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Acrylamide
CASRN 79-06-1
Contents
0286
Acrylamide; CASRN 79-06-1
Health assessment information on a chemical substance is included in IRIS only
after a comprehensive review of chronic toxicity data by U.S. EPA health
scientists from several Program Offices and the Office of Research and
Development. The summaries presented in Sections I and II represent a
consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Acrylamide
File On-Line 09/26/1988
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) on-line 03/01/1991
Inhalation RfC Assessment (I.B.) message 11/01/1990
Carcinogenicity Assessment (II.) on-line 07/01/1993
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
Last Revised -- 03/01/1991
The oral Reference Dose (RfD) is based on the assumption that thresholds exist
for certain toxic effects such as cellular necrosis. It is expressed in units
of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanning
perhaps an order of magnitude) of a daily exposure to the human population
(including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime. Please refer to the Background
Document for an elaboration of these concepts. RfDs can also be derived for
the noncarcinogenic health effects of substances that are also carcinogens.
Therefore, it is essential to refer to other sources of information concerning
the carcinogenicity of this substance. If the U.S. EPA has evaluated this
substance for potential human carcinogenicity, a summary of that evaluation
will be contained in Section II of this file.
___I.A.1. ORAL RfD SUMMARY
Critical Effect Experimental Doses* UF MF RfD
-------------------- ----------------------- ----- --- ---------
Nerve damage NOEL: 0.2 mg/kg/day 1000 1 2E-4
mg/kg/day
Rat Subchronic LOAEL: 1 mg/kg/day
Drinking Water Study
Burek et al., 1980
*Conversion Factors: None
___I.A.2. PRINCIPAL AND SUPPORTING STUDIES (ORAL RfD)
Burek, J.D., R.R. Albee, J.E. Beyer, et al. 1980. Subchronic toxicity of
acrylamide administered to rats in the drinking water followed by up to 144
days of recovery. J. Environ. Pathol. Toxicol. 4: 157-182.
Acrylamide was administered in drinking water to male and female Fischer 344
rats (10/sex/dose) at dose levels of 0, 0.05, 0.2, 1, 5, or 20 mg/kg/day for
90 days. Additional groups of male rats (10/dose) were treated at the same
dose levels and held, without treatment, for another 144 days to ascertain
whether recovery could occur. For microscopic examination of nerve tissue,
male rats only, were treated at the same dose levels for 3 months; the control
and high dose groups consisted of nine rats each, while three rats were used
in all other treatment groups.
At the conclusion of the latter study, the left sciatic nerve was examined
under light and electron (EM) microscopy for damage. No significant adverse
effects were seen in the 0.05 or 0.2 mg/kg/day groups, while the 5 and 20
mg/kg/day groups had frank nerve degeneration. In the 1 mg/kg/day group, a
slight, but significant, increase in peripheral axolemnal invaginations were
observed under EM, but not when using light microscopy. After 144 days of
recovery (no acrylamide treatment), the lesions observed at the 20 mg/kg/day
dose level had partially or completely reversed. At lower doses, there
appeared to be a complete reversal. A NOEL of 0.2 and a LOAEL of 1 mg/kg/day
were established using EM.
In the main portion of the study (Burek et al., 1980) hind limb splaying was
observed only in the 20 mg/kg/day group on day 22 of the study. Significant
decreases in packed cell volume (PCV), red blood cell (RBC), and hemoglobin
(Hgb) were seen in female rats at the 5 mg/kg/day dose level. Serum
cholinesterase was decreased in females at the 20 mg/kg/day level. There were
no decreases in serum cholinesterase in any other group. In addition, no
changes in blood urea nitrogen or serum alanine aminotransaminase were noted
in any group. At the high dose level, PCV, RBC, and Hgb concentration were
decreased.
A chronic study conducted by the Dow Chemical Co. (1985) gave similar results.
Groups of male Fischer 344 rats (n=3) were given acrylamide in their drinking
water at doses of 0, 0.01, 0.1, 0.5, or 2 mg/kg/day for 2 years. Rats were
sacrificed after 3, 6, 12, 18, and 24 months of treatment. After sacrifice,
the tibial nerve was observed under light and EM. At 3, 6, and 12 months, the
rats on 2 mg/kg/day displayed early signs (axolemmal invaginations) of nerve
damage using EM. However, at 18 and 24 months, there was a marked increase in
spontaneous nerve damage in control rats, obscuring any possible differences,
as judged by EM, among the treatment groups. The authors postulated that the
small numbers (n=3) of rats in each experimental group and the small size (0.1
cm) of the examined samples may have accounted for the results. Nevertheless,
using EM, the 18 and 24 months results are indeterminate. Using light
microscopy, however, a 2-year NOEL of 0.5 mg/kg/day was established. Although
a 2-year study, it was not selected for use in the RfD calculation, since the
NOEL was found using light microscopy, a fairly insensitive measure of
structural integrity.
