August, 1987

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

    1,3-Dichloropropene                                       Augus t,  1987



    CAS No.   542-75-6

    Structural Formula

                   C1CH2       H                    C1CH2       Cl
                        \     '                         \     /
                         c = c                            c » c
                        /     \                          /    \
                       H       Cl                       H       H

                        (trans)                           (cis)

                          (approximately 46% trans/42% cis)
            Dichloro-1,3-propene;  1,3-dichloro-1-propene;  Telone?  Telone II;
            Dow Telone;  cis/trans-1,3-dichloropropene;  1,3-D;  DCP;  D-D
            (approximately 28% cis/27% trans).
         0  The pesticide 1 , 3-dichloropropene (DCP)  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 DCP has increased due to cancellation of  the once widely
            used product containing ethylene  dibromide (EDB) and dibromochloro-
            propane (DBCP) (U.S. EPA, 1986a).

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

    Properties  (Dow Chemical USA, 1977,  1982; Patty,  1981)
            Chemical Formula
            Molecular Weight                  11.0.98 (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/mL
            Vapor Pressure (25°C)             27.3 mm 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
            Log Octanol/Water Partition       25
            Flash Point                       about 28°C
            Conversion Factor (25'C)           1  mg/L.= 220 ppm;  1  ppm » 4.54 mg/m3

     1,3-Dichloropropene                                        August,  1987


          0  In  California  (Maddy et al.f 1982),  54 wells were examined in areas
             where  Telone or D-D were used  for  several  years.   The well water did
             not have measurable amounts of DCP (<0.1 ppb).

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

     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, 19865;
             U.S. EPA, 1986c).

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



          0  Toxicity studies  indicate that DCP is absorbed  from skin, respiratory
             and gastrointestinal systems  (Patty, 1981).

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


          0  Radiolabeled  [C14] D-D  (55% DCP) was administered orally in arachis
             oil in rats.   After 4 days, most of the administered dose was recovered
             for the most part in  urine and there were  insignificant amounts  (less
             than 5%) remaining in  the gut, feces,  skin and  carcass (Hutson et al.,


          0  cis-Dichloropropene 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.  The main  urinary metabolite (92%)  was N-acetyl-
             S-[ (cis)-3-chloroprop-2-enyl]  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  (Climie  and Morrison,  1978).

          0  In  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.

    1,3-Dichloropropene                                       August, 1987
                                    /          '
            In two studies (Hutson et al., 1971; Cliraie and Morrison, 1978)
            f4c]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-DCP was excreted in the urine.

            The only known human fatality occurred a few hours after accidental
            ingestioh 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 high vapor concentrations result 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. (1980) 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 >5 years exposure.  Sperm counts and percent normal
            sperm forms were the major variables evaluated.  Although the study  .
            participation rate for the exposed group was only 64%, no adverse
            effects on fertility were observed.
       Short-term Exposure

         0  DCP is moderately toxic via single-dose oral administration.  A
            technical product containing 92% cis-/trans-DCP was fed as a 10%
            solution in corn oil to rats.  The oral LDsos in male and female rats
            were 713 and 740 mg/kg, respectively  (Torkelson and Oyen, 1977).  In
            another study, the oral LD5Q in the mouse for both males and females
            was 640 mg/kg (Toyoshima et al., 1978).

       Dermal/Ocular Effects

         e  The percutaneous LD^gS for male and female mice were greater than
            1,211 mg/kg (Toyoshima et al., 1978).

         e  The percutaneous administration of DCP in rabbits (3 g/kg) resulted
            in mucous nasal discharge, depressed  respiration and decreased body
            movements.  The LD5g by this route was 2.1 g/kg (Torkelson and Oyen,

1,3-Dichloropropene                                        August,  1987

        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.
        Eye irritation was reversible 8 days post-instillation.  The dermal
             in rabbits was 504 mg/kg (Dow, 1978; Hanley et al., 1987).
   Long-term Exposure

     0  Rats,  guinea pigs,  rabbits and dogs were exposed to 4.5 or 13.6 mg/m3
        DCP in air for 7 hours per day, and 5 days per week for 6 months.
        The only effect noted was a slight apparently reversible microscopic
        renal lesion in male rats exposed to the high dose (Torkelson and
        Oyen,  1977).

     0  Fischer 344 rats and CD-1 albino mice were exposed to Telone II
        (Production Grade)  by inhalation exposure, 6 hours per day for 13
        weeks at concentrations of 11.98, 32.14, and 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
        lesion is unknown (Coate et al., 1979).

