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Toxicity Effects

CAS Registry Number: 107-18-6

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 2.

Names 1

  • 1-Propen-3-Ol
  • 2-Propen-1-Ol
  • 2-Propenol
  • 2-Propenyl Alcohol
  • 3-Hydroxypropene
  • Allyl alcohol
  • Allylic Alcohol
  • Vinyl Carbinol

Human Toxicity Excerpts

  • CASE REPORTS: At least three cases of accidental poisoning have been described following acute inhalation exposures to unknown concentrations of allyl alcohol. ...Dyspnea, difficulties in ocular accommodation and general malaise in one individual /has been reported/. /Investigators/ also documented nausea, vomiting, and "slight haemoptysis" after two workers spilled allyl alcohol on a floor and on their clothing. In each case, these individuals recovered without sequelae. ...[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • CASE REPORTS: Oral ingestion of allyl alcohol by a 55-yr-old man resulted in death within 100 min. At autopsy, bloody, reddish fluid was found in mouth, larynx, esophagus, and trachea. The mucous membranes of the trachea, stomach, and duodenum were congested and inflamed. The stomach contained a pungent green-black fluid, and all internal organs exhibited a strong pungent odor. Toxicological analysis of blood identified allyl alcohol ... Total amounts of allyl alcohol in gastric contents, bile, and urine were 3.6 g, 15 mg, and 0.5 mg, respectively. The concentration in blood was 309 mg/L. Acrolein was not detected in gastric contents and only in small amounts in bile and urine. The concentration of acrolein in blood was 7.2 mg/L. Death was attributed to acrolein-induced acute cardiotoxicity, similar to that previously documented in animal experiments.[Toennes SW et al; J Anal Toxicol 26 (1): 55-7 (2002)] **PEER REVIEWED** PubMed Abstract
  • CASE REPORTS: The U.S. Chemical Safety and Hazard Investigation Board (CSB) conducted a comprehensive investigation of a runaway chemical reaction at MFG Chemical (MFG) in Dalton, Georgia on April 12, 2004 that resulted in the uncontrolled release of a large quantity of highly toxic and flammable allyl alcohol and allyl chloride into the community. Five people were hospitalized and 154 people required decontamination and treatment for exposure to the chemicals. This included police officers attempting to evacuate the community and ambulance personnel who responded to 911 calls from residents exposed to the chemicals.[Kaszniak M, Vorderbrueggen J et al; J Hazard Mater 159 (1): 2-12 (2008)] **PEER REVIEWED** PubMed Abstract
  • HUMAN EXPOSURE STUDIES: /Allyl alcohol exposure/ studies were carried out on groups of volunteers (numbers of the staff or medical students). /Doses administered were/ 0.78, 6.25, 12.5, or 25 ppm. The age range was 19 to 39, with a mean of 22. All participants were in apparent good health before and during the experimental period, which extended over 50 days. All of the exposed subjects were under the supervision of physician. The eyes were visually inspected after each exposure. Physical examination of the chest was made at the conclusion of the day's run, or when subjective complaints were elicited. Group of five to seven subjects were exposed from one to three times a week for exactly five minutes, during which time they noted the degree of subjective response at one-minute intervals. Evaluation was made by checking: absent, slight, moderate, severe, or extreme. ... Exactly five minutes was allowed for vaporization and equilibration before the subjects entered /the exposure room/, and at least 10 minutes was allowed for evacuating the vapors after the subjects were dismissed. In no case was there any pulmonary discomfort or noticeable effect on the central nervous system. Eye irritation, occurring immediately, was not more than slight until the level of 25 ppm was reached, although nose irritation was regarded as at least moderate by four of seven subjects at 12.5 ppm. Olfactory cognition was checked off as more than moderate only at 6.25 ppm, and by only two of five subjects.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 220 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: ... There is also no evidence for histamine release following exposure to allyl alcohol.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Vapors are quite irritating to eyes, nose, and throat. Eye irritation may be accompanied by complaints of photophobia and pain in the eyeball; pain may not begin until 6 hr after exposure.[Prager, J.C. Environmental Contaminant Reference Databook Volume 2. New York, NY: Van Nostrand Reinhold, 1996., p. 55] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: ...Absorbed through intact skin in toxic and even lethal concentration. Dermatitis of variable types and degrees results, in addition to first and second-degree burns with vesiculation.[Arena, J.M. and Drew, R.H. (eds.) Poisoning-Toxicology, Symptoms, Treatments. 5th ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 275] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: ...Concentration likely to be injurious, in short period of time will be painful to eyes and nose.[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 381] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Absorption through the skin leads to deep muscle pain, presumably due to spasm. Lacrimation, retro-bulbar pain, photophobia, and blurring of vision may be associated with exposure to vapors, and corneal injury has been described.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 222 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Absorption through the skin leads to deep muscle pain, presumably due to spasm.[Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974., p. 299] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: May be fatal if absorbed through skin or inhaled. Irritating to skin, eye, and respiratory system. May cause pulmonary edema if inhaled. Health effects may be delayed.[National Fire Protection Association; Fire Protection Guide to Hazardous Materials. 14TH Edition, Quincy, MA 2010, p. 49-14] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Potential symptoms of overexposure are eye irritation, tissue damage; irritation of upper respiratory system and skin; pulmonary edema.[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 52] **PEER REVIEWED**
  • SIGNS AND SYMPTOMS: Severe eye irritation results from exposure to 25 ppm ...5 ppm is slightly irritating to some individuals. Corneal necrosis has been reported to result in temporary blindness. ...Skin penetration may lead to serious systemic injury (visceral congestion, periportal congestion of the liver, hematuria, and nephritis)... /allyl alcohol/ produces a syndrome of lacrimation, photophobia, blurred vision, and retrobulbar pain. Although these symptoms persist for some hours following exposure, neither increased sensitivity nor tolerance appear to develop.[American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 3] **PEER REVIEWED**
  • SURVEILLANCE: In air moderately contaminated with allyl alcohol (concentration unspecified), men complained of excessive secretion of tears, pain behind the eyes, sensitivity to light, and some blurring of vision.[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 520] **PEER REVIEWED**
  • SURVEILLANCE: The breath of eight male volunteer subjects was analyzed to determine the levels of trace organic compounds in the respired air. 2-Propen-1-ol was found at 0.52 and 9.5 ug/hr in expired air from one subject that was a smoker and from one non-smoking subject, respectively. 2-Propen-1-ol was not found in the breath of the other 6 subjects. 2-Propen-1-ol was categorized as a chemical that is thought to result from or be related to normal human metabolism.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 222 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**

