Molecular Formula. C3H5NO
CAS No 79-06-1
RTECS No AS3325000
Abbreviations. AA (acrylamide); PAA ( polyacrylamide).
Synonyms. Acrylic acid, amide; Ethylenecarboxamide; 2-Propenamide.
Properties. Colorless, odorless crystals. Water solubility is 204 g/100 ml, soluble in alcohol. When hydrolyzed, AA forms acrylic acid. Concentrations of 0.01 to 0.5 mg/I give water neither color or opalescence nor any unrequired odor. A concentration of 0.001 to 0.01 mg/l gives water no foreign taste.1
Applications. Used in the manufacture of articles intended for use in contact with food.
AA is predominantly used as a monomer in the production of polyacrylamide (PAA), a number of copolymers and synthetic rubber. Polymers of AA are used in the production of lacquers, paints, adhesives, and dentistry compositions. PAA are also used as grouting agents in the construction of drinking water reservoirs and wells.
Exposure. Residual AA monomer occurs in PAA coagulants used in the treatment of drinking water. Generally, the maximum authorized dose of polymer is 1.0 mg/l corresponding to a maximum theoretical concentration of 0.0005 mg/I monomer in water. Practical concentration may be lower by a factor of 2 to 3. This applies to the anionic and non-anionic PAA, but residual levels from cationic PAA may be higher. Additional human exposure might result from food owing to the use of PAA in food processing.
Acute Toxicity. LD50 is reported to be 120 to 180 mg/kg BW in rats, 100 to 170 mg/kg BW in mice, 150 to 170 mg/kg BW in guinea pigs, and 150 to 280 mg/kg BW in rabbits.1-3 ,05 In 12 hours after administration of 50 to 200 mg/kg BW, poisoned animals displayed impaired hind limb functioning, convulsions, and diffuse damage to different sections of the NS. Gross pathology examination revealed circulatory disturbances in the parenchymatous organs and brain matter as well as signs of parenchymatous dystrophy of the liver and kidneys. The treatment caused marked lysis of tigroidal matter in the cerebellum neurons.2
The acute effect threshold for the change in STI value appeared to be 40 mg/kg BW. Cats seem to be more sensitive to AA than rats and monkeys.
Repeated Exposure.
Observations in man. Five individuals were exposed through ingestion and external use of well water contaminated with AA. Signs of intoxication included confusion, disorientation, memory disturbances, hallucinations, and truncal ataxia. All exposed persons recovered completely within 4 months.4
Animal studies. AA exhibited pronounced cumulative properties: administration of 1/5 and l/20 LD 50 resulted in Kacc of 2.2 and 2.4, respectively (by Kagan). According to Lim method, Kacc appeared to be l.07 in mice, and 1.56 in rats.1
AA produces prominent effects in the neuromuscular domain. It is shown to reduce the amount of large-diameter fibers in the peripheral nerves and to cause their degeneration. Doses of 50 to 100 mg/kg BW impair functioning of the hind legs, but the front legs remain unimpaired even with a 400 mg/kg BW dose.3 Repeated administration of doses up to 50 mg/kg BW by any route produced neuropathy of the peripheral nerves in the majority of laboratory animals including non-antropoidal monkeys. Changes observed seem to be reversible but secondary effects include atrophy of the skeletal muscles. Administration of 300 mg AA/kg BW produced muscular weakness in the limbs and the loss of reflexes. A dose of 100 mg AA/kg BW in the feed caused retardation of BW gain.
