Polybrominated Diphenyl Ethers Data Sheet

Source of Exposure

Polybrominated diphenyl ethers (PBDE’s) compose a group of 209 possible isomers. Like Polychlorinatedbiphenyls the comercial products are mixtures of the isomers and are called arachlors. Each individual isomer is a congener.

Polybrominated Diphenyl Ethers (PBDE’s) are a class of chemicals that have replaced polychlorinated biphenyls and polybrominated biphenyls as fire retardants. PBDE’s are used in electronics, electrical cables, carpets, furniture, and textiles. Because of their widespread use typical Americans come in contact with them daily. Worldwide, DecaPBDE’s are the most widely used, followed by Penta and Octa. 95% of the PentaPBDE’s produced annually are used in the USA and research shows that the Penta’s are the most likely to be absorbed by and build up in living organisms.

The environmental rate of increase in the concentration of PBDE’s is increasing exponentially, doubling every 2 to 5 years. Researchers in Sweden found a 60 fold increase in the concentrations of PBDE’s in breast milk between 1972 and 1997. Canadian researchers reported a 15-fold increase in breast milk of women in Vancouver, BC between 1992 and 2002.

The average PBDE concentrations found in breast tissue, blood, and breast milk samples from studies of U.S. women are the highest yet reported in the world. The San Fransico Bay area has the highest environmental concentrations in the U.S.

Symptoms

Potential health effects of PBDE’s have only just begun to be studied, but they have been shown to cause permanent brain damage to fetuses exposed in utero and to be thyroid disrupters. Recent animal research has shown that exposure to low levels of PBDE’s can cause permanent neurological and developmental damage including deficits in learning, memory and hearing, changes in behavior, and delays in sensory-motor development.

A growing body of evidence shows a very low threshold for PBDE to cause permanent impacts to the development of the nervous system. Understanding of the mechanisms involved is lacking but several different mechanisms, including mimicking thyroid hormones, increasing their rate of clearance from the body, and interfering with intracellular communication have been proposed. Early exposure to PBDE has been found to delay the onset of puberty in male and female rats and decrease the weight of the male reproductive organs. Other health effects that have been found in laboratory animals include retarded fetal weight gain, enlarged livers, and raised serum cholesterol. In utero exposures have been associated with serious harm to the fetus, including limb and ureter malformation, enlarged hearts, bent ribs, fused stemebrae, delayed bone hardening, and lower weight gain.

The few studies that have looked at changes in organ structure have found that semi-chronic PBDE exposure can cause thyroid hyperplasia and enlarged livers at 10 mg/kg-day and other adverse effects such as hyaline degeneration, focal necrosis and deformation in the kidney, hyperplastic nodules in the liver, decreased hemoglobin and red blood cell counts at higher doses.

Blood Concentrations

General population data does not exist at this time. Measurable concentrations exist in exposed individuals with higher concentrations in adipose tissue and breast milk. However, PBDE levels may differ greatly between countries and geographic regions due to variables such as dietary customs and agricultural practices.

Samples

Blood specimens, because of their availability and probable diagnostic value with regard to extent of chronic and acute exposures to PBDE’s, present a convenient tissue for study, providing meaningful data pertinent to the fields of environmental toxicology and clinical ecology. PBDE’s can also be analyzed in breast milk to determine infant exposure and in adipose tissue to look at body burden. 2,2’,4,4’ Tetra and 2,2’,4,4’,5 Penta are analyzed as markers for exposure. 2,2’,4,4’ Tetra is the most abundant congener in the environment and 2,2’,4,4’,5 Penta is the most toxic congener identified up to this point in time

Toxic Concentrations

Concentration that are known to be toxic have yet to be determined. However, malformations of the fetus were consistently seen at levels much lower than doses harmful to the mothers – the lowest being 2 and 5 mg/kg-day respectively.

References

Lunder, Sonya; Sharp, Renee. “Tainted Catch” publication of The Environmental Working Group, 2003.

Darnerud, P.O.; Eriksen, G.S.; Johannesson, T.; Larsen, P.B.; Viluksela, M. 2001. Polybrominated diphenyl ethers: occurrence, dietary exposure, and toxicology. Environ. Health Perspect. 109(Suppl1): 49-68.

Strandman,T.; Koistinen, J.; Vartiainen, T. 2000. Polybrominated diphenyl ethers (PBDEs) in placenta and human milk. Organohalogen Compounds. 47.61-64.

Ohta, S.; Ishizuka, D.; Nishimura, H. et al. 2002. Comparison of polybrominated diphenyl ethers in fish, vegetables, and meats and levels in human milk of nursing women in Japan. Chemosphere, 46(5): 689-96.

Noren, K. and Meironyte, D. 2000. Certain organochorine and organobromine contaminates in Swedish human milk in perspective of past 20-30 years. Chemosphere. 40: 1111-1123.

Meironiti, C.; Bergman, A. 1999. Analysis of Polybrominated Dipenyl Ethers in Swedish Human Milk, 1972-1997. Journal of Toxicology and Environmental Health. Part A, 58:329-341.

Ryan, J.J.; Patry, B.; Mills, P.; Beaudoin, N.G. 2002. Recent trends in levels of Brominated Diphenyl Ethers (BDEs) in Human Milks from Canada. Organohalogen Compounds. 58:173-6.

Kruger C. 1998. Polybrominated biphenyls and polybrominated diphenyl ethers: Detection and quantitation in selected foods. University of Munster, Munster, Germany. Thesis. In National Institute for Environmental Health Sciences (NIEHS) 2001. Toxicological Summary for Selected Polybrominated Diphynyl Ethers. Submitted by Bonne Carson, Integrated Laboratory Systems, Research Triangle Park, North Carolina. March, 2001.

Laws et al. 2003. Study on the dffects of DE71 on female rat pubertal development – presented at the Society of Toxicologist meeting. As cited by L.S. Birnbaum in “New findings on PBDEs”. Talk presented at the Bominated Flame Retardants and Foam Furniture Conference and Roundtable. San Francisco, CA. April 29-30, 2003.

Stoker, etal. 2003. . Study on the dffects of DE71 on male rat pubertal development – presented at the Society of Toxicologist meeting. As cited by L.S. Birnbaum in “New findings on PBDEs”. Talk presented at the Bominated Flame Retardants and Foam Furniture Conference and Roundtable. San Francisco