     0  Solutions of Telone (78.5% DCP) in propylene glycol were administered
        by gavage to 1 0 rats/sex/dose for six days per week for a period of 1 3
        weeks.  The dose levels were 1, 3, 10 and 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
        result in any major adverse effects.  No significant effects on body
        weight, food consumption, hematology and histopathology were noted.
        However, at the 10 mg/kg/day dose, the relative weight of the kidney
        of males was still higher than controls.  The authors conclude that
        the no-toxic-effect level for DCP was between 3 and 10 mg/kg/day.
        The actual observed No-Observed-Adverse-Effect-Level  (NOAEL) was
        3 mg/kg/day  (Til et al,  1973).

     0  The National Toxicology Program  (NTP, 1985) evaluated the chronic
        toxicity and carcinogenicity of Telone  II in rats and mice.  These
        studies utilized Telone  II fumigant containing approximately 89%
        cis- and trans-DCP.  Groups of 52 male and female F344/N rats (doses
        0, 25 or 50 mg/kg)  and 50 male and female B6C3F! mice  (doses 0, 50
        or 100 mg/kg) were gavaged with Telone  II in corn oil, 3 days per
        week up to 104 weeks.  Arcillary studies were conducted in which
        dose groups containing five male and female rats were killed after
        receiving Telone II 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 was considered inade-
        quate due to the deaths of vehicle control animals.  Many chronic
        toxicity parameters (hematology/ clinical chemistry) were not deter-
        mined.  The DCP used in  the NTP  study had a different stabilizer from
        the current Telone II.

1,3-Dichloropropene                                       August, 1987


   Reproductive Effects

     0  Groups of male and female Wistar rats were exposed to technical D-D
        at 0,  64, 145 and 443 mg/m3 (0,  14, 12 and 94 ppm) for 5 days per
        week over 10 weeks.  Male 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 sizes and weights
        were normal and pup survival over 4 days was not influenced by exposure
        (Clark et al., 1980).

   Developmental Effects

     0  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
        days 6 to 15.  Maternal body weight gain was depressed in all of the
        DCP-exposed rats in a dose-related manner.  Therefore, the Lowest-
        Observed-Adverse-Effect-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.

     0  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
        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-ppm groups.
        Therefore, the NOAEL was 20 ppm DCP.  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.


     0  Tests of commercial formulations containing DCP (DeLorenzo et al.,
        1975; Flessel, 1977; Neudecker et al., 1977; Brooks et al., 1978;
        Sudo et al., 1978; Stolzenberg and Hine, 1980), a mixture of pure
        cis-DCP and trans-DCP  (DeLorenzo et al., 1975), and pure cis-DCP
        (Brooks et al, 1978) were positive in the Salmonella typhimurium
        strains TA1535 and TA100 with and without metabolic activation.
        These results indicate that DCP acts by base-pair substitution and
        is a direct acting mutagen.

     0  DCP may be a mutagen that acts via frame shift mutation indicated
        by studies  (DeLorenzo et al,  1975) in which positive results were
        obtained for TA1978 (with and without metabolic activation) for a
        commercial mixture of DCP and a mixture of pure cis- and trans-DCP.

1,3-Dichloropropene                                        August,  1987

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

     •  sudo et al. (1978)  tested  DCP in  a  reverse mutation assay with
        J3. coli B/r Wp2  with negative results.

     0  DCP  was negative for reverse  mutation in the mouse host-mediated test
        with S. typhimurium G46  in studies  by Shirasu et al. (1976) and Sudo
        et al7 (1978).


     0  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 DCP).  No  increased mortality occurred in
        treated animals.  Neoplastic  lesions  associated with Telone II included
        squamous cell papillomas of the forestomach (male  rats:  1/52; 1/52;
        9/52; female  rats:  0/52;  2/52; 3/52),  squamous cell carcinomas of
        the  forestomach  (male rats:   0/52;  0/52; 4/52) and neoplastic nodules
        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-    N
        stomach 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, 1985).

