The following information was generated from the Hazardous Substances Data Bank 

(HSDB), a database of the National Library of Medicine's TOXNET system 

(http://toxnet.nlm.nih.gov) on October 30, 2009. 

Query: The chemical name was identified. 

The following terms were added from ChemIDplus: 

methyldiglyme 

dimethyl carbitol 

dimethoxydiglycol 

CAS Registry Number: 111-96-6 

NAME: DIETHYLENE GLYCOL DIMETHYL ETHER 

HSN: 72 

RN: 111-96-6 

HUMAN HEALTH EFFECTS: 

HUMAN TOXICITY EXCERPTS: 

 /GENOTOXICITY/ 2-Methoxyethanol and bis(2-methoxyethyl)ether were 

 subjected to the ... unscheduled DNA synthesis (UDS) assay in human 

 embryo fibroblasts ... UDS in fibroblasts were not increased by either 

 compound. [McGregor DB et al; Toxicol. Appl. Pharmacol. 70 (2): 303-16 

 (1983)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=6623472" 

 target=new>PubMed Abstract 

 /OTHER TOXICITY INFORMATION/ The ethers of diethylene glycol are lower in 

 toxicity than the ethers of ethylene glycol, but they have many similar 

 characteristics. /Diethylene glycol ethers/ [International Labour Office. 

 Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, 

 Switzerland: International Labour Office, 1983., p. 975] **PEER REVIEWED** 

 

 /EPIDEMIOLOGY STUDIES/ Ethylene glycol ethers (EGEs) including diglyme are 

 used in the manufacture of semiconductors. Epidemiological studies of 

 semiconductor populations evaluated potential adverse reproductive 

 outcomes. ... In each of these studies, workers were exposed to mixtures 

 including diglyme but not to diglyme alone. ... Exposure to EGEs was 

 determined using questionnaires from subjects about the work performed and 

 an assessment of the work environment by industrial hygienists, but no 

 measurements of personal or area exposures were made. Workers in the 

 fabrication area were considered exposed to EGEs. For the retrospective 

 study, information on pregnancy outcomes and potential confounders (age, 

 smoking, ethnicity, education, income, year of pregnancy, and stress) was 

 obtained through a comprehensive interviewer-administered interview of 

 female employees. The prospective study of early fetal loss and fecundity 

 (probability of conception per menstrual cycle) was conducted in a subset 

 of female employees from five plants. Daily diaries and measurements of 

 daily urinary human chorionic gonadotrophin (hCG) levels for 6 months were 

 collected in addition to the comprehensive interview. Of the 891 medically 

 verified pregnancies identified for the retrospective study, 774 (86.9%) 

 were live births, 113 (12.7%) were spontaneous abortions, and 4 (0.4%) 

 were stillbirths. The overall unadjusted relative risk (RR) for 

 spontaneous abortions was 1.45 (95% confidence interval [CI] = 1.02–2.05) 

 and changed little after adjusting for confounders (adjusted RR =1.43; 95% 
 CI = 0.95–2.09). When stratified by work group, the risk of spontaneous 

 abortion was statistically significantly increased for female workers in 

 the photolithography group (RR = 1.67; 95% CI = 1.04–2.55) and in the 

 etching group (RR = 2.08; 95% CI = 1.27–3.19). For women working with 

 higher levels of EGE only in masking, the risk for spontaneous abortion 

 was increased 3-fold (RR = 3.38; 95% CI = 1.61–5.73). In the prospective 

 study, no statistically significant differences were detected in the 

 overall rate of spontaneous abortions between fabrication and 

 non-fabrication workers or when pregnancy outcomes were examined by work 

 group. However, the ability to conceive was lower among female workers 

 exposed to EGEs (fertility rate [FR] = 0.37; 95% CI = 0.11–1.19). 

 /Ethylene glycol ethers/ [International Programme on Chemical Safety; 

 Concise International Chemical Assessment Document Number 41: Diethylene 

 Glycol Dimethyl Ether (2002). Available from, as of February 20, 2007: 

 http://www.inchem.org/pages/cicads.html ] **PEER REVIEWED** 

 /EPIDEMIOLOGY STUDIES/ Painters exposed to the solvent 2-methoxyethanol, 

 which is also a metabolite of diglyme, were found to have an increased 

 prevalence of oligospermia and azoospermia. ... Semen samples from 73 

 painters and 40 controls from a shipyard were analysed. The painters were 

 exposed by inhalation to 0–17.7 mg 2-methoxyethanol/ cu m (mean 2.6 mg/cu 

 m) and to 0–80.5 mg 2-ethoxyethanol (= ethylene glycol monoethyl ether)/cu 

 m (mean 9.9 mg/cu m). Skin contact with 2-methoxyethanol and 

 2-ethoxyethanol was also considered possible. Exposure to numerous other 

 substances, including organic solvents and metals, was also known to 

 occur. While no effects were seen in hormone levels or in sperm viability, 

 motility, and morphology, the prevalence of those with oligospermia 

 differed between the groups. The proportion of men with a sperm density 

 100 million/cm3 was higher in the exposed group than in the unexposed 

 group (33% vs. 20%; P = 0.20). The proportion of those with oligospermia 

 among painters who did not smoke compared with controls was 36% vs. 16% (P 

 = 0.05). The proportion of those with oligospermia was similar between 

 painters and controls who smoked (30% vs. 38%; P = 0.49). The proportion 

 of painters with azoospermia was 5% compared with 0% in the controls. 

 /2-Methoxyethanol/ [International Programme on Chemical Safety; Concise 

 International Chemical Assessment Document Number 41: Diethylene Glycol 

 Dimethyl Ether (2002). Available from, as of February 20, 2007: 

 http://www.inchem.org/pages/cicads.html ] **PEER REVIEWED** 

PROBABLE ROUTES OF HUMAN EXPOSURE: 

 NIOSH (NOES Survey 1981-1983) has statistically estimated that 207 workers 

 (52 of these are female) are potentially exposed to diethylene glycol 

 dimethyl ether in the US(1). Occupational exposure to diethylene glycol 

 dimethyl ether may occur through inhalation and dermal contact with this 

 compound at workplaces where diethylene glycol dimethyl ether is produced 

 or used(SRC). Monitoring data indicate that the general population may be 

 exposed to diethylene glycol dimethyl ether via inhalation of vehicle 

 exhaust and ingestion of contaminated drinking water(SRC). [(1) NIOSH; 

 NOES. National Occupational Exposure Survey conducted from 1981-1983. 

 Estimated numbers of employees potentially exposed to specific agents by 

 2-digit standard industrial classification (SIC). Available at 

 http://www.cdc.gov/noes/ as of Jan 2007.] **PEER REVIEWED** 

EMERGENCY MEDICAL TREATMENT: 
EMERGENCY MEDICAL TREATMENT: 

 

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MICROMEDEX. All Rights Reserved. Any duplication, replication, "downloading," 

sale, redistribution or other use for commercial purposes is a violation of 

Micromedex' rights and is strictly prohibited.<p>The following Overview, *** 

GLYCOL ETHERS ***, is relevant for this HSDB record chemical. 

LIFE SUPPORT: 

 o This overview assumes that basic life support measures 

 have been instituted. 

CLINICAL EFFECTS: 

 0.2.1 SUMMARY OF EXPOSURE 

 0.2.1.1 ACUTE EXPOSURE 

 A) Based on animal comparative data, the glycol ethers may 

 be more acutely toxic than ethylene glycol; however, 

 this model does not account for toxicity of 

 metabolites. Toxicity in humans following ingestions 

 may be dependent on the metabolic products. 

 1) Human overdose experience is limited to extremely 

 large ingestions in adults. Experience with smaller 

 amounts or low concentrations is insufficient to 

 predict whether animal data suggesting significant 

 acute toxicity are relevant to humans. 

 B) CNS depression, renal injury, hyperventilation, 

 hemolysis, and metabolic acidosis have occurred after 

 large ingestions. Onset of symptoms may be delayed for 

 up to 18 hours. 

 0.2.3 VITAL SIGNS 

 0.2.4 HEENT 

 0.2.4.1 ACUTE EXPOSURE 

 A) Eye irritation is generally slight, but may be severe 

 with the propyl ether. 

 0.2.5 CARDIOVASCULAR 

 0.2.5.1 ACUTE EXPOSURE 

 A) Severe hypotension and ventricular dysrhythmias are 

 rare effects of large ingestions of ethylene glycol 

 butyl ether (EGBE). 

 0.2.6 RESPIRATORY 

 0.2.6.1 ACUTE EXPOSURE 

 A) ARDS was reported in one case after ingestion of 500 mL 

 of 9.1% ethylene glycol butyl ether (EGBE). 

 0.2.7 NEUROLOGIC 

 0.2.7.1 ACUTE EXPOSURE 

 A) Ataxia, tremor, somnolence, lethargy, headache, 

 dysarthria, blurred vision, coma, and personality 
 changes have been reported after chronic inhalation. 

 B) Coma has been described after ingestion of 30 to 100 mL 

 of pure glycol ethers in adults. 

 0.2.8 GASTROINTESTINAL 

 0.2.8.1 ACUTE EXPOSURE 

 A) Hemorrhagic gastritis was seen in a case of fatal 

 poisoning with methyl ether. 

 0.2.9 HEPATIC 

 0.2.9.1 ACUTE EXPOSURE 

 A) Fatty degeneration of the liver was noted on autopsy 

 after a poisoning with methyl ether. 

 0.2.10 GENITOURINARY 

 0.2.10.1 ACUTE EXPOSURE 

 A) Renal tubular necrosis with proteinuria has been seen 

 following oral ingestion. Oxalate crystals were seen in 

 the urine in one patient. 

 0.2.11 ACID-BASE 

 0.2.11.1 ACUTE EXPOSURE 

 A) Metabolic acidosis has been consistently described 

 after large oral ingestions. 

 0.2.12 FLUID-ELECTROLYTE 

 0.2.12.1 ACUTE EXPOSURE 

 A) Hypocalcemia and hypokalemia have been noted. 

 0.2.13 HEMATOLOGIC 

 0.2.13.1 ACUTE EXPOSURE 

 A) Hemolytic anemia, non-hemolytic anemia, 

 thrombocytopenia, and DIC have been reported in 

 overdose. 

 0.2.20 REPRODUCTIVE HAZARDS 

 A) Teratogenic effects have been observed at maternally 

 non-toxic doses for the methyl ether and ethyl ether of 

 ethylene glycol. 

 0.2.21 CARCINOGENICITY 

 0.2.21.1 IARC CATEGORY 

 A) IARC Carcinogenicity Ratings for CAS111-76-2 (IARC, 

 2004): 

 1) IARC Classification 

 a) Listed as: 2-Butoxyethanol 

 b) Carcinogen Rating: 3 

 1) The agent (mixture or exposure circumstance) is not 

 classifiable as to its carcinogenicity to humans. 

 This category is used most commonly for agents, 

 mixtures and exposure circumstances for which the 

 evidence of carcinogenicity is inadequate in humans 

 and inadequate or limited in experimental animals. 

 Exceptionally, agents (mixtures) for which the 

 evidence of carcinogenicity is inadequate in humans 

 but sufficient in experimental animals may be placed 

 in this category when there is strong evidence that 

 the mechanism of carcinogenicity in experimental 

 animals does not operate in humans. Agents, mixtures 

 and exposure circumstances that do not fall into any 

 other group are also placed in this category. 

 B) IARC Carcinogenicity Ratings for CAS109-86-4 (IARC, 

 2004): 

 1) Not Listed 

 C) IARC Carcinogenicity Ratings for CAS110-80-5 (IARC, 
 2004): 

 1) Not Listed 

 D) IARC Carcinogenicity Ratings for CAS109-59-1 (IARC, 

 2004): 

 1) Not Listed 

 0.2.22 GENOTOXICITY 

 A) Ethylene glycol n-butyl ether and the aldehyde 

 metabolite of ethylene glycol monomethyl ether 

 (methoxyacetaldehyde) displayed mutagenic potency in the 

 Salmonella typhimurium assay. In contrast, EGME, EGEE, 

 EALD, BALD and the acid metabolites gave negative 

 responses with all strains of Salmonella typhimurium 

 used in the assay (Hoflack et al, 1995). 

LABORATORY: 

 A) Blood ethanol, methanol, and ethylene glycol levels may 

 be useful in assessing concurrent ingestions, but are not 

 useful in assessing glycol ether toxicity. 

TREATMENT OVERVIEW: 

 0.4.2 ORAL EXPOSURE 

 A) Emesis is contraindicated due to rapid GI absorption and 

 potential for rapid progression to coma. 