___I.A.3. UNCERTAINTY AND MODIFYING FACTORS (ORAL RfD)
UF -- The UF of 1000 allows for uncertainty in the extrapolation of dose
levels from laboratory animals to humans (10A), uncertainty in the threshold
for sensitive humans (10H), and uncertainty in the effect of duration when
extrapolating from subchronic to chronic exposure (10S). The chronic study
did not adequately address the latter uncertainty because of the lack of a
sensitive measurement of the critical effect.
MF -- None
___I.A.4. ADDITIONAL COMMENTS (ORAL RfD)
Female Fischer 344 rats were given acrylamide in their drinking water at doses
of 0, 0.5, 2, or 5 mg/kg/day for 10 weeks throughout gestation and lactation
(Nalco Chemical Co., 1985). At the highest dose level, there were decreases
in body weight and body weight gain and an increase in pre-implantation loss.
At the 2 mg/kg/day dose, the females had a decreased number of litters
(decreased fecundity index), but no effects were noted at 0.5 mg/kg/day. This
section of the study demonstrated a NOEL of 0.5 mg/kg/day and a LOAEL of 2
mg/kg/day. In a second part of this study, male Fischer 344 rats were given
acrylamide in drinking water at doses of 0, 0.5, 2.0, or 5.0 mg/kg/day for 10
weeks. A NOEL of 0.5 mg/kg/day and a LOAEL (lower body weight gain and ataxia)
of 2.0 were found.
Rats were given acrylamide (0, 1.5, 2.8, or 5.8 mg/kg/day) for 80 days (Smith
et al., 1986). A NOEL of 1.5 mg/kg/day and a LOAEL of 2.8 mg/kg/day (post-
implantation loss) were established.
___I.A.5. CONFIDENCE IN THE ORAL RfD
Study -- High
Data Base -- Medium
RfD -- Medium
The principal study was very well-designed for the evaluation of a large
number of endpoints and employed a sensitive measure of the most appropriate
endpoint. The study also used more than the minimum number of treatment
groups and included a long post-treatment recovery period. Although the
extensive data base includes studies covering all important toxicologic
endpoints and supports the choice of critical effect, it is assigned a medium
confidence level since there are no accepted chronic studies. Confidence in
the RfD is rated medium only because of the lack of a sensitive measure of the
critical effect for chronic exposure.
___I.A.6. EPA DOCUMENTATION AND REVIEW OF THE ORAL RfD
Source Document -- This assessment is not presented in any existing U.S. EPA
document.
Other EPA Documentation -- None
Agency Work Group Review -- 02/24/1988
Verification Date -- 02/24/1988
___I.A.7. EPA CONTACTS (ORAL RfD)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
The health effects data for acrylamide were reviewed by the U.S. EPA
RfD/RfC Work Group and determined to be inadequate for derivation of an
inhalation RfC. The verification status of this chemical is currently not
verifiable. For additional information on health effects of this chemical,
interested parties are referred to the EPA documentation listed below.
U.S. EPA. 1985. Drinking Water Criteria Document for Acrylamide Office of
Drinking Water, Washington, DC. NTIS PB 89-192041/AS.
U.S. EPA. 1985. Health and Environmental Effects Profile for Acrylamide.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste
and Emergency Response, Washington, DC. NTIS PB 88-170824/AS.
Agency Work Group Review -- 09/20/1990
EPA Contacts:
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
Last Revised -- 07/01/1993
Section II provides information on three aspects of the carcinogenic
assessment for the substance in question; the weight-of-evidence judgment of
the likelihood that the substance is a human carcinogen, and quantitative
estimates of risk from oral exposure and from inhalation exposure. The
quantitative risk estimates are presented in three ways. The slope factor is
the result of application of a low-dose extrapolation procedure and is
presented as the risk per (mg/kg)/day. The unit risk is the quantitative
estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m
air breathed. The third form in which risk is presented is a drinking water
or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1
in 1,000,000. The rationale and methods used to develop the carcinogenicity
information in IRIS are described in The Risk Assessment Guidelines of 1986
(EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries
developed since the publication of EPA's more recent Proposed Guidelines for
Carcinogen Risk Assessment also utilize those Guidelines where indicated
(Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to
Section I of this IRIS file for information on long-term toxic effects other
than carcinogenicity.
