March  31,  1987
                                   VINYL  CHLORIDE

                               Health  Advisory  Draft
                              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.

    Vinyl Chloride
                 March 31, 1987
         This Health Advisory (HA)  is based on information presented in the
    Office of Drinking Water's Health Effects Criteria Document (CD) for vinyl
    chloride (U.S.  EPA,  1985a).  The HA and CD formats are similar for easy
    reference.  Individuals  desiring further information on the toxicological
    data base or rationale for risk characterization should consult the CD.  The
    CD is available for  review at each EPA Regional Office of Drinking Water
    counterpart (e.g., Water Supply Branch or Drinking Water Branch),  or for a
    fee from the National Technical Information Service, U.S. Department of
    Commerce,  5285  Port  Royal Rd.,  Springfield,  VA 22161,  PB t 86-118320/AS.  The
    toll-free number is  (800) 336-4700; in the Washington, D.C. area:  (703) 487-4650,
    CAS No.   75-01-4
    Structural Formula
                                      i  I
                                      H  H
            Monochloroethylene,  chloroethene
            Vinyl chloride and polyvinyl chloride (PVC)  are used as raw materials
            in the plastics,  rubber,  paper,  glass and automotive industries.
            In addition,  vinyl chloride and  PVC are used in the manufacture of
            electrical wire insulation and cables,  piping,  industrial and household
            equipment, medical supplies, food packaging  materials and building
            and construction products.  Vinyl chloride copolymers and PVC are
            distributed and processed in a variety of forms,  including dry resins,
            plastisol (dispersions in plasticizers),  organosol (aispersions in
            plasticizers  plus volatile solvent),  and  latex  (a colloidal dispersion
            in water used to coat paper, fabric or leather) (U.S. EPA, 1985a).
    Properties  (U.S. EPA (1985a)

            Chemical Formula
            Molecular Weight
            Physical State
            Boiling Point
            Melting Point
            Vapor Pressure
            Specific Gravity
            Water Solubility
            Taste Threshold (water)
            Odor Threshold (water)
            Conversion Factor (air)

            *Amoore and Hautala (1983)
2,530 mmHg at 20C
1.1 g/L water at 28C
not available
3.4 mg/L*
1  ppm = 2.6

     Vinyl Chloride                                             March 31, 1987


             Vinyl chloride is a synthetic chemical with no natural sources.

             Since 1979,  yearly production of vinyl chloride has been approximately
             7 billion Ibs (U.S. ITC,  1983).  Vinyl chloride is polymerized, and
             little is released to the environment.  Environmental releases will
             be limited to the areas where vinyl chloride is produced and used.

             Vinyl chloride released to the air is degraded in a matter of a few
             hours (U.S.EPA,  1980a).  Vinyl chloride released to surface waters
             migrates to  the  atmosphere in a few hours or days where it undergoes
             photochemical oxidation.   Vinyl chloride which is released to the
             ground does  not  adsorb onto soil and migrates readily to ground
             water.  Evidence from laboratory studies suggests that vinyl chloride
             in ground water  may degrade to C02 and Cl~ (Vogel and McCarty, 1985).
             Vinyl chloride is expected to remain in ground water for months to
             years.  Vinyl chloride has been reported to be a degradation product
             of trichloroethylene and  tetrachloroethylene in ground water (Parsons,
             1984).  Vinyl chloride does not bioaccumulate in individual animals
             or food chains.

             Vinyl chloride does not occur widely in the environment because of
             its rapid degradation and limited release.  Vinyl chloride is a
             relatively rare  contaminant in ground and surface waters with higher
             levels found in  ground water.  The Ground Water Supply Survey of
             drinking water supplies have found that less than 2% of all ground
             water derived public water systems contain vinyl chloride at levels
             of 1  ug/L or higher.  Vinyl chloride almost always co-occurs with
             trichloroethylene.  Public systems derived from surface water also
             have  been found  to contain vinyl chloride but at lower levels.  No
             information  on the levels of vinyl chloride in food have been identi-
             fied.  Based upon the limited uses of vinyl chloride and its physical
             chemical properties, little or no exposure is expected from food.
             Vinyl chloride occurs in  air in urban areas and near the sites of its
             production and use.  Atmospheric concentrations are in the ppt
             range (U.S.  EPA,  1979).

             The major source of exposure to vinyl chloride is from contaminated
             Vinyl  chloride  is  absorbed  rapidly  in rats  following ingestion and
             inhalation (Withey,  1976; Duprat  et al.,  1977).

