August, 1968
                                1,3-OXCHLOROPROPBNK

                                  Health Advisory
                              Office of Drinking Hater
                        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.
   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.  Bxcess cancer risk
   estimates may also be calculated using  the one-felt, Heibull, 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
   assumption*, the estimates that are derived can differ by several orders of
   magnitude*

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    1,3-0ichloroprop«n«                                       August, 1988

                                         -2-


ZX. GENERAL INFORMATION AND PROPERTIES

    CAS No.    542-75-6

    Structural Foraula

                   C1CH2       H                    aCH2       Cl
                       >      /                        ^      /
                         c - c                            c - c
                        '     *                          t     \
                       H       Cl                       H       H

                        (trans)                           (eis)

                                 1/3-Dichloropropene
                          (approximately 46% trans/42% cis)
    Synonyms
            Dichloro-1,3-propene;  1,3-dlchloro-1-propene;  cis/trans-1,3-dichloro-
            propene;  1,3-0;  OCP;  D-0 (approximately  28% cis/27% trans)
    Uses
         •   OCP is the active ingredient in Telone*,  a registered trademark of
            the Dow Chemical Company.

         •   The pesticide  1, 3-dichloropropene (OCP) is a broad spectrum soil
            fumigant to control  plant  pests.   Its major use  is for nematode
            control on crops grown  in  sandy soils of  the Eastern,  Southern  and
            western U.S.

         0   The usage of OCP has increased due to cancellation of  the  once  widely
            used product containing ethylene dibromide (BOB)  and dibromochloro -
            propane (DBCP)  (U.S. EPA,  1986a).

         •   Estimated usage of OCP  containing products in  1984 to 1985 ranged from
            about 34 to 40  million  pounds (U.S.  EPA,  1986a).

    Properties  (Dow Chemical USA,  1977, 1982; Clayton and Clayton, 1981)
            Chemical  Formula
            Molecular Height                  110.98  (pure  isomers)
            Physical  State (25«C)              Pale yellow to yellow  liquid
            Boiling Point                     about 104-C (104.3*C,  cis;  112*C, trans)
            Density (25«C)                    1.21 g/mt
            Vapor Pressure (25*C)              27.3mm-Hg
            Specific  Gravity                  about 1.2 (20/20*C)
            Water Solubility (25°C)            0.1 to  about  0.25% (1  to  2.5  g/L)
                                                reported; miscible with most organic
                                                solvents
            Log Octanol/Water Partition       25
              Coefficient
            Conversion Factor (25*C)(air)      1  mg/L  » 220  ppm;  1 ppm -4.54 mg/n3

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1,3-Dlchloropropene                                       August,  1988

                                     -3-


oeeurrence

     •  In California (Madefy et al., 1982), 54 wells ware examined in areas
        where Telone or 0-0 were used for several years.  The well water did
        not have measurable aoouats of OCP «0.1 ppb).

     •  Monitoring data from New York have shown positive results for OCP in
        ground water (U.S. EPA, 1986b).

     •  In deep well sampling in southern California (65 to 1/200 foot depths),
        no DCP was detected.  In shallow wells (3 to 4 meters) around potato
        fields in Suffolk County/ NY, OCP was detected up to 138 days after
        application (OPP, 1988).

     •  OCP has been found in 41 of 1/088 surface water staples analyzed and
        in 10 of 3/949 ground water samples (STORBT, 1988).  Samples were
        collected in 800 surface water locations and 2/506 ground water
        locations; OCP was found in 13 states.  The range of concentrations
        found In ground water was 0.2 ug/L to 90 ug/L.  nie 85th percentlle
        of all non-zero samples was 1.3 ug/L in surface water and 3.4 ug/L
        in ground water*  This information is provided to give a general
        impression of the occurrence of this chemical in ground and surface
        waters as reported in the STORET database.  The individual data
        points retrieved were used as they came from STORET and have not been
        confirmed as to their validity.  STORBT data is often not valid when
        individual numbers are used out of the context of the entire sampling
        regime/ as they are here.  Therefore/ this information can only be
        used to form an impression of the intensity and location of sampling
        for a particular chemical.