Addition of 10 to 50 mg AA/kg BW to the diet of young rats had no clear toxic effect (ARC 19-93). The doses of l.0, 4.0, or 60 mg/kg BW were administered ilp to Long-Evans rats for 13 weeks. Treatment with A. caused time- and dose-related changes in muscle tone and equilibrium, and produced axonal degeneration in peripheral nerves and within long tracts of the spinal cord.5
Short-term Toxicity. Young rats were given a dose of 31 mg/kg BW for 3 months. The treatment caused retardation of BW gain and anemia. Gross pathology examination revealed edema of the mucosa and submucosa of the stomach and small intestine, moderate epithelial sloughing in the large intestine, dystrophic changes in the brain, parenchymatous dystrophy in the liver and kidneys, and increased relative weights of the liver.6,7 Rats exposed to AA solution at dose levels of 5.0 to 20 mg/kg BW for 3 months became weak and dragged their hind legs. The treatment caused retardation of BW gain. Histology examination revealed the loss of axones, and degeneration and demyelination of the peripheral nerves.8 Administration of 10 mg/kg BW to male rats 3 times a week for 13 weeks resulted in retardation of BW gain observed seven weeks after the onset of treatment.9
In one study, macaques received an overall dose of 320 to 450 mg/kg BW until toxic effect developed.8 Animals displayed reduced BW gain preceded by neurological disturbances, including loss of equilibrium, tremors, reduction in activity, and coordination disorder. The vibration sensitivity threshold was increased, but there was no change in sensitivity to electrostimulation. A dose of 0.2 mg/kg BW appeared to be ineffective in a 3-month experiment in rats. 19
Long-term Toxicity. Rats were fed 100 to 400 mg AA/kg BW for 6 to 48 weeks. The treatment disrupted nervous conduction in the hind legs and caused degenerative changes in the peripheral NS. Recovery began a long time after administration had ceased (IARC 19-99). Baboons received 10 to 20 mg AA/kg BW with their drinking water for 29 to 192 days. The treated animals displayed weakness and ataxia of their limbs, weakness of the eye muscles, and later, development of tetraplegia. Histology examination revealed an extensive effect on the peripheral nerves.11 The NOAEL in rat chronic toxicity studies was reported to be 0.2 mg/kg8 or 0.3 mg/kg BW. 05
Immunotoxicity. Novikov and Ostapova found no sensitizing effect during acute or chronic administration of AA.' XXX 7,12 With repeated administration of 12 mg AA/kg BW there were changes in the immune reactivity. A dose of 0.l mg/kg BW caused an increase in the amount of plaque-forming cells, but a dose of 0.01 mg/kg BW had no such effect.
Reproductive Toxicity.
Gonadotoxicity. AA affects germ cells and impairs reproductive function. The dose of 500 mg/kg BW led to a reduction in the testicle weights. A marked degeneration of the seminiferous tubules was observed. 13,14 The NOEL of l.5 mg/kg BW was identified based on the absence of DLM in male sperm. Rumyantzev et al. 2 did not observe a gonadotoxic effect at dose levels up to 0.05 mg A./kg BW.
Embryotoxicity. No adverse effect of AA on the offspring development was found in the study where Porton rats were given AA during gestation with their feed at doses of 0.2 to 0.4 g AA/kg BW with the simultaneous administration of an i/v dose of 0.l g/kg BW on days 9, 14, or 21 of gestations.5
Maternal toxicity at the highest dose level was demonstrated in mice gavaged with 3.0 to 45 mg/kg BW on days 6 to 17 of gestation, and in rats given 2.5 to 15 mg/kg BW on days 6 to 20 of gestation. BW was decreased and hind limb splaying occurred in mice only.15 In another study, the NOEL for embryotoxic effect was found to be 2.0 mg/kg BW. 1
Swiss CD-1 mice were provided drinking water containing 3.0, 10, or 30 ppm AA during and after a 14-week cohabitation. The last litter was reared and dosed after weaning until mating at 2.5 months of age, with same level of compound given to the parents. In the F0 generation, the treatment caused an 11% decrease in pup number without measurable neurotoxicity. Female fertility was not affected. Larger changes were observed in the fertility-related endpoints in the F1 mice than in the F0 generation. There was no concomitant change in organ weights or sperm parameters.16
Teratogenicity. No fetal abnormalities were shown after oral administration of high doses17,18
Mutagenicity. Despite the fact that AA is structurally similar to the mutagens and carcinogens acrylonitrile and vinyl chloride, and is capable to react with nucleophilic sites or compounds, published data on its mutagenicity are contradictory.
In vivo cytogenetics. In the dominant lethal assay, mice were exposed ilp to 1.5 to 2.2 mg/kg BW. The treatment produced no increase in the incidence of early death or pre-implantation losses.19 AA is reported to produce mutagenic effect in the germ cells of mice which were given it at a dose level of 500 mg/kg in the diet for 3 weeks. 13
AA induced gene mutations in mammalian cells and CA in vitro and in vivo. 5 It appeared to be a clastogenic agent inducing CA, DLM, SCE, and unscheduled DNA synthesis. There was no increase of micronuclei in CD- I mice. 20
Shelby et al. found AA to produce DLM and translocations in early spermatozoa and late spennatides of the mouse, but not at earlier stages.21-23 DLM studies revealed fertility effects that could be explained by a male-mediated increase in postimplantation loss. Dominant lethality occurred without structural effects on the reproductive system and without detectable neural histopathology. 16 According to Hurt et al., 24 AA caused unscheduled DNA synthesis in pachytene spermatocytes of rats. AA produced a DNA repair response in the in vivo spermatocyte but not in either the in vitro or in vivo hepatocyte DNA repair assay.
