820K88105                            AU9USt- 1987
                                     AMETRYN               DRAFT
                                                           •^•1^%I   B
                                 Health Advisory
                             Office of Drinking Water
                       U.S. Environmental Protection Agency
        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

        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 accuratel> than another.
   Because each  model is based on differing assumptions, the estimates that are
   derived can differ by several orders of magnitude.

                                                                August,  1987

    CAS No.  834-12-8

    Structural Formula
     0  N-ethyl-Nt-(1-methylethyl)-6-(methylthio)-1,3,5-triazine-2,4-diamine;
        Ametrex; Ametryne; Cemerin;  Crisatine; Evik SOW; Gesapax (WSSA, 1983;
        Meister, 1983).


     0  A selective herbicide for control of broadleaf and grass weeds in
        pineapple, sugarcane, bananas and plantains.  Also used as a post-
        directed spray in corn, as a potato vine dessicant and for total
        vegetation control (WSSA, 1983).

Properties   (WSSA, 1983)

        Chemical Formula
        Molecular Weight
        Physical State
        Boiling Point
        Melting Point
        Vapor Pressure
        Specific Gravity
        Water Solubility
        Log Octanol/Water Partition
        Taste Threshold
        Odor Threshold
        Conversion Factor              — •


     0  Ametryn has been found in 3 of 1,246 surface water samples analyzed
        and in 27 of 653 ground water samples (STORET, 1987).  Samples were
        collected at 211 surface water locations and 544 ground water
        locations, and ametryn was found in 6 states.  The 85th percentile of
                                           Colorless crystals
                                           84 to 85°C

                                           8.4 x 10~7 mm Hg

                                           185 mg/L
                                           -1.72 (calculated)

     Ametryn                                                     August* 1987


             all nonzero samples  was 0.1  ug/L in surface water and 210 ug/L in
             ground water sources.   The maximum concentration found was 0.1 ug/L
             in surface water  and 450 ug/L in ground water.

     Environmental Fate

          0  In aqueous solutions,  ametryn is stable to natural sunlight,  with a
             half-life of greater than 1  week.  When exposed to artificial light
             for 6 hours,  75%  of  applied  ametryn remained.   One photolysis product
             was identified  as 2-ethylamino-4-hydroxy-6-isopropylaminos-triazine
             (Registrant CBI data).

          0  Ametryn is stable to photolysis on soil (Registrant CBI data).

          0  Soil metabolism of ametryn,  under aerobic conditions, proceeds with
             a half-life of  greater than 2 to 3 weeks.  Metabolic products include
             2-amino-4-isopropylamino-6-methylthio-s-triazine, 2-amino-4-ethylamino-
             6-methylthio-s-triazine and 2,4-diamino-6-methylthio-triazine.  Under
             anaerobic conditions the rate of metabolism decreases (t-|/2 = 122 days)
             (Registrant CBI data).

          0  Under sterile conditions ametryn does not degrade appreciably.  There-
             fore, microbial degradation is a major degradation pathway (Registrant
             CBI data).

          0  Neither ametryn nor  its hydroxy metabolite leach past 0 to 6 in. depth
             with normal rainfall.   However, since both compounds are persistent
             they may leach  under exaggerated rainfall or flood and furrow irrigation.
             This behavior is  seen with other triazines (Registrant CBI data).

          0  Ametryn's Freundlich soil-water partition coeficient values,  Kd, range
             from 0.6 in sands to 5.0 in silty clay soils.   Specifically,  the Kd
             for a sandy loam  is  4.8, and for 2 silty loams, 3.8 and 2.8,

          0  In the laboratory, Ametryn has a half-life of  36 days.  In the field,
             Ametryn degraded  with a half-life of 125 to 250 days (Registrant CBI


          8  Oliver et al.  (1969)  administered 14C-labeled ametryn orally to
             Sprague-Dawley rats.   Investigators stated that ametryn was admini-
             stered by stomach tube to animals at dosage levels from 1  to 4 mg
             per animal.  When the label was in the ring,  32.1* was excreted in
             the feces, indicating that over 70% had been  absorbed.  When the
             label was in the ethyl or isopropyl side chains,  only 2 to 5% was
             excreted in  the feces.

