August,  1987
                                      PROPHAM

                                  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, logit or  probit models.  There is no current
   understanding of the biological mechanisms involved in cancer to suggest that
   any one of these models is able 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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    Propham                                                        August, 1987

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II. GENERAL INFORMATION AND PROPERTIES

    CAS No.   122.-42-9

    Structural Formula
                                        0

                                      N-C-0-CH(CH3)2

                                      H

           Phenyl 1-methylethyl carbamate;  isopropyl-N-phenylcarbamate

    Synonyms

         0  IPC;  Aglrmin;  Ban-Hoe;  Beet-Kleen; Birgin; Chem-Hoe; Collavin;
            Ortho grass killer; Premalox;  Profam; Prophos; Tixit; Triherbide;
            Tuberit;  USAF  d-9 (Meister,  1983).

     Uses

           0  Pre- and postemergence herbicide for control  of  weeds  in alfalfa,
             clover, flax, lettuce, safflower,  spinach,  sugarbeets, lentils and
             peas and on fallow land (Meister,  1983).

     Properties   (Meister, 1983; Cohen, 1984; CHEMLAB,  1985;  TDB, 1985)

             Chemical Formula               C10H132N
             Molecular Weight               179.21
             Physical State  (25C)       White crystals
             Boiling Point (at 25 mm Hg)    
             Melting Point                  87C
             Vapor Pressure  (25C)
             Specific Gravity  (20C/20C)    1.09
             Water Solubility  (25C)        250 mg/L
             Log Octanol/Water Partition    1.22 (calculated)
               Coefficient
             Taste Threshold
             Odor Threshold
             Conversion Factor              

     Occurrence

           0  Propham has been found in 2 of 431  surface  water samples analyzed
             and in 10 of 431 ground water samples  (STORET, 1987).  Samples were
             collected at 107 surface water locations and  395 ground water locations,
             and propham was found in three states.  The 85th percentile of all
             non-zero samples was 2 ug/L in surface  water  and 10 ug/L in ground
             water sources.  The maximum concentration found  in surface water was
             2 ug/L, and in ground water it was 10 ug/L.

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Prophara                                                         August,  1987

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Environmental Fate

     0  Ring-labeled 14c-propham (purity unspecified), at 4 ppm in unbuffered
        distilled water declined to 2.4 ppm during 14 days of irradiation
        with a Pyrex-filtered light (uncharacterized) at 25C (Gusik, 1976).
        Degradation products included isopropyl 4-hydroxycarbanilate (3.5% of
        applied propham),  isopropyl 4-aminobenzoate (approximately 0.1%),
        1-hydroxy-2-propylcarbanilate (approximately 0.1%), and polymeric
        materials (10 to 12%).   No degradation occurred in the dark control
        during the same period.

     0  Under aerobic conditions,  ring-labeled 14C-propham (test substance
        uncharacterized),  at 2 ppm, degraded with a.half-life of 2 to 7 days in
        silt loam soil, (Hardies,  1979;  Hardies and Studer, 1979a), 4 to 7 days
        in loam soil (Hardies and  Studer,  1979b), and 7 to 14 days in sandy
        loam soil (Hardies and Studer,  1979c) when incubated in the dark at
        approximately 25C and 60% of water holding capacity.

     0  Under anaerobic conditions, ring-labeled I^C-propham (test substance
        uncharacterized) declined  from 8.5 to <5% of the applied radioactivity
        during 60 days of  incubation in silt loam soil in the dark at approxi-
        mately 25C and 60% of water holding capacity (Hardies 1979; Hardies
        and Studer, 1979a).  Under anaerobic conditions, ring-labeled 14C-
        propham (test substance  uncharacterized) declined from approximately
        0.08 to approximately 0.04 ppm during 61 days of incubation in loam
        soil in the'dark at approximately 25C and 60% of water holding
        capacity (Hardies  and Studer, 1979b); in sandy loam soil, the decline
        was from approximately 0.06 to 0.03 ppm during 63 days of incubation
        (Hardies and Studer, 1979c).

