Diethylene Glycol

Diethylene glycol (DEG) is a clear, odorless, hygroscopic liquid with the chemical formula C4H10O3. In automotive products it most commonly appears as a co-solvent in antifreeze and engine coolant, typically at 1.5 to 5 percent of the finished formula. The bulk of a consumer coolant is still ethylene glycol or propylene glycol; DEG sits alongside the primary glycol to improve low-temperature flow, help dissolve the corrosion-inhibitor package, and round out the freeze-point curve. It also shows up in some DOT 3 brake fluids, where DEG-based borate esters serve as the hygroscopic base fluid, and in selected hydraulic and heat-transfer fluids.

The reason formulators reach for DEG is practical chemistry. It is miscible with water in all proportions, has a high boiling point (about 245 C), and dissolves both polar inhibitors and the dye packages used to color coolants. It is produced at industrial scale as a byproduct of ethylene oxide hydration, the same reaction that yields mono-ethylene glycol.

What the SDS classifications mean

In Section 2 of a typical DEG SDS, the substance carries H302 (harmful if swallowed) under the GHS oral acute toxicity category 4. The published oral LD50 in rats is in the range of 12,500 mg/kg, which is well above the threshold that would trigger a stronger category. There is no inhalation or skin sensitizer classification for the pure substance under GHS, and it is not listed as a carcinogen by IARC, NTP, or OSHA.

DEG has a very low vapor pressure (about 0.001 mmHg at 20 C), which is why it is not counted as a volatile organic compound (VOC) under U.S. EPA Method 24 and similar regulatory definitions. At room temperature, the airborne concentration above an open container is small. The flash point is around 138 C, so it is not classified as a flammable liquid for transport purposes.

Historical context: the pharmaceutical incidents

DEG has a long and documented public-health record, almost entirely from pharmaceutical contamination rather than industrial or automotive use. The 1937 Elixir Sulfanilamide incident in the United States, in which a sulfanilamide preparation was dissolved in diethylene glycol and sold as a syrup, caused more than 100 deaths and prompted the Federal Food, Drug, and Cosmetic Act of 1938. Subsequent contamination events have followed a similar pattern: DEG substituted for glycerin or propylene glycol in liquid medications such as cough syrup or acetaminophen suspension. Documented incidents include Haiti in 1996, Panama in 2006, and a series of pediatric cough-syrup deaths reported by the WHO across The Gambia, Indonesia, and Uzbekistan in 2022 and 2023.

These events are listed here because they are the dominant signal in the public toxicology literature on DEG, not because they map onto automotive use. The exposures involved oral ingestion of contaminated medicines at gram-per-dose levels in vulnerable populations, often children. Retail antifreeze at 1.5 to 5 percent DEG is a different exposure scenario, governed by the SDS classification of the finished mixture (where ethylene glycol is the dominant hazard driver) and by accidental-ingestion controls such as the bittering agent denatonium benzoate required in most U.S. states.

Metabolism and treatment

The mechanism of DEG toxicity is well characterized. Hepatic alcohol dehydrogenase oxidizes DEG first to 2-hydroxyethoxyacetic acid (HEAA) and then to diglycolic acid. Diglycolic acid is the metabolite most closely associated with the proximal-tubule kidney injury seen in DEG poisoning cases. Unlike ethylene glycol, DEG metabolism does not produce significant oxalate, so calcium oxalate crystalluria is not the dominant clinical finding.

Documented antidotal therapies are the same ones used for ethylene glycol poisoning: fomepizole (4-methylpyrazole), which inhibits alcohol dehydrogenase, and ethanol, which competes for the same enzyme. Hemodialysis is used to clear both the parent compound and the diglycolic acid metabolite. These treatments are described in ATSDR and clinical toxicology references.

Where DEG specifically appears in car care

The substantive automotive uses are: ethylene-glycol-based coolants of all generations (IAT, OAT, HOAT, NOAT, P-HOAT) where DEG functions as a minor co-solvent; DOT 3 brake fluid, where DEG-based borate ester chemistry is the dominant base; some hydraulic brake-clutch fluids; and certain industrial heat-transfer fluids that overlap with automotive use. DOT 4 and DOT 5.1 brake fluids shift toward higher-boiling glycol ethers and use less DEG. DOT 5 is silicone-based and contains none.

Environmental profile

DEG is classified as readily biodegradable under OECD 301B and 301F test protocols, with reported degradation typically above 70 percent within 28 days. Reported aquatic toxicity is low: published EC50 and LC50 values for fish, daphnia, and algae are commonly above 100 mg/L, which places it outside the GHS aquatic-hazard categories. It is not bioaccumulative (log Kow approximately -1.98), not persistent under normal environmental conditions, and not ozone-depleting.

Further reading

Primary sources for DEG toxicology and environmental data: the manufacturer SDS for the specific product in hand, the ATSDR Toxicological Profile for ethylene glycol and propylene glycol (which discusses DEG in context), the WHO Concise International Chemical Assessment Document for diethylene glycol, U.S. EPA IRIS and ChemView entries, and the OECD SIDS Initial Assessment Report for diethylene glycol.

Related: Is Brake Fluid Toxic? Read the full SDS breakdown of the DOT 3 brake fluids this glycol forms the base of.