             Using  statistical  modeling,  Withey  and Collins  (1976)  concluded that,
             for rats,  a  total  liquid  intake containing  20 ppm (wt/wt)  vinyl
             chloride  would  be  equivalent to an  inhalation exposure of  about 2 ppm
             (vol/vol)  for 24 hours.

Vinyl Chloride                                             March 31,  1987



     0  Upon either inhalation or ingestion of 14C-vinyl chloride in rats,  the
        greatest amount of 1 4C activity was found 72 hours after treatment
        in liver followed by  kidney,  muscle,  lung and fat (Watanabe et al.,
        1976a,b).  Another study of inhalation exposure of rats to 14c-vinyl
        chloride showed the highest 14C activity immediately after treatment
        in liver and kidney,  followed by spleen and brain (Bolt et al., 1976).


     0  Bartsch and Montesano (1975)  reported two possible metabolic pathways
        for vinyl chloride, one involving alcohol dehydrogenase, the other
        involving mixed function oxidase.  Hefner et al, (1975) concluded
        that the dominant pathway at  lower exposure levels probably involves
        alcohol dehydrogenase.

     0  Vinyl chloride metabolism is  saturable (Hefner et al.,  1975;  Watanabe
        et al., 1976a; Bolt et-al., 1977).

     0  Chloroethylene oxide,  presumably through  mixed-function oxidase,  may
        be the main metabolite capable of alkylating intracellular macro-
        molecules (Laib and Bolt, 1977).


     0  Rats administered vinyl chloride by ingestion or inhalation exhale
        greater amounts of unmetabolized vinyl chloride as the dose is
        increased (Watanabe et al., 1976a, b).

     0  Vinyl chloride metabolites are excreted mainly in the urine.  In
        rats, urinary metabolites include N-acetyl-S-(2-hydroxyethylcysteine)
        and thiodiglycolic acid (Watanabe et al., 1976a).



     0  Cancer findings in humans are described under Carcinogenicity.

     0  Mutagenic effects in  humans are described under Mutagenicity.

     0  Developmental studies in humans are described under Developmental

     0  At high inhalation exposure levels, e.g., 40900 ppm (104-2,344 mg/m3),
        workers have experienced dizziness, headaches, euphoria and narcosis
        (U.S. EPA, 1985a).

     0  Symptoms of chronic inhalation exposure of workers to the vinyl
        chloride-polyvinyl chloride industry include hepatotoxicity (Marstellar^
        et al. 1975), acro-osteolysis (Lilis et al., 1975), central nervous

Vinyl Chloride                                             March 31, 1987

        system disturbances, pulmonary insufficiency, cardiovascular toxicity,
        and gastrointestinal toxicity (Miller et al., 1975; Selikoff and
        Hammond, 1975; Suciu et al., 1975).  Data on dose-responses in humans
        are scarce because few measurements of ambient vinyl chloride levels
        in the workplace were made before 1975 (Mancuso,  1975).
Short-term Exposure
     0  Inhalation exposure to high levels (ca. 100,000 ppm or 260,417
        of vinyl chloride can induce narcosis and death, and,  to lower doses,
        ataxia, narcosis, congestion and edema in lungs and hyperemia in
        liver in several species (U.S. EPA, 1985a).

Long-term Exposure

     0  Administration of vinyl chloride monomer to rats by gavage for 13
        weeks resulted in hematologic, biochemical and organ weight effects
        at doses above 30 mg/kg (Feron et al., 1975).

     0  Inhalation exposure of rats, guinea pigs, rabbits and  dogs to 50 ppm
        (130 mg/m3) vinyl chloride, 7 hours/day, 130 exposures in 139 days,
        did not induce toxicity as  judged by appearance, mortality, growth,
        hematology, liver weight and pathology.  Rats exposed  to 100 ppm
        (260 mg/m3) 2 hours/day for six months, had increased  liver weights
        (Torkelson et al., 1961).

Reproductive Effects

     0  Potential effects on reproductive capacity have not been studied.

Developmental Effects

     0  Infante et al. (1975a,b) reported an association between human
        exposure to vinyl chloride  and birth defects and fetal loss, but this
        association was contradicted by Edmonds et al. (1975)  and Hatch et
        al. (1981).

     0  Inhalation exposure of rats and rabbits to vinyl chloride concentrations
        as high as 2,500 ppm (6,500 mg/m3) on days 5 to 15 (rats) and 6 to
        18 (rabbits) of gestation and mice to vinyl chloride levels as high as
        500 ppm (1,300 mg/m3) on days 5 to 15 of gestation did not induce
        teratogenic effects but did increase skeletal variants in high dose nice
        (John et al., 1977) .

