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Administrative data

Description of key information

Magnesium methanolate rapidly hydrolyzes in aqueous environments. Toxicity is mediated by its degradation products MeOH and Mg(OH)2 and assessed for these products.


Oral: LOAEL subacute = 2340 mg/kg/bw in monkeys (mortality 7/7 after 3 d exposure)

Inhalation: NOAEC chronic = 0.013 mg/L air in monkeys (7 to 29 months exposure)


In the key study, a parental, reproduction and developmental NOAEL of at least 1000 mg/kg/day was determined. Based on the low toxicity revealed with this test, no further testing for toxicity with other routes of exposure is justified.

Key value for chemical safety assessment

Additional information


Animal data


Seven male monkeys received daily doses of 2340 mg/kg bw methanol as 30% aqueous solution by oral gavage for three days. Under the test conditions, this dosage was lethal for all seven animals (Rao et al., 1977).


In a whole-body inhalation study in monkeys exposed to 0.013, 0.13, and 1.3 mg/L for 21 hours/day, 7 days/week for 7, 19, and 29 months, several general clinical signs as well as degenerative effects in the brain (at 0.13 and 1.3 mg/L), slight peripheral nerve damage (at 0.13 and 1.3 mg/L), very slight degeneration of the optic nerve (concentrations not noted), increased fat granules and slight fibrosis in the liver (all concentrations) as well as Sudan positive granules in the kidney were observed (at 0.13 and 1.3 mg/L). Also, a slight myocardial disorder (at 0.13 and 1.3 mg/L) and localized effects in the trachea and possible slight fibrosis in the lungs (concentrations not noted) were observed. Although the statistical significance of the effects cannot be verified from the limited study report, the effects observed appear to be associated with methanol (NEDO, 1987).

In a short-time experiment, monkeys were exposed up to 20 days for 21 hours per day to methanol vapour. Coma and lethality were observed at concentrations > 9.31 mg/(L*d). In the brain, necrosis of the basal ganglia and cerebral edema were observed at 6.65 mg/(L*d) and at 3.99 mg/(L*d), hyperplasia and fibrosis around myelin sheaths of the basal ganglia as well as a slight to moderate increase in astroglia cells were observed. The optic nerve showed atrophy at > 3.99 mg/(L*d), along with reduction in myelin fibers. In the liver, fibrosis was observed at 6.65 mg/(L*d) and mild fatty degeneration was observed at 3.99 mg/(L*d). In the kidney, partly vacuolated hyaline degeneration was observed at 6.65 mg/(L*d) (NEDO, 1987). The liver and kidney effects were recorded at doses already overtly toxic in humans and, hence, are of low relevance.

In rats exposed to methanol up to 6.65 mg/L for 6 hours per day, five days per week for 28 days, no adverse effects were observed except local nasal irritation and increased relative spleen weights, which were observed only at the middle dose. The estimated blood level of methanol was about 250 mg/L under this condition (Andrews et al., 1987).

In a whole-body inhalation study in mice exposed for 12 months to concentrations of 0.013, 0.13, and 1.3 mg/L for 20 hours/day, slight changes in clinical signs, body and organ weights, and some changes in histopathology were observed, but these effects were considered to be toxicologically irrelevant (NEDO, 1987). In rats exposed in the same manner, slight changes in body weight and organ weights were observed at the highest dose. The NOEC was 0.13 mg/L, the NOAEC was 1.3 mg/L for rats and mice in these studies (NEDO, 1987). Again, these effects are of low relevance in the light of the onset of human toxicity already at lower doses. The species-related differences are very obvious between rodents and primates.

The latter demonstrating a 100-fold greater susceptibility for methanol-related effects due to differences in metabolism of methanol. In rodents, methanol is metabolized to carbon dioxide to a great extent, whereas in primates, formate accumulation is responsible for the observed effects.

Human data

In male and female workers exposed to methanol for 0.3 to 7.8 years, the highly exposed workers (4.7 - 7.3 mg/L) more often complained of blurred vision, headache and nasal irritation during or after work. Nobody stated to suffer from photophobia. The examination of the eye fundus failed to reveal retinal changes. Among three workers exposed to about 1.0 to 1.6 mg/L and one worker exposed to 0.12 to 3.6 mg/L, two showed retarded pupil reflex and one exhibited mild mydriasis (Kawai et al., 1991). Other common complaints were forgetfulness and skin sensitivity (IPCS/WHO, 1997).

A health hazard evaluation was conducted by the National Institute for Occupational Safety and Health (NIOSH) to determine if vapours from duplicating fluid (99% methyl alcohol) used in direct-process spirit duplicating machines were causing adverse health effects among teacher aides (Frederick et al., 1984). The teacher aides reported significantly more blurred vision, headache, dizziness, and nausea than the comparison group. Concentrations of airborne methyl alcohol ranged from 0.48 to 4.0 mg/L. Additional studies also showed that headaches were associated with occupations that involve the operation of duplicating machines (NTP, 2003; IPCS/WHO, 1997).

Repeated dose toxicity: via oral route - systemic effects (target organ) neurologic: eyes (retina, optic nerve)

Repeated dose toxicity: inhalation - systemic effects (target organ) cardiovascular / hematological: heart; digestive: liver; neurologic: brain (multiple sections)


A combined repeated dose reproductive toxicity screening study (OECD TG 422) study was performed with magnesium hydroxide to assess sub-acute oral toxicity in rats. No test substance related effects were observed at the highest dose tested, which was equal to the limit dose of 1000 mg/kg bw. In addition, 90 day oral studies in rats and mice are available with the structural analogue magnesium chloride, which showed no significant toxic effects up to dose levels of 1600 mg/kg bw of test substance for males and 1531 mg/kg bw test substance for females and 5410 mg/kg bw for males and 6810 mg/kg bw for females, respectively.


Justification for classification or non-classification

Magnesium methanolate

Magnesium methanolate rapidly hydrolyzes in aqueous environments. Toxicity is mediated by its degradation products MeOH and Mg(OH)2 and assessed for these products.

Based on the classification of MeOH, magnesium methanolate is classified as acute toxic by oral, dermal and inhalative exposure, and capable of inducing serious irreversible effects upon single exposure by the oral, dermal and inhalation route.

CLP: STOT single exposure category 1 (route of exposure: oral, inhalation)


Chronic studies in monkeys clearly demonstrate the potential of methanol to cause neurological and myocardial effects, but these studies were conducted at a much longer daily exposure time than ususal. Therefore, it is conceivable that the observed effects were more severe than in comparable studies with shorter daily exposure times, because the biologically available dose of methanol was much higher. Furthermore, the different susceptibilities of primates and rodents have to be considered.

Although there is a clear potential of methanol to cause adverse health effects especially in primates, the experimental studies in animals do not provide clear evidence for the necessity for classification.

However, methanol is classified as acute toxic by oral, dermal and inhalative exposure, and capable of inducing serious irreversible effects upon single exposure by the oral, dermal and inhalation route.

Due to the much higher sensitivity of humans to CNS- and optic nerve toxicity, the rodent studies are of little relevance to the human situation.

CLP: STOT single exposure category 1 (route of exposure: oral, inhalation)


A key oral repeated dose toxicity study on magnesium hydroxide with rats yielded a NOAEL of at least 1000 mg/kg bw/day after 28 days of exposure. According to Regulation (EC) No. 1272/2008, classification is applicable when significant toxic effects are seen to occur at 100 mg/kg bw/day or less for an oral rat study, which means that the NOAEL does not trigger classification. Therefore, it can be concluded that magnesium hydroxide should not be classified for repeated dose toxicity.