux & Davison, 1975) and 68.8% (Bakke
    et al., 1980) of the administered dose was recovered in urine 24 h and
    48 h after dose administration, respectively.

    6.2  Metabolic transformation

         Propachlor is rapidly metabolized. Its metabolism in animal
    species has been studied by Bakke & Price (1979), Pekas et al. (1979),
    Bakke et al. (1981a,b,c), Rafter et al. (1983a,b), Aschbacher &
    Struble (1987) and Davison et al. (1988, 1990). Most of the animal
    species studied metabolize propachlor through the mercapturic acid
    pathway (MAP). The intestinal microflora is involved in the metabolism
    of MAP intermediates (Bakke et al., 1981c). Metabolites of propachlor,
    in which chlorine from the parent compound (2-chloro-
    isopropylacetanilide) is removed by a nucleophilic displacement
    (Rafter et al., 1983a) by a cysteine group or methylsulfonyl group
    (CH3SO2), are present in the urine of rats dosed orally with
    propachlor (Larsen & Bakke, 1979). It has been shown that a cysteine
    conjugate of propachlor is the source of sulfur in methylsulfonyl-
    containing metabolites, but that the carbon in the methylsulfonyl
    group does not come from the cysteine moiety. Propachlor is conjugated
    firstly with glutathione and the reaction is mediated by glutathione
    transferases. The glutathione conjugation provides a means for
    inactivation of reactive electrophiles. Glutathione conjugates have
    the required physico-chemical properties for biliary excretion and
    will generally be present, together with their catabolites
    cysteinyl-glycine, cysteine and  N-acetylcysteine-mercapturic acid,
    in relatively high concentrations in the bile (Rafter et al., 1983a).
    After excretion with the bile, they are metabolized in the intestine
    where the C-S lyase present cleaves the cysteine conjugate, allowing
    further metabolism of sulfur to a methylsulfonyl-containing moiety
    (Larsen & Bakke, 1979).

         The C-S lyase enzyme systems have been isolated in rat liver and
    bacteria demonstrating that they are of bacterial origin. As a good
    example, C-S lyase from  Fusobacterium necrophorum, one of the pure
    intestinal bacteria, has been isolated and characterized as a key
    enzyme in mammalian metabolism (Larsen et al., 1983). This is
    confirmed by the fact that in germ-free rats (Bakke et al., 1980)
    (Fig. 2) and rats treated by antibiotics (Larsen & Bakke, 1981) 14C
    was excreted from 14C-propachlor as MAP metabolites, but there were
    no methylsulfonyl-containing metabolites in urine. Inextractable
    residues were eliminated in the faeces. This shows that MAP
    metabolites are available as substrates for the intestinal microflora.
    Of the MAP metabolites studied, the glutathione and cysteine
    conjugates are the best substrates both for production of
    2-mercapto- N-isopropyl-acetanilide and for parallel formation of
    insoluble 14C residues (Larsen & Bakke, 1983) which are excreted in
    the faeces.

    FIGURE 2

         In normal rats dosed with propachlor, the above-mentioned final
    metabolites were formed when MAP metabolites underwent a number of
    reactions: carbon-sulfur bond cleavage by microflora, S-methylation,
    S-oxidation, ring and alkyl-hydroxylation, glucuronide conjugation,
    N-dealkylation and amide cleavage (Rafter et al., 1983b).

         Fig. 3 shows the proposed metabolic pathway for the formation of
    methylsulfonyl metabolites in rats and pigs (Aschbacher & Struble,

    1987) and Fig. 4 the metabolism in normal rats treated with propachlor
    proposed by Bakke et al. (1980).

         The tissue in which propachlor enters the mercapturic acid
    pathway has not been determined. The liver is an obvious site for
    glutathione conjugation, but the intestine cannot be excluded (Bakke
    et al., 1980). Organ perfusion studies have demonstrated that all
    enzymes necessary for the formation of mercapturic acid conjugates are
    present in the kidneys of both chickens and rats (Davison et al.,
    1988, 1990) and in the livers of rats (Davison et al., 1990). Rat
    caecal contents are similar to those of the pig with respect to C-S
    lyase activity, which explains the general similarity of their
    metabolic transformations (Larsen & Bakke, 1983).

         When pig caecal contents were incubated with the glutathione
    conjugate of propachlor, the formation of both insoluble residues and
    the thiol increased with increase in incubation period (Table 9).
    Digestive peptidases extracted during isolation of the metabolites
    were thought to be the explanation for the presence of the cysteine
    conjugate in the zero time samples, because no cysteine conjugate was
    isolated from heat-treated caecal contents. A decrease in glutathione
    concentration with increased incubation time was also evident and was
    confirmation of a product-precursor relationship. This decrease in
    glutathione conjugate concentration was assumed to be caused by
    formation of cysteine conjugate (82%), due to cleavage by peptidase
    activity, in the caecum (Larsen & Bakke, 1983).

         In summary, three or more enterohepatic cycles for propachlor
    metabolism in normal rats have been described. In the first,
    propachlor is metabolized via the mercapturic acid pathway and the
    conjugates are excreted in the bile. The second cycle is initiated
    when the biliary mercapturic acid pathway metabolites are metabolized
    by microbial/intestinal C-S lyase into reabsorbable metabolites
    (possibly 2-mercapto- N-isopropylacetanilide). The reabsorbable
    metabolites are further metabolized to glucuronides by glucuronidase
    enzymes, and these are secreted with the bile. These biliary
    glucuronides subsequently initiate the third cycle in the
    enterohepatic circulation of propachlor metabolites.

         No doubt the intestinal microorganisms complicate the metabolism
    of propachlor (in comparison with the situation in germ-free and
    antibiotic-treated rats) and create new non-polar compounds from the
    products of the mercapturic acid pathway, which are reabsorbed into
    the blood. These new compounds have to be converted again into polar
    products in order to be excreted (Bakke et al., 1980).

    FIGURE 3
    FIGURE 4
        Table 9.  Incubation of the glutathione conjugate of propachlor with pig caecal contents for various durationsa
    Metabolites recovered                                            Incubation time

                                       0             20 min        40 min        1 h           2 h           4 h

    2-Mercapto-N-isopropylacetanilide  7.7b          14.5b         23.0b         28.3b         34.7b         43.4c
                                       (5.1-10.6)    (5.5-22.8)    (15.8-36.0)   (22.9-38.7)   (21.8-44.0)   (38.7-49.2)

    Glutathione conjugate              26.8          36.0          20.8          28.8          21.5          16.5
      of propachlor                    (15.8-38.1)   (18.1-51.6)   (13.3-25.3)   (16.6-42.3)   (14.0-32.2)   (14.8-19.2)

    Cysteine conjugate of              47.5          32.5          35.1          20.9          11.9          3.8
      propachlor                       (36.0-51.5)   (21.3-43.7)   (30.5-41.9)   (12.0-27.9)   (10.9-12.5)   (2.2-5.6)

    Non-extractable 14C                13.1          12.9          16.0          16.6          25.4          33.9
      residues                         (13.0-13.4)   (9.9-17.8)    (13.5-20.5)   (15.0-18.9)   (22.8-28.2)   (31.5-35.8)

    a From: Larsen & Bakke (1983).
    b Isolated as 2-carboxymethylthio- N-isopropylacetanilide
    c Isolated as 2-(13C)-carboxymethylthio- N-isopropylacetanilide
      Pigs were gilts. Results are shown as a percentage of the substrate. Values given in parentheses represent the range of values
      obtained from 14C-recovery measurements.
         More recent studies carried out by Aschbacher & Struble (1987) on
    the metabolism of propachlor in pigs have proved the similarity, i.e.
    the formation of methylsulfonyl-containing metabolites, with the
    metabolism of rats, but have also revealed some differences.

         A pig with a cannulated bile duct, which was dosed orally with
    14C-propachlor, excreted 7.6% of the dose in the bile compared with
    approximately 75% in the case of the rats. When enterohepatic
    circulation was prevented in the bile of cannulated pigs,
    CH3SO2-containing metabolites of propachlor were excreted in the
    urine. As mentioned above, enterohepatic circulation is necessary for
    the production of methylsulfonyl-containing metabolites in rats. In
    experiments with germ-free pigs dosed orally with 14C-propachlor, it
    was shown that they did not excrete urinary CH3SO2 metabolites, which
    indicated involvement of the intestinal flora in the production of
    these metabolites, as occurs in rats. Non-biliary excretion of
    metabolites of propachlor into the lumen of the intestine probably
    occurred. It is presumed that propachlor is absorbed by the mucosal
    cells and conjugated with glutathione and that some of this conjugate
    moves directly into the lumen of the intestinal tract by simple
    diffusion, where it becomes the substrate of bacterial beta-lyase. The
    presence of glutathione transferase has been demonstrated previously
    in subcellular fractions of mucosal tissue homogenates.

          In situ intestinal absorption of propachlor and non-biliary
    excretion of metabolites into the intestinal tract of rats, pigs and
    chickens was studied by Struble (1991). Propachlor was absorbed from
     in situ intestinal loops of rats and pigs, the absorption half-times
    being 7.5 and 16.5 min, respectively. Water-soluble 14C-labelled
    metabolites that accumulated in the intestinal loops accounted for
    31%, 53% and 25% of the initial 14C in rats, pigs and chickens,
    respectively. Propachlor- S-cysteine was identified as the major
    metabolite in the pig intestinal lumen (43% of the water-soluble
    14C). It was concluded that the intestinal metabolism and intestinal
    excretion of water-soluble metabolites of propachlor are important
    physiological processes that occur in a variety of animal species.
    These processes provide a route by which metabolites of xenobiotics
    may reach the intestinal lumen in animals that are poor biliary
    excretors. These studies demonstrated that although bile may be the
    major route by which MAP metabolites are made available to the
    intestinal microflora in the rat, an extrahepatic route exists in the

         Davison (1991) conducted a study using six anaesthetized 2- to
    21-day-old male Guernsey calves weighing 28 to 61 kg in which either
    the left kidney was perfused (via the left renal artery) or the left
    ureter was perfused with metabolites of propachlor. The glutathione
    conjugate of propachlor (2- S-glutathionyl- N-acetyl-acetanilide)
    was metabolized in both kidney and ureter to the cysteine conjugate.
    When the mercapturic acid conjugate of propachlor was presented to the
    kidney, it was eliminated in urine. First-pass metabolism and
    elimination of the glutathione conjugate by the kidney was 16% of the

    dose, whereas first-pass elimination of the mercapturic acid was 33%.
    Absorption of the glutathione conjugate of propachlor or its
    metabolites, or of glycine by the ureter was nil. The cattle may be
    unable to form mercapturic acids from glutathione conjugates of some
    xenobiotics, which may result in their being more easily poisoned by
    these xenobiotics than chickens, pigs and rats.

         The glutathione conjugate of 2-chloro- N-isopropyl[1-14C]acet-
    anilide (14C-propachlor) was perfused through a calf kidney  in situ
    by Bakke et al. (1990). Twenty-three per cent of the dose was excreted
    in the perfused kidney urine as the cysteine conjugate; no mercapturic
    acid was detected. A 5-day-old calf dosed orally with 14C-propachlor
    excreted 70% of the dose in the urine as the cysteine conjugate; again
    no mercapturic acid was detected. Rumen microflora were established in
    the calf when it was 5 weeks older and the experiment was repeated.
    The same results were obtained.

    6.3  Elimination and excretion

         When 14C-propachlor was given to rats, 56-64% of the dose was
    excreted in urine in the first 24 h and 5.7-7.0% in 24-48 h. In the
    faeces, 8-13% and 2.2-7.7% were eliminated in 0-24 h and 24-48 h,
    respectively; 0.4% of the 14C was eliminated as CO2 and 5-11% was in
    the carcass. In total 80-97% was eliminated in 48 h (Lamoureux &
    Davison, 1975).

         According to Bakke et al. (1980), the metabolites of propachlor
    formed in normal rats treated with propachlor are excreted mainly
    through urine (68%) and faeces (19%). Eleven urinary metabolites were
    isolated from rats given 14C-labelled propachlor orally. The major
    metabolite was the mercapturate (17%), and six of the metabolites were
    2-methylsulfonylacetanilides. Faecal residues (19%) of the
    administered dose, insoluble in common solvents or by treatment with
    diluted acid or base, were also determined.

         Rats with cannulated bile ducts secreted 66% of an oral dose of
    propachlor in the bile as the glutathione conjugate (2), cysteine
    conjugate (3), mercapturate (4) and the mercapturate sulfoxide (5)
    (see Table 10). Germ-free rats given orally 14C-labelled propachlor
    excreted 98% of the dose in the urine and faeces within 48 h. Three
    metabolites were isolated from the excreta and the faecal radioactive
    metabolites were water soluble. The major metabolite was mercapturate
    (4) and the other metabolites were the cysteine conjugate (3) (present
    only in the faeces) and mercapturate sulfoxide (5) (Bakke et al.,
    1980). Mercapturate sulfoxide was isolated from the excreta of
    germ-free rats by Feil et al. (1981), who also demonstrated its
    presence in the bile of rats and urine of chickens and pigs dosed with
    propachlor. The metabolite was characterized by mass and nuclear
    magnetic resonance spectro-metry on samples isolated from rats.

        Table 10.  Comparison of the excretion of single oral doses of 14C-propachlor
               by control rats with fistulated bile ducts, and germ-free ratsa

    Metabolite                             Recovery of 14C (% dose)b
                            Control rats          rats            Germ-free rats
                        Urine        Faeces       Bile         Urine        Faeces
    Glutathione                                   37
      conjugate (2)b

    Cysteine                                      13                        19
      conjugate (3)

    Mercapturate (4)    17                        12           63.1         3.7

    Mercapturate                                   4            5.7          5.4
      sulfoxide (5)

    Non-extractable                  19

    Other metabolites   51

        Total           68           19           66           68.8         32.1

    a From: Bakke et al. (1980)
    b Metabolite designations are those used in Figs. 1 and 3.
             As in the case of the glutathione and cysteine conjugates, the
    sulfoxide is not excreted at detectable levels by normal rats and was
    detected only in the bile (Bakke et al., 1981a). It may become a
    substrate for the intestinal flora, but the ultimate  in vivo fate of
    this metabolite is unknown.

