August, 1987
                                       DIURON

                                  Health Advisory
                              Office of Drinking Water
                        U.S. Environmental Protection Agency
I. INTRODUCTION
        The Health Advisory (HA) Program,  sponsored by the Office of Drinking
   Water (ODW), provides information on the health effects, analytical method-
   ology and treatment technology that would be useful in dealing with the
   contamination of drinking water.  Health Advisories describe nonregulatory
   concentrations of drinking water contaminants at which adverse health effects
   would not be anticipated to occur over specific exposure durations.  Health
   Advisories contain a margin of safety to protect sensitive members of the
   population.

        Health Advisories serve as informal technical guidance to assist Federal,
   State and local officials responsible for protecting public health when
   emergency spills or contamination situations occur.  They are not to be
   construed as legally enforceable Federal standards.  The HAs are subject to
   change as new information becomes available.

        Health Advisories are developed for one-day, ten-day, longer-term
   (approximately 7 years, or 10% of an individual's lifetime) and lifetime
   exposures based on data describing noncarcinogenic end points of toxicity.
   Health Advisories do not quantitatively incorporate any potential carcinogenic
   risk from such exposure.  For those substances that are known or probable
   human carcinogens, according to the Agency classification scheme (Group A or
   B), Lifetime HAs are not recommended.  The chemical concentration values for
   Group A or B carcinogens are correlated with carcinogenic risk estimates by
   employing a cancer potency (unit risk) value together with assumptions for
   lifetime exposure and the consumption of drinking water.  The cancer unit
   risk is usually derived from the linear multistage model with 95% upper
   confidence limits.  This provides a low-dose estimate of cancer risk to
   humans that is considered unlikely to pose a carcinogenic risk in excess
   of the stated values.  Excess cancer risk estimates may also be calculated
   using the one-hit, Weibull, logi't or probit models.  There is no current
   understanding of the biological mechanisms involved in cancer to suggest that
   any one of these models is cible to predict risk more accurately than another.
   Because each model is based on differing assumptions, the estimates that are
   derived can differ by several orders of magnitude.

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    Diuron                                                      August,  1987

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II. GENERAL INFORMATION AND PROPERTIES

    CAS No.  330-54-1

    Structural Formula
                       N'-(3,40ichlorophenyi)-N,N-dimethylurea

    Synonyms

         0  Crisuron; Dailon; Di-on; Dichlorfendism;  Diurex, Drexel; Duran;
            Dynex; DCMU; Herbatox; HW 920; Karmex; Sup'r flo; Telvar, Urox D;
            Vonduron (Meister, 1983).

    Uses

         0  Pre-emergence herbicide  (Meister, 1984).

    Properties   (Meister, 1984; Windholz et al.,  1983}
            Chemical Formula
            Molecular Weight               233.10
            Physical State  (at 25°C)       White crystalline solid
            Boiling Point
            Melting Point                  158-159°C
            Vapor  Pressure  (20°C)          3.1 x 10-6 nun Hg
            Specific Gravity               —
            Water  Solubility  (25°C)        42 mg/L
            Log Octanol/Water Partition    —
              Coefficient
            Taste  Threshold
            Odor Threshold                 --
            Conversion Factor              —
    Occurrence
             Diuron  has  been  found  in  none of  the  8 surface water  samples  analyzed
             and  in  25 of  939 ground water samples  (STORET, 1987).   Samples  were
             collected at  6 surface water locations and  930 ground water locations,
             and  diuron  was found only in California and Georgia.  The  85th  percentile
             of all  non-zero  samples was  1 ug/L  in ground water  sources only.   The
             maximum concentration  found  in  ground water was  5 ug/L.

             Diuron  residues  as  a result  of  agricultural practice  have been  detected
             in ground waters in California  in wells at  low (e.g., 2 to 3  ppb)
             levels  (California  Department of  Food and Agriculture,  1986).

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Environmental Fate

     0  Radiolabeled diuron and its degradation products 3-(3,4-dichlorophenyl)-
        1-methylurea (DCPMU) and 3-(3,4-dichlorophenyl)urea (DCPU) had half-lives
        of 4 to 8, 5, and 1 month,  respectively, in aerobic soils maintained
        at 18 to 29°C and moisture  levels at approximately field capacity
        (Walker and Roberts, 1978;  Elder, 1978).   3,4-Dichloroaniline (DCA)
        was identified as a minor degradation product of diuron (Belasco,
        1967; Belasco and Pease, 1969;  Elder, 1978).  Increasing soil organic
        matter content appears to increase the rate of decline of diuron
        phytotoxic residues (McCormick, 1965; Corbin and Upchurch, 1967;
        McCormick and Hiltbold, 1966; Liu et al., 1970).