   Ametryn                                                 «   August,  1987



        0  Oliver et al.  (1969) administered ring-labeled ametryn orally  to
           male and female Sprague-Dawley rats and measured distribution  of
           label in tissues at 6, 48 and 72 hours after dosing.  Tissue distri-
           bution at 6 hours was greatest in kidney, followed by liver, spleen,
           blood, lung, fat, carcass, brain, and muscle.  Blood levels  remained
           relatively constant for 72 hours after dosing, while all other tissue
           levels dropped rapidly to <0.1% of dose per gram of tissue.


        0  Oliver et al.  (1969) administered 14C-labeled ametryn orally to
           groups of six  male and six female Sprague-Dawley rats.  When the
           label was in the isopropyl side chain, 41.9% of the label  appeared as
           C02.  When the label was in the ethyl side chain,  18.1% of the label
           appeared as CO2.  This indicated that the side chains were extensively
           metabolized.   When the ring was uniformly labeled with carbon-14 and
           the compound fed orally to rats, 58% was excreted  in the urine but it
           was not determined whether excretion of the original compound  or
           metabolites had occurred.
           Oliver  et  al.  (1969) studied  the  excretion  of  ametryn  utilizing
           uniformly  labeled compound with 14C-ametryn in  the ring or  in  the
           ethyl or isopropyl side chains.   Forty-eight hours after oral  dosing
           of  six  male  and  six female Sprague-Dawley rats,  57.6%  of the ring
           labeled activity had been excreted  in  the urine with 32.1%  excreted
           in  the  feces (total 89.7% of  dose).  When the  fed compound  was labeled
           in  the  side  chains, however,  much of the  14C was excreted in expired
           air as  carbon  dioxide.  When  fed  compound labeled in the isopropyl
           side chain,  rats excreted 41.9% of  the label in expired air 20% in
           the urine,  2%  in the feces and 7% remained  in  the carcass  (total
           70.9%)  at  48 hours.  When the ethyl side chain contained the label,
           18.1% of the label was excreted as  carbon dioxide, 45% in the  urine,
           5%  in the  feces  and 9% remained in  the carcass (total  77.1% of dose).
           After 72 hours,  total recovery was  approximately 88% for both  of the
           side-chain labeled compounds.
            No information was  found  in  the available  literature  on the health
            effects  of ametryn  in humans.
       Short-term Exposure

         0  The following acute oral 1.050  values .for ametryn in rats  were
            reported:   Charles River CD rats,  1,207 mg/kg  (males),  1,453 mg/kg

Ametryn                                                     August, 1987

        (females)  (Grunfeld,  1981); mixed male and female rats (strain not
        specified),  1,750 mg/kg (Stenger and Planta, 1961a); male and female
        Wistar rats,  1,750 mg/kg (Consultox Laboratories Limited, 1974).

     0  Piccirillo (1977) reported the results of a 28-day feeding study in
        male and female mice.   Animals were 5 weeks of age and weighed
        21 to 28 g at the beginning of the study.  Animals (five/sex/dose)
        were fed diets containing 0, 100, 300, 600, 1,000, 3,000, 10,000 or
        30,000 ppm of ametryn  (technical).  Based on the assumption that 1 ppm
        in the diet of mice is equivalent to 0.15 mg/kg/day (Lehman, 1959),
        these doses  correspond to 0, 15, 45, 90, 150, 450, 1,500 or 4,500
        mg/kg/day.  At 30,000  ppm in the diet, all animals died within 2
        weeks.  At 10,000 ppm, 3 of the 10 died within 2 weeks.  No other
        deaths occurred at any other dose level.  Clinical signs in the two
        highest dose groups included hunched appearance, stained fur and
        labored respiration.   At the 3,000-ppm dose level, only 1 of the
        10 animals showed clinical signs of toxicity.  Body weight gain was
        comparable in all survivors by the end of week 4.  Gross pathology in
        animals that died showed a dark-red mucosal lining of the gastro-
        intestinal tract and ulcerated areas of the gastric mucosa.  There
        was no histopathological examination of tissues in this study.