         Bakke et al. (1981c) reported differences between some species
    concerning the metabolism of propachlor in the MAP. Clear but
    unexplained differences are that rats excrete no cysteine conjugate
    and chickens form no methylsulfonyl-containing metabolites, whereas
    sheep excrete large amounts of cysteine conjugate in urine.

         Nadeau & Pantano (1986) carried out a study to determine the
    rates and routes of excretion of orally administered synthetic
    14C-labelled propachlor plant metabolites in lactating goats and to
    quantify and identify the radioactive metabolites in the goat milk,
    tissues, urine and faeces. The daily dose level for the three treated
    goats was 15 mg/kg administered on 5 consecutive days (the actual dose
    levels for the treated goats were 13, 14.5 and 13 mg/kg,
    respectively). Each treated goat received a total of 130.5 mg of the

    13C/14C-labelled propachlor plant metabolites mixture during the
    dosing period. A control animal received placebo capsules. The
    radioactivity eliminated in faeces accounted for 72.1, 64.5 and 57.9%
    of the administered dose, respectively (average 64.8%), and that
    excreted in urine accounted for 35.8, 28.1 and 32.3% (average 32.1%).
    The percentage of the dose eliminated through faeces and urine
    averaged 96.9%.

         The radioactivity found in the milk accounted for only 0.084,
    0.10 and 0.13% (average 0.10%) of the administered dose. These values
    corresponded to metabolite concentrations in the milk of 11.9, 14.8
    and 18.0 µg/litre (average 14.9 µg/litre). The metabolic
    concentrations (µg/kg) in the tissues were: kidney 51.9, liver 30.4,
    muscle 8.5, fat 19.5 and blood 50.1. The loss of radioactivity from
    tissues, milk and excrement occurred rapidly, and after 5 days of
    depuration the milk and tissue radioactivity levels were below the
    limit of detection, except in the case of the liver (5.7 µg/kg).

    6.4  Metabolism in laying hens

         Since crops treated with propachlor are used in animal feed, it
    is important to know the fate of propachlor in animal feed.

         The purpose of the study by Bleeke et al. (1987) was to examine
    the metabolic fate of propachlor plant metabolites in laying hens and
    to determine whether they accumulate or persist in the eggs or edible
    tissues. The compounds used for feeding were the three major
    metabolites of propachlor found in sorghum, i.e. [( N-iso-propyl)-
    phenylamino] oxacetic acid, sodium salt (I), {{[( N-iso-propyl)-
    phenylamino]acetyl}sulfinyl} lactic acid, sodium salt (II) and
    2-[( N-isopropyl)-phenylamino] 2-oxoethane sulfonic acid, sodium salt

         The first study involved dosing chickens at a level of 5 mg/kg
    diet for 6 consecutive days. Data for bioaccumulation and excretion of
    plant metabolites were obtained from this study. A second group of
    chickens, dosed at a level of 25 mg/kg diet (nominal dose) on 6
    consecutive days, provided eggs and tissues with higher residues for
    metabolic characterization. Each group consists of five hens. Control
    groups received a single gelatine capsule per day. The total recovery
    of 14C radioactivity was good in both studies.

         An average of 87.4% of the total administered dose was recovered
    from the chickens fed 5 mg/kg approximately 1 day after the last dose,
    and 97.9% was recovered from the chickens fed 25 mg/kg, primarily in
    the excreta. The eggs contained low residue levels; those from
    chickens fed 5 mg/kg contained residues below the minimum quantifiable
    limit (MQL) of 1.7 µg/kg. The level in the egg yolks reached an
    average of 5.5 µg/kg by day 6 but by day 12 the residues in the yolk
    had fallen below 1.6 µg/kg.

         In the high-dose group, the residues in the egg white levelled
    off at about 4 µg/kg on day 2, while those in the egg yolk increased
    to a level of 27.3 µg/kg on day 6.

         Tissues also contained low levels of residues. In the low-dose
    group, the highest levels were found in the kidney and they averaged
    only 6 µg/kg. The residue levels in the liver measured an average of
    1.9 µg/kg and those in the fat 3.5 µg/kg. The residues in other fat
    samples and organs were below the MQL (1.4-1.6 µg/kg). Residues in the
    breast muscle were below the minimum detectable limit (7 µg/kg) and
    those in the blood were 6-7 µg/kg.


    7.1  Single exposure

    7.1.1  Oral

         The acute oral toxicity of propachlor for the rat, mouse and the
    rabbit has been examined. According to the WHO hazard classification
    of pesticides and as far as its acute oral toxicity to rats is
    concerned, propachlor is slightly hazardous (Group III) (WHO, 1990).
    LD50 values in various animal species reveal a higher susceptibility
    for the mouse and the rabbit than for the rat (Table 11). The LD50
    for rats ranges from 950 to 2176 mg/kg.

         The clinical picture of acute oral intoxication by propachlor has
    been described in three species of experimental animals: mice, rabbits
    and rats (Panshina, 1973). When propachlor is given at lethal or toxic
    doses, the main symptoms concern the central nervous system. In mice
    and rabbits, a state of excitement, trembling and light convulsions is
    observed 15 min after a toxic or lethal dose of propachlor. This
    gradually increases, breathing becomes difficult and death follows in
    fseveral hours. Intoxication in rats takes a different course: a state
    of immobility and head and body tremors are accompanied by the sudden
    onset of convulsions and death occurs within 24 h. This clinical
    picture was confirmed by Strateva (1974,a,b).

         Kronenberg (1988) reported clear signs of irritation to the
    gastrointestinal tract and lungs that were evident at necropsy in
    animals that died during the study. Histoenzymological changes
    expressed as decreased enzyme activity were in full agreement with the
    morphological picture (Strateva et al., 1974a,b).

    7.1.2  Dermal

         Results of studies in rabbits on the acute dermal toxicity of
    propachlor and its formulations indicate that the dermal LD50 ranges
    from 4000 mg/kg for a 65% WP formulation (Auletta & Rinehart, 1979) to
    20 000 mg/kg for technical propachlor (94.5%) (Braun & Rinehart,
    1978). Test animals exhibited moderate to severe erythema, severe
    oedema and necrotic skin at the dermal application sites at a dose
    level of 2800 mg/kg. Motor activity decrease and ataxia were noted at
    dose levels of 2000 to 5600 mg/kg.
        Table 11.  Oral LD50 values for laboratory mammals

    Species                LD50 (mg/kg)a                  Reference
    Rat                    1056 (834-1278)               Panshina (1973, 1977)

                           950 (860-1050)                Strateva (1974b)

                           1340                          Mirkova (1975)

    Table 11 (contd).
    Species                LD50 (mg/kg)a                  Reference
                           2176 ± 220                    Lehotzky et al. (1979)

    Rat (Sprague-Dawley)   840 (419-1261)                Blaszcak (1988)
                           (in corn oil)

                           1700 (1265-2135)              Blaszcak (1988)
                           (in 1% methylcellulose)

    Rat (Fischer-344)      550 (252-848) in corn oil     Blaszcak (1988)

                           1359 (1009-1691)              Blaszcak (1988)
                           (in 1% methylcellulose)

    Rat (both sexes)       4000                          Heenehan et al. (1979)

    Rat (both sexes)       3269                          Branch et al. (1982a)

    Mouse                  306 (275-337)                 Panshina (1973, 1977)

                           290 (240-350)                 Strateva (1974b)

    a The concentration is based on the percentage active ingredient.
      Figures in parentheses indicate the range of values.
             Using groups of 16 Wistar rats, Baynova et al. (1977) studied the
    acute dermal toxicity of a single application of propachlor 65 WP
    (10-20% in aqueous suspension) with doses of 1500-4000 mg/kg body
    weight (active ingredient). There was no mortality, and no signs of
    intoxication were observed. No haematological or biochemical tests
    were performed.

         Propachlor and Satecid 65 WP caused severe dermatitis, ulceration
    and necrosis in the skin of rabbit and ears of mice. None of the
    compounds exhibited contact sensitization effects on guinea-pigs
    (Lehotzky et al., 1979).

    7.1.3  Inhalation

         In a study by Bechtel (1991), technical propachlor (96.8%) was
    dissolved in dimethylsulfoxide (DMSO) to generate an aerosol and
    administered to five male and five female Sprague-Dawley rats in a
    nose-only chamber at an analytically determined concentration of 1.2
    mg/litre for 4 h. Control rats (five of each sex) were exposed to an
    atmosphere of aerosolized DMSO for the same duration. Particle size
    measurements on the propachlor/DMSO aerosol indicated a mass median
    aerodynamic diameter of 3.5 µm, with 96% of the particles being less
    than 10 µm and 1.8% less than 1 µm in diameter (Bechtel, 1991). No

    treatment-related deaths occurred. Clinical signs included laboured
    respiration and nasal discharge; all animals appeared normal by
    post-exposure day 2. A transient weight loss was noted in both treated
    and control animals during the first two days of the study, but normal
    body weight was observed thereafter. No abnormalities were apparent
    during postmortem examination of the animals.

         In another acute inhalation study, three groups of Charles River
    CD rats (five rats of each sex per group) were exposed to test
    atmospheres of a propachlor formulation (44% active ingredient) for 4
    h (Kaempfe, 1991). During the exposure period, animals were housed in
    a 250-litre New York University style stainless steel chamber, and
    were exposed to analytically confirmed concentrations of 0.18, 0.67
    and 1.0 mg propachlor/litre in the breathing zone of the chamber. At
    least 82% of the particles were less than 10 µm in diameter. No
    animals died at the two lower exposure levels, whereas four out of ten
    rats died at 1.0 mg/litre. Clinical observations during the
    post-exposure period included ocular opacities, perinasal
    encrustation, rapid or shallow respiration, perioral wetness and focal
    loss of hair from animals in the highest exposure group. Fourteen days
    after exposure, all surviving animals had body weights higher than the
    pre-exposure (day 0) values with the exception of females in the
    1.0-mg/litre group, which exhibited body weight depression. There were
    no abnormal findings in rats that died during the test or were
    sacrificed at 14 days. Based on the mortality observed, the LC50 was
    slightly greater than 1.0 mg/litre.

    7.2  Short-term exposure

    7.2.1  Oral  Dogs

         To assess potential subchronic toxicity, propachlor (96.1% pure)
    was administered via the diet to five groups of two male and two
    female beagle dogs for 4 weeks (Daly & Knezevich, 1984). Dietary
    concentrations of propachlor were 0, 100, 500, 1000 and 1500 mg/kg
    (equivalent to 0, 2.5, 12.5, 25, and 37.5 mg/kg body weight per day).
    No mortality or clinical signs of toxicity related to treatment
    occurred during this study. Food consumption was initially decreased,
    but only in the females treated with 1000 and 1500 mg/kg (equal to 25
    and 37.5 mg/kg body weight) and the males treated with 1000 mg/kg. The
    consumption had returned to normal by the end of the study. Body
    weight varied markedly. The decreased body weight and/or weight gain
    noted in males fed 12.5 or 25 mg/kg body weight per day, and females
    fed 37.5 mg/kg per day could have been treatment related.
    Haematological examination showed slightly increased platelet counts
    in high-dose males. No treatment-related gross pathological effects
    were noted at sacrifice.

         Following the 4-week pilot feeding study in beagle dogs, a 90-day
    feeding study was undertaken (Naylor & Ruecker, 1986). Propachlor
    (96.1% purity) was administered in the diet to groups of six dogs of
    each sex per group for 90 days. Nominal dietary concentrations were 0,
    100, 500 and 1500 mg/kg. There was no mortality or clinicopathological
    or histopathological changes related to the treatment. The dose level
    of 1500 mg/kg (45 mg/kg body weight) was a no-observed-adverse-effect
    level (NOAEL).  Rodents

         Propachlor (65% WP) was given orally by gavage to white rats at
    daily doses of 21, 53 and 106 mg/kg body weight for 4 months, and its
    cumulative effect was studied by Panshina (1973). Later, Strateva
    (1974a, 1976) carried out a short-term study (45 days) at dose levels
    of 50, 100 and 200 mg/kg body weight given orally by gavage to 104
    Wistar rats (divided into four groups (three experimental and one
    control) with equal numbers of both sexes), and a long-term oral study
    (6 months) at dose levels of 0.05, 0.5, 5 and 20 mg/kg body weight
    given to 220 Wistar rats divided into five groups (four experimental
    and one control).

         Strateva (1976) found a decrease in haemoglobin content and
    number of erythrocytes, slight leucocytosis and an increased number of
    neutrophils. The threshold dose for rats in long-term studies was 5
    mg/kg body weight.

         Panshina (1976) carried out a 10-month study on white rats given
    propachlor by gavage at doses of 1, 3.5 and 10.6 mg/kg body weight.
    Slight leucocytosis was found within 4-7 months. The first two doses
    provoked a decreased activity of catalase and peroxidase as well as an
    increase in nicotinamide adenine dinucleotide in brain and heart
    tissue homogenates. No changes in haemoglobin content or number of
    erythrocytes were noted. There were no alterations to the
    pathomorphological picture.

         Baynova et al. (1978a) compared the effects of continuous and
    intermittent oral dosing of propachlor (65% WP) on white rats (equal
    numbers of both sexes). The number of animals per group was not given.
    The scheme of the experimental design is given in Table 12.

    Table 12.  Experimental design of the study by Baynova et al. (1978a)
    Group                          Duration of  Daily dose  Dose (fraction
                                   study        (mg/kg)     of the LD50)
    Control                         4 months         -          -
    I (dosing every week)           4 months        70          1/20
    II (dosing every second week)   4 months       140          1/10
    III (dosing every second week)  8 months        70          1/20
    Control                         8 months         -          -

         Continuous administration of propachlor led to more marked
    changes in the main parenchymous organs than intermittent
    administration. These changes were characterized by decreased activity
    of oxido-reductive tissue enzymes. The hexabarbital sleeping time,
    which characterized the detoxification function of the liver, showed
    a statistically significant reduction. Propachlor administration at
    120 mg/kg body weight for 6 consecutive days to male and female rats
    increased the levels of both cytochrome and microsomal protein content
    (Nenov & Baynova, 1978) as a result of the induction of mixed-function
    oxidase in the liver (Baynova et al., 1978a).