     0  B6C3Fi mice of each sex  were  gavaged  with Telone II in corn oil at
        doses of 0, 50 and 100  mg/kg/day  for  104 weeks.  A total of 50 mice/sex
        were used  for each dose  group. Due to excessive mortality in control
        male mice  from myocardial  inflammation approximately 1 year after the
        initiation of the study, conclusions  pertaining to oncogenicity were
        based on concurrent control data  and  NTP historical control data.
        Neoplastic lesions associated with  the administration of Telone II
        included squamous cell  papillomas of  the forestomach (female mice:
        0/50; 1/50; 2/50),  squamous cell  carcinomas of the forestomach  (female
        mice:  0/50;  0/50;  2/50),  transitional cell carcinomas of the urinary
        bladder (female  mice:   0/50;  8/50;  21/48), and alveolar/bronchiolar
        adenomas (female mice:   0/50; 3/50; 8/50).  The increased incidence
        of forestomach  tumors  was  accompanied by an increased incidence of
        stomach epithelial cell hyperplasia in males and females at  the
        highest dose level tested  (100 mg/kg/day), and the increased incidence
        of urinary bladder transitional  cell  carcinoma was accompanied  by a
        positive trend  for bladder hyperplasia in male and female mice  of
        both treated groups (50 and  100  mg/kg/day)  (NTP, 1985).

     0  Thirty female Ha:ICR  Swiss mice  received weekly subcutaneous injections
        of cis-DCP.  The dose  was  3 mg DCP/mouse in 0.05 mL trioctanoin
        delivered  to the left  flank.   After 77 weeks, there was an increased
        incidence  of fibrosarcomas at the site of injection.  Six of the
        30 exposed mice  developed  the tumors.  There were no similar lesions
        in the controls  (Van Duuren,  1979).

   1,3-Dichloropropene                            .           August, 1987


        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)


           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, 1 00 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                                               N

        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 HA value for a 10-kg child (30 ug/L) be
   used as a conservative estimate of the Ten-day HA value.

   Longer-term Health Advisory

        The Til et al. (1973) 90-day subchronic feeding study in rats has been
   selected to serve as the basis for calculating the Longer-term HA for DCP.
   This study resulted in a LOAEL of 10.0 mg/kg/day based on increased relative
   kidney weight in males.  No adverse biological 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*° agAq/day) (10 kg) = QfQ3 mg/L (30 ug/L)
                             (100) (10) (1 L/day)

1,3-Dichloropropene                                       August,  1987

     3.0 mg/kg/day = NOAEL based  on the absence of increased  relative kidney
                     weights in rats.

             10 kg = assumed body weight of a child.

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

                10 = modifying factor,  selected since this was the only
                     useful feeding study available and the study design was
                     not ideal for assessing exposure via drinking water.

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

     For a 70-kg adult:

       Longer-term HA = (3.0 mg/kg/day) (70 kg) = ,105 mg/L (105 ug/L)
                         (100) (10) (2 L/day)


     3.0 mg/kg/day = NOAEL 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 NAS/ODW
                     guidelines for use with a NOAEL from an animal study.

                10 = modifying factor, selected since this was the only
                     useful feeding study available and the study design was
                     not ideal for assessing exposure via drinking water.

           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 w.ter 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

1,3-Dichloropropene                                       August, 1987

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, 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 NOAEL of 3.0 mg/kg/day, as determined in that study, the
DWEL is calculated as follows:
Step 1:  Determination of the Reference Dose (RfD)

                   RfD =  (3.0 mg/kg/day) _ Q.0003 mg/kg/day
                          (1,000) (10)


     3.0 mg/kg/day = NOAEL based on the absence of increased relative kidney
                     weights in rats.

             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.

                10 = modifying factor selected since this was the only useful
                     feeding study available and the study design was not
                     ideal for assessing exposure via drinking water.

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

            DWEL = (0.0003 mg/kg/day) (70 kg) , ,011 mg/L (n ug/L)
                           (2 L/day)


        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 HAs are not recommended for Group A or B carcinogens.  DCP is
a Group B, probable human carcinogen.  The estimated cancer risk associated
with lifetime exposure to drinking water containing DCP at 11 ug/L is

       1,3-Dichloropropene                                        August,  1987


       approximately 5.5  x  10-5.   This  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

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

            0  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"^ (mg/kg/day)~^ was

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

            0  The forestomach tumor  data  in male rats used to calculate the q-|*
               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).  It 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, Weibull, probit and logit models,


            0  The ACGIH  recommended  1  ppm  (5 mg/m3) as a Threshold Limit Value for
               DCP (Patty,  1981).


            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 (USEPA, 1986e) both for volatile organic compounds in
               water should be suitable for analysis of DCP.  Both are standard
               purge and  trap capillary column gas chromatographic techniques.


            0  There are  no specific  publications on treatment of 1,3-DCP.  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).