     0  Stenger and Planta (1961b) reported a 28-day study of the toxicity
        of ametryn in rats. Dose levels of 100, 250 or 500 mg/kg/day were
        administered 6 days/week by gavage to groups of five male and five
        female rats.   The study indicated that there was a control group but
        no data were given. At the 500-mg/kg/day dose level, animals became
        emaciated, weight gain was limited and 7 of 10 rats died.  Histo-
        pathological examination of the animals that died indicated severe
        vascular congestion, centrilobular liver necrosis and fatty degeneration
        of individual liver cells.  At 250 mg/kg/day, 1 of 10 rats died
        during the study and there was depressed growth rate in the survivors.
        Histological examination of liver, kidney, spleen, pancreas, heart,
        lung, intestine and gonads showed no major degenerative changes.  No
        effects were reported  in animals administered 100 mg/kg/day, which
        was identified as the  No-Observed-Adverse-Effect-Level (NOAEL) in
        this study.

     0  Ceglowski  et al.  (1979) administered single oral doses of 88 or 880
        mg/kg of ametryn to mice 5 days before, on the day of or 2 days after
        immunization with sheep erythrocytes ('purity not specified).  All
        mice receiving the highest dose (880 mg/kg) of ametryn had significant
        depression of splenic  plaque-forming cell numbers when assayed 4 days
        later.  Animals receiving the low dose showed no effect.   Similarly,
        animals receiving 88 mg/kg for 8 or 28 consecutive days prior to
        immunization exhibited no significant reduction in antibody plaque

   Dermal/Ocular Effects

     0  Two of six rabbits showed mild skin irritation when ametryn was left
        in contact with intact or abraded skin (500 mg/2.5 cm2) for 24 hours
        (Sachsse and Ullmann,  1977).

Ametryn                                                     August, 1987

     0  In a sensitization study with Perbright White guinea pigs (Sachsse
        and Ullmann, 1977), 10 male and 10 female guinea pigs weighing 400
        to 450 g received 10 daily intracutaneous 0.1-mL injections of 0.1%
        ametryn in polyethylene glycol:saline (70:30).  Fourteen days after
        the last dose,  animals were challenged by an occlusive dermal applica-
        tion of ametryn or by an intradermal challenge.  Animals showed no
        sensitization reaction following the dermal application of the challenge
        dose but there was a positive response after the intradermal challenge«

     0  Kopp (1975) found that ametryn (technical grade) placed in the eyes
        of rabbits produced slight conjunctiva! redness at 24 hours.  This
        cleared completely within 72 hours.

     0  Sachsse and Bathe (1976) applied 2,150 mg/kg or 3,170 mg/kg ametryn
        in suspension to the shaved backs of five male and five female rats
        weighing 180 to 200 g.  Hie occlusive covering was removed at
        24 hours, the skin was washed and animals were observed for 14 days.
        There was no local irritation or adverse reaction, and at necropsy
        there were no gross changes in the skin.  The acute dermal LDgQ in
        male and female rats was reported to be >3,170 mg/kg.

     e  Ametryn (2,000 mg/kg) was applied daily to the skin of five male and
        five female rats weighing approximately 200 g (Consultox Laboratories
        Limited, 1974).  After 14 days of treatment, no deaths had occurred
        and no other effects were reported.  The 14-day dermal LDsg was re-
        ported to be >2,000 mg/kg/day.

   Long-term Exposure

     0  Domenjoz (1961) administered ametryn in water via stomach tube
        6 days/week for 90 days to Meyer-Arendt rats (1 2/sex/dose).  Ttie
        initial material was 50% ametryn in a powder vehicle.  Two dose
        levels of the material (20 or 200 mg/kg/day) provided dose levels of
        ametryn of 10 or 100 mg/kg/day.  Two control groups were included;
        one group received water only and the other received the powder
        vehicle only suspended in water.  Over the 90-day period, all animals
        gained weight at comparable rates and there was no visible effect on
        appearance or behavior.  One control rat and one rat in the 100-mg/kg
        dosage group died.  This death was not considered compound-related.
        At the 90-day necropsy, organ-to-body weight ratios were comparable
        to controls.  Liver, Sidney, spleen, heart, gonads, small intestine,
        colon, stomach, thyroid and lung were microscopically examined.  The
        Lowest-Observed-Adverse-Effect-Level (LOAEL) was associated with fatty
        degeneration of the liver.  Based on this study, a LOAEL of 100 mg/kg/day
        (the highest dose tested) was identified.  All tissues were comparable
        to controls at the lowest dose (10 mg/kg/day), which was identified
        as the NOAEL.

   Reproductive Effects

     e  No information was found in the available literature on the reproduc-
        tive effects of ametryn.