     0  A developmental effects study with vinyl chloride in rats exposed by
        inhalation to 600 or 6,000  ppm (2,160 or 21,160 mg/m3) 4 hours daily
        on gestation days 9 through 21 was negative for teratogenicity and
        inconclusive for fetotoxicity (Radike et al., 1977).

   Vinyl Chloride                                             March 31,  1987



        0  Chromosomal effects of vinyl chloride exposure in workers is  conflicting
           in that positive (Ducatmann et al.,  1975;  Purchase et al., 1975) and
           negative (Killian et al.,  1975; Picciano et al.,  1977) results have
           been reported.  Picciano et al. (1977) reported exposures of  0.13 to
           15.2 ppm (0.34 to 40 rng/rn^, time-weighted averages) for 1 to  332

        0  Vinyl chloride is mutagenic, presumably through active metabolites in
           various systems including metabolically activated systems witn S_. typhi-
           murium (Bartsch et al.,  1975);  _E.  coli (Greim et al.,  1975);  yeast
           (Loprieno et al., 1977); germ cells  of Drosophija (Verburgt and
           Vogel, 1977);  and Chinese hamster  V79 cells (Hubermann et al., 1975).

        0  Dominant lethal studies  with vinyl chloride in CD-1 mice were negative
           (Anderson et al., 1976).


        0  Increases in the occurrence of  liver angiosarcomas as  well as in tumors
           of the brain,  lung, and  hematopoietic and lymphopoietic tissues have
           been associated with occupational  exposure to the vinyl chloride-
           polyvinyl chloride industry in humans (IARC,  1979).  The initial
           report of a link between vinyl chloride exposure and cancer in humans
           by Creech and Johnson (1974),  as well as subsequent reports by others,
           indicates the high risk  and specificity of association with liver
           angiosarcoma,  a very rare tumor in humans.

        0  Ingestion of vinyl chloride monomer  in the diet by rats at feeding
           levels as low as 1.7 and 5 mg/kg/day over their lifespan induced
           hepatocellular carcinomas  and liver  angiosarcomas, respectively, as
           well as other adverse hepatic effects (Feron et al., 1981).  Til
           et al. (1983) extended the Feron et al. (1981) work to include lower
           doses and did not find a significant (P<0.05)  increase in carcinogenic
           effects at feeding levels  as high  as 0.13 mg/kg/day.  Administration
           of vinyl chloride monomer by gastric intubation for at least  52 weeks
           resulted in carcinogenic effects in  liver and other tissue sites in
           rats (Feron et al., 1981;  Maltoni  et al.,  1981).

        0  Chronic inhalation of vinyl chloride has induced cancer in liver and
           other tissue sites in rats and mice  (Lee et al.,  1977, 1978;  Maltoni
           et al.,  1981).


        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:

Vinyl Chloride                                             March 31, 1987
              HA = (NOAEL or LOAEL) x (BW) = _ mg/L ( _ Ug/L)
                     (UF) x ( _ L/day)
        NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Ef fact-Level
                         in mg/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

     There are insufficient data for calculation  of a One-day Health Advisory.
The Ten-day HA of 2.6 mg/L is proposed as a conservative estimate for a
One-day HA.

Ten-day Health Advisory

     Inhalation data by Torkelson et al. (1961) were not selected for the
Ten-day HA calculation because of preference for  studies with oral exposure.
Feron et al. (1975)  reported a subchronic toxicity study in which vinyl
chloride monomer (VCM) dissolved in soybean oil was administered by gavage to
male and female Wistar rats, initially weighing 44 g, at doses of 30, 100 or
300 mg/kg once daily, 6 days per week for 13 weeks.  Several hematological,
biochemical and organ weight values were significantly (P<0.05 or less)
different in both mid- and high-dose animals compared to controls.  The NOAEL
in this study was identified as 30 mg/kg.

     The Ten-day HA, as well as the One-day HA, for a 1 0-kg child is calculated
as follows:

         Ten-day HA = (30 mg/kg/day (6/7) (10 kg) = 2i6   /L (2,500 ug/L)
                          (100) (1 L/day)
        30 mg/kg/day = NOAEL based on absence of biochemical and organ weight
                       effects in rats exposed orally to vinyl chloride.

                 6/7 = expansion of 6 days/week treatment in the Feron et al.
                       (1975) study to 7 days/week to represent daily exposure.

               10 kg = assumed body weight of a child.
                 100 = uncertainty factor, chosen in accordance with NAS/ODW
                       guidelines for use with a NOAEL from an animal study.