         A special study on the morphological changes in kidneys was
    carried out. Propachlor (65% WP) was administered by gavage to male
    white rats (10 animals per group and 1 control) at doses equivalent to
    6, 12 and 60 mg/kg body weight for 3 months (Maleva & Zlateva, 1982).
    Dose-dependent morphological changes were found in the proximal
    convoluted renal tubules. The tubules were deformed and the epithelial
    cells were vacuolized and dystrophic. A decreased cellular content of
    ribonucleoproteins was also observed and pycnosis and caryolysis of
    nuclei were seen. In the lumen, desquamated epithelia and hyalin
    cylinders were found. The intestine was slightly swollen in certain

         The subchronic toxicity of propachlor (96.1% purity) has also
    been evaluated in Sprague-Dawley CD rats (30 of each sex per group)
    fed diets containing 0, 300, 1500 or 7500 mg/kg for 90 days (Reyna &
    Ribelin, 1984a). No animals died. A statistically significant
    reduction in body weight was observed in animals fed 1500 mg/kg (8%
    for males and females) and 7500 mg/kg (59% for males and 36% for
    females). Food consumption was significantly depressed for animals at
    the highest dose level for the first month of the study, but recovered
    during the remainder of the study. After 6 weeks, reduced haemoglobin,
    haematocrit, mean corpuscular haemoglobin and haematocrit, and an
    increase in reticulocytes were observed in females at all dose levels
    and in high-dose males. The anaemia was less evident in high-dose
    males and was only present in high-dose females at study termination.
    Significantly reduced lymphocyte counts were observed at week 6 for
    high-dose males and mid- and high-dose females, and at study
    termination for all groups. Levels of serum enzymes (SGPT, SAP, GGT),
    cholesterol and total bilirubin were significantly increased for
    high-dose animals at weeks 6 and 13 and there were significant
    reductions in total protein, glucose, creatinine and albumin. No
    histological changes were observed in the liver. Organ weights (with
    the exception of female livers) were reduced, relative to controls,
    for high-dose animals, and spleens were extremely small and
    treatment-related in size in about 65% of the animals. No histological
    changes were observed in the tissues examined, which included the
    spleen.  Mice

         The subchronic toxicity of propachlor (96.1% pure) was evaluated
    in four groups of Charles River CD-1(R) mice (30 mice of each sex
    per group) (Reyna & Ribelin, 1984b). Dietary levels were 0, 500, 1500
    and 5000 mg/kg. No mortality or adverse clinical signs were observed
    during the study. A statistically significant reduction (10%) in body
    weight was observed in the mid- and high-dose males and females during
    the study. Food consumption was also reduced during the first month
    for mid- and high-dose animals. A dose-related statistically
    significant reduction in the number of white blood cells was observed
    in both sexes at all dose levels, except low-dose females, at the
    7-week sampling period. At study termination, this reduction was
    evident in mid- and high-dose animals but was statistically
    significant only for high-dose males. Liver weights were increased for
    males at all dietary levels and for mid- and high-dose females. There
    was an accompanying statistically significant increase in the
    incidence of centrilobular hepatocellular hypertrophy for mid- and
    high-dose males, based on histological examination. No other
    microscopic changes that could be considered treatment related were
    evident in tissues. For males, the kidney to body weight ratio was
    decreased at the high-dose level.

    7.2.2  Dermal

         A 21- and 90-day short- and longer-term dermal toxicity study on
    Wistar rats (12 animals in each tested group plus 1 control) using
    propachlor (65% wettable powder) administered 5 days per week was
    carried out by Baynova et al. (1977). The doses applied were 50, 200
    and 500 mg/kg in aqueous suspensions in the 21-day experiment, and 10,
    25 and 50 mg/kg in the 90-day study. The dermal application was
    performed uncovered (Draize, modification of Noakes). By the end of
    day 21, anaemia was found at dose levels of 200 and 500 mg/kg, but
    there was no methaemoglobinaemia. The same doses induced a
    statistically significant decrease in the activity of certain enzymes
    (SGOT, SGPT, OCT and AP). Dermal application of propachlor at dose
    levels of 25 and 50 mg/kg to the skin of white rats (two groups of 12
    animals) for 90 days did not provoke any changes in concentrations of
    red blood cells and haemoglobin, but there were decreases in SGOT,
    SGPT, LAP, AP and catalase. Decreased sulfur-containing enzymes were
    found in tissue homogenates (liver and kidney). Decreases in the
    levels of LDH, SDH, AcP and glucose-6-phosphate dehydrogenase were
    determined histochemically. There was no evidence of clinical signs of
    intoxication after repeated dermal application of the herbicide, but
    the occurrence of the above-mentioned enzymatic changes demonstrated
    the penetration of this herbicide through the dermal barrier. The
    hexabarbital sleeping time was statistically significantly shortened
    at the mid- and high-dose levels, thereby confirming the induction of
    mixed-function oxidases reported by Nenov & Baynova (1978).

         A threshold dermal dose of 25 mg/kg (1% aqueous suspension of
    propachlor 65 WP) and a no-observed-effect level (dermal) of 10 mg/kg
    (0.5% aqueous suspension) were determined in 90-day experiments by
    Baynova et al. (1977).

    7.3  Skin and eye irritation; sensitization

    7.3.1  Skin irritation

         Single application to Wistar rats (three rats of each sex per
    group) of propachlor 65 WP at doses of 1500, 2000, 3000 and 4000 mg/kg
    in 10 or 20% aqueous suspension, under the open modified method of
    Noakes, did not cause any local irritative effects (Baynova et al.,

         Panshina (1973) reported a strong irritative effect of propachlor
    after single and repeated application. Single applications to rabbits
    of 16% propachlor 65 WP in aqueous suspension at doses of 500, 700,
    and 1000 mg/kg led to hyperaemia and even ulceration in the skin of
    some animals. Ten applications of a 32% aqueous suspension of
    propachlor at a level of 200 mg/kg had the same effect on the skin.
    Seventeen applications of a 6.5% aqueous suspension at 100 mg/kg did
    not result in mortality, and only slight hyperaemia was seen in the
    treated skin area of the rabbits.

         Primary irritation and contact sensitization effects of Satecid
    65 WP containing 65% propachlor were investigated in rabbits, mice and
    rats, and these were compared with the effects of technical grade
    propachlor, propachlor with analytical purity, and the vehicle alone
    (Lehotzky et al., 1979). Propachlor had strong to very strong
    irritating effects on intact and scarified skin as well as on the eye
    mucosa of rabbits and mice. The symptoms included erythema, oedema and
    penetrating ulcer. Technical grade propachlor had the most potent
    irritating effect.

         Heise et al. (1983) conducted parallel experiments with two
    propachlor preparations, one produced in the USA and the other in
    Hungary, using an aqueous suspension applied under occlusion to the
    skin of rabbits for 24 h. The irritant dose (ID50) for the USA
    preparation was 2% and for the Hungarian preparation 0.6%.

         Several dermal irritation studies have been carried out with
    technical propachlor and its formulations, each of which involved the
    use of six New Zealand white rabbits (2.5 to 3.5 kg). All application
    sites were scored for erythema, eschar and oedema formation. For
    technical propachlor (94.5% pure) a slight degree of dermal irritation
    was observed (2.5/8.0 score) (Braun et al., 1979a); for a 20%
    formulation of propachlor (again 94.5% pure) there was a slight degree
    of dermal irritation (1.8/8.0 score) (Braun et al., 1979b); for a 65%
    formulation a moderate degree of dermal irritation (3.4/8.0 score)
    (Braun et al., 1979c); and for a 42% formulation corrosive effects
    were observed (Branch et al., 1982b).

    7.3.2  Skin sensitization

         A modification of the maximalization test of Magnusson & Kligman
    (1969) for identification of allergens was used by Heise et al.
    (1983). Guinea-pigs (12 female and 12 male) were treated by
    intramuscular injection of 0.2% propachlor aqueous suspension (using
    preparations from both the USA and Hungary together with Freund
    adjuvant), by subcutaneous injection of 0.05% aqueous suspension and
    by epicutaneous application of a 1% water suspension of both
    preparations for 6 weeks, both on healthy and scarified skin. A
    challenge single application was given two weeks after the last
    application using 0.2 ml of an 1% aqueous suspension of each
    formulation. There was no significant difference between the reactions
    to the two preparations. A challenge dose did not induce a reaction.

         The dermal sensitization potential of propachlor was evaluated in
    guinea-pigs using the Buehler procedure (Auletta, 1983). For the
    induction phase, 0.2 ml of undiluted propachlor (95.7% purity) was
    applied dermally using the closed patch technique to the shaved backs
    of five male and five female Hartley albino guineapigs. The
    applications were made for 6 h/day, 3 days/week, for 3 weeks. Two
    weeks after the final dose, additional 0.2 ml doses of 25% propachlor
    in ethanol (challenge dose) were applied to previously untreated areas
    on those guinea-pigs that had received the induction doses and to six
    others (three males and three females) which served as irritation
    controls. Two positive control groups, treated with 1-chloro-2,4-
    dinitrobenzene (DNCB) as positive control, were used. The negative
    control group (five males and five females) was treated with saline
    for the induction doses and challenged with acetone. All animals had
    slight to moderate dermal irritation following the third induction
    dose of propachlor, and some of them exhibited severe irritation,
    including oedema, necrosis and exfoliation. Following application of
    the challenge dose, one out of ten animals had an irritation score of
    1 (slight), eight animals had a score of 2 (moderate) and one animal
    had a score of 3 (severe) at 24 h. Nine of these animals exhibited
    oedema. At 78 h, two animals had very low scores, six animals had
    scores of 1, and two scores of 2. Six of these animals exhibited
    oedema. Similar results were obtained when 20 and 40% propachlor
    formulations were tested for sensitization in guinea-pigs (Auletta et
    al., 1984a,b).

    7.3.3  Eye irritation

         Molnar & Paksy (1978) studied the effect of Satecid 65 WP on the
    eye mucosa of CFY male albino rats using the Evans blue diffusion
    technique. The aqueous suspension caused strong conjunctivitis at the
    minimum concentration of 0.01%.

         In a study by Auletta (1984), technical propachlor (96.1% pure)
    was ground to a fine powder and introduced in the conjunctival sac of
    the right eye of six (two males and four females) albino New Zealand
    White rabbits. The left eye served as the control. The treated eyes

    were rinsed 24 h later. Five of the animals exhibited severe
    conjunctival irritation (redness, necrosis, chemosis and discharge),
    five exhibited opacity and/or ulceration, and five had iridial damage.
    Two animals exhibited neovascular-ization of the cornea and one
    bulging of the cornea, indicative of increased intraocular pressure.
    After 21 days of observation one animal continued to exhibit
    conjunctival redness and one corneal opacity and bulging of the
    cornea. The eyes of the remaining animals had minimal conjunctival

         In an eye irritation test on six New Zealand white rabbits using
    technical propachlor (94.5%), 0.1 cm3 was instilled into one eye of
    each rabbit and ocular reactions were observed on days 1, 2, 3, 4, 7,
    10 and 14. According to Draize scores, all treated eyes were assigned
    positive scores for corneal opacity and ulceration, conjunctival
    redness, chemosis and necrosis. Two eyes were assigned positive scores
    for iritis. Three eyes exhibited pannus, and corneal bulge was
    observed in two eyes. Four eyes were clear of signs of irritation by
    day 14 and two eyes showed signs of irritation at the termination of
    the study (Braun, 1979).

         US EPA (1984b) reviewed the existing data and concluded that
    propachlor is corrosive to the rabbit eye, corneal opacity being
    irreversible after 7 days.

    7.4  Reproduction, embryotoxicity and teratogenicity

    7.4.1  Reproduction  Biochemical and histopathological studies on gonads

         The effect of propachlor 65 WP on protein content, activity of
    5-nucleotidase and ATP in testis homogenate was evaluated by Maleva &
    Stereva (1977), Stereva & Maleva (1977) and Zlateva & Maleva (1978,
    1979). Each test group consisted of 20 male Wistar rats, administered
    orally (by gavage) 12 or 60 mg propachlor/kg body weight per day for
    6 months. A control group consisted of the same number of animals. At
    the end of the experiment, there were dose-dependent statistically
    significant changes in the biochemical indices studied (a decrease in
    protein content and an increase in 5-nucleotidase and ATPase activity)
    and these were accompanied by histomorphological changes, i.e.
    disorganization of the seminiferous epithelium. After prolonged dosing
    some dystrophic and degenerative changes in the gonad tissue and the
    appearance of multinuclear giant cells with central chromatolysis were
    observed. Adverse effects on the mitotic division of spermatogonia and
    blockage of meiosis in the earlier phases were found (Zlateva &
    Maleva, 1978, 1979).

         In subchronic toxicity studies, there was no microscopic evidence
    of testicular pathology in dogs administered the equivalent of 45 mg
    propachlor/kg diet per day (Naylor & Ruecker, 1986), in rats fed the
    equivalent dose of 250-310 mg/kg diet per day in the food (Reyna &

    Ribelin, 1984a), or in mice fed the equivalent of 400 to 600 mg/kg
    diet per day (Reyna & Ribelin, 1984b).  Reproduction studies

         A two-generation rat reproduction study was undertaken to
    evaluate the effects of propachlor (96.3% pure) (Rao, 1981). Four
    groups of 30 male and 30 female 6-week-old Fischer-344 rats (F0
    generation) were exposed to diets adjusted weekly to provide dose
    levels of 0, 0.3, 3 and 30 mg propachlor/kg body weight per day for
    100 days and were then allowed to mate to produce the F1 generation.
    The F1 weanlings were similarly dosed for 120 days prior to
    breeding. The F1 adults were mated twice to produce F2a and F2b
    litters. At weaning of F1, F2a and F2b litters, 10 pups of each
    sex at each dose level were sacrificed and selected organs were
    examined histologically. No signs of toxicity in any animals were
    found during the study. A significant decrease in food consumption and
    body weight of adult F1 males dosed with 30 mg/kg per day was found.
    No adverse effects in any of the treated groups over two generations
    were noted with respect to gestation length, number of live pups
    delivered, neonatal survival, litter weight and sex ratio. Decreased
    pregnancy rates (fertility index) were observed in mid-dose (60%) and
    high-dose (63%) F1 females following the first mating (F2a
    litter), in comparison with 83% in the control rats. Test animals
    continued to be treated with propachlor and were remated to produce a
    second (F2b) litter. Pregnancy rates for the F2b litter were 83%
    for controls and 83, 83 and 80% for low-, mid- and high-dose groups,

         No treatment-related gross necropsy findings were noted. Slight
    increases in absolute and/or relative liver weights were noted in
    high-dose F0 adults, mid- and high-dose F1 adults and high-dose
    F2a weanlings. Hypertrophy of the centrolobular hepatocytes was
    noted during microscopic examination of livers from the high-dose F0
    and F1 adult females. There was no evidence of compound-related
    microscopic changes in the testes and ovaries of test animals for
    either generation.

