Summary of Meeting Paper

The 1996 Annual Meeting of the Society for Risk Analysis-Europe

Comparing Ethylene Glycol (EG) and Propylene Glycol (PG) Using Toxicity As a Basis for Risk Management Decisions. E.A. McKenna, EA, Hunt Valley, MD USA; J.S. LaKind, EA Engineering, Science, and Technology (EA), Silver Spring, MD USA; D.F. Bodishbaugh, EA, Hunt Valley, MD USA; R.P. Hubner, EA Engineering, Science, and Technology (EA), Silver Spring, MD USA; A.H. Kim, EA, Lafayette, CA USA; D.F. Ludwig, EA, Hunt Valley, MD USA; G. Wright, ARCO Chemical Company, Newtown Square, PA USA; B.S. Suedel, Dames & Moore, York, PA USA; and R.G. Tardiff, EA Engineering, Science, and Technology (EA), Silver Spring, MD USA


Ethylene glycol (EG) and propylene glycol (PG) are principal components of aircraft deicing and anti-icing fluids and of motor vehicle antifreeze. Consideration of the relative toxicity of these two compounds can play a role in the selection EG versus PG formulations, and forms the basis for managing risks at personal, regulatory, and industrial levels. Individuals make personal purchasing decisions based on their perception of the relative risks of such products to humans and animals (including pets). This process may be influenced by the common practice of many veterinarian offices to outline the toxicity of EG-based antifreeze and promote purchase of PG-based antifreeze to safeguard pets. At a regulatory level, both national and international regulations for EG abound, while fewer, and less restrictive, regulations exist for PG-based formulations. Industries (e.g., airlines) use toxicity data to form the basis for selecting deicing/anti-icing formulations, and a national military (USAF) policy exists which requires the phasing out of EG-based fluids in favor of PG-based fluids based on the former's potential to pose a human health hazard via airfield runoff.

This review of the toxicity of EG, PG, and associated formulations was undertaken to assess the scientific basis for supporting the use of one over the other. The weight of the evidence presented in this paper supports the conclusion that PG-based fluids are preferable to EG-based fluids from a toxicological standpoint.


Use and misuse of EG in commercial products are responsible for a number of human deaths yearly from acute exposures. Human case studies reporting death caused by exposure to PG have not been found in the scientific literature.

The acute oral toxicity of EG in humans is well-documented, and follows a defined series of stages including central nervous system (CNS) dysfunction with severe metabolic acidosis, cardiopulmonary failure, and acute renal failure. While the stages of acute EG poisoning in humans have been well recorded, the stages may overlap and death can result at any stage. The lowest reported minimum lethal dose (MLD) of EG is 1.57 g/kg, and accidental and intentional deaths have been attributed to ingestion of EG. Based on the MLD, EG appears to be more toxic in humans than experimental animal species on a weight-normalized basis. No acute inhalation exposure studies to EG in humans have been reported, although EG caused upper respiratory irritation, slight headaches, and lower backaches in volunteers exposed to as much as 140 mg/m3 (37 mg/kg-day) for 30 days. Dermal contact with EG produced mild to no skin irritation, and minimal sensitization potential.

Acute PG toxicity, in contrast to that of EG, is not well-defined but includes CNS effects (e.g., CNS depression) and lactic acidosis from high doses. No deaths from oral, dermal, or inhalation exposure to PG have been reported. Acute oral exposure to high-dose PG has resulted in hematological effects. No acute toxicities have been reported from the inhalation of PG vapors or aerosols. Mild skin irritation has been reported from dermal contact with PG in various patch tests, and the ability of PG to cause allergic sensitization in humans remains debatable.


The acute toxicity of EG in experimental animals closely mirrors the acute effects seen in humans, including CNS, cardiopulmonary, and renal effects. The oral LD50 ranged from 4.0 g/kg in rats to as high as 15.4 g/kg in mice. Rats exposed to a high concentration of saturated EG vapor (500 mg/m3 in rats) for 28 hours showed signs of irritation to the eyes and respiratory tract, and mice and rats exposed to 398 Mg/M3 EG for 16 weeks (eight hours/day, five days/week) had intestinal irritation and immune system effects. Dermal application of EG to rabbits produced mild or no irritation.

The acute toxicity of PG includes CNS effects, hematological effects, respiratory effects, and microscopic renal and hepatic changes in laboratory animals. The minimum lethal dose in the rat was 19.8 g/kg and 20 g/kg in the rabbit. The LD50 ranged from 10-20 g/kg in dogs to 33.5 g/kg in rats. No adverse effects from inhalation of PG have been found in the scientific literature. Dermal exposure to PG produced mild irritation.


EG toxicity includes primarily reproductive, developmental, and chronic renal effects. Adverse reproductive effects have been reported following oral EG exposure of both mice and rats, with no studies via inhalation and dermal exposures. Developmental effects encompass developmental malformations and teratogenicity in mice following oral exposure, with several variations and a single malformation observed after inhalation. Dermal exposure also resulted in developmental variations, but does not appear to result in teratogenic effects in mice. Chronic EG toxicity due to oral exposure results in renal effects in two species of animals, while no studies of effects via other routes were located.

Predominant effects of non-acute PG exposure encompass primarily hematological effects. No effects have been noted for reproductive or developmental endpoints from exposures by the oral route. Reproductive or developmental studies of animals exposed to PG via other routes were not found. No chronic renal effects have been noted, and minimal qualitative effects on the liver have been reported. Slight hematological effects were seen in dogs only after high-dose oral exposure and in rats after high-dose inhalation exposure. The primary significant hematological effects noted have been in a highly sensitive species, the cat, whose capacity for metabolizing PG differs greatly from that of humans. Hence, cats are not considered a representative species for modeling PG effects in humans.


Very little chronic toxicity data exist for ethylene and propylene glycols or glycol formulations to aquatic species. Most published studies are best characterized as acute or subacute exposures. Based on available data, the relative acute toxicities of EG and PG are very similar. LC50s values for freshwater and marine fish invertebrates and algae for EG range from 7,900 mg/L-111,000 mg/L and LC50s for PG range from 10,000 mg/L-79,700 mg/L. The acute toxicities of commercial ethylene glycol and propylene glycol aircraft deicer/anti-icer formulations are also similar across groups of organisms encompassing producer (algae) and consumer species (daphnids, minnows). The range of acute LC50 values across all taxa for propylene glycol Type I deicers (50% diluted, deicer formulations applied hot to aircraft to break-up ice which has already formed) is comparable to that for ethylene glycol Type I deicers. The ranges of toxicity reported for ethylene and propylene glycol Type II anti-icers (non-diluted, anti-ice formulations applied cold to aircraft to prevent ice formation prior to takeoff) are also similar, although Type II toxicity appears to be more variable. All Type I deicers tested are of very low acute toxicity (freshwater LC50 > 1000 Mg/L), while virtually all Type II anti-icers are more acutely toxic (50 < freshwater LC50 < 1000 mg/L). Based upon the limited available data, no general distinction can be made between aquatic toxicities of ethylene and propylene glycol formulations. There is considerable variability in the observed toxicities of different commercial formulations, especially those of Type II. The chemical factors which account for this variability are unknown.