     0  Degradation of diuron phytotoxic residues is much (28 to 50%) slower
        in flooded soil than in aerobic soil (Imamliev and Bersonova, 1969;
        Wang et al., 1977).

     8  Diuron has a low-to-intermediate mobility in fine to coarse-textured
        soils and freshwater sediments (Hance 1965a; Hance, 1965b; Harris and
        Sheets, 1965; Harris, 1967; Helling and Turner, 1968; Grover and
        Hance, 1969; Gerber et al., 1971; Green and Corey, 1971; Helling,
        1971; Guth, 1972; Grover, 1975; Helling, 1975).  Mobility is correlated
        with organic matter content and  (CEC).  Soil texture apparently is not,
        by itself, a major factor governing the mobility of diuron in soil.

     0  In a study using radiolabeled material, the diuron degradation products
        (96% pure) had K^ values of 66 and 115 in silty clay loam soils,
        indicating that they are relatively immobile or less mobile than diuron
        (Elder, 1978).

     8  In the field, diuron residues  (nonspecific method used) generally
        persisted for up to 12 months in soils that ranged in texture from sand
        to silt loam treated with diuron at 0.8 to 4 Ib/A (Cowart, 1954; Hill
        et al., 1955; Weed et al.,  1953; Weed et al., 1954; Miller et al.,
        1978).  These residues may  leach in soil to a depth of 120 cm (4 feet).
        Diuron was detectable  (3 to 74 ppb) in runoff-water sediment and soil
        samples for up to 3 years after  the last application to pineapple-
        sugarcane fields in Hawaii  (Mukhtar, 1976; Green et al., 1977).

     8  Phytotoxic residues persisted for up to 12 months in soils ranging in
        texture from sand to silty  clay loam to boggy meadow soil following
        the last of one to six annual applications of diuron at 1 to 18 Ib/A
        (Weldon and Timmons, 1961;  Dalton et al., 1965; Bowmer, 1972; Dawson
        et al., 1978; Arle et al.,  1965; Wang and Tsay, 1974; Spiridonov et al.,
        1972; Addison and Bardsley, 1968; Cowart, 1954; Hill et al., 1955;
        Weed et al, 1953; Weed et al., 1954).  Diuron persistence in soil
        appears to be a function of application rate and amount of rainfall
        and/or irrigation water.  Three degradation products (DCPMU, DCPU,
        and DCA) were identified in soil (planted to cotton) that had received
        multiple applications of diuron  (80% wettable powder totaling 5 to 5.7
        Ib/A (Dalton et al., 1965).

     ••  Diuron persists in irrigation-canal soils for 6 or more months following
        application at 33 to 46 kg/ha  (Evans and Duseja, 1973a; Evans and

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     Diuron                                                      August, 1987

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             Duseja, 1973t>; Bowmer and Adeney, 1978a; Bowmer and Adeney,
             1978b).  The relative percentages of diuron and its degradates DCPMU
             and DCPU were 60-90:10-25:1-30 in clay and sandy clay soils, 4.5 to 17
             weeks after treatment.  Diuron levels in water samples were highest
             (0.5 to 8 ppm) in the initial flush of irrigation-water.  These levels
             declined rapidly, probably as a function of dilution and not degradation,


III. PHARMACOKINETICS

     Absorption

          0  Diuron is absorbed through the gastrointestinal tract of rats and dogs.
             Hodge et al.  (1967) fed diuron to rats and dogs at dietary levels
             from 25 to 2,500 ppm and from 25 to 1,250 ppm active ingredient (a.i.),
             respectively, for periods up to two years.  These doses are equivalent
             to 1.25 to 125 mg/kg/day for the rat and 0.635 to 31.25 mg/kg/day for
             the dog.  Urinary and fecal excretion products after one week to 2
             years  accounted for  about 10% of the daily dose ingested.  The
             excretion data provided evidence that gastrointestinal absorption
             ocurred in rats and dogs.