Environmental Fate

     •  Available data indicate that DCP does leach to ground water.  However,
        the relative hydrolytic instability of the parent compound would
        mitigate the potential for extensive contamination (U.S. EPA/ I986b;
        U.S. EPA/ 1986c).

     •  The half-life of  1,3-OCP in soil was reported by Laskowski et al.
        (1982) to be approximately 10 days while Van Oijk (1974) reported
        3 to 37 days depending on soil conditions and analytical methods.

     •  OCP hydrolyses as a function of temperature not as a function of pH.
        At 10«C, the half-life is 51 days while at 20*C it is 10 to 13 days.
        Chloroallyl alcohol is the main hydrolytic degradate.  Some phololysis
        of OCP does occur (OPP/ 1988).

     0  In laboratory aerobic soil metabolism studies/ OCP degrades to
        chloroallyl alcohol in 20 to 30 days where soil pH is between 5.0 and
        7.0, the temperature is between 15 and 20*C and the organic matter
        content is from  1.5 to 11.6 percent in sandy loam or clay soils.  In
        anaerobic soil metabolism studies, OCP degrades to chloroallyl alcohol
        to less than 8 percent in 30 days.  For anaerobic aquatic metabolism
        studies/ the half-life was reported to be about 20 days at pBs of
        6.9 to 7.5 (OPP/  1988).

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     1,3-Oichloropropene                                       Auguat, 1983
          •  In • field dissipation study done in the Netherlands, OCP (220-250 lb/T
             injected into the soil at 9 to 19 on depths was found to move rapidly
             downward over a 2 week period.  In a similar study in Delano, CA, DCP
             was injected at 1,310 1/ha to 1,638 1/ha (-Ib/A) to 81 em.  Samples
             at 14 days noted the presence of OCP (up to 0.5 ppm) at all depths to
             8 feet (OPP, 1988).


III. PHARMACOKINETICS

     Absorption

          •  Toxicity studies indicate that OCP is absorbed from skin, respiratory
             and gastrointestinal systems (Clayton and Clayton, 1981).

          •  Oral administration of DCP in rats resulted in approximately 90%
             absorption of the administered dose (Hutson et •!., 1971).

     Distribution

          •  Radiolabeled 14C D-D (55% DCP) was administered orally in arachis
             oil in rats.  After 4 days, most of the administered dose, based on
             measured radioactivity, was recovered primarily in orine and there
             were insignificant amounts (less than 5%) remaining in the gut,
             feces, skin and carcass (Rutson et al., 1971).

     Metabolism

          •  cis-Dichlorqpropene in corn oil was given as a single oral dose
             (20 mg/kg bw) to two female Wistar rats.  Urine and feces were
             collected separately.  Die main urinary metabolite (92%) was N-*cetyl-
             S-[(cis)-3-chloroprop-2-enylJ cysteine.  The cis-DCP has also been
             shown to react with glutathione in the presence of rat liver cystol
             to produce S[(cis)-3-chloroprop-2-enyl]glutathione.  The cis-DCP is
             probably biotransformed to an intermediate glutathione conjugate and
             then follows the mercapturic acid pathway and is excreted in the
             urine as a cysteine derivitive (Climie and Morrison, 1978).

          •  Zn a study conducted by Dietz et al. (1984) rats and mice administered
             (via gavage) up to 50 and 100 mg DCP/kg bw, respectively, demonstrated
             no evidence of metabolic saturation.
     Excretion
             Zn two studies (Hutson et al., 1971} Climie and Morrison,  1978)
             1*C cis- and/or trans-DCP, administered orally in rats, were excreted
             primarily in the urine in 24 to 48 hours.  When pulmonary  excretion
             was evaluated (Hutson et al., 1971), the cis and trans isomers were
             3.9% and 23.6% of the administered dose, respectively.  Most of  the
             cis-OCP was excreted in the urine.

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    1,3-Oichloropropene                                       August,  1988

                                         -5-
ZV. mm.TH
    Humana
         •  The only known human fatality occurred a few hours after accidental
            infection of D-D mixture.  The dosage was unknown.'  Symptoms were
            abdominal pain, vomiting, muscle twitching and pulmonary edema.
            Treatment by gastric lavage failed (Gosselin et al., 1976).