 B) GASTRIC LAVAGE: Consider after ingestion of a 

 potentially life-threatening amount of poison if it can 

 be performed soon after ingestion (generally within 1 

 hour). Protect airway by placement in Trendelenburg and 

 left lateral decubitus position or by endotracheal 

 intubation. Control any seizures first. 

 1) CONTRAINDICATIONS: Loss of airway protective reflexes 

 or decreased level of consciousness in unintubated 

 patients; following ingestion of corrosives; 

 hydrocarbons (high aspiration potential); patients at 

 risk of hemorrhage or gastrointestinal perforation; and 

 trivial or non-toxic ingestion. 

 C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 

 mL water/30 g charcoal). Usual dose: 25 to 100 g in 

 adults/adolescents, 25 to 50 g in children (1 to 12 

 years), and 1 g/kg in infants less than 1 year old. 

 D) Correct severe acidosis (pH < 7.1) with IV NaHCO3. 1 to 

 2 mEq/kg is a useful starting dose. Monitor ABGs. 

 E) Ethanol (ETOH) may inhibit the formation of toxic 

 metabolites, but there are no controlled human studies 

 documenting efficacy. 

 1) LOADING DOSE - Administer 7.6 to 10 mL/kg of 10% ETOH 

 in D5W IV over 30 minutes. 

 2) MAINTENANCE DOSE - Administer 1.39 mL/kg/hr of 10% ETOH 

 in D5W by IV infusion. Aim at achieving and maintaining 

 100 to 130 mg/dL blood ethanol levels. 

 3) PRECAUTION - Monitor blood glucose and ETOH levels. 

 F) HEMODIALYSIS - Consider hemodialysis in patients with 

 severe toxicity. Maintenance ETOH dose must be modified 

 during dialysis. INDICATIONS: a) severe acid-base and/or 

 fluid-electrolyte abnormalities despite conventional 

 therapy; or b) renal failure. 

 0.4.3 INHALATION EXPOSURE 

 A) INHALATION: Move patient to fresh air. Monitor for 

 respiratory distress. If cough or difficulty breathing 

 develops, evaluate for respiratory tract irritation, 
 bronchitis, or pneumonitis. Administer oxygen and assist 

 ventilation as required. Treat bronchospasm with inhaled 

 beta2 agonist and oral or parenteral corticosteroids. 

 0.4.4 EYE EXPOSURE 

 A) DECONTAMINATION: Irrigate exposed eyes with copious 

 amounts of room temperature water for at least 15 

 minutes. If irritation, pain, swelling, lacrimation, or 

 photophobia persist, the patient should be seen in a 

 health care facility. 

 0.4.5 DERMAL EXPOSURE 

 A) OVERVIEW 

 1) DECONTAMINATION: Remove contaminated clothing and wash 

 exposed area thoroughly with soap and water. A 

 physician may need to examine the area if irritation or 

 pain persists. 

RANGE OF TOXICITY: 

 A) Adults have developed severe toxicity after ingestion of 

 30 to 100 mL, and death after 240 mL (methoxyethanol). 

ANIMAL TOXICITY STUDIES: 

NON-HUMAN TOXICITY EXCERPTS: 

 /LABORATORY ANIMALS: Acute Exposure/ Wistar rats (males and females) were 

 exposed to diglyme vapors in an "inhalation risk test" using air 

 "saturated" with diglyme and an exposure period of 7 hours. After 

 exposure, animals were maintained for a 14-day observation period after 

 which they were sacrificed and subjected to a gross necropsy. All animals 

 survived exposure and a 14-day observation period. No macroscopic findings 

 were observed at necropsy 14 days after the exposure. Clinical signs were 

 restlessness, narrowing of palpebral fissures, and irregular breathing in 

 rats. Based on the vapor pressure the concentration could have been as 

 high as 3800 ppm (21 mg/L) but the /actual/ nominal concentration 

 calculated by the weight loss of test material and the flow rate of the 

 apparatus ... calculates to 11.14 mg/L or about 2000 ppm. [EPA/Office of 

 Pollution Prevention and Toxics; High Production Volume (HPV) Challenge 

 Program's Robust Summaries and Test Plans. Available from the Database 

 Query page at: http://www.epa.gov/hpv/pubs/hpvrstp.htm on Diglyme as of 

 February 7, 2007] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Young adult ChR-CD male rats were 

 administered /diglyme/ by intragastric intubation as a water solution in 

 single doses ranging from 1500 to 23000 mg/kg. Surviving animals were 

 observed for 14 days and were sacrificed and necropsied. ... / All animals 

 given doses higher than 7,500 mg/kg died./ Clinical effects /observed 

 at/ lethal doses/ include/ ataxia, loss of muscle tone, lethargy, 

 prostration, labored respirations, and belly-to-cage posture at 7,500 

 mg/kg and above; pallor at 17,000 mg/kg and above; loss of righting reflex 

 at 25,000 mg/kg. /Clinical effects observed at/ nonlethal doses included 

 lethargy, belly-to-cage posture and ruffled fur at 1,500 mg/kg and above; 

 prostration at 5,000 mg/kg on day of dosing; ruffled fur at 5,000 mg/kg on 

 day after dosing; weight loss 1-2 days at 2,250 mg/kg and above. Diglyme 

 is slightly toxic when administered orally to young adult ChR-CD male rats 

 in single doses; its Approximate Lethal Dose is 7,500 mg/kg of body 

 weight. [EPA/Office of Pollution Prevention and Toxics; High Production 

 Volume (HPV) Challenge Information System (HPVIS). Available from the 

 Database Query page at: http://www.epa.gov/hpvis/index.html on 

 Ethane,1-1'-oxybis[2-methoxy- (CAS # 111-96-6) as of February 21, 2007.] 
 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Acute Exposure/ Described as slightly irritating in 

 the rabbit skin and eye irritation tests. [European Chemicals Bureau; 

 IUCLID Dataset, bis (2-methoxyethyl) ether (CAS # 111-96-6) p.28-9. 

 Available from, as of February 7, 2007: http://ecb.jrc.it/esis/esis.php ] 

 **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... In an in 

 vivo mouse sperm abnormality test, groups of 10 male B6C3F1 mice were 

 exposed for 7 hr/day to vapor concentrations of 250 ppm for 5 days or 1000 

 ppm for 4 days. Because of toxicity in the high-exposure group, exposure 

 was reduced by 1 day. The mice were maintained for 35 days without further 

 exposure, then sacrificed and examined. Significant increases in sperm 

 head abnormalities were observed in the highest exposure group, but no 

 significant exposure-related effects were observed in the low-exposure 

 group. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V7 

 211] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The onset of 

 testicular pathology in the rat and possible recovery over an 8 wk period 

 were evaluated after the administration of up to 20 daily oral doses of 

 bis(2-methoxyethyl)ether (diglyme) at 5.1 mmol/kg body weight (684 mg/kg 

 body weight). Primary and secondary spermatocyte degeneration and 

 spermatidic growth cells were observed after six to eight treatments. In 

 addition, the testes-to-body weight ratio was significantly reduced by the 

 tenth day of treatment and continued to be depressed eight weeks after 

 discontinuation of the treatment. Testicular LDH-X activity, a pachytene 

 spermatocyte marker enzyme, was significantly decreased in animals by the 

 eighteenth day of treatment with diglyme. [Cheever KL et al; Toxicol Ind 

 Health 5 (6): 1099-110 (1989)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... To assess the 

 inhalation toxicity of diglyme, groups of 20 male and 10 female rats were 

 exposed by nose-only inhalation 6 hr/day, 5 days/wk for 2 wk to either 0 

 (control), 110, 370 or 1100 ppm diglyme. To compare potency, 

 2-methoxyethanol was also tested at 300 ppm. Rats were sacrificed either 

 immediately following exposure, after a 14-day recovery period, or after 

 42 and 84 days of recovery (males only). ... Exposure to diglyme produced 

 a variety of concentration-related hematological, clinical chemical and 

 histopathological changes in both sexes. The most striking effect produced 

 in all test groups was cellular injury involving the testes, seminal 

 vesicles, epididymides and prostate. Although these effects were more 

 severe at the higher concentrations tested, partial or complete recovery 

 was seen by 84 days post-exposure. Changes in the hematopoietic system 

 occurred in both sexes and involved the bone marrow, spleen, thymus, 

 leucocytes and erythrocytes. The testicular effects of diglyme were 

 somewhat less pronounced than those seen with 2-methoxyethanol. The 

 no-observed-effect level (NOEL) for repeated inhalation exposure to 

 diglyme in female rats is 370 ppm. For males, all concentrations tested 

 produced effects to the reproductive system, hence a no-observed-effect 

 level could not be demonstrated. [Valentine R et al; Food Chem Toxicol 37 

 (1): 75-86 (1999)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=10069485" 
 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In four male 

 JCL-ICR mice that received diglyme in the drinking-water for 25 days at a 

 level of 2% (approximately 7000 mg/kg body weight, assuming an intake of 7 

 mL/day and a body weight of 20 g), the number of total white blood cells 

 was more than doubled compared with controls. This increase was not, 

 however, statistically significant. [International Program on Chemical 

 Safety/Commission of the European Communities; International Chemical 

 Safety Card on Diethylene Glycol Dimethyl Ether (2002). Available from, as 

 of February 20, 2007: http://www.inchem.org/pages/icsc.html ] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In this 

 study, measured concentrations of 0, 3.1, 9.9, 30, or 98 ppm were used to 

 expose rats by inhalation for 10 exposures followed by a 14-day recovery 

 period. Mean body weights of rats exposed to 98 ppm were significantly 

 lower than those of controls at the end of the exposure period. The 

 weights of testes, seminal vesicles, prostate, and epididymides were 

 similar to controls. Microscopic examination of the testes revealed 

 minimal or mild testicular atrophy in the 100 ppm group. Findings at lower 

 concentrations were not considered to be compound related. It was 

 concluded that the target organ is the male reproductive system and the 

 NOEL for male rats is 30 ppm under these conditions. [EPA/Office of 

 Pollution Prevention and Toxics; High Production Volume (HPV) Challenge 

 Information System (HPVIS). Available from the Database Query page at: 

 http://www.epa.gov/hpvis/index.html on Ethane,1-1'-oxybis[2-methoxy- (CAS 

 # 111-96-6) as of February 21, 2007.] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The 

 reproductive toxicity potential of chemicals were screened in Female CD-1 

 mice: ethylene glycol dimethyl ether, diethylene gycol dimethyl ether, 

 triethylene glycol dimethyl ether, diethylene glycol diethyl ether. The 

 dose lethal to 10% of the mice was the maximum tolerated dose. Pregnant 

 mice received eight doses, once daily, of the chemicals based on their 

 maximum tolerated doses. Ethylene glycol dimethyl ether, diethylene glycol 

 dimethyl ether, and triethylene glycol dimethyl ether had LD50s of 2525.8, 

 2978.7, and 4136.7 mg/kg, respectively, and maximum tolerated doses of 

 2000.0, 2000.0, and 3500 mg/kg, respectively. These compounds 

 significantly affect reproductive indices. No ethylene glycol dimethyl 

 ether, diethylene glycol dimethyl ether, or triethylene glycol dimethyl 

 ether groups delivered any viable pups. Diethylene glycol diethyl ether 

 moderately, but not significantly, reduced reproductive indices. Maternal 

 lethality was significant in ethylene glycol dimethyl ether and diethylene 

 glycol dimethyl ether groups. [Plasterer MR et al; J Toxicol Environ 

 Health 15 (1): 25-38 (1985)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... 

 Diethylene glycol dimethyl ether (0, 25, 50, 100 or 175 mg/kg/day) was 

 administered by gavage in distilled water to timed-pregnant New Zealand 

 White rabbits (15-22 dams/group) during major organogenesis (gestational 

 days 6-19). Exposure of New Zealand White rabbit to diethylene glycol 

 dimethyl ether at 25 mg/kg/day during major organogenesis produced no 

 adverse maternal or developmental effects. Doses of 50 and 100 mg/kg/day 

 were associated with adverse developmental effects, but did not produce 

 distinctive evidence of maternal toxicity. The incidence of adverse 

 developmental effects was further increased at a dose associated with 
 increased maternal mortality (eg, 175 mg/kg/day). The principal 

 manifestations of developmental toxicity were increased resorptions and a 

 higher incidence of major malformations among surviving fetuses. [Price 

 CJ; Govt Reports Announcements & Index Issue 20 (1987)] **PEER 

 REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... 