     Distribution


          0  Hodge et al.  (1967) fed diuron (80% wettable powder) for 2 years
             to rats at dietary levels of 25 to 2,500 ppm a.i. and to dogs at
             dietary levels of 25 to 1,250 ppm a.i.  Assuming that 1 ppm in the
             diet is equivalent to 0.05 mg/kg/day in rats and 0.025 mg/kg/day in
             dogs, this corresponds to doses of 1.25 to 125 mg/kg/day in rats and
             0.625 to 31.25 mg/kg/day in dogs (Lehman,  1959).  Analysis of tissue
             samples for diuron residues revealed levels ranging from 0.2 to 56 ppm,
             depending on  dose. This constituted only a minute fraction of
             the total dose ingested.  The authors concluded that there was little
             diuron storage in tissues.

     Metabolism


          0  Geldmacher von Mallinckrodt and Schlussier (1971) analyzed the urine
             of a woman who had ingested a dose cf 38 mg/kg of diuron along with
             20 mg/kg of aminotriazole.  The urine was  found to contain
             1-(3,4-dichlorophenyl)-3-methylurea and 1 -(3,4-dichlorophenyl)-urea,
             and may also  have contained some 3,4-dichloroaniline.  No unaltered
             diuron was detected.

          0  Hodge  et al.  (1967) fed diuron (80% wettable powder) to male beagle
             dogs at a dietary level of 125 ppm active  ingredient for 2 years.
             Assuming that 1  ppm in the diet is equivalent  to 0.025 mg/kg/day
              (Lehman, 1959),  this corresponds to a dose of  3.1 mg/kg/day.  Analysis
             of urine at weeks one to four or after  two years revealed the major
             metabolite was N-(3,4-dichlorophenyl)-urea.  Small amounts of

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    Diuron                                                      August,  1987

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            N-(3,4-dichlorophenyl)-N'-methylurea,  3,4-dichloroanaline,
            3,4-dichlorophenol  and  unmetabolized diuron also were detected.
    Excretion
         0  Hodge et al.  (1967)  fed  diuron (80% wettable powder) for 2 years
            to rats at dietary levels  of 25 to 2,500 ppm and to dogs at dietary
            levels of 25  to  1,250  ppm.   Assuming that 1  ppm in the diet is equivalent
            to 0.05 mg/kg/day in rats  and 0.025 mg/kg/day in dogs, this corresponds
            to doses of 1.25 to  125  mg/kg/day in rats and 0.625 to 31.25 mg/kg/day
            in dogs (Lehman, 1959).  In rats, urinary excretion (6.3 to 492 ppm,
            depending on  dose) was consistently greater than fecal excretion
            (1.0 to 204 ppm).  In  dogs, urinary excretion (6.3 to 307 ppm) was
            similar to fecal excretion (7.9 to 308 ppm).  For both rats and dogs,
            combined urinary and fecal excretion accounted for only about 10% of
            the daily diuron ingestion.
IV. HEALTH EFFECTS

    Humans
            No information was  found  in the available literature on the health
            effects of diuron in humans.
    Animals
       Short-term Exposure

         0  Acute oral LD50 values of 1,017 mg/kg and 3,750 mg/kg have been
            reported in albino rats by Boyd and Krupa (1970), NIOSH (1985) and
            Taylor (1976a), respectively.  Signs of central nervous system
            depression were noted after treatment.

         0  Hodge et al. (1967) administered single oral doses of recrystallized
            diuron in peanut oil to male CR rats.  The approximate lethal dose was
            5,000 mg/kg, and the LDgg was 3,400 mg/kg.  Survivors sacrificed after
            14 days showed large and dark-colored spleens with numerous foci of
            blood formation.

         0  Hodge et al. (1967) administered oral doses of 1,000 mg/kg of
            recrystallized diuron five times a week for 2 weeks (10 doses) to
            six male CR rats.  At necropsy, 3 or 11 days after the final dose,
            the spleens were large, dark and congested, and foci of blood formations
            were noted in both the spleen and bone marrow.