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

Vinyl Chloride                                             March 31, 1987


Longer-term Health Advisory

     The Longer-term HA can be calculated from the -lifetime feeding study in
rats by Til et al. (1983).  Til et al. (1983) have extended the earlier work
by Feron et al. (1981) to include lower doses with basically the same protocol
used in the latter study.  Carcinogenic and noncarcinogenic effects were evi-
dent with a vinyl chloride dietary level of 1.3 mg/kg/day.  At dietary levels
of 0.014 and 0.13 mg/kg/day, increased incidences of basophilic foci of cellu-
lar alteration in the liver of female rats were evident.  However, basophilic
foci by themselves are concluded not to represent an adverse effect on the
liver in the absence of additional effects indicative of liver lesions such
as those found in the 1.3 mg/kg/day group; and a dose-related increase in
basophilic foci was not evident.  Therefore,  the dose of 0.13 mg/kg/day is
identified as the NOAEL for noncarcinogenic effects for the Longer-term HA

     Using the 0.13 mg/kg/day NOAEL from the Til et al. (1983) study, the
Longer-term HA for a 10-kg child is calculated as follows:

       Longer-term HA = (0.13 mg/kg/day) (10 kg) = 0>013   /L (13   /L)
                            (100) (1  L/day)
        0.13 mg/kg/day = NOAEL based on absence of adverse liver effects
                         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.

               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 = (0'13 mg/kg/day) (70 kg) = 0.046 mg/L (46 ug/L)
                            (100) (2 L/day)
        0.13 mg/kg/day = NOAEL based on absence of adverse liver effects
                         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.

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

Vinyl Chloride                                             March 31, 1987


Lifetime Health Advisory

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

     Because vinyl chloride is classified as a human carcinogen (IARC Group 1
and EPA Group A), a Lifetime Health Advisory is not recommended.

Evaluation of Carcinogenic Potential

     0  Applying the criteria described in EPA's guidelines for assessment of
        carcinogenic risk (U.S. EPA, 1986), vinyl chloride may be classified
        in Group A:  Human carcinogen.  This category is for agents for which
        there is sufficient evidence to support the causal association between
        exposure to the agents and cancer.

     0  The IARC (1979) has concluded that there is sufficient evidence to
        classify vinyl chloride as a human carcinogen in its Category 1.

     0  EPA's Carcinogen Assessment Group (CAG) recently has recalculated its
        excess carcinogenic risk estimates resulting  from lifetime exposure
        to vinyl chloride through the drinking water  (U.S. EPA, 19S5a).  CAG
        based its preliminary revised estimates on the Feron et al. (1981)
        study.  The total number of tumors, considering tumors of the lung
        and liver,  in rats exposed through the diet was used to calculate the
        excess cancer risk.   Using the 95% upper limit Cq-j* = 2.3 (mg/kg/day)-1 j
        with the linearized multistage model,  they calculated that consuming
        2 liters of water per day with vinyl chloride concentration of 1.5  ug/L,
        0.15 ug/L and 0.015 ug/L would increase the risk of one excess cancer
        per 10,000 (10-4),  100,000 (10-5) Or 1,000,000 (10-6) people exposed,
        respectively, per lifetime.  The CAG is presently reassessing the
        cancer risk estimate based on the Feron et al.  (1981) study by taking
        into account the more recent data by Til et al.  (1983) which, as

     Vinyl Chloride                                             March 31, 1987

             described previously, is an extension of the earlier Feron et al.
             (1981) work to include lower doses.

          0  Maximum likelihood estimates as well as 95% upper limits of cancer
             risks by the multistage model are presented.  Expressing risk as
             cases/lifetime/person, examples would be 0.01  mg/kg/day or 0.35 mg/L
             exposure associated with risks of 1 .6 x 1 0"2 (MLE) and 1.9 x 10-2
             (UL) and 0.001  mg/kg/day exposure associated with risks of 1.6 x 10-3
             (MLE) and 1.9 x 10-3 (UL).

          0  Cancer risk estimates (95% upper limit) with other models are presented
             for comparison with that derived with the  multistage.  For example,
             one excess cancer per 1,000,000 (10"6)  is  associated with exposure
             to vinyl chloride in drinking water at levels  of 50 ug/L (probit),
             0.5 ug/L (logit), and 0.02 ug/L (Weibull).   While recognized as
             statistically alternative approaches, the  range of risks described by
             using any of these modeling approaches has  little biological signifi-
             cance unless data can be used to support the selection of one model
             over another.  In the interest of consistency  of approach and in
             providing an upper bound on the potential  cancer risk, the EPA has
             recommended use of the linearized multistage approach.


          0  The National Academy of Sciences (NAS,  1977) estimated a 10-6 risk
             (95% upper bound estimate) from lifetime exposure to 1 ug vinyl
             chloride/L drinking water with the multistage  model and the lifetime
             ingestion study in rats by Maltoni et al.  (1981).