    7.4.2  Embryotoxicity and teratogenicity  Rats

    a)  Single dose treatment

         Mirkova (1975) reported embryotoxic and teratogenic effects of
    propachlor 65 WP in Wistar rats following single-dose treatment (675
    mg/kg body weight) on each of the first 16 days of gestation.
    Significantly increased lethality and frequency of haematomas,
    predominantly in the head of the fetuses, and reduced cranio-caudal
    size were observed when the treatment was performed from days 1 to 4
    and on days 8, 10 and 12 of gestation (8 to 12 animals per test group

    and 57 controls). The effect was more marked following treatment on
    the first day of pregnancy. A weak teratogenic effect was observed
    with a single dose, which included the induction of external
    malformations (day 11, brachygnatia), abnormality of internal organs,
    i.e. hydrocephalus (days 9, 11, 12 and 13 of gestation), defects in
    skeletal ossification, i.e. non-ossification of sternum (day 9), and
    delayed ossification of parietal bones (days 11, 12 and 13 of

    b)  Repeated dose treatment

         Wistar rats were treated daily with 67.5, 135 or 270 mg
    propachlor/kg body weight on days 1-7 or 8-16 of gestation (six test
    groups of 10 animals each). In a second set of experiments, a daily
    treatment of 33.7, 67.5, 135 and 270 mg/kg body weight was given
    throughout the gestation period (1-21 days) (Mirkova, 1975).
    Propachlor induced embryotoxicity at all dose levels of repeated
    treatment during the pre-implantation stages of embryogenesis (days
    1-7 of gestation). This was expressed as raised lethality and
    haemorrhages, predominantly in the head of the fetus, and reduced
    weight and cranio-caudal size. The effects were significantly reduced
    when administration was performed during the period of organogenesis
    (8-16 days). Propachlor showed low teratogenic activity, producing
    external malformations of the tail (short, curved tail), skeletal
    abnormalities (non-ossified parietal and occipital bones) and
    hydrocephalus, at all three dose levels during the pre-implantation
    stage (days 1-7 of gestation). A slight degree of internal
    hydrocephalus was observed with doses of 135 and 270 mg/kg on days
    8-16 of gestation.

         Using a similar treatment regimen, Ivanova-Chemishanska et al.
    (1975) reported similar changes. No embryotoxic or teratogenic effect
    was seen at a dose level of 10 mg/kg body weight given daily to rats
    throughout the pregnancy (Medved, 1977; Panshina, 1985).

         Teratogenic effects of technical propachlor were assessed in
    pregnant Charles River COBS CD rats using a control and three
    treatment groups consisting each of 25 females (Schardein & Wahlberg,
    1982). Propachlor (96.5% pure) levels of 20, 60 and 200 mg/kg body
    weight were administered orally by gavage as a single daily dose on
    days 6-19 of gestation in a constant volume of 10 ml/kg corn oil. The
    control group received the same dose of corn oil. Survival in the
    control, low-dose and mid-dose groups was 100%. One female in the
    high-dose group died on gestation day 18 due to an intubation error.
    There were no differences in mean maternal body weight gain. No
    changes were evident at gross necropsy that could be considered
    treatment related. There were no differences between treated and
    control groups with respect to the mean number of viable fetuses,
    post-implantations loss, total implantations, corpora lutea, fetal
    body weights, sex ratio distribution, and in the number of litters or
    fetuses with external, visceral or skeletal malformations and/or
    developmental and genetic variations.  Mice

         When Balb/c mice (8-12 in each test group and 18 control pregnant
    females) were treated with a single dose of 675 mg propachlor/kg body
    weight on each of days 8-13 of gestation, and at dose levels of 33.7,
    67.5, 135 and 270 mg/kg body weight per day from days 1 to 21, a
    significant increase in post-implantational lethality and reduced
    fetal weight and cranio-caudal size were observed at all dose
    regimens. With both single and repeated doses, there was a
    statistically significant increase in the frequency of internal
    hydrocephalus, but only at a dose level of 675 mg/kg in a single
    application on days 9 and 11 of gestation and on daily application at
    270 mg/kg from days 1 to 18 of pregnancy (Mirkova, 1975).  Rabbits

         Pregnant New Zealand White rabbits randomly assigned to a control
    and three treatment groups (each consisting of 16 rabbits) were used
    to determine the teratogenic potential of propachlor (95.6% pure)
    (Schardein, 1982). Dose levels of 5, 15 and 50 mg/kg were administered
    orally by gavage as a single daily dose on days 7-19 of gestation at
    a constant volume (0.5 ml/kg dissolved in corn oil). The control group
    received only 0.5 ml/kg corn oil. On gestation day 29, the number and
    location of viable and non-viable fetuses, early and late resorptions,
    number of total implantations and the number of corpora lutea were
    recorded. All fetuses were examined for external, soft tissue and
    skeletal malformations and for genetic or developmental variations.

         Mortality (between 3 and 26 days of gestation) was recorded in
    the control as well as the treated groups, i.e. two in the control
    group, three at 5 mg/kg, three at 15 mg/kg and two at 50 mg/kg. Two
    rabbits from the low-dose group and one from the mid-dose group
    aborted on gestation days 22 to 25. Ante-mortem observations gave no
    indication of a treatment-related effect at any dosage level.

         Results of the reproductive parameters revealed slight to
    moderate increases in the number of post-implantation losses and the
    number of early resorptions in the mid- and high-dose groups when
    compared with controls (Table 13). Single animals with resorptions
    only were also found at the two highest dose levels. This resulted in
    a subsequent decrease in the average number of viable fetuses in the
    mid- and high-dose groups when compared with controls. Although the
    number of post-implantation losses fell within the range of historical
    control frequencies, all the above parameters were considered to imply
    a mild embryotoxic response. No effects were observed in the number of
    late resorptions, total implantations, number of corpora lutea, fetal
    sex distribution or the mean fetal body weights. Examination of the
    fetuses revealed no external, skeletal or soft tissue malformations,
    or genetic and developmental variations that could be considered to be
    related to treatment. These abnormalities observed were low in
    frequency and within the range of historical control values. A
    statistically significant increase in the total number of litters with

    malformations was observed in the mid-dose group when compared to the
    control group. This trend, however, was not found in the high-dose
    group and the malformations in the group given 15 mg/kg per day were
    considered to be incidental to treatment.

        Table 13.  Mean number of resorptions (late and early),
               post-implantation losses and total implantations in
               New Zealand rabbits (Schardein, 1982)
    Dose           Fetuses        Resorptions   Post-implantation  Total
    (mg/kg)   viable  non-viable  late  early   losses             implantation
     0        8.0     0.0         0.3   0.3     0.6                8.6
     5        7.9     0.0         0.0   0.4     0.4                8.3
    15        5.2a    0.1         0.0   1.4     1.4                6.6
    50        5.9     0.0         0.2   0.9     1.1                7.0

    a P < 0.05
        7.5  Mutagenicity and related end-points


          Many in vitro  and in vivo  studies on the genotoxicity of
     propachlor have been reported. It has been found to be clastogenic
     in in vivo  lower test systems and plant assays. It is cytotoxic
     and also shows a weakly positive clastogenic response in in vitro
     mammalian tests, inducing chromosomal aberrations in Chinese hamster
     ovary cells. Variable results do not allow any definite conclusions
     to be drawn. However, on the basis of negative results in many in
    vivo  assays in mammalian test systems, the available experimental
     data provide insufficient evidence of a mutagenic potential. Data
     on mutagenicity testing are summarized in Table 14.

    7.5.1  Bacterial test systems

          Salmonella mutation assays using standard tester strains
    (TA1535; TA1538; TA98 and TA100), both with and without metabolic
    activation with rat liver S9, were negative for formulations and
    technical grades of propachlor (Plewa et al., 1984; Flowers, 1984).
    No mutagenicity was observed with extracts of plants treated with

         Negatives results for propachlor in spot tests using  Salmonella
     typhimurium test strains were also reported by Njagi & Gopalan
    (1980) and Eisenbeis et al. (1981).

        Table 14.  Summary of mutagenicity testing

    Test materiala                           Test system                              Resultc         Reference
                                                                               -S9    +S9    1S
    Gene mutation in Prokaryotes

    Propachlor U                            Ames spot test                     -                    Njagi & Gopalan (1980)
    Propachlor U                            Ames spot test                     -      -             Eisenbeis et al. (1981)
    Propachlor T                            Ames plate test                    -      -             Flowers (1984)
    Propachlor T                            Ames plate test                    -      -      -
    Propachlor + Cyanazineb                 Ames plate test                                  +      Plewa et al. (1984)

    Gene mutation in plants

    Propachlor C                            maize Wx locus                     -                    Plewa et al. (1984)

    Gene mutation in mammals ( in vitro)

    Propachlor T                            CHO/HGPRT                          -      -             Flowers (1985)

    Chromosome effects in plants

    Propachlor U                             Vicia faba cytogenetics           +                    Njagi & Gopalan (1981)
    Propachlor U                            maize cytogenetics                 +                    Lapina et al. (1984)
    Propachlor U                            maize chlorophyll mutations        +                    Lapina et al. (1984)

    Chromosome effects in mammals ( in vitro)

    Propachlor T                            CHO cytogenetics                   -      +             Li & Meyers (1987)

    Chromosome effects in mammals ( in vivo)

    Propachlor U                             in vivo mouse bone marrow cyt.    +                    Pilinskaya et al. (1980)
    Propachlor T                             in vivo rat bone marrow cyt.      -                    Ernst & Blazak (1985)

    Table 14 (contd).

    Test materiala                           Test system                              Resultc         Reference
                                                                               -S9    +S9    1S
    DNA damage/recombination in yeast

    Propachlor T                            gene conversion                    -             +      Gentile et al. (1977)
    Propachlor T                            gene conversion                    -      -      +      Plewa et al. (1984)
    Propachlor C                            gene conversion                    -      -      +      Plewa et al. (1984)
    Propachlor + Cyanazine                  gene conversion                                  -      Plewa et al. (1984)

    DNA damage in mammals ( in vitro)

    Propachlor T                             in vitro hepatocyte UDS           -                    Steinmetz & Mirsalis (1984)
    Propachlor T                             in vivo/in vitro hepatocyte UDS   -                    Steinmetz & Mirsalis (1986)

    a T = technical grade; C = commercial grade; U = unspecified grade
    b Propachlor and cyanazine were both of commercial grade.
    c +S9 and -S9 = with or without rat liver S9 activation mixture;
      1S = with maize 1S fraction
    7.5.2  Yeast assays

         Propachlor was not recombinogenic when tested at 1000 mg/litre in
     Saccharomyces cerevisae strain D4 (ade 2-1, ade 2-2; trp 5-12, trp
    5-27) either with or without a liver microsomal activation system
    (Gentille et al., 1977).

         Extracts of plants treated with propachlor cause a weak
    recombinogenic activity (Gentille et al., 1977). Maize extracts
    treated with 25 ppm propachlor increased the rate of mitotic gene
    conversion at the ade locus in  S. cerevisae strain D4 approximately
    4-fold over the control levels. Extracts of plants treated with a
    technical grade of propachlor (1.306 x 10-4 mol/litre) and
    formulated grade (1.306 x 10-3 mol/litre) induced a significant
    increase in gene conversion at the ade locus and a lower increase at
    the trp locus in  S. cerevisae D4. Results for both formulated and
    technical grades of propachlor were negative after mammalian S9
    activation (Plewa et al., 1984).

    7.5.3  Plant assays

         Njagi & Gopalan (1981) studied the cytogenic and cytological
    effects of propachlor at a wide range of concentrations (10, 50, 100,
    500, 1000, 5000 and 10 000 ppm) in root-tip meristematic cells of
     Vicia faba. At a concentration of 100 ppm, propachlor induced,
    within 2 h, chromosomal aberrations, such as anaphase bridge
    formation, micronuclei as well as inhibition of mitosis, formation of
    highly pycnotic nuclei and premature chromosome condensation. The
    mutagenic properties of propachlor were not detectable in the field
    experiments using reverse mutations at the wx-C locus in maize as the
    genetic end-point. Lapina et al. (1984) also reported that propachlor
    induced mitotic chromosomal aberrations in the root-tip meristematic
    cells of an inbred F2 strain of maize. At a concentration of 10-3
    mol/litre and within 2 h of treatment of maize grains, propachlor
    increased the rate of mitotic chromosomal aberrations more than 4-fold
    over the control levels. The main types of cytogenetic damage included
    single bridges (72%) and fragments (28%). Propachlor did not show
    evidence of being significantly cytotoxic.

    7.5.4  Cultured mammalian cell CHO/HGPRT assay

         Propachlor (96.1%) was tested in a gene mutation assay in
    cultured mammalian cells (CHO/HGPRT assay), both in the presence and
    absence of mammalian metabolic activation, at doses ranging from 10-60
    mg/litre. It was found to be cytotoxic at some of the higher
    concentrations tested, but no mutagenicity was observed (Flowers,

    7.5.5  In vitro unscheduled DNA synthesis in primary rat hepatocyte

         Steinmetz & Mirsalis (1986) studied the potential of propachlor
    to induce unscheduled DNA synthesis (UDS) in primary rat hepatocyte
    cultures. They used ten concentrations of propachlor (95.8% pure)
    ranging from 0.1 to 5000 mg/litre and, in another assay, five
    concentrations ranging from 0.1 to 50 mg/litre. Results of this study
    showed a cytotoxic effect of propachlor at concentrations of 50
    mg/litre or more, but there was no evidence of UDS induction.