         •  Inhalation of DCP at high vapor concentrations resulted in gasping,
            refusal to breathe, coughing, substernal pain and extreme respiratory
            distress at vapor concentrations over 1,500 ppm (Gosselin et al.,
            1976).

         •  Venable et al. (1980J studied 64 male workers exposed to three carbon
            compounds including DCP to determine if fertility was adversely
            affected.  The exposed study population was divided into <5 years
            exposure and >S years exposure.  Sperm counts and percent normal
            sperm forms were the major variables evaluated*  Although the at'udy
            participation rate for the exposed group was only 64%, no adverse
            effects on fertility were observed.
    Animals
       Short-term Exposure

         •  DCP is moderately toxic via single-dose oral administration.  A
            technical product containing 92% cls-/trans-DCP was administered by
            gavage as a 10% solution in corn oil to rats.  The oral LDgQS in male
            and female rats were 713 and 740 mg/Tcg, respectively (Torkelson and
            Oyen, 1977).  In another study, the oral LDso in the mouse for botn
            males and females was 640 mg/kg (Toyoshlma et al., 1978).

       Dermal/Ocular Effects

         •  The percutaneous LOsos for male and female mice dosed with DCP were
            greater than 1,211 mg/kg (Toyoshima et al., 1978).

         •  The percutaneous administration of DCP in rabbits (3 g/kg) resulted
            in mucous nasal discharge, depressed respiration and decreased body
            movements.  The 1.050 by this route was 2. 1 gAg (Torkelson and Oyen,
            1 977) .

         •  Primary eye irritation and primary dermal irritation studies in
            rabbits indicated that DCP causes severe conjunctival irritation,
            moderate transient corneal injury and slight skin erythema/edema.
            Bye irritation was reversible 8 days post-instillation.  The dermal
            LD50 in rabbits was 504 mg/kg (Dow, 1978).

       Long-term Exposure

         •  Rats, guinea pigs, rabbits and dogs were exposed to 4.5 or 13.6
            DCP in air for 7 hours per day, and 5 days per week for 6 months

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1,3-Oichloropropene                                        Augupt,  1968

                                     -6-
       The only  effect  noted was  alight  cloudy availing of ranal tubular
       epithelium in mala rats axpoaad to  tha  high  doaa (Torkalaon and Cyan,
        1977).

       Fiachar 344 rata and CD-I  albino  mice were exposed to Telone ZZ
        (Production Grade) by inhalation  expoaure, 6 hours per day for  13
       weeks at  concentrations of 11.98, 32.14, or  93.02 ppm.   Gross pathology
       revealed  an Increased incidence of  kidney discoloration in the  treated
       male rats relative to the  control group.  The significance of this
       leaion is unknown (Coate et al.,  1979).

       Solutions of Telone (78.5% DCP) in  propylene glycol were administered
       by gavage to  10  rats/sex/doae  for aix daya per week for a period of
        13 weeks.  The dose levels were  1,  3,  10 or  30 mg/kg/day.  The  control
       groups were given propylene glycol.  The daily administration of DCP
       to rats by stomach intubation  up  to a dosage of 30 mg/kg/day did not
       reault in any major adverae effects.  No significant effects on body
       weight, food consumption,  hematology and histopathology were noted.
       However,  at the  10 and 30  mg/kg/day doses, the relative weight  of the
       kidney of males  was higher than controla.  The authors conclude that
       the no-toxic-effect level  for  OCP was between 3 and 10 mgAg/day.
       The actual Ho-Observed-Adverse-Effect-Level  (NOAEL) was 3 mgAg/day
        (Til et al, 1973).  This is the only study that can be used to  develop
       a reference dose.  However, because the design does not ideally
       addresa drinking water, a  modifying factor will be used.