 Diethylene glycol dimethyl ether (0, 62.5, 125, 250, or 500 mg/kg/day) was 

 administered by gavage in distilled water to timed-pregnant CD-1 mice 

 during major organogenesis (gestational days 6-15). No maternal deaths, 

 morbidity, or treatment-related clinical signs were observed. Reduced 

 maternal weight gain during treatment at greater than or equal to 250 

 mg/kg/day was primarily attributed to compromised pregnancy status 

 resulting in reduced gravid uterine weight. Maternal weight gain during 

 gestation corrected for gravid uterine weight, and relative liver weight 

 (% body weight) were not affected. Average fetal body weight/litter was 

 significantly reduced at greater than or equal to 125 mg/kg/day. The 

 percentage of postimplantation loss/litter (5, 8, 7, 12, and 50% for 

 control through high dose) and the percentage of malformed live 

 fetuses/litter (0.4, 0, 2, 24, and 96%) were significantly increased at 

 greater than or equal to 250 mg/kg/day. Developmental defects involved 

 primarily the neural tube, limbs and digits, craniofacial structures, 

 abdominal wall, cardiovascular system, urogenital organs, and both the 

 axial and appendicular skeleton. Oral administration of diethylene glycol 

 dimethyl ether during major organogenesis did not produce any distinctive 

 signs of maternal toxicity, but did produce selective and profound adverse 

 effects upon fetal growth, viability and morphological development at 

 greater than or equal to 125 mg/kg/day. [Price CJ et al; Fundam Appl 

 Toxicol 8 (1): 115-26 (1987)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Male rats 

 were exposed to 0, 110, 370, or 1100 ppm bis(2-methoxyethyl)ether 

 (diglyme) 6 hr/day, 5 days/week for 2 weeks. One group of male rats was 

 exposed to 300 ppm 2-methoxyethanol for 2 weeks as a positive control. 

 Exposed rats were killed after 10 days of exposure and 14, 42, or 84 days 

 post-exposure, respectively. At 110 ppm diglyme, spermatocytes in 

 pachytene and meiotic division at spermatogenic stages XII-XIV were mainly 

 affected. At 370 ppm diglyme, affected germ cells were similar to those 

 seen at 110 ppm diglyme, but round spermatids at spermatogenic stages 

 I-VII were also affected. The testes regained normal spermatogenesis by 84 

 days post exposure. At 1100 ppm diglyme or 300 ppm 2-methoxyethanol marked 

 testicular atrophy was found affecting all spermatogenic stages. Damaged 

 seminiferous tubules were lined with regenerating pachytene spermatocytes 

 at 14 days post exposure and with spermatocytes and round spermatids after 

 42 days post exposure. Most but not all testes in rats exposed to 300 ppm 

 2-methoxyethanol or 1100 ppm diglyme had normal morphology after 84 days 

 post exposure. Based on the observation of germ cell damage, spermatozoa 

 population in the epididymal tubules, reversibility of spermatogenesis 

 after various post exposure periods, testicular toxicity induced by 300 

 ppm 2-methoxyethanol was more severe than that seen at 370 ppm diglyme but 

 was slightly less remarkable than that of 1100 ppm diglyme. [Lee KP et al; 

 Toxicol 59 (3): 239-58 (1989)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Time-mated 

 CD-1 mice were orally dosed on gestation day 11 (plug= 0) with distilled 

 water (control) or one of four glycol ethers at a dose of 4 mmol/kg: 

 ethylene glycol monomethyl ether, 304 mg/kg, ethylene glycol dimethyl 
 ether, 361 mg/kg, diethylene glycol dimethyl ether 537 mg/kg, triethylene 

 glycol dimethyl ether, 713 mg/kg. Fetuses were collected on gestation day 

 18. Fetuses were cleared and stained to examine paws. There were no signs 

 of treatment-related maternal toxicity, and intrauterine survival was 

 unaffected by glycol ether treatments. Fetal body weights were 

 significantly reduced only in litters treated with ethylene glycol 

 dimethyl ether. There was no treatment-related pattern of gross external 

 malformations other than paw defects. Only triethylene glycol dimethyl 

 ether failed to produce a significant incidence of malformations. Paw 

 defects were present in 87.5% of ethylene glycol monomethyl ether treated 

 litters (68.5% of fetuses), 86.7% of ethylene glycol dimethyl ether 

 treated litters (33.8% of fetuses), and 77.8% of diethylene glycol 

 dimethyl ether treated litters (39.7% of fetuses). Hindpaw defects 

 predominated over forepaw, and syndactyly was the most common 

 malformation. The incidences of oligodactyly and short digits were also 

 significantly increased. The similarity of malformations produced by these 

 methyl-substituted glycol ethers may be attributable to in vivo conversion 

 to a common teratogen, methoxyacetic acid. [Hardin BD, Eisenmann CJ; 

 Teratol 35 (3): 321-8 (1987)] **PEER REVIEWED** 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ 

 2-Methoxyethanol and bis(2-methoxyethyl)ether were subjected to the... 

 dominant lethal test in male rats, ... and the sperm abnormality test in 

 mice. In vivo test animals were exposed to atmospheric concentrations of 

 25 or 500 ppm 2-methoxyethanol and 250 or 1000 ppm 

 bis(2-methoxyethyl)ether. ...There was evidence from the dominant lethal 

 tests that both compounds have profound effects upon male rat fertility 

 during the meiotic phase. Pregnancy frequency was greatly reduced and 

 preimplantation losses were large. In addition, there was evidence of 

 postimplantation losses. Sperm abnormalities were increased in mice 

 exposed to both compounds, but particularly bis(2-methoxyethyl)ether. 

 These effects on male reproductive cells were confined to the higher 

 concentrations of both compounds. [McGregor DB et al; Toxicol Appl 

 Pharmacol 70 (2): 303-16 (1983)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=6623472" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... To assess 

 the potential developmental toxicity of diglyme (diethylene glycol 

 dimethyl ether), groups of pregnant Crl:CD BR rats were exposed to either 

 0 (control, room air only), 25, 100, or 400 ppm diglyme by inhalation for 

 6 hr/day for Days 7 through 16 of gestation (day on which the copulation 

 plug was detected was designation Day 1 G). All female rats were 

 euthanized on day 21G and the fetuses were examined. An additional group 

 of rats was treated with 25 ppm 2-methoxethanol (2ME) to serve as a 

 positive control and for comparison of relative potencies. Maternal 

 toxicity evident as depressed feed consumption at 400 ppm and increased 

 liver weights at 100 ppm. There were no dams in the 400 ppm group with 

 live fetuses (all litters consisted on resorbed conceptuses). Embryo 

 viability was unaffected by concentrations of diglyme as high as 100 ppm. 

 2ME produced increased liver weights and depressed feed consumption at 25 

 ppm. Embryo-fetal toxicity was evident as a concentration-related decrease 

 in fetal weight at diglyme concentrations as high as 100 ppm (and with 

 2ME). There were no fetuses derived from the 400 ppm diglyme-treated dams. 

 A low incidence of structural malformations was observed in all diglyme 
 groups (as well as with 2ME). The incidence of variations, (primarily 

 delayed skeletal ossification and rudimentary ribs) was increased in the 

 25 and 100 ppm diglyme groups. The incidence and severity in the diglyme 

 and 2ME groups exposed to 25 ppm was essentially the same suggesting 

 similar potency for producing structural variations. In this study, 

 diglyme was embryolethal at 400 ppm; a level that otherwise was only 

 marginally toxic to the dam. Maternal and fetal toxicity also were 

 demonstrated at 100 ppm. Although the fetal defects detected following 

 diglyme exposure at 25 ppm were not significantly different from control 

 values (with the exception of the incidence of skeletal developmental 

 variations), the pattern, type, and incidence of variations were similar 

 to those seen at 100 ppm, suggesting that 25 ppm was an effect level that 

 approaches the lower end of the developmental toxicity response curve. 

 Therefore, the no-observable-effect level (NOEL) for diglyme exposure in 

 the dam is 25 ppm and a NOEL was not clearly demonstrated for the 

 conceptus. [Driscoll CD et al; Drug Chem Toxicol 21 (2): 119-36 (1998)] 

 **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=9598295" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... In the 

 present study, 0, 25, 50, 100, or 175 mg/kg/day diethylene glycol dimethyl 

 ether (diEGdiME) ... was administered by gavage in distilled water to 

 timed-pregnant New Zealand white rabbits (15-25 dams/group) during major 

 organogenesis [Gestational Days (gd) 6-19]. Treated females were 

 euthanized on gd 30, uterine contents were examined, and live fetuses were 

 examined for morphological alterations. ... Evidence of maternal toxicity, 

 per se, was observed only at 175 mg/kg/day with 15% mortality among 

 treated females compared to 4% among controls. No significant maternal 

 toxicity was observed in the 25 mg/kg/day group, and only minimal maternal 

 toxicity (decreased maternal weight gain during treatment) was observed at 

 50 and 100 mg/kg/day compared to the vehicle control group. The 

 no-observed-adverse-effect level for developmental toxicity in rabbits for 

 diEGdiME was 50 mg/kg/day. The incidences of prenatal mortality and 

 malformed live fetuses were significantly above controls at 100 and 175 

 mg/kg/day. Malformations observed most frequently included fusion of ribs 

 to each other and hydronephrosis; clubbing of the limbs without underlying 

 bone deformities, a variation, was also observed. [Schwetz BA et al; 

 Fundam Appl Toxicol 19 (2): 238-45 (1992)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=1516781" 

 target=new>PubMed Abstract 

 /LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Pregnant CD-I 

 mice were treated by gavage at a dosage of 3000 mg/kg/day from day 7 to 14 

 of gestation. Maternal mortality was nearly 25% in the treated mice, and 

 none of the surviving mice delivered any viable offspring. [Bingham, E.; 

 Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John 

 Wiley & Sons. New York, N.Y. (2001)., p. V7 212] **PEER REVIEWED** 

 /GENOTOXICITY/ Bis(2-methoxyethyl) ether was tested for mutagenicity using 

 the Salmonella/microsome preincubation assay, using the standard protocol 

 approved by the National Toxicology Program. Bis(2-methoxyethyl) ether was 

 tested in ...5 Salmonella typhimurium strains (TA 1535, TA 1537, TA 97, TA 
 98, and TA 100) in the presence and absence of rat and hamster liver S-9, 

 at doses of 0.1, 0.33, 1.0, 3.3, and 10 mg/plate. Bis(2-methoxyethyl) 

 ether was negative in these tests and the highest ineffective dose tested 

 in any Salmonella typhimurium strain was 10 mg/plate. [Mortelmans K et al; 

 Environ Mutagen 8: 1-119 (1986)] **PEER REVIEWED** 

 /GENOTOXICITY/ Described as negative in the Escherichia coli WP2 uvrA 

 mutation test with metabolic activation [European Chemicals Bureau; IUCLID 

 Dataset, bis (2-methoxyethyl) ether (CAS # 111-96-6) p.39. Available from, 

 as of February 7, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER 

 REVIEWED** 

 /GENOTOXICITY/ 2-Methoxyethanol and bis(2-methoxyethyl)ether were 

 subjected to the following assays for genetic toxicity: Ames' test, ... 

 sex-linked recessive lethal (SLRL) test in Drosophila, ... /and/ bone 

 marrow metaphase analysis in male and female rats. In vivo test animals 

 were exposed to atmospheric concentrations of 25 or 500 ppm 

 2-methoxyethanol and 250 or 1000 ppm bis(2-methoxyethyl)ether. Point 

 mutations in Ames' test ... were not increased by either compound, while 

 the SLRL test gave ambiguous results which deserve further investigation. 

 Chromosomal aberration frequencies were not increased in rat bone marrow. 

 [McGregor DB et al; Toxicol. Appl. Pharmacol. 70 (2): 303-16 (1983)] 

 **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=6623472" 

 target=new>PubMed Abstract 

NATIONAL TOXICOLOGY PROGRAM STUDIES: 

 ... Diethylene glycol dimethyl ether (0, 62.5, 125, 250 or 500 mg/kg/day) 

 was administered to CD-1® mice by gavage (by mouth) on gestational days 

 (gd) 6-15. Mice were monitored daily during treatment for evidence of 

 maternal toxicity and were sacrificed on gd 17 (20-24 confirmed 

 pregnancies per group). ... Diethylene glycol dimethyl ether-treated dams 

 failed to exhibit treatment-related clinical signs, death, or differences 

 from control in corrected maternal body weight gain (i.e., gestational 

 weight gain minus gravid uterine weight) or relative maternal liver 

 weight. However, intact maternal body weight (i.e., including gravid 

 uterine weight) was reduced at 250 and 500 mg diethylene glycol dimethyl 

 ether/kg/day on gd 15 and 17, as were maternal weight gain during 

 treatment and gestation. Gravid uterine weight in diethylene glycol 

 dimethyl ether-treated groups was significantly reduced at all doses in a 

 dose-related manner. There were dose-related and significant increases at 

 250 and 500 mg/kg/day in the percentage of nonlive implants per litter 

 (4.88%, 8.41%, 7.05%, 12.02% and 50.41% in the vehicle control through 

 high-dose groups, respectively), as well as the percentage of adversely 

 affected implants per litter (5.25%, 8.41%, 9.35%, 32.29% and 96.93% 

 nonlive or malformed in the vehicle control through high-dose groups, 

 respectively). The mean live litter size was significantly less than 

 control at 500 mg/kg/day and was marginally reduced at all lower dose 

 levels. The average fetal body weight per litter was significantly reduced 

 at and above 125 mg diethylene glycol dimethyl ether/kg/day. Examination 

 of fetuses for anatomical malformations revealed a dose-dependent trend 

 toward an increased percentage of malformed live fetuses per litter, and 

 the difference from control was statistically significant in the 250 and 

 500 mg diethylene glycol dimethyl ether/kg/day groups. The mean percent 

 malformed live fetuses per litter was 0.37%, 0.00%, 2.47%, 23.86% and 
 95.82% in the vehicle through high-dose groups, respectively. The 

 proportion of litters with gross, visceral or skeletal malformations was 

 increased at the high dose, and the proportion of litters with gross or 

 skeletal malformations was increased in the 250 mg/kg/day group. The types 

 of malformations observed in the present study were quite diverse. Major 

 malformations affected primarily the development of the neural tube, limbs 

 and digits, craniofacial structures, abdominal wall, cardiovascular 

 system, urogenital organs, and both the axial and appendicular skeleton. 

