Journal of Toxicology: Clinical Toxicology
ISSN: 0731-3810 (Print) (Online) Journal homepage: http://www.tandfonline.com/loi/ictx19
Clinical Evaluation of Pediatric Ethylene Glycol Monobutyl Ether Poisonings Bonnie S. Dean & Edward P. Krenzelok To cite this article: Bonnie S. Dean & Edward P. Krenzelok (1992) Clinical Evaluation of Pediatric Ethylene Glycol Monobutyl Ether Poisonings, Journal of Toxicology: Clinical Toxicology, 30:4, 557-563, DOI: 10.3109/15563659209017941 To link to this article: http://dx.doi.org/10.3109/15563659209017941
Published online: 25 Sep 2008.
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Citing articles: 4 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ictx19 Download by: [RMIT University Library]
Date: 17 April 2016, At: 22:49
CLINICAL TOXICOLOGY, 30(4), 557-563 (1992)
CLINICAL EVALUATION OF PEDIATRIC ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
Downloaded by [RMIT University Library] at 22:49 17 April 2016
Bonnie S. Dean, R.N., B.S.N. ; Edward P. Krenzelok, Pharm.D. Pittsburgh Poison Center; Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania
ABSTRACT Ethylene glycol butyl ether, CAS 111-76-2, an ingredient in many popular commercial window/glass cleaners, is known to produce equal if not greater toxicity than ethylene glycol when administered to animals. Treatment recommendations for human poisonings are based upon animal data and include the use of ethanol therapy to inhibit the production of toxic metabolites. No human experiential data exist to accurately assess human toxicity or to verify treatment modalities. A 5 month retrospective review of all glass cleaner ingestions reported to a regional poison information center disclosed 24 pediatric patients, ages 7 mo to 9 y, who ingested 5-300 mL of a liquid glass cleaning product containing ethylene glycol butyl ether. All ingestions were reported within 5 min of ingestion, and all 24 children were asymptomatic at that time and subsequently. The product concentrations of ethylene glycol butyl ether ranged from 0.5% to 9.9%. Two of the 24 children ingested > 15 mL and were treated by gastric emptying and 24 h hospital observation. Neither hospitalized child suffered symptoms consistent
Address reprint requests to: Bonnie S. Dean, R.N., B.S.N., Pittsburgh Poison Center, Children’s Hospital of Pittsburgh, One Children’s Place, 3705 Fifth Avenue @ DeSoto Street, Pittsburgh, PA 15213.
557 Copyright
Q
1992 by Marcel Dekker, Inc.
558
DEAN AND KRENZELOK
with hemolysis, nervous system depression, acidosis, or renal compromise. Dilution with oral fluids at home is considered appropriate treatment of pediatric ingestions of < 10 mL of a commercial liquid glass/window cleaners containing < 10% ethylene glycol butyl ether. (Key Words: ethylene glycol mmbutyl ether; CAS 111-76-2;poisoning, human.)
Downloaded by [RMIT University Library] at 22:49 17 April 2016
INTRODUCTION Ethylene glycol monobutyl ether (EGBE, 2-butoxyethanol, butyl cellosolve, CAS 111-76-2) combines the solubility characteristics of both ethers and alcohols and is extensively used in various industrial and commercial applications (1). Many contemporary household glass/window cleaners contain EGBE in concentrations ranging from 0.5% to 10.0%(Table 1). While human toxicity data is limited to two case reports (2,3), the available animal data suggests that administered EGBE is five to six times more toxic than ethylene glycol (4). Whether these figures can or should be extrapolated to humans and especially children who accidently ingest liquid glass cleaners is unclear. A potentially toxic dose of 18.5 mL of 10%EGBE is proposed (5) despite limited human toxicity data and the uncorroborated concern that EGBE is metabolized to ethylene glycol in humans. The purpose of this study was to determine if gastric emptying and aggressive intervention are necessary in children who have suffered casual exposures to EGBE-containing products.