       The National Toxicology Program  (NTP,  1985)  evaluated the chronic
       toxicity  and carcinogenicity of Telone  ZZ in rats and mice.  These
       studies utilized Telone ZZ fumigant containing approximately 89%
       cis- and  trans-OCP.  Groups of 52 male  and female F344/M rats (doses
       0, 25 or  50 mg/kg) and 50  male and  female B6C3F1 mice (doses 0, 50
       or 100 mg/kg) were gavaged with Telone  ZZ in corn oil, 3 days per
       week up to 104 weeks.  Ancillary  studies were conducted in which
       dose groups containing five male  and female  rats were killed after
       receiving Telone ZZ for 9, 16, 21,  24 or 27  months.  Toxic effects
        (noncarcinogenic) included basal  cell or epithelial hyperplasia of
       the forestomach  of rats and mice  at all treatment levels of DCP.
       Epithelial hyperplasia of  the  urinary bladder of mice occurred  at
       both treatment levels in males and  females.   Kidney hydronephrosis
       also occurred in mice.  The study in male mice waa considered
       inadequate due to the deatha of vehicle control animals.  Many
       chronic toxicity parameters (hematology/ clinical chemistry) were not
       determined.   The DCP used  in the  NTP study h«d a different stabilizer
        from the  current Telone ZZ.

       Scott et  al.  (1987) exposed groups  of male and female B6C3F1 mice
        (70 animals/sex/exposure concentration) to vapors of Telone ZZ* soil
        fumigant  for  6 hours/day,  5 days/week  for up to 24 months at 0, 5,
        20 or 60  ppm.   Urinary bladder effects  including hyperplasia of
       bladder epithelium were noted  in  both  sexes  at 20 and 60 ppm.  Hyper-
       trophy and hyperplasia of  the  nasal respiratory mucosa were observed
        in most 60 ppm  exposed mice of both sexes and in 20 ppm exposed
        females.  Hyperplasia of the epithelial lining of the nonglandular
       portion of the  stomach was observed in 60 ppm exposed males.

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1,3-Oichloropropene                                       August,  1968

                                     -7-
              •t  al.  (1987)  exposed group* of 70 male and female Fischer 344
       rat*  to vapors of Telone II* soil fumlgant for 6 hours/day,  5 days/week
       for up to 24  months  at  targeted concentration* of 0,  5,  20 or 60 ppm.
       the MOAIL was 20 ppm.   The highest do*e caused hlstopathological
       changes in nasal tissue as well as a decrease in body weight gain
       during the first year of this study.  Males and females  exposed to*
       60 ppa showed decreased thickness and erosions of the nasal  epithelium
       as well as minimal submucosa fibrosis.

   Reproductive Effects

     •  Groups of male and female Histar rats were exposed to technical D-D
       at 0, 64, 145 and 443 mg/m3 (0, 14,  12 or 94 ppa) for 5  days per week
       over  10 weeks.   Hale mating indices, fertility indices and reproductive
       indices were  not affected by D-D exposure.   No gross  morphological
       changes were  seen in sperm.   Female mating, fertility and other
       reproductive  indices were normal.   Litter sices and weights  were
       normal and pup survival over 4 days was not influenced by exposure
       (Clark et al.,  1980).

     •  Breslin et al.  (1987) exposed by inhalation groups (F0)  of 30 males
       and 40 females for 10 weeks, 6 hours/day, 5 days/week to Telone II*
       at concentrations of 0, 10,  30 and 90 ppm prior to breeding.   Exposure
       was increased to 7 days/week during breeding at weeks 11 to  13.
       Exposure  of PI  male  and female parents to Telone 12*  began after
       weaning (approximately  week 32 of the study) and continued for
       12 weeks  (5 days/week and 6 hours/day),  The NQAEL for reproductive
       effects in the  study was *90 ppa,  the highest dose tested.   Conception
       indices of females were somewhat reduced in the Fj and ?2 generations.
       At 90 ppm, both males and females developed hyperplasia  of respiratory
       epithelium and focal degeneration of olefactory tissue.   Decreased
       body  weight was observed in males and females exposed to 90  ppm.