    7.5.6  In vitro test for induction of chromosomal aberrations using
           Chinese hamster ovary cells

         Propachlor was tested for its potential to induce chromosomal
    aberrations in cultured Chinese hamster ovary (CHO) cells treated with
    propachlor (97.4% pure) at concentrations of 5, 10 or 15 mg/litre for
    5 h both in the presence and absence of exogenous activation (Li &
    Meyers, 1987). As indicated both by decrease in mitotic index and
    lengthening of average cell generation times, the highest treatment
    level was cytotoxic both in the presence and absence of activation. In
    the non-activated study, no statistically significant increases in the
    percentage of cells with structural aberrations or in average
    structural aberrations per cell were observed at any treatment level.
    In the study with S9 activation (15 mg propachlor/litre), the average
    number of aberrations per cell was statistically elevated at 12 h and
    24 h (P < 0.05 test). Chromatid and chromosome gaps were not
    included. The percentage of cells with structural aberrations
    following treatment at 15 mg/litre was statistically elevated at 12 h
    but not at 24 h. No apparent dose-response relationship was observed
    at either harvest time. Under these conditions, propachlor was
    considered to be negative in the assay without exogenous metabolic
    activation and a weak clastogen with activation.

    7.5.7  In vivo rat bone marrow cytogenetic assay

         Ernst & Blazak (1985) conducted an  in vivo rat bone marrow
    cytogenetic assay using technical grade propachlor (95.6% pure) at
    dose levels of 0, 0.05, 0.2 and 1 mg/kg body weight. The results were
    evaluated for mitotic index (based on at least 1000 cells per animal)
    and 60 cells per animal were examined for chromosomal aberrations.
    Chromatid and isochromatid gaps were recorded for each cell, but these
    were not considered chromosomal aberrations. The results showed that
    propachlor does not induce chromosomal damage in male or female
    Fischer-344 rats under the conditions used in this study.

    7.5.8  Acute in vivo mouse bone marrow cytogenicity assay

         Pilinskaya et al. (1980) studied the cytogenetic effect of
    propachlor on the bone marrow of mice treated orally with 10, 50 and
    100 mg/kg body weight. The metaphase frequency of aberration at the
    lowest dose applied was 2.67 ± 0.66 compared with 0.7 ± 0.19 in the

    control. At this dose level an approximately 4-fold increase in the
    frequency of chromosome aberrations was observed. No statistically
    significant changes were found at a dose level of 1 mg/kg.

    7.5.9  In vivo/in vitro hepatocyte DNA repair assay

         Steinmetz & Mirsalis (1986) presented data on the  in vivo/in
     vitro hepatocyte DNA repair assay. Propachlor (97.7% pure) was
    suspended in corn oil and administered by gavage to five groups of
    male Fischer-344 rats at dose levels of 25, 250, 300, 400 and 1000
    mg/kg. A positive control group received 2-acetyl aminofluorene
    (2-AAF) (50 mg/kg) while a negative one was given corn oil. The
    results were negative.

    7.6  Long-term toxicity and oncogenicity studies

    7.6.1  Rat

         Propachlor (96% pure) was administered via the diet to four
    groups of 60 male and 60 female Charles River CD SDBR rats at
    concentrations of 0, 10, 50 and 500 mg/kg (equivalent to 0, 0.5, 2.6
    and 27 mg/kg body weight) (Hamada, 1987a). A complete battery of
    haematological, clinical chemistry and urinalysis tests was carried
    out every 6 months for 2 years. No treatment-related effects were
    noted on survival, incidence of clinical and ophthalmoscopic
    observations, body weight gain or food consumption. Haematological and
    clinical chemistry parameters and urinalysis data of treated animals
    were comparable to control values. Thyroid and liver weights were
    slightly increased in high-dose males at the 12-month interim
    sacrifice but not at the end of the study. An increased incidence of
    liver changes (centrilobular hypertrophy, clear cell cytoplasmic
    alteration and eosinophilic cytoplasmic alteration) was observed in
    high-dose males and females. A slightly higher incidence of thyroid
    c-cell tumours (adenomas and carcinomas) noted in high-dose animals
    was within the testing laboratories' historical range for such
    tumours. All other organ weight changes and gross and microscopic
    pathological findings were comparable to controls. An increase in
    benign granulosa/theca cell tumours was observed for high-dose females
    (4/60) compared to controls (0/60). The historical control data for
    this tumour ranged from 0/80 to 4/96. On the basis of these results,
    50 mg/kg diet (2.6 mg/kg body weight) can be considered the
    no-observed-effect level (NOEL) for rats. 

    7.6.2  Mouse

         When propachlor (96.1% pure) was administered in the diet to male
    and female CD1 mice at dose levels of 10, 50 and 500 mg/kg (equivalent
    to 1.6, 8.1 and 81.3 mg/kg for males and 2.0, 10.5 and 104.9 mg/kg for
    females) for 18 months, no histological changes were noted (Hamada et
    al., 1987b). The survival of all treated male groups was similar to
    that of controls. Female survival was lower than that of controls in
    all treated groups. There was a significant increase in segmented

    neutrophilic leucocytes in the 500-mg/kg group at 12 months, but this
    change was not evident at study termination. At the end of the study,
    ratio of liver (with gall bladder) to body weight was increased in the
    50- and 500-mg/kg group females, and the ratio of kidney to body
    weight was decreased in males of the highest-dose group. The NOEL was
    considered to be 10 mg/kg (1.6 mg/kg per day).

    7.6.3  Dog

         In a study by Naylor & Ruecker (1986), propachlor was
    administered daily via the diet to four groups of six male and six
    female beagle dogs for 12 months (0, 25, 250 and 1000 mg/kg diet). No
    mortality occurred during the study. Absolute body weights were lower
    than those of controls at study termination (approximately 14% for
    males and 8% for females in the high-dose group and 5% for males in
    the mid-dose group. A slight increase in emesis and/or stool change
    was noted in treated dogs. No other changes in clinical and
    pathological parameters were observed that could be related to
    treatment. Based on the body weight depression at the high dose, a
    dietary level of 250 mg/kg (9 mg/kg body weight) was considered a
    no-observed-adverse-effect level (NOAEL) in this chronic study.

    7.7  Miscellaneous studies

         Propachlor has a strong inhibitory effect on the proliferation of
    L1210 mouse leukaemia cells  in vitro (the ID50 for cell
    proliferation is < 3 x 10-7 mol/litre). Propachlor also inhibits
    significantly the uptake of leucine, thymidine and uridine. The
    inhibitory effect of propachlor is largely reversible, i.e. cells
    grown in propachlor and then washed free of the compound return to an
    almost normal rate of proliferation (Zilkah et al., 1981).

         It has been demonstrated that propachlor treatment also causes
    L1210 cells to accumulate in the G1 phase. This effect is dose
    dependent; a concentration of 10 µmol/litre causes more than 90% of
    cells to accumulate in the G1 phase (Zilkah et al., 1985).

         The combined effect of propachlor and vibration has been studied.
    Propachlor was given orally to Wistar rats (20 animals in each group)
    at doses equivalent to 6, 12 and 60 mg/kg body weight per day for 3
    months, and the animals were exposed to low-frequency vibration (15
    Hz) during the last 30 days of the study. The results were compared
    with those obtained from groups of rats subjected to the effect of 15
    Hz vibration daily for 30 days, as well as with those of groups of
    rats dosed only with propachlor. It was found that the combined
    exposure (with 12 or 60 mg propachlor/kg) caused more severe
    haemodynamic alterations and degenerative (even necrotic) changes in
    the epithelial cells of the renal tubules, either in the proximal or
    distal convoluted tubules (Maleva & Zlateva, 1982).

         In a study by Baynova et al. (1978b), groups of 20 white rats
    were pretreated with oral doses of 4 ml/kg 40% ethanol (one tenth of

    the LD50), 6 days per week, for 4 months. Propachlor was then given
    daily at a dose level of 140 mg/kg (one tenth of the LD50), 6 days
    per week, every other week for a further 4-month period. The controls
    were subjected to 8 months of treatment with ethanol and 4 months of
    intermittent (every second week) treatment with propachlor using the
    same doses as in the combined experiment. Both experiments had
    untreated control groups. The combined treatment led to a reduction of
    the hepatotoxic effect. This was probably due to induction of
    mixed-function oxidases and to a more rapid biotransformation in the
    hepatocytes. It has also been found that propachlor (140 mg/kg for 6
    days) reduces the hexabarbital sleeping time by speeding up its
    metabolism in the hepatic endoplasmic reticulum as a result of
    induction of the mixed-function oxidase system in the liver cell
    microsomes (Nenov & Baynova, 1978).


    8.1  Occupational exposure

         There have been few reports dealing with the effects of
    propachlor on humans.

         Von Schubert (1979) reported a case of contact eczema on the
    palms, wrists and forearms of a 29-year-old agricultural worker who
    had been in contact with propachlor for 8 days. Once this contact
    ceased, the skin lesions disappeared.

         Iden & Schroeter (1977) patch-tested 17 patients, predomi-nantly
    farmers, who had been exposed simultaneously to many types of
    herbicides. Seven showed a positive patch test reaction and five
    others had an irritant reaction to propachlor. One of these farmers,
    who was highly sensitive to propachlor, used to develop generalized
    airborne contact dermatitis each spring when his neighbours used this
    product. Farkasdy et al. (1976) and Dombay & Farkasdy (1978) examined
    dermatologically 79 workers manufacturing Satecid 65 WP (65%
    propachlor). Of these, 19% showed contact dermatitis attributed to
    propachlor exposure. Patch testing was carried out on 67 workers of
    this group, 12 of whom showed monovalent and bivalent hypersensitivity
    reaction to propachlor. Photosensitization tests were negative in 28
    of the cases tested. Three years later, the same authors examined 108
    workers who were continuously exposed to Satecid in the same factory
    without finding any sign of sensitization.

         Jung et al. (1989) patch-tested 19 allergic cases and one
    irritative case with occupational contact eczema, who were exposed to
    different types of herbicides. Two of them showed positive testing to
    Satecid 65 WP. One of these two was only exposed to the substance for
    10 days and the other for 6 months.

    8.2  General population exposure

         No reports on general population exposure are available.


    9.1  Microorganisms

    9.1.1  Soil

         The effects of propachlor with regard to changes in numbers of
    four types of soil bacteria (aerobic nitrogen-fixing, aerobic
    cellulose-decomposing, ammonifying and nitrifying) was studied by
    Helmeczi (1977). The studies were carried out using pseudomycelial
    chernozem soil with maize plants. For the purpose of the microbial
    examinations, samples from the field were taken three times a year
    (after spraying propachlor in spring, summer, and autumn at a rate of
    8-10 kg/ha) from the upper 20-cm layer of the soil. Sampling was
    carried out under sterile conditions and samples were collected in
    sterile vessels. The nitrifying bacteria had the greatest sensitivity
    to propachlor, their number decreasing considerably from 2720 to 610
    per g soil in 1974 and from 4510 to 1920 per g soil in 1975. The
    aerobic cellulose-decomposing bacteria were the least sensitive, their
    numbers, with respect to the control bacteria, increasing to a small

         Long-term studies in smolnista and alluvial soils have been
    carried out to establish the effects of propachlor on useful soil
    microorganisms and the processes of nitrification (Bakalivanov &
    Kostov, 1981). These studies were conducted under laboratory
    conditions at 20 °C and 60-70% soil moisture for a period of 10 days.
    The concentration of propachlor used was 80 mg/kg soil. The results
    showed an inhibitory effect on nitrification and weaker effect on soil
    microorganisms (bacteria, actinomycetes and microscopic fungi). High
    adsorption of propachlor to clay minerals reduced the toxic effect on

         Rankov & Velev (1976) studied the effect of propachlor on the
    biological activity of soil microorganisms and showed that inhibition
    was greater at a temperature of 2 to 4 °C than at 20 to 22 °C.

    9.1.2  Water

         The acute toxicity of propachlor to  Selenastrum capricornutum
    Printz has been assessed in two studies. In the first (Richards &
    Kaiser, 1984), the 96-h EC50 for growth in algae was calculated to
    be 0.029 mg/litre with 95% confidence intervals of 0.021-0.038
    mg/litre. The no-observed-effect concentration (NOEC) was calculated
    to be 0.01 mg/litre. In the second study (Zschaler & Jonas, 1990), the
    72-h EC50 for growth was 5.3 mg/litre and the NOEC 1.9 mg/litre for
    a propachlor formulation containing 65% active ingredient. The
    differences in toxicity observed between the two studies may be either
    because the 65% formulation is less toxic than technical propachlor or
    because the duration of the second study was 24 h shorter.

    9.2  Aquatic organisms

    9.2.1  Aquatic invertebrates

         Thompson & Forbes (1979a) determined a 24-h LC50 of 11 mg/litre
    and a 48-h LC50 of 7.8 mg/litre for the water flea  Daphnia magna.
    The NOEC in this study was < 5.6 mg/litre. A 48-h LC50 of 6.9
    mg/litre in the same species was reported by Mayer & Ellersieck
    (1986). The same authors reported a 48-h LC50 of 0.79 mg/litre for
    the midge larva  Chironomus plumosus. Another midge larva  Chironomus
     riparius was reported to show a 24-h LC50 of 5.2 mg/litre and a
    48-h LC50 of 1.8 mg/litre (Buhl & Faerber, 1989).

