Senior Toxicology Advisor, Toxicology and Regulatory Affairs, Health, Safety and Environment Department, 451 Florida Street, Baton Rouge, Louisiana. Fax: (225) 388-7686. E-mail: marcia_hardy{at}albemarle.com
To the Editor: May 13, 2004
Drs. Eriksson and Viberg responded to a Letter to the Editor (Vijverberg and van den Berg) regarding their report of neurobehavioral effects of decabromodiphenyl ether (Deca) in neonatal mice (Toxicol. Sci. 76, 112120; Viberg et al., 2003). They commented that toxicity data on highly brominated diphenyl ethers are very sparse. However, Deca, the most highly brominated diphenyl ether possible, has a large data set. Its database includes mammalian acute, repeated dose, and lifetime studies in more than one species; absorption-distribution-elimination studies; developmental toxicity studies, and mutagenicity studies, among others (Hardy, 2002
; Hardy et al., 2002
). Deca's potential environmental effects have also been studied in acute studies in fish, daphnia, and algae, and in repeated dose studies in earthworms, plants, and sediment organisms (Hardy, 2002
).
Drs. Eriksson and Viberg also commented that their work showed Deca could be absorbed and that this was contrary to their belief that it was "... not present in our environment and also assumed not to be taken up in an organism." Almost 10 years ago, the World Health Organization's Environmental Health Criteria Document on polybrominated diphenyl ethers (WHO, 1994) included data on Deca's environmental monitoring results (Deca was detected in some Japanese sediments, and near its U.S. manufacturer). In 2000, more monitoring results were available that indicated Deca was detected mainly in sediments near point sources (Hardy, 2000
). Information on Deca's potential for absorption dates back to the mid-1970 s (Norris et al., 1973
, 1975
). Some years later, the U.S. National Toxicology Program published its report (NTP, 1986
) on a two-year study on Deca that included an ADME study subsequently published by El Dareer et al. (1987)
. This body of work going back 2030 years demonstrates that DBDPO is poorly bioavailable, but that its availability is not absolute zero. Current detection of minute levels of Deca in biota does not contradict this finding (Jakobsson et al., 2002
).
Finally, Drs. Erikkson and Viberg raise the question of risk. Mere detection of a substance does not equate to risk. As we all learned in our first toxicology course: "the dose makes the poison." Levels of Deca reported in humans indicate that any exposures are far below those causing no harm whatsoever (NAS, 2000). Also incumbent in any risk evaluation is the concept of riskbenefit. Deca is used solely as a flame retardant to prevent or slow development of fires in various products. In the U.S. alone, Deca is estimated to prevent nearly 300 fire deaths each year (Clarke, 1997
). With someone in the U.S. dying in a fire every two and half hours (Karter, 2003
), fires represent a significant risk to life and limb.
ACKNOWLEDGMENTS
Dr. Hardy is employed by Albemarle Corporation in its Health, Safety and Environment Department. Albemarle Corporation is a specialty chemicals manufacturer. Its product line includes flame retardants, including decabromodiphenyl ether.
REFERENCES
Clarke, F. (1997). The life safety benefits of brominated flame retardants in the United States. Final Report to the Chemical Manufacturers Association Brominated Flame Retardant Industry Panel. Benjamin/Clarke Associates.
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NTP (National Toxicology Program). (1986). Toxicology and Carcinogenesis Studies of Decabromodiphenyl Oxide (CAS No.1163195) in F344/N Rats and B6C3F1 Mice (Feed Studies). National Toxicology Program Technical Report Series No.398. U.S. Department of Health and Human Sciences. Public Health Service. National Institutes of Health. Research Triangle Park, NC.
Viberg, H., Fredriksson, A., Jakobsson, E., Orn, U., and Eriksson, P. (2003). Neurobehavioral derangements in adult mice receiving decabrominated diphenyl ether (PBDE 209) during a defined period of neonatal brain development. Toxicol. Sci. 76, 112120.
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