         0  Hodge et al. (1967) fed Wistar rats (five/sex/dose) diuron (purity
            not specified) in the diet for 42 days at dose levels of 0, 200, 400,
            2,000, 4,000 or 8,000 ppm a.i.  Assuming that 1 ppm in the diet is
            equivalent to 0.05 mg/kg/day (Lehman, 1959), this corresponds to
            doses of 0, 10, 20, 100, 200 or 400 mg/kg/day.  Following treatment
            body weight, clinical chemistry, food consumption, hematology,
            urinalysis and histology were evaluated.  No effects were observed at

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Diuron                                                      August,  1987

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        400 ppm  (20 mg/kg/day) or less.  At 2,000 ppm  (100 mg/kg/day) or
        greater, red blood cell counts and hemoglobin  values were decreased.
        A marked inhibition of growth occurred in the  4,000 ppm  (200 mg/kg/day)
        or greater dosage groups, and there was increased mortality at 8,000
        ppm.  Based on these data, a No-Observed-Adverse-Effect-Level (NOAEL)
        of 400 ppm (20 mg/kg/day) and a Lowest-Observed-Adverse-Effect-Level
        (LOAEL) of 2,000 ppm (100 mg/kg/day) were identified.

   Dermal/Ocular Effects

     0  Taylor (1976b) applied diuron (98% pure) to the intact or abraded skin
        of eight albino rabbits at dose levels of 1,000 to 2,500 rag/kg for 24
        hours.  After treatment, a slight erythema was observed, but no other
        symptoms of toxicity were noted during a 14-day observation period.
        The dermal LD5Q was reported as >2,500 mg/kg.

     0  Larson (1976) applied diuron (98% pure) at doses of 1, 2.5, 5 or 10
        n»9/kg to intact abraded skin of rabbits for 24 hours.  Adverse effects
        were not detected in exposed animals.

     0  In studies conducted by DuPont (no date), diuron (50% water paste)
        was not irritating to intact skin and was moderately irritating to
        abraded skin of guinea pigs.  No data were available on  skin
        sensitization.  See also DuPont (1961).

     0  In studies conducted by Larson and Schaefer (1976), 10 mg of a fine
        dry powder of diuron (98% a.i.) was instilled  into the conjunctival
        sac of one eye of each of six New Zealand White rabbits.  Ocular
        irritation was not detected within 72 hours.

   Long-term Exposure

     0  Hodge et al.  (1967) fed albino Charles River rats  (five/sex/dose)
        diuron (98%"pure) for 90 days at dietary levels of 0, 50, 500 or
        5,000 ppm.  Assuming that 1 ppm in the diet is equivalent to 0.05
        ing/kg/day  (Lehman, 1959), this corresponds to  doses of 0, 2.5, 25 or
        250 mg/kg/day.  Following treatment, body weight, food consumption,
        clinical chemistry and histopathology were evaluated.  No adverse
        effects were observed in any parameter at 50 ppm.  At 500 ppm there
        were no effects on males, but females gained less weight than controls
        and appeared cyanotic.  At the 5,000-ppm dose  level, body weights
        were reduced in both sexes, spleens were enlarged and exhibited
        hemosiderosis, and there was clinical and pathological evidence of
        chronic methemoglobinemia.  Based on these data, a NOAEL of 50 ppm
        (2.5 mg/kg/day) and a LOAEL of 500 ppm (25 mg/kg/day) were identified.

     0  Hodge et al.  (1967) fed diuron (80% wettable powder) to groups of
        Charles River rats (20/sex/dose) for 90 days at dietary  levels of 0,
        250 or 2,500 ppm active ingredient.  Assuming  that 1 ppm in the diet
        is equivalent to 0.05 mg/kg/day (Lehman, 1959), this corresponds to
        doses of 0, 12.5 or 125 mg/kg/day.  At 2,500 ppm, both males and
        females ate less and gained less weight did than controls.  There was
        a slight decrease in red blood cell count, greater in females than in

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        males.  No effect on food consumption or weight gaiir was noted at
        250 ppm, but hematological changes were evident in females.  This
        study identified a LOAEL of 250 ppm (12.5 mg/kg/day), the lowest
        dose tested.

     8  In a 2-year feeding study conducted by Hodge et al. (1964a, 1967),
        beagle dogs (two males/dose and three females/dose) were administered
        technical diuron (80% a.i.) in the diet at dose levels of 0, 25, 125,
        250 or 1,250 ppm active ingredient.  Assuming that 1 ppm in the diet
        of dogs is equivalent to 0.025 mg/kg/day (Lehman, 1959), this corresponds
        to doses of diuron of 0, 0.625, 3.12, 6.25 or 31.25 mg/kg/day.
        Following treatment, body weight, clinical chemistry, hematology,
        organ weight, gross pathology and histopathology were evaluated.  No
        adverse effects were reported at 25 ppm in any parameter measured.
        Abnormal blood pigment  was observed at 125 ppm or greater.  ,Hemato-
        logical alterations (depressed red blood cells (RBC), hematocrit and
        hemoglobin) were observed at 250 ppm or greater.  In the 1,250 ppm
        group, a slight weight loss occurred as well as increased erythrogenic
        activity in bone marrow and hemosiderosis of the spleen.  Based on
        these data, a NOAEL of 25 ppm  (0.625 mg/kg/day) and a LOAEL of 125 ppm
        (3.12 mg/kg/day) were identified.