   Developmental  Effects

     •  Hanley et al. (1987) investigated the effects of inhalation  exposure
       to DCP on fetal development in rats.  Pregnant Fischer 344 rats  were
       exposed to 0, 20, 60 and 120 ppm DCP for 6 hr/day during gestation
       day*  6 to 15.  Maternal body weight gain was depressed in all of  the
       DCP««xposed rats in  a dose-related manner.   Therefore, the Lowest-
       Observed-Adver*e-Sffect Level (LOAEL) for this effect was 20 ppm DCP.
       There was also significant depression of feed consumption in all
       exposed rats, along  with decreases in water"consumption  in rats
       exposed to 120 ppm DCP.  At 120 ppm there were significant increases
       in relative kidney weights and decreases in absolute  liver weights in
       all exposed rats. There was a statistical increase in the incidence
       of delayed ossification of the vertebral centra of rats  exposed  to
       120 ppm DCP.   This effect is of little toxicological  significance due
       to maternal toxicity observed at 120 ppm DCP.

     •  Hanley et al. (1987) also studied the effects of Inhalation  exposure
       to DCP on fetal development in rabbits.  Pregnant New Zealand White
       rabbits were  exposed to 0, 20, 60 or 120 ppm DCP for  6 hr/day during

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1,3-Dichloropropene                                        August,  1988

                                     -8-
        gestation  days  6  through  18.   In  rabbits,  evaluation of  maternal
        weight  gain over  the entire exposure period  indicated significant
        exposure-related  decreases in  both  the 60- and 120-vpm groups.
        Therefore, the  KOAIL was  20 ppm OCP.   Statistically  significant
        decreases  in  the  incidence of  delayed  ossification of the  hyoid and
        presence of cervical spurs among  the exposed group were  considered
        within  normal variability in rabbits.

   Mutaqenicity

     •   Tests of commercial formulations  containing  DCP  (DeLorenzo et al.,
        1975; Flessel,  1977; Neudecker et al.,  1977; Brook*  et al.,  1978;
        Sudo et al.,  1978; Stolzenberg and  Bine, 1980),  a mixture of pure
        cia-OCP and tran*-OCP  (DeLorenzo  et al., 1975),  and  pure cis-OCP
        (Brook* et al,  1978) were poeitive  in  the  Salmonella typhimurium
        •train* TA1535  and TA100  with and without  metabolic  activation.
        These result* indicate that DCP act* by base^alr substitution  and
        is  a direct acting mutagen.

     •   OCP may be a  mutagen that acts via  frame shift mutation  since studies
        by  DeLorenzo  at al. (1975) reported poeitive result* in  TA1978  (with
        and without metabolic activation) for  a commercial mixture of OCP and
        a mixture  of  pure ci«- and tran*-OCP*

     •   A commercial  mixture of DCP and pure cis-OCP were also positive with
        and without metabolic activation  in Salmonella typhimurium strain TA98
        (PIeasel,  1977; Sudo et al., 1978;  Brooks  st al., 1978).

     •   Sudo et al. (1978) tested OCP in  a  reverse mutation  assay with
        B.  coll B/r Hp2 with negative results.

     •   OCP was negative  for reverse mutation  in the mouse host-mediated test
        with £. typhimurium G46 in studies  by  Shirasu  et al.  (1976) and Sudo
        et  alT  (1978).

   Carcinogenicity

     •   F344 rats  of  each sex were gavaged  with Telone II in corn oil at
        doses of 0, 25  and 50 mg/kg/day for 3  days per week.   A  total of
        77  rats/sex were  used for each dose group  (52  animals/sex/group were
        dosed for  104 weeks in the main oncogenicity study,  and  an ancillary
        study where 5 animals/sex/ group  were  sacrificed after 9, 16, 21, 24
        and 27  months'  exposure to OCP).  No increased mortality occurred In
        treated animals,  aaoplastie lesions associated  with Telone II  Included
        squamous cell papillomas  of the forestomach  (male rats:  1/52;  1/S2i
        9/52; female  ratsi  0/52; 2/52; 3/52),  squamous  cell carcinoma*  of
        the forestomach (male rats:  0/52;  0/52; 4/52) and neoplastic nodule*
        of  the  liver  (male rats:  1/52; 6/52;  7/52).   The increased incidence
        of  forestomach  tumors was accompanied  by a positive  trend for fore-
        •tomach basal cell hyperplasia in male and female rats of both  treated
        groups  (25 and  50 mg/kg/day).  The  highest dose  level  tested in  rats
        (50 mg/kg/day)  approximated a maximum  tolerated  dose level (NTP,  198S).

