March  31,  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.

    Acrylamide                                                 March  31,  1987

         This  HA is  based  on  information  presented  in  the  Office of  Drinking
    Water's  draft Health Effects  Criteria Document  (CD)  for Acrylamide (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 #  86-117744/AS. The toll-free number is  (800)
    336-4700;  in the Washington,  D.C.  area: (703) 487-4650.


    CAS No.    79-06-1

    Chemical Structure
                                      H H 0
                                      I  Mi
             '                                 ^^ H

         0   2-Propenamide, acrylic amide,  acrylic acid amide, akrylamid, ethylene
            carboxamide and propinoic acid amide.


         0   As the monomer,  in:
              Soil stabilizers

         0  As the polyacrylamide, in:
              Flocculant production - drinking water and wastewater treatment plants
              Additive  for enhanced oil recovery
              Fog dissipator
              Soil stabilizer
              Paper and paperboard strengthener
              Adhesive/binder component
              Metal coating
              Food packaging
              Photography applications
              Chromatography gel
              Electrophoresis gel
              Dye applications

    Properties   (Windholz, 1976;  Verschueren,  1983)

            Chemical Formula                       C3H5NO
            Molecular  Weight                       71.08
            Physical State (room temp.)            white crystals
            Boiling Point (at 25 mmHg)             125  C
            Melting Point                         84.5 C
            Vapor Pressure (25C)                  0.007 mmHg

     Acrylamide                                               March 31, 1987

             Specific Gravity (30C)                 1.122 g/mL
             Water Solubility (30C)                 2155 g/L
             Chloroform Solubility (30C)           26.6 g/L
             Benzene Solubility (30C)               3.46 g/L
             Octanol/Water Partition  Coefficient    
             Taste Threshold (water)
             Odor Threshold (water)
             Odor Threshold (air)
             Conversion Factor                       1  mg/m3 = 0.34 ppm
             Conversion Factor                       1  ppm = 2.95 mg/m3

             The production of acrylamide in 1982 was estimated to be 86 million
             pounds (U.S. ITC, 1984).  Acrylamide is used primarily in the produc-
             tion of polyacrylamide polymers and co-polymers.  It is also used as
             a grouting agent, and approximately 1 million pounds is used for this
             purpose (U.S. EPA,  1984).

             Acrylamide monomer  occurs  as a contaminant in polyacrylamide.  The
             monomer may be released to the environment during its production, its
             use in manufacturing polymers and during the use of polyacrylamides.
             However, the major  source  of release occurs as a result of its use as
             a grout.  No information on production and manufacture releases is
             available.  Due to  the low vapor pressure of acrylamide, no releases
             to air are expected (U.S.  EPA, 1984).

             Acrylamide has been shown  to biodegrade in surface waters within a
             few days (Brown and Rhead,  1979).  Waters which routinely receive
             acrylamide releases will degrade it even more readily.  Hydrolysis of
             acrylamide to acrylic acid has been reported to occur, but is likely
             to be a relatively  slow reaction (Brown and Rhead 1979; Brown et al.

             Acrylamide has not  been surveyed for in U.S. food and drinking water.
             Based upon standards recommended by EPA for polymers used in drinking
             water,  the levels of acrylamide monomer in drinking water have been
             reported to occur up to 0.5 ug/L (U.S. EPA,  1980).  One study in
             England has reported tap water levels of acrylamide in the low ug/L
             range (Brown and Rhead, 1979) .  No information has been identified
             on the occurrence of acrylamide in food.  Low levels of acrylamide
             also may occur in some foods from the use of polyacrylamides in the
             manufacture of those foods  (U.S. EPA, 1984).
             When acrylamide  (10  mg/kg)  was  administered  to  rats  per  os,  it was
             absorbed rapidly and completely from the  gastrointestinal tract
             (Miller  et al.,  1982).

Acrylamide                                                   March 31, 1987

     0  By comparing the blood levels of acrylamide after iv or dermal
        administration, it was calculated that approximately 25% of either
        applied dose (2 or 50 mg/kg) was absorbed through the skin (Ramsey et
        al., 1984).