1 , 3-Dichloropropene                                       August, 1987

Brooks, T.N., B.J. Dean, A.S. Wright et al.*  1978.  Toxicity studies with
     dichloropropenes:  mutation studies with 1,3-D and cis-1 , 3-dichloropropene
     and the influence of glutathione on the mutagenicity of cis-1 , 3-dichloro-
     propene in Salmonella typhimurium;  Group research report (Shell Research,
     Ltd.)  TLGR.0081 78.  Unpublished study by Shell Chemical Co., Washington,
     DC.  MRID 61059.

Clark, D., D. Blair and S. Cassidy.*  1980.  A 10 week inhalation study of
     mating behavior, fertility and toxicity in male and female rats:  Group
     research report (Shell Research, Ltd.) TLGR.80.023.  Unpublished study
     Dow Chemical U.S.A., Midland, MI.  MRIDs 117055, 103280, 39691.

Climie, I.J.G., and B.J. Morrison.*  1978.  Metabolism studies on (Z)1 , 3-dichloro-
     propene in the rat:  Group research report (Shell Research, Ltd.) TLGR.010U
     78.  Unpublished study by Dow Chemical U.S.A., Midland, MI.  MRID 32984.

Coate, W.B., D.L. Keenan, R.J. Hardy and R.W. Voelker.*  1979.  Inhalation-
     toxicity study in rats and mice:  Telone II:  Project No. 174-127.
     Final report.  Unpublished study by Hazleton Laboratories America, Inc.,
     for Dow Chemical U.S.A., Midland, MI. MRID 119191.

DeLorenzo, F., S. Degl Innocenti and A. Ruocco.*  1975.  Mutagenicity of
     pesticides containing 1 , 3-dichloropropene:  University of Naples, Italy.
     Submitted by Dow Chemical U.S.A., Midland, MI.  MRID 119179.

Dietz, F.K., E.A. Hermann and J.C. Ramsey.  1984.  The pharmacokinetics of
     14c-1 , 3-dichloropropene in rats and mice following oral administration.
     Toxicologist.  4:585 (Abstract no.).

Dow Chemical U.S.A.*  1977.  Telone II soil fumigant:  Product chemistry.
     MRID 00119178.

Dow Chemical U.S.A.*  1978.  Summary of human safety data.  Summary of studies
     099515-1 and 09951 5-J.  Unpublished study Dow Chemical U.S.A., Midland, MI.
     MRID 39676.

Dow Chemical U.S.A.  1982.  A data sheet giving the chemical and physical
     properties of the chemical.  A complete statement of the names and
     percentages by weight of each active inert ingredient in the formulation
     to be shipped.  Dow Chemical U.S.A., Midland, MI.  MRID 115213.

Flessel, P.*  1977.  Letter dated Apr. 8, 1977:  Subject:  Mutagen testing
     program, mutagenic activity of Telone II in the Ames Salmonella assay.
     Prepared by Calif. Dept. Health, submitted by Dow Chemical U.S.A.,
     Midland, MI.  MRIDs 120906, 67534.

Gosselin, R.E., B.C. Hodge, R.P. Smith and M.N. Gleason.  1976.  Clinical
     toxicology of commercial products.  4th ed.  Baltimore, MD:  The Williams
     and Wilkins Co., p. 120.

1,3-Dichloropropene                                       August, 1987
Hanley, T.R.,  J.A.  John-Greene,  J.T.  Young, L.L. Calhoun and K.S. Rao.   1987.
     Evaluation of  the effects of inhalation exposure to 1,3-dichloropropene
     on fetal  development in rats and rabbits.  Fundamental and Applied
     Toxicology.  8:562-570.

Hutson, D.H.,  J.A.  Moss and B.A. Pickering.*  1971.  The excretion and retention
     of components  of the soil fumigant D-D and their metabolites in the rat.
     Food Cosmet.  Toxicol.  9:677-680.  Dow Chemical U.S.A., Midland, MI.
     MRID 39690.

Laskowski, D., C.  Goring, P. McCall and R. Swan.  1982.  Terrestrial environment.
     Environ.  Risk  Anal. Chem.  25:198-240.

Maddy, K., H.  Fong, J. Lowe, D.  Conrad and A. Fredrickson.  1982.  A study
     of well water  in selected California communities for residues of
     1,3 dichloropropene, chloroallyl alchohol, and 49 organophosphate or
     chlorinated hydrocarbon pesticides.  Bull. Environ. Contam. Toxicol.