 The two most frequently observed malformations were fused ribs in 74% of 

 high dose fetuses and exencephaly in 54% of high dose fetuses. In summary, 

 exposure of timed-pregnant CD-1® mice to diethylene glycol dimethyl ether 

 throughout major organogenesis produced no notable evidence of maternal 

 toxicity. The lowest dose level, 62.5 mg/kg/day, appeared to be a no 

 observed effect level for indices of fetal development. At higher doses, 

 diethylene glycol dimethyl ether produced profound adverse effects upon 

 fetal growth ( greater than or equal to 125 mg/kg/day), fetal viability 

 (greater than or equal to 250 mg/kg/day), and fetal morphological 

 development (greater than or equal to 250 mg/kg/day). At the highest dose, 

 all 23 litters contained at least one malformed fetus compared to 1 of 21 

 control litters, and 94% of the high-dose fetuses were malformed compared 

 to 0.35% of the fetuses in the control group. Thus, diethylene glycol 

 dimethyl ether posed an extreme degree of risk to the embryo or fetus at 

 dose levels which did not cause observable toxicity to the maternal 

 organism. [Department of Health & Human Services/National Institute of 

 Environmental Health Sciences, National Toxicology Program; Teratologic 

 Evaluation of Diethylene Glycol Dimethyl Ether (CAS NO. 111-96-6) 

 Administered to CD-1® Mice on Gestational Days 6 through 15, NTP Study No. 

 TER85061 (August 30, 1985 ) Available from, as of August 15, 2002: 

 http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-C685-

88B4D7EAC975BD44 

 ] **PEER REVIEWED** 

 In the present study, diethylene glycol dimethyl ether (0, 25, 50, 100 or 

 175 mg/kg/day ) was administered by gavage in distilled water to 

 timed-pregnant New Zealand White (NZW) rabbits (15-22 dams/group) during 

 major organogenesis (gestational days (gd) 6-19) based on preliminary 

 rangefinding studies. Treated females were sacrificed on gd 30, uterine 

 contents were examined, and live fetuses examined for malformations. 

 Evidence of maternal toxicity, per se, was observed only at 175 mg/kg/day 

 . At this high dose, the mortality among treated females was 15.4% as 

 compared to 4% among controls. No significant maternal toxicity was 

 observed in the 25 mg/kg/day group, and only minimal maternal toxicity 

 (maternal weight gain during treatment) was observed at 50 mg/kg/day as 

 compared to the vehicle control group. However, even these lower doses 

 appeared to contribute to significant dose-related trends for indices of 

 maternal body weight, weight gain, and gravid uterine weight maternal. The 

 lowest dose of diethylene glycol dimethyl ether (25 mg/kg/day ) appeared 

 to be a no-observed-effect level (NOEL) for developmental toxicity in New 

 Zealand White rabbits. At 50 mg/kg/day , apparent adverse effects on 

 prenatal growth, viability and morphological development were in accord 

 with significant dose-response relationships observed across all groups. 

 At 100 and 175 mg/kg/day , adverse effects upon fetal weight were in 

 accord with significant dose-response relationships, but individual 

 treatment groups did not differ significantly from controls. The incidence 

 of resorptions and malformed live fetuses, as well as other cumulative 

 indices which included these endpoints, were significantly above controls 

 at 100 and 175 mg/kg/day . Major malformations affected the development of 
 the digits, craniofacial structures, abdominal wall, cardiovascular 

 system, urogenital organs and axial skeleton. The most frequently observed 

 individual defects were fusion of ribs to each other (19%), hydronephrosis 

 (23%), and clubbing of the limbs (19%) without underlying bone deformities 

 (i.e., of presumed neuromuscular origin). In conclusion, exposure of New 

 Zealand White rabbits to diethylene glycol dimethyl ether at 25 mg/kg/day 

 during major organogenesis produced no adverse maternal or developmental 

 effects. Doses of 50 and 100 mg/kg/day were associated with adverse 

 developmental effects, but did not produce distinctive evidence of 

 maternal toxicity. The incidence of adverse developmental effects was 

 further increased at a dose associated with increased maternal mortality 

 (e.g., 175 mg/kg/day). The principal manifestations of developmental 

 toxicity were increased resorptions and a higher incidence of major 

 malformations among surviving fetuses. [Department of Health & Human 

 Services/National Institute of Environmental Health Sciences, National 

 Toxicology Program; Diethylene glycol dimethyl ether (CAS No. 111-96-6) 

 Administered to New Zealand White Rabbits on Gestation Days 6 Through 19, 

 NTP Study No. TER86062 (May 5, 1987) Available from, as of August 15, 

 2002: 

 http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-C685-

88B4D7EAC975BD44 

 ] **PEER REVIEWED** 

NON-HUMAN TOXICITY VALUES: 

 LD50 Mouse oral 2978 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 bis (2-methoxyethyl) ether (CAS # 111-96-6) p.26. Available from, as of 

 February 7, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED** 

 LD50 Rat oral 4760 mg/kg bw [European Chemicals Bureau; IUCLID Dataset, 

 bis (2-methoxyethyl) ether (CAS # 111-96-6) p.25. Available from, as of 

 February 7, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER REVIEWED** 

 LC50 Rat inhalation > 11 mg/L/7 hr [European Chemicals Bureau; IUCLID 

 Dataset, bis (2-methoxyethyl) ether (CAS # 111-96-6) p.27. Available from, 

 as of February 7, 2007: http://ecb.jrc.it/esis/esis.php ] **PEER 

 REVIEWED** 

ECOTOXICITY VALUES: 

 LC50 Rana brevipoda porosa /(Frog)/ 8300 mg/kg bw for 48 hr /Conditions of 

 bioassay not specified in source examined/ [Verschueren, K. Handbook of 

 Environmental Data on Organic Chemicals. Volumes 1-2. 4th ed. John Wiley 

 & Sons. New York, NY. 2001, p. 845] **PEER REVIEWED** 

 LC50 Leuciscus idus /(Ide)/ > 2000 mg/L for 96 hr /Conditions of 

 bioassay not specified in source examined/ [Verschueren, K. Handbook of 

 Environmental Data on Organic Chemicals. Volumes 1-2. 4th ed. John Wiley 

 & Sons. New York, NY. 2001, p. 845] **PEER REVIEWED** 

TSCA TEST SUBMISSIONS: 

 Subchronic toxicity was evaluated in 5 groups of 20 male CD rats exposed 

 nose-only by inhalation to diglyme (diethylene glycol dimethyl ether) at 

 air concentrations of 0, 3.1, 9.9, 30, and 98 ppm for 6 hours/day, 5 

 days/week, over 2 weeks. An interim sacrifice of 10 rats from each 

 treatment group was performed immediately after the last dosing. The 

 remaining 10 rats were sacrificed after a 14-day observation period. No 

 mortalities were reported. A slight depression in body weight and body 

 weight gain was observed during days 1 to 12 of the study in the group 
 exposed to 98 ppm (p < 0.05). After the 2-week recovery period, 

 testicular atrophy and exfoliated degenerative germ cells were observed 

 among the rats exposed to 98 ppm. No treatment-related clinical signs, 

 gross lesions, or organ weight changes were observed. Hematology, 

 urinalysis, and clinical chemistry results were not reported.[Haskell 

 Lab.; Subchronic Inhalation Toxicity Study with Diglyme with Cover Letter 

 Dated 05/16/89 (1989), EPA Document No. FYI-OTS- 0589-0553, Fiche No. 

 OTS0000553-2] **UNREVIEWED** 

 Reproductive toxicity was evaluated in groups of 10 pregnant Charles River 

 CD female mice receiving an oral gavage dose of diethylene glycol dimethyl 

 ether at 10 ml/kg body weight on gestation days 7 through 14. Maternal 

 mortality, clinical observations and gross necropsy were not reported. 

 There was a significant reduction (p < 0.05) in the number of live pups 

 per litter.[Department of Health & Human Services; Results of Testing 

 Fifteen Glycol Ethers in a Short-Term In Vivo Reproductive Toxicity Assay 

 With Attachments, EPA Doc. 40-8385037, Fiche No. OTS0521552] 

 **UNREVIEWED** 

METABOLISM/PHARMACOKINETICS: 

METABOLISM/METABOLITES: 

 The effect of enzyme induction on the metabolism of 

 bis(2-methoxyethyl)ether (diglyme) was studied in rats. Male 

 Sprague-Dawley rats were administered 5.1 mmol/kg diglyme or 0.1% 

 phenobarbital in their drinking water for 22 days. Other rats were 

 pretreated with 5.1 mmol/kg diglyme or 0.1% phenobarbital administered in 

 their drinking water for 22 days, and then given a single oral dose of 5.1 

 mmol/kg (14)C labeled diglyme. Urine samples were collected at 6 to 96 

 hours post dosing and analyzed for diglyme metabolites. Phenobarbital and 

 diglyme caused significant decreases in hexobarbital sleeping time, 

 phenobarbital showing the greater effect. Pretreatment with phenobarbital 

 or diglyme did not significantly affect cumulative excretion of (14)C 

 activity. Cumulative excretion of methoxyacetic acid, a minor metabolite, 

 was significantly increased by both phenobarbital and diglyme, 

 phenobarbital showing the greater effect. /It was concluded/ that 

 pretreating rats with diglyme or phenobarbital increases the extent of 

 cleavage of the ether bond in diglyme, forming 2-methoxyethanol, a 

 precursor of methoxyacetic acid, a putative reproductive toxicant. 

 [Cheever KL et al; Toxicol and Ind Health 5 (3): 601-7 (1989)] **PEER 

 REVIEWED** 

 The testicular toxicity of bis(2-methoxyethyl)ether (diglyme) was studied 

 in rats. Male Sprague-Dawley-rats were given 0.051, or 5.1 mmol/kg (14)C 

 labeled diglyme orally. Approximately 86 to 90% of each dose was excreted 

 in the urine over 96 hours. Less than 5% of the doses was excreted in the 

 feces. Only trace amounts of radiolabel were found in the expired air as 

 volatile organic compounds. The principal urinary metabolites were 

 (2-methoxyethoxy)acetic acid and methoxyacetic acid which accounted for 

 around 70 and 6% of the doses, respectively. Smaller amounts of 

 N-(methoxyacetyl)glycine, diglycolic acid, 2-methoxyethanol, and 

 2-(2-methoxyethoxy)ethanol were found. Only unchanged diglyme was found in 

 the volatile organic fraction of the expired air. ... Diglyme metabolism 

 proceeds primarily through an O-demethylation pathway, followed by 

 oxidation to (2-methoxyethoxy)acetic acid. The lack of toxicity of 

 2-(2-methoxyethoxy)ethanol and (2-methoxyethoxy)acetic acid suggests that 

 the testicular toxicity of diglyme may be due to methoxyacetic acid, a 
 minor metabolite. [Cheever KL; Toxicol and Appl Pharmacol 94 (1): 150-9 

 (1988)] **PEER REVIEWED** 

 The metabolism of ... bis(2-methoxyethyl)ether (diglyme) was studied in 

 isolated rat hepatocytes and in the intact rat. Male Sprague-Dawley rats 

 (190-220 g) were used in both studies. Hepatocytes, isolated by a two-step 

 in situ collagenase perfusion of the liver, were cultured as monolayers 

 and incubated with [14C]diglyme at 1, 10, 30, and 50 uM for up to 48 hr. 