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   1,3-Oichloroprop«ne                                       August, 1988

                                        -9-
           B6C3P)  mica of each aax were gavaged with Talon* 11 in corn oil 'at
           doses of 0, 50 and 100 ag/kg/day for 104 waeka.   A total of SO mice/sex
           wars used for each dose group*   Ou« to excessive mortality ia control
           mala mice from ayocazdlal inflammation approximately 1 year aftar the
           initiation of tha study, conclusions partalalng to oncogeniclty ware
           baaed on concurrent control data and WP historical control data.
           Hsoplaatic laaiona aaaociatad with tha administration of Talone IX
           included aquaaous call papillomaa of the foraatomach (female alee:
           0/50; 1/50» 2/50), aquamous cell carcinoaac of tha forestoaach (feaale
           alee:  0/50; 0/50; 2/50), tranaitional cell earcinomaa of tha urinary
           bladder (female aices   0/50; 8/SOi 21/48), and alveolar/bronchlolar
           adenoaaa (female alee:  0/50; 3/50} 8/50).  the inereaaed incidence
           of forastoaach tuaora  waa accompanied by an increased incidence of
           atoaach epithelial call hyperplaaia in aalea and femalea at the
           hlgheat doae level teated (100 ag/kg/day), and tha inereaaed Incidence
           of urinary bladder tranaitional call carcinoma waa accompanied by a
           positive trend for bladder hyperplaaia in mala and female alee of
           both treated groupa (50 and 100 mg/kg/day).  Incidences of neoplasms
           were not significantly inereaaed in aale mice (NTF, 1985).

           Thirty  female Ha:ZCR Arias mice received weekly subcutaneous injections
           of cis-OCP.  the doae  was 3 ag OCP/aouae In 0.05 al. trioetanoin
           delivered to the left  flank.  After 77 weeks, there was an inereaaed
           incidence of fibrosarcomas at the site of injection.  Six of the
           30 exposed alee developed the tumors.  Thar* were no similar lesions
           in the  controls (Van Duuren, 1979).

           Scott et al. (1987) exposed groupa of aala and female B6C3F1 alee (70
           anlaals/sex/doae) to vapors of Telone XI* for 6 hours/day, 5 days/week
           for up  to 24 months at 0, 5, 20 or 60 ppa.  The only tuaorigenic
           effect  was an Increased incidence in benign lung tumors (bronchio-
           loalveolar adenomas) in the 60 ppm exposed males.  There were no
           tuaorigenlc effects in the lower-dose males or at any of the doses In
           females.

           Lomax et al. (1987) exposed Fisher 344 rats (70 rats/•ex/dose) to
           vapors  of Telone IX*  (0, 5, 20 and 60 ppa).  The two year exposure by
           inhalation did not result In increases In timior incidence.
V. QUANTIFICATIOM OF TOXICOLOGICAL EFFECTS

        Health advisories (HAs) are generally determined for one-day, ten-day,
   longer-ten (up to 7 years) and lifetime exposures if adequate data are
   available that identify a aensitive noncarcinogenic end point of toxlcity.
   The HAs for noncarcinogenic toxicants are derived using the following formula:

                 HA . (HOABL or LOAEL) x (BW) » 	^/j, ,	 ug/u
                        (OF) x (     L/day)
   where:
           NOAEL or LOAEL - Mo- or Lowest-Observed-Adverse-Bffeet Level
                            in ag/kg bw/day.

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 i TJ-QlchloTopropene                                       August,

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

                    OF - uncertainty factor (10, 100, 1,000 or  10,000),
                         la accordance with Z9\ or NAS/OOU guidelines.

             .. _ L/day - assumed daily water consumption of a child
                         {) Vday) or aa adult (2 L/day).