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Non-Human Toxicity Excerpts

  • ALTERNATIVE and IN VITRO TESTS: ... /Investigators sought/ to determine the expression profile of uptake and efflux transporters in mouse liver following treatment with allyl alcohol (AlOH), a periportal hepatotoxicant. This study also investigated the role of Kupffer cells in AlOH hepatotoxicity, and whether changes in transport protein expression by AlOH are dependent on the presence of Kupffer cells. C57BL/6J mice received 0.1 mL clodronate liposomes to deplete Kupffer cells or empty liposomes 48 h prior to dosing with 60 mg/kg AlOH, i.p. Hepatotoxicity was assessed by plasma ALT and histopathology. Hepatic transporter mRNA and protein expression were determined by branched DNA signal amplification assay and Western blotting, respectively. Depletion of Kupffer cells by liposomal clodronate treatment resulted in heightened susceptibility to AlOH toxicity. Exposure to AlOH increased mRNA levels of several Mrp genes, while decreasing organic anion transporting polypeptides (Oatps) mRNA expression. Protein analysis mirrored many of these mRNA changes. The presence of Kupffer cells was not required for the observed changes in uptake and efflux transporters induced by AlOH. Immunofluorescent analysis revealed enhanced Mrp4 staining exclusively in centrilobular hepatocytes of AlOH treated mice. These findings demonstrate that Kupffer cells are protective from AlOH toxicity and that induction of Mrp4 occurs in liver regions away from areas of AlOH damage independent of Kupffer cell function. These results suggest that Kupffer cell mediators do not play a role in mediating centrilobular Mrp4 induction in response to periportal damage by AlOH.[Campion et al; Toxicol Appl Pharmacol 236 (1): 49-58 (2009)] **PEER REVIEWED** PubMed Abstract Full text: PMC4404030
  • ALTERNATIVE and IN VITRO TESTS: ...Liver slices were prepared from male Sprague-Dawley rats, male Dunkin-Hartley guinea-pigs and from samples of Cynomolgus monkey and human liver ... /and/ were cultured with the test compounds for 24 hr in a dynamic organ culture system. ...At /the/ concentrations ... examined, ... rat liver slices were less susceptible to allyl alcohol toxicity. ...[Price RJ et al; Arch Toxicol 71 (1-2): 107-11 (1996)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: ...The action of allyl alcohol (100-500 uM) on isolated hepatocytes was studied using cells maintained at either 95 or 21% O2. Allyl alcohol toxicity, as indexed by trypan blue uptake, lactate dehydrogenase release, and ATP content, did not differ in the two groups of cells, suggesting that O2 dependency of allyl alcohol toxicity involves other cell types. ...[Przybocki JM et al; Toxicol Appl Pharmacol 115 (1): 57-63 (1992)] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: ...The effects of ethanol and allyl alcohol on primary mouse hepatocytes were investigated. No cytotoxicity was observed by ethanol treatments, but more toxicity to cells was found in the response to allyl alcohol treatment. The expression of cytochrome P450 2E1 (CYP2E1), phase I enzyme was examined in response to ethanol and allyl alcohol. Both xenobiotics induced CYP2E1 up to 1.5 to approximately 5 fold at the protein level. ...[Yang JW et al; Biosci Biotechnol Biochem 65 (7): 1528-33 (2001)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: /Lipopolysaccharide/ (LPS) treatment did not affect the activity of alcohol dehydrogenase and did not affect the rate of production of NADH in isolated /rat/ livers perfused with allyl alcohol; thus, LPS does not appear to increase the metabolic bioactivation of allyl alcohol into acrolein. On the other hand, pretreatment with 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, abolished the hepatotoxicity of allyl alcohol in LPS-treated rats, indicating that production of acrolein was needed for LPS enhancement of the toxicity of allyl alcohol. Pretreatment of rats with gadolinium chloride (10 mg/kg), a known inactivator of Kupffer cell phagocytic function, decreased LPS augmentation of the response to allyl alcohol. ...The results suggest that the LPS-induced enhancement of allyl alcohol hepatotoxicity occurs through a Kupffer cell-dependent mechanism.[Sneed RA et al; Toxicol Appl Pharmacol 144 (1): 77-87 (1997)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: Allyl alcohol-induced LDH leakage from isolated rat hepatocytes was preceded by ... a loss of mitochondrial membrane potential. Addition of dithiothreitol (DTT) prevented the drop in membrane potential and completely prevented cell killing by allyl alcohol. In contrast, cyclosporin A and trifluoperazine delayed the loss of membrane potential without affecting cytolethality. The results indicate that a drop in mitochondrial membrane potential is not essential for allyl alcohol lethality. The mitochondrial dysfunction produced by allyl alcohol appears to be the consequence of an earlier event in the toxicity that is reversible by DTT.[Rikans LE et al; Toxicol Lett 81 (2-3): 159-65 (1995)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: Possible effect of bone marrow cells on liver regeneration was studied in mice injected with a mixture of hepatotoxins (allyl alcohol and CCl4) in a dose equal to LD50. The mixture of hepatotoxins was used to minimize the restitution regeneration of the liver. The dose of allyl alcohol causing (in combination with CCl4) maximum liver damage was selected beforehand. Increasing the dose of allyl alcohol in the two-component mixture resulted in more severe necrosis of the liver. The maximum dose of alcohol (50 mg/kg) in combination with CCl4 caused irreversible injury to the liver leading to 100% mortality after 2-4 days. In radiation chimeras reconstituted by bone marrow cell transplantation, in which liver damage was induced by a mixture of hepatotoxins containing the maximum dose of allyl alcohol, ... normalization of liver tissue structure and function /was observed/. ...[Todriya TV, Nikolaeva TL; Bull Exp Biol Med 141 (4): 475-8 (2006)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: Reversal by dithiothreitol (DTT) of allyl alcohol cytotoxicity was investigated in isolated rat hepatocytes. Allyl alcohol-induced protein sulfhydryl loss, bleb formation, and cell death were prevented by DTT, when it was added to hepatocytes 30 min after the toxicant. The protective effect of DTT also was demonstrated in cells that were washed after 30 min of exposure to allyl alcohol. DTT reversed the cell surface protrusions that formed during exposure to allyl alcohol, but reversal of blebbing did not insure that the cells would remain viable. Glutathione disulfide was not formed in allyl alcohol-treated cells, and DTT reversal of cytotoxicity occurred without restoring glutathione levels. Moreover, protection against allyl alcohol toxicity required the continuous presence of DTT. The results suggest that initial events in the toxic process are reversible, and that DTT can prevent cytotoxicity if added to hepatocytes before irreversible damage occurs; however, the mechanism by which DTT exerts its protection is not clear.[Rikans LE, Cai Y; Toxicology 86 (1-2): 147-61 (1994)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The activity of alcohol dehydrogenase (ADH) with 2-propen-1-ol as substrate was measured in liver cystolic fractions of rats representing young adulthood, middle age and old age. 2-Propen-1-ol-induced hepatotoxicity was more severe in old male rats than in young male rats, as measured by release of hepatic enzymes from injured cells and loss of hepatic microsomal cytochrome P-450. The extent of toxicity in female rats was greater than in males and unaffected by aging. ADH activities were 1.7+/-0.1, 2.3+/-0.1 and 2.6+/-0.1 umol/min/g of liver in males rats aged 4, 14 and 25 months, respectively. ADH activities in young adult and old female rats were 3.8+/-0.1 and 3.7+/-0.1 umol/min/g of liver. There was good correlation between liver ADH activity and 2-propen-1-ol-induced hepatotoxicity, measured as release of sorbitol dehydrogenase into the bloodstream. Cytosolic free NAD+/NADH ratios in male rats were not significantly different among the three age groups; the ratios were lowest in young adult female rats. Low Km aldehyde dehydrogenase activities in liver mitochondrial and cytosolic fractions were similar among the three age groups of male rat, and the activities in female rats were not substantially different. The results indicated that increased ADH activity is the principal cause of the age associated enhancement of 2-propen-1-ol hepatotoxicity in male rats.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 131 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • ALTERNATIVE and IN VITRO TESTS: The influence of aging on the toxicity of allyl alcohol was studied in hepatocytes isolated from male Fischer 344 rats. Initial values for trypan blue uptake, lactate dehydrogenase (LDH) release, alanine aminotransferase release, and glutathione content were similar in cells isolated from rats aged 5, 15, or 26 months. Incubation with 0.1 to 0.8 mM allyl alcohol resulted in a dose- and time-dependent loss of viability. Inhibition by pyrazole of allyl alcohol-induced lactic dehydrogenase (LDH) release from hepatocytes also was affected by age. Total protection was observed for cells from young rats whereas no protection was found for those of old rats. Cells from middle-aged rats were between the extremes.[Rikans LE, Hornbrook KR; Toxicol Appl Pharmacol 84 (3): 634-9 (1986)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The possible involvement of thiols and adenine nucleotides in the selective toxicity to periportal regions by allyl alcohol was evaluated in isolated perfused rat livers. Infusion of allyl alcohol (350 uM) for 20 min depleted hepatic glutathione content by 95% in both regions of the liver lobule yet damage was undetectable as indexed by release of lactate dehydrogenase or uptake of trypan blue. Perfusion for an additional 40 min in the absence of allyl alcohol resulted in lactate dehydrogenase release (2400 U/l) and uptake of trypan blue by 75% of hepatocytes in periportal regions of the liver lobule; however dye was not taken up by cells in pericentral areas. Because the content was depleted in the undamaged pericentral area, it was concluded that thiol depletion alone cannot explain local toxicity to periportal regions by allyl alcohol.[Belinsky SA et al; J Pharmacol Exp Ther 238 (3): 1132-7 (1986)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The role of altered energy homeostasis in the lethality of allyl alcohol to isolated rat hepatocytes was studied. ATP, ADP, AMP, and viability loss (leakage of lactate dehydrogenase into the medium) were measured in isolated hepatocytes of fed or fasted rats exposed to 0.5 mM allyl alcohol. Adenine mononucleotides and cytotoxicity were determined also in hepatocytes incubated with allyl alcohol in the presence of 4 mM sodium azide or 15 mM fructose. Allyl alcohol-induced cell death in hepatocytes of fed rats was preceded by slight decreases in ATP content and energy charge (16% and 12%, respectively). More substantial decreases in these parameters occurred in parallel with cell killing, but the effect of allyl alcohol on energy status did not exceed the effect produced by a nonlethal concentration of sodium azide. Neither azide nor fructose affected the development of allyl alcohol cytotoxicity. Moreover, allyl alcohol-induced cytotoxicity was similar in hepatocytes of fed and fasted rats. The results suggest that altered energy homeostasis is a consequence rather than a cause of allyl alcohol-induced hepatocyte lethality.[Rikans LE et al; J Toxicol Environ Health 44 (1): 1-11 (1995)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: The toxicity of allyl alcohol was studied in freshly isolated renal epithelial cells prepared from male and female rats. Cells from female rats demonstrated a greater susceptibility to allyl alcohol toxicity as assessed by glutathione depletion and loss of cell viability. The sensitivity of female rat renal cells appears to relate to the higher activity of alcohol dehydrogenase found in the female rat kidney, which metabolizes allyl alcohol to the highly reactive aldehyde, acrolein. Pyrazole, an inhibitor of alcohol dehydrogenase, abolished the cytotoxic effects of allyl alcohol whereas inhibition of aldehyde dehydrogenase by disulfiram treatment was found to increase the sensitivity of renal cells to the effects of allyl alcohol. ...[Ohio Y et al; Chem Biol Interact 52 (3): 289-99 (1985)] **PEER REVIEWED** PubMed Abstract
  • ALTERNATIVE and IN VITRO TESTS: Two hepatotoxicants, allyl alcohol and bromobenzene, were studied using an in vitro system of cultured liver slices from control and phenobarbital-treated rats, respectively. Dose- and time-dependent increases in media lactate dehydrogenase (LDH), and decreases in slice K+ content and in protein synthesis were observed in rat liver slices incubated with either compound at concentrations between 0.1 and 1 mM over a period of 6 hr. Additionally, the toxicity of either bromobenzene or allyl alcohol, evaluated at 4 hr, was inhibited when slices were preincubated for 30 min with beta-ethyl-2,2-diphenylvalerate hydrochloride (SKF 525-A) (0.1 mM) or pyrazole (1.0 mM), respectively.[Smith PF et al; Toxicol Appl Pharmacol 87 (3): 509-22 (1987)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: ... Genetic toxicology studies were conducted in Salmonella typhimurium, Drosophila melanogaster, cultured Chinese hamster ovary cells, rat bone marrow erythrocytes, and mouse peripheral blood erythrocytes /with allyl acetate, allyl alcohol, and acrolein/. ... Allyl alcohol was not mutagenic in four strains of S. typhimurium, with or without S9 metabolic activation. ... Equivocal results were obtained in strains TA100 and TA1535 with 10% induced hamster liver S9. Negative results were obtained with TA97, TA98, and TA1538 under all test conditions ... No significant increases in micronucleated erythrocytes were noted in bone marrow samples from male rats administered allyl alcohol by intraperitoneal injection for 3 days. ... No increases in the frequencies of micronucleated normochromatic erythrocytes were observed in the peripheral blood of male or female mice administered allyl alcohol or acrolein by gavage for 14 weeks. ...[Irwin RD; Toxic Rep Ser (48): 1-73, A1-H10 (2006)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Allyl alcohol is a direct-acting mutagen in Salmonella typhimurium (strain TA100). /It/ is an equipotent mutagen for cultured V79 cells as is its metabolite, acrolein.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol mutagenicity /was tested in a/ Salmonella typhimurium reverse mutation microsomal assay at a concentration of 50 ug/plate with and without S9 activation. /Mutagenicity was observed/ in more than one of five strains.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol mutagenicity /was tested in a/ forward mutation assay in Aspergillus nidulans at concentrations of 10, 20, or 40 uL/plate. All results were negative.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol mutagenicity /was tested in a/ forward mutation assay in Streptomyces coelicolar at concentrations of 2, 10, 20, or 100 uL/plate. All results were negative.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol mutagenicity /was tested in/ Salmonella typhimurium TA 1535, TA 1537, TA 1538, TA98, and TA100 strains /at a/concentration of 0.05 uL/plate with and without S9 activation. Results were negative.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol was mutagenic in the Ames bacterial test and in mammalian cells in culture. There was no evidence of mutation in male rats treated orally.[BIBRA working group; TA:Toxicity profile. BIBRA Toxicology International:5 (1995).] **PEER REVIEWED**
  • GENOTOXICITY: Allyl alcohol was tested positive for mutagenicity on Chinese hamster V-79 cells at concentrations /between/ 1-2 uM. 6-Thioguanine was used as an indicator.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • GENOTOXICITY: Five industrial and agricultural chemicals including allyl alcohol were tested for their ability to induce reverse mutations in Salmonella typhimurium and forward mutations in Streptomyces coelicolor and Aspergillus nidulans. Allyl alcohol was completely negative in all test systems.[Principe P et al; J Sci Food Agric 32 (8): 826-32 (1981)] **PEER REVIEWED** PubMed Abstract
  • GENOTOXICITY: Male F344 rats were given 2-propen-1-ol at 5, 10 or 20 mg/kg bw (n=5/treatment) by i.p. injection on 3 consecutive days. The control group (n=4) received physiological saline. Bone marrow was collected 24 hr after the final treatment. Two thousand polychromatic erythrocytes (PCEs) were examined microscopically and scored for the presence of micronuclei. Cyclophosphamide (7.5 mg/kg bw) was used as positive control (i.p. injection on 3 consecutive days). ... There was no statistically significant difference in the number of micronuclei per 1000 PCEs in rats given 2-propen-1-ol at 5, 10 or 20 mg/kg bw/d by i.p. injection on 3 consecutive days. Animals given 40, 60 or 80 mg/kg died prior to scheduled study termination. A satisfactory response was obtained with the positive control group (24.2MN-PCEs per 1000 PCEs; P=0.0001). Under the conditions of the study, no increase in micronucleated polychromatic erythrocytes was detected in male F344 rats given 2-propen-1-ol at doses of up to 20 mg/kg bw/d for three consecutive days.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 188 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • GENOTOXICITY: Mutagenicity of vinyl compounds were tested in 5 strains of Salmonella typhimurium. Allyl alcohol was mutagenic in more than 1 strain.[Lijinsky W, Andrews AW; Teratog, Carcinog, Mutagen 1 (3): 259-67 (1980)] **PEER REVIEWED**