          0  The final RMCL by the U.S. EPA Office of Drinking Water is zero, the
             proposed MCL is 1 ug/L, and the practical quantitation level is 1 ug/L
             (U.S. EPA, 1985b).

          0  Ambient water quality critera (U.S. EPA,  1980b) are 20,  2 and 0.2 ug/L
             for risks of 10"^, 10"^, and 10"^, respectively, assuming consumption
             of 2 liters of  water and 6.5 grams of contaminated fish per day by a
             70 kg adult.

          0  A  workplace standard of 1  ppm (time-weighted average)  was set by OSHA
             in 1974 based on the demonstration of angiosarcoma of the liver in
             vinyl chloride  workers (Federal Register.   39:35890).

          0  The ACGIH (1982) has recommended a TLV of  5 ppm (10 mg/m3).

             Analysis of vinyl chloride is by  a purge  and trap gas  chromatographic
             procedure used for the determination of volatile organohalides in
             drinking water (U.S.  EPA,  1985c).   This method calls  for the bubbling
             of an inert gas through a  sample  of water and trapping the purged
             vinyl chloride on an  adsorbent material.   The adsorbent material is

      Vinyl Chloride
March 31, 1987
              heated to drive off the vinyl chloride onto a gas chromatographic
              column.  This method is applicable to the measurement of vinyl chloride
              over a concentration range of 0.06 to 1500 ug/L.   Confirmatory analysis
              for vinyl chloride is by mass spectrometry (U.S.  EPA, 1985d).  The
              detection limit for confirmation by mass spectrometry is 0.3 ug/L.
           0  The value of the Henry's  Law Constant for vinyl chloride (6.4
              atm-m3/mole) suggests  aeration as  a potential removal technique
              for vinyl chloride  in  water (ESE,1984).   Removals  of  up to 99.27%
              were achieved at 9C using a pilot packed tower aerator.  In similar
              studies,  vinyl chloride was removed from ground water using a
              spray aeration system  with total VOC concentration was 100 to
              200 ug/L  (ESE,  1984).   Greater than 99.9% VOC removal was  obtained
              using a four-stage  aeration system; each stage employed 20 shower
              heads with a pressure  drop of approximately  10 pounds per  square
              inch.  In-well aeration has also demonstrated up to 97% removal of
              vinyl chloride using an air-lift pump.   However,  practical considera-
              tions are likely to limit the application of this  (Miltner, 1984).

           0  The concentration of vinyl chloride in  southern Florida ground  water
              declined  by 25% to  52% following passage through lime softening basins
              and filters (Wood and  DeMarco,  1980).   Since vinyl chloride is  a
              highly volatile compound, it is probably volatilized  during treatment
              (ESE,  1984).

           0  Adsorption techniques  have been less successful than  aeration in
              removing  vinyl chloride from water.  In  a pilot study,  water from a
              ground water treatment plant was passed  through a  series of four
              30-inch granular activated carbon  (Filtrasorb 400) columns (Wood and
              DeMarco,  1980;  Symons,  1978);  the  empty  bed  contact time was approxi-
              mately six minutes  per column.   Influent vinyl chloride concentrations
              ranged from below detection to  19  ug/1;  erratic removal was reported.
              To  maintain effluent concentrations below 0.5 ug/1,  the estimated
              column capacity to  breakthrough was 810, 1,250, 2,760 and  2,050 bed
              volumes for empty bed  contact times of 6,  12,  19 and  25 minutes,
              respectively.  In addition,  the estimated service  life of  the acti-
              vated carbon was low.   Similarly,  poor removal of  vinyl chloride was
              achieved  using an experimental  synthetic resin, Ambersorb  XE-340,
              (Symons,  1978).

           0  Treatment technologies for the  removal of vinyl chloride from water
              have not  been extensively evaluated except on an experimental level.
              Available information  suggests  aeration  merits further investigation.
              Selection of individual or combinations  of technologies to achieve
              vinyl chloride  removal must be  based on  a case-by-case  technical
              evaluation,  and  an  assessment of the economics involved.

    Vinyl Chloride                                             March 31,  1987



    ACGIH.  1982.   American Conference of Governmental Industrial Hygienists.
         Threshold limit values  for chemical substances and physical agents in
         the workroom environment.   Cincinnati,  OH.

    Amoore,  J.E.,  and E. Hautala.   1983.   Odor as  an aid to chemical safety:
         Odor thresholds compared with threshold limit values  and volatilities
         for 214 industrial chemicals  in  air and water dilution.   J. Appl.  Toxicol.