Neudecker, T., A.  Stefani and D. Heschler.  1977.  In vivo mutagenicity  of
     soil nematocide 1,3-dichloropropene.  Experientia.  33:1084-1085.

NTP.  1985.  National Toxicology Program.  NTP Technical report on the toxi-
     cology and carcinogenesis studies of Telone II in F344/N rats and B6C3F-)
     mice (gavage studies).  NTP TR 269, NIH Pub. No. 85-2525, May, 1985.

Patty.  1981.   Patty's Industrial hygiene and toxicology.  3rd ed., New  York,
     NY:  Wiley-Interscience Co.  Vol. 2B, pp. 3573-3577.

Shirasu, Y.,  M. Moriga and K. Kato.*  1976.  Mutagenicity testing on D-D in
     microbial systems.  Prepared by Institute of Environmental Toxicology,
     submitted by Shell Chemical Co., Washington, DC.  MRID 61050.

Stolzenberg,  S. and C. Hine.  1980.  Mutagenicity of 2- and 3-carbon halo-
     genated compounds in Salmonella/mammalian microsome test.  Environmental
     Mutagenesis.  2:59-66.

Sudo, S., M. Nakazawa and M. Nakazono.*   1978.  The mutagenicity test on
     1,3-dichloropropene in bacteria test systems.  Prepared by Nomura Sogo
     Research Institute, submitted by Dow Chemical U.S.A., Midland, MI.
     MRID 39688.

Til, H.P., M.T. Spanjers, V.J. Feron and P.J. Reuzel.  1973.*  Subchronic
     (90-day) toxicity study with Telone in albino rats:  Report No. R4002.
     Final report.   Unpublished study (Central  Institute for Nutrition
     and Food Research) submitted by Dow Chemical U.S.A., Midland, MI.
     MRIDs 39684,  67977.

Torkelson, T.R., and F. Oyen.  1977.*  The toxicity of 1,3-dichloropropene is
     determined by repeated exposure of laboratory animals.  American  Industrial
     Hygiene Association Journal.  38:217-223.  Dow Chemical U.S.A., Midland,  MI.
     MRID 39686.

1,3-Dichloropropene                                       August,  1987
Toyoshima, S., R. Sato and S. Sato.  1978.  The acute toxicity test on
     Telone II in mice.  Unpublished study by Dow Chemical U.S.A., Midland,  MI,
     MRID 39683.

U.S. EPA.  1980.  U.S. Environmental Protection Agency.  Carbon adsorption
     isotherms for toxic organics.  EPA-60018-80-023.  Apr.  1980.

U.S. EPA.  1986a.  U.S. Environmental Protection Agency.  1,3-Dichloropropene,
     a digest of biological and economic benefits and regulatory implications.
     Benefits and Use Division, Office of Pesticide Programs.

U.S. EPA.  1986b.  U.S. Environmental Protection Agency.  1,3-Dichloropropene;
     initiation of special review; availability of registration standard;
     notice.  Fed. Reg.  51(195).-36161.  October 8, 1986.

U.S. EPA.  1986c.  U.S. Environmental Protection Agency.  Guidance for the
     reregistration of pesticide products containing 1,3-dichloropropene as
     the active ingredient.  Office of Pesticides and Toxic  Substances,
     Washington, DC.  September 1986, 111 pp.

U.S. EPA.  1986d.  U.S. Environmental Protection Agency.  Volatile organic
     compounds in water by purge and trap capillary gas chromatography/mass
     spectrometry.  Office of Drinking Water, Washington, DC.  Aug. 1986.

U.S. EPA.  1986e.  U.S. Environmental Protection Agency.  Volatile organic
     compounds in water by purge and trap capillary column gas chromatography
     with photoionization and electrolytic conductivity detectors in series.
     Office of Drinking Water, Washington, DC.

Van Dijk, H.  1974.  Degradation of 1,3-dichloropropenes in  soil.  Agro-
     Ecosystems.  1:193-204.

Van Duuren, B.L., B.M. Goldschmidt and G. Loewengart.*  1979.  Carcinogenicity
     of halogenated olefinic and aliphatic hydrocarbons in mice.  Journal of
     the National Cancer Institute.  63(6):1433-1439.  MRID  94723.

Venable, J.R., C.D McClimans, R.E. Flake and D.B. Demick.*   1980.  A fertility
     study of male employees engaged in the manufacture of glycerine.  Journal
     of Occupational Medicine.  22(2):87-91.  Dow Chemical U.S.A., Midland,
     MI:  MRID 117052.
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