  • GENOTOXICITY: Several alpha-, beta-unsaturated carbonylic compounds and their corresponding allylic alcohols were tested in a modified Salmonella typhimurium assay with and without metabolic activation by S9 mix. Allyl alcohol exerted a significant direct mutagenic activity (750 revertants/uM).[Lutz D et al; Mutat Res 93 (2): 305-15 (1982)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: ... Administration of allyl alcohol (30 or 40 mg/kg, ip) to rats caused extensive hepatic necrosis localized primarily to periportal regions. To test the involvement of Kupffer cells in the genesis of this injury, male rats (200-350 g) were treated with gadolinium chloride (GdCl3, 10 mg/kg, iv) which diminishes Kupffer cell function and number. The extent of hepatic damage assessed by light microscopy and serum enzymes, aspartate aminotransferase and alanine aminotransferase, was markedly attenuated by pretreatment of rats with GdCl3 24 hr prior to allyl alcohol injection. Thus, O2-dependent hepatic necrosis caused by allyl alcohol involves the presence of Kupffer cells. Since GdCl3 did not prevent toxicity in the perfused liver, circulating blood elements may also contribute to injury of the liver by allyl alcohol in vivo.[Przybocki JM et al; Toxicol Appl Pharmacol 115 (1): 57-63 (1992)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: .../Single/ 5, 10 and 25 mg/kg doses of... allyl alcohol /was administered/ to obese Sprague-Dawley rats and age-matched non-obese controls. Alanine aminotransferase activity (ALT) in plasma was ten-fold more elevated in obese animals than in non-obese animals given the 25 mg/kg dose (P<0.05). ...The minimum dose required to produce elevated ALT (DMIN) was 50% lower for obese animals (DMIN 6.47 +/- 2.75 vs. 13.3 +/- 0.96 mg allyl alcohol; P<0.05). In a subsequent experiment, allyl alcohol was administered to obese rats based on ideal body weight, which is defined as the mean total body weight of an age-matched non-obese animal. With this dosing normalization, the 25 mg/kg ideal body weight doses translated to administration of a fixed dose of 13.5 mg allyl alcohol to obese rats. Obese rats treated in this fashion exhibited more severe necrosis in the periportal zone (median necrosis score 2 versus 0-1, P<0.05) and increased mortality over controls (44% versus 0%; P<0.05).[Salazar DE et al; Int J Obes Relat Metab Disord 18 (1): 25-33 (1994)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: ...The study comprised 130 male Wistar rats divided randomly into 2 groups: I (n=10) sham and II (n=120) /allyl alcohol/ (AA) injection (ip: 0.62 mmol/kg) and rhinogastric administration of /carbon tetrachloride/ (CCl4) (0.66 mL/kg, 1:1 volume dilution in corn oil). After injection was completed, animals of group II were assigned in 12 categories and sacrificed 2, 4, 6, 12, 18, 24, 33, 48, 57, 81, and 153 hr after. Tissue was obtained from the left anterior lobe and the hilum of the liver, and histological examination included H&E, silver methenamine and van Giesson stains. Liver sections from group II (AA+CCl4) demonstrated periportal together with pericentral necrosis; the peak was 57 hr after injection. In all 120 cases, H&E stain showed evidence of regeneration originated from zone 2, extending to zone 1 and occasionally to zone 3, and accomplished mainly by non-necrotic cell proliferation. Sections from the liver hilum showed thrombosis of the portal vein, whereas the hepatic artery and its branches developed a variety of changes. Initially (2, 4 hr), endothelial hypertrophy was observed which was followed by focal fibrinoid necrosis of the arterial wall (6 hr). Later on (9-153 hr) the following findings were present: hyperplasia and non-isometric cytoplasmic vacuolisation of media, disruption of the elastic lamina, aggregation of foam cells and macrophages in intima, media, and focally in adventitia of hepatic artery; and lymphocytic inflammation of intimal and periadventitial area. In 2 cases (153 hr) hepatic artery thrombosis was present. Additionally to liver parenchymal changes, simultaneous administration of allyl-alcohol and carbon tetrachloride in rats results /in/ vascular changes mainly in the hepatic artery and its branches. During liver parenchymal regeneration, the hepatic artery and its branches develop microscopic features that morphologically resemble those of atherosclerosis. These changes may result in hepatic artery thrombosis and or obstruction.[Papalambros E et al; Int Angiol 19 (2): 166-70 (2000)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: / Male Fischer-344 rats (150-200 g) and male B6C3F1 mice(20-25 g)/ were dosed orally with 25-200 mg/kg of 2-propen-1-ol. Corn oil was used as a vehicle. The animals were anesthetized with ether 24 hr after dosing and blood was taken from the inferior vena cava and analyzed for SGPT activity. Histopathlogical evaluation of liver was performed. Although statistically significant increases in SGPT activities were observed in both rats and mice at 50 and 75 mg/kg, the magnitude of these increases at 50 or 75 mg/kg was considerably greater in rats. Mice given 100 to 220 mg/kg of 2-propen-1-ol died within 24 hr after administration. Therefore in mice it was not possible to identify a nonlethal dose of 2-propen-1-ol that resulted in extensive liver damage. Histopathological examination confirmed a marked species difference in 2-propen-1-ol-induced hepatic injury. Doses of 25, 50 and 75 mg/kg of 2-propen-1-ol were not hepatotoxic in mice. In rats, periportal necrosis was evident in 9 of 12 animals treated with 2-propen-1-ol. The severity of the injury was greater at the 50 and 75 mg/kg doses that at the 25 mg/kg dose.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 130 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /A dose of/ 0.05 mL/kg of allyl alcohol administered orally to mice caused depletion of hepatic glutathione activity. The extent of depletion was 44.5% of control values.[Siegers CP et al; Proc Eur Soc Toxicol 18 (Clin Toxicol): 160-2 (1977)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /Allyl alcohol administered at/ 30 mg/kg orally in rats cause marked periportal necrosis which was associated with losses of alcohol dehydrogenase and succinate dehydrogenase activities in liver. Benzo(a)pyrene hydroxylase and hepatic content of cytochrome p450 were decreased showing inhibition of xenobiotic metabolism.[Lake BG et al; Biochem Soc Trans 6 (1): 145-7 (1978)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /At/ 0, 1, 3, 24, and 72 hr after oral administration to rats of 1 mL/100 g body weight of 1% allyl alcohol, livers contained 1.05, 1.088, 1.37, 1.21, and 1.51 (arbitrary) units of malonic aldehyde and 4.30, 5.68, 10.97, 6.67, and 7.13 (arbitrary) units of conjugated dienes. Alanine aminotransferase activity was very high during this period. Necrosis in the hepatocyte and Kupffer cell cytoplasm was observed from the 4th hr after administration which shows that the onset of lipid peroxidation precedes necrosis.[Kopylova TN, Vicupe Z; Eksp Med (Riga) 3: 58-61 (1978)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: /On the skin of rabbits,/ 0.5 mL (undiluted allyl alcohol) was applied to intact and scarified areas. The areas were covered with patches of gauze. One rabbit of three showed a slight ertythema where allyl alcohol had been applied to the intact skin 24 hours previously. This had disappeared by the end of the 48 hours, and no other reactions were noted.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: 2-Propen-1-ol /was administerd/ to twenty male Ssc: CF-1 mice /via/ inhalation (normal or via tracheal cannula) in doses of 0.42, 2.00, 4.55, /or/ 15.10 ppm (normal) 3.62 (cannula) for 30 minutes. 2-Propen-1-ol induced a decrease in the respiratory rate due to sensory irritation in normal (non-cannulated) mice. The effects were very rapid, normally reaching a plateau within the first 10 minutes. After exposure, the sensory irritating responses died away very rapidly. No pulmonary irritation was observed at concentrations up to the RD50 in cannulated mice, therefore the respiratory depression observed was due entirely to the chemical's sensory irritating effect. Groups of 4 mice used for each exposure level. Sensory irritation of the upper respiratory tract causes a characteristic pause before exhalation and thereby a decrease in respiratory rate. This bradypnea occurs reflexively from stimulation of the trigeminal nerve endings in the nasal mucosa. ... If exposures were carried out in animals via tracheal cannula, the bypass of the nasal trigeminal nerve endings excludes the development of sensory irritation of the upper respiratory tract. Stimulation of pulmonary receptors by airborne irritants in mice results in a different reflex decrease in respiratory rate due to a pause between the end of expiration and the beginning of the following inspiration resulting in a net decrease in respiratory rate proportional to the log of the concentration of the irritants.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 154 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: A histologic, histochemical and electron microscopic study was carried out on the rat exocrine pancreas 6-96 h after a single allyl alcohol intake. Histologically, acidophilia, necrosis and vacuolation of the pancreatic acinar cells were observed. Histochemically, a low but evident alcohol dehydrogenase activity could focally be demonstrated in the pancreatic acinar cell cytoplasm of the experimental and control rats. By electron microscopy, cytoplasmic lipid droplets, mitochondrial degeneration and necrosis were found in the acinar cells. Focal cytoplasmic degradation and vacuolation were seen in acinar, centroacinar and ductular cells of the pancreas. ...[Nizze H et al; Digestion 19 (6): 359-69 (1979)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: A single oral intubation of 10 mg allyl alcohol proved fatal to adult male hamsters. The oral LD50 in adult rats is 64 mg/kg. /It was reported/... that a single topical application of 25 to 200 mg allyl alcohol/kg body weight to the clipped skin of rabbits produced only slight local erythema, but no other signs of toxicity. ...The rabbit dermal LD50 /was listed/ as 45 mg/kg (0.053 mL/kg). Some animal studies suggest that percutaneous absorption with liquid allyl alcohol can lead to serious systemic injury (periportal necrosis and congestion in the liver, hematuria, nephritis). In one such instance, muscular spasms, localized pain, erythema, and hyperemia followed direct skin contact with allyl alcohol; however, no follow-up or clinical examination findings were conducted. /One researcher/ considered skin penetration by allyl alcohol to be dangerous; skin contact causes chemical burns when evaporation is prevented or reduced. Instillation of 0.05 mL allyl alcohol into rabbit eyes produced conjunctival erythema, swelling of the nicotinic membrane, and corneal sloughing. Corneal opacity developed in some of these rabbits but was said to resolve within one week. /Another study/ found corneal necrosis over 75% of the surface after instillation of 0.02 mL into rabbit eyes. Rat LC50 values for 1-, 4-, and 8-hour exposures were 1060, 165, and 76 ppm, respectively, and signs of intoxication included tremors, convulsions, diarrhea, coma, pulmonary and visceral congestion, and varying degrees of hepatotoxicity. Repeated inhalation trials 7 hr/day at 60 ppm induced gasping during the first few exposures, persistent eye irritation, and death of one of the ten exposed rats. Monkeys died after inhaling 1000 ppm for 3 to 4 hours. Middle-aged and older animals are more susceptible to allyl alcohol-induced hepatotoxicity than are young animals. Marked species differences are also recognized; rats are significantly more sensitive to allyl alcohol-induced liver damage than mice, an effect due to the three-fold greater biotransformation of allyl alcohol to acrolein and acrylic acid in rats than in mice. The RD50 values range from 1.6 to 3.9 ppm for the vapor of allyl alcohol in OFI, ICR, and CFI mice exposed between 5 and 30 minutes. There was no evidence for overt pulmonary damage in mice exposed at the RD50. From the highest statistical correlation between RD50s and TLVs for 40 sensory irritants, /it was/ concluded that these values correspond to a TLV of 0.05 to 0.1 ppm for allyl alcohol.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 (2010)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: After first depressing dogs with paraldehyde in order to delay vomiting, it was found that 0.05 mL of 2-propen-1-ol in 1% solution causes death in about seven hours. ... The symptoms of 2-propen-1-ol poisoning are similar to those commonly ascribed to wood alcohol especially the marked hyperemia of the gastric mucosa, intense vomiting convulsive movements and coma. One animal receiving a sublethal dose, developed in two days an opacity, apparently of the cornea, with blindness in one eye. This cleared up in two days more.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 157 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Allyl alcohol (20 mg/kg) enhanced mitotic activity of adrenocortical cells in rats after 24 hr but activity returned to normal values within following 12 hr.[Danz M et al; Exp Pathol 12: 301-8 (1976)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Allyl alcohol was slightly irritating to intact and abraded skin of rabbits. In rabbits, 0.02 mL of the undiluted material produced severe injury, including corneal necrosis. ...[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 518] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: An acute, whole-body inhalation study for allyl alcohol in Sprague-Dawley rats was designed to support derivation of AEGL values, with emphasis on establishing NOAELs for irreversible effects of different exposure concentrations and durations. Groups of 10 rats were exposed for 1 hour (0, 50, 200, or 400 ppm), 4 hours (0, 20, 50, or 100 ppm), or 8 hours (0, 10, 20, or 50 ppm). Clinical evaluations were performed during exposure and in an open field within 22-71 minutes after termination of exposure. Clinical pathology, gross necropsy, and histopathology (nasal tissues, larynx, trachea, lungs/bronchi, liver, and kidneys) were evaluated 14 days after exposure. Mortality was limited to 1 male exposed for 8 hours to 50 ppm. Clinical findings of gasping, rales, increased respiration noted at higher exposure levels were rapidly reversed. No treatment-related findings were observed in the liver and kidneys, or in the lungs of surviving animals. Histopathology in the nasal cavity was noted at all exposure levels following 1, 4, or 8 hours of exposure. Mild nasal inflammation was found at the lowest exposure levels (50-ppm/1-hour, 20-ppm/4-hour, and 10-ppm/8-hour). These effects were considered reversible and were not associated with related clinical signs. Severe, irreversible nasal olfactory epithelial lesions were present in 50 ppm/8-hour males. The NOELs for irreversible effects were 400-ppm/1-hour, 100-ppm/4-hour, and 20-ppm/8-hour. The incidence of severe findings was positively dependent on both concentration and the exposure duration. In contrast, the incidence of mild reversible findings did not appear to be dependent on duration.[Li AA et al; Inhal Toxicol 24 (4): 213-26 (2012)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: Cyclic(C)AMP was studied in male Sprague-Dawley rats administered a single dose of allyl alcohol. Adrenal (C)AMP concentration increased 10 hr after intoxication compared to controls. In final stage of experiment (30-39 hr after application) all intoxication was associated with significant increases in adrenal (C)AMP concentration.[Danz M, Kittlick P-D; Exp Pathol 13 (2-3): 139-44 (1977)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Graded amounts /(32-55 mg/kg bw)/ of a 1% solution of 2-propen-1-ol were administered by intraperitoneal injection to groups of 10 male /Long-Evans/ rats (178-200 g). Surviving animals were observed for up to 10 days. ... The main clinical sign was described as apathy, along with anxiety. Coma and diarrhea preceded death in moribund animals. Gross post mortem findings in decedent animals included: edema and congestion of the lungs, visceral congestion, presence of mucus in the intestinal tract, discolored liver (some necrosis) and swollen, discolored kidneys. Histopathological examination of tissue from decedent animals revealed: lung congestion, liver damage (congestion and necrosis of periportal sinusoids, central pallor and necrosis), presence of heme casts and cloudy swelling in the kidney. Similar (but less frequent) lesions were present in animals that survived the 10 day observation period. ...