 For the in vivo study, rats were given single oral doses of [14C]diglyme 

 at 5.1 mmol/kg bw, and urine was collected for up to 96 hr. Radioactive 

 compounds in the culture medium or in the urine were separated by high 

 performance liquid chromatography and quantified with an in-line 

 radioactivity monitor. Metabolites were identified by comparison of their 

 chromatographic retention times and their mass spectra with those of 

 authentic compounds. The principal metabolite from hepatocytes and in the 

 urine was (2-methoxyethoxy)acetic acid (MEAA). This metabolite accounted 

 for approximately 36% of the radioactivity in the 48-hr culture medium and 

 about 67% of the administered dose in the 48-hr urine. Other prominent 

 metabolites common to both systems included 2-(2-methoxyethoxy)ethanol, 

 methoxyacetic acid (MAA), 2-methoxyethanol, and diglycolic acid. The 

 diglyme metabolite profiles from urine and from hepatocytes were 

 qualitatively similar, demonstrating that, in the rat, hepatocytes serve 

 as a good model system for predicting the urinary metabolites of diglyme. 

 Moreover, MEAA was shown to be the metabolite best suited for use as a 

 short-term biological marker of exposure to diglyme. [Richards DE et al; 

 Arch Toxicol 67 (8): 531-7 (1993)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=8285851" 

 target=new>PubMed Abstract 

 An embryotoxic oral dose of bis(2-methoxyethyl) ether (DGDME), 3.73 

 mmol/kg bw (500 mg/kg), administered on the 11th day of gestation to 

 pregnant CD-1 mice was metabolized predominantly by O-demethylation to 

 2-(2-methoxyethoxy)ethanol with subsequent oxidation to 

 (2-methoxyethoxy)acetic acid. Urinary excretion of this metabolite over 48 

 hr amounted to 63 +/- 2% of the dose. A smaller percentage of the 

 administered dose was metabolized at the central ether linkage to produce 

 2-methoxyethanol, which was further metabolized by alcohol dehydrogenase 

 to methoxyacetic acid. Urinary excretion of methoxyacetic acid, a potent 

 developmental toxicant, amounted to 28 +/- 1% of the administered dose by 

 48 hr and was the second most prominent urinary metabolite. Unchanged 

 DGDME and methoxyacetic acid were detected in the embryonic tissues from 

 these animals, and embryos harvested after the initial 6-hr period showed 

 detectable amounts of only methoxyacetic acid. The average amount of 

 methoxyacetic acid per embryo was calculated to be 1.5 +/- 1.0 umol (5.9 

 mmol/kg bw) at the 6-hr termination time. This finding suggests that the 

 reported teratogenic effects of DGDME are due to methoxyacetic acid 

 formed, either in the fetus or by hepatic metabolism in the dam with 

 subsequent distribution to the embryonic tissue. ... [Daniel FB et al; 

 Fundam Appl Toxicol 16 (3): 567-75 (1991)] **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=1855627" 

 target=new>PubMed Abstract 

 The principal pathway of biotransformation of diglyme involves 
 O-demethylation with subsequent oxidation to form the main metabolite 

 2-methoxyethoxyacetic acid, which accounts for about 60-70% of the dose in 

 the urine of rats and pregnant mice after 48-96 hr. In addition, cleavage 

 (O-dealkylation) of the central ether bond results in the formation of 

 2-methoxyethanol, which is subsequently oxidized to 2-methoxyacetic acid. 

 This metabolite accounts for about 5-15% of the dose in the urine of rats 

 after 48-96 hr. ... Also, humans may form this metabolite in higher 

 concentrations. Based on nmol 2-methoxyethanol generated per nmol P-450, 

 human microsomes were found to be 7 times more effective than rat 

 microsomes in converting diglyme to 2-methoxyethanol. ...Repeated doses of 

 diglyme or induction with phenobarbital or ethanol increases the cleavage 

 of the central ether linkage of diglyme as a result of cytochrome P-450 

 enzyme induction in the liver. Although the main metabolite in rat urine 

 is 2-methoxyethoxyacetic acid, numerous studies indicate that 

 2-methoxyacetic acid is the metabolite responsible for the toxicity of 

 diglyme for the male reproductive organs. [International Programme on 

 Chemical Safety; Concise International Chemical Assessment Document 

 Number 41: Diethylene Glycol Dimethyl Ether (2002). Available from, as of 

 February 20, 2007: http://www.inchem.org/pages/cicads.html ] **PEER 

 REVIEWED** 

 Although the main metabolite in rat urine is 2-methoxyethoxyacetic acid, 

 numerous studies indicate that 2-methoxyacetic acid is the metabolite 

 responsible for the toxicity of diglyme for the male reproductive organs. 

 2-methoxyacetic acid was transferred to the fetus and found as the sole 

 metabolite in the fetus (no parent compound was detected in the fetus 

 either) after dosing diglyme to mice at day 11 or 12 of pregnancy. The 

 highest levels for the average embryo (whole embryos analysed) were 

 detected at 6 hr after dosing. Significantly lower amounts were detected 

 in blood taken from the dam at that time point. [International Programme 

 on Chemical Safety; Concise International Chemical Assessment Document 

 Number 41: Diethylene Glycol Dimethyl Ether (2002). Available from, as of 

 February 20, 2007: http://www.inchem.org/pages/cicads.html ] **PEER 

 REVIEWED** 

ABSORPTION, DISTRIBUTION & EXCRETION: 

 The major route of elimination is through the urine. Ninety-six hours 

 after oral application of 6.84 mg diglyme/kg body weight to male 

 Sprague-Dawley rats, 90% of the dose was excreted via urine, 3.6% as 

 carbon dioxide, and 2.9% in the feces. Only 1.7% of the dose remained in 

 the carcass. [International Programme on Chemical Safety; Concise 

 International Chemical Assessment Document Number 41: Diethylene Glycol 

 Dimethyl Ether (2002). Available from, as of February 20, 2007: 

 http://www.inchem.org/pages/cicads.html ] **PEER REVIEWED** 

 Although the main metabolite in rat urine is 2-methoxyethoxyacetic acid, 

 numerous studies indicate that 2-methoxyacetic acid is the metabolite 

 responsible for the toxicity of diglyme for the male reproductive organs. 

 2-methoxyacetic acid was transferred to the fetus and found as the sole 

 metabolite in the fetus (no parent compound was detected in the fetus 

 either) after dosing diglyme to mice at day 11 or 12 of pregnancy. The 

 highest levels for the average embryo (whole embryos analysed) were 

 detected at 6 hr after dosing. Significantly lower amounts were detected 

 in blood taken from the dam at that time point. [International Programme 

 on Chemical Safety; Concise International Chemical Assessment Document 

 Number 41: Diethylene Glycol Dimethyl Ether (2002). Available from, as of 
 February 20, 2007: http://www.inchem.org/pages/cicads.html ] **PEER 

REVIEWED** 

 ... The skin absorption rates of a group of glycol ethers /were evaluated/ 

 in vitro ... using the Franz cell method with human skin. ... A permeation 

 profile was obtained and steady state, lag time and permeation constant 

 flux was calculated for ... ethylene glycol diethyl ether (EGDEE) and 

 diethylene glycol dimethyl ether (DEGDME). ... solvents were tested in 

 their pure form and with 70% acetone. ... For all solvents tested the lag 

 time was less than 2 hr, and for the majority of them was about 60 min ... 

 Flux at steady state ranged between 0.017 +/- 0.005 and 3.435 +/- 1.897 

 mg/cm(2)/hr and permeation rate was from 0.0192 to 1.02 x 10(-3) cm/hr ... 

 [Larese Filon F et al; Int Arch Occup Environ Health 72 (7): 480-4 (1999)] 

 **PEER REVIEWED** <a 

 

href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=

Abstract&list_uids=10541914" 

 target=new>PubMed Abstract 

BIOLOGICAL HALF-LIFE: 

 The /diglyme/ metabolite 2-methoxyacetic acid has shown evidence of 

 accumulation in animals and humans. In humans, its half-life was 

 calculated as 77.1 hr. [International Programme on Chemical Safety; 

 Concise International Chemical Assessment Document Number 41: Diethylene 

 Glycol Dimethyl Ether (2002). Available from, as of February 20, 2007: 

 http://www.inchem.org/pages/cicads.html ] **PEER REVIEWED** 

PHARMACOLOGY: 

ENVIRONMENTAL FATE & EXPOSURE: 

ENVIRONMENTAL FATE/EXPOSURE SUMMARY: 

 Diethylene glycol dimethyl ether's production and use as a solvent and an 

 anhydrous reaction medium for organo-metallic synthesis or as a 

 solubilizer may result in its release to the environment through various 

 waste streams. If released to air, a vapor pressure of 2.96 mm Hg at 25 

 deg C indicates diethylene glycol dimethyl ether will exist solely as a 

 vapor in the atmosphere. Vapor-phase diethylene glycol dimethyl ether will 

 be degraded in the atmosphere by reaction with photochemically-produced 

 hydroxyl radicals; the half-life for this reaction in air is estimated to 

 be 22 hours. Diethylene glycol dimethyl ether does not contain 

 chromophores that absorb at wavelengths > 290 nm and therefore is not 

 expected to be susceptible to direct photolysis by sunlight. If released 

 to soil, diethylene glycol dimethyl ether is expected to have very high 

 mobility based upon an estimated Koc of 15. Volatilization from moist soil 

 surfaces is not expected to be an important fate process based upon an 

 estimated Henry's Law constant of 5.2X10-7 atm-cu m/mole. Diethylene 

 glycol dimethyl ether may volatilize from dry soil surfaces based upon its 

 vapor pressure. Biodegradation of diethylene glycol dimethyl ether in soil 

 and water may be an important environmental fate process based on a study 

 done where it was degraded 33% after 25 days and a 7 day lag period using 

 an activated sludge from an industry producing the chemical. If released 

 into water, diethylene glycol dimethyl ether is not expected to adsorb to 

 suspended solids and sediment based upon the estimated Koc. Volatilization 

 from water surfaces is not expected to be an important fate process based 

 upon this compound's estimated Henry's Law constant. An estimated BCF of 3 

 suggests the potential for bioconcentration in aquatic organisms is low. 
 Hydrolysis is not expected to be an important environmental fate process 

 since this compound lacks functional groups that hydrolyze under 

 environmental conditions. Occupational exposure to diethylene glycol 

 dimethyl ether may occur through inhalation and dermal contact with this 

 compound at workplaces where diethylene glycol dimethyl ether is produced 

 or used. Monitoring data indicate that the general population may be 

 exposed to diethylene glycol dimethyl ether via inhalation of vehicle 

 exhaust and ingestion of contaminated drinking water. (SRC) **PEER 

 REVIEWED** 

PROBABLE ROUTES OF HUMAN EXPOSURE: 

 NIOSH (NOES Survey 1981-1983) has statistically estimated that 207 workers 

 (52 of these are female) are potentially exposed to diethylene glycol 

 dimethyl ether in the US(1). Occupational exposure to diethylene glycol 

 dimethyl ether may occur through inhalation and dermal contact with this 

 compound at workplaces where diethylene glycol dimethyl ether is produced 

 or used(SRC). Monitoring data indicate that the general population may be 

 exposed to diethylene glycol dimethyl ether via inhalation of vehicle 

 exhaust and ingestion of contaminated drinking water(SRC). [(1) NIOSH; 

 NOES. National Occupational Exposure Survey conducted from 1981-1983. 

 Estimated numbers of employees potentially exposed to specific agents by 

 2-digit standard industrial classification (SIC). Available at 

 http://www.cdc.gov/noes/ as of Jan 2007.] **PEER REVIEWED** 

ARTIFICIAL POLLUTION SOURCES: 

 Diethylene glycol dimethyl ether's production and use as a solvent and an 

 anhydrous reaction medium for organo-metallic synthesis(1) or as a 

 solubilizer(2) may result in its release to the environment through 

 various waste streams(SRC). [(1) Lewis RJ Sr; Hawley's Condensed Chemical 

 Dictionary 14th ed. John Wiley & Sons, Inc. New York, NY p. 373 (2001) 

 (2) Ashford RD; Ashford's Dictionary of Industrial Chemicals. London, 

 England: Wavelength Publications Ltd., p. 301 (1994)] **PEER REVIEWED** 

ENVIRONMENTAL FATE: 

 TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc 

 value of 15(SRC), determined from a log Kow of -0.36(2) and a 

 regression-derived equation(3), indicates that diethylene glycol dimethyl 

 ether is expected to have very high mobility in soil(SRC). Volatilization 

 of diethylene glycol dimethyl ether from moist soil surfaces is not 

 expected to be an important fate process(SRC) given an estimated Henry's 

 Law constant of 5.2X10-7 atm-cu m/mole(SRC), derived from its vapor 

 pressure, 2.96 mm Hg(4), and assigned value for water solubility of 1X10+6 

 mg/L (miscible)(5). Diethylene glycol dimethyl ether is expected to 

 volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). 