METHODS All accidental pediatric ingestions of EGBE-containing products reported to the Pittsburgh Poison Center (PPC) were documented on the data collection form of the American Association of Poison Control Centers for December 1990 through April 1991. Cases reported by either the lay public or health care professionals were included. Poisonings involving the ingestion of multiple products and/or pharmaceuticals were excluded from the review. A minimum of one follow-up call by the PPC professional staff was completed with each incident to accurately determine medical outcome. The following data points were critically reviewed: age of the patient; amount
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
559
TABLE 1
Downloaded by [RMIT University Library] at 22:49 17 April 2016
Common Commercial EGBE-Containing Glass Cleaners PfOdUCt Window Kleen Sears Window Cleaner Tektor Window Cleaner Windex with Ammonia-D Windex with Vinegar-D Lemon Fresh Windex with Ammonia-D Windex Professional Strength Multi-Surface SOS Glass Works Sparkle Glass Glass Plus Glance Glass Cleaner
96 EGBE < 3% 15% 16% 5% 9%
Manufacturer State Chemical Brulin and Company Ridgeway Chemical Drackett Products Drackett Products
15 mL. A 14 mo old child, reportedly ingesting 30 mL of a glass cleaner containing < 10% EGBE ( 3 mL EGBE), was treated by gastric emptying with syrup of ipecac and a 24 h hospitalization. A second child, age 2 y o swallowed a reported 300 mL of an 8% EGBE-containing glass cleaner (-24 mL EGBE) and,
-
560
DEAN AND KRENZELOK
following gastric lavage, was hospitalized for 24 h. Hemolysis, central nervous system depression, metabolic acidosis, and renal compromise, consistent findings of EGBE toxicity in animals, did not occur in either. The remaining 22 pediatric patients were treated at home with simple dilution and remained asymptomatic through 48 h of telephone follow-up.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
DISCUSSION EGBE is a glycol ether frequently encountered as an ingredient in a variety of common household products including glass/window cleaners. EGBE is oxidized via the alcohol dehydrogenase to butoxyaldehyde (BAL), an intermediate that is further oxidized to butoxyacetic acid (BAA) in a reaction presumably catalyzed by the aldehyde dehydrogenases (1,a). Ghanayem et al. identified the presence of two additional urinary metabolites of EGBE, namely butoxyethanol-glucuronide (BEG), and butoxyethanolsulfate (BES) (Figure 1) (7). The hematopoietic system is the major target of EGBE acute toxicity in some but not all animal species (8). Early animal experiments demonstrated that BAA increased erythrocyte fragility and produced hemolytic anemia, hemoglobinuria and kidney enlargement with nonspecific histologic alterations (6-8). These in vivo hemolytic effects were later discovered to be age dependent, with older rats being significantly more sensitive than younger rats (9,lO). On in vitro study, human erythrocytes are resistant to the hemolytic effects of BAA, even at concentrations several times that causing hemolysis of erythrocytes from rats, mice, rabbits, and baboons (11,12). Human data indicating significant conversion to ethylene glycol and oxalate is limited to the case report by Rambourg-Schepens e? aZ. of oxaluria following the ingestion of 250-500 mL of a 12% EGBEcontaining glass cleaner (2). This finding was absent in a strikingly similar human poisoning reported by Gijsenberg et aZ. (3). Rambourg-Schepens et aZ. suggest that large ingestions of EGBE might actually saturate traditional metabolism, and propose the possibility of a secondary metabolic pathway, converting EGBE to ethylene glycol and then further metabolic conversion to oxalates (2). Medinsky et aZ. studied in vivo differences of 2-methoxyethanol (ME), 2-ethoxyethanol (EE), and 2-butoxyethanol (EGBE)
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
561
I
Metabolic Pathways of Monobutyl Ether
1 Glucuronyl Transferase (BEG) 1
1 Sulfo Transferase (BES) I
f
Downloaded by [RMIT University Library] at 22:49 17 April 2016
IEthylene Glycol Monobutyl Ether (EGBE) 1
1
Alcohol Dehydrogenase
1
Butoxyacetaldehyde (BAL) =,HIP* I
1
Aldehyde Dehydrogenase
1 Butoxyacetic Acid (BAA) I
Figure 1.