[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 151 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Graded amounts /(75-130 mg/kg bw; 79-140 mg/kg bw)/ of a 1% solution of 2-propen-1-ol were administered by gavage (dosing needle) to groups of 5 male Long-Evans rats (body weights: 111-143 g or 170-252 g; two studies). Surviving animals were observed for up to 10 days. ... The main clinical sign was described as apathy, along with anxiety. Coma and diarrhea preceded death in moribund animals. Gross post mortem findings in decedent animals included: edema and congestion of the lungs, visceral, congestion, presence of mucus in the intestinal tract, discolored liver (some necrosis) /and/ swollen, discolored kidneys. Histopathological examination of tissue from decedent animals revealed: lung congestion, liver damage (congestion and necrosis of periportal sinusoids, central pallor and necrosis), presence of heme casts and cloudy swelling in the kidney. Similar (but less frequent) lesions were present in animals that survived the 10 day observation period. ...[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 144 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: In rats a single dose of allyl alcohol (100 uL/kg) was given to produce periportal liver damage. The prothrombin index was reduced to a minimum after 12 hr and reestablished after 24 hr. The galactose elimination capacity was not changed. Hepatic glutathione content was unchanged for the first 24 hr but was then elevated two-fold. Microsomal D-nitroanisole demethylase showed a slight initial increase and a subsequent reduction. Thus, in chemical liver damage ribosomal function is more vulnerable than cytosolic phosphorylation of carbohydrate.[Poulsen HE, Korsholm B; Acta Pharmacol Toxicol 54 (2): 120-3 (1984)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Instillation of 0.05 mL allyl alcohol into rabbit eyes produced conjuntival erythema, swelling of the nicotinic membrane, and corneal sloughing. Corneal opacity developed in some of these rabbits but was said to resolve in one week.[American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 2] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Male CD-1 mice were tested with carbon tetrachloride (1mL/kg, ip), or allyl alcohol (0.05 mL/kg, ip) or both 24 hr prior to sacrifice. The livers were removed, homogenized and mitochondrial preparations were fractionated. The mitochondrial pellet from allyl alcohol-treated livers was characterized by a preponderance of condensed mitochondria whether carbon tetrachloride was given also or not. The mitochondrial fraction from carbon tetrachloride-treated mice failed to utilize oxygen whereas that fraction from mice given allyl alcohol did not differ from control in either its basal oxygen consumption (state 4) or oxygen utilization after the addition of adenosine diphosphate (state 3). State 4 respiration differed slightly but significantly from control in mitochondria from mice given both allyl alcohol and carbon tetrachloride whereas state 3 respiration was greatly and significantly decreased from that of control values. Electron micrographs of liver slices from mice given allyl alcohol or the combination of allyl alcohol and carbon tetrachloride showed normal mitochondrial morphology.[Rutkowski JV et al; Toxicology 40 (1): 25-30 (1986)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: Male CD1 mice and male CD rats were administered allyl alcohol, 0.05 mL/kg in corn oil, ip, 24 hr prior to sacrifice. Pentobarbital sleeping time, serum glutamic pyruvic transaminase (SGPT), histologic evidence of liver necrosis, and respiratory activity of liver mitochondria were used as indices of hepatotoxicity. Allyl alcohol treatment resulted in a significant decrease in pentobarbital sleeping time in mice (p<0.05), but significantly prolonged the sleeping time in rats (p<0.005). SGPT was significantly elevated in treated mice (3-fold, p<0.05) and rats (20-fold). There was no visible liver necrosis in mice; livers from treated rats showed variable necrosis. Micrographs of mitochondria from treated rats showed flocculent densities in the matrix compartment. Mitochondria from control mice and rats and treated mice had normal state 3 respiratory activity and normal respiratory control. In treated rats state 3 respiratory activity was depressed relative to the control value and respiratory control was absent, indicating inability to carry out oxidative phosphorylation.[Jacobs JM et al; Toxicol Lett 38 (3): 257-64 (1987)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: Male NMRI mice were fed a sucrose diet for 48 hr in order to reduce the hepatic glutathione content and to level off its diurnal variation. After administration of allyl alcohol (AA: 1.1 mmol/kg), hepatic glutathione (24.3 +/- 7.0 nmol GSH/mg protein) was almost totally lost within the first 15 min (less than 0.5 nmol GSH/mg protein). Subsequently, a massive lipid peroxidation was observed, ie, the animals exhaled 414 +/- 186 nmol ethane/kg/hr compared to 0.9 +/- 0.8 of controls, and the hepatic TBA-reactive compounds had increased from 55 +/- 16 pmol/mg protein in controls to 317 +/- 163 after 1 hr. Concomitantly, a 40-45% loss of the polyunsaturated fatty acids (arachidonic and docosahexaenoic acid) in the liver lipids was observed. About 80% of the cytosolic alcohol dehydrogenase activity and about 50% of the microsomal p450-content were destroyed. In vivo-inhibition of alcohol dehydrogenase by pyrazole or induction of aldehyde dehydrogenase by phenobarbital abolished allyl alcohol-induced liver damage as well as glutathione depletion and lipid peroxidation, while inhibition of aldehyde dehydrogenase by cyanamide made a subtoxic dose of allyl alcohol (0.60 mmol/kg) highly toxic. In vitro, acrolein alone failed to initiate lipid peroxidation in soy bean phospholipid liposomes or in mouse liver microsomes. Thus, acrolein not only impairs the glutathione defense system but also directly destroys cellular proteins and evokes lipid peroxidation by an indirect iron-dependant mechanism.[Jaeschke H et al; Biochem Pharmacol 36 (1): 51-7 (1987)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: Male Sprague-Dawley rats /were given intraperitoneal injections/ of 0.05 mL 2-propen-1-ol in corn oil. 2-Propen-1-ol reduced hepatic cytochrome p450 in liver, and the activities of ethylmorphine demethylase, benzphetamine demethylase, benzo[a]pyrene hydroxylase, and ethoxyresorufin deethylase. No significant decrease in epoxide hydrolase or glucuronyltransferase activities were observed. The activities of cytosolic conjugating enzymes (glutathione-, sulfo- and acetyltransferases) also were minimally affected by toxic liver injury. ...[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 155 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Rapid drop in carotid blood pressure, definite reduction in respiratory rate and amplitude, and increase in hemoconcentration (hematocrit), but no increase in concentration of histamine in plasma, followed iv injection of 40 mg/kg into a dog.[Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963., p. 1487] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Rats were dosed orally with 1 mL/100g bw of a 1% solution of 2-propen-1-ol. Livers were removed and analysed for malonic aldehyde and conjugated dienes at 0, 1, 3, 24 and 72 hr after administration. 0, 1, 3, 24, and 72 hr after oral administration livers contained 1.05, 1.088, 1.37, 1.21, and 1.51 (arbitrary) units of malonic aldehyde and 4.30, 5.68, 10.97, 6.67, and 7.13. (arbitrary) units of conjugated dienes. Alanine aminotransferase activity was very high during this period. Necrosis in the hepatocyte and Kupffer cell cytoplasm was observed from the 4th hr after administration which shows that the onset of lipid peroxidation precedes necrosis.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 119 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Single necrogenic doses of allyl alcohol admin to Fischer 344 rats were used to produce cell specific injury in centrilobular hepatocytes, periportal hepatocytes, and bile duct cells, respectively. Allyl alcohol administration increased serum alanine aminotransferase activity but had no effect on serum gamma-glutamyl transferase activity.[Leonard TB et al; Am J Pathol 116 (2): 262-9 (1984)] **PEER REVIEWED** PubMed Abstract Full text: PMC1900544
  • LABORATORY ANIMALS: Acute Exposure: The effect of acute exposure of rats to allyl alcohol (0.05 mL/kg, ip) on the activity of enzymes of hepatic phase I (cytochrome p450-linked microsomal monooxygenases, epoxide hydrolase) and phase II (glucuronyl-, glutathione-, acetyl- and sulfotransferases) biotransformation were studied in rats. Allyl alcohol reduced hepatic cytochrome p450 in liver, and the activities of ethylmorphine demethylase, benzphetamine demethylase, benzo[a]pyrene hydroxylase, and ethoxyresorufin deethylase. No significant decrease in epoxide hydrolase or glucuronyltransferase activities were observed. The activities of cytosolic conjugating enzymes (glutathione-, sulfo- and acetyltransferases) also were minimally affected by toxic liver injury.[Gregus Z et al; J Pharmacol Exp Ther 222 (2): 471-9 (1982)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: The livers of rats showed periportal necrosis and elevation of hepatic glutathione within 24 hr following the administration of allyl alcohol.[Atzori L et al; Boll Soc Ital Biol Sper 56 (21): 2218-22 (1980)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: The time course of allyl alcohol induced toxicity was studied in freshly isolated rat hepatocytes incubated with 0.4 and 0.8 mM allyl alcohol. The sequence of events was as follows: an initial rapid decrease of 65 to 75% in glutathione concentration within 10 min, a subsequent increase in malondialdehyde (final concentration 60 times greater than initial values) and decrease in protein sulfhydryl groups (at 20 min with 0.8 mM and at 0.4 mM of allyl alcohol), and the eventual loss of membrane integrity at 30 min with the higher dose and at 45 min with the lower dose. ...[Hormann VA et al; Toxicol Appl Pharmacol 98 (3): 375-84 (1989)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Acute Exposure: Three hours after oral administration to rats of 1 mL/100 g body weight of 2-propen-1-ol, cytochrome p450 was increased by 33% in liver microsomes. Aminopyrine demethylase and dimethylaniline demethylase were stimulated. Activity of microsomal hydroxylation system gradually decreased.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 140 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Three hr after oral administration to rats of 1 mL/100 g body weight of allyl alcohol, cytochrome p450 was increased by 33% in liver microsomes. Aminopyrine demethylase and dimethylaniline demethylase were stimulated. Activity of microsomal hydroxylation system gradually decreased.[Gorshtein ES et al; Eksp Med (Riga) 3: 15-20 (1978)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: By inhalation, repeated exposure of rats to 40, 60 and 100 ppm caused gasping, severe depression and nasal discharge, and at highest levels some animals died by 10th exposure. ... /Rats, rabbits, guinea pigs and dogs were/ exposed to ...7 ppm 7 hr/day for 6 months. ...Liver showed cloudy swelling and focal necrosis, and kidney necrosis of convoluted tubules and proliferation of interstitial tissue; these changes were mild and reversible.[Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 379] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Gavage administration of allyl alcohol in ethanol:corn oil to a group of 20 male hamsters (beginning at 8 weeks of age) at 2 mg/week killed 7 of these animals within 48 weeks. There were no tumors of the forestomach or pancreas duct in any of these animals (an observation consistent with that made in 20 hamsters given only the vehicle), but adenoma/carcinoma of the adrenal cortex was seen in 4 of the 13 survivors (compared to 8 such tumors in the 20 controls). Incorporation of allyl alcohol at 300 ppm in the drinking water of groups of 20 male and 20 female F344 rats (until their natural death or sacrifice in extremis) at 80 to 126 weeks (males) or 59 to 126 weeks (females), (total lifetime dose/rat = 3.2 grams), failed to demonstrate an increase in the incidence of neoplastic changes compared to untreated, concurrent controls (no statistical comparisons were provided). Among the treated rats, there were six hepatocellular carcinomas/yperplastic nodules in the females and three in the males, compared to two each in the female and male controls. For the other sites studied (adrenal cortex, pituitary, blood), the incidence of tumors or leukemia in the treated rats was no different than that in the controls.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Male and female F344 rats (20/group) were given allyl alcohol in the drinking water at a concentration of 0 or 300 mg/L for 106 weeks. The incidence of tumors was similar to that in controls. Male and female hamsters (20/group) were dosed by oral gavage with 2 mg allyl alcohol/wk for 60 weeks. The incidence of tumors did not increase significantly compared to controls.[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 520] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Groups of Wistar rats (15/sex/treatment level) were exposed to 2-propen-1-ol in the drinking water at 0 (control), 50, 100, 200 or 800 ppm for 15 weeks. At the end of the appropriate treatment period, animals were killed by exsanguination following an overnight fast and subject to a post-mortem examination. This included gonadal weights and histopathological examination of testis, ovary and uterus. The calculated mean intake of 2-propen-1-ol over the course of the study (based on body weight and water intake data) was: Males: 0, 4.8, 8.3, 14.0, 48.2 mg/kg bw/d; Females: 0, 6.2, 6.9, 17.1 and 58.4 mg/kg bw/d. Absolute organ weights (including gonadal weights) were generally decreased in males, and to a lesser extent in females, in a time- and treatment related manner. Relative organ weights (including gonadal weights) were generally increased to a statistically significant extent in high dose animals of both sexes at study termination. These changes appeared secondary to a reduction in water intake (presumably due to unpalatability of the treatment solution) and body weight, that was particularly pronounced in high dose animals. No histopathological abnormalities were reported for testis, ovary or uterus. No treatment-related changes were present in gonadal weights or histopathology in male and female rats given allyl alcohol at received doses of up to 48.2, 58.4 mg/kg bw/d.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 203 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Litters sired by male rats treated with a dose of 0.86% allyl alcohol 7 days/wk to week 12 and 5 days/wk from week 13 to 33 did not develop any malformations. No adverse reproductive effects were observed.[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 519] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Male Sprague-Dawley (SD) rats (9-11 wk old) were given 0.85% saline (control group; n=6) or 2-propen-1-ol (25 mg/kg bw/d) by oral gavage (10 ml/kg bw; 7 d/wk for 12 wk, 5 d/wk to wk 15). Each male was caged with 2 virgin females (until a sperm-positive smear was obtained; up to 6 nights) on wk 1-11. After mating was complete the males were subject to a gross postmortem examination and hematological screen. Sperm parameters were also assessed (no further methodological details). Males treated with 2-propen-1-ol were sacrificed in wk 15, while controls were maintained until wk 33 (dosed 5 d/wk, in support of a parallel experiment). On GD20, females from mating weeks 1-11 were killed and the uteri examined for total number of corpora lutea, total implants, live/dead fetuses, late / early deaths (calculated as a percentage of the total implants from the pregnant females in each group). Each fetus was weighed and examined. Abnormal fetuses were photographed (Polaroid) prior to removal of a sample of liver (chromosomal preparation) and preservation for skeletal staining and evaluation. The abnormal fetal index was calculated as a percentage of the total number of term fetuses observed at post-mortem. When karyotype abnormalities were observed, the chromosome(s) involved were identified according to the standard karyotype of the Norway rat. Litter data were analyzed using Fisher's exact test. ... The authors note that paternal exposure to a mutagenic agent resulted in changes in chromosomal structure and/or number, which may be manifest as fetal abnormalities or changes in karyotype. ... Mean body weight was lower in male rats given 2-propen-1-ol (569+/-49 g) compared to controls (635+/-74 g); this may, in part, have reflected the 18 wk age difference at sacrifice. Relative liver weight was increased 26% (P<0.05), and relative spleen weight 22% (P<0.05), with non-significant increases in relative kidney and testis weights. Red cell count, mean cell volume, percentage cell volume and hemoglobin concentration were unaffected by treatment with 2-propen-1-ol. White cell counts were similar in treated and control animals, however a differential count revealed a significant increase in percentage of lymphocytes with a corresponding significant decrease in eosinophils and neutraphil counts. The authors comment that these changes in differential count were within the normal range for the SD rat. Total sperm count and epididymal sperm concentration were unaffected by treatment. There was a total of 1669 live implants from 125 pregnancies in the controls (13.4 implants/litter) versus 1371 live implants from 108 litters in the 2-propen-1-ol-treated group (12.7 implants/litter) (non significant). Mean preimplantation loss was comparable in control (12.8+/-5.4%) and treated (11.7+/-6.2%) groups. The rate of post-implantation loss (dominant lethality) varied between 2.2-13.2% in the controls, with a mean for the whole study (13 matings) of 6.2%. The comparable range for the male rats given 2-propen-1-ol was 1.7-8.7%, with an overall mean of 4.1%. The incidence of runted, abnormal and grossly abnormal fetuses was comparable in the control and treated groups. The abnormalities seen in the litters of the three groups of treated animals were diagnosed as: anasarca (massive edema), exencephaly, craniofacial and skeletal, abnormality. The combined incidence of gross abnormalities was not statistically significantly different between the control (n=0) and treated (n=3) groups. The authors note that the incidence of grossly abnormal fetuses (0.22%) was within the historic range for this strain of rat (not reported) and were therefore considered to be spontaneous in origin. Karyotypic abnormalities were present in 3 of 12 slides prepared from abnormal fetuses from the treated group whereas no abnormal karyotype was present in 5 slides from the controls ... The abnormalities from the 2-propen-1-ol