__II.A. EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
___II.A.1. WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification -- B2; probable human carcinogen
Basis -- Based on inadequate human data and sufficient evidence of
carcinogenicity in animals; significantly increased incidences of benign
and/or malignant tumors at multiple sites in both sexes of rats, and
carcinogenic effects in a series of one-year limited bioassays in mice by
several routes of exposures. The classification is supported by positive
genotoxicity data, adduct formation activity, and structure-activity
relationships to vinyl carbamate and acrylonitrile.
___II.A.2. HUMAN CARCINOGENICITY DATA
Inadequate. There are two studies on the relationship of workers exposed
to acrylamide and cancer mortality. A basic limitation of both studies is
that the design is insufficient to derive an inference of relative risk.
In the first study (Collins, 1984), a standardized proportional mortality
ratio (SPMR) was used to analyze the data on two study groups: a long duration
exposure group of 10 individuals and a short duration/intermittent exposure
group of 52 individuals. Results from the study indicated no significant
excesses of mortality from cancer (all types combined) in either group. The
mortality from cancer of the lung and CNS appeared to be slightly elevated;
however, the SPMRs were not significantly different from expected values, due
to the small size of the groups. Other limitations in this study include an
under representation of the worker population potentially at risk for
exposure-related effects, incomplete ascertainment of causes of death for
group members, and incomplete acrylamide exposure data.
In another study (Sobel et al., 1986), the mortality experience of 371
employees assigned to acrylamide monomer and polymerization operations during
the late 1950s and 1960s was examined. Whereas 38 deaths were expected (based
on the U.S white male mortality rates), a total of 29 deaths had been observed
up until 1982. The mortality in the total cohort from cancer was somewhat in
excess (11 observed vs. 7.9 expected); however, this appeared due to excess
cancer mortality in a subgroup with previous exposure to organic dyes. The
epidemiologic evidence of this study is considered insufficient to assess the
carcinogenicity of acrylamide because of the small cohort, multiple chemical
exposures and limited follow-up; furthermore, 167 cohort members had <1 year
employment and another 109 had only l-4 years of employment.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. In an adequately designed 2-year carcinogenesis bioassay
(Johnson et al., 1984, 1986), acrylamide (>98% purity) was administered in
drinking water to F344 rats (60/sex/dose) at doses of 0, 0.01, 0.1, 0.5 and
2.0 mg/kg/day. An MTD appeared to have been achieved based on decreased body
weight gain, decreased survival and the observance of several toxic effects in
the high dose group. There were transient symptoms of a viral infection
(sialodacryoadenitis virus) in some rats beginning on day 210 of the study;
however, all animal groups were equally affected. This viral infection did
not significantly affect the body weight, survival or tumor incidences of F344
rats (Rao et al., 1988).
Acrylamide induced statistically significant increases in the incidences
of several tumor types in test rats of both sexes when compared with control
animals. In males, significantly increased incidences of tumors included the
following: scrotal mesotheliomas in the two highest doses (11/53 and 10/54 at
the two highest doses vs. 3/57 in the control), adrenal pheochromocytomas in
the high dose (10/54 vs. 3/57), and thyroid adenomas in the high dose (7/54
vs. 1/57). In high dose females, gliomas and astrocytomas of the CNS (9/61
high dose vs. 1/60 control), adenomas and adenocarcinomas of the mammary gland
(28/60 vs. 10/60;), adenomas and adenocarcinomas of the thyroid gland (5/50
vs. 1/54;), adenocarcinomas of the uterus (5/49 vs. 1/56), and papillomas and
carcinomas of the oral cavity (8/60 vs. 0/60) were significantly increased.
A series of mouse skin papilloma and lung adenoma assays showed that
acrylamide initiated skin tumorigenesis in both SENCAR and Swiss-ICR mice, and
induced lung tumors in SENCAR, Swiss-ICR and A/J mouse strains (Bull et al.,
1984a,b; Robinson et al., 1986). Bull et al. 1984a administered a total of 0,
75, 150, and 300 mg acrylamide/kg during 6 applications over a 2-week period
via gavage, intraperitoneal injection (i.p.), or dermal application to groups
of female SENCAR mice, followed by triweekly applications of 1 ug TPA (12-o-
tetradecanoyl-phorbal-13-acetate) for 20 weeks. Acrylamide initiated skin
tumorigenesis in Swiss-ICR mice (by gavage) and induced lung neoplasms in
Swiss-ICR mice (by gavage) and A/J mice (by gavage and i.p.). A dose-response
increase in skin tumors was observed in the mice; Bull et al. (1984a,b) found
that skin tumor development was dependent on promotion by TPA whereas lung
tumor induction was not. Robinson et al. (1986) noted significant increases
of skin and lung tumors in SENCAR mice administered 50 mg/kg of acrylamide by
a single i.p. injection followed by treatment with TPA.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Acrylamide has been shown to be a clastogenic agent, inducing chromosomal
aberrations, dominant lethality, sister-chromatid exchanges and unscheduled
DNA synthesis in various in vivo and in vitro systems. Acrylamide also
produces cell transformation in vitro and causes amplification of SV40 DNA
inserts of SV40-transformed Chinese hamster cells. Furthermore, there is
evidence that [C14]-acrylamide binds covalently to DNA and protein in rodents
(Dearfield et al., 1988).
