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Toxicity Summary for Dimethyl Ether (DME); HP DME Propellant

Technical Information
Dimethyl ether has a low order of toxicity on both an acute

A lifetime inhalation toxicity and carcinogenicity bioassay7

and chronic basis. Although an ACGIH TLV® has not been

was completed at DuPont’s Haskell Laboratory. In theestablished for DME, a value of 1,000 ppm (v/v; 8-hr TWA)

lifetime inhalation study in rats, DME produced slight

seems appropriate based on its low toxicity potential.

hemolytic (blood) effects at 25,000 ppm (2.5% DME) andChemours has established a 1,000 ppm Acceptable

was negative for carcinogenicity. The no-observable-Exposure Limit (AEL) for its workplace environment.

adverse-effect-level (NOAEL) for this lifetime inhalation

The main physiological action of DME is that of “weakanesthesia” at high inhaled levels. Its 4-hour LC50 for rats
is 164,000 ppm1. DME can also, in gross misuse
situations, sensitize the heart to the body’s own adrenaline,

study was 2000 ppm (0.2% DME) and based on anincrease in body weight and decrease in survival in malerats exposed at 10,000 and 25,000 ppm, and on the blood
effects seen at the 25,000 ppm exposure level.

similar to the action mental screening studies using dogs

In a study8 to evaluate developmental toxicity, pregnant

and simulating stress with a large injected dose ofrats were exposed to DME at 0, 1,250, 5,000, 20,000, oradrenaline; cardiac sensitization was observed only at

40,000 ppm on days 6-15 of gestation. There was slightinhaled concentrations of 200,000 ppm and higher .

evidence of both maternal and fetal toxicity at the two

2

The toxicity of DME on a repeated exposure basis is also
very low. In a 10-day (6 hours/day, 5 days/week) inhalation
study3, rats showed a decrease in body weight gain andslight evidence of anesthesia, but no histopathologic

highest levels. However, no evidence of teratogenicity wasseen at any test level. A similar investigation9 in another rat
strain at exposure levels ≤28,000 ppm DME also showedno evidence of teratogenic potential.

evidence of tissue damage at 50,000 ppm; no significant

DME has also been tested for genotoxic activity inadverse effects occurred at 10,000 ppm. In a four-week

in vitro bacterial assays.1 It was not mutagenic in several

study and in a 90-day study , rats showed no gross,

S. typhimurium strains with or without metabolic activation.

clinical, or histopathologic evidence of toxicity at exposure

In pharmacokinetic investigations10, 11 in animals andlevels ≤10,000 ppm and ≤20,000 ppm, respectively. Otherhumans, DME has shown no evidence of accumulation in

investigators exposed rats for 6 hours/day, 5 days/week fortissues and appears to have a very short biological half-life.

4530 weeks at 0, 200, 2,000, or 20,000 ppm DME. Except
for a slight liver weight decrease and slight serum SGPT
increase at 20,000 ppm, there were not adverse effects
attributable to exposure at any test level.

In conclusion, on the basis of animal toxicity studies andhuman experience to date, DME appears to have a very low
degree of reactivity in biological systems. An 8-hour
exposure limit of 1,000 ppm (v/v) in the workplace shouldpose no special hazard.

References1.

Unpublished DuPont Haskell Laboratory Data, 1979.

2.

Reinhardt, C. F., et al. Arch Environ. Hlth. 22: 265-279,1971.

3.

Unpublished DuPont Haskell Laboratory Data, 1980.

4.

Unpublished Data. CIVO Institute (TNO). Zeist,Netherlands,1980.

5.

Reuzel, P. G. J., et al. Aerosol Rep. 20 (1): 23-28, 1981.

6.

Collins, C. J., et al. Toxicology 11 (1): 65-71, 1978.

7.

Unpublished DuPont Haskell Laboratory Data, 1986.

8.

Unpublished DuPont Haskell Laboratory Data, 1981.

9.

Keoter, H. B., et al. Unpublished Data CIVO Institute(TNC). Zeist, Netherlands, 1981.

10. Bohnenn, L. J. M. Aerosol Rep. 18(12): 413-421, 1979.
11. Eckerd, R., et al. Arch. Pharmacol., 307 (Suppl.), R19,1979.
12. Daly, Jr., J. J. and Kennedy, Jr., G. L. Chemical Times &Trends: 40-44, 54, January 1987.

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Replaces: H-04236
C-10917 (7/16)