     0  Recently, it was reported that 26% of a 0.5% solution of acrylamide
        was absorbed through the skin of rats in 24 hours.  An additional 35%
        was present in the skin and, potentially, available for absorption.
        Using excised skin preparations, they found that 67% (54% absorbed
        and 13% present in skin after washing) of the acrylamide was either
        absorbed or available for absorption  (Frantz et al., 1985).


     0  After acrylamide was administered to rats by gavage, the highest
        concentrations were found in red blood cells, with lower amounts
        found in all other tissues examined (Ramsey et al., 1984).

     0  Results reported by Hashimoto and Aldridge (1970) indicate that acryla-
        mide is bound covalently to proteins or other cellular macromolecules.

     0  Acrylamide freely crosses the placenta in pregnant female rats,
        rabbits, dogs and pigs (Edwards, 1976; Ikeda et al., 1983) and is
        uniformly distributed throughout dog and pig fetal tissue (Ikeda
        et al., 1983).

     0  Autoradiographic studies revealed that, after oral administration of
        120 mg/kg, acrylamide was widely distributed in male and female mice.
        The fetuses of pregnant mice were uniformly labeled, except that there
        was a concentration of acrylamide in fetal skin (Marlowe et al., 1986).


     0  In rats, acrylamide is metabolized primarily by conjugation with
        cellular glutathione (Miller et al.,  1982).

     0  The major metabolite (greater than 50%) of acrylamide is the mercapturic
        acid, N-acetyl-S-(3-amino-3-oxypropyl) cysteine (detected in the urine
        of rats given acrylamide orally or intravenously (Miller et al., 1982;
        Ramsey et al., 1984).

     0  Another metabolite resembling cysteine-5-propionamide has been
        tentatively identified (Dixit et al., 1982).
        In rats, excretion of acrylamide and its metabolic products occurs
        primarily via the urine (Miller et al., 1982; Ramsey et al., 1984).

        Over 60% of a dose of acrylamide, administered either orally or iv,
        appeared in the urine of rats within 24 to 72 hours (Miller et a-1.,
        1982; Ramsey et al., 1984).

    Acrylamide                                                March  31,  1987

         0  Minor routes  (less  than 6%)  of  acrylamide  elimination in  rats  include
            fecal excretion (Miller et al., 1982)  and  release of  the  amide carbon
            as CO2 following oxidation (Hashimoto  and  Aldridge,  1970;  Ramsey
            et al.,  1984).


    Humans                                                                      !

            Acrylamide  intoxication has  been  reported  in  five individuals  (three
            adults and  two  children) exposed  via ingestion of drinking water
            contaminated with 400 ppm acrylamide (Igisu et al., 1975).   All  three
            adults exhibited symptoms of widespread  central and peripheral nervous
            system dysfunction.  The children apparently  consumed less  water than
            the adults  and  were  less severely affected.

            Additional  reports on human  exposure to  acrylamide deal primarily
            with dermal or  inhalation exposure of  workers.  The predominant
            effects  included dysfunction of the central and/or peripheral  nervous
            systems.  Quantitative  data  on  dose and  duration of exposure generally
            were not available in these  reports (Auld  and Bedwell, 1967; Garland
            and Patterson,  1967; Fullerton, 1969;  Davenport et al.,  1976;  Kesson
            et al.,  1977).
            Evaluation  of  the  toxicological data base  for  acrylamide  indicates
            that this chemical is  a  cumulative  poison.  It has  been shown  that
            when the  total dose of acrylamide administered over either  short  or
            longer  periods of  time reaches 100  to  150  mg/kg,  signs of neuropathology
            begin to  appear in many  species tested (U.S.  EPA,  1985a).
    Short-term Exposure
            Reported  acute  oral LD50  values  for  rats, guinea pigs  and  rabbits
            range  from  150  to  180 mg/kg  (McCollister et  al., 1964).  Acute  oral
            LD50 values  for mice have been reported to range from  107  to  170 mg/kg
            (NIOSH, 1976; Hashimoto et al.,  1981).