 Diethylene glycol dimethyl ether was degraded 33% after 25 days and a 7 

 day lag period using an activated sludge from an industry producing the 

 chemical(6), indicating that biodegradation may be an important 

 environmental fate process in soil(SRC). [(1) Swann RL et al; Res Rev 85: 

 17-28 (1983) (2) Hansch C et al; Exploring QSAR. Hydrophobic, Electronic, 

 and Steric Constants. ACS Prof Ref Book. Heller SR, consult. ed., 

 Washington, DC: Amer Chem Soc p. 299 (1995) (3) Lyman WJ et al; Handbook 

 of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 

 4-9 (1990) (4) Daubert TE, Danner RP; Data Compilation, Tables of 

 Properties of Pure Compounds, NY, NY: Design Inst for Phys Prop Data, Am 

 Inst for Phys Prop Data (1989) (5) Riddick JA et al; Organic Solvents NY: 

 John Wiley & Sons Inc (1984) (6) Roy D et al; J Environ Sci Health 

 Part A 29:129-47 (1994)] **PEER REVIEWED** 
 AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value 

 of 15(SRC), determined from a log Kow of -0.36(2) and a regression-derived 

 equation(3), indicates that diethylene glycol dimethyl ether is not 

 expected to adsorb to suspended solids and sediment(SRC). Volatilization 

 from water surfaces is not expected(3) based upon an estimated Henry's Law 

 constant of 5.2X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 

 2.96 mm Hg(4), and assigned value for water solubility of 1X10+6 mg/L 

 (miscible)(5). According to a classification scheme(6), an estimated BCF 

 of 3(SRC), from its log Kow(2) and a regression-derived equation(7), 

 suggests the potential for bioconcentration in aquatic organisms is 

 low(SRC). Diethylene glycol dimethyl ether was biodegraded 33% after 25 

 days and a 7 day lag period using an activated sludge from an industry 

 producing the chemical(8), indicating that biodegradation may be an 

 important environmental fate process in water(SRC). [(1) Swann RL et al; 

 Res Rev 85: 17-28 (1983) (2) measured log Kow ref e.g. Hansch C et al; 

 Exploring QSAR. Hydrophobic, Electronic, and Steric Constants. ACS Prof 

 Ref Book. Heller SR, consult. ed., Washington, DC: Amer Chem Soc p. 299 

 (1995) (3) Lyman WJ et al; Handbook of Chemical Property Estimation 

 Methods. Washington, DC: Amer Chem Soc pp. 4-9, 15-1 to 15-29 (1990) (4) 

 Daubert TE, Danner RP; Data Compilation, Tables of Properties of Pure 

 Compounds NY, NY: Design Inst for Phys Prop Data, Am Inst for Phys Prop 

 Data (1989) (5) Riddick JA et al; Organic Solvents NY: John Wiley & 

 Sons Inc (1984) (6) Franke C et al; Chemosphere 29: 1501-14 (1994) (7) 

 Meylan WM et al; Environ Toxicol Chem 18: 664-72 (1999) (8) Roy D et al; J 

 Environ Sci Health Part A 29:129-47 (1994)] **PEER REVIEWED** 

 ATMOSPHERIC FATE: According to a model of gas/particle partitioning of 

 semivolatile organic compounds in the atmosphere(1), diethylene glycol 

 dimethyl ether, which has a vapor pressure of 2.96 mm Hg at 25 deg C(2), 

 is expected to exist solely as a vapor in the ambient atmosphere. 

 Vapor-phase diethylene glycol dimethyl ether is degraded in the atmosphere 

 by reaction with photochemically-produced hydroxyl radicals(SRC); the 

 half-life for this reaction in air is estimated to be 22 hours(SRC), 

 calculated from its rate constant of 1.75X10-11 cu cm/molecule-sec at 25 

 deg C(3). Diethylene glycol dimethyl ether does not contain chromophores 

 that absorb at wavelengths > 290 nm and therefore is not expected to be 

 susceptible to direct photolysis by sunlight(4). [(1) Bidleman TF; Environ 

 Sci Technol 22: 361-367 (1988) (2) Daubert TE, Danner RP; Data 

 Compilation, Tables of Properties of Pure Compounds, Design Inst for Phys 

 Prop Data, Am Inst for Phys Prop Data, NY, NY (1989) (3) Atkinson R; J 

 Phys Chem Ref Data. Monograph No. 1 (1989) (4) Silverstein RM, Bassler GC; 

 Spectrometric Id Org Cmpd NY: J Wiley & Sons Inc p. 148-69 (1963)] 

 **PEER REVIEWED** 

ENVIRONMENTAL BIODEGRADATION: 

 AEROBIC: Diethylene glycol dimethyl ether had a 37.0% COD removal at 30 

 deg C from a starting concentration of 600 mg COD/L (time period not 

 given) indicating little degradation compared to 95% degradation of 

 ethylene glycol monophenyl ether(1). Diethylene glycol dimethyl ether was 

 degraded 33% after 25 days and a 7 day lag period using an activated 

 sludge from an industry producing the chemical(2). 40% was removed in a 1% 

 salt solution after 25 days with a 20 day lag period, higher salt 

 concentrations inhibited the degradation of diethylene glycol dimethyl 

 ether(2). [(1) Cowan RM, Kwon J; pp. 273-82 in Hazard Ind Wastes, 31st 

 Technomic Pub Co., Inc., p 273-82 (1999) (2) Roy D et al; J Environ Sci 

 Health Part A 29: 129-47 (1994)] **PEER REVIEWED** 
ENVIRONMENTAL ABIOTIC DEGRADATION: 

 The rate constant for the vapor-phase reaction of diethylene glycol 

 dimethyl ether with photochemically-produced hydroxyl radicals has been 

 measured as 1.75X10-11 cu cm/molecule-sec at 25 deg C(1). This corresponds 

 to an atmospheric half-life of about 22 hours at an atmospheric 

 concentration of 5X10+5 hydroxyl radicals per cu cm(1). Diethylene glycol 

 dimethyl ether is not expected to undergo hydrolysis in the environment 

 due to the lack of functional groups that hydrolyze under environmental 

 conditions(2). Diethylene glycol dimethyl ether does not contain 

 chromophores that absorb at wavelengths > 290 nm and therefore is not 

 expected to be susceptible to direct photolysis by sunlight(3). [(1) 

 Atkinson R; J Phys Chem Ref Data. Monograph No. 1 (1989) (2) Lyman WJ et 

 al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer 

 Chem Soc pp. 7-4, 7-5, 8-12 (1990) (3) Silverstein RM, Bassler GC; 

 Spectrometric Id Org Cmpd NY: J Wiley & Sons Inc p. 148-69 (1963)] 

 **PEER REVIEWED** 

ENVIRONMENTAL BIOCONCENTRATION: 

 An estimated BCF of 3 was calculated in fish for diethylene glycol 

 dimethyl ether(SRC), using a log Kow of -0.36(1) and a regression-derived 

 equation(2). According to a classification scheme(3), this BCF suggests 

 the potential for bioconcentration in aquatic organisms is low(SRC). [(1) 

 Hansch C et al; Exploring QSAR. Hydrophobic, Electronic, and Steric 

 Constants. ACS Prof Ref Book. Heller SR, consult. ed., Washington, DC: 

 Amer Chem Soc p. 299 (1995) (2) Meylan WM et al; Environ Toxicol Chem 18: 

 664-72 (1999) (3) Franke C et al; Chemosphere 29: 1501-14 (1994)] **PEER 

 REVIEWED** 

SOIL ADSORPTION/MOBILITY: 

 The Koc of diethylene glycol dimethyl ether is estimated as 15(SRC), using 

 a log Kow of -0.36(1) and a regression-derived equation(2). According to a 

 classification scheme(3), this estimated Koc value suggests that 

 diethylene glycol dimethyl ether is expected to have very high mobility in 

 soil. [(1) Hansch C et al; Exploring QSAR. Hydrophobic, Electronic, and 

 Steric Constants. ACS Prof Ref Book. Heller SR, consult. ed., Washington, 

 DC: Amer Chem Soc p. 299 (1995) (2) Lyman WJ et al; Handbook of Chemical 

 Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 4-9 (1990) 

 (3) Swann RL et al; Res Rev 85: 17-28 (1983)] **PEER REVIEWED** 

VOLATILIZATION FROM WATER/SOIL: 

 The Henry's Law constant for diethylene glycol dimethyl ether is estimated 

 as 5.2X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 2.96 mm 

 Hg(1), and assigned value for water solubility of 1X10+6 mg/L 

 (miscible)(2). This Henry's Law constant indicates that diethylene glycol 

 dimethyl ether is expected to be essentially nonvolatile from water 

 surfaces(3). Diethylene glycol dimethyl ether's estimated Henry's Law 

 constant indicates that volatilization from moist soil surfaces is not 

 expected to occur(SRC). The potential for volatilization of diethylene 

 glycol dimethyl ether from dry soil surfaces may exist(SRC) based upon its 

 vapor pressure(1). [(1) Daubert TE, Danner RP; Data Compilation, Tables of 

 Properties of Pure Compounds. NY, NY: Design Inst for Phys Prop Data, Am 

 Inst for Phys Prop Data (1989) (2) Riddick JA et al; Organic Solvents NY: 

 John Wiley & Sons Inc (1984) (3) Lyman WJ et al; Handbook of Chemical 

 Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 

 15-29 (1990)] **PEER REVIEWED** 
ENVIRONMENTAL WATER CONCENTRATIONS: 

 DRINKING WATER: Diethylene glycol dimethyl ether was listed as a 

 contaminant found in drinking water(1). [(1) Kool HJ et al; Crit Rev Env 

 Control 12: 307-57 (1982)] **PEER REVIEWED** 

EFFLUENT CONCENTRATIONS: 

 Diethylene glycol dimethyl ether was found at concentrations of 400 mg/L 

 in activated sludge from the waste treatment facility of the industry 

 producing the chemical(1). [(1) Roy D et al; J Environ Sci Health Part A 

 29: 129-47 (1994)] **PEER REVIEWED** 

 Diethylene glycol dimethyl ether in diluted vehicle exhaust from a 

 light-duty truck using different fuel types(1). Testing Phase diesel + 

 diethylene glycol diethyl ether diesel diesel + diethylene glycol dimethyl 

 ether diesel + 2-ethylhexyl nitrate Cold start Not detected Not detected 

 66 ug/cu m 17 ug/cu m Hot start Not detected Not detected 74 ug/cu m 15 

 ug/cu m [(1) Cao X-L, Zhu J; Chemosphere 45: 911-7 (2001)] **PEER 

 REVIEWED** 

ENVIRONMENTAL STANDARDS & REGULATIONS: 

TSCA REQUIREMENTS: 

 Section 8(a) of TSCA requires manufacturers of this chemical substance to 

 report preliminary assessment information concerned with production, 

 exposure, and use to EPA as cited in the preamble in 51 FR 41329. [40 CFR 

 712.30; U.S. National Archives and Records Administration's Electronic 

 Code of Federal Regulations. Available from, as of March 1, 2007: 

 http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

 Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and 

 Safety Data Reporting Rule. The section 8(d) model rule requires 

 manufacturers, importers, and processors of listed chemical substances and 

 mixtures to submit to EPA copies and lists of unpublished health and 

 safety studies. Diethylene glycol dimethyl ether is included on this list. 