         The effects of propachlor on daphnia reproduction was assessed in
    a 21-day life-cycle study (Thun, 1990a). In this study, there was
    decreased reproductive performance at concentrations from 0.29 to 2.6
    mg/litre; the NOEC for reproduction was considered to be 0.097

    9.2.2  Fish

         Thompson & Forbes (1979b) determined 24-h, 48-h and 96-h LC50
    values for rainbow trout ( Onchorynchus mykiss) of 0.75, 0.28 and
    0.17 mg/litre, respectively. Thun (1990b) conducted a 21-day study on
    rainbow trout and found that fish died at concentrations between 0.11
    and 0.3 mg/litre. No deaths related to exposure occurred at
    concentrations between 0.009 and 0.075 mg/litre. The NOEC was
    considered to be 0.019 mg/litre. Mayer & Ellersieck (1986) reported a
    96-h LC50 of 0.23 mg/litre for the channel catfish  (Channa

    9.3  Terrestrial organisms

    9.3.1  Terrestrial invertebrates

         The toxicity of propachlor to earthworms was assessed in a 14-day
    study (Thun et al., 1991). Propachlor (97.8% pure) was added to the
    soil at five concentrations ranging from 100 to 1000 mg/kg, and 40
    worms were added to the soil at each concentration. Worms were removed
    from the soil at 7 and 14 days and examined for any adverse effects.
    Body weights were measured at the beginning and end of the test. The
    LC100 was 560 mg/kg and the LC0 218 mg/kg; the NOEC was 100 mg/kg.

         The contact LD50 of propachlor for honey bees was reported to
    be 311 µg/bee (Kenaga, 1979).

         Under laboratory conditions, Tanke & Franz (1978) studied the
    side effects of propachlor on some beneficial insects by measuring the
    reduction of the beneficial capacity of three enthomophagous insects.
    The egg parasite  Trichogramma cacoeciae March reacted very strongly
    in laboratory as well as in field conditions to the effects of the
    herbicide. Contact toxicity tested using residues of propachlor on

    glass plates (residue level not stated) caused a reduction of the
    degree of parasitization leading to total mortality of the population
    in contaminated cages. In a study on the contact toxicity of the spray
    deposit on single leaves as well as on whole plants, the
    parasitization of  Trichogramma was reduced by 100 and 83%,
    respectively. The direct toxic effect should be distinguished from a
    repellent effect, which is probably more important in the field. In
    addition to this direct contact effect of spray deposits, systemic
    application also caused an effect after transport of the herbicide
    through the soil and the plant. This was demonstrated by a reduction
    of the degree of parasitization compared with untreated controls.

         Propachlor does not seem to have any influence on  Chysopa carnea
    Steph larvae. No effect was visible either in tests of contact
    toxicity or contaminated sandy soil, in choice studies on a repellent
    action of the residue or after topical application of the preparation.
    After oral application through an artificial food chain, no influence
    could be demonstrated. Only overdosage increased the mortality rate of
    the test larvae. No repellent effect of the herbicide on adults was
    demonstrated (Tanke & Franz, 1978).

         The syrphid  Epistrophe balteata DeG was more sensitive. Both in
    contact toxicity studies and in studies for a possible repellent
    effect, an influence of propachlor on the larval stages was shown.
    Oral intake through an artificial food chain did not have an effect on
    the larvae. When the herbicide was sprayed directly on the plant, an
    increase in larval mortality was observed. Adults of this syrphid also
    showed reactions to herbicides; during egg deposition, females avoided
    surfaces previously treated (Tanke & Franz, 1978).

         The potential toxicity of a 65% formulation of propachlor to
     Aleochara bilineta Gyll was assessed by Pietrzik (1991). The imagos
    were dug into moist sand and the test substance was added at
    recommended use rates (8 kg in 400 litres/ha water). For the
    assessment of parasitical capacity, pupae of  Delia antiqua were dug
    into the sand. At the termination of the test, the sum of hatched
     Aleochara larvae in the pupae was determined. These were compared to
    the number of control organisms treated with tap water. The parasitic
    capacity of the test beetles was decreased by 11.4% when compared to

    9.3.2  Birds

         Palazzolo (1964) reported data for pheasants indicating an acute
    oral LD50 of 735 mg/kg body weight. Increased respiration, loss of
    reflexes, mydriasis, salivation and intermittent tonic/clonic
    convulsions were found among birds receiving dose levels of 900 and
    1350 mg/kg. The onset of symptoms occurred approximately 15 min
    following dosing and persisted until death 3-5 h later. Kenaga (1979)
    reported an LD50 of 512 mg/kg for Mallard duck and Beavers & Fink
    (1979) reported an LD50 for Bobwhite quail of 137 mg/kg body weight
    for a 65% propachlor formulation.

         When propachlor was administered in the diet to quail or Mallard
    ducks for five consecutive days, the LC50 for both species of birds
    was more than 5620 mg/kg diet (Beavers & Fink, 1983a,b). For the
    quail, a dietary level of 5620 mg/kg is approximately equivalent to a
    dose of 1400 mg/kg per day. The data presented above indicate that the
    quail is more susceptible to exposure to propachlor via stomach tube
    than via the diet.


    10.1  Conclusions

    *    Under conditions of normal use, the general population is not
         likely to be exposed to propachlor.

    *    Those occupationally exposed to propachlor should take adequate
         safety and hygienic precautions in order to protect the skin, eye
         and respiratory tract.

    *    Propachlor is rapidly degraded in the environment under most
         conditions. It persists longer in cold dry environments. The
         conjugated  N-isopropylaniline metabolite persists longer than
         the parent compound. Propachlor does not bioconcentrate or

    *    Propachlor is highly toxic to some aquatic organisms. Exposure of
         aquatic organisms under conditions of normal use is low, the
         maximum expected concentrations being several orders of magnitude
         lower than the no-observed-effect concentrations. Direct
         contamination of water courses will kill aquatic organisms and
         should be avoided. Propachlor poses a low hazard to birds,
         earthworms and honey-bees.

    10.2  Recommendations for protection of human health

         Workers should be educated about the hazards of propachlor and
    systematically trained to practice safety and personal hygiene and to
    use protective equipment.


    *    The results of the existing animal studies on mutagenicity are
         inconclusive and more research is needed.

    *    Studies should be performed in laboratory animals to determine
         the potential neurotoxic effects of propachlor.

    *    Only validated analytical methods for residues of propachlor
         should be used.

    *    Epidemiological studies on occupationally exposed workers are

    *    There is a need to develop methods of biological monitoring for
         evaluating human exposure to propachlor.

    *    Research is needed to clarify the exposure of workers in the
         production and agricultural use of propachlor. Studies should
         also include examination of health effects at the measured
         exposure levels.


         In the WHO recommended classification of pesticides by hazard,
    technical propachlor is classified in Class III as slightly hazardous
    in normal use (WHO, 1990). A data sheet on propachlor has been issued
    (WHO/FAO, 1989).

         Neither the FAO/WHO Joint Meeting on Pesticide Residues (JMPR)
    nor the International Agency for Research on Cancer (IARC) has so far
    evaluated propachlor.


    Aschbacher PW & Struble CB (1987) Evidence for involvement of
    non-biliary excretion into the intestine of the formation of
    methyl-sulphonyl containing metabolites of 2-chloro- N-
    isopropylacetanilide (propachlor) by swine and rats. Xenobiotica,
    13(2): 115-126.

    Auletta CS (1983) A propachlor dermal sensitization study in
    guinea-pigs (Project No. 4236-83). East Millstone, New Jersey,
    Bio/dynamics Inc. (Unpublished proprietary report submitted to WHO by
    Monsanto International Services, Brussels).

    Auletta CS (1984) Eye irritation study with propachlor in rabbits
    (Project No. 5050-84). East Millstone, New Jersey, Bio/dynamics Inc.
    (Unpublished proprietary report submitted to WHO by Monsanto
    International Services, Brussels).

    Auletta CS & Rinehart WE (1979) Acute dermal toxicity study in rabbits
    (Project No. 4892-77). East Millstone, New Jersey, Bio/dynamics Inc.
    (Unpublished proprietary report submitted to WHO by Monsanto
    Agricultural Services, Brussels).

    Auletta CS, Erickson J, & Webb M (1984a) A closed-patch repeated
    insult dermal sensitization study in guinea-pigs (modified Buehler
    method) (Project No. 4946-84). East Millstone, New Jersey,
    Bio/dynamics Inc. (Unpublished proprietary report submitted to WHO by
    Monsanto International Services, Brussels).

    Auletta CS, Erickson J, & Webb M (1984b) A closed-patch repeated
    insult dermal sensitization study in guinea-pigs (modified Buehler
    method) (Project No. 4540-83). East Millstone, New Jersey,
    Bio/dynamics Inc. (Unpublished proprietary report submitted to WHO by
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    submitted to WHO by Monsanto International Services, Brussels).

    Steinmetz L & Mirsalis C (1986) Evaluation of the potential of
    propachlor to induce unscheduled DNA synthesis in the  in vivo- in
     vitro rat hepatocyte DNA repair assay (Project No. LSC-2021). Menlo
    Park, California, Stanford Research Institute, 37 pp (Unpublished
    proprietary report submitted to WHO by Monsanto International
    Services, Brussels).

    Stereva M & Maleva E (1977) [Biochemical studies on changes in gonads
    of male white rats under combined action of low frequency vibrations
    and intoxication with Ramrod. II. Dynamic in changes of 5-nucleotidase
    activity.] In: [Proceedings of the National Scientific Session of
    Chemists with Medical Direction, Part I], pp 133-139 (in Bulgarian).

    Strateva A (1974a) [Hygienic-toxicologic study on Ramrod aiming its
    hygienic standardization in water.] Sofia, University of Sofia
    (Dissertation) (in Bulgarian).

    Strateva A (1974b) [Amid preparations with herbicide action.
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    Exp Med Morphol, 13(2): 123-129 (in Russian).

    Strateva A (1975) [On some toxicologic properties of Ramrod and their
    significance on its hygienic standardization in waters.] Hyg
    Zdraveopazvane, 18(4): 401-405 (in Russian).

    Strateva A (1976) [The experimental determination of MAC of Ramrod in
    water.] Gig i Sanit, 4: 85-87 (in Russian).

    Strateva A, Velisarov A, & Georgiev A (1974) [Morphological and
    enzymohistochemical investigations on some internal organs of
    experimental animals under the effect of Ramrod in acute experiment.]
    Hyg Zdraveopazvane, 17(3): 283-286 (in Russian).

    Struble CB (1991)  In situ intestinal absorption of
    2-chloro-N-isopropylacetanilide (propachlor) and non-biliary excretion
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    Xenobiotica, 21: 85-95.

    Tanaka FS, Wien RG, & Mansager ER (1981) Survey for surfactant effects
    on the photodegradation of herbicides in aqueous media. J Agric Food
    Chem, 29: 227-230.

    Tanke W & Franz JM (1978) [Side effects of herbicides on economically
    useful insects.] Entomophaga, 23(3): 275-280 (in German).

    Thompson CM & Forbes AD (1979a) Acute toxicity of propachlor to
     Daphnia magna. Columbia, Missouri, ABC-Laboratories Inc., 40 pp
    (Unpublished proprietary report No. 24708, submitted to WHO by
    Monsanto International Services, Brussels).

    Thompson CM & Forbes AD (1979b) Acute toxicity of propachlor to
    Rainbow trout  Salmo gairdneri. Columbia, Missouri, ABC-Laboratories
    Inc., 40 pp (Unpublished proprietary report No. 24019, submitted to
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    Thun S (1990a) Propachlor 21-day reproduction test in  Daphnia
    (Project Number XX-89-126). Walsrode, Germany, IBR Forschung GmbH
    (Unpublished proprietary report of Monsanto Agricultural Company,
    submitted to WHO by Monsanto International Services, Brussels).

    Thun S (1990b) Prolonged fish toxicity test in the rainbow trout
    ( Salmo gairdneri) (Project Number XX-89-163). Walsrode, Germany, IBR
    Forschung GmbH (Unpublished proprietary report of Monsanto
    Agricultural Company, submitted to WHO by Monsanto International
    Services, Brussels).

    Thun S, Lemke G, & Fulst S (1991) Acute toxicity in earthworms
    according to OECD 207. (Project Number IB-90-566). Walsrode, Germany,
    IBR Forschung GmbH (Unpublished proprietary report of Monsanto
    Agricultural Company, submitted to WHO by Monsanto International
    Services, Brussels).

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    Villarreal DT, Turco RF, & Konopka A (1991) Propachlor degradation by
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    Council, pp 171-177.

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    Warholic DT, Gutenmann WH, & Lisk DJ (1983) Propachlor herbicide
    residue studies in cabbage using modified analytical procedure. Bull
    Environ Contam Toxicol, 31: 585-587.

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    World Health Organization, 7 pp (WHO/VBC/DS/87.78).

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    British Crop Protection Council.

    Yu Ching Chien, Booth GM, Hansen DJ, & Larsen JR (1975) Fate of
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    Zhukova PS & Shirko TS (1979) [Herbicide residues in soil and
    vegetables.] Khim Sel'skom Khoz, 17(6): 46-50 (in Russian).

    Zilkah S, Osband ME, & Mccaffrey RP (1981) Characterization of the
    inhibitory effects of the phytotoxic agent propachlor on L1210 cell
    proliferation. Cancer Lett. (Irel), 13(3): 241-248.

    Zilkah S, Osband ME, Mccaffrey RP, & Shapiro H (1985) The effect of
    the plant cell inhibitor propachlor on the cell cycle of LI210 cells
    as evaluated by flow cytometry. Life Sci, 6: 2111-2115.

    Zimdahl RL & Clark SK (1982) Degradation of three acetanilide
    herbicides in soil. Weed Sci, 30: 545-548.

    Zlateva M & Maleva E (1978) [Late changes in the gonads of male white
    rats upon combined treatment with low frequency vibrations and Ramrod
    intoxication.] Med Fizkult, pp 85-91 (in Bulgarian).

    Zlateva M & Maleva E (1979) Disorders in the processes of division and
    differentiation of seminiferous epithelium in case of chronic
    intoxication with Ramrod. Exp Med Morphol, 18(1): 35-39.

    Zlateva M, Maleva E, & Stareva M (1978) Changes of adenosine
    triphosphatase activity in the testes of albino rats under combined
    influence of low-frequency vibration and intoxication with the
    herbicide Ramrod. Rev Toxicol Eur Res, 6(78): 375-378.

    Zschaler R & Jonas W (1990) Growth inhibition test with algae (Project
    No. NC-90-592). Hamburg, Natec Institut für
    Naturwissenschaftlich-technische Dienste GmbH. (Unpublished
    proprietary report of Monsanto Agricultural Company, submitted to WHO
    by Monsanto International Services, Brussels).