and found that with increased alkyl chain length, the contribution to ethylene glycol by the dealkylase reaction decreases, whereas the contribution of the dehydrogenase reaction to the production of acetic acid metabolism increases (13). They concluded that while a small percentage of ethylene glycol appeared in the urine of the rats ingesting drinking water with EGBE, BAA was the predominant metabolite excreted (13). The relative resistance of the ether linkage also makes it unlikely that significant amounts of EGBE are metabolically converted to ethylene glycol in humans (14). Gas chromatography using pentafluorobenzy1 chloride with electron dense capture has been employed to detect the presence of BAA in the urine. This assay requires several urine samples from an individual for accurate verification (15). In animal studies, ethanol treatment favors retention of unmetabolized EGBE, attributed to the inhibition of alcohol dehydrogenases (15,16). The role of ethanol therapy in human toxicity requires re-evaluation. This small series of 24 healthy children does not provide conclusive evidence regarding the toxicity of large ingestions of EGBE-containing
562
DEAN AND KRENZELOK
products. Individuals with congenital hemolytic anemias merit consideration. It is evident, however, that pediatric ingestions of less than 10 mL of a commercially available glass/window cleaner containing C 10% EGBE, do not require gastric emptying or other aggressive interventions.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
ACKNOWLEDGEMENTS This work was presented at the American Academy of Clinical Toxicology, The American Association of Poison Control Centers, The American Board of Medical Toxicology and the Canadian Association of Poison Control Center’s Annual Scientific Meeting October 1-4, 1991, in Toronto, Ontario, Canada.
REFERENCES 1.
2.
3. 4. 5.
6. 7.
8.
Ghanayem BI, Burka LT, Sanders JM, Matthews HB. Metabolism and disposition of ethylene glycol monobutyl ether (2-butoxyethanol) in rats. Drug Metab Dispos 1987;15:478-484. Rambourg-Schepens MO, Buffet M, Bertault R, et a1. Severe ethylene glycol butyl ether poisoning. Kinetics and metabolic pattern. Human Toxicol 1988;7: 187-189. Gijsenbergh FP, Jenco M, Veulemans H, et a1. Acute butylglycol intoxication: A case report. Hum Toxicol 1989;8:243-245. Clayton GD, Clayton FE. Patty’s Indwtrial Hygiene and Toxicology, 3rd ed., New York: John Wiley and Sons, 1981. Smolinske SC. Ethylene glycol butyl ether (Management Treatment Protocol). In: POISINDEX InJonnation System. Rumack BH, Spoerke DG, eds. Denver, CO Micromedex, Inc., (edition expires November 30, 1991). Carpenter CP, Pozzani UC, Wwil CS, et al. The toxicity of butyl cellosolve solvent. Arch Ind Health 1956;14:114-131. Ghanayem BI, Burka LT, Matthews HB. Metabolic basis of ethylene glycol monobutyl ether (2-butoxyethanol) toxicity: Role of alcohol and aldehyde dehydrogenases. J Phamcol Escp Ther 1987; 242:222-231. Ghanayem BI, Burka LT, Thompson MB, et al. Hematotoxicity of 2-butoxyethanol (BE). Effects of age, metabolism, and tolerance development. Phamcologist 1986;28:205.
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS 9.
563
Ghanayem BI, Blair PC, Thompson MB, Maronpot RR, Matthews
HB. Effect of age on the toxicity and metabolism of ethylene glycol 10.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
11. 12.
13. 14. 15. 16.
monobutyl ether (2-butoxyethanol) in rats. Toxicol Appl Pharmucol 1987;91:222-234. Ghanayem BI, Sanders JM, Clark AM, et al. Effects of dose, age, inhibition of metabolism and elimination on the toxicokinetics of 2-butoxyethanol and its metabolites. J Phurmacol B p Ther 199O;253:136-143. Ghanayem BI. Metabolic and cellular basis of 2-butoxyethanolinduced hemolytic anemia in rats and assessment of human risk in vitro. Biochem Phurmucol 1989;38: 1679-1684. Ward S,Wall C, Ghanayem BI. Effects of 2-butoxyethanol (BE) and its toxic metabolite, 2-butoxyacetic acid (BAA) on blood from various mammals in vivo and in vitro. Toxicologist 1992;12:282. Medinsky MA, Singh G, Bechtold WE, et al. Disposition of three glycol ethers administered in drinking water to male F344/N rats. Toxicol Appl Phamcol 1990;102:443-455. ECETOC. The toxicology of glycol ethers and its relevance to man: An updating of ECETOC technical report no. 4. report no. 17. April 1985. Johanson G,Wallen M, Byfalt Nordqvist M. Elimination kinetics of 2-butoxyethanol in the perfused rat liver-dose dependence and effect of ethanol. Toxicol Appl Pharmucol 1986;83:315-320. Romer KG, Balge F, Freundt KJ. Ethanol-induced accumulation of ethylene glycol monoalkyl ethers in rats. Drug Chem Toxicol 1985;8:255-264.