One-day Health Advisory

     There are not sufficient data to derive a One-day Health Advisory value
for DCP.  It is recommended that the Longer term HA value for a 10-kg child
(30 ug/L, calculated below) be used at this time as a conservative estimate
of the One-day HA value.

Ten-day Health Advisory

     There are not sufficient data to derive a Ten-day HA value for DCP.
It is recommended that the Longer-term BA value for a 10-*g child (30 ug/L.
calculated below) be used as a conservative estimate of the Ten-day HA value.

Longer-term Health Advisory

     The Til et al. (1973) 13 weeks subehronlc gavage study in rats has been
selected to serv« as the basis for calculating the Longer-term HA for DCP.
This study resulted in a LOA2L of 10.0 sig/kg/day based on Increased relative
kidney weight in males.  No adverse effects were noted at the next lowest
dose (3.0 mg/kg/day).  Therefore, the NOAEL is 3.0 mg/kg/day.

     Based on the NOAEL of 3.0 mg/kg/day determined in this study, the Longer-
term HAs are calculated as follows:

     For a 10-kg child:

        Longer-term HA • (3.0 m^/kg/day) (10 k
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 ',3-Olchloropropena                                       August,  1968

                                      -11-


     For •  70-kg adult:

       Longer-term HA •  <3'° aq/lcq/dav)  (70 ko)  .  0.105 mg/L  (100  ua/L)
                          (100)  (10)  (2 L/day)                      *

where:

     3.0 mgAg/dey • NGAEL based on the absence  of Increased relative  kidney
                     weights in rats*

             70 kg • assumed body weight of an adult.

                100 • uncertainty factor, chosen  In accordance with EPA or
                     HAS/ODW guidelines for use  with a NGAEL from  an animal
                     study'

                10 - Modifying factor, selected  since this was the only useful
                     gavage study available and  classified as suppleaentary
                     data.  Also there were considerable toxlcological -data gaps.

          .2 I/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^tep process.  Step  1 determines the Reference Use
(RfD), formerly called the Acceptable Daily Intake (ADI).  The RfO 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 NQAEL (or LQAEL), identified from a chronic  (or subchroaic) study, divided
by an uncertainty factor(a).  From the RfD, a Drinking Hater Equivalent Level
(DUEL) can  be determined  (Step 2).  A OKEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarclnogenic health effects would not be expected to occur.
The DUEL 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.  If the contaminant is classified as a Group A or
B carcinogen, according to the Agency's classification scheme of carcinogenic
potential,  then caution should be exercised in assessing the risks associated
with lifetime exposure to this chemical.  For Group C carcinogens, an additional
safety factor of 10 is added to the DWEL.

     The Lifetime HA for a 70-kg adult has been determined on the basis of
the study in rats by Til et al. (1973), as described above.

     Using  the NQAEL of 3.0 mg/kg/day, as determined in that study, the
DUEL is calculated as follows:

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 1,3-Oichloropropene                                        August,  1988

                                      -12-


 Btep 1t  Dstsrmination of the Reference  Dose  {RfD)

                   RfD .  (3.0 mg/kq/day) . 0.0003 mgAg/day
                           (1,000)  (10)

where:

     3.0 mgAg/day • NOAEL based on the absence of increased relative kidney
                     weights in rats.

             1,000 - uncertainty factor, chosen in accordance with EPA or
                     NAS/ODH guidelines for use with a NOA£L from an animal
                     study of less-than•lifetime duration.

                10 • modifying factor selected since this was the only useful
                     gavage study available and classified as supplementary
                     data.  Also there were considerable toxicological data gaps.

Step 2:  Determination of the Drinking Hater Equivalent Level (OWED

           DWEL • (0-0003 mq/kq/day)  (70 kg) . <011   /L (10   /L)
                          (2 L/day)

where:

        0.0003 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 BAs are not recommended for Group A or B carcinogens.  DCP is
a Group B2, probable human carcinogen.  The estimated cancer risk associated
with lifetime exposure to drinking water containing DCP at 10 ug/L is
approximately 5.0 x 10-3.  ihiB estimate represents the upper 95% confidence
limit using the linearized multistage model,  the actual risk is unlikely to
exceed this value.

