Diethanolamine (DEA)
Diethanolamine (DEA) is a secondary amine classified within the group of organic compounds known as ethanolamines, which possess both amine and alcohol properties. It is a high-production chemical commonly found in metalworking fluids, pesticides, antifreeze, pharmaceuticals, and various personal care products like lotions and shampoos. DEA is also used in the manufacturing of fatty acid derivatives such as cocamide DEA and lauramide DEA, which serve as emulsifiers and foaming agents.
Exposure to DEA primarily occurs through skin contact, inhalation of vapors and aerosols, and ingestion. While studies have shown that DEA increases the risk of liver and kidney cancers in mice, the relevance of these findings to humans is unclear due to insufficient epidemiological evidence. DEA is not believed to directly damage genetic material; instead, it may disrupt cellular processes by causing choline deficiency, which can lead to changes associated with tumor development.
Regulatory responses to DEA have varied; the U.S. has implemented limitations on its concentration in products for skin contact, while the European Union has banned DEA and related compounds in cosmetics due to potential carcinogenic risks. Overall, understanding DEA's applications, exposure risks, and regulatory context is crucial for consumers and industry professionals alike.
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Diethanolamine (DEA)
ALSO KNOWN AS: Diethylolamine, 2,2 -hydroxyethylamine, diolamine, bis-2-hydroxyethylamine, iminodiethanol
RELATED CANCERS: Liver and kidney cancer in mice
DEFINITION: Diethanolamine (DEA) is a secondary amine in a class of organic compounds known as ethanolamines, which combine the properties of amines and alcohols. A high-production chemical, DEA is a component of metalworking fluids, pesticides, antifreeze, pharmaceuticals, and personal care products. Its fatty acid derivatives, including cocamide DEA, lauramide DEA, DEA-Cetyl Phosphate, and oleamide DEA, are emulsifiers or foaming agents.
Exposure routes: Principally through dermal contact, inhalation of vapor and aerosols, ingestion
Where found: Intermediates in agricultural and photographic chemicals, personal care products (such as lotions, creams, shampoos, and hair dyes), textile processing, pharmaceuticals, metalworking fluids, industrial gas treatments
At risk: Workers in diethanolamine manufacturing facilities, metal industry workers exposed to lubricating liquids, consumers of personal care products and some tobacco products
Etiology and symptoms of associated cancers: Diethanolamine increases the risk of liver cancers (hepatocellular or carcinoma) and kidney cancers (renal tubule adenoma) in mice. The cancer risk to humans has not been firmly established by adequate epidemiological studies. DEA does not damage the genetic material; rather, it perturbs cellular processes by causing a deficiency of choline, an essential nutrient in mammals. Choline depletion is known to induce changes in deoxyribonucleic acid (DNA) methylation, stimulate DNA synthesis, generate free radicals, and enhance susceptibility to oxidative damage—all events linked to tumorigenesis. Because rodents are more sensitive to choline deficiency than humans, the relevance of the mouse tumor findings to humans is unclear.
DEA’s potential carcinogenicity may stem from its ability to interact with nitrites. As contaminants or preservatives in commercial formulations, nitrites react with DEA to form nitrosodiethanolamine (NDELA), a that induces tumors of the liver, nasal cavity, and kidney in laboratory animals. The National Toxicology Program has listed nitrosodiethanolamine as reasonably anticipated to be a human carcinogen.
History: The industrial synthesis of ethanolamines depends on the wide-scale production of the primary reactant, ethylene oxide, discovered in 1859 by the French chemist Charles Adolphe Wurtz. In 1999, after a two-year carcinogenesis study, the National Toxicology Program reported that dermal applications of DEA or cocamide DEA induced liver and kidney cancers in mice. As early as 1979, the US Food and Drug Administration urged the cosmetics industry to remove DEA-derived nitrosamines from its products, but it has not strictly enforced the policy. Instead, the DEA limited the concentration of DEA in substances intended to directly contact the skin to 5 percent. Additionally, DEA may not be used in products containing N-nitrosating agents. These decisions have been confirmed by expert panels in the twenty-first century. In contrast, the European Union enacted legislation to ban DEA and nitrosodiethanolamine from cosmetics and toiletries, citing concerns about the potential for conversion to carcinogenic nitrosamines.
Bibliography
"Diethanolamine." US Environmental Protection Agency, www.epa.gov/sites/default/files/2016-09/documents/diethanolamine.pdf. Accessed 20 June 2024.
"Diethanolamine." US Food and Drug Administration, 25 Feb. 2022, www.fda.gov/cosmetics/cosmetic-ingredients/diethanolamine. Accessed 20 June 2024.
Kamendulis, Lisa M., and James E. Klaunig. "Species Differences in the Induction of Hepatocellular DNA Synthesis by Diethanolamine." Toxicological Sciences, vol. 87, no. 2, 2005, pp. 328–336. doi.org/10.1093/toxsci/kfi252.
"NIOSH Pocket Guide to Chemical Hazards: Diethanolamine." CDC, National Institute for Occupational Safety and Health, 2019, www.cdc.gov/niosh/npg/npgd0208.html. Accessed 20 June 2024.
US Dept. of Health and Human Services, Natl. Toxicology Program. "NTP Toxicology and Carcinogenesis Studies of Diethanolamine (CAS No. 111-42-2) in F344/N Rats and B6C3F1 Mice (Dermal Studies)." NTP Technical Reports Series 478 (1999): 1–212.
Yar, M., N. Mushtaq, and S. Afzal. "Synthesis, Reactions, Applications, and Biological Activity of Diethanolamine and Its Derivatives." Russian Journal of Organic Chemistry, vol. 49, no. 7, 2013, pp. 949–967. DOI:10.1134/S1070428013070014.