            An  acute  oral LD$Q for acrylamide  in male F-344 rats was reported  to
            be  202.5  (range of 188.9  to  217.3) mg/kg (Pryor et al., 1983).

            Single doses of acrylamide,  administered at  levels as  low  as  25 mg/kg,
            have been shown to significantly increase binding of the neurotrans-
            mitter 3H-spiroperidol in rat brains (Agrawal et al.,  1981).

            Single doses of acrylamide (1 to 100 mg/kg), administered  via ip
            injection,  were shown to  cause significant inhibition  of retrogade
            axonal transport in rats  at  doses  of 25 mg/kg or greater.  Doses of
            1,  5, or  15  mg/kg  caused  no  inhibition of transport (Miller et  al.,

Acrylamide                                                  March 31, 1987


     0  Cats given acrylamide in the diet at levels of 20 mg/kg/day for 2 or
        3 weeks developed hind limb weakness and general unsteadiness of the
        posterior half of the body which usually progressed to hind limb
        paralysis (Leswing and Ribelin, 1969).  Microscopically, the affected
        nerves exhibited degeneration of myelin and axons.

     0  Dogs that were given acrylamide orally at levels of 5 mg/kg/day
        developed ataxia and muscular weakness by day 21 of treatment;
        de-myelination of nerves was evident af-ter 60 days (Thomani et al.,

     0  Rats administered acrylamide in their drinking water displayed hind
        limb splaying after 14 days of treatment at a dose of 30 mg/kg/day.
        Microscopic changes in peripheral nerves were observed in animals
        dosed at 10 and 30 mg/kg/day.  A NOAEL of 3 mg/kg/day was identified
        (Gorzinski et al., 1979).

     0  Monkeys treated with an average dose of 7.1 mg/kg/day (administered
        orally in fruit juice) developed signs of visual impairment after  28
        days; ataxia and motor impairment occurred after 46 to 65 days of
        exposure (Merigan et al.,  1982).

Long-term Exposure

     0  Most adverse health effects of acrylamide appear to be the result  of
        damage to central or peripheral nerve tissue.  The most  characteristic
        effects are weakness and ataxia in hind limbs, progressing to paralysis
        with continued  exposure  (Pryor et al.,  1983;  Thomann et  al.,  1974;
        McCollister et  al.,  1964).

     0  The subacute  (5 days/wk  for 4 wks) and subchronic  (5 days/wk  for
        15 wks) LDsos for acrylamide are 32.0  (25.8  to  38.2) and 17.0 (15.3
        to  18.7) mg/kg, respectively  (Pryor  et al.,  1983).

      0  Acrylamide administered  in drinking  water  to rats  at levels  of
        1 mg/kg/day for 90 days  caused no external signs of toxicity, but
        histologic evidence  of neuropathy was noted  (axolemmal  invaginations)
         (Burek et al.,  1980).  The NOAEL in  this study was determined to be
        0.2 mg/kg/day.

        Cats  receiving  oral  doses  of  1 mg/kg/day for 125 days developed
        ataxia  (Kuperman,  1958).

      0  Cats  fed  0.7  mg/kg/day  for 240 days  developed hind limb weakness;  a
        NOAEL of  0.2  mg/kg/day  was identified  in this study  (McCollister
        et  al.,  1964).

 Reproductive  Effects

      0  Mice,  dosed  orally  with  acrylamide  at  10.1 mg/kg/day  for 8 to 10  weeks,
         displayed testicular atrophy and significant reduction  in testes
         weight with  degeneration of the  epithelial cells  of  the seminiferous
         tubules  (Hashimoto et al., 1981).

Acrylamide                                               March 31, 1987


Developmental Effects

     0  Acrylamide,  administered by gavage at 20 mg/kg/day to pregnant rats on
        days 7 through 16 of gestation,  significantly reduced 3H-spiroperidol
        binding in the striatal tissue of 2-week-old pups (Agrawal and Squibb,


       Acrylamide did not elicit mutagenic activity in the Salmonella Ames
        test in strains TA 98, TA 100, TA 1535 and TA 1537 with or without
        microsomal activation (Bull et al., 1984a).