    Anderson,  D.,  M.C.E. Hodge and  I.F.H. Purchase.   1976.   Vinyl chloride:
         Dominant  lethal studies in male  CD-1  mice.   Mutat. Res.   40:359-370.

    Bartsch,  H., C. Malaveille and  R.  Montesano.   1975.  Human, rat and  mouse
         liver-mediated mutagencity of vinyl chloride in S_. typhimurium  strains.
         Int.  J.   Cancer.  15:429-437.

    Bartsch,  H., and R. Montesano.   1975.  Mutagenic and carcinogenic effects of
         vinyl chloride.  Mutat. Res.  32:93-114.

    Bolt,  H.M.,  H. Kappus,  A. Buchter  and W. Bolt.   1976.   Disposition of
         (1,2-140 vinyl chloride in the  rat.   Arch. Toxicol.   35:153-162.

    Bolt,  H.M.,  R.J. Laib,  H. Kappus and  A. Buchter.  1977. Pharmacokinetics of
         vinyl chloride in the rat. Toxicol.   7:179-188.

    Creech,  J.L.,  and M.N.  Johnson. 1974.  Angiosarcoma of the liver in the
         manufacture of polyvinyl chloride.  J.  Occup. Med. 20:338-340.

    Ducatman,  A.,  K. Hirschhorn  and I.J.  Selikoff.   1975.   Vinyl  chloride expo-
         sure  and  human chromosome  aberrations.   Mutat. Res. 31:163-168.

    Duprat,  P.,  J.P. Fabry,  D. Gradiski and J.L.  Magadur.   1977.   Metabolic
         approach  to industrial  poisoning:  blood  kinetics  and distribution of
         14c-vinyl chloride monomer (V.C.M.).   Acta. Pharmacol. Toxicol.  Suppl.
         (Kbh) 41(1):142-143.

    Edmonds,  L.D., H. Falk  and J.E. Nissim.  1975.   Congenital malformations  and
         vinyl chloride.  Lancet.   2:1098.

    ESE, 1984. Environmental Science and  Engineering.   Technologies and  costs for
         the removal of volatile organic  chemicals from potable water supplies.
         (Draft)  ESE No. 84-912-0300.   Prepared for  U.S. EPA,  Science and Technology
         Branch, CSD, ODW,  Washington, DC.

    Federal  Register.  39:35890.

    Feron, V.J., A.J. Speek, M.I. Williams,  D.  van Battum and  A.F.  de Groot.
         1975.  Observations on  the oral  administration and toxicity of  vinyl
         chloride  in rats.   Fd.  Cosmet. Toxicol.  13:633-638.

Vinyl Chloride                                             March 31, 1987

                                     -1 3-
Feron, V.J., C.F.M. Hendrikson, A.J. Speek, H.P. Til and B.J. Spit.  1981.
     Lifespan oral toxicity study of vinyl chloride in rats.  Fd. Cosmet.
     Toxicol. 19:317-331.

Greim, H., G. Bonse, Z. Radwan, D. Reichert and D. Henschler.  1975.
     Mutagenicity In vitro and potential carcinogenicity of chlorinated
     ethylenes as a function of metabolic oxirane formation.  Biochem.
     Pharmacol. 24:2013-2017.

Hatch, M./ J. Kline and Z. Stain.  1981.  Power considerations in studies of
     reproductive effects of vinyl chloride and some structural analogs.
     Environ. Health Perspec.  41:195-201.

Hefner, R.E., Jr, P.G. Watanabe and P.J. Gehring.  1975.  Preliminary studies
     on the fate of inhaled vinyl chloride monomer in rats.  Ann. NY. Acad.
     Sci.  246:135-148.

Huberman, E., H. Bartsch and L. Sachs. 1975. Mutation induction in Chinese
     hamster V79 cells by two vinyl chloride metabolites, chloroethylene
     oxide and 2-chloro-acetaldehyde.  Int. J. Cancer.  16:639-644.

IARC.  1979.  International Agency for Research on Cancer.  IARC monographs
     on the evaluation of carcinogenic risk of chemicals to man.  Vol. 19.
     pp. 377-438.  Lyon, France.

Infante, P.F., J.K. Wagoner and R.J. Waxweiler.  1976a.  Carcinogenic,
     mutagenic and teratogenic risks associated with vinyl chloride.  Mutat.
     Res.  41:131-142.

Infante, P.P., J.K. Wagoner,  R.J. Waxweiler, A.J. McMichael and H. FaIk.
     1976b.  Genetic risks of vinyl chloride.  Lancet.  1:734-735.

John, J.A., F.A. Smith, B.K.J. Leong and B.A. Schwetz.  1977.  The effects
     of maternally inhaled viny chloride on embryonal and fetal development
     in mice, rats and rabbits.  Toxicol. Appl. Pharmacol.  39;497-513.

