March 31, 1987
820K87121
ACRYLAMIDE
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members of the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for One-day, Ten-day, Longer-term
(approximately 7 years, or 10% of an individual's lifetime) and Lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
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.
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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.
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 79-06-1
Chemical Structure
H H 0
I Mi
H-C=C-C-N
' ^^ H
Synonyms:
0 2-Propenamide, acrylic amide, acrylic acid amide, akrylamid, ethylene
carboxamide and propinoic acid amide.
Uses;
0 As the monomer, in:
Grouts
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 (25°C) 0.007 mmHg
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Specific Gravity (30°C) 1.122 g/mL
Water Solubility (30°C) 2155 g/L
Chloroform Solubility (30°C) 26.6 g/L
Benzene Solubility (30°C) 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
Occurrence
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.
1980b).
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).
III. PHARMACOKINETICS
Absorption
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).
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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).
Distribution
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).
Metabolism
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).
Excretion
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).
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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).
IV. HEALTH EFFECTS
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).
Animals
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.,
1983).
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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.,
1974).
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).
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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,
1981).
Mutagenicity
° 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
mgA
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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.
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
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)
where:
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
routes.
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)
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where:
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)
where:
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:
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Longer-term HA = (0.2 mg/kg/day) (10 kg)_ = 0.02 mg/L (20 ug/L)
(100) (1 L/day)
where:
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)
where:
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.
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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
(1,000)
where:
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)
where:
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
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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.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
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).
VII. ANALYTICAL METHODS
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.
VIII. TREATMENT
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.
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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 20°C), 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
reactivity.
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.
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IX. REFERENCES
Agrawal, A.K., P.K. Seth, R.E. Squibb, H.A. Tilson, L.L. Uphouse and S.C. Bondy.
1981. Neurotransmitter receptors in brain regions of acrylamide-treated
rats. I: Effects of a. single exposure to acrylamide. Pharmacol.
Biochem. Behav. 14:527-531.
Agrawal, A.K., and R.E. Squibb. 1981. Effects of acrylamide given during
gestation on dopamine receptor binding in rat pups. Toxicol. Lett.
7:233-238.
Auld, R.B., and S.F. Bedwell. 1967. Peripheral neuropathy with sympathetic
overactivity from industrial contact with acrylamide. Can. Med. Assoc. J.
96:652-654.
Brown, L., and M. Rhead. 1979. Liquid chromatographic determination of
acrylamide monomer in natural and polluted aqueous environment. Analyst.
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