Evaluation of Carcinogenic Potential

     •  DCP may be classified as a B2, probable human carcinogen baaed on
        sufficient evidence of tumor production in two rodent species and two
        routes of administration.

     8  Data on an increased incidence of squamous cell papilloma or carcinoma
        of the forestomach in rats exposed to DCP (NCI, 1985) were used for a
        quantitative assessment of cancer risk due to DCP.  Based on the data
        from this study and using the linearized multistage model, a carcinogenic
        potency factor (q^) for humans of 1.75 x 10~* (mgAg/day)*1 was
        calculated.

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       1,3-Oichloroprop«ne                                        Auguit,  1988

                                            -13-
            •  The drinking water concentrations  corresponding to increased lifetime
              cancer  risks of 10-4,  io-5 and  10-6 (one  excess cancer per one million
              population)  for a 70Hcg  adult consuming 2 L/day are 20 ug/L, 2 ug/L
              and 0.2 ug/L, respectively.

            •  The forestomach timwr  data in male rats used  to calculate  the qj*
              value  (NCI,  1985) consisted of  the 2-year study data excluding the
              ancillary studies data.  The ancilliary studies involved serial
              sacrifice of animals (at 9, 16, 21, 24  and 27 months).  Zt is not
              appropriate  to include these data  in the  lifetime  predictive model
              used (multistage).

            0  For comparison purposes, drinking  water concentrations associated
              with an excess risk of 10-6 were 0.2 ug/L, 3.6  mg/L, 0.03  ug/L and
              0.004 ug/L for the one-hit, Neibull, probit and logit models,
              respectively.


  VI.   OTHER CRITERIA, GDIDANCE AMD STANDARDS

            •  The ACGZH recommended  1  ppm (5  mg/m*) as  a Threshold Limit Value for
              DCP (Clayton and Clayton,  1981).


 VII.   ANALYTICAL METHODS

            0  No specific  methods have been published by U.S. EPA for analysis of
              DCP in water." However,  EPA Method 524.2  (U.S.  EPA, 1986d) and EPA
              Method 502.2 (USBPA, 1986e) both for volatile organic compounds in
              water should be suitable for analysis of  DCP.   Both are standard
              purge and trap capillary column gas chromatographlc techniques.
              While an estimated detection limit has  not been calculated for the
              two isomers  of 1,3-^lichloropropene, work  done with 1,1-^lichloropropene
              would indicate a range for 1,3HXP of 0.02 to 0.05 ug/L.


VIII.   TREATMENT TECHNOLOGIES

            •  There are no specific  publications on treatment of 1,3-OCP.   However,
              adequate treatment by  granular  activated  carbon (GAC) should be
              possible.  Freundlich  carbon absorption isotherms  for DCP  indicate
              reasonably high adsorption capacity (U.S. EPA,  1980).

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1,3-0ichloroprop«n«                                        August,  1988

                                      -14-


ZZ. MTEREHCBS
Breslin, W.J., R.D. Xirk, C.M. Streeter, J.F. Cjuast and J.R.  Ssabo.*   1987.
     Telone ZZ soil fumlgant:  two-generation inhalation reproduction  study
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Brooks, T.M., B.J. Dean and A.S. Wright.*   1978.  Toxicity studies with
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Clark, D., D. Blair and S. Cassidy.*  1980.  A 10 week inhalation study of
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1,3-Oichloropropene                                       August,  1968

                                     -15-
Plessel, ?•*  1977.  tetter dated Apr. 8,  1977t  Subject:  Mutagen  testing
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 1,3-Oichloropropene                                        August,  1988

                                      -16-
Stott, H.T., K.A. Johnson, X».L. Calhoun, S.K. Weiss and  L.B.  Frauson.*   1987.
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  3-Oichloroprop«n«
August, 1988
                                      -1.7-
Van Duuren, B.L., B.M. Goldsehnldt and G. Loewengart.*   1979.  Carcinogenic!ty
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•Confidential Business  Information  submitted to  the Office of Peeticide
 Programs.

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