     0  Hodge et al.  (1964b, 1967) administered technical diuron (80% a.i.)
        in the diet of rats (35/sex/dose) for 2 years at dose levels of 0,
        25, 125, 250 or 2,500 ppm active ingredient.  Assuming that 1 ppm in
        the diet of rats is equivalent to 0.05 mg/kg/day (Lehman, 1959), this
        corresponds to doses of diuron of 0, 1.25, 6.25, 12.5 or 125 mg/kg/day.
        Following treatment, body weight, clinical chemistry, hematology,
        food  consumption, urinalysis, organ weights and histopathology were
        evaluated.  No adverse effects were reported at 25 ppm  (1.25 mg/kg/day)
        for any parameters measured.  Abnormal blood pigments  (sulfhemoglobin)
        were  observed at 125 ppm  (6.25 mg/kg/day) or greater.  Hematological
        changes  (decreased RBC, reduced hemoglobin), growth depression,
        hemosiderosis of the spleen and increased mortality were observed at
        250 ppm  (12.5 mg/kg/day) or greater.  Based on these data, a NOAEL of
        25 ppm  (1.25  mg/kg/day) and a LOAEL of 125 ppm  (6.25 mg/kg/day) were
        identified.

    Reproductive Effects

     0  Hodge et al.  (1964b, 1967) studied the effects of diuron (80% wet-
        table powder) in a three-generation reproductio'n study in rats.
        Animals were  supplied food containing 125 ppm active ingredient.
        Assuming that 1 ppm in  the diet of rats is equivalent  to 0.05 mg/kg/
        day  (Lehman,  1959), this corresponds to a dose of 6.25 mg/kg/day.
        Fertility rate, body weight, hematology and histopathology were
        monitored.  No effect was seen on  any parameter except body weight,
        which significantly decreased  in the F2D and F3a litters.  A LOAEL
        of  125 ppm  (6.25 mg/kg/day) was identified.

    Developmental Effects

     0  Khera et al.  (1979) administered by gavage a formulation containing
        80% diuron at dose levels of 125,  250 or 500- mg/kg of  formulation to

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  Diuron                                                       August,  1987

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           pregnant Wistar rats  (14  to  18/dose)  on days  6 through 15 of gestation.
           Vehicle (corn oil)  controls  (19  dams)  were  run concurrently.  No
           maternal or teratogenic effects  were  observed at 125 mg/kg/day.
           Developmental effects  appeared to  increase  in all treatment groups,
           i.eo   wavy ribs,  extra ribs  and  delayed ossification.   The incidence
           of wavy ribs was  statistically significant  at 250 mg/kg and greater.
           Maternal and fetal  body weights  decreased significantly at 500 mg/kg
           (p <0.05).  A NOAEL was not  determined from this study for fetotoxic
           effects; hence, a LOAEL of  125 mg/kg  of formulation per day was
           identified.

      Mutagenicity

        0  Andersen et al. (1972) reported  that  diuron did not exhibit mutagenic
           activity in T4 bacteriophage test  systems  (100 ug/plate)  or in tests
           with  eight histidine-requiring mutants of Salmonella typhimurium
           (small crystals applied directly to surface of plate).

        0  Fahrig (1974) reported that  diuron (purity  not specified) was not
           mutagenic in a liquid  holding test for mitotic gene conversion in
           Saccharomyces cerevisiae, in a liquid holding test for forward mutation
           to streptomycin resistance  in Escherichia coli, in a spot test for
           back  mutation in £. marcescens or  in  a spot test for forward mutation
           in _E. coli.

        0  Recent studies by DuPont  (1985)  did not detect evidence of mutagenic
           activity for diuron in reversion tests in several strains of £.
           typhimurium (with or  without metabolic activation), in a Chinese
           hamster ovary/hypoxanthine  guanine phosphoribosyl-transferase (CHO/HGPRT)
           forward gene mutation  test or in unscheduled  DNA synthesis tests in
           primary rat hepatocytes.  However, in an in vivo cytogenetic test in
           rats, diuron was observed to cause clastogenic effects.