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Male and female Crj:CD(SD)IGS rats were given 2-propen-1-ol daily by gavage at doses of 0 (vehicle), 2, 8 or 40 mg/kg bw/day for 14 days before mating to 42 days (males) or from 14 days before mating to day 3 of lactation (females). No deaths were observed. Clinical signs in males and females include salivation, decrease in locomotor activity, irregular respiration, lacrimation, and loose stool /in the/ 40 mg/kg/day groups. Total litter loss / occurred/ from dam in this treatment group. No abnormality /was observed/ at the 2 and 8 mg/kg/day groups. All all treated groups, body weight and food consumption was similar with that of control groups. No toxicological significances at testis and epididymis was found in males at all treated groups. In females, /there was/ an extension of the mean estrous cycle and an increase of famales with irregular estrous cycles in the 40 mg/kg/day groups. No abnormality /was observed/ in delivery and lactation. The NOAEL for general toxicity and reproductive and developmental toxicity is considered to be 8 mg/kg/day.[Organization for Economic Cooperation and Development; Screening Information Data Set for Allyl Alchol, (107-18-6) p. 195 (May 2006). Available from, as of May 21, 2012: http://www.inchem.org/pages/sids.html] **PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: Timed-gestation pregnant Sprague-Dawley rats (225-250) were obtained from Charles River Canada Inc. The day on which spermatozoa were found in the vaginal smear was considered day zero of pregnancy. On day 13 the rats were laparotomized under anesthesia (ether) and the uteri exposed. Embryos in one uterine horn received an intraamniotic injection (10 uL; 30-gauge needle) of 2-propen-1-ol (10, 100 or 1000 ug/fetus in 0.9% NaCl in 5, 8 and 7 litters, respectively) while those in the other horn were untreated. Saline injected controls were also included in the study and treated in a similar manner (intraamniotically injected or sham treated). The uterus was repositioned and the laporotomy closed (nylon sutures). Rats were sacrificed on day 20 of gestation (ether overdose) and the number of dead or resorbed fetuses recorded. Live fetuses were examined for external malformations, blotted dry and weighed. ... Approx. 24% of the saline-injected control fetuses and 12% of the sham control fetuses were resorbed; 6% and 5%, respectively, were malformed. ... 2-Propen-1-ol treatment caused a dose dependent increase in the incidence of resorbed fetuses, with significance found at 100 ug and 1000 ug/fetus (treated uterine horn versus untreated contralateral horn). While no tabulated results are available, interpolation from graphical data included in the publication indicates that the mean number of dead or resorbed fetuses was 0.3, 0.5 (P<0.05) and 0.6 (P<0.05) in the 10 (5 litters), 100 (8 litters) and 1000 (7 litters) ug/fetus groups. The occurrence of dead or resorbed fetuses also increased in a treatment-related manner in the fetuses from the contra-lateral (untreated) uterine horn : <0.1, 0.2, 0.4 for the low, intermediate and high dose groups. Two fetuses from 7 high dose litters were malformed (limb defects; non-significant). Two contralateral controls (untreated) from 8 intermediate dose litters were also malformed (omphalocele, edema, micromelia of the limbs, clubfoot, short neck and micrognathia; the other had a minor forelimb defect). There was one maternal death at the high dose of 2-propen-1-ol the day after surgery and treatment of the embryos; this was the only evidence of maternal toxicity. A treatment related increase in dead and resorbed fetuses was reported following intraamniotic injection of 10, 100 or 1000 ug 2-propen-1-ol/fetus on GD13. ...[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • LABORATORY ANIMALS: Neurotoxicity: Allyl alcohol was investigated for its property as sensory irritant in Ssc:CF-1 mice. The concentration of the chemical necessary to depress the respiratory rate by 50% (RD50) due to sensory irritation of the upper respiratory tract was 3.9 ppm. No pulmonary irritation was found at the concn causing a 50% decrease in respiratory rate.[Nielsen GD et al; Acta Pharmacol Toxicol 54 (4): 292-8 (1984)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ... Inbred wild-type FVB/N mice were either treated with alpha-naphthyl-isothiocyanate (ANIT), allyl alcohol (AA), carbon tetrachloride (CCl(4)), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC), and silica, or subjected to common bile duct ligation (CBDL) to induce hepatic injury. Liver biopsies were performed every 4 wk to evaluate hepatic fibrosis over a period of 6 mo. Cumulative cirrhosis and survival curves were constructed by life table method and compared with Wilcoxon test. Under the dosages used, there was neither mortality nor cirrhosis in AA and silica-treated groups.[Chang ML et al; World J Gastroenterol 11 (27): 4167-72 (2005)] **PEER REVIEWED** PubMed Abstract Full text: PMC4615437
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: ... Of 40 male adult rats, 30 were injected with 0.62 mmol/kg of allyl alcohol ip twice a week, the remaining 10 with normal saline as controls. Ten rats were killed at each of 4, 8, and 16 weeks later. ... After 4 weeks, periportal fibrosis was produced in only 6 out of 10 rats, and was mild in extent. However, after 8 weeks, 8 out of 9 survivors showed moderate to severe fibrosis ... The extent of fibrosis correlated significantly with the amount of collagen and /transforming growth factor/ (TGF)beta1 mRNA expression in liver tissues. ...[Jung SA et al; Scand J Gastroenterol 35 (9): 969-75 (2000)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: .../Investigators/ evaluated the specificity of the 15-day intact adult male rat assay, using a negative control chemical, allyl alcohol, a known hepatotoxicant that was not expected to induce endocrine effects. Male rats were dosed for 15 days via oral gavage with 0, 10, 30, 40, or 50 mg/kg/day allyl alcohol. The endpoints evaluated included final body and organ weights, serum hormone concentrations, and a limited histopathology assessment. No mortality or adverse clinical signs were observed. Mean final body weight for rats in the 50-mg/kg/day dose group was decreased to 90% of control. Mean relative liver weights were increased at 40 and 50 mg/kg/day (115% and 117% of control, respectively). Serum testosterone and DHT concentrations were statistically significantly decreased at 50 mg/kg/day (72% of control). Serum prolactin concentrations were statistically significantly decreased at 40 mg/kg/day (58% of control), but not at 50 mg/kg/day. There were no effects on the other endpoints evaluated. Consistent with previous guidance for interpreting the 15-day intact adult male rat assay, histological and weight changes of target organs were given a higher weight-of-evidence than changes in serum hormone concentrations alone. Therefore, with only minimal changes in serum hormone concentrations and no effects on organ weights or microscopic alterations, the results of allyl alcohol in the 15-day intact adult male rat assay were considered negative and consistent with the predicted results.[O'Connor JC et al; Birth Defects Res B Dev Reprod Toxicol 83 (2): 117-22 (2008)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: /Rats were exposed to 20, 40, 60, 100, or 150 ppm /of allyl alcohol via/ inhalation for 7 hours/day for 2 to 12 weeks. The NOAEL /was determined to be/ 20 ppm; the LOAEL was 40 ppm.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: A 15-week drinking-water study conducted in male and female Wistar rats given 50, 100, 200, or 800 ppm allyl alcohol ad libitum found increased relative kidney weight (and reduced urinary output) in animals given 100 ppm or more, perhaps due to reduced fluid intake. Hepatotoxicity was evident only after ingestion of >100 ppm. ...A series of repeated inhalation trials /were conducted/ with allyl alcohol in dogs, rats, rabbits, and guinea pigs at 7 hours/day, 5 days/week for 5 weeks or for 6 months at 2 or 7 ppm. Based on the severe irritation of mucous membranes and the eyes noted in these animals exposed at 7 ppm, but no detectable injury at 2 ppm, these authors recommended that occupational TWA exposures not exceed 2 ppm for an 8-hour workshift and that short-term exposures in workplace air not exceed 5 ppm.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 (2010)] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Groups of 10 male and 10 female B6C3F1 mice were administered 0, 8, 16, 32, 62.5, or 125 mg/kg allyl acetate, 0, 3, 6, 12, 25, or 50 mg/kg allyl alcohol, or 0, 1.25, 2.5, 5, 10, or 20 mg/kg acrolein in 0.5% methylcellulose by gavage, 5 days per week for 14 weeks. ... In the allyl alcohol mouse study, one 50 mg/kg female died due to a gavage accident; all other animals survived to the end of the study. ... All other early deaths, except one male and one female administered 10 mg/kg, were unrelated to chemical administration. The concentration of 3-hydroxypropyl mercapturic acid (3-HPM) in the urine of mice was determined after the first dose of chemical and at the end of the 14-week study. At both time points, the concentrations of 3-HPM in the urine of animals that received allyl acetate or allyl alcohol increased linearly with dose. ... Since urine volumes were not recorded during the urine collection, complete quantitation of these data was not possible. The mean body weight gain of male mice in the 50 mg/kg group in the allyl alcohol study was also less than that of the vehicle controls. Final mean body weights and mean body weight gains of ... female mice in the allyl alcohol studies ... generally similar to those of the respective vehicle controls. ... Male and female mice administered 12 mg/kg allyl alcohol or greater had significantly increased incidences of squamous hyperplasia of the forestomach epithelium. Incidences of portal cytoplasmic vacuolization were significantly increased in 50 mg/kg male mice and female mice in the 25 and 50 mg/kg groups. ...[DHHS/NTP; NTP Technical Report on the Comparative Toxicity Studies of Allyl Acetate, Allyl Alcohol, and Acrolein (CAS Nos. 591-87-7,107-18-6, and 107-02-8) Administered by Gavage to F344/N Rats and B6C3F1 Mice. Technical Report Series No. 48 (2006) NIH Publication No. 06-4413 U.S. Department of Health and Human Services, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 http://ntp.niehs.nih.gov/ntp/htdocs/ST_rpts/tox048.pdf] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Groups of 10 male and 10 female F344/N rats were administered 0, 6, 12, 25, 50, or 100 mg allyl acetate/kg body weight, 0, 1.5, 3, 6, 12, or 25 mg/kg allyl alcohol, or 0, 0.75, 1.25, 2.5, 5, or 10 mg/kg acrolein in 0.5% methylcellulose by gavage, 5 days per week for 14 weeks. ... In the allyl alcohol study, all rats survived to the end of the study except one 6 mg/kg female. ... The concentration of 3-hydroxypropyl mercapturic acid (3-HPM) in the urine of rats ... was determined after the first dose of chemical and at the end of the 14-week study. At both time points, the concentrations of 3-HPM in the urine of animals that received allyl acetate or allyl alcohol increased linearly with dose. ... Since urine volumes were not recorded during the urine collection, complete quantitation of these data was not possible. Final mean body weights and mean body weight gains of dosed female rats in the allyl acetate studies, /and/ male and female rats in the allyl alcohol studies were generally similar to those of the respective vehicle controls. The liver weights of male rats administered 25 mg/kg allyl alcohol ... were significantly greater than those of the vehicle controls. ... Female rats administered 25 mg/kg allyl alcohol spent more time in diestrus and less time in metestrus than the vehicle controls. ... Male and female rats administered 6 mg/kg allyl alcohol or greater had significantly increased incidences of squamous hyperplasia of the forestomach epithelium. Female rats in the 25 mg/kg group had significantly increased incidences of bile duct hyperplasia and periportal hepatocyte hypertrophy in the liver.[DHHS/NTP; NTP Technical Report on the Comparative Toxicity Studies of Allyl Acetate, Allyl Alcohol, and Acrolein (CAS Nos. 591-87-7,107-18-6, and 107-02-8) Administered by Gavage to F344/N Rats and B6C3F1 Mice. Technical Report Series No. 48 (2006) NIH Publication No. 06-4413 U.S. Department of Health and Human Services, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 http://ntp.niehs.nih.gov/ntp/htdocs/ST_rpts/tox048.pdf] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Groups of 15 male and 15 female /Wistar/ rats were given 0 (control), 50, 100, 200 or 800 ppm allyl alcohol in the drinking water for 15 weeks. There were no effects attributable to allyl alcohol in the results of the hematological examinations or analyses of serum. There was a dose-related reduction in the fluid intake at all treatment levels in both sexes, while growth and food consumption were reduced in both sexes given 800 ppm and in males give 200 ppm. Males given 100 ppm or above and females given 200 or 800 ppm produced less urine than the controls in a period without water or following a water load. The only changes in organ weight that could be attributed to treatment were increased values for the relative weights of liver, spleen and kidney. All 3 organs were affected in both sexes given 800 ppm and the kidneys were also affected in both sexes given 200 ppm and in females given 100 ppm. No effects attributable to allyl alcohol treatment were seen at autopsy or in the histopathological examination. The /NOAEL/ established in this study was 50 ppm of the drinking water, a level equivalent to an intake in rats of between 4.8 and 6.2 mg allyl alcohol/kg/day.[Carpanini F MB et al; Toxicology 9 (1-2): 29-46 (1978)] **PEER REVIEWED** PubMed Abstract
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Rabbits /were administered/ allyl alcohol /orally via/ drinking water in doses of 0.005, 0.05, or 2.5 mg/kg/day for 8 months. /The highest dosage of/ 2.5 mg/kg produced liver hemorrhage and necrosis dystrophy of the epithelium of kidneys convoluted tubules, and diffuse reticular-endothelial hyperplasia in the gulp of the spleen suggesting the rabbit is more sensitive to repeated allyl alcohol exposures than the rat.[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Rats /were exposed/ to 0.15 to 70 mg/kg/day equivalent of allyl alcohol for 90 days. Decreased body weight gamin (42 and 70 mg/kg), well localized areas of hepatic necrosis with regeneration (70 mg/kg) and increased relative liver and/or kidney weights (29, 42, and 70 mg/kg).[European Chemicals Bureau; IUCLID Dataset, Allyl alcohol (107-18-6) (2000 CD-ROM edition). Available from, as of May 15, 2012: http://esis.jrc.ec.europa.eu/] **PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Validation of the 15-day intact adult male rat screening assay (IAMRSA), an endocrine activity screen, was extended beyond the 28 substances evaluated to date. Two independent laboratories evaluated specificity using allyl alcohol (AA), a putative negative control, and DE-71 (technical grade pentabromodiphenyl ether) for comparison with previous pubertal assays that demonstrated thyroid effects. Male rats (15/group) were gavaged daily with AA (0, 10, 30, or 40 mg/kg/day) or DE-71 (0, 3, 30, or 60 mg/kg/day) for 15 days. Body and organ weights and serum hormone concentrations were measured, and a limited histopathological assessment was conducted. AA results were considered negative at doses that did not exceed the maximum tolerated dose (MTD); effects reported were dose-related decreases in weight gain, increased liver weights and, although the pattern varied across studies, alterations in some androgen-sensitive endpoints in the high-dose where the maximum tolerated dose was exceeded. ...[Becker RA et al; Birth Defects Res B Dev Reprod Toxicol 95 (1): 63-78 (2012)] **PEER REVIEWED** PubMed Abstract