 [40 CFR 716.120; U.S. National Archives and Records Administration's 

 Electronic Code of Federal Regulations. Available from, as of March 1, 

 2007: http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

ATMOSPHERIC STANDARDS: 

 This action promulgates standards of performance for equipment leaks of 

 Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical 

 Manufacturing Industry (SOCMI). The intended effect of these standards is 

 to require all newly constructed, modified, and reconstructed SOCMI 

 process units to use the best demonstrated system of continuous emission 

 reduction for equipment leaks of VOC, considering costs, non air quality 

 health and environmental impact and energy requirements. Diethylene glycol 

 dimethyl ether is produced, as an intermediate or final product, by 

 process units covered under this subpart. [40 CFR 60.489; U.S. National 

 Archives and Records Administration's Electronic Code of Federal 

 Regulations. Available from, as of March 1, 2007: 

 http://www.gpoaccess.gov/ecfr ] **PEER REVIEWED** 

CHEMICAL/PHYSICAL PROPERTIES: 

MOLECULAR FORMULA: 

 C6-H14-O3 [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th 

 Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] **PEER 
 REVIEWED** 

MOLECULAR WEIGHT: 

 134.17 [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of 

 Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: 

 Merck and Co., Inc., 2001., p. 557] **PEER REVIEWED** 

COLOR/FORM: 

 Colorless liquid [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 

 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] 

 **PEER REVIEWED** 

ODOR: 

 Mild odor [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th 

 Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] **PEER 

 REVIEWED** 

BOILING POINT: 

 162 deg c at 760 mm Hg; 116 deg C at 200 mm Hg; 75 deg c at 35 mm Hg; 20 

 dg C at 3 mm Hg [O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of 

 Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: 

 Merck and Co., Inc., 2001., p. 557] **PEER REVIEWED** 

MELTING POINT: 

 -68 deg C [Lide, D.R., G.W.A. Milne (eds.). Handbook of Data on Organic 

 Compounds. Volume I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V3: 

 2648] **PEER REVIEWED** 

DENSITY/SPECIFIC GRAVITY: 

 Sp gr: 0.9451 at 20 deg C/20 deg C [O'Neil, M.J. (ed.). The Merck Index - 

 An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, 

 Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 557] **PEER 

 REVIEWED** 

OCTANOL/WATER PARTITION COEFFICIENT: 

 log Kow = -0.36 [Hansch, C., Leo, A., D. Hoekman. Exploring QSAR - 

 Hydrophobic, Electronic, and Steric Constants. Washington, DC: American 

 Chemical Society., 1995., p. 25] **PEER REVIEWED** 

SOLUBILITIES: 

 Miscible with alcohol, ether, hydrocarbon solvents [O'Neil, M.J. (ed.). 

 The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 

 13th Edition, Whitehouse Station, NJ: Merck and Co., Inc., 2001., p. 

 557] **PEER REVIEWED** 

 Soluble in benzene [Lide, D.R. CRC Handbook of Chemistry and Physics 86TH 

 Edition 2005-2006. CRC Press, Taylor & Francis, Boca Raton, FL 2005, 

 p. 3-168] **PEER REVIEWED** 

 In water, miscible [Riddick, J.A., W.B. Bunger, Sakano T.K. Techniques of 

 Chemistry 4th ed., Volume II. Organic Solvents. New York, NY: John Wiley 

 and Sons., 1985., p. 299] **PEER REVIEWED** 

SPECTRAL PROPERTIES: 

 Index of refraction: 1.4097 at 20 deg C/D [Lide, D.R., G.W.A. Milne 

 (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd ed. CRC 

 Press, Inc. Boca Raton ,FL. 1994., p. V3: 2648] **PEER REVIEWED** 
 IR: 18544 (Sadtler Research Laboratories IR Grating Collection) [Lide, 

 D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume 

 I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V3: 2648] **PEER 

 REVIEWED** 

 NMR: 9286 (Sadtler Research Laboratories Spectral Collection) [Lide, D.R., 

 G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume I. 3rd 

 ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V3: 2648] **PEER REVIEWED** 

 MASS: 61161 (NIST/EPA/MSDC Mass Spectral database, 1990 version) [Lide, 

 D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume 

 I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V3: 2648] **PEER 

 REVIEWED** 

 Raman: 259 (Sadtler Research Laboratories spectral collecction) [Lide, 

 D.R., G.W.A. Milne (eds.). Handbook of Data on Organic Compounds. Volume 

 I. 3rd ed. CRC Press, Inc. Boca Raton ,FL. 1994., p. V3: 2648] **PEER 

 REVIEWED** 

VAPOR PRESSURE: 

 2.96 mm Hg at 25 deg C (est) [Daubert, T.E., R.P. Danner. Physical and 

 Thermodynamic Properties of Pure Chemicals Data Compilation. Washington, 

 D.C.: Taylor and Francis, 1989.] **PEER REVIEWED** 

VISCOSITY: 

 1.089 cP at 20 deg C [Lewis, R.J. Sr.; Hawley's Condensed Chemical 

 Dictionary 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., 

 p. 373] **PEER REVIEWED** 

OTHER CHEMICAL/PHYSICAL PROPERTIES: 

 Diethylene glycol dimethyl ether dissolves vinyl chloride copolymers, 

 postchlorinated poly (vinyl chloride), polymethacrylate, polystyrene, 

 polychloroprene, and cellulose acetate. It does not dissolve rubber and 

 polyethylene, and swells poly(vinyl chloride). It also dissolves sodium 

 borohydride, other covalent inroganic metal compounds, and sodium. 

 [Gerhartz, W. (exec ed.). Ullmann's Encyclopedia of Industrial Chemistry. 

 5th ed.Vol A1: Deerfield Beach, FL: VCH Publishers, 1985 to Present., p. 

 VA24: 498 (1997)] **PEER REVIEWED** 

 Henry's Law constant = 5.23X10-7 atm-cu m/mol at 25 deg C (est) [SRC; The 

 Physical Properties Database (PHYSPROP). Syracuse, NY: Syracuse Res Corp. 

 Available from, as of Dec 15, 2006: http://www.syrres.com/esc/physprop.htm 

 ] **PEER REVIEWED** 

 Hydroxyl radical reaction rate constant = 1.75X10-11 cu cm/molec-sec at 25 

 deg C [Atkinson R; J Phys Chem Ref Data Monograph No. 1 (1989)] **PEER 

 REVIEWED** 

CHEMICAL SAFETY & HANDLING: 

FIRE POTENTIAL: 

 Combustible [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th 

 Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] **PEER 

 REVIEWED** 

NFPA HAZARD CLASSIFICATION: 
 Health: 1.1= Materials that, on exposure, would cause significant 

 irritation, but only minor residual injury, including those requiring the 

 use of an approved air-purifying respirator. These materials are only 

 slightly hazardous to health and only breathing protection is needed. 

 [Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 

 Fire Protection Association, 2002., p. 325-44] **PEER REVIEWED** 

 Flammability: 2. 2= This degree includes materials that must be moderately 

 heated before ignition will occur and includes Class II and IIIA 

 combustible liquids and solids and semi-solids that readily give off 

 ignitible vapors. Water spray may be used to extinguish fires in these 

 materials because the materials can be cooled below their flash points. 

 [Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: National 

 Fire Protection Association, 2002., p. 325-44] **PEER REVIEWED** 

 Reactivity: 1. 1= This degree includes materials that are normally stable, 

 but that may become unstable at elevated temperatures and pressures and 

 materials that will react with water with some release of energy, but not 

 violently. Fires involving these materials should be approached with 

 caution. [Fire Protection Guide to Hazardous Materials. 13 ed. Quincy, MA: 

 National Fire Protection Association, 2002., p. 325-44] **PEER REVIEWED** 

FLASH POINT: 

 153 DEG F (67 DEG C) (CLOSED CUP) [Fire Protection Guide to Hazardous 

 Materials. 13 ed. Quincy, MA: National Fire Protection Association, 2002., 

 p. 325-44] **PEER REVIEWED** 

EXPLOSIVE LIMITS & POTENTIAL: 

 Presence of carbon dioxide in solutions of the hydride in dimethyl or 

 bis(2-methoxyethyl)ether can cause a violent decomposition on warming the 

 residue from evaporation. Presence of aluminum chloride tends to increase 

 the vigour of decomposition to explosion. [Bretherick, L. Handbook of 

 Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 

 1990, p. 40] **PEER REVIEWED** 

HAZARDOUS REACTIVITIES & INCOMPATIBILITIES: 

 Glycol ethers, glycols, ketones, and alcohols undergo violent 

 decomposition in contact with 68-72% perchloric acid [Fire Protection 

 Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection 

 Association, 2002., p. 491-142] **PEER REVIEWED** 

 Light, heat and oxygen (air) promote formation of potentially explosive 

 peroxides. These may be removed by stirring with a suspension of iron 

 oxide in aqueous alkali. [Bretherick, L. Handbook of Reactive Chemical 

 Hazards. 4th ed. Boston, MA: Butterworth-Heinemann Ltd., 1990, p. 662] 

 **PEER REVIEWED** 

 Presence of carbon dioxide in solutions of the hydride in dimethyl or 

 bis(2-methoxyethyl) ether can cause a violent decomposition on warming the 

 residue from evaporation. Presence of aluminium chloride tends to increase 

 the vigour of decomposition to explosion. Lithium tetrahydroaluminate may 

 behave similarly, but is generally more stable. [Bretherick, L. Handbook 

 of Reactive Chemical Hazards. 4th ed. Boston, MA: Butterworth-Heinemann 

 Ltd., 1990, p. 40] **PEER REVIEWED** 

 The peroxide-free ether, being dried by distillation at 162 DEG C under 

 inert atmosphere at ambient pressure, exploded violently when the heating 
 bath temperature had been raised to 200 DEG C towards the end of 

 distillation. This was attributed to local overheating of an insulating 

 crust of hydride in contact with oxygen-containing organic material. 

 [Bretherick, L. Handbook of Reactive Chemical Hazards. 4th ed. Boston, MA: 

 Butterworth-Heinemann Ltd., 1990, p. 43] **PEER REVIEWED** 

 Glycol ethers, glycols, ketones, and alcohols undergo violent 

 decomposition in contact with 68-72% perchloric acid [Fire Protection 

 Guide to Hazardous Materials. 13 ed. Quincy, MA: National Fire Protection 

 Association, 2002., p. 491-142] **PEER REVIEWED** 

HAZARDOUS DECOMPOSITION: 

 When heated to decomposition it emits toxic fumes of /nitrogen oxides/. 

 [Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 

 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 

 2004., p. 507] **PEER REVIEWED** 

DISPOSAL METHODS: 

 SRP: The most favorable course of action is to use an alternative chemical 

 product with less inherent propensity for occupational exposure or 

 environmental contamination. Recycle any unused portion of the material 

 for its approved use or return it to the manufacturer or supplier. 

 Ultimate disposal of the chemical must consider: the material's impact on 

 air quality; potential migration in soil or water; effects on animal, 

 aquatic, and plant life; and conformance with environmental and public 

 health regulations. **PEER REVIEWED** 

OCCUPATIONAL EXPOSURE STANDARDS: 

NIOSH RECOMMENDATIONS: 

 NIOSH recommends reducing exposure to lowest feasible concn & 

 preventing contact with the skin. /Glycol ethers/ [NIOSH/CDC. NIOSH 

 Recommendations for Occupational Safety and Health Standards 1988, Aug. 

 1988. (Suppl. to Morbidity and Mortality Wkly. Vol. 37 No. 5-7, Aug. 26, 

 1988). Atlanta, GA: National Institute for Occupational Safety and Health, 

 CDC, 1988., p. 16] **PEER REVIEWED** 

MANUFACTURING/USE INFORMATION: 

MAJOR USES: 

 Solvent; reaction medium for Grignard and similar syntheses. [O'Neil, M.J. 

 (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and 

 Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006.., p. 

 537] **PEER REVIEWED** 

 Diethylene glycol dimethyl ether is used as a solvent in chemical 

 reactions involving metals and organometallic compounds. [Gerhartz, W. 

 (exec ed.). Ullmann's Encyclopedia of Industrial Chemistry. 5th ed.Vol A1: 

 Deerfield Beach, FL: VCH Publishers, 1985 to Present., p. VA24 498] **PEER 

 REVIEWED** 

 Solubilizer [Ashford, R.D. Ashford's Dictionary of Industrial Chemicals. 

 London, England: Wavelength Publications Ltd., 1994., p. 301] **PEER 
 REVIEWED** 

 Used in production of plastics. [Sheftel, V.O.; Indirect Food Additives 

 and Polymers. Migration and Toxicology. Lewis Publishers, Boca Raton, FL. 

 2000., p. 671] **PEER REVIEWED** 

MANUFACTURERS: 

 Arch Chemicals, Inc., 501 Merritt 7, P.O. Box 5204, Norwalk, CT 

 06856-5204, (203) 229-2900; Performance Products; Production site: 

 Brandenburg, KY 40108 /Glycol ethers/ [SRI Consulting. 2006 Directory of 

 Chemical Producers-United States. Menlo Park, CA. 2006, p. 657] **PEER 

 REVIEWED** 

 The Dow Chemical Co., 2030 Dow Center, Midland, MI 48642, (989) 636-1000; 

 Production sites: Midland, MI 48667; Plaquemine, LA 70764; Seadrift, TX 

 77983; Taft, LA 70057 /Glycol ethers/ [SRI Consulting. 2006 Directory of 

 Chemical Producers-United States. Menlo Park, CA. 2006, p. 657] **PEER 

 REVIEWED** 

 Eastman Chemical Co., P.O. Box 511, Kingsport, TN 37662, (423) 229-2000; 

 Eastman Div., Eastman Rd., Kingsport, TN; Production site: Longview, TX 

 75607 /Glycol ethers/ [SRI Consulting. 2006 Directory of Chemical 

 Producers-United States. Menlo Park, CA. 2006, p. 657] **PEER REVIEWED** 

 Equistar Chemicals, LP, /subsidiary of Lyondell Chemical Co.,/ One Houston 

 Center, 1221 McKinney St., Suite 700, Houston, TX 77010, (713) 652-7200; 

 Production site: Bayport, TX 77507 /Glycol ethers/ [SRI Consulting. 2006 

 Directory of Chemical Producers-United States. Menlo Park, CA. 2006, p. 