Killian, D.J., D.J. Picciano and C.B. Jacobson.  1975.  Industrial monitoring:
     A cytogenetic approach.   Ann. N.Y. Acad. Sci.  269:4-11.

Laib, R.J., and H.M. Bolt. 1977.  Alkylation of RNA by vinyl chloride metabo-
     lites in vitro and in vivo;  Formation of 1-N'-etheno-adenosine.
     Toxicology.  8:185-195.

Lee, C.C., J.C. Bhandari,  J.M. Winston, W.B. House,  R.L. Dixon and J.5. Woods.
     1977.  Inhalation toxicity of vinyl chloride and vinylidene chloride.
     Environ. Health Perspect.  21:25-32.

Lee, C.C., J.C. Bhandari,  J.M. Winston, W.B. House,  R.L. Dixon and J.S. Woods.
     1978.  Carcinogenicity of vinyl chloride and vinylidene chloride.
     J. Toxicol. Environ.  Health.  4:15-30.

Lilis,  R., H. Anderson, W.J.  Nicolson,  S. Daum,  A.S.  Fischbein and I.J. Seli-
     koff.  1975.  Prevalence of disease among vinyl chloride and polyvinyl
     chloride workers.  Ann.  N.Y. Acad. Sci.  246:22-41.

Vinyl Chloride                                             March 31, 1987         '


Loprieno, N., R. Barale, S. Baroncelli, H. Bartsch, G. Bronzetti, A. Cammellini,^B
     C. Corsi, D. Frezza, R. Nieri, C. Leporini, D. Rosellini and A.M. Rossi.
     1977.  Induction of gene mutations and gene conversions by vinyl chloride
     metabolites in yeast.  Cancer Res.  253-257.

Maltoni, C., G. Lefemine, A. Ciliberti, G. Cotti and D. Carretti.  1981.
     Carcinogenicity bioassays of vinyl chloride monomer:  a model of risk
     assessment on an experimental basis.  Environ.  Health Perspec.  41:3-31.

Mancuso, T.F.  1975.  Comments for opening of discussion on "neoplastic
     effects."  Ann. N.Y. Acad. Sci.  246:251-254.

Marsteller, H.J., w.K. Lelbach, R. Muller and P. Gedigk.  1975.  Unusual
     splenomegalic liver disease as evidence by peritoneoscopy and guided
     liver biopsy among polyvinyl chloride production workers.  Ann. N.Y.
     Acad. Sci.  246:95-134,

Miller, A., A.S. Tiersten, M. Chuang,  I.J. Selikoff and R. Warshaw.  1975.
     Changes in pulmonary function in workers exposed to vinyl chloride and
     polyvinyl chloride.  Ann. N.Y. Acad. Sci.  246:42-52.

Miltner, R., 1984.  Personal -communication, U.S. EPA Technical Support
     Division, ODW, Cincinnati, OH.  Cited in Technologies and Costs for the
     Removal of Volatile Organic Chemicals from Potable Water Supplies by
     Environmental Science and Engineering.

NAS.  1977.  National Academy of Sciences.  Drinking Water and Health.
      Volume 1, National Academy Press.  Washington, DC. pp. 783-787.

Parsons, F., P.R. Wood and J. DeMarco.  1984.  Transformation of Tertrac-
     hloroethene and Trichloroethene in Microcosms and Groundwater, J.A.W.W.A.,
     Vol. 26 No. 2, pg 56f.

Picciano, D.J., R.E. Flake, P.C. Gay and D.J. Killian.  1977.  Vinyl chloride
     cytogenetics.  J. Occup. Med.  19:527-530.

Purchase, IF.H,, C.R. Richardson and D. Anderson.  1975.  Chromosomal and
     dominant lethal effects of vinyl chloride.  Lancet.  2(7931):410-411.

Radike et al.  1977.  Transplacental effects of vinyl chloride in rats.
     Annual Report, pp. 183-185.  USPHS-ES-00159.  Center for Study of the
     Human Environment, Dept. Environ. Health, University of Cincinnati
     Medical Center.

Selikoff, I.J., and E.G. Hammond, eds.  1975.  Toxicity of vinyl chloride-
     polyvinyl chloride.  Ann. N.Y. Acad. Sci., Vol. 246.

Suciu, I., L. Prodan, E. Ilea, A. Paduracu and L. Pascu.  1975.  Clinical
     manifestations in vinyl chloride poisoning.  Ann. N.Y. Acad. Sci.