     0  In the hepatocyte primary culture DNA repair test, acrylamide did not
        exert mutagenic effects (Miller and McQueen,  1986).

     0  Acrylamide induced chromosome breaks and aberrations in spermatogonia
        of mice exposed to 75 mg/kg/day in the diet for two or three weeks
        (Shiraishi,  1978).

     0  In a dominant lethal study,  male rats received acrylamide at 0, 15,
        30 or 60 mg/L for 80 days in their drinking water (0, 1.5, 2.8 or 5.8
        mgA9/day; Smith et al., 1986).   The males were mated to untreated
        females which were killed on day 14 of gestation.  A significant
        increase in preimplantation loss was noted in females mated to males
        treated at 60 mg/L.  Significant post-implantation loss was observed
        in females mated to the mid- and high-dose males (30 and 60 mg/L).
        The authors  concluded that acrylamide produces dominant lethality in
        the male rat.  This effect was noted at dose levels at which no
        hindlimb splaying was evident or significant histopathological lesions
        of the sciatic nerve occurred as determined by light microscopy.

Carcinogenici ty

     0  Groups of male and female Fischer 344 rats received drinking water
        containing acrylamide monomer at 0,  0.01,  0.1,  0.5 or 2.0 mg/kg/day
        for 2 years  (Johnson et al., 1986).  After a year, significant
        depression of body weight was observed in the highest dose males.
        Distal neuropathy was observed in the peripheral nerves of animals in
        this group.   Tumor incidence was not increased significantly in the
        groups receiving 0.01 or 0.1  mg/kg/day.  Male rats receiving 0.5
   Acrylamide                                                   March 31,  1987

        0  Male and female mice that received acrylamide orally or intraperitoneally
           at average daily doses of 2.7,  5.4 or 10.7 mg/kg/for eight weeks
           showed statistically significant increases in the incidence of lung
           adenomas (Bull et al., 1984a).   Acrylamide was more potent by gavage
           than by systemic routes.


        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-Effeet-Level
                            in mg/kg bw/day.

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

                       UF = uncertainty factor (10, 100 or 1,000), in
                            accordance with NAS/ODW guidelines.

                	 L/day = assumed daily water consumption of a child
                            (1 L/day) or an adult (2 L/day).

        No adequate dose-response data representing the oral route of exposure
   are available from which to develop short term risk assessments.  However, in
   view of substantial chemical disposition evidence showing that acrylamide is
   absorbed rapidly and completely by virtually any route of exposure, it is
   considered acceptable to use data generated following exposure via other

   One-day Health Advisory

        The results of Miller et al.  (1983) are considered appropriate for use
   in calculating the One-day HA.   In this study, male Sprague-Dawley rats  (five
   animals per dose) were  injected  intraperitoneally with a single dose  of
   acrylamide  (1 to  100 mg/kg) and  the rate  of retrograde axonal transport of
   iodinated nerve growth  factor was  measured.  The authors determined  that
   significant inhibition  of transport occurred at or above doses of 25  mg/kg,
   while  no significant changes were seen at or below 15 mg/kg.  A NOAEL of
   15 mgAg was  identified.

        The One-day HA for  the 10 kg child is calculated as follows:

             One-day HA =  (15 mg/kg/day) (10  kg) =  , .5 mg/L  (^ 50o ug/L)
                              (100)  (1 L/day)

Acrylamide                                                  March 31, 1987


        15 mg/kg/day = NOAEL, based on absence of neurotransport inhibition
                       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.

Ten-day Health Advisory

     The results of Gorzinski et al. (1979) are considered appropriate for
use in calculating the Ten-day HA.  In this study, acrylamide was administered
at levels of 0, 1, 3, 10 or 30 mg/kg/day in drinking water to male and female
CDF Fischer 344 rats for 21 consecutive days.  Based upon histological exam-
ination of peripheral nerves using both light and electron microscopy, it
was determined that axon degeneration and demylenization occurred at the 10
and 30 mg/kg/day dose levels while no significant changes were apparent at
the 0, 1 or 3 mg/kg/day dose levels.  A NOAEL of 3 mg/kg/day was identified.

