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2-Methoxyethanol (EGME)

Molecular Formula. C3H802 M=76.11
CAS No 109-86-4
RTECS No KL5775000
Abbreviations. ME, MAA (2-methoxyacetic acid).

Synonyms and Trade Names. Ethylene glycol, monomethyl ether; Methyl cellosolve; Methyl glycol; Methyl oxitol; Monomethyl ethylene glycol ether; Monomethyl glycol.

Properties. Colorless, transparent, volatile liquid with a mild non-residual odor. Soluble in water and ethanol. Does not affect transparency and color of water; does not form foam and film on the water surface. Odor perception threshold is 14.3 mg/l or <0.09 mg/1.010 According to other data, organoleptic threshold is 100 mg/l.01

Applications. ME has wide industrial and consumer applications. It is used as a solvent in the production of nitro- and acetyl cellulose, natural and artificial resins. Used in the manufacture of protective epoxy resin coatings for metals. A surfactant.

Acute Toxicity. LD50 is found to be 2.46 to 3.25 g/kg BW in male rats, 3.4 g/kg BW in female rats, 0.89 to 1.425 g/kg BW in rabbits, and 0.95 g/kg BW in guinea pigs.1,2 High doses caused anuria. Death occurred in rabbits in 2 to 4 days after poisoning.

Observations in man. ME affects hematology parameters and CNS functions.

Repeated Exposure. Gross pathology examination in rats exposed to 100 or 150 mg/kg BW for three weeks revealed reduced weights of the visceral organs, normochromic, normocytic anemia, hemorrhagic changes in the bone marrow and ovarian atrophy.3 Inflammatory changes were observed in the bladder mucosa.4

Decrease in liver weights was observed in Wistar rats administered 300 mg ME/kg BW for 20 days. The activity of cytosolic ADH was increased.5

In 2-week studies, F344 rats and B6C3F, mice received ME in their drinking water. Consumption values ranged from 100 to 400 mg/kg BW (rats) and 200 to 1300 mg/kg BW (mice). There were no effects on survival. Decrease in BW gain in rats was reported. The treatment caused thymic and testicular atrophy in males of both species.6

Short-term Toxicity. In 13-week studies, histology changes were observed in the testes, thymus, and hematopoietic tissues. There was progressive anemia, effect on the testes, spleen, and adrenal gland (in females only). The NOAEL in rats was not reached, since testicular degeneration in males and decreased thymus weights occurred at the lowest concentration administered. The NOAEL for testicular degeneration and increased hematopoiesis in the spleen was 2000 ppm in mice

Long-term Toxicity. Chronic exposure causes hemodynamic injuries and dystrophic changes in the brain, liver, kidneys, myocardium, etc. ME produced hematological disorders in both humans and experimental animas.7 Medinsky et al. believe hematotoxic effects to be due to the MAA metabolite of ME.8

Immunotoxicity. ME has been shown to be immunosuppressive in rats but not in mice, with oxidation of ME to MAA being a prerequisite for immunosuppression. Oral and dermal exposure to ME revealed the ability of the immune system to mount an effective humoral immune response.15

MAA, the main metabolite of ME, is shown to cause immunodepressive effect when administered by gavage to young adult F344 rats. Thymic involution is reported."

Repeated high dose oral exposure to MAA does not suppress humoral immunity in the mouse.9

Rats given doses greater than 100 mg ME/kg BW displayed significant thymic depression.10 Dose-related increase in natural killer cells cytotoxic activities and decrease in specific antibody production in rats were reported."

Mice, however, appeared to be insensitive to the immunosuppressive effects of ME and MAA, at the doses producing such effects in rats.12,13 House did not observe changes in the immunological functions or host resistance in B6C3F1 female mice dosed by gavage 10 times over 2 weeks with 25 to 100 mg ME or MAA per kg BW.14 Nevertheless, thymic involution was revealed at 50 to 100 mg/kg BW doses.

F344 rats were gavaged with 25 to 200 mg ME/kg BW in distilled water for 4 consecutive days. The treatment caused a reduction in thymus weights at the doses of 50 to 200 mg/kg BW, while spleen weights were reduced in rats that were dosed at 200 mg/kg BW. The lymphoproliferative responses to phytohaemagglutinin, pokeweed mitogen, and Salmonella typhimirium were increased at the 200 mg/kg BW.

Reproductive Toxicity. ME produces a dose-related embryotoxic and teratogenic effect in mice, hamsters and guinea pigs.

Embryotoxicity. ME is metabolized to the active compound MAA, which readily crosses the placenta and impairs fetal development. Pregnant mice were exposed to 100, 150, or 200 mg ME/kg BW from gestation days 10 to 17. The treatment caused a significant thymus atrophy and cellular depletion in fetal mice. ME inhibited thymocyte maturation. ME-induced immunodepression may result from targeting of multiple hematopoietic compartments.'