Batiste-Allentom et al .25 reported that AA produced a significant increase in Dr. melanogaster wing spot somatic mutation and recombination assay. However, according to Vogel and Nivard, AA was found to be a substance of relatively low DNA reactivity in a Dr. melanogaster assay. 26
In vitro genotoxicity. According to Knaap et al.,27 AA exhibits no mutagenic activity in different test systems, including Salmonella mutagenicity assay and test on gene mutations in murine lymphoma cells. Glycidamide, a mutagenic metabolite of AA, induced DNA repair in the in vitro hepatocyte DNA repair assay and produced a strong unscheduled DNA synthesis response. 23
Carcinogenicity. There was an increased incidence of lung adenomas in mice exposed to average daily doses of 2.7 to 10.7 mg/kg BW. 28
In a 2-year study, rats were administered 0.5 to 2.0 mg/kg BW via drinking water. Increased rates of scrotal mesotheliomas, mammary gland tumors, thyroid adenomas, uterine adenocarcinomas, clitoral gland adenomas, and oral papillomas were found .29 AA is considered to be a genotoxic carcinogen (WHO, 1991).
Carcinogenicity classifications. An IARC Working Group concluded that there is sufficient evidence for the carcinogenicity of AA in experimental animals and there is inadequate evidence for the Car cinogenicity of AA in humans.
The Annual Report of Carcinogens issued by the U.S. Department of Health and Human Services (1998) defines AA to be a substance which may reasonably be anticipated to be a carcinogen, i.e., a substance for which there is a limited evidence of Carcinogenicity in humans or sufficient evidence of Carcinogenicity in experimental animals.
IARC: 2A;
U.S. EPA: B2;
EU: 2.
Chemobiokinetics. Following ingestion, AA is readily absorbed from the GI tract and widely distributed in the body fluids. Accumulation in the liver and kidneys as well as in the male reproductive system has been demonstrated. AA is likely to cross the placenta. Less than 1.0% of the administered dose accumulates in the NS. AA is found mainly in the muscles and skin. Male rats were given 50 mg 14C- AA/kg BW. Rapid absorption from the GI tract was reported. After 28 hours the highest activity was found in gastric contents, followed by stomach, lung, bone marrow, and skin. After 144 hours the availability of the highest total activity was lung > pancreas >adrenal >esophagus. Kidney is the major route of elimination. 10% of activity was excreted in feces. 30
AA is electrophilic and, subsequently, undergoes reactions with nucleophiles. In rats, biotransformation of AA occurs through glutathione conjugation and decarboxylation. The major metabolite is N-acetyl-S (3-amino-3-oxypropyl)cysteine, which accounted for 48% of the oral dose.31 Despite much research it is still unclear whether the parent compound or a metabolite is responsible for the observed toxic etfects. 32 AA is mainly excreted as metabolites in the urine and bile.
Regulations.
U.S FDA (1998) regulates AA as an indirect food additive, a component of food-contact surfaces for single and repeated use. PAA has been approved for various applications. MPC in food contact PAA solutions: 0.02% (1990); MPC for PAA food additive: 0.05 to 0.2%.
US FDA has established regulations for use of AA: It can be used (l) in washing or to assist in the peeling of fruits and vegetables using lye if the concentration does not exceed 10 mg/l in the wash water and if no more than 0.2% AA is present; (2) in adhesives as a component (monomer) of articles intended for use in packaging, transporting, or holding food in accordance with the conditions prescribed in 21 CFR part 175.105; as (3) a component (monomer) of the uncoated or coated food-contact surface of paper and paperboard intended for use in producing, manufacturing, packaging, processing, preparing, treating, packing, transporting, or holding dry food in accordance with the conditions prescribed in 21 CFR part 176.180; (4) as a monomer in the manufacture of semirigid and rigid acrylic and modified acrylic plastics in the manufacture of articles intended for use in contact with food in accordance with the conditions prescribed in 21 CFR part 177.1010. (5) AA-sodium acrylate resins can be used as boiler water additives in the preparation of articles that will be in contact with food, if the water contains not more than 0.05% by weight of AA; (6) PAA can be used as a film former in the imprinting of soft-shell gelatin capsules if no more than 0.2% of the monomer is present; (7) homopolymers and copolymers of AA may be safely used as food packaging adhesives, providing the amount used does not exceed that "reasonably required to accomplish the intended effect"; (8) AA-acrylic acid resins may be safely used as components in the production of paper or paperboard used for packaging food, providing the resin contains less than 0.2% residual monomer and that the resin does not exceed 2.0% by weight of the paper or paperboard.
EU (1990). AA is available in the List of authorized monomers and other starting substances which may continue to be used for the manufacture of plastic materials and articles intended to come into contact with foodstuffs pending a decision on inclusion in Section A (Section B).
Great Britain (1998). AA is authorized without time limit for use in the production of polymeric materials and articles in contact with food or drink or intended for such contact. The specific migration of this substance shall be not detectable (when measured by a method with a detection limit of 0.01 mg/kg).