     0  14c-Propham (purity unspecified) at 0.2 to 20 ppm was adsorbed to two
        silt loams, a silty clay loam,  a sandy clay loam, and two sandy loam
        soils with Freundlich K  values of 0.74 and 2.72, 1.77, 0.65, and 0.27
        and 1.58, respectively (Hardies and Studer, 1979d).  Ring-labeled
        1 'kVpropham (purity unspecified) was very mobile (>98% of applied
        propham in leachate) in  30.5-cm columns of sandy clay loam and sandy loam
        soil leached with  20 inches of water (Hardies and Studer, 1979e).  It
        was less mobile in columns of Babcock silt loam (42.3% in leachate),
        silty clay loam (approximately 62% at 11- to 27-cm depth), and Wooster
        silt loam (approximately 54% at 7.6- to 15-cm depth) soils.  Aged
        (30-day) residues  were relatively immobile in Wooster silt loam soil;
        <1% of the applied radioactivity moved from the treated soil.

      0 Propham residues dissipated from the upper 6 inches of sandy loam,
        sandy clay loam, silty loam, and silty clay loam field plots with
        half-lives of 42 to 94,  57 to 160, 42 to 147, and approximately
        21  to 42 days, respectively, following application of propham (ChemHoe
        135, 3 Ib/gal F1C) at 4  and 8 Ib active ingredient (a.i.) per acre
        in September-November, 1977 (Pensyl and Wiedmann, 1979).  Residues
        were nondetectable (<0.02  ppm)  within 164 to 283 days after treatment
        at all rates and sites.   In general, propham residues in the 6- to
        12-inch depth were <0.04 ppm.  Propham (3 Ib/gal F1C) applied at
        6  Ib a.i./A in mid-May dissipated with a half-life of 10 to 15 days in

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     Propham                                                       August, 1987
             the 0- to 6-inch depth of silt loam soil (Wiedmann and Pensyl, 1981)
             Ring-labeled 14C-propham (formulated as ChemHoe 135) applied at 4 Ib
             a.i./A dissipated with a half-life of <7 days in the upper 3 inches
             of silt loam soil treated in November, 1981 (Wiedmann et al., 1982).
             The second half -life occurred approximately 133 days post-treatment.
III. PHARMACOKINETICS
     Absorption
             After oral administration of 1 , 1 00 mg/kg 1 4C-isopropyl-labeled propham
             (99% a.i.) to rats (1,100 mg/kg), ,88% of the label appeared in urine
             within 4 days.  After oral doses of 1,100 mg/kg of 1 4C-phenyl-labeled
             propham, 96% was excreted in urine and 2% was excreted in feces
             (Chen, 1979).

             Fang et al.  (1972) reported that in rats given oral doses (ranging
             from less than 4 mg/kg to 200 mg/kg) of 14C-propham (99% a.i.)
             80 to 85% was excreted in urine and 5% was expired in air, indicating
             that propham is well absorbed (85 to 98%) from the gastrointestinal
             tract.
     Distribution
             Chen. (1979) administered single oral doses of 14C-phenyl- or
             1 4C-isopropyl-labeled propham (1,100 mg/kg 99% a.i.) to rats.  Trace
             amounts of both 1 ^-phenyl- or 14C-isopropyl-labeled (0.5 to 1.2%)
             propham were present in the liver, kidneys, muscle and carcass after
             48 hours.

             Paulson and Jacobsen (1974) administered single oral doses of
             1 4C -propham (100 mg/kg 99% a.i.) to goats.  Six hours later, only low
             levels (0.2%) were detectable in milk.
     Metabolism
             Chen (1979) administered single oral doses of 1 4C-phenyl-labeled
             propham (1,100 mg/kg 99% a.i.) to rats by gavage.  Most of the dose
             (96%) was excreted in urine as metabolites.  The primary metabolites
             identified were the sulfate ester conjugate and the glucuronide
             conjugate of isopropyl 4-hydroxycarbanilate, which accounted for 78
             and 1.3%, respectively, of the total primary metabolites recovered.
             Similar studies in rats (single oral dose of 100 mg/kg) by Paulson et
             al. (1972) support the rapid metabolism and excretion of propham.  In
             these studies a third metabolite (the sulfate ester of 4-hydroxy-
             acetanilide) and a fourth (unidentified) metabolite were found to
             account for 12.3% and 8.9%, respectively, of the total metabolites
             detected in urine.  The data demonstrate that ring hydroxylation at
             the 4-position and subsequent conjugation as well as hydrolysis and
             subsequent N^acetylation occurred prior to excretion.