Vinyl Chloride                                             March 31, 1987

Symons, J.M.  1978.  Interim Treatment Guide for Controlling Organic
     Contaminants in Drinking Water Using Granular Activated Carbon.  U.S.
     EPA Office of Research and Development, MERL, DWRD, Cincinnati, OH.
     Cited in U.S. EPA SNARL Document for Vinyl Chloride (Draft) and in U.S.
     EPA May, 1983.  Treatment of Volatile Organic Compounds in Drinking
     Water.  Report No. EPA-600/8-83-019, Office of Research and Development,
     MERL, DWRD, Cincinnati, OH.

Til, H.P., H.R. Immel and V.J. Feron.  1983.  Lifespan oral carcinogenicity
     study of vinyl chloride in rats.  Final report.  Civo Institutes TNO.
     Report No. V 83.285/291099.

Torkelson, R.R., F. Oyen and V.K. Rowe.  1961.  The toxicity of vinyl chloride
     as determined by repeated exposure of laboratory animals.  Amer. Ind.
     Hyg. Assoc. J. 22:354-361.

U.S. EPA.  1979.  U.S. Environmental Protection Agency.  Water related
     environmental fate of 129 priority pollutants.  Office of Water Planning
     and Standards.  EPA-440/4-79-029.

U.S. EPA.  1980a.  U.S. Environmental Protection Agency.  Vinyl chloride
     Occurrence in drinking Water,  food and air.  Office of Drinking Water.

U.S. EPA.  1980b.  U.S. Environmental Protection Agency.  Ambient water quality
     criteria for vinyl chloride.  Office of Water Regulations and Standards.
     EPA 440/5-80-078.

U.S. EPA.  1985a.  U.S. Environmental Protection Agency.  Final draft for
     the drinking water criteria document on vinyl chloride (Office of
     Drinking Water).  TR-540-162.

U.S. EPA.  1985b.  U.S. Environmental Protection Agency.  National primary
     drinking water regulations; Volatile synthetic organic chemicals; Final
     rule and proposed rule.  Federal Register.  50(219):46880-46933.
     November 13.

U.S. EPA.  1985c.  U.S. Environmental Protection Agency.  Method 502.1.
     Volatile halogenated organic compounds in water by purge and trap gas
     chromatography.   Environmental Monitoring and Support Laboratory, Cincin-
     nati, Ohio 45268.  June 1985.

U.S. EPA.  1985d.  U.S. Environmental Protection Agency.  Method 524.1.
     Volatile organic compounds in  water by gas chromatography/mass
     spectroraetry.  Environmental Monitoring and Support Laboratory,  Cincin-
     nati, Ohio 45268.  June 1985.

U.S. EPA.  1986.  U.S. Environmental Protection Agency.  Guidelines for
     carcinogenic risk assessment.   Federal Register 51(185):33993-34003.
     September 24.

U.S. ITC.  1983.  U.S. International Trade Commission.  Synthetic organic
     chemicals United States production,  1982.  USTIC Publication 1422.
     Washington, D.C. 20436.  1983.

Vinyl Chloride                                             March 31, 1987


Verburgt, F.G., and E. Vogel.  1977.  Vinyl chloride mutagenesis in Drosophila
     melanogaster.  Mutat. Res.  48:327-333.

Vogel, T., and P. McCarty.  1985.  Biotransformation of Tetrachloroethylene
     to Trichloroethylene, Dichloroethylene, Vinyl Chloride, and Carbon
     Dioxide Under Methanogenic Conditions, Applied and Environmental
     Microbiology, Vol 49 No.5.

Watanabe, P.G., G.R. McGowan and P.J. Gehring.  1976a.  Fate of (1 4C) vinyl
     chloride after single oral administration in rats.  Toxicol.  Appl.
     Pharraacol.  36:339-352.

Watanabe, P.G., G.R. McGowan, E.O. Madrid and P.J. Gehring.  1976b.  Fate of
     O^C) vinyl chloride following inhalation exposure in rats.  Toxicol.
     Appl. Pharmacol.  37:49-59.

Withey, J.R.  1976.  Pharmacodynamics and uptake of vinyl chloride  monomer
     administered by various routes to rats.  J. Toxicol. Environ.  Health.

Withey, J.R., and B.T. Collins.  1976.  A statistical assessment of the
     quantitative uptake of vinyl chloride monomer from aqueous solution.
     J. Toxicol. Environ. Health.  2:311-321.

Wood, P.R., and J. DeMarco.  1980.  Effectiveness of various adsorbents in
     removing organic compounds from water. 1:  Removing purgeable  halogenated
     organics.  In: Activated Carbon Adsorption of Organics from the Aqueous
     Phase. Volume 2.  Ann Arbor Science, pp. 85-114.