    1.  Identité, modalités d'utilisation, propriétés physiques et
        chimiques, méthodes d'analyse

         Le propachlor est un herbicide dérivé de l'acétanilide qu'on
    utilise depuis 1965 en traitement de pré-levée et en traitement
    précoce de post-levée. Il est principalement formulé en poudre
    mouillable, liquide (concentré en suspension) et granulés. On
    l'utilise en agriculture pour détruire les graminées annuelles et
    certaines adventices à feuilles larges dans des cultures comme le
    maïs, le sorgho, les potirons, le lin et les fleurs.

         Le propachlor est légèrement soluble dans l'eau et facilement
    soluble dans la plupart des solvants organiques. Il est peu volatil,
    non inflammable et stable au rayonnement ultra-violet. La méthode
    d'analyse la plus pratique est la chromatographie en phase gazeuse
    avec détection par capture d'électrons après extraction et
    purification par des méthodes appropriées.

    2.  Transport, distribution et transformation dans l'environnement

         Le propachlor ne semble pas subir de dégradation photochimique à
    la surface du sol. Il se volatilise en présence de vent lorsque la
    surface du sol est encore humide.

         Il n'est que modérément adsorbé aux particules du sol et aux
    matières organiques, d'où un risque de lessivage à travers le sol
    jusqu'aux eaux souterraines. Toutefois toutes les études montrent que
    ce risque est faible en pratique. Il faut des précipitations très
    importantes pour que les résidus se déplacent de 30 cm à l'intérieur
    du sol. Selon la plupart des auteurs, la majorité des résidus
    demeurent à moins de 4 cm de profondeur. Les caractéristiques du sol
    influent beaucoup sur la mobilité du composé. Le lessivage se produit
    surtout dans des sols sableux pauvres en matières organiques.

         On a étudié en laboratoire et sur le terrain l'entraînement du
    propachlor par ruissellement. Une des études a montré que la présence
    de matières organiques dans le sol réduisait de 7 à 1 % de la quantité
    appliquée, la concentration de l'herbicide dans l'eau de
    ruissellement. L'incorporation de propachlor dans le sol réduit
    également les pertes par ruissellement (de 3 à 0,8 % selon une étude).

         En ce qui concerne la réduction de la concentration de propachlor
    dans le sol et dans l'eau, le facteur de loin le plus important est sa
    dégradation par les micro-organismes. On a montré que bactéries et
    champignons étaient responsables de la dégradation de ce composé. Peu
    de bactéries sont apparemment capables d'utiliser le propachlor comme
    seule source de carbone. On a également isolé des bactéries qui sont
    en mesure d'utiliser des métabolites telluriques du propachlor.

         Les principaux métabolites qui se forment dans le sol sont des
    acides oxaniliques et sulfoniques solubles dans l'eau. Il peut se
    former un grand nombre d'autres métabolites mais ils ne représentent
    qu'une faible proportion du total.

         Le propachlor disparaît rapidement du sol et on a fait état de
    demi-vies allant jusqu'à trois semaines. La plupart des études
    indiquent une dégradation pratiquement complète en moins de six mois.
    Les conditions écologiques influent sur la vitesse de dégradation qui
    est favorisée par une température élevée et une forte humidité du sol.
    Les résultats qui indiquent une persistance élevée du propachlor dans
    le sol ont été obtenus à basse température et dans des sols secs. La
    présence de nutriments en quantité suffisante dans le sol est
    également nécessaire à la dégradation du propachlor.

         Un des métabolites, la  N-isopropylaniline conjuguée est
    beaucoup plus persistante que le composé initial. On a retrouvé des
    résidus de ce métabolite jusqu'à deux ans après l'épandage de
    propachlor à titre expérimental à des doses plus élevées que celles
    que l'on utilise normalement en agriculture.

         Dans les conditions normales d'utilisation, le propachlor ne
    devrait pas être entraîné à travers le sol par lessivage jusqu'aux
    nappes souterraines et ne demeure pas dans le sol. Des conditions
    exceptionnelles (température très basse ou sécheresse) peuvent
    prolonger la persistance du propachlor et de ses métabolites.

         Dans les conditions normales, le propachlor ne subit pas de
    dégradation photochimique importante dans l'eau. Cependant, en
    présence de photosensibilisateurs, cette dégradation photochimique
    peut se produire. Le propachlor est stable à l'hydrolyse. Il est peu
    probable qu'il se volatilise à partir de l'eau du fait de sa forte
    solubilité dans l'eau et de sa faible tension de vapeur.

         Comme dans le sol, c'est principalement par dégradation
    biologique que le propachlor s'élimine de l'eau. Sa vitesse
    d'élimination est donc liée à la population microbienne. Une étude
    effectuée sur de l'eau contenant peu de bactéries a permis d'obtenir
    une demi-vie d'environ cinq mois. Une autre étude a montré qu'au bout
    de six semaines, il n'y avait toujours pas d'ouverture du cycle. Des
    études de laboratoire portant sur des modèles d'écosystèmes ont montré
    que le propachlor était presque complètement dégradé en l'espace de 33

         Plusieurs études portant sur différentes espèces végétales ont
    montré que le propachlor était rapidement métabolisé par les plantes
    intactes ainsi que par des tissus végétaux excisés. Les voies
    métaboliques se sont révélées analogues chez tous les végétaux
    étudiés, tout au moins pendant les six à 24 premières heures,
    conduisant à des métabolites hydrosolubles. On n'a pas observé de
    décomposition métabolique du reste  N-isopro-pylaniline. Seule une
    très faible proportion (< 1 % selon une étude) des métabolites a été

    retrouvée dans les fruits de ces végétaux; ils étaient concentrés en
    grande majorité dans les racines et les feuilles. Les principaux
    métabolites produits par les plantes sont identiques à ceux qui
    prennent naissance dans le sol. On sait que ces métabolites peuvent
    être fixés à partir du sol et un certain nombre d'études ne permettent
    pas de déterminer avec certitude si les métabolites analysés
    proviennent de la plantes ou du sol.

         Bien que, d'après le coefficient de partage octanol/eau, ce
    composé ait une tendance modérée à la bioaccumulation, on a montré
    qu'il n'y avait ni bioconcentration ni bioamplification chez les êtres

    3.  Concentrations dans l'environnement et exposition humaine

         Les rapports d'analyse du propachlor dans l'air au cours de
    l'épandage sont rares et insuffisants.

         Aux Etats-Unis d'Amérique, la concentration du propachlor dans
    les eaux de surface et les eaux souterraines est toujours faible, les
    maxima atteignant 10 µg/litre dans les eaux de surface et 0,12
    µg/litre dans les eaux souterraines. Le concentration la plus forte
    enregistrée lors d'une étude sur les eaux de ruissellement était de 46

         Les résidus de propachlor dans les denrées alimentaires sont
    généralement inférieurs à la limite de détection de la méthode
    d'analyse (0,005 mg/kg). L'expérimentation a permis de retrouver des
    résidus de l'ordre de 0,005 mg/kg dans des tomates, des poivrons, des
    oignons et des choux.

         Le dosage du propachlor dans l'atmosphère de la zone de travail
    de conducteurs de tracteur pendant l'épandage du composé a donné des
    résultats allant de 0,1 à 3,7 mg/m3.

    4.  Cinétique et métabolisme

         Chez les mammifères, le propachlor peut être absorbé au niveau
    des voies respiratoires, des voies digestives et de la peau. Il ne
    s'accumule pas dans l'organisme et devient indétectable au bout de 48

         La plupart des espèces animales (rats, porcs, poulets)
    métabolisent le propachlor par la voie de l'acide mercapturique (MAP).
    Il se forme des conjugués de cystéine par conjugaison avec le
    glutathion et on a avancé que ces conjugués jouaient le rôle
    d'intermédiaires dans la formation métabolique des acides
    mercapturiques. La métabolisation du conjugué cystéinique du
    propachlor se poursuit, notamment sous l'action de la C-S lyase
    bactérienne qui intervient également dans la formation des métabolites
    terminaux contenant le groupement méthylsulfonyle, métabolites qui
    sont principalement excrétés dans l'urine (68 % de la dose initiale de

    propachlor) et, sous forme de résidus insolubles, dans les matières
    fécales (19 %). La C-S lyase du propachlor est sans action chez les
    rats axéniques.

         On a montré qu'il y avait un certain nombre de différences dans
    le métabolisme du propachlor chez le rat et le porc. La bile est la
    principale voie d'élimination des métabolites mercapturiques chez le
    rat, mais on a montré qu'il existait une voie métabolique
    extra-biliaire chez le porc.

         Des études de métabolisme effectués sur des veaux ont montré que
    ces animaux pourraient être incapables de former de l'acide
    mercapturique à partir des conjugués du glutathion, ce qui les
    rendrait plus sensibles à l'intoxication par le propachlor.

    5.  Effets sur les animaux d'expérience et les systèmes d'épreuves in

         Le propachlor est légèrement toxique en cas d'exposition aiguë
    par voie orale (la DL50 pour le rat varie de 950 à 2176 mg/kg de
    poids corporel). Les signes d'intoxication aiguë proviennent
    principalement d'effets sur le système nerveux central (excitation et
    convulsions suivies d'une dépression). Chez des rongeurs, la toxicité
    aiguë par inhalation est faible (CL50 = 1,0 mg/litre). Le propachlor
    provoque de graves irritations des yeux et de la peau.

         Des rats, des souris et des chiens ont été soumis à une
    exposition de longue ou de courte durée au propachlor. Les organes
    cibles sont le foie et les reins. Chez le chien, la dose sans effet
    nocif observable a été de 45 mg/kg de poids corporel lors d'une étude
    de trois mois où l'animal était exposé par la voie alimentaire. Lors
    d'une étude d'une année sur des chiens, la dose sans effet nocif
    observable a été estimée à 9 mg/kg de poids corporel (200 ppm dans la
    nourriture). Lors d'une étude sur des rats exposés de la même manière
    pendant 24 mois au propachlor, la dose sans effet observable a été
    évaluée à 50 mg/kg de nourriture (2,6 mg/kg de poids corporel). Lors
    d'une étude semblable effectuée sur des souris pendant 18 mois, on a
    évalué à 1,6 mg/kg de poids corporel (10 ppm) la dose sans effet

         Le propachlor ne s'est révélé cancérogène ni pour la souris ni
    pour le rat. Dans la plupart des systèmes d'épreuve mammaliens, sa
    réponse mutagène est négative tout en étant positive dans quelques
    autres cas. Les données expérimentales disponibles de fournissent pas
    une preuve suffisante de son pouvoir mutagène.

         Administré en dose unique (675 mg/kg) à des rats et à des souris,
    le propachlor a donné lieu à des signes d'embryotoxicité. On a
    également observé des effets embryotoxiques lors d'études où du
    propachlor avait été administré à plusieurs reprises (35,7 à 270
    mg/kg). Toutefois, lors d'une autre étude sur des rats, où les doses

    variaient de 20 à 200 mg/kg, aucun effet embryotoxique n'a été

         Aux doses respectives de 12 et 60 mg/kg de poids corporel, le
    propachlor (en poudre mouillable) a entraîné une réduction de la
    teneur en protéines et un accroissement de l'activité de l'ATPase et
    de la 5-nucléotidase dans des homogénats de testicules de rats,
    provoquant également une dégénérescence du tissu testiculaire. Lors
    d'une étude de reproduction portant sur deux générations, on n'a pas
    véritablement obtenu la preuve d'effets indésirables.

    6.  Effets sur l'homme

         On a signalé quelques dermatites de contact et dermatites
    allergiques chez des agriculteurs et des ouvriers de production
    exposés au propachlor (Ramrod et Satecid). Des tests cutanés ont été
    effectués parmi un certain nombre d'entre eux, avec un résultat
    positif, qui révèle une réaction d'irritation et une hypersensibilité
    mono- et bivalente.

         On n'a pas eu connaissance de symptômes ou de maladies, soit chez
    des personnes exposées de par leur profession, soit dans la population
    générale - à part les quelques cas d'effets cutanés chez les ouvriers
    professionnellement exposés.

    7.  Effets sur les êtres vivant dans leur milieu naturel

         Des études portant sur la microflore terricole ont montré que les
    bactéries nitrifiantes constituaient le groupe le plus sensible aux
    effets inhibiteurs du propachlor, leur nombre étant réduit d'un
    facteur 3 à 4 après épandage de 8 à 10 kg de propachlor par hectare.
    Ce sont les bactéries décomposant la cellulose qui étaient les moins
    sensibles. La forte adsorption du propachlor aux particules d'argile
    présentes dans le sol et une température élevée sont deux facteurs qui
    réduisent les effets inhibiteurs.

         Chez l'algue  Selenastrum capricornutum, on a fait état d'une
    CE50 à 96 heures de 0,02 mg/litre (pour la croissance) et d'une
    concentration sans effet observable de 0,01 mg/litre. D'après une
    deuxième étude portant sur une formulation de propachlor et menée
    pendant 72 heures, le risque pour cette même algue serait nettement

         Pour la daphnie  Daphnia magna, on donne des CL50 de 7,8 ou
    6,9 mg/litre et une concentration sans effet observable inférieure à
    5,6 mg/litre. La concentration sans effet observable sur la
    reproduction était de 0,097 mg/litre. Pour des larves de deux espèces
    de moucherons, on a obtenu pour la CL50 des valeurs respectives de
    0,79 et 1,8 mg/litre.

         Chez la truite arc-en-ciel la CL50 à 96 heures est de 0,17
    mg/litre et la concentration sans effet observable sur 21 jours, de
    0,019 mg/litre.

         Le propachlor est considéré comme modérément à fortement toxique
    pour les organismes aquatiques.

         Le propachlor n'est pas toxique pour les lombrics aux
    concentrations présentes dans le sol par suite d'un usage normal (la
    concentration sans effet observable est de 100 mg/kg de terre). La
    DL50 par contact pour les abeilles (311 µg/abeille) montre que le
    propachlor ne constitue pas un danger pour ces insectes. En revanche,
    des études menées en laboratoire et sur le terrain montrent que des
    parasites utiles peuvent souffrir des effets du propachlor.