In Germany, PAA flocculents must not contain more than 0.05% of the monomer.11 The addition of PAA is limited to l.0 mg/I in treated water. The concentration of the monomer will therefore not exceed 0.0005 mg/l in finished water. The level of PAA used in foodstuff packaging is limited to 0.3% and the level of residual AA monomer in polyacrylamide to 0.2%.
Recommendations.
WHO (1996). Guideline value for drinking water: 0.0005 mg/l. Generally, AA cannot be detected at concentrations of 0.001 mg/l or less, but can be controlled by product specification.33
U.S. EPA (1999): Health Advisory for a longer-term exposure is 0.04 mg/l.
The UK Committee on Carcinogenicity (1993) recommended that the level of AA monomer in PAA used for drinking water treatment should be reduced to the lowest practicable level.34
Standards.
EU(1990). SML: Not detectable (Detection limit is 0.01 mg/kg).
U.S. EPA (1999). MCL: TT; MCLG: zero.
Russia (1995). MAC and PML: 0.01 mg/l.
References:
l. Kozeyeva, E. E., Production and Experimental Investigations on Hygienic Assessment of Acrylamide, Author's abstract of thesis, Moscow, 1980, 23 (in Russian).
2. Rumyantsev, G. I., Novikov, S. M., Kozeeva, E. E., et al., Experimental study of biological effects of acrylamide, Gig. Sanit, 9, 38, 1980 (in Russian).
3. Tilson, H. and Cabe, P., The effects of acrylamide given acutely or in repeated doses on fore- and hindlimb function of rats, Toxicol. Appl. Pharmacol., 47, 253, 1979.
4. Igusu, H., Goto, I., Kawamura, Y., et al., Acrylamide encephaloneuropathy due to well water pollution, J Neurol. Neurosurg. Psychiatr., 38, 581, 1975.
5. Zenick, H., Hope, E., and Smith, M. K., Reproductive toxicity associated with acrylamide treatment in male and female rats, J Toxicol. Environ. Health, 17, 457, 1986.
6. Loshchenkova, l. F., in Physiology of Autonomic Nervous System, Kuibyshev, Issue No 1, 1979, 321 (in Russian).
7. Ostapova, l. F., Pharmaceutical Kinetics, Toxicology, and Pharmaceutical Dynamics of Acrylamide, Methacrylamide, and Diacetone Acrylamide, Author's abstract of thesis, Yaroslavl', 1981, 333 (in Russian).
8. Burek, J. D., Albee, R. R., Beyer, J. E., et al., 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, 1980.
9. Moser, V. C., Antony, D. C., Sette, W. F., and MacPhail, R. C., Comparison of subchronic neurotoxicity of 2-hydroxyethyl acrylate and acrylamide in rats, Fundam. Appl. Toxicol., 18, 343, 1992.
10. Maurissen, J. P., Weiss, B., Davis, H. T., et al., Somatosensory thresholds in monkeys exposed to acrylamide, Toxicol. Appl. Pharmacol., 71, 266, 1983.
11. Hopkins, A., The effect of acrylamide on the peripheral nervous system of the baboon, J Neurol. Neurosurg. Psychiatr., 33, 805, 1970.
12. Novikov, S. M., Problems of Occupational Safety and Industrial Toxicology in Production and Use of Acrylamide, Author's abstract of thesis, Moscow, 1974, 23 (in Russian).
13. Shiraishi, Y., Chromosome aberrations induced by monomeric acrylamide in bone marrow and germ cells of mice, Mutat. Res., 57, 313, 1978.
14. McCollister, D. D., Oyen, F., and Rowe, V. K., Toxicology of acrylamide, Toxicol. Appl Pharmacol., 6, 172, 1964.
15. Field, E. A., Price, C. J., Sleet, R. B., et al., Developmental toxicity evaluation of acrylamide in rats and mice, Fundam. Appl Toxicol., 14, 502, 1990.
16. Chapin, R. E., Fail, P. A., George, J. D., Grizzle, T. B., Heindel, J. J., Harry, G. J., Collins, B. J., and Teague, J., The reproductive and neural toxicities of acrylamide and three analogues in Swiss mice, evaluated using the continuous breeding protocol, Fundam. Appl Toxicol, 27, 9, 1995.
17. Edwards, P. M., The insensitivity of the developing rat fetus to the toxic effects of acrylamide, Chem.-Biol. Interact., 12, 13, 1976.
18. Kankaanpaa, J., Elovaara, E., Hemminki, K., et al., Embryotoxicity of acrolein, acrylonitrile, and acrylamide in developing chick embryos, Toxicol Lett., 4, 93, 1979.
19. Epstein, S. S., Arnold, E., Andrea, J., Bass, W., and Bishop, Y., Detection of chemical mutagens by the dominant lethal assay in the mouse, Toxicol. Appl. Pharmacol., 23, 288, 1972.