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LC50 Mouse inhalation 500 mg/cu m/ 2hr[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 109] **PEER REVIEWED**
  • LC50 Rat inhalation 1060 ppm/1 hr /from table/[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 518] **PEER REVIEWED**
  • LC50 Rat inhalation 165 ppm/4 hr[USEPA; Health and Environmental Effects Profile for Allyl alcohol p.36 (1985) ECAO-CIN-P121] **PEER REVIEWED**
  • LC50 Rat inhalation 76 ppm/8 hr /from table/[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 518] **PEER REVIEWED**
  • LD50 Mouse ip 60 mg/kg[Dunlap MK et al; AMA Arch Ind Health 18: 303-11 (1958) as cited in USEPA; Health and Environmental Effects Profile for Allyl alcohol p.36 (1985) ECAO-CIN-P121] **PEER REVIEWED**
  • LD50 Mouse iv 78 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 109] **PEER REVIEWED**
  • LD50 Mouse oral 85 mg/kg[Worthing, C. R. (ed.). Pesticide Manual. 6th ed. Worcestershire, England: British Crop Protection Council, l979., p. 9] **PEER REVIEWED**
  • LD50 Mouse oral 96 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 109] **PEER REVIEWED**
  • LD50 Rabbit dermal 45 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 109] **PEER REVIEWED**
  • LD50 Rabbit percutaneous 89 mg/kg[Farm Chemicals Handbook 1989. Willoughby, OH: Meister Publishing Co., 1989., p. C-16] **PEER REVIEWED**
  • LD50 Rat intraperitoneal 37 mg/kg[Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 109] **PEER REVIEWED**
  • LD50 Rat oral 64 mg/kg[O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 52] **PEER REVIEWED**