ISSN: 0731-3810 (Print) (Online) Journal homepage: http://www.tandfonline.com/loi/ictx19
Clinical Evaluation of Pediatric Ethylene Glycol Monobutyl Ether Poisonings Bonnie S. Dean & Edward P. Krenzelok To cite this article: Bonnie S. Dean & Edward P. Krenzelok (1992) Clinical Evaluation of Pediatric Ethylene Glycol Monobutyl Ether Poisonings, Journal of Toxicology: Clinical Toxicology, 30:4, 557-563, DOI: 10.3109/15563659209017941 To link to this article: http://dx.doi.org/10.3109/15563659209017941
Published online: 25 Sep 2008.
Submit your article to this journal
Article views: 19
View related articles
Citing articles: 4 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ictx19 Download by: [RMIT University Library]
Date: 17 April 2016, At: 22:49
CLINICAL TOXICOLOGY, 30(4), 557-563 (1992)
CLINICAL EVALUATION OF PEDIATRIC ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
Downloaded by [RMIT University Library] at 22:49 17 April 2016
Bonnie S. Dean, R.N., B.S.N. ; Edward P. Krenzelok, Pharm.D. Pittsburgh Poison Center; Children’s Hospital of Pittsburgh, Pittsburgh, Pennsylvania
ABSTRACT Ethylene glycol butyl ether, CAS 111-76-2, an ingredient in many popular commercial window/glass cleaners, is known to produce equal if not greater toxicity than ethylene glycol when administered to animals. Treatment recommendations for human poisonings are based upon animal data and include the use of ethanol therapy to inhibit the production of toxic metabolites. No human experiential data exist to accurately assess human toxicity or to verify treatment modalities. A 5 month retrospective review of all glass cleaner ingestions reported to a regional poison information center disclosed 24 pediatric patients, ages 7 mo to 9 y, who ingested 5-300 mL of a liquid glass cleaning product containing ethylene glycol butyl ether. All ingestions were reported within 5 min of ingestion, and all 24 children were asymptomatic at that time and subsequently. The product concentrations of ethylene glycol butyl ether ranged from 0.5% to 9.9%. Two of the 24 children ingested > 15 mL and were treated by gastric emptying and 24 h hospital observation. Neither hospitalized child suffered symptoms consistent
Address reprint requests to: Bonnie S. Dean, R.N., B.S.N., Pittsburgh Poison Center, Children’s Hospital of Pittsburgh, One Children’s Place, 3705 Fifth Avenue @ DeSoto Street, Pittsburgh, PA 15213.
557 Copyright
Q
1992 by Marcel Dekker, Inc.
558
DEAN AND KRENZELOK
with hemolysis, nervous system depression, acidosis, or renal compromise. Dilution with oral fluids at home is considered appropriate treatment of pediatric ingestions of < 10 mL of a commercial liquid glass/window cleaners containing < 10% ethylene glycol butyl ether. (Key Words: ethylene glycol mmbutyl ether; CAS 111-76-2;poisoning, human.)
Downloaded by [RMIT University Library] at 22:49 17 April 2016
INTRODUCTION Ethylene glycol monobutyl ether (EGBE, 2-butoxyethanol, butyl cellosolve, CAS 111-76-2) combines the solubility characteristics of both ethers and alcohols and is extensively used in various industrial and commercial applications (1). Many contemporary household glass/window cleaners contain EGBE in concentrations ranging from 0.5% to 10.0%(Table 1). While human toxicity data is limited to two case reports (2,3), the available animal data suggests that administered EGBE is five to six times more toxic than ethylene glycol (4). Whether these figures can or should be extrapolated to humans and especially children who accidently ingest liquid glass cleaners is unclear. A potentially toxic dose of 18.5 mL of 10%EGBE is proposed (5) despite limited human toxicity data and the uncorroborated concern that EGBE is metabolized to ethylene glycol in humans. The purpose of this study was to determine if gastric emptying and aggressive intervention are necessary in children who have suffered casual exposures to EGBE-containing products.