20. Dearfield, K. L., Abernathy, C. O., Ottley, M. S., et al., Acrylamide: its metabolism, developmental and reproductive effects, genotoxicity, and carcinogenicity, Mutat. Res., 195, 45, 1988.
21. Shelby, M. D., Cain, K. T., Hughes, L. A., et al., Dominant lethal effects of acrylamide in male mice, Mutat. Res., 173, 35, 1986.
22. Shelby, M. D., Cain, K. T., Cornett, C. V., et al., Acrylamide: induction of heritable translocations in male mice, Environ. Mutagen., 9, 363, 1987.
23. Butterworth, B. E., Eldridge, S. R., Sprankle, C. S., Working, P. K., Bentley, K. S., and Hurt, M. E., Tissue-specific genotoxic effects of acrylamide and acrylonitrile, Environ. Molec. Mutagen., 20, 148, 1992.
24. Hurt, M. E., Bentloy, K., and Working, P. K., Effects of acrylamide and acrylonitrile on unscheduled DNA synthesis in rat spermatocytes, Environ. Mutagen., 9, 49, 1987.
25. Batiste-Allentom, M., Xamena, N., Creus, A., and Marcos, A., Genotoxic evaluation of ten carcinogens in the Drosophila melanogaster with spot test, Experiertia, 51, 73, 1995.
26. Vogel, E. W. and Nivard, N. J., Performance of 181 chemicals in a Drosophila assay predominantly monitoring interchromosomal mitotic recombination, Mutagenesis, 8, 57,1993.
27. Knaap, A., et al., in The 14 `h Annual Conf Europ. Soc. Environ. Mutagens., Abstracts, Moscow, 1984, 247 (in Russian).
28. Bull, R. J., Robinson, M., Laurie, R. D., et al., Carcinogenic effects of acrylamide in SENCAR and A/J mice, Cancer Res., 44, 107, 1987.
29. Johnson, K. A., Gorzinski, S. J., Bodner, K. M., et al., Chronic toxicity and oncogenicity study on acrylamide incorporated in the drinking water of Fischer 344 rats, Toxicol. Appl. Pharmacol., 85, 154, 1986.
30. Kady, A. M., Kardos, S., Johnson, L. R., Friedman, M., and Abdel-Rahman, M. S., Pharmacokinetics of acrylamide after oral exposure in male rats, in Toxicologist, Abstracts of SOT 1996 Annual Meeting, Abstract No 204, Issue of Fundam. Appl. Toxicol., 30, Part 2, March 1996.
31. Miller, M. J., Carter, D. E., and Sipes, I. G., Pharmacokinetics of acrylamide in Fischer 344 rats, Toxicol Appl. Pharmacol., 63, 36, 1982.
32. Calleman, C. J., Bergmark, E., and Costa, L. G., Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation, Chem. Res. Toxicol., 3, 406, 1990.
33. Revision of the WHO Guidelines for Drinking Water Quality, Report on the Consolidation Meeting on Organics and Pesticides, Medmenham, UK, January 30-31, 1992, 11
34. 1992 Annual Report of the Committee on Toxicity, Mutagenicity, Carcinogenicity of Chemicals in Food. Consumers Products and the Environment, Dept. of Health, HMSO, London, 1993, 72.
page source: Indirect Food Additives and Polymers: Migration and Toxicology V.O. Sheftel 2000
ACRYLAMIDE
MSDS Number: A1550 --- Effective Date: 03/01/00
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1. Product Identification
Synonyms: 2-Propenamide; ethylene carboxamide; acrylic amide; vinyl amide
CAS No.: 79-06-1
Molecular Weight: 71.09
Chemical Formula: CH2CHCONH2
Product Codes:
J.T. Baker: 4080, 4081, 5530
Mallinckrodt: 7717
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2. Composition/Information on Ingredients
Ingredient CAS No Percent Hazardous
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Acrylamide 79-06-1 100% Yes
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3. Hazards Identification
Emergency Overview
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WARNING! HARMFUL IF SWALLOWED, INHALED OR ABSORBED THROUGH SKIN. AFFECTS CENTRAL AND PERIPHERAL NERVOUS SYSTEMS AND REPRODUCTIVE SYSTEM. CAUSES IRRITATION TO SKIN, EYES AND RESPIRATORY TRACT. SUSPECT CANCER HAZARD. MAY CAUSE CANCER. Risk of cancer depends on level and duration of exposure. POSSIBLE BIRTH DEFECT HAZARD. MAY CAUSE BIRTH DEFECTS BASED ON ANIMAL DATA. THERMALLY UNSTABLE. MAY POLYMERIZE EXPLOSIVELY IF HEATED TO THE MELTING POINT.