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    Propham                                                        August, 1987

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    Excretion
            14c-Propham is rapidly excreted primarily in the urine of rats.  Peak
            urinary concentrations were reached 6 hours post-treatment.  It was
            found that 96% and 2% of the administered dose of 14C-propham (100
            mg/kg 99% a.i.) was excreted in the urine and feces, respectively (Chen,
            1979; Paulson et al.,  1972).

            Fang et al. (1972) reported that after oral administration of ring-
            or chain-14C-labeled propham (99% a.i.) to rats, 80 to 85% of the
            administered dose was excreted in the urine over a 3-day period.  In
            animals dosed with 14C-isopropyl-labeled propham, 5% was detected as
            expired carbon dioxide.
IV. HEALTH EFFECTS
    Humans
            No information was found in the available literature on the health
            effects of propham in humans.
    Animals
       ghort-term Exposure

         0  Terrell and Parke (1977)  administered single oral doses of propham
            (technical grade, purity  not specified) to groups of 10 male and 10
            female rats and monitored adverse effects for 14 days.  Doses of
            2,000 mg/kg produced loss of righting reflex, ptosis, piloerection,
            decreased locomotor activity, chronic pulmonary disease and rugation
            and irregular thickening  of the stomach.  The acute oral LDso values
            in male and female rats were reported to be 3,000  232 mg/kg and
            2,360 118 mg/kg, respectively. A No-Observed-Adverse-Effect-Level
            (NOAEL) cannot be derived from the study because the doses used were
            too high, and adverse effects were found at all doses tested.

         0  Brown and Gross (1949) reported that when a single dose of 1,140
            m9/fcg propham (purity not specified) was administered orally to rats
            (number not specified), no adverse effects were observed.  Doses of
            2,200 to 3,320 mg/kg resulted in periods of light anesthesia.  Deep
            anesthesia was produced when 4,420 mg/kg of propham was administered,
            with subsequent death of  38% of the test animals.

         0  The acute inhalation LC5Q value in albino rats was reported to
            be 10.71 mg/L (PPG Industries, 1978).

       Dermal/Ocular Effects

         0  The acute dermal LD5Q value in albino rabbits was reported to be
            greater than 3,000 mg/kg  (PPG Industries, 1978).

         0  Propham (3% aqueous solution) was slightly irritating when applied to
            the skin and eyes of albino rabbits (PPG Industries, 1978).

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Propham                                                        August, 1987

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   Long-term Exposure

     0  Tisdel et al. (1979) fed Sprague-Dawley rats (30/sex/dose) propham
        (technical grade, purity not specified) in the diet at 0,  250, 1,000
        or 2,000 ppm for 91 days.  Assuming that 1 ppm in the diet of rats is
        equivalent to 0.05 mg/kg/day (Lehman, 1959), these levels  are equivalent
        to 0, 12.5, 50 or 100 mg/kg/day.  Following treatment, body weight,
        organ weight, growth, clinical chemistry, gross pathology  and histo-
        pathology were evaluated.  No effects were reported at 1,000 ppm
        (50 mg/kg/day) or lower in any parameters measured.  At the highest
        dose (2,000 ppm or 100 mg/kg/day) there was a significant  increase in
        spleen weight (p <0.05) and in spleen-to-body weight ratio (p <0.01)
        in males, and a 70% inhibition of plasma cholinesterase (p <0.01)  in
        females at 45 days.  Based on" the above data, a NOAEL of 1,000 ppm
        (50 mg/kg/day) was identified.


   Reproductive Effects

     0  In a report of a three-generation rat reproduction study,  Ravert
        (1978) reported data from the ?2 to weaning of the F2b generation.
        Sprague-Dawley rats (10 males or 20 females/dose) were administered
        technical grade propham (purity not specified) in the diet at dose
        levels of 0,  87.5, 250, 750 or 1,500 ppm for 9 weeks prior to breeding
        for each parental generation.  Assuming that 1 ppm in the  diet of
        rats is equivalent to 0.05 mg/kg/day (Lehman, 1959), these levels  are
        equivalent to 0, 4.4,  12.5,  37.5 or 75 mg/kg/day.  It was  not clear
        whether the test animals were also fed propham-containing  diets
        during pregnancies or through weaning of offspring.  No effects were
        reported on fertility,  mortality or pup development at any dose level
        tested.