     The Ten-day HA for the 10 kg child is calculated as follows:

           Ten-day HA = 13 mg/kg/day)(10 kg) = 0.3 mg/L (300 ug/L)
                           (100)(1 L/day)


        3 mg/kg/day = NOAEL, based on absence of neuropathy 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.

Longer-term Health Advisory

     The results of Burek et al. (1980) are considered appropriate for use in
deriving the Longer-term HA.  In this study, acrylamide was administered in
drinking water for 90 days to male and female CDF rats at dose levels of
0, 0.05, 0.2, 1,  5 or 20 mg/kg/day.  Electron microscopy revealed that animals
dosed at 1  mg/kg/day exhibited axolemmal invaginations of peripheral nerves.
No significant alterations were observed at the 0, 0.05 and 0.2 mg/kg/day
dose levels.  Thus, based on the most sensitive measure of toxicity employed
in these studies (ultrastructural examination of peripheral motor nerves), it
was concluded that 0.2 mg/kg was the NOAEL.

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

Acrylamide                                               March 31,  1987


        Longer-term HA = (0.2 mg/kg/day) (10 kg)_ = 0.02 mg/L (20 ug/L)
                             (100) (1  L/day)


        0.2 mg/kg/day = NOAEL,  based on absence of neuropathy 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 the 70 kg adult is calculated as follows:

        Longer-term HA = (0'2 mg/kg/day) (70 kg) = 0.07 mg/L (70 ug/L)
                             (100) (2 L/day)


        0.2 mg/kg/day = NOAEL,  based on absence of neuropathy 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.

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.

Acrylamide                                                  March 31, 1987

                                     -1 1-
     The study by Burek at al. (1980) is the most appropriate from which to
derive the DWEL.  The experimental details are described in the Longer-term
Health Advisory section.  An additional uncertainty factor of 10 is included
in order to accommodate for use of a less-than-lifetime study.  From the
results of the study, a NOAEL of 0.2 mgA<3 was identified.

     The RfD and DWEL are calculated as follows:

Step 1:  Determination of the Reference Dose (RfD)

                   RfD = (0.2 mg/kg/day) = Q.0002 mgAg/day

        0.2 mgAg/day = NOAEL.

                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.

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

            DWEL = (0.002 mg/kg/day)(70 kg) = 0.007   /L (7 u /L)
                          (2 L/day)


                70 kg = assumed body weight of an adult.

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

Step 3:  Determination of the Lifetime Health Advisory

     Acrylamide may be classified in group B2:   Probable Human Carcinogen.
Therefore, a Lifetime HA is not recommended for acrylamide.

     The estimated excess cancer risk associated with lifetime exposure to
drinking water containing acrylamide at 7 ug/L is approximately 7 x 10~4.
This estimate represents the upper 95% confidence limit from extrapolations
prepared by EPA'3 Carcinogen Assessment Group using the linearized, multistage
model.  The actual risk is unlikely to exceed this value,  but there is consid-
erable uncertainty as to the accuracy of risks  calculated  by this methodology.

Evaluation of Carcinogenic Potential

     0  The data from the Bull et al.  (1984a,b)  and the Johnson et al.  (1986)
        studies in mice and rats show that acrylamide has  significant carcino-
        genic potential.

     0  On the basis  of the results observed in the rat drinking water study
        (Johnson et al., 1986),  EPA's Carcinogen Assessment Group (CAG) has
        prepared a draft quantitative risk assessment of acrylamide exposure
        (U.S. EPA,  1985c).   In this draft assessment,  CAG  derived several

      Acrylamide                                                 iMarch 31, 1987


              carcinogenic potency factors from different sets of dose-response
              data.  CAG recommended,  however, that the human potency factor (q-|*)
              of 3.7 (mg/kg/day)~1 derived from the combination of tumor incidence
              data on mammary gland,  thyroid and uterus in the females be used for
              estimating the increased lifetime risk of human exposure to acrylamide.
              Assuming that a 70 kg adult ingests 2 L of water per day over a 70-year
              lifetime, the estimated excess cancer risk at 10~4, 1 0~5 and 10~6 would
              be 1  ug/L,  0.1  ug/L and  0.01  ug/L,  respectively. (These estimates
              were made by the Office of Drinking Water).  While recognized as
              statistically alternative approaches, the range of risks described by
              using any of these modelling 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 Agency has
              recommended use of the linearized multistage approach.

