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Acrylamide (CASRN 79-06-1)

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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 First 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

Rat Subchronic
Drinking Water Study

Burek et al., 1980

NOEL: 0.2 mg/kg/day

LOAEL: 1 mg/kg/day
1000
1
2E-4
mg/kg/day

*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 Studies/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
Database — 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 database 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 IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_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 IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_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 Human Carcinogenicity

__II.A.1. Weight-of-Evidence Characterization

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.

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_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
Dose (mg/kg)/day
Human Equivalent
Dose (mg/kg)/day
Tumor
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.

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_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.

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_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. EPA Review (Carcinogenicity Assessment)

Agency Work Group Review — 10/29/1986, 05/25/1988

Verification Date — 05/25/1988

__II.D.3. EPA Contacts (Carcinogenicity Assessment)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_III.  [reserved]
_IV.  [reserved]
_V.  [reserved]

_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.

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_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.

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_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.

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_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. database 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
08/01/1995 II.D.2. EPA's RfD/RfC and CRAVE workgroups were discontinued in May, 1995. Chemical substance reviews that were not completed by September 1995 were taken out of IRIS review. The IRIS Pilot Program replaced the workgroup functions beginning in September, 1995.
04/01/1997 III., IV., V. Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary Data were removed from IRIS on or before April 1997. IRIS users were directed to the appropriate EPA Program Offices for this information.
02/22/2001 I., II. This chemical is being reassessed under the IRIS Program.

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_VIII.  Synonyms

Substance Name — Acrylamide
CASRN — 79-06-1
Primary Synonym — 2-Propenamide
Last Revised — 09/26/1988

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