J.T. Baker SAF-T-DATA(tm) Ratings (Provided here for your convenience)
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Health Rating: 3 - Severe (Cancer Causing)
Flammability Rating: 1 - Slight
Reactivity Rating: 3 - Severe (Explosive)
Contact Rating: 3 - Severe (Life)
Lab Protective Equip: GOGGLES; LAB COAT; VENT HOOD; PROPER GLOVES
Storage Color Code: Yellow Stripe (Store Separately)
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Potential Health Effects
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Acrylamide is a suspected human carcinogen, severe neurotoxin, and causes irritation of the eyes, skin (is readily absorbed), and respiratory tract.
Inhalation:
May cause drowsiness, tingling sensations, fatigue, weakness, stumbling, slurred speech, and shaking. May cause central and peripheral nervous system damage. Severe intoxications may cause permanent nerve damage. Causes irritation to the respiratory tract. May affect reproductive system and act as a teratogen.
Ingestion:
Toxic! May cause systemic poisoning with symptoms paralleling those of inhalation.
Skin Contact:
May cause irritation and redness. Can be absorbed through the skin causing systemic poisoning; symptoms may parallel inhalation.
Eye Contact:
Solutions may cause irritation.
Chronic Exposure:
Prolonged or repeated exposure through any route may cause muscular weakness, incoordination, skin rashes, excessive sweating of hands and feet, cold hands, peeling of the skin, numbness, abnormal skin or muscle sensations, fatigue, and cause central and peripheral nervous system damage. Suspect cancer hazard. May cause cancer. May affect the reproductive system and act as a teratogen.
Aggravation of Pre-existing Conditions:
Persons with pre-existing skin disorders, eye problems or central or peripheral nervous system conditions may be more susceptible to the effects of this substance.
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4. First Aid Measures
Because of the toxic and highly absorptive nature of acrylamide, quickly providing first aid helps to minimize health effects.
Inhalation:
Remove to fresh air. If not breathing, give artificial respiration. If breathing is difficult, give oxygen. Call a physician.
Ingestion:
Induce vomiting immediately as directed by medical personnel. Never give anything by mouth to an unconscious person. Call a physician.
Skin Contact:
Immediately flush skin with plenty of soap and water for at least 15 minutes while removing contaminated clothing and shoes. Get medical attention. Wash clothing before reuse. Thoroughly clean shoes before reuse.
Eye Contact:
Immediately flush eyes with plenty of water for at least 15 minutes, lifting lower and upper eyelids occasionally. Get medical attention immediately.
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5. Fire Fighting Measures
Fire:
Flash point: 138C (280F) CC
Autoignition temperature: 240C (464F)
Combustible solid.
Explosion:
Not considered an explosive hazard, but an explosion may occur upon polymerization. Polymerization may be caused by exposure to heat, U.V. light, oxidizers, or peroxides.
Fire Extinguishing Media:
Water spray, dry chemical, alcohol foam, or carbon dioxide.
Special Information:
In the event of a fire, wear full protective clothing and NIOSH-approved self-contained breathing apparatus with full facepiece operated in the pressure demand or other positive pressure mode.
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6. Accidental Release Measures
Remove all sources of ignition. Ventilate area of leak or spill. Wear appropriate personal protective equipment as specified in Section 8. Spills: Clean up spills in a manner that does not disperse dust into the air. Use non-sparking tools and equipment. Reduce airborne dust and prevent scattering by moistening with water. Pick up spill for recovery or disposal and place in a closed container. US Regulations (CERCLA) require reporting spills and releases to soil, water and air in excess of reportable quantities. The toll free number for the US Coast Guard National Response Center is (800) 424-8802.
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7. Handling and Storage
Keep in a tightly closed container. Store in a cool, dry, ventilated area away from sources of heat or ignition. Protect against physical damage. Store separately from reactive or combustible materials, and out of direct sunlight. Isolate from oxidizing materials and peroxides. Store away from acids and alkalies. Wear special protective equipment (Sec. 8) for maintenance break-in or where exposures may exceed established exposure levels. Wash hands, face, forearms and neck when exiting restricted areas. Shower, dispose of outer clothing, change to clean garments at the end of the day. Avoid cross-contamination of street clothes. Wash hands before eating and do not eat, drink, or smoke in workplace. Containers of this material may be hazardous when empty since they retain product residues (dust, solids); observe all warnings and precautions listed for the product.
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8. Exposure Controls/Personal Protection
Airborne Exposure Limits:
Acrylamide:
-OSHA Permissible Exposure Limit (PEL):
0.3 mg/m3 (TWA) (skin)
-ACGIH Threshold Limit Value (TLV):
0.03 mg/m3 (TWA) (skin)
Listed as A3, animal carcinogen
Ventilation System:
A system of local and/or general exhaust is recommended to keep employee exposures below the Airborne Exposure Limits. Local exhaust ventilation is generally preferred because it can control the emissions of the contaminant at its source, preventing dispersion of it into the general work area. Please refer to the ACGIH document, Industrial Ventilation, A Manual of Recommended Practices, most recent edition, for details.