      Carcinogenicity

        0  Hodge et al. (1964b,  1967)  fed Wistar rats  (35/sex/dose) diuron (80%
           wettable powder) in the diet at  levels of  0,  25, 125,  250 or 2,500 ppm
           a.i.  for 2 years.  Assuming  that 1 ppm in  the diet of rats corresponds
           to 0.05 mg/kg/day (Lehman,  1959),  this corresponds to doses of 0,
           1.25, 12.5 or 125 mg/kg/day. There was some early mortality in males
           at 250 and 2,500 ppm,  but the authors ascribed this to viral infection.
           Histological examination  of  tissues showed  no evidence of changes
           related to diuron;  however,  only 10 animals or fewer were examined
           per group.  Tumors  and neoplastic  changes observed were similar in
           exposed and control groups,  and  the authors concluded  there was  no
           evidence that diuron  was  carcinogenic in rats.


V. QUANTIFICATION OF TOXICOLOGICAL  EFFECTS

        Health Advisories (HAs)  are  generally determined for one-day, ten-day,
   longer-term  (approximately  7  years)  and  lifetime exposures if adequate data

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are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula:

              HA = (NOAEL or LOAEL) x (BW) . 	   „  (	   /L,
                     (UF) x (	 L/day)

where:

        NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
                         in mg/kg bw/day.

                    BW = assumed body weight of a child (10 kg) or
                         an adult (70 kg).

                    UF = uncertainty factor (10,  100 or 1,000), in
                         accordance with NAS/ODW guidelines.

             ____ L/day = assumed daily water consumption of a child
                         (1 L/day) or an adult (2 L/day).

One-day Health Advisory

     No suitable information was found in the available literature for use in the
determination of the One-day HA value for diuron.  It is, therefore, recommended
that the Ten-day HA value for a. 10-kg child, calculated below as 1.0 mg/L
(1,000 ug/L) be used at this time as a conservative estimate of the One-day
HA value.

Ten-day Health Advisory

     The study by Khera et al.  (1979) has been selected to serve as the
basis for the Ten-day HA for diuron.  In this study, pregnant rats were
administered diuron (80%) on days 6 through 15 of gestation at dose levels
of 125, 250 or 500 mg/kg/day.  Developmental effects appeared to increase in
the diuron-treated groups as compared to the control group, i.e. wavy ribs,
extra ribs and delayed ossification.  The incidence of wavy ribs was
statistically significant at 250 mg/kg/day (p <0.05).  Fetal and maternal
body weights were decreased at 500 mg/kg  (p <0.05).  A NOAEL was not determined
from this study at the lowest dose tested (LOT) based on developmental toxicity;
hence, the LOAEL for this study was 125 mg/kg/day  (LOT).

     Using a LOAEL of 125 ma/kg/day, the Ten-day HA for a 10-kg child is
calculated as follows:

     Ten-Day HA ^ (125 mg/kg/day)  (10 kg) (0.80) . uo   /L (1 000 ug/L)
                         (1,000)  (1 L/day)
where:
        125 mg/kg/day = LOAEL, based on fetotoxicity in rats exposed to
                        diuron via the diet for days 6 through 15 of gestation.

                10 kg = assumed body weight of a child.

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 Diuron                                                      August,  1987

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                  0.80  = correction factor to account for 80% active ingredientc

                 1,000  = uncertainty factor,  chosen in accordance with NAS/ODW
                         guidelines for use with a LOAEL from an animal study.

               1  L/day  = assumed daily water consumption of a child.

 Longer-term Health  Advisory

      The 90-day  feeding study in rats by Hodge et al. (1967) has been chosen
 to serve as the  basis  for determination of the Longer-term HA values for diuron,
 In this study,  five animals  per sex were fed diuron (98% pure) at dose levels
 of 0, 2.5,  25 or 250 mg/kg/day.  Based on decreased weight gain and
 methemoglobinemia,  this study identified a NOAEL of 2.5 mg/kg/day and a LOAEL
 of 25 mg/kg/day. These values are supported by the 42-day feeding study of
 Hodge et al. (1964b),  in which a NOAEL of 20 mg/kg/day and a LOAEL of 100
 mg/kg/day were identified.  This study was not selected, however, since the
 duration of exposure was only 42 days.

