Report Date: June 1992
The following abstract presents results of a study conducted by a contract laboratory for the National Toxicology Program. The findings have not been peer reviewed and were not evaluated in accordance with the levels of evidence criteria established by NTP in March 2009. The findings and conclusions for this study should not be construed to represent the views of the NTP or the U.S. Government.
Diethanolamine is a viscous, colorless liquid which is formed by ammonolysis of ethylene oxide. Diethanolamine is extensively used in pharmaceutical ointments and skin cleaners. It has been approved for use in numerous cosmetic formulations. Furthermore, it is permitted as a secondary direct food additive from use in delinting cottonseed. Diethanolamine is also widely used as a dispensing agent in various agriculture chemicals including herbicides. As a direct result of its wide spread consumer and industrial usages, large amounts of diethanolamine are discharged directly into water and sewage.
Diethanolamine was nominated to the NTP for toxicological evaluation and was selected for immunotoxicity studies by the chemical manager. The purpose of these studies was to determine if diethanolamine had an effect on the immune system by performing a range-finding study. If diethanolamine produced an effect on the immune system, doses to be used in the full protocol study would be determined.
Female B6C3F1 mice were exposed to DEA in doses between and including 100 and 1500 mg/kg by the oral route daily for 14 days. Body weights, selected organ weights and selected hematologic assays were used to indicate overall toxicity. The IgM spleen antibody-forming cell response and the cytotoxic T lymphocyte response were used as indicators of immune status.
DEA in doses above 800 mg/kg produced morbidity and mortality. DEA has a marked effect on the erythroid cells which is most likely related to inhibition of synthesis of this cell lineage. DEA produced a dose-dependent increase in liver weight and a decrease in thymus weight. DEA produced a dose-dependent decrease in the IgM AFC response in vivo with a no-effect level at 100 mg/kg and a dose-dependent decrease in the in vitro-generated IgM AFC response with a no-effect level at 10-9 M. DEA produced a dose-dependent decrease in the CTL response with a no-effect level at 800 mg/kg.