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Absorption, Distribution And Excretion

  • ... A single oral intubation of 120 mg/kg allyl alcohol in male Long-Evans rats produced circulating concentrations of 9 to 15 ug/mI at 15 to 120 minutes after exposure. Peak blood concentrations were achieved at 30 to 60 minutes. Following intravenous injection of 30 mg/kg body weight in rats, the parent alcohol was cleared rapidly from the circulation such that within 60 minutes it could no longer be detected in blood. Kodama and Hine concluded that the rate of allyl alcohol metabolism in rats was far slower than that of ethanol.[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • ... Urinary 3-hydroxypropyl mercapturic acid accounts for about 28% of an oral (64 mg/kg) dose of allyl alcohol. ...[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • ...Absorbed through intact skin in toxic and even lethal concentrations.[Arena, J.M. and Drew, R.H. (eds.) Poisoning-Toxicology, Symptoms, Treatments. 5th ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 275] **PEER REVIEWED**
  • Allyl alcohol is apparently oxidized readily since within few min after iv injection of rats with the dosage of 30 mg/kg, vena cava blood contained average concentration of about 24 ug/mL; within 15 min concentration was about 4 ug/mL and within 1 hr the alcohol had almost disappeared from the blood. During constant iv infusion the allyl alcohol disappeared at rate of about 23 mg/hr. During the period of 15-120 min after admin of single oral dose of allyl alcohol (120 mg/kg) to rats, mean concentration of this alcohol in the portal vein was between 9 and 15 ug/mL.[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4668] **PEER REVIEWED**

