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Cosmetic, Toiletry, and Fragrance Association, Washington, D. C., USA
1Correspondence: Cosmetic, Toiletry, and Fragrance Association, 1101 17th St., NW, Suite 300, Washington, D.C. 20036-4702, USA. E-mail: baileyj{at}ctfa.org
The paper by Craciunescu et al. reporting altered neurogenesis and apoptosis in fetal mouse hippocampus following diethanolamine (DEA) exposure in utero (1)
grossly overestimates potential human exposure to DEA from personal care products and implies a risk from their use that is not supported by the data.
In contrast to the authors’ reference to DEA at levels of 1–25% in cosmetic formulations, DEA per se is rarely if ever used in personal care products. There is potential for exposure to DEA in personal care products from the use of alkanolamides of DEA, which are condensation products of DEA and fatty acids (for example, cocamide DEA, a reaction product of DEA and coconut oil-derived fatty acids). These ingredients are primarily used in rinse-off applications such as shampoos and hair dyes, and may contain free DEA as a component/contaminant of the ingredients, generally in the range of 0.2–10%.
Dermal penetration studies using human skin have demonstrated that penetration of DEA from cosmetic formulations under realistic use conditions is consistently very low (2
, 3)
. For example, in the case of a model shampoo formulation, the percentage of the applied dose of DEA that could be absorbed systemically ranged from 0.011 to 0.034% (2)
. Using a slightly different protocol, researchers at the US FDA reported dermal penetration values for DEA in a shampoo of 
0.1 % (3)
. This contrasts with mouse skin, which has been shown to be highly permeable to DEA (4)
.
The paper by Craciunescu et al. provides exposure estimates of 8–200 mg/kg/day from daily use of shampoo (1)
. In fact, using the values above to calculate the amount of DEA that would be absorbed from daily use of shampoo results in a very different conclusion. If the shampoo is assumed to contain a DEA condensate ingredient at 10%, with free (unbound) DEA present in the ingredient at 10% (both high-end estimates) (5)
, and the daily application of shampoo is 12.80 grams (6)
, the resulting DEA exposure for a 60 kg person would be in the range of 0.2–2 µg/kg/day.
This value can then be compared to the 20 mg/kg/day no-effect level in mice reported in Craciunescu et al. (1)
to demonstrate a safety factor well in excess of 1000 for DEA exposure from shampoo. The use of additional DEA-containing products would be expected to contribute equally small amounts of DEA, and a wide margin of safety would still exist. Further, the hypothesized mechanism behind the adverse developmental effects reported by Craciunescu et al. is choline deficiency (1)
, to which humans are believed to be less susceptible than rodents (7
8
9)
, thereby increasing the safety factor further. Thus the inference that the use of consumer products containing DEA by pregnant women may present a risk to the unborn is without merit and not supported by the data.
FOOTNOTES
The opinions expressed in editorials, essays, letters to the editor, and other articles comprising the Up Front section are those of the authors and do not necessarily reflect the opinions of FASEB or its constituent societies. The FASEB Journal welcomes all points of view and many voices. We look forward to hearing these in the form of op-ed pieces and/or letters from its readers addressed to journals@faseb.org.
REFERENCES
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