   Ametryn                                                     August,  1987


      Developmental Effects

        •  No information was  found  in the available literature on the  developmental
           effects  of ametryn.


        0  Anderson et al. (1972)  reported that ametryn was not mutagenic in
           eight strains  of  Salmonella typhimurium.   No metabolic activating
           system was utilized.

        0  Simmons  and Poole (1977)  also reported that ametryn was not  mutagenic
           in five  strains of  Salmonella typhimurium (TA 98, 100, 1535, 1537 and
           1538), with or without  metabolic  activation provided by an S9 fraction
           from rats pretreated  with Aroclor 1254.

        0  Shirasu  et al. (1976) reported ametryn was not mutagenic in  the
           rec-assay system utilizing two strains of Bacillus subtilis, in
           reversion assays  utilizing auxotrophic strains of Escherichia coli
           (WP2) and in _S. typhimurium strains TA 1535, 1536, 1537 and
           1538 (without  metabolic activation).


        0  No information was  found  in the available literature on the  carcinogenic
           effects  of ametryn.


        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) . 	   /L (	   /L)
                         (UP) x (    L/day)
           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).

Ametryn                                                     August, 1987


One-day Health Advisory

     No data were found in the available literature that were suitable for
determination a One-day HA value for ametryn.  It is, therefore, recommended
that the Ten-day HA value for the 10-kg child (8.6 mg/L, calculated below) be
used at this time as a conservative estimate of the One-day HA value.

Ten-day Health Advisory

     The study by Stenger and Planta (1961b) has been selected to serve as
the basis for determination of the Ten-day HA value for the 10-kg child.
This study identified a NOAEL of 100 mg/kg/day, based on normal weight gain
and absence of histological evidence of injury in rats following 28 days of
exposure by gavage.  The study also identified a LOAEL of 250 mg/kg/day,
based on reduced body weight gain, although no major histological changes
were noted.  One death occurred in the 250-mg/kg/day group, but it could not
be determined if this was compound-related.  The NOAEL identified in this
study (100 mg/kg/day) is supported by the 28-day feeding study in rats by
Piccirillo (1977), which identifed a NOAEL of 150 mg/kg/day and a LOAEL of
450 mg/kg/day, and by the study of Ceglowski et al. (1979), which identified
a NOAEL of 88 mg/kg/day and a LOAEL of 880 mg/kg/day.

     Using the NOAEL of 100 mg/kg/day, the Ten-day HA for a 10-kg child is
calculated as follows:

      Ten-day HA = (100 mg/kg/day) (10 kg)  (6/7) z 8.6 mg/L (8,600 ug/L)
                          (100)  (1 L/day)


        100 mg/kg/day • NOAEL, based on absence of effects on weight gain
                        or histology in rats dosed by gavage for 28 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 a study in animals.

                  6/7 * conversion from 6 to 7 days.

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

Longer-term Health Advisory

     The 90-day oral dosing study in rats by Domenjoz (1961) has been selected
to serve as the basis for determination of the Longer-term HA.  At two dose
levels  (10 or 100 mg/kg/day), no deaths were reported and no other effects
were noted during the 90-day period.  Terminal necropsy findings and histo-
logical examination of tissues from treated animals were comparable to
controls.  At the highest dose tested, there was fatty degeneration in the
livers examined.  Based on these data, a NOAEL of 10 mg/kg/day (the lowest
dose tested) was identified.

  Ametryn                                                   August, 1987


     The Longer-term HA for a 10-kg child is calculated as follows:

     Longer-term HA » (10 mg/kg/day) (10 kg) (6/7) . 0>86 mg/L (860   /L)
                            (100) (1 L/day)
         10 mg/kg/day = NOAEL,  based on the absence of histological evidence
                        of toxicity in rats exposed to ametryn via gavage 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 a study in animals.

                  6/7 = conversion from 6 to 7 days of exposure.

              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 = (10 mg/kg/day) (70 kg) (6/7) . 3   /L (3,000 ug/L)
                            (100) (2 L/day)


         10 mg/kg/day = NOAEL,  based on the absence of histological evidence
                        of toxicity in rats exposed to ametryn via gavage for
                        90 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 a study in animals.

                  6/7 = conversion from 6 to 7 days of exposure.