           0  Applying the criteria described in EPA's guidelines for assessment
              of carcinogenic risk (U.S. EPA, 1986), acrylamide is classified in
              Group B2:  Probable human carcinogen.  Group B2 contains substances
              with sufficient evidence of carcinogencity in animals and inadequate
              evidence from human studies.


           0  Polyacrylamide  products  used  as coagulant aids in the treatment
              of drinking water should not have a residual monomer content
              greater than 0.5 ug/L (U.S. EPA, 1980).


           0  There is  no standardized method for the determination of acrylamide
              in drinking water.  An analytical procedure for the determination of
              acrylamide  has  been reported  in the literature (Brown and Rhead,  1979).
              This procedure consists  of bromination, extraction of the brominated
              product from water with  ethyl acetate and quantification using high
              performance liquid chromatography (HPLC) with an ultraviolet detector.
              The concentration of the ethyl acetate to dryness and dissolution in
              a small volume  of distilled water prior to HPLC analysis allows the
              detection of acrylamide  at concentrations of 0.2 ug/L.
              Croll et al.  (1974)  conducted laboratory experiments to determine the
              effectiveness of conventional treatments such as coagulation and rapid
              gravity sand  filtration for removal of acrylamide.   Several 400 ml samples
              of Thames River water (pH 7.5)  containing 25 mg/L kaolin were coagulated
              by adding 32  mg/L alum and 2 mg/L of an acrylamide-based polymer with a
              residual acylamide monomer content of 0.19%.  Only  about 5% of the
              residual monomer was removed by this method, suggesting that full-scale
              water plants  using conventional treatment techniques would not be
              successful in removing acrylamide from drinking water.

Acrylamide                                                 March 31, 1987

        The removal of acrylamide from water by adsorption was studied by
        Brown et al. (1980a) using various adsorbants including granular
        activated carbon (GAC) and synthetic resins.  The data indicated
        that GAC may be an effective treatment process.  GAC removed 94 to
        96% of the acrylamide from a sample containing 0.5 mg/L and 68 to
        70% from a sample containing 10 mg/L.  The adsorption of acrylamide
        was not affected significantly by changes in pH.  No significant
        adsorption was achieved by any of the resins tested,  including the
        XAD-2 resin.

        In a laboratory experiment conducted by Croll et al.  (1974),
        water containing 6 ug/L acrylamide (at pH 5.0)  was dosed with
        8 mg/L powdered activated carbon (PAC) and mixed for 30 minutes.
        Only 13% of the acrylamide was removed.  These data indicate that PAC
        may not be effective for acrylamide removal from drinking water
        under conditions used generally in water treatment plants.

        No data were found on the removal of acrylamide by aeration.   Since
        its Henry's Law Constant is 4.38 x 10~3 atm (at 20C),  aeration
        probably would not be very effective.

        Croll et al. (1974)  evaluated the effects of some chemical oxidacive
        treatments on removal of acrylamide.  Potassium permanganate and ozone
        were found to be highly effective in removing the substance.   Additional
        data to optimize these processes are needed.  Oxidative degradation
        products also should be identified and evaluated for toxicity and

        Selection of individual or combinations of technologies to achieve
        acrylamide reduction must be based on a case-by-case technical
        evaluation and an assessment of the economics involved.

    Acrylamide                                                  March 31,  1987

                                         -1 4-


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Acrylamide                                                  March 31, 1987

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Acrylamide                                                 March 31, 1987

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Acrylamide                                                      March 31,  1987

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