METHODS All accidental pediatric ingestions of EGBE-containing products reported to the Pittsburgh Poison Center (PPC) were documented on the data collection form of the American Association of Poison Control Centers for December 1990 through April 1991. Cases reported by either the lay public or health care professionals were included. Poisonings involving the ingestion of multiple products and/or pharmaceuticals were excluded from the review. A minimum of one follow-up call by the PPC professional staff was completed with each incident to accurately determine medical outcome. The following data points were critically reviewed: age of the patient; amount
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
559
TABLE 1
Downloaded by [RMIT University Library] at 22:49 17 April 2016
Common Commercial EGBE-Containing Glass Cleaners PfOdUCt Window Kleen Sears Window Cleaner Tektor Window Cleaner Windex with Ammonia-D Windex with Vinegar-D Lemon Fresh Windex with Ammonia-D Windex Professional Strength Multi-Surface SOS Glass Works Sparkle Glass Glass Plus Glance Glass Cleaner
96 EGBE < 3% 15% 16% 5% 9%
Manufacturer State Chemical Brulin and Company Ridgeway Chemical Drackett Products Drackett Products
15 mL. A 14 mo old child, reportedly ingesting 30 mL of a glass cleaner containing < 10% EGBE ( 3 mL EGBE), was treated by gastric emptying with syrup of ipecac and a 24 h hospitalization. A second child, age 2 y o swallowed a reported 300 mL of an 8% EGBE-containing glass cleaner (-24 mL EGBE) and,
-
560
DEAN AND KRENZELOK
following gastric lavage, was hospitalized for 24 h. Hemolysis, central nervous system depression, metabolic acidosis, and renal compromise, consistent findings of EGBE toxicity in animals, did not occur in either. The remaining 22 pediatric patients were treated at home with simple dilution and remained asymptomatic through 48 h of telephone follow-up.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
DISCUSSION EGBE is a glycol ether frequently encountered as an ingredient in a variety of common household products including glass/window cleaners. EGBE is oxidized via the alcohol dehydrogenase to butoxyaldehyde (BAL), an intermediate that is further oxidized to butoxyacetic acid (BAA) in a reaction presumably catalyzed by the aldehyde dehydrogenases (1,a). Ghanayem et al. identified the presence of two additional urinary metabolites of EGBE, namely butoxyethanol-glucuronide (BEG), and butoxyethanolsulfate (BES) (Figure 1) (7). The hematopoietic system is the major target of EGBE acute toxicity in some but not all animal species (8). Early animal experiments demonstrated that BAA increased erythrocyte fragility and produced hemolytic anemia, hemoglobinuria and kidney enlargement with nonspecific histologic alterations (6-8). These in vivo hemolytic effects were later discovered to be age dependent, with older rats being significantly more sensitive than younger rats (9,lO). On in vitro study, human erythrocytes are resistant to the hemolytic effects of BAA, even at concentrations several times that causing hemolysis of erythrocytes from rats, mice, rabbits, and baboons (11,12). Human data indicating significant conversion to ethylene glycol and oxalate is limited to the case report by Rambourg-Schepens e? aZ. of oxaluria following the ingestion of 250-500 mL of a 12% EGBEcontaining glass cleaner (2). This finding was absent in a strikingly similar human poisoning reported by Gijsenberg et aZ. (3). Rambourg-Schepens et aZ. suggest that large ingestions of EGBE might actually saturate traditional metabolism, and propose the possibility of a secondary metabolic pathway, converting EGBE to ethylene glycol and then further metabolic conversion to oxalates (2). Medinsky et aZ. studied in vivo differences of 2-methoxyethanol (ME), 2-ethoxyethanol (EE), and 2-butoxyethanol (EGBE)
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS
561
I
Metabolic Pathways of Monobutyl Ether
1 Glucuronyl Transferase (BEG) 1
1 Sulfo Transferase (BES) I
f
Downloaded by [RMIT University Library] at 22:49 17 April 2016
IEthylene Glycol Monobutyl Ether (EGBE) 1
1
Alcohol Dehydrogenase
1
Butoxyacetaldehyde (BAL) =,HIP* I
1
Aldehyde Dehydrogenase
1 Butoxyacetic Acid (BAA) I
Figure 1.