              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

Ametryn                                                     August, 1987

        concentration equals 10% of influent concentration) occurred after
        896 bed volumes (BV).  When a bi-solute ametryn-propham solution was
        passed over the same column, ametryn breakthrough occurred after 240 BV.

        In a laboratory study (Nye, 1984) GAC was employed as a possible
        means of removing ametryn from contaminated wastewater.  Ihe results
        show that the column exhaustion capacity was 111.2 mg ametryn adsorbed
        on 1 g of activated carbon.

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

    Ametryn                                                     August, 1987



    Anderson,  K.J.,  E.G.  Leighty and M.T.  Takahasi.   1972.  Evaluation of herbicides
         for possible mutagenic activity.   J. Agr.  Food Chem.  20:649-656.

    Ceglowski, W.S., D.D.  Ercegrovich and  N.S. Pearson.  1979.  Effects of pesticides
         on the reticuloendothelial system.   Adv.  Exp. Med. Biol.  121:569-576.

    CFR.   1985.  Code of  Federal Regulations.  July  1, 1985.  40 CFR 180.258.
         pp. 300-301.

    Consultox Laboratories Limited.*  1974.   Ametryn:   Acute oral and dermal toxieity
         evaluation.  Unpublished study.   MRID 00060310.

    Domenjoz, R.  1961.*   Ametryn:   Toxieity in long-term administration.  Unpub-
         lished study. MRID 00034838.

    Grunfeld,  Y.  1981.*   Ametryn 80 w.p.:  Acute oral toxieity in the rat.
         Unpublished study.  MRID 00100573.

    Kopp, R.W.*  1975. Acute eye irritation potential study in rabbits.  Final
         Report.  Project No. 915-104.   Unpublished  study.  MRID 00060311.

    Lehman, A.J.  1959.   Appraisal of the  safety of  chemicals in foods, drugs and
         cosmetics.   Association of Food and Drug Officials of the United States.

    Meister, R., ed.  1983.  Farm chemicals  handbook.   Willoughby, OH:  Meister
         Publishing Co.

    Nye,  J.C.   1984.  Treating pesticide-contaminated  wastewater.  Development
         and evaluation of a system.  American Chemical Society.

    Oliver, W.H., G.S. Born and P.L. Zeimer.  1969.   Retention, distribution, and
         excretion of ametryn.  J.  Agr. Food Chem.   17:1207-1209.

    Piccirillo, V.J.*  1977.  28-day pilot feeding study in mice.  Final Report.
         Project No. 483-126.  Unpublished study.   MRID 00068169.

    Sachsse, K. and R. Bathe.*  1976.  Acute dermal  LD50 in the rat of technical
         G34162.  Project No. Siss. 5665.   Unpublished study.  MRID 00068172.

    Sachsse, K. and L. Ullmann.*  1977.  Skin irritation in the rabbit after
         single application of technical  grade G34162.  Unpublished study.
         MRID 00068174.

    Shirasu, Y., M.  Moriya, K. Kato, A. Furuhashi  and  T. Kada.  1976.  Mutagenic
         screening of pesticides in the microbial  system.  Mutat. Res.  40:19-30.

    Simmons, V.F. and D.  Poole.*  1977.  In-vitro and  in-vivo microbiological
         assays of six Ciba-Geigy chemicals.  SRI project LSC-5686.  Final. Report.
         Unpublished study.  MRID 00060642.

    Stenger, P. and V. Planta.*  1961 a.  Oral toxieity in rats.  Unpublished
         Study.  MRID 00048226.

Ametryn                                                     August,  1987

Stenger, P. and V. Planta.*  1961b.  Subchronic toxicity test no. 257.
     Unpublished study.  MRID 00048228.

STORET.  1987.

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. EPA Method #1 - Determination of nitrogen and phosphorus
     containing pesticides in ground water by GC/NPD,  January 1986 draft.
     Available from U.S. EPA's Environmental Monitoring and Support Laboratory,
     Cincinnati, OH.

WSSA.  1983.  Weed Science Society of America.  Herbicide handbook.  5th
     ed.  Champaign, IL:  Weed Society of America,  pp. 16-19.

Whittaker, K.F.  1980.  Adsorption of selected pesticides by activated  carbon
     using isotherm and continuous flow column systems.  Ph.D. Thesis,  Purdue
 •Confidential Business  Information  submitted  to  the Office of  Pesticide