Acrylamide is structurally analogous to vinyl carbamate and acrylonitrile;
they all contain a vinyl group which may interact with cellular macromolecules
via activation to an epoxide.
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Oral Slope Factor -- 4.5 per (mg/kg)/day
Drinking Water Unit Risk -- 1.3E-4 per (ug/L)
Extrapolation Method -- Linearized multistage procedure, extra risk
Drinking Water Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 8E-1 ug/L
E-5 (1 in 100,000) 8E-2 ug/L
E-6 (1 in 1,000,000) 8E-3 ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- CNS, mammary and thyroid glands, uterus, oral cavity (combined)
Test Animals -- rat/Fischer 344, female
Route -- drinking water
Reference -- Johnson et al., 1986
Administered Human Equivalent Tumor
Dose (mg/kg)/day Dose (mg/kg)/day Incidence
---------------- ---------------- ---------
0 0 13/60
0.01 0.001 18/60
0.1 0.015 14/60
0.5 0.076 21/60
2.0 0.305 46/60
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
Tumors at a particular site were added into the pool only when the tumor
site had statistically significantly increased incidence at least at the high
dose level (treated vs. control). The dose response curves for each sex based
on the pooled tumor incidence (benign and malignant) data comprise the data
sets of choice for risk assessment. The female was the more sensitive sex (as
there were significantly increased tumor incidences at a greater number of
sites than in the males) and was, therefore, chosen for the risk estimate. A
transpecies conversion factor of 7.05 was used (the cube root of the ratio of
human to rat body weights, or 70 kg/0.2 kg).
There was no indication that the doses used should be adjusted to reflect
different patterns of distribution or metabolism; the distribution of
acrylamide appears to be quantitatively the same regardless of route of
exposure (Dearfield et al., 1988).
The unit risk should not be used if the water concentration exceeds 8E+1
ug/L, since above this concentration the unit risk may not be appropriate.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
Four doses over a reasonable range and a sufficient number of animals were
tested. Many of the tumors were malignant, including gliomas and astrocytomas
of the CNS which rarely occur in rats.
Slope factors calculated from six data sets based on tumor incidences at
individual sites in males and females ranged from 2.9E-1 per (mg/kg)/day to
2.3 per (mg/kg)/day.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
___II.C.1. SUMMARY OF RISK ESTIMATES
Inhalation Unit Risk -- 1.3E-3 per (ug/cu.m)
Extrapolation Method -- Linearized multistage procedure, extra risk
Air Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 8E-2 ug/cu.m
E-5 (1 in 100,000) 8E-3 ug/cu.m
E-6 (1 in 1,000,000) 8E-4 ug/cu.m
___II.C.2. DOSE-RESPONSE DATA FOR CARCINOGENICITY, INHALATION EXPOSURE
Calculated from oral data.
___II.C.3. ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
The unit risk should not be used if the air concentration exceeds 8
ug/cu.m, since above this concentration the unit risk may not be appropriate.
___II.C.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE)
This inhalation risk estimate is based on oral data.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1987, 1988
The 1987 Drinking Water Criteria Document on Acrylamide has received Agency
and SAB review.
The 1988 Draft Preliminary Assessment of Health Risks from Exposure to
Acrylaminde has received Agency review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 10/29/1986, 05/25/1988
Verification Date -- 05/25/1988
___II.D.3. U.S. EPA CONTACTS (CARCINOGENICITY ASSESSMENT)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_VI. BIBLIOGRAPHY
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
Last Revised -- 08/01/1991
__VI.A. ORAL RfD REFERENCES
Burek, J.D., R.R. Albee, J.E. Beyer, et al. 1980. Subchronic toxicity of
acrylamide administered to rats in the drinking water followed by up to 144
days of recovery. J. Environ. Pathol. Toxicol. 4: 157-182.
Dow Chemical Company. 1985. Acrylamide: A two-year drinking water chronic
toxicity-oncogenicity study in Fischer 344 rats. Electron microscopy portion.