F344 rats were treated on days 6 to 15 of gestation by dosed feed or gavage (doses 12.5 to 100 mg/kg BW). This exposure caused only a small decrease in maternal BW gain during treatment. Litter weights and postnatal survival were decreased (100 mg/kg BW group); percentage of resorption was increased in 50 and 100 mg/kg BW dosed groups. The number of the live pups was decreased in 25 to 100 mg/kg BW dosed groups. 1'

Monkey were dosed with up to 55 mg ME/kg BW on gestation days 20 to 45. All pregnancies at the highest dose ended in death. One of the fetuses at the highest dose had a missing digit on each forelimb. The LOAEL was considered to be 12 mg/kg BW in this study.18

Teratogenicity. Time-mated CD-1 mice were orally dosed on gestation day 11 with distilled water (control) or ME at a dose of 304 mg/kg BW. There were no signs of treatment-related maternal toxicity, and intrauterine survival was unaffected by the treatments. There was no treatment-related pattern of gross external malformations other than paw defects. Paw defects were present in ME-treated litters (68.5% 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 methyl-substituted glycol ethers is proposed to be attributable to in vivo conversion to a common teratogen, methoxyacetic acid.33

Bifurcated or split cervical vertebrae were found in the offspring of female mice treated on days 7 to 14 of gestation. The LOAEL of 31 mg/kg BW was established.19 The NOAEL for induction of malformations after a single administration on gestation day 11 was 100 mg/kg BW.4

Gonadotoxicity. ME causes testicular atrophy, degenerative changes in the germinal epithelium, pathological changes in the sperm head, and infertility.20

Rats and guinea pigs received a single oral dose of 200 mg/kg BW. The treatment induced spermatocyte degeneration in 24 and 96 hours after dosing, respectively.21

ME was found to deplete the spermatocytes of rats and mice which were given a single oral dose of 0.5 to 1.5 g/kg BW. This treatment produced morphologic abnormalities in rat spermatozoa that had been exposed as spermatocytes.22

In a 5-week study, male mice were exposed to oral doses of 0.5 to 4.0 g/kg BW. Male Dutch rabbits received the doses of 12.5, 25, 37.5, or 50 mg ME/kg BW in the drinking water for 12 weeks. The treatment caused oligospermia in the highest dose groups. No notable histopathology was found. A marked disruption in spermatogenesis increased above 25 mg ME/kg BW. The NOAEL of 12.5 mg/kg BW was established in this study�

The NOAEL of 0.5 mg/kg BW for testicular atrophy was identified.24 The ineffective dose for lesions and degeneration in primary spermatocytes and spermatids in male rats dosed for 11 days appeared to be 0.05 g/kg BW.25

Mutagenicity.

In vivo cytogenetics. B6C3F1 mice received the doses of 35 to 2500 mg ME/kg BW during acute and subchronic oral exposure. The treatment did not cause induction of CA even after ME administration in cytotoxic doses.26

ME is shown to increase the rate of DLM in rats. It produced damage in mouse sperm head morphology following inhalation exposure. Equivocal results are observed in Dr. melanogaster (NTP-82).

In vitro genotoxicity. ME gave negative results in mutagenicity assays with Salmonella typhymurium strains TA 98, TA 100, and TA 102 either with or without S9 mix.27,28 At high concentrations, it induced SCE in Chinese hamster ovary cells with and without S9 fraction. 6 Methoxyacetaldehyde, a metabolite of ME, was mutagenic in a subline of Chinese hamster ovary cells.29 It displayed mutagenic potency in Salmonella typhimurium strain TA 97a with or without S9 mix at high concentrations.28

Chemobiokinetics.

Observations in man. MAA is found in the urine of 7 male volunteers exposed to 5.0 ppm ME30 but it was not found in human urine in acute poisoning cases.

Animal studies. ME is metabolized via alcohol dehydrogenase to methoxyacetaldehyde and via aldehyde dehydrogenase to MAA, which seems to be a major oxidative metabolite. The urine appears to be a major route of excretion.16'31

According to Medinsky et al., ethylene glycol, a metabolite of ME, is a result of dealkylation of the ether occurred prior to oxidation to MAA. Ethylene glycol was excreted in urine, representing approximately 21% of the dose administered.$ Biotransformation of ME has also been detected in testes from Wistar rats and one strain of mice, but not in testes from hamsters, guinea pigs, rabbits, dogs, cats, or humans. Testes from all these species readily converted the aldehyde metabolite of ME to MAA

ME is removed mainly in the urine, it does not accumulate in the testes Excretion also occurs via exhalation as CO2. Less than 5.0% ME was exhaled unchanged.

Ethylene Glycol Monomethyl Ether (EGME)
 

 

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