      Using a NOAEL  of  2.5 mg/kg/day, the Longer-term HA for a 10-kg child
 is calculated as follows:

        Longer-term  HA  - (2'5 mg/kg/day) (10 kg) = 0.25 mg/L (250 ug/L)
                             (100) (1 L/day)

 where:

         2.5 mg/kg/day  = NOAEL, based on absence of effects on weight gain or
                         blood chemistry in rats exposed to diuron via the
                         diet for 90 days.

                 10  kg  = assumed body weight of a child.

                   100  = uncertainty factor, chosen in accordance with NAS/ODW
                         guidelines for use with a NOAEL from an animal study.

               1  L/day  = assumed daily water consumption of a child.

The Longer-term HA for  a 70-kg adult is calculated as follows:

        Lon<:er-term  HA  = (2.5 mg/kg/day) (70 kg) = 0.875 mg/L (875 ug/L)
                             (100) (2 L/day)
 where:
         2.5 mg/kg/day = NOAEL, based on absence of effects on weight gain or
                         blood chemistry in rats exposed to diuron via the
                         diet for 90 days.

                 70 kg = assumed body weight of an adult.

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Diuron                                                      August, 1987

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                  100 = uncertainty factor, chosen in accordance with NAS/ODW
                        guidelines  for use with a NOAEL from an animal study.

              2 L/day = assumed daily water consumption of an adult.

Lifetime Health Advisory

     The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure.  The Lifetime HA
is derived in a three-step process.  Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI).  The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s).  From  the RfD, a Drinking Water Equivalent Level
(DWEL) can be determined (Step 2).   A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult.  The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC).  The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals.  If the contaminant is classified as a
Group A or B carcinogen, according  to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986a), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.

     The 2-year feeding study in dogs by Hodge et al. (1964a, 1967) has been
selected to serve as the basis for  the Lifetime HA for diuron.  In this
study, dogs (three/sex/dose) were fed diuron at doses of 0.625, 3.12, 6.25 or
31.15 mg/kg/day of active ingredient.  Hematological alterations were observed
at 3.12 mg/kg/day or greater, and this was identified as the LOAEL.  No effects
were reported at 0.625 mg/kg/day in any parameter measured, and this was
identified as the NOAEL.  This value is supported by a lifetime study in rats
by the same authors (Hodge et al.,  1964b).  In this study, rats were fed
diuron at dose levels of 0, 1.25, 6.25, 12.5 or 125 mg/kg/day for 2 years.
Hematological changes were observed at 6.25 mg/kg/day or greater, and a NOAEL
of 1.25 mg/kg/day was identified.

     Using a NOAEL of 0.625 mg/kg/day, the Lifetime HA is calculated as
follows:

Step 1:  Determination of the Reference Dose (RfD)

                 RfD = (0.625 mq/kg/day) = 0<002 mg/kg/day
                         (100) (3)                    y   y
where:
        0.625 mg/kg/day = NOAEL, based on absence of hematological effects in
                          dogs exposed to diuron via the diet for 2 years.

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                                     -12-
                    100 = uncertainty factor chosen  in  accordance  with NAS/ODW
                          guidelines for use with a  NOAEL  from an  animal  study.

                      3 = additional uncertainty factor used  in  the Office of
                          Pesticide Programs  (U.S. EPA,  1987).   This  factor
                          is used to account for a lack of adequate chronic
                          toxicity studies in the data  base preventing estab-
                          lishment of the most sensitive toxicological end
                          point.

Step 2:  Determination of the Drinking Water Equivalent Level  (DWEL)

            DWEL =  (0*002 mg/kg/day) (70 kg) = 0.07  mg/L (70  ug/L)
                            (2 L/day)

where:

        0.002 mg/kg/day = RfD.

                  70 kg = assumed body weight of an  adult.

                2 L/day = assumed daily water consumption  of  an  adult.

Step 3:  Determination of the Lifetime Health Advisory

            Lifetime HA =  (0.07 mg/L)  (20%) = 0.014  mg/L (14  ug/L)

where:

        0.07 mg/L = DWEL.

               20% = assumed relative source contribution from water.