         Le propachlor est plus toxique pour les oiseaux lorsqu'on
    l'introduit directement dans l'estomac que lorsqu'on l'administre dans
    la nourriture. La DL50 aiguë varie de 137 à 735 mg/kg de poids
    corporel pour différentes espèces. Quant à la CL50 lors d'une
    exposition par voie alimentaire, elle dépasse 5620 mg/kg de nourriture
    chez les oiseaux.

         Le propachlor ne constitue pas un danger pour les oiseaux dans la
    nature, même sous forme de granulés.


    1.  Identidad, modalidades de uso, propiedades físicas y químicas y
        método analíticos

         El propacloro es un herbicida derivado de la acetanilida
    utilizado desde 1965 que actúa en las plantas antes de nacer o poco
    después. Las principales formulaciones son de polvo humectable,
    líquido fluido (concentrado en suspensión) y gránulos. Se aplica en la
    agricultura a la lucha contra las gramíneas anuales y algunas malas
    hierbas de hoja ancha en varios cultivos, como los de maíz, sorgo,
    calabaza, lino y flores ornamentales.

         El propacloro es ligeramente soluble en agua y se disuelve
    fácilmente en la mayoría de los disolventes orgánicos. Su volatilidad
    es escasa, no es inflamable y es estable a la radiación ultravioleta.
    El método más práctico de análisis es la cromatografía de gases con
    detección por captura de electrones, después de aplicar procedimientos
    apropiados de extracción y purificación.

    2.  Transporte, distribución y transformación en el medio ambiente

         Según la información disponible, el propacloro no se fotodegrada
    sobre la superficie del suelo. El producto se volatiliza cuando hay
    viento y la superficie del suelo está todavía mojada.

         La adsorción sobre las partículas del suelo y la materia orgánica
    es sólo moderada. Debido a esto, es posible la lixiviación a través
    del perfil del suelo hacia el agua subterránea. Sin embargo, todos los
    estudios indican que en la práctica es poco probable que esto ocurra.
    Se requiere una precipitación muy abundante para hacer descender los
    residuos 30 cm en el perfil del suelo. La mayoría de los autores
    señalan que la mayor parte de los residuos se mantienen en una capa
    superficial del suelo de 4 cm. Las características del suelo influyen
    mucho en el desplazamiento del producto. La lixiviación se produce en
    su mayor parte en suelo arenoso con poca materia orgánica.

         Se ha estudiado el arrastre del propacloro por el agua tanto en
    el laboratorio como sobre el terreno. En un estudio, la materia
    orgánica del suelo redujo el arrastre del herbicida aplicado del 7% al
    1%. Su incorporación al suelo también redujo la pérdida por arrastre
    del agua (del 3% al 0,8% en un estudio).

         El factor que más contribuye, con diferencia, a reducir los
    niveles de propacloro en el suelo y el agua es la degradación por los
    microorganismos. Se ha comprobado que en la degradación de la
    sustancia intervienen tanto bacterias como hongos. Son pocas las
    bacterias que parecen tener capacidad para usar el propacloro como
    única fuente de carbono. También se han aislado bacterias que pueden
    utilizar los metabolitos del propacloro presentes en el suelo.

         Los metabolitos predominantes entre los que se forman en el suelo
    son los ácidos oxanílico y sulfónico, solubles en agua. Pueden
    formarse otros muchos metabolitos, pero representan una proporción
    pequeña del total.

         El propacloro desaparece con rapidez del suelo, habiéndose
    registrado semividas de hasta tres semanas. En la mayoría de los
    estudios se señala que la degradación es casi completa en menos de
    seis meses. Las condiciones del medio ambiente influyen en la
    velocidad de degradación, que se ve favorecida por los valores
    elevados de la temperatura y el contenido de humedad del suelo. Los
    estudios en los que se describía una permanencia más prolongada del
    propacloro en el suelo se realizaron en condiciones de baja
    temperatura o suelo seco. También es necesaria una cantidad suficiente
    de nutrientes en el suelo para la degradación.

         El metabolito conjugado  N-isopropilanilina es mucho más
    persistente que el producto del que procede. Se han encontrado
    residuos de este metabolito hasta dos años después de la aplicación
    experimental de dosis de propacloro más altas de las que se utilizan
    normalmente en la agricultura.

         Con el uso normal no es previsible que el propacloro llegue por
    lixiviación a través del suelo hasta el agua subterránea, y no se
    mantiene mucho tiempo en el suelo. En condiciones excepcionales de
    baja temperatura o sequedad, el propacloro y sus metabolitos pueden
    permanecer más tiempo en él.  En condiciones normales, el propacloro
    no sufre una fotodegradación significativa en el agua. En presencia de
    fotosensibilizadores puede fotodegradarse. El propacloro es estable
    desde el punto de vista hidrolítico. No es probable la volatilización
    a partir del agua, debido a la elevada solubilidad en ella y la baja
    tensión de vapor del producto.

         Al igual que en el suelo, la principal ruta de pérdida de
    propacloro del agua es la degradación biótica. La velocidad de
    desaparición del propacloro del agua depende, pues, de la población
    microbiana. En un estudio realizado con un pequeño número de bacterias
    presentes en el agua se obtuvo una semivida de unos cinco meses. En
    otro estudio, a las seis semanas no se había roto el anillo. En
    estudios de laboratorio con modelos de ecosistemas se observó una
    degradación casi completa en un período de 33 días.

         En varios estudios con distintas especies vegetales se vio que el
    propacloro se metabolizaba con rapidez tanto en las plantas intactas
    como en tejidos vegetales extirpados. Las rutas metabólicas eran
    análogas en todas las plantas estudiadas, por lo menos durante las
    primeras 6-24 horas, produciendo metabolitos hidrosolubles. No se
    observó degradación metabólica del fragmento de la
     N-isopropilanilina. En los frutos de las plantas solamente se
    encontró una proporción muy pequeña (< 1% en un estudio) de los
    metabolitos; en su mayor parte estaban en las raíces y el follaje. Los
    principales metabolitos producidos en las plantas son idénticos a los

    que se forman en el suelo. Se sabe que las plantas absorben esos
    metabolitos del suelo, y en algunos estudios había dudas acerca de si
    los metabolitos medidos procedían de la planta o del suelo.

         Aunque del coeficiente de reparto en octanol y agua parece
    deducirse un potencial moderado de bioacumulación, los estudios
    realizados indican que no hay ni bioconcentración ni bioamplificación
    en los organismos.

    3.  Niveles medioambientales y exposición humana

         Las mediciones descritas de la concentración del propacloro en el
    aire durante la aplicación son pocas e inadecuadas.

         Las concentraciones en el agua superficial y subterránea en los
    Estados Unidos fueron siempre bajas, con un máximo de 10 µg/litro en
    la superficial y de 0,12 µg/litro en la subterránea. La mayor
    concentración registrada en el agua en un estudio del arrastre fue de
    46 µg/litro.

         Los residuos de propacloro en los alimentos suelen ser inferiores
    al límite de detección del método analítico (0,005 mg/kg). En estudios
    experimentales se han identificado concentraciones de residuos del
    orden de 0,05 mg/kg en tomates, pimientos, cebollas y coles.

         Las concentraciones de propacloro en el aire de la zona de
    trabajo de los conductores de tractores que aplicaban la sustancia
    oscilaban entre 0,1 y 3,7 mg/m3.

    4.  Cinética y metabolismo

         Los mamíferos pueden absorber el propacloro por los tractos
    respiratorio y gastrointestinal, así como a través de la piel. El
    producto no se acumula en el organismo, en el que no es detectable a
    las 48 horas.

         La mayoría de las especies animales (ratas, cerdos, pollos)
    metabolizan el propacloro siguiendo la vía de los ácidos
    mercaptúricos. Mediante conjugación con el glutatión se forman
    productos conjugados de cisteína, que se han señalado como posibles
    intermediarios en la formación metabólica de ácidos mercaptúricos. La
    C-S liasa bacteriana participa en el ulterior metabolismo del sistema
    conjugado del propacloro con la cisteína y en la formación de los
    metabolitos finales con metilsulfonilo, que se excretan sobre todo en
    la orina (68% de la dosis de propacloro), y de residuos insolubles,
    que se excretan en las heces (19%). La propacloro C-S liasa es
    inactiva en ratas sin microorganismos.

         En los estudios realizados se observaron algunas diferencias en
    cuanto al metabolismo entre las ratas y los cerdos. La bilis es el
    principal camino de eliminación de los metabolitos de la vía de los

    ácidos mercaptúricos en las ratas, pero se ha demostrado que en los
    cerdos existe una vía metabólica extrabiliar.

         En estudios metabólicos con terneros se observó que pueden ser
    incapaces de formar ácidos mercaptúricos a partir de los productos
    conjugados del glutatión, por lo que pueden ser más susceptibles a la

    5.  Efectos en los animales de experimentación y en sistemas de prueba
        in vitro

         El propacloro es ligeramente tóxico en la exposición oral aguda
    (la DL50 en ratas va de 950 a 2176 mg/kg de peso corporal). Los
    signos de intoxicación aguda son predominantemente efectos sobre el
    sistema nervioso central (excitación y convulsiones, seguidas de
    depresión). La toxicidad aguda por inhalación en roedores es baja
    (CL50 = 1,0 mg/litro). El propacloro produjo efectos graves de
    irritación en los ojos y la piel.

         El propacloro se ha ensayado en estudios de exposición de corta
    y larga duración en ratas, ratones y perros. Los órganos sobre los que
    actuaba eran el hígado y los riñones. En un estudio de administración
    con los alimentos a perros durante tres meses, el nivel sin efectos
    adversos observados (NOAEL) fue de 45 mg/kg de peso corporal. En otro
    estudio de un año, también en perros, el NOAEL fue de 9 mg/kg de peso
    corporal (250 ppm en la dieta). El nivel sin efectos observados (NOEL)
    en un estudio de alimentación de ratas durante 24 meses fue de 50
    mg/kg de la dieta (2,6 mg/kg de peso corporal). En un estudio en el
    que administró el producto a ratones con los alimentos durante 18
    meses, el NOEL fue de 1,6 mg/kg de peso corporal (10 ppm).

         No se encontraron efectos carcinogénicos del propacloro en
    ratones y ratas. En la mayoría de los sistemas de prueba de mamíferos
    la respuesta mutagénica fue negativa, obteniéndose resultados
    positivos en un pequeño número de ensayos. Los datos experimentales
    disponibles no aportan suficientes pruebas de su potencial mutagénico.

         En pruebas de dosis única (675 mg/kg) con ratones y ratas se
    demostró la embriotoxicidad del propacloro. También se detectaron
    efectos embriotóxicos en tratamientos con dosis repetidas (35,7-270
    mg/kg). Sin embargo, en otro estudio en ratas, con una gama de dosis
    de 20-200 mg/kg, no se observó embriotoxicidad.

         Con niveles de 12 y 60 mg/kg de peso corporal, el propacloro
    (polvo humectable) provocó una disminución del contenido de proteínas
    y un aumento de la actividad de la ATPasa y la 5-nucleotidasa en un
    homogeneizado de testículo de rata y cambios degenerativos en los
    testículos. En un estudio de reproducción de dos generaciones no se
    obtuvieron pruebas definitivas de efectos adversos.

    6.  Efectos en la especie humana

         Se ha descrito un pequeño número de casos de dermatitis de
    contacto y alérgica en agricultores y trabajadores expuestos al
    propacloro durante la producción (Ramrod y Satecid). En algunos de
    ellos se efectuaron pruebas del parche y la reacción fue positiva, con
    irritación e hipersensibilidad monovalente y bivalente.

         No se han notificado casos de síntomas o enfermedades entre las
    personas expuestas profesionalmente o en la población general, salvo
    un pequeño número de informes de sus efectos cutáneos en trabajadores
    expuestos profesionalmente.

    7.  Efectos en los seres vivos del medio ambiente

         En varios estudios sobre los microorganismos del suelo, las
    bacterias nitrificantes fueron el grupo más sensible a los efectos
    inhibidores del propacloro, reduciéndose su número a la tercera o
    cuarta parte tras la aplicación de 8-10 kg/ha de propacloro. Las menos
    sensibles fueron las bacterias celulolíticas. La adsorción elevada
    sobre las partículas de arcilla del suelo y la temperatura alta
    reducen los efectos inhibidores.

         En el alga  Selenastrum capricornutum se ha registrado una CE50
    a las 96 horas de 0,02 mg/litro para el crecimiento y una
    concentración sin efectos observados (NOEC) de 0,01 mg/litro. De un
    segundo estudio de 72 horas realizado con una formulación, parece
    desprenderse que el peligro es mucho menor para este mismo organismo.

         Se ha informado de unos valores de la CL50 para  Daphnia magna
    de 7,8 y 6,9 mg/litro y una NOEC de < 5,6 mg/litro. En las larvas de
    dos especies de moscas enanas, los valores registrados de la CL50
    fueron de 0,79 y 1,8 mg/litro.

         La CL50 para la trucha arcoiris a las 96 horas es de 0,17
    mg/litro, y la NOEC en un estudio de 26 días fue de 0,019 mg/litro.

         Se considera que el propacloro tiene una toxicidad entre moderada
    e intensa para los organismos acuáticos.

         La exposición a las concentraciones de propacloro que cabe prever
    en el suelo no es tóxica para las lombrices de tierra si la aplicación
    es normal (la NOEC es de 100 mg/kg de suelo). La DL50 por contacto
    para las abejas (311 µg/abeja) demuestra que el propacloro no
    representa un peligro para estos insectos. En estudios de laboratorio
    y de campo se han detectado efectos adversos del propacloro en algunos
    insectos parasitarios beneficiosos.

         El propacloro es más tóxico para las aves cuando se administra
    mediante sonda gástrica que cuando se incorpora a la dieta. Los
    valores de la DL50 aguda para distintas especies de aves oscilan

    entre 137 y 735 mg/kg de peso corporal. Los valores de la CL50 en la
    administración con los alimentos fueron superiores a los 5620 mg/kg de
    la dieta.

         El propacloro no representa un peligro para las aves en el campo,
    ni siquiera con la formulación granulada.

    See Also:
       Toxicological Abbreviations
       Propachlor (HSG 77, 1992)