2,2'-iminodiethanol or 

Diethanolamine (DEA), a chemical compound belonging to the class of chemical compounds alkanolamines, is a water-soluble molecule obtained by a reaction process of ethylene oxide with ammonia. DEA shows reactive capacity is an aminoalcohol as it combines the properties of alcohols and amines.

It appears as a colourless transparent or yellowish liquid.

Safety

Some of the scientific literature warns of the possible danger of DEA (1), while a 1998 study by the National Toxicology Program (NTP) did not establish a link between DEA and cancer risk in humans.

What it is used for and where

It is used as a surfactant in cosmetics and a corrosion inhibitor in industrial applications.

Cosmetics

pH adjuster. This ingredient tends to restore the pH of a cosmetic formulation to its optimal value. The correct pH value is an essential determinant for lipid synthesis in the stratum corneum. The average physiological pH value of the face ranges between 5.67 and 5.76. The hair fibre has a pH value of 3.67.

Other uses

• Chemical acid gas absorber 
• Leather and synthetic fibre softener
• Complexing agent for silver, lead, cadmium and zinc plating

The most relevant studies on this ingredient have been selected with a summary of their contents:

Diethanolamine studies

Synonyms:

• 2,2'-Iminodiethanol
• 2-(2-Hydroxyethylamino)ethanol
• Ethanol, 2,2'-iminobis-
• 2,2'-Dihydroxydiethylamine

Trade name:

• Dabco DEOA-LF
• H2dea
• Niax DEOA-LF

CAS: 111-42-2

References______________________________________________________________________

(1) Craciunescu CN, Wu R, Zeisel SH. Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus. FASEB J. 2006 Aug;20(10):1635-40. doi: 10.1096/fj.06-5978com.

Abstract. Diethanolamine (DEA) is present in many consumer products such as shampoo. Dermal administration of DEA diminishes hepatic stores of the essential nutrient choline, and we previously reported that dietary choline deficiency during pregnancy reduces neurogenesis and increases apoptosis in the hippocampus of fetal rats and mice. Therefore, DEA could also alter brain development. Timed-pregnant C57BL/6 mice were dosed dermally from gestation day 7 through 17 with DEA at 0, 20, 80, 160, 320, and 640 mg/kg body/day. At doses of DEA > 80 mg/kg body/day, we observed decreased litter size. In fetuses (embryonic day 17) collected from dams treated dermally with 80 mg/kg body/day DEA, we observed decreased neural progenitor cell mitosis at the ventricular surface of the ventricular zone of the hippocampus [to 56+/-14% (se) histone 3 (H3) phosphorylation as compared to controls; P < 0.01]. We also observed increased apoptosis in fetal hippocampus (to 170+/-10% of control measured using TUNEL and to 178+/-7% of control measured using activated caspase 3; P < 0.01). Thus, maternal exposure to DEA reduces the number of neural progenitor cells in hippocampus by two mechanisms, and this could permanently alter memory function in offspring of mothers exposed to this common ingredient of shampoos and soaps.