Evaluation  of Carcinogenic  Potential

      0  Hodge  et al.  (1964b,  1967) fed rats  (35/sex/dose)  diuron in  the diet
        at  ingested doses of  up to 125 mg/kg/day for 2  years.  Histological
        examinations did not  reveal increased frequency of tumors; however,
        fewer  than  half of  the survivors were examined.

      0  The International Agency for Research on Cancer has not  evaluated the
        carcinogenic potential of diuron.

      0  Applying the criteria described in EPA's guidelines for  assessment
        of  carcinogenic risk  (U.S. EPA, 1986a), diuron  may be classified  in
        Group  D:  not classified.  This category is  for substances with
        inadequate  animal evidence of carcinogenic!ty.

      0  Structurally related  analogue(s)  (e.g., linuron) of diuron appears to
        reflect some oncogenic activity.   In  addition,  a Russian study by
        Rubenchik et. al.  (1973) reported  gastric carcinomas  and pancreatic
        adenomas in rats  (strain not designated) given  450 mg/kg/  day for

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      Diuron                                                      August, 1987

                                           -13-
              22 months.   However,  the actual  data for the study is unavailable
              for Agency  review.


  VI.  OTHER CRITERIA,  GUIDANCE  AND  STANDARDS

           0  An Acceptable Daily Intake  (ADI) of 0.002 mg/kg/day,  based on a
              NOAEL of 0.625 mg/kg  from a dog  study and an uncertainty factor of
              300 has  been calculated  (U.S. EPA,  I986b).

           0  Residue  tolerances have  been established for diuron in or on agricul-
              tural commodities that range from 0.1 to 7 ppm (U.S.  EPA, 1985).


 VII.  ANALYTICAL METHODS

           0  Analysis of diuron is by a  high-performance liquid chromatographic
              (HPLC) method applicable to the  determination of certain carbaraate
              and urea pesticides in water samples (U.S. EPA,  1986c).  This method
              requires a  solvent extraction of approximately 1 L of sample with
              methylene chloride using a  separatory funnel.  The methylene chloride
              extract  is  dried  and  concentrated to a volume of 10 mL or less.  HPLC
              is used  to  permit the separation of compounds, and measurement is
              conducted with an ultraviolet (UV)  detector.  The method detection
              limit has not been determined for diuron, but it is estimated that the
              detection limits  for  analytes included in this method are in the
              range of 1  to 5 ug/L.


VIII.  TREATMENT TECHNOLOGIES

           0  Available data indicate  that granular-activated carbon (GAC) and
              powdered activated carbon (PAC)  adsorption and chlorination effectively
              remove diuron from water.

           0  El-Dib and  Aly (1977b) determined experimentally the Freundlich
              constants for diuron  on  GAC. Although the values do not suggest a
              strong adsorption affinity  for  activated carbon, diuron is better
              adsorbed than other phenylurea  pesticides.

           0  El-Dib and  Aly (1977b) calculated,  based on laboratory tests, that
              66 mg/L  of  PAC would  be  required to reduce diuron concentration by
              98%, and 12 mg/L  of PAC  to  reduce diuron concentration by 90%.

           8  Conventional water treatment techniques of coagulation with ferric
              sulfate, sedimentation and  filtration proved to be only 20% effective
              in removing diuron from  contaminated water  (El-Dib and Aly, 1977a).
              Aluminum sulfate  was  reportedly  less effective than ferric sulfate.
                                                                    •»
           0  Oxidation with chlorine  for 30  minutes removed 70% of diuron at a pH 7.
              Under the same conditions,  80%  of diuron was oxidized by "chlorine
              dioxide  (EL-Dib and Aly, 1977a).  Chlorination,  however, will produce
              several  degradation products whose.environmental toxic impact should

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                                     -14-
        be evaluated prior to selection of oxidative chlorination for treatment
        of diuron-contaminated water.

        The treatment technologies cited above for the removal of diuron from
        water are available and have been reported to be effective.  However,
        selection of individual or combinations of technologies to attempt
        diuron removal from water must be based on a case-by-case technical
        evaluation and an assessment of the economics involved.

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                                         -15-


IX. REFERENCES

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                                     -16-
DuPont.*  1985.  E. I. du Pont de Nemours & Co.,  Inc.  Mutagenicity  studies
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                                     -17-
Grover, R., and R.J. Hance.  1969.  Adsorption of some herbicides by soil and
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                                     -18-
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                                     -19-
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•Confidential Business Information submitted to the Office of Pesticide
 Programs.

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