   Developmental Effects

     0  Ravert and Parke (1977) administered technical propham (purity not
        specified) by gavage to pregnant Sprague-Dawley rats (16 to 20/dose),
        at levels of  0,  37.6,  376 or 1,879 mg/kg/day on days 6 through
        15 of gestation.  End points that were monitored included  maternal
        and fetal body weight and the number of corpora lutea, implants, live
        fetuses and dead fetuses.   Fetuses were also examined for  soft-tissue
        and skeletal  anomalies.  The only effects detected were reduced
        maternal and  fetal body weights and higher resorption rates at the
        highest dose  tested (1,879 mg/kg) and increased incidences of incomplete
        ossification  of the parietal and frontal bones of the skull at 375.8
        and 1,879 mg/kg.  An apparent NOAEL appears to be 37.6 mg/kg/day.
        However,  in this experiment,  the high dose (1,879 mg/kg/day is too
        high (i.e., one-half of the  LDso);  nearly two-thirds of the pregnant
        rats at this  dose died  prior to scheduled sacrifice.  Further,  the dose
        intervals are also relatively large.   Therefore,  a reliable NOAEL  can
        not be determined accurately due to the large difference in dosages
        tested and the marginal effect noted at 376 mg/kg/day (For more
        information on the developmental effects,  see Worthing,  1979).

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   Propham                                                       August,  1987

                                        -7-


      Mutagenicity

        0  Using the Ames  Salmonella  test, Margard  (1978)  reported  that propham
           (purity not specified,  1,000  ug/plate) did  not  show any  indications
           of mutagenic activity either  with  or  without activation.

        0  When propham (100 ug/mL, purity not specified)  was  applied to cultures
           containing BALB/c 3T3 cell lines,  no  clonal transformation was evident
           (Margard,  1978).

        0  Friedrick and Nass (1983)  reported that  propham (1.1  to  2.2 mM)  did
           not induce mutation in  S49 mouse lymphoma cells.

      Carcinogenicity

        0  Innes et al. (1969) administered propham to C57BL/6XC3H/AMF or
           C57BL/6XAKR mice  (18/sex)  in  the diet at 560 ppm  for 18  months.
           Assuming that 1 ppm in  the diet of mice  is  equivalent to 0.15 mg/kg/day
           (Lehman, 1959), this corresponds to a dose  of about 84 mg/kg/day.
           The incidence of  tumors was not significantly increased  (p >0.05)
           for any tumor type in any  sex-strain  subgroup or  in the  combined
           sexes of either strain. This duration of exposure  and this dose
           level may not be  sufficient for detecting late-occurring tumors.

        0  Hueper (1952) fed 15 Osborne  Mendel rats (sex not specified) dietary
           propham (20,000 ppm, purity not specified)  for  18 months.   The animals
           were alternately  placed from  1 to  2 months  on the diet followed by
           1  to 2 weeks on normal  diet.   Assuming that 1 ppm in the diet of rats
           is equivalent to  0.05 mg/kg/day  (Lehman, 1959), the dietary level was
           equivalent to 1,000 mg/kg/day.  The time-weighted average can not be
           calculated due  to a lack of detailed  reporting  of the study design.
           No tumors were  observed in 6  of 8  surviving rats  that were evaluated
           histologically.  This study is limited by the low number of animals
           used, the poor  survival rate, short duration, limited histopathological
           examination and method  of  treatment.

        0  Van Esch and Kroes (1972)  fed groups  of  23  to 26  golden  hamsters 0 or
           0.2% propham (2,000 ppm, purity not specified)  in the diet for
           33 months.  Assuming that  1 ppm in the diet of  hamsters  is equivalent
           to 0.04 mg/kg/day (Lehman, 1959),  these  levels  are  equivalent to 0 or
           80 mg/kg/day.  Based on histological  examination, the authors reported
           no significant  increase in tumor incidence.