Personal Respirators (NIOSH Approved):
If the exposure limit is exceeded, a half-face respirator with an organic vapor cartridge and high efficiency dust/mist filter may be worn for up to ten times the exposure limit or the maximum use concentration specified by the appropriate regulatory agency or respirator supplier, whichever is lowest. A full-face piece respirator with an organic vapor cartridge and high efficiency dust/mist filter may be worn up to 50 times the exposure limit, or the maximum use concentration specified by the appropriate regulatory agency, or respirator supplier, whichever is lowest. For emergencies or instances where the exposure levels are not known, use a full-face piece positive-pressure, air-supplied respirator. WARNING: Air-purifying respirators do not protect workers in oxygen-deficient atmospheres. This compound possibly exists in both particulate and vapor phase. A gas/vapor cartridge should be used in addition to the particulate filter. If the vapor concentration alone exceeds the exposure limits, use a supplied air respirator, because warning properties are unknown for these compounds.
Skin Protection:
Rubber or neoprene gloves and additional protection including impervious boots, apron, or coveralls, as needed in areas of unusual exposure.
Eye Protection:
Use chemical safety goggles and/or full face shield where dusting or splashing of solutions is possible. Maintain eye wash fountain and quick-drench facilities in work area.
Other Control Measures:
Comments: Stress good personal cleanliness and housekeeping to prevent skin contact. Wear clean work clothing daily. Do not home launder. If clothes become contaminated, remove at once, wash the skin with soap and water and launder clothing before reuse. Destroy contaminated leather goods.
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9. Physical and Chemical Properties
Appearance:
Colorless crystals.
Odor:
Odorless.
Solubility:
216 g/l00 g water @ 30C (86F)
Specific Gravity:
1.1222 @ 30C/4C
pH:
No information found.
% Volatiles by volume @ 21C (70F):
0
Boiling Point:
125C (257F)
Melting Point:
84.5C (183F)
Vapor Density (Air=1):
2.4 @ 175C
Vapor Pressure (mm Hg):
0.007 @ 20C (68F)
Evaporation Rate (BuAc=1):
No information found.
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10. Stability and Reactivity
Stability:
May polymerize explosively. Thermally unstable. Polymerization may be caused by exposure to heat, U.V. light, oxidizers, or peroxides. May be stabilized with hydroquinone, t-butylpyrocatechol, N-phenyl-2-naphthylamine, or other antioxidants.
Hazardous Decomposition Products:
Burning may produce ammonia, carbon monoxide, carbon dioxide, nitrogen oxides. Hydrogen gas.
Hazardous Polymerization:
Acrylamide readily polymerizes on exposure to heat, U.V. light, oxidizers, or peroxides.
Incompatibilities:
Acids, oxidizing agents, and bases. Spontaneously reacts with hydroxyl-, amino-, and sulfhydryl- containing compounds.
Conditions to Avoid:
Heat, shock, UV light, ignition sources, and incompatibles.
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11. Toxicological Information
For Acrylamide: oral rat LD50: 124 mg/kg; skin rabbit LD50: 1680 uL/kg; investigated as a tumorigen, mutagen, reproductive effector.
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---NTP Carcinogen---
Ingredient Known Anticipated IARC Category
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Acrylamide (79-06-1) No Yes 2A
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12. Ecological Information
Environmental Fate:
When released into the soil, this material is expected to leach into groundwater. When released into the soil, this material may biodegrade to a moderate extent. This material is not expected to significantly bioaccumulate. When released into the air, this material may be removed from the atmosphere to a moderate extent by wet deposition.
Environmental Toxicity:
This material is not expected to be toxic to aquatic life. The LC50/96-hour values for fish are over 100 mg/l.
--------------------------------------------------------------------------------
13. Disposal Considerations
Whatever cannot be saved for recovery or recycling should be handled as hazardous waste and sent to a RCRA approved incinerator or disposed in a RCRA approved waste facility. Processing, use or contamination of this product may change the waste management options. State and local disposal regulations may differ from federal disposal regulations. Dispose of container and unused contents in accordance with federal, state and local requirements.
--------------------------------------------------------------------------------
14. Transport Information
Domestic (Land, D.O.T.)
-----------------------
Proper Shipping Name: ACRYLAMIDE
Hazard Class: 6.1
UN/NA: UN2074
Packing Group: III
Information reported for product/size: 12KG
International (Water, I.M.O.)
-----------------------------
Proper Shipping Name: ACRYLAMIDE, SOLID
Hazard Class: 6.1
UN/NA: UN2074
Packing Group: III
Information reported for product/size: 12KG
International (Air, I.C.A.O.)