Final report dated August 13.
Nalco Chemical Company. 1985. Preliminary report of draft results from the
FO breeding and dominant lethal assay. EPA Document Control No. 8EHQ-0785-
0560.
Smith, M.K., H. Zenick, R.J. Preston, E.L. George and R.E. Long. 1986.
Dominant lethal effects of subchronic acrylamide administration in the male
Long-Evans rat. Mutat. Res. 173(4): 273-277.
__VI.B. INHALATION RfD REFERENCES
U.S. EPA. 1985. Drinking Water Criteria Document for Acrylamide Office of
Drinking Water, Washington, DC. NTIS PB 89-192041/AS.
U.S. EPA. 1985. Health and Environmental Effects Profile for Acrylamide.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste
and Emergency Response, Washington, DC. NTIS PB 88-170824/AS.
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Bull, R., M. Robinson, R. Laurie, et al. 1984a. Carcinogenic effects of
acrylamide in Sencar and A/J mice. Cancer Res. 44: 107-111.
Bull, R., M. Robinson and J. Stober. 1984b. Carcinogenic activity of
acrylamide in the skin and lung of Swiss-ICR mice. Cancer Lett. 24: 209-212.
Collins, J.J. 1984. A Proportional Mortality Ratio Analysis of Workers
Exposed to Acrylamide at the Warners Plant. Epidemiology Section, American
Cyanamid Company.
Dearfield, K.L., C.O. Abernathy, M.S. Ottley, J.H. Brantner and P.F. Hayes.
1988. Acrylamide: Its metabolism, developmental and reproductive effects,
genotoxicity and carcinogenicity. Mutat. Res. 195: 45-77.
Johnson, K.A., S.J. Gorzinski, K.M. Bodner and R.A. Campbell. 1984.
Acrylamide: A two year drinking water chronic toxicity - oncogenicity study in
Fisher 344 rats. Dow Chemical Company. Final Report. September 21.
Johnson, K., S. Gorzinski, K. Bodner, et al. 1986. Chronic toxicity and
oncogenicity study on acrylamide incorporated in the drinking water of Fischer
344 rats. Toxicol. Appl. Pharmacol. 85: 154-168.
Rao, G.N., J. Edmondson and J.K. Haseman. 1988. Influence of viral infection
on tumor incidences, body weight and survival of Fischer 344 rats.
Toxicologist. 8: 166.
Robinson, M., R.J. Bull, G.L. Knutsen, R.P. Shields and J. Stober. 1986. A
combined carcinogen bioassay utilizing both the lung adenoma and skin
papilloma protocols. Environ. Health Perspect. 68: 141-145.
Sobel, W., G.G. Bond, T.W. Parsons and F.E. Brenner. 1986. Acrylamide cohort
mortality study. Br. J. Ind. Med. 43: 785-788. [This study was also
submitted under section 8(d) of the Toxic Substances Control Act on April 28,
1986.]
U.S. EPA. 1987. Final Draft for the Drinking Water Criteria Document on
Acrylamide. Office of Drinking Water, Washington, DC.
U.S. EPA. 1988. Draft Preliminary Assessment of Health Risks from Exposure to
Acrylamide. Office of Toxic Substances. Washington, DC. March.
_VII. REVISION HISTORY
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
09/26/1988 I.A. Oral RfD summary on-line
09/26/1988 II. Carcinogen summary on-line
06/01/1989 II.D.2. Work group review date added
09/01/1990 II. Text edited
09/01/1990 III.A. Health Advisory on-line
09/01/1990 VI. Bibliography on-line
10/01/1990 I.B. Not verified; data inadequate
11/01/1990 I.B. Inhalation RfC message on-line
11/01/1990 VI.B. Inhalation RfC references on-line
01/01/1991 II. Text edited
01/01/1991 II.C.1. Inhalation slope factor removed (global change)
03/01/1991 I.A.5. Data Base corrected to medium; text revised
08/01/1991 VI.C. References clarified
01/01/1992 IV. Regulatory Action section on-line
07/01/1993 II.D.1. Source Document and Review Statement clarified
VIII. SYNONYMS
Substance Name -- Acrylamide
CASRN -- 79-06-1
Primary Synonym -- 2-Propenamide
Last Revised -- 09/26/1988
79-06-1
Acrylamide
ACRYLIC AMIDE
AKRYLAMID
AMID KYSELINY AKRYLOVE
ETHYLENECARBOXAMIDE
PROPENAMIDE
2-Propenamide
RCRA WASTE NUMBER U007
UN 2074
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0286.HTM
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