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
   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) =  	 mg/L (	  ug/L)
                        (UF) x (   L/day)

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Propham                                                        August, 1987

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where:

        NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
                         in rag/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 information was found in the available literature that was suitable
for determination of the One-day HA value for propham.  It is, therefore,
recommended that the Ten-day HA value for a 10-kg child, 5 mg/L, be used at
this time as a conservative estimate of the One-day HA value.

Ten-day Health Advisory

     The Longer-term HA of 5 mg/L for a 10-kg child, calculated below,
is used for the 10-day HA because the apparent NOAEL (37.6 mg/kg/day) in
the teratology study by Ravert and Parke (1977) was not necessarily the
highest NOAEL, due to the large difference between the doses selected (a
ten-fold difference between 37.6 and 376 mg/kg/day).

Longer-term Health Advisory

     The study by Tisdel et al. (1979) has been selected to serve as the
basis for the Longer-term HA value for propham.  In this study, rats were fed
propham in the diet for 91 days.  At 100 mg/kg/day, plasma cholinesterase was
inhibited (70%) and spleen-to-body weight ratios were increased.  No effects
were observed at 50 mg/kg/day.  This NOAEL is supported by the NOAEL of 75
mg/kg/day identified in the three-generation reproduction study in rats by
Ravert (1978).

     Using a NOAEL of 50 mg/kg/day, the Longer-term HA for a 10-kg child is
calculated as follows:

       Longer-term HA = J50 mg/kg/day) (10 kg) , 5>0 mg/L (5,000 ug/L)
                            (100) (1 L/day)
where:
        50 mg/kg/day = NOAEL, based on the absence of inhibition of cholin-
                       esterase or effects on organ weights in rats fed
                       propham in the diet for 91 days.

               1 0 kg = assumed body weight of a child.

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Propham                                                        August, 1987

                                     -9-


                 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:

      Longer-term HA = (50 mg/kg/day) (70 kg) =17.5 mg/L (17,500 ug/L)
                           (100) (2.L/day)

where:

        50 mg/kg/day = NOAEL, based on the absence of inhibition of cholin-
                       esterase or effects on organ weights in rats fed
                       propham in the diet for 91 days.

               70 kg = assumed body weight of an adult.

                 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.

     No chronic study was found in the available literature that was suitable
for determination of the Lifetime HA value for propham.  The chronic studies
by Innes et al. (1969), Hueper (1952) and Van Esch and Kroes (1972) did not
provide adequate data on noncarcinogenic end points.  In the absence of
appropriate chronic data, the 90-day study by Tisdel et al. (1979), which

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Propham                                                        August, 1987

                                     -10-


identified a NOAEL of 50 mg/kg/day and was selected to serve as the basis for
the Longer-term HA, has also been selected for deriving the Lifetime HA.

     Using this study, the Lifetime HA is calculated as follows:

Step 1:  Determination of the Reference Dose  (RfD)

                    RfD =  (50 mg/kg/day) = Q.017 mg/kg/day
                            (1,000) (3)

where:

        50 mg/kg/day = NOAEL, based on the absence of any cholinesterase
                       inhibition or effects on organ weights in rats fed
                       propham in the diet for 91 days.

               1,000 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a NOAEL from an animal study
                       of less-than-lifetime duration.

                   3 = additional uncertainty factor used in the Office of
                       Pesticide Programs (OPP) Guidance for Establishing RfD
                       dated May 1, 1987 as an Addendum, to TOX SOP #1002).
                       This factor is used to account for a lack of adequate
                       chronic toxicity studies in the data base, preventing
                       establishment of the most sensitive toxicological end
                       point.

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

           DWEL =  (0*017 mg/kg/day) (70 kg) = 0.595 mg/L (595 ug/L)
                          (2 L/day)
where:

        0.017 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 =  (0.595 mg/L)"(20%) = 0.12 mg/L (120 ug/L)

where:

        0.595 mg/L = DWEL.

              20%  = assumed relative source contribution from water.

Evaluation of Carcinogenic Potential

     0  The International Agency for Research on Cancer (IARC, 1976) evaluated
        propham and concluded that the carcinogenic potential is indeterminate.

