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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

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Toxicological information

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Description of key information

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - dermal (%):
Absorption rate - inhalation (%):

Additional information

Oral absorption

Toxicokinetic behavior of monopropylene glycol and its structural homologue tripropylene glycol upon oral administration to rats was investigated in a well-conducted and well-reported study (Dow Chemical Company, 1995). In this study, two groups of 5 male rats were administered a single oral dose of either radiolabeled (14C) tripropylene glycol or non-radiolabeled monopropylene glycol by gavage in water at target concentrations 40 mg/kg bw and 50 mg/kg bw, respectively. The excreta were collected for ca. 24 hours post-dosing. After sacrifice 24 hours post-dosing the remaining radioactivity in tissues was determined for the first group and urine was analyzed for free and acid-abile conjugates of mono-, di- and tripropylene glycol for both groups.

While the absorption of monopropylene glycol has not been specifically investigated in the study, the data on tripropylene glycol indicate that it is rapidly adsorbed if administered by gavage, based on the average recovery of ca. 91% of the14C label administered from excreta, CO2, skin, tissues and carcass after ca. 24 hours post-dosing sacrifice. The absorption of tripropylene glycol via oral route was calculated to amount to at least 86%, based on 5% of the administered dose recovered in faeces. As monopropropylene glycol has a significantly lower molecular weight, its absorption from the gut is expected to occur even faster.Toxicokinetic behavior of monopropylene glycol in humans and experimental animals was also evaluated by the NTP CERHR expert panel (National Toxicology Program, 2004a), which concluded that available data indicate rapid and extensive absorption.Therefore a value of 100% for oral absorption shall be used for risk assessment for monopropylene glycol.


No data on the distribution of monopropylene glycol were reported in the study; however, in case of tripropylene glycol, approximately 10% of the radiolabeled dose was recovered in tissues and carcass, with the liver and kidney having the greatest amount of radiolabel per gram of tissue 24 hours after dosing (ca. 0.2 and 0.1%, respectively). The14C concentration in blood was approximately 6.4 and 2.8 -fold lower than in liver and kidney, respectively. The expert panel of NTP CERHR (National Toxicology Program, 2004a) concluded that monopropylene glycol is rapidly distributed into total body water.

Metabolism and excretion

In the study with rats administered monopropylene glycol and radiolabeled tripropylene glycol, the data on the animals administered monopropylene glycol indicate that approximately 11% of the monopropylene glycol administered was recovered in the urine as free monopropylene glycol with < 1% of the dose recovered as acid-labile conjugates. In the study with radiolabeld tripropylene glycol, twenty-four hours after administration of a single oral dose of 40 mg/kg bw to male rats, only 5.8% of the dose was recovered as unmetabolized parent compound in the urine, while 7.2% was recovered as acid-labile conjugates of tripropylene glycol, 5.1% and 3.3% as free and acid-labile conjugates of dipropylene glycol and 3.3% and 0.6% as free and acid-labile conjugates of monopropylene glycol, respectively. A large fraction (21%) of the14C-tripropylene glycol dose was catabolized all the way to14CO2, indicating considerable breakdown of tripropylene glycol.

According to the NTP CERHR expert panel report (National Toxicology Program, 2004a), the rate-determining step in the metabolism is alcohol dehydrogenase which, when saturated, switches from a first order process into a zero order process. Saturation of metabolism appears to occur in rats and rabbits at a dose of about 1600 to 2000 mg/kg bw, whereas in humans this seems to happen at a dose of about 200 mg/kg bw. In accordance with a zero order process, the half-life of propylene glycol in humans and rats increases from about 1.5 hours to more than 5 hours with increasing doses above metabolic saturation. By a NAD-dependent reaction, alcohol dehydrogenase converts propylene glycol to lactaldehyde, which is further metabolized to lactate.

Since propylene glycol has a chiral center, technical grade propylene glycol results in the formation of 50/50 D, L-lactate. L-lactate is indistinguishable from endogenous lactate, which is a good substrate for gluconeogenesis. D-lactate is less readily converted to glucose than L-lactate, which prolongs its half-life leading, under conditions of prolonged exposure, to D-lactic acidosis. It is difficult to cause L-lactic acidosis even with very high doses of propylene glycol because of its efficient detoxification via gluconeogenesis. The second reason for lack of development of L-lactic acidosis is the saturation of alcohol dehydrogenase, which results in a constant rate of lactate production. Due to removal of L-lactate by gluconeogenesis, a further increase in lactate levels is not possible after saturation of metabolism.

The excretion of propylene glycol is species-dependent. Humans clear about 45% of propylene glycol via kidney, and in dogs, up to 88%. In rats and rabbits, very little of the parent compound is excreted by the kidney until saturation of metabolism occurs. Inhibition of alcohol dehydrogenase by pyrazole increases urinary excretion of propylene glycol to 75% in rats, as expected. Since propylene glycol has very low intrinsic toxicity, saturation of metabolism plays a protective role in its toxicity since the conversion of propylene glycol to the more toxic lactate (particularly D-lactate) is slowed.

Inhalation route of exposure


Only limited data addressing the absorption of monopropylene glycol by inhalation are available. Bau et al. (1971) reported that less than 5% of a technetium-labeled aerosol containing 10% monopropylene glycol in deionized water was taken up by human volunteers after inhalation for 1 hour in a mist tent. The authors measured the aerosol mass median diameter to be 4.8 -5.4 microns, a size small enough to have enabled penetration to the deep lung. Ninety percent of the dose was found in the nasopharynx and it rapidly entered the stomach with very little entering the lungs. Monopropylene glycol was not directly measured, not allowing the determination of absorption through the nasal mucosa. However, the low dose rate from inhalation exposure and the small surface area would not lead to significant absorption of monopropylene glycol.


Dermal route of exposure.


An in vitro skin penetration study (El du Pont de Nemours and Company, 2007; Fasano et al, 2011) with the monopropylene glycol, using human cadaver skin and performed under infinite dose conditions, was available for assessment. A nominal dose of 1200 µL/cm2(ca. 1.2 g/cm2)of the neat substance was applied for 24 hours under occlusive conditions to 6 skin replicates representing 5 human subjects. By the conclusion of the 24-hour exposure interval, only a negligible portion of the applied dose of neat monopropylene glycol (0.14%) had penetrated through the skin into the receptor fluid. The integrity of human skin, as determined by electrical impendance (EI), was affected by continuous exposure to monopropylene glycol under occlusive conditions. The ratio of the post-EI values was 0.33, confirming that the barrier properties of the stratum corneum were altered by monopropylene glycol.

In general, monopropylene glycol was detected in receptor fluid within about an hour of application (lag time ~ 6 hours ); steady-state penetration, which was represented by no less than 4 data points, was determined to be 95.4 µg/cm2/h (r2=0.999).This represents the maximum flux for neat monopropylene glycol.

Based on the slope at steady-state (95.4 µg/cm2/h) and the concentration of monopropylene glycol in the applied solution, taken as its density (1,036,000 µg/cm3), the permeability coefficient for neat monopropylene glycol was calculated to be 9.21×10-5cm/h.

Based on the results of the study, a value of 40% for dermal absorption has been chosen by expert judgment to be used in the risk assessment. This value has been chosen as an average value between the percentage of dermal absorption obtained in the study and the maximal oral absorption (corresponding to 100%), and is considered to represent a worst-case approach.