-----------------------------
Proper Shipping Name: ACRYLAMIDE
Hazard Class: 6.1
UN/NA: UN2074
Packing Group: III
Information reported for product/size: 12KG
--------------------------------------------------------------------------------
15. Regulatory Information
--------\Chemical Inventory Status - Part 1\---------------------------------
Ingredient TSCA EC Japan Australia
----------------------------------------------- ---- --- ----- ---------
Acrylamide (79-06-1) Yes Yes Yes Yes
--------\Chemical Inventory Status - Part 2\---------------------------------
--Canada--
Ingredient Korea DSL NDSL Phil.
----------------------------------------------- ----- --- ---- -----
Acrylamide (79-06-1) Yes Yes No Yes
--------\Federal, State & International Regulations - Part 1\----------------
-SARA 302- ------SARA 313------
Ingredient RQ TPQ List Chemical Catg.
----------------------------------------- --- ----- ---- --------------
Acrylamide (79-06-1) 5000 1,000* Yes No
--------\Federal, State & International Regulations - Part 2\----------------
-RCRA- -TSCA-
Ingredient CERCLA 261.33 8(d)
----------------------------------------- ------ ------ ------
Acrylamide (79-06-1) 5000 U007 No
Chemical Weapons Convention: No TSCA 12(b): No CDTA: No
SARA 311/312: Acute: Yes Chronic: Yes Fire: No Pressure: No
Reactivity: Yes (Pure / Solid)
WARNING:
THIS PRODUCT CONTAINS A CHEMICAL(S) KNOWN TO THE STATE OF CALIFORNIA TO CAUSE CANCER.
Australian Hazchem Code: 2PE
Poison Schedule: No information found.
WHMIS:
This MSDS has been prepared according to the hazard criteria of the Controlled Products Regulations (CPR) and the MSDS contains all of the information required by the CPR.
--------------------------------------------------------------------------------
16. Other Information
NFPA Ratings: Health: 2 Flammability: 2 Reactivity: 2
Label Hazard Warning:
WARNING! HARMFUL IF SWALLOWED, INHALED OR ABSORBED THROUGH SKIN. AFFECTS CENTRAL AND PERIPHERAL NERVOUS SYSTEMS AND REPRODUCTIVE SYSTEM. CAUSES IRRITATION TO SKIN, EYES AND RESPIRATORY TRACT. SUSPECT CANCER HAZARD. MAY CAUSE CANCER. Risk of cancer depends on level and duration of exposure. POSSIBLE BIRTH DEFECT HAZARD. MAY CAUSE BIRTH DEFECTS BASED ON ANIMAL DATA. THERMALLY UNSTABLE. MAY POLYMERIZE EXPLOSIVELY IF HEATED TO THE MELTING POINT.
Label Precautions:
Do not breathe dust.
Do not get in eyes, on skin, or on clothing.
Keep container closed.
Use only with adequate ventilation.
Wash thoroughly after handling.
Keep away from heat, sparks and flame.
Protect from U.V. light, oxidizers and peroxides.
Label First Aid:
If swallowed, induce vomiting immediately as directed by medical personnel. Never give anything by mouth to an unconscious person. If inhaled, remove to fresh air. If not breathing, give artificial respiration. If breathing is difficult, give oxygen. In case of contact, immediately flush eyes or skin with plenty of water for at least 15 minutes while removing contaminated clothing and shoes. Wash clothing before reuse. In all cases, get medical attention.
Product Use:
Laboratory Reagent.
Revision Information:
MSDS Section(s) changed since last revision of document include: 14, 16.
Disclaimer:
************************************************************************************************
Mallinckrodt Baker, Inc. provides the information contained herein in good faith but makes no representation as to its comprehensiveness or accuracy. This document is intended only as a guide to the appropriate precautionary handling of the material by a properly trained person using this product. Individuals receiving the information must exercise their independent judgment in determining its appropriateness for a particular purpose. MALLINCKRODT BAKER, INC. MAKES NO REPRESENTATIONS OR WARRANTIES, EITHER EXPRESS OR IMPLIED, INCLUDING WITHOUT LIMITATION ANY WARRANTIES OF MERCHANTABILITY, FITNESS FOR A PARTICULAR PURPOSE WITH RESPECT TO THE INFORMATION SET FORTH HEREIN OR THE PRODUCT TO WHICH THE INFORMATION REFERS. ACCORDINGLY, MALLINCKRODT BAKER, INC. WILL NOT BE RESPONSIBLE FOR DAMAGES RESULTING FROM USE OF OR RELIANCE UPON THIS INFORMATION.
************************************************************************************************
Prepared by: Environmental Health & Safety
Phone Number: (314) 654-1600 (U.S.A.)
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