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      Propham                                                 August, 1987

                                          -11-


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


  VI. OTHER CRITERIA, GUIDANCE AND STANDARDS

           0  No information on other existing criteria, guidelines and standards
              was found in the available  literature.


 VII. ANALYTICAL METHODS

           0  Analysis of propham is by a high-performance liquid chromatographic
              (HPLC) method applicable to the determination of certain carbamate
              and urea pesticides in water samples (U.S. EPA, 1986b).  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.
              Compounds are separated by  HPLC, and measurement is conducted with a
              UV detector.  The method detection limit has not been determined for
              propham, 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 (GAG) adsorption
              will remove propham from water.

           0  Whittaker (1980) experimentally determined adsorption isotherms for
              propham on GAG.

           0  Whittaker (1980) reported the results of studies with GAG columns
              operating under bench scale conditions.  At a flow rate of
              0.8 gal/min/sq ft and an empty bed contact time of 6 minutes, propham
              breakthrough (when effluent concentration equals 10% of influent
              concentration) occurred after 720 bed volumes (BV).

           0  In the same study, Whittaker (1980) reported the results for seven
              propham bi-solute solutions when passed over the same GAC continuous-
              flow column.

           0  The studies cited above indicate that GAC adsorption ia the most
              promising treatment technique for the removal of propham from water.
              However, selection of individual or combinations of technologies for
              propham removal from water  must be based on a case-by-case technical
              evaluation and an assessment of the economics involved.

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    Propham                                                        August, 1987

                                         -12-


IX. REFERENCES

    Brown, J.H. and P. Gross.*  1949.  Acute toxicity .study of isopropyl n-phenyl
         carbamate.  Unpublished study.  MRID 00075264.

    CHEMLAB.  1985.  The Chemical Information System, CIS, Inc., Bethesda, MD.

    Chen, Y.*  1979.  Summary of animal metabolism of IPC.  Unpublished study.
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    Cohen, S.Z.  1984.  List of potential groundwater contaminants.  Memorandum
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    Fang, S.C., E. Fallin, M.L. Montgomery et al.*  1972.  Metabolic studies of
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    Fang, S.C. and E. Fallin. 1974.  Metabolic studies of 14C-labeled propham
         and chlorophropham in the female rat.  Pest. Biochem. Physiol. 4:1-11.

    Friedrick, U. and G. Nass.  1983.  Evaluation of a mutation test using S49
         mouse lymphoma cells and monitoring simultaneously the induction of
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         Mutat. Res.  110:147-162.

    Gusik, F.F.*  1976.  Photolysis of carbon 14 ring-labeled isopropyl carbanilate
          (IPC) in water.  Unpublished study received Sept. 17, 1979 under 748-224;
         submitted by PPG Industries, Inc., Barberton, OH; CDL:240988-C.  MRID
         00115466.

    Hardies, D.E.*  1979.  Metabolism of isopropyl carbanilate on a Wooster silt
         loam soil:  BR 21422.  Unpublished study received Sept. 17, 1979 under
         748-224; submitted by PPG Industries, Inc., Barberton, OH; CDL:240988-1.
         MRID 00115472.

    Hardies, D.E. and D.Y. Studer.*  1979a.  Metabolism of isopropyl carbanilate
         on a Woodburn silt loam soil:  BR 21448.  Unpublished study received
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    Hardies, D.E. and D.Y. Studer.*  1979b.  Metabolism of isopropyl carbanilate
         on an Altvan loam soil:  BR 21531.  Unpublished study received Sept. 17,
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    Hardies, D.E. and D.Y. Studer.*  1979c.  Metabolism of isopropyl carbanilate
         on a Hanford sandy loam:   BR 21566.  Unpublished study received
         Sept. 17, 1979 under 748-224; submitted by PPG Industries, Inc., Barberton,
         OH; CDL:240988-G.  MRID 00115470.

    Hardies, D.E. and D.Y. Studer.*  1979d.  Absorption of isopropyl carbanilate
         on five soil types:  BR 21590.  Unpublished study received Sept. 17,
         1979 under 748-224; submitted by PPG Industries, Inc., Barberton, OH;
         CDL:240987-C.  MRID 00038945.