 657] **PEER REVIEWED** 

 Lyondell Chemical Co., 1221 McKinney St., Suite 700, Houston, TX 77010, 

 (713) 652-7200; Production site: Bayport, TX /Glycol ethers, propylene 

 glycol monoethers only/ [SRI Consulting. 2006 Directory of Chemical 

 Producers-United States. Menlo Park, CA. 2006, p. 657] **PEER REVIEWED** 

 Shell Chemical Co., One Shell Plaza, P.O. Box 2463, Houston, TX 

 77252-2463, (713) 241-6161; Production site: Geismar, LA 70734 /Glycol 

 ethers; plant is currently idle/ [SRI Consulting. 2006 Directory of 

 Chemical Producers-United States. Menlo Park, CA. 2006, p. 657] **PEER 

 REVIEWED** 

METHODS OF MANUFACTURING: 

 Ethylene glycol ethers are produced by reacting ethylene oxide with 

 alcohols in the presence of either acidic or basic catalysts. Temperature, 

 pressure, mole ratios of reactants, and catalysts are chosen to yield the 

 desired product mix. [CHEMICAL PRODUCTS SYNOPSIS: Glycol Ethers, 1983] 

 **PEER REVIEWED** 

 Diethylene glycol + dimethyl sulfate (ether formation) [Ashford, R.D. 

 Ashford's Dictionary of Industrial Chemicals. London, England: Wavelength 

 Publications Ltd., 1994., p. 301] **PEER REVIEWED** 

 Ethylene glycol monoethers are usually produced by reaction of ethylene 

 oxide with the appropriate alcohol. A mixture of homologues is obtained 

 ... The glycol monoethers can be converted to diethers by alkylation with 

 common alkylating agents, such as dimethyl sulfate or alkyl halides ( 

 Williamson synthesis). Glycol dimethyl ethers are formed by treatment of 
 dimethyl ether with ethylene oxide. /Ethers/ [Ullmann's Encyclopedia of 

 Industrial Chemistry. 6th ed.Vol 1: Federal Republic of Germany: Wiley-VCH 

 Verlag GmbH & Co. 2003 to Present, p. V12 601 (2003)] **PEER 

 REVIEWED** 

GENERAL MANUFACTURING INFORMATION: 

 Diglyme can be effectively used as an odor-attractant solvent without 

 reducing the attractiveness of the chemical additive, eg, decanoic acid, 

 trimethylammonium decanoate, and trimethylamine. Odorants dissolved in 

 diglyme can be added to aqueous solutions, such as coyote urine. Also, 

 diglyme has a low freezing point so its use as an odor solvent increases 

 the temperature range in which an odor can be effectively used. [Scrivner 

 JH et al; J Wildl Manage 49 (2): 519-21 (1985)] **PEER REVIEWED** 

FORMULATIONS/PREPARATIONS: 

 Grade: Technical [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 

 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] 

 **PEER REVIEWED** 

U. S. PRODUCTION: 

 (1972) PROBABLY GREATER THAN 4.54X10+5 GRAMS **PEER REVIEWED** 

 (1975) PROBABLY GREATER THAN 4.54X10+5 GRAMS **PEER REVIEWED** 

 (1982) 4.72X10+10 g /Diethylene glycol ethers/ [CHEMICAL PRODUCTS 

 SYNOPSIS: Glycol Ethers, 1983] **PEER REVIEWED** 

 (2006) 1,612 million lb annual capacity /Glycol ethers/ [SRI Consulting. 

 2006 Directory of Chemical Producers-United States. Menlo Park, CA. 2006, 

 p. 657] **PEER REVIEWED** 

 Production volumes for non-confidential chemicals reported under the 

 Inventory Update Rule. Year Production Range (pounds) 1986 >1 million - 10 

 million 1990 >1 million - 10 million 1994 >1 million - 10 million 1998 >1 

 million - 10 million 2002 >1 million - 10 million [US EPA; 

 Non-confidential Production Volume Information Submitted by Companies for 

 Chemicals Under the 1986-2002 Inventory Update Rule (IUR). Ethane, 

 1,1'-oxybis[2-methoxy- (111-96-6). Available from, as of March 6, 2007: 

 http://www.epa.gov/oppt/iur/tools/data/2002-vol.htm ] **PEER REVIEWED** 

 This chemical is listed as a High Production Volume (HPV) (65FR81686). 

 Chemicals listed as HPV were produced in or imported into the U.S. in 

 > 1 million pounds in 1990 and/or 1994. The HPV list is based on the 

 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438). 

 [EPA/Office of Pollution Prevention and Toxics; High Production Volume 

 (HPV) Challenge Program. Available from, as of March 6, 2007: 

 http://www.epa.gov/hpv/pubs/general/opptsrch.htm ] **PEER REVIEWED** 

U. S. IMPORTS: 

 (1984) 9.43X10+9 g /Diethylene glycol esters, ethers, etc/ [BUREAU OF THE 

 CENSUS. U.S. IMPORTS FOR CONSUMPTION AND GENERAL IMPORTS 1984 p.361] 

 **PEER REVIEWED** 

LABORATORY METHODS: 
ANALYTIC LABORATORY METHODS: 

 Gas chromatography is likely to be the analytical method for final 

 analysis. Infrared absorption is sometimes used. /Glycol ethers/ [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. 3910] **PEER REVIEWED** 

SAMPLING PROCEDURES: 

 In instances where materials are very soluble in water, samples of air can 

 be taken effectively by scrubbing through water. /Glycol ethers/ [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. 3910] **PEER REVIEWED** 

SPECIAL REFERENCES: 

SPECIAL REPORTS: 

 Hardin BD, Lyon JP; Environmental Health Perspectives 57: 273-5 (1984). 

 Proceedings from a NIOSH symposium on the toxic effects of glycol ethers 

 are reviewed. 

 European Chemicals Bureau; IUCLID Dataset, bis (2-methoxyethyl) ether (CAS 

 # 111-96-6) p.28-9. Available from the Database Query page at: 

 http://ecb.jrc.it/esis/esis.php as of February 7, 2007. 

 EPA/Office of Pollution Prevention and Toxics; High Production Volume 

 (HPV) Challenge Program's Robust Summaries and Test Plans. Available 

 from the Database Query page at: http://www.epa.gov/hpv/pubs/hpvrstp.htm 

 on Diglyme as of February 7, 2007 

 International Programme on Chemical Safety; Concise International Chemical 

 Assessment Document Number 41: Diethylene Glycol Dimethyl Ether (2002). 

 Available from the Database Query page at: 

 http://www.inchem.org/pages/cicads.html as of February 20, 2007. 

SYNONYMS AND IDENTIFIERS: 

RELATED HSDB RECORDS: 

 97 [2-METHOXYETHANOL] (metabolite) 

SYNONYMS: 

 BIS(2-METHOXYETHYL) ETHER [O'Neil, M.J. (ed.). The Merck Index - An 

 Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, 

 NJ: Merck and Co., Inc., 2006.., p. 537] **PEER REVIEWED** 

 DIGLYCOL METHYL ETHER [Lewis, R.J. Sr.; Hawley's Condensed Chemical 

 Dictionary 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., 

 p. 373] **PEER REVIEWED** 

 DIGLYME [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 14th 

 Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] **PEER 

 REVIEWED** 

 DIMETHYL CARBITOL **PEER REVIEWED** 

 ETHANE, 1,1'-OXYBIS(2-METHOXY- [Bingham, E.; Cohrssen, B.; Powell, C.H.; 

 Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, 
 N.Y. (2001)., p. V7 210] **PEER REVIEWED** 

 ETHANOL, 2,2'-OXYBIS-, DIMETHYL ETHER **PEER REVIEWED** 

 ETHER, BIS(2-METHOXYETHYL) **PEER REVIEWED** 

 GLYME-2 **PEER REVIEWED** 

 2-(2-METHOXYETHOXY)-1-METHOXYETHANE **PEER REVIEWED** 

 (2-METHOXYETHYL) ETHER **PEER REVIEWED** 

 POLY-SOLV **PEER REVIEWED** 

 2,5,8-TRIOXANONANE [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's 

 Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. 

 (2001)., p. V7 210] **PEER REVIEWED** 

 DIMETHYLDIGLYCOL [Verschueren, K. Handbook of Environmental Data on 

 Organic Chemicals. Volumes 1-2. 4th ed. John Wiley & Sons. New York, 

 NY. 2001, p. 844] **PEER REVIEWED** 

 DIMETHOXYDIETHYLENEGLYCOL [Verschueren, K. Handbook of Environmental Data 

 on Organic Chemicals. Volumes 1-2. 4th ed. John Wiley & Sons. New 

 York, NY. 2001, p. 844] **PEER REVIEWED** 

 DYME [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 

 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V7 210] 

 **PEER REVIEWED** 

 DGdiME [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology 

 Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V7 

 210] **PEER REVIEWED** 

 DIETHYL GLYCOL DIMETHYL ETHER [Lewis, R.J. Sr. (ed) Sax's Dangerous 

 Properties of Industrial Materials. 11th Edition. Wiley-Interscience, 

 Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 507] **PEER REVIEWED** 

FORMULATIONS/PREPARATIONS: 

 Grade: Technical [Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 

 14th Edition. John Wiley & Sons, Inc. New York, NY 2001., p. 373] 

 **PEER REVIEWED** 

ADMINISTRATIVE INFORMATION: 

HAZARDOUS SUBSTANCES DATABANK NUMBER: 72 

LAST REVISION DATE: 20071011 

LAST REVIEW DATE: Reviewed by SRP on 5/14/2007 

UPDATE HISTORY: 

 Complete Update on 2007-10-11, 44 fields added/edited/deleted 

 Complete Update on 03/05/2003, 2 fields added/edited/deleted. 

 Field Update on 02/14/2003, 1 field added/edited/deleted. 

 Field Update on 11/08/2002, 1 field added/edited/deleted. 

 Complete Update on 05/13/2002, 1 field added/edited/deleted. 

 Complete Update on 02/13/2002, 1 field added/edited/deleted. 

 Complete Update on 01/18/2002, 3 fields added/edited/deleted. 

 Field Update on 01/14/2002, 1 field added/edited/deleted. 
 Complete Update on 08/09/2001, 1 field added/edited/deleted. 

 Complete Update on 05/16/2001, 1 field added/edited/deleted. 

 Complete Update on 03/28/2000, 1 field added/edited/deleted. 

 Complete Update on 02/08/2000, 1 field added/edited/deleted. 

 Complete Update on 02/02/2000, 1 field added/edited/deleted. 

 Complete Update on 11/18/1999, 1 field added/edited/deleted. 

 Complete Update on 09/21/1999, 1 field added/edited/deleted. 

 Complete Update on 08/26/1999, 1 field added/edited/deleted. 

 Complete Update on 03/19/1999, 1 field added/edited/deleted. 

 Complete Update on 09/11/1998, 1 field added/edited/deleted. 

 Complete Update on 06/02/1998, 1 field added/edited/deleted. 

 Complete Update on 02/25/1998, 1 field added/edited/deleted. 

 Complete Update on 10/17/1997, 1 field added/edited/deleted. 

 Complete Update on 09/17/1997, 1 field added/edited/deleted. 

 Complete Update on 05/08/1997, 1 field added/edited/deleted. 

 Complete Update on 03/27/1997, 1 field added/edited/deleted. 

 Complete Update on 01/24/1997, 1 field added/edited/deleted. 

 Complete Update on 12/12/1996, 33 fields added/edited/deleted. 

 Field Update on 10/12/1996, 1 field added/edited/deleted. 

 Complete Update on 01/18/1996, 1 field added/edited/deleted. 

 Complete Update on 12/19/1994, 1 field added/edited/deleted. 

 Complete Update on 03/25/1994, 1 field added/edited/deleted. 

 Field update on 12/10/1992, 1 field added/edited/deleted. 

 Complete Update on 11/06/1991, 44 fields added/edited/deleted. 

 Complete Update on 05/07/1991, 41 fields added/edited/deleted. 

 Complete Update on 04/16/1990, 1 field added/edited/deleted. 

 Field update on 03/06/1990, 1 field added/edited/deleted. 

 Complete Update on 05/26/1987, 25 fields added/edited/deleted. 

 Created 19830401 by SYS