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Metabolism/Metabolites

  • ... Urinary 3-hydroxypropyl mercapturic acid accounts for about 28% of an oral (64 mg/kg) dose of allyl alcohol. ...[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • Allyl alcohol is metabolized by alcohol dehydrogenase to acrolein; it is also converted to malondialdehyde. ... The characteristic periportal liver necrosis produced by exposure to allyl alcohol is preceded by rapid depletion of intracellular glutathione. This glutathione depletion is a prerequisite for the production of allyl alcohol-induced toxicity as evidenced by the administration of N-acetylcysteine and other sulfur-containing metabolic precursors of glutathione which prevent allyl alcohol and acrolein-induced hepatotoxicity in cultured cells and in intact animals. ...[American Conference of Governmental Industrial Hygienists. Documentation of the TLV's and BEI's with Other World Wide Occupational Exposure Values. CD-ROM Cincinnati, OH 45240-4148 2010.] **PEER REVIEWED**
  • In rats, allyl alcohol is metabolized to acrolein by alcohol dehydrogenase. ...Acrolein can react with glutathione to form the corresponding thiol ether, which can be further metabolized to mercapturic acids and excreted in the urine. In the presence of NADPH and liver and lung microsomes, allyl alcohol and acrolein were oxidized to the corresponding epoxides, glycidol, and glycidaldehyde, respectively.[Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 519] **PEER REVIEWED**
  • Rates of allyl alcohol metabolism in periportal and pericentral regions of the liver lobule were measured to determine whether the zonal toxicity due to allyl alcohol results from its selective metabolism in periportal regions. Infusion of allyl alcohol into perfused livers from fed, phenobarbital-treated rats caused an increase in nicotinamide adenine dinucleotide, reduced form (NADH) fluorescence (366 leads to 450 nm) measured with a large-tipped (2 mm) light guide placed on the surface of the liver. A linear increase in NADH fluorescence was observed when 25-150 uM allyl alcohol was infused; however, when allyl alcohol exceeded 200 uM, oxygen uptake by the liver was inhibited 30-40%, and a large increase in NADH fluorescence occurred. /4-Methylpyrazole (80 umol), an inhibitor of alcohol dehydrogenase, prevented the fluorescence increased due to allyl alcohol in both regions, indicating that the changes were due entirely to NADH generated from alcohol dehydrogenase-dependent allyl alcohol metabolism./ Using the correlation (r= 0.91) between rates of allyl alcohol uptake and the increase in NADH fluorescence established for the whole organ, local rates of allyl alcohol metabolism were 23 and 31 umoles/g/hr in periportal and pericentral regions, respectively. Since allyl alcohol is metabolized in both regions of the liver lobule, the hypothesis that the zone specific hepatotoxicity results from its exclusive metabolism to acrolein in periportal regions seems unlikely.[Belinsky SA et al; Mol Pharmacol 25 (1): 158-64 (1984)] **PEER REVIEWED** PubMed Abstract
  • Rats treated with single ip doses (0.05 mL/kg) of allyl alcohol showed significantly greater hepatic necrosis and elevation of plasma glutamic-pyruvic transaminase (GPT) levels 24 hr later than rats given the same dose of deuterium-labeled allyl alcohol (d2-allyl alcohol). The covalent binding of radiolabel to hepatic proteins of rats treated with (14)C-allyl alcohol was three-fold greater than that in rats given the same dose of d2-(14)C-allyl alcohol. The formation of acrolein and acrylic acid by hepatic 9000X g and cytosol fractions from d2-allyl alcohol was significantly less than that from allyl alcohol. ...[Patel JM et al; Drug Metab Dispos 11 (2): 164-6 (1983)] **PEER REVIEWED** PubMed Abstract
  • The biotransformation of allyl alcohol was studied in rat liver and lung preparation. Acrylic acid was formed from allyl alcohol. Lung and liver microsomal epoxidation products were also identified.[Patel JM et al; Drug Metab Dispos 8 (5): 305-8 (1980)] **PEER REVIEWED** PubMed Abstract

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Footnotes

1 Source: the NTP's CEBS database.

2 Source: the National Library of Medicine's Hazardous Substance Database, 02/28/2017.

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