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                                     -13-
Hardies, D.E. and D.Y. Studer.*  1979e.  A laboratory study of the leaching of
     isopropyl carbanilate in soils.  Unpublished study prepared and submitted
     on Nov. 1, 1984, by PPG Industries, Inc., Chemical Division, Barberton,
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Hueper, W.C.*  1952.  Carcinogenic studies on isopropyl-n-phenyl-carbamate.
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IARC.  1976.  International Agency for Research on Cancer.  IARC monographs
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Innes, J., B. Ulland, M.G. Valerio, L. Petrucelli, L. Fishbein, E. Hart and
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Lehman, A.j.  1959.  Appraisal of the safety of chemicals in foods, drugs and
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Margard, W.*  1978.  Summary report on in vitro bioassay of selected compounds.
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Meister, R., ed.  1983.  Farm chemicals handbook.  Willoughby, OH:  Meister
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Paulson, G. and A. Jacobsen.*  1974.  Isolation and identification of
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Paulson, G., A. Jacobsen and R. Zaylskie.*  1972.  Propham metabolism in the
     rat and goat:  Isolation and identification of urinary metabolites.
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Pensyl, J. and J.L. Wiedmann.*  1979.  Field dissipation of IPC and PPG-124
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PPG Industries, Inc.*  1970.  Primary rabbit eye irritation study.  Inter-
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PPG Industries, Inc.*  1978.  Study:  IPC toxicity to test subjects.
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Ravert, J.*  1978.  Three generation reproductive study of IPC in Sprague
     Dawley rats.   Unpublished study.  MRID 00115425.

Ravert, J. and G.  Parke.*  1977.  Investigation of teratogenic and toxic
     potential of IPC-50%-rats.  Unpublished study.  MRID 00115434.

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                                     -1 4-
Ryan, A.J.  1971.   The metabolism  of carbamate pesticides.  CRC Grit.  Rev.
     Toxicol.  1:33-51.

STORET.   1987.

TDB.  1985.  Toxicology Data Bank.  Medlars II.  National Library of  Medicine's
     National  Interactive Retrieval Service.

Terrell,  Y., and G. Park.*  1977.  Acute oral toxicity in rats (IPC technical).
     Unpublished study.  MRID 00115421.

Tisdel, M., G. Rao, G. Thomson et al.*  1979.  IPC  (propham) subchronic oral
     dosing study  in rats.  Unpublished study.  MRID  00128777.

U.S. EPA.   1986a.  U.S. Environmental Protection Agency.  Guidelines  for
     carcinogen risk assessment.  Fed. Reg.  51(185)33992-34003.  September 24.

U.S. EPA.   1986b.  U.S. Environmental Protection Agency.  U.S. EPA Method  #4
     - Determination of Pesticides in Ground Water  by HPLC/UV, January 1986
     draft.  Available from U.S.  EPA's Environmental Monitoring and  Support
     Laboratory, Cincinnati, OH.

Van Esch, G.J., and R. Kroes.  1972.  Long-term toxicity studies of chloro-
     propham and propham in mice  and hamsters.  Food  Cosmet. Toxicol.
     10:373-381.

Whittaker, K.F.  1980.  Adsorption of selected pesticides by activated carbon
   .  using isotherm and continuous flow column systems.  Ph.D. Thesis.
     Lafayette, IN:  Purdue University.

Wiedmann, J.L., and J. Pensyl.*   1981.  Dissipation of IPC and PPG-124 in  soil
     treated with  ChemHoe 135   Spring 1980:  BR 22412.  Unpublished study
     received  Dec. 20, 1982 under 748-224; submitted  by PPG Industries, Inc.,
     Barberton, OH; CDL:249100-A.  MRID 00121299.

Wiedmann, J.L., D. Mattle, D.R. Coffman and J. Pensyl.*  1982.  Determination
     of IPC and PPG-124 residues  in soil treated with carbon 14 labeled
     Chemhoe 135:  BR 22882.  Unpublished study received Dec. 20, 1982 under
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Worthing, C.R.  1979.  Pesticide  manual, 6th ed.  British Crop Protection
'     Council,  Worchestershire, England.
Confidential Business Information submitted to the Office of Pesticide
 Programs.

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