and found that with increased alkyl chain length, the contribution to ethylene glycol by the dealkylase reaction decreases, whereas the contribution of the dehydrogenase reaction to the production of acetic acid metabolism increases (13). They concluded that while a small percentage of ethylene glycol appeared in the urine of the rats ingesting drinking water with EGBE, BAA was the predominant metabolite excreted (13). The relative resistance of the ether linkage also makes it unlikely that significant amounts of EGBE are metabolically converted to ethylene glycol in humans (14). Gas chromatography using pentafluorobenzy1 chloride with electron dense capture has been employed to detect the presence of BAA in the urine. This assay requires several urine samples from an individual for accurate verification (15). In animal studies, ethanol treatment favors retention of unmetabolized EGBE, attributed to the inhibition of alcohol dehydrogenases (15,16). The role of ethanol therapy in human toxicity requires re-evaluation. This small series of 24 healthy children does not provide conclusive evidence regarding the toxicity of large ingestions of EGBE-containing
562
DEAN AND KRENZELOK
products. Individuals with congenital hemolytic anemias merit consideration. It is evident, however, that pediatric ingestions of less than 10 mL of a commercially available glass/window cleaner containing C 10% EGBE, do not require gastric emptying or other aggressive interventions.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
ACKNOWLEDGEMENTS This work was presented at the American Academy of Clinical Toxicology, The American Association of Poison Control Centers, The American Board of Medical Toxicology and the Canadian Association of Poison Control Center’s Annual Scientific Meeting October 1-4, 1991, in Toronto, Ontario, Canada.
REFERENCES 1.
2.
3. 4. 5.
6. 7.
8.
Ghanayem BI, Burka LT, Sanders JM, Matthews HB. Metabolism and disposition of ethylene glycol monobutyl ether (2-butoxyethanol) in rats. Drug Metab Dispos 1987;15:478-484. Rambourg-Schepens MO, Buffet M, Bertault R, et a1. Severe ethylene glycol butyl ether poisoning. Kinetics and metabolic pattern. Human Toxicol 1988;7: 187-189. Gijsenbergh FP, Jenco M, Veulemans H, et a1. Acute butylglycol intoxication: A case report. Hum Toxicol 1989;8:243-245. Clayton GD, Clayton FE. Patty’s Indwtrial Hygiene and Toxicology, 3rd ed., New York: John Wiley and Sons, 1981. Smolinske SC. Ethylene glycol butyl ether (Management Treatment Protocol). In: POISINDEX InJonnation System. Rumack BH, Spoerke DG, eds. Denver, CO Micromedex, Inc., (edition expires November 30, 1991). Carpenter CP, Pozzani UC, Wwil CS, et al. The toxicity of butyl cellosolve solvent. Arch Ind Health 1956;14:114-131. Ghanayem BI, Burka LT, Matthews HB. Metabolic basis of ethylene glycol monobutyl ether (2-butoxyethanol) toxicity: Role of alcohol and aldehyde dehydrogenases. J Phamcol Escp Ther 1987; 242:222-231. Ghanayem BI, Burka LT, Thompson MB, et al. Hematotoxicity of 2-butoxyethanol (BE). Effects of age, metabolism, and tolerance development. Phamcologist 1986;28:205.
ETHYLENE GLYCOL MONOBUTYL ETHER POISONINGS 9.
563
Ghanayem BI, Blair PC, Thompson MB, Maronpot RR, Matthews
HB. Effect of age on the toxicity and metabolism of ethylene glycol 10.
Downloaded by [RMIT University Library] at 22:49 17 April 2016
11. 12.
13. 14. 15. 16.
monobutyl ether (2-butoxyethanol) in rats. Toxicol Appl Pharmucol 1987;91:222-234. Ghanayem BI, Sanders JM, Clark AM, et al. Effects of dose, age, inhibition of metabolism and elimination on the toxicokinetics of 2-butoxyethanol and its metabolites. J Phurmacol B p Ther 199O;253:136-143. Ghanayem BI. Metabolic and cellular basis of 2-butoxyethanolinduced hemolytic anemia in rats and assessment of human risk in vitro. Biochem Phurmucol 1989;38: 1679-1684. Ward S,Wall C, Ghanayem BI. Effects of 2-butoxyethanol (BE) and its toxic metabolite, 2-butoxyacetic acid (BAA) on blood from various mammals in vivo and in vitro. Toxicologist 1992;12:282. Medinsky MA, Singh G, Bechtold WE, et al. Disposition of three glycol ethers administered in drinking water to male F344/N rats. Toxicol Appl Phamcol 1990;102:443-455. ECETOC. The toxicology of glycol ethers and its relevance to man: An updating of ECETOC technical report no. 4. report no. 17. April 1985. Johanson G,Wallen M, Byfalt Nordqvist M. Elimination kinetics of 2-butoxyethanol in the perfused rat liver-dose dependence and effect of ethanol. Toxicol Appl Pharmucol 1986;83:315-320. Romer KG, Balge F, Freundt KJ. Ethanol-induced accumulation of ethylene glycol monoalkyl ethers in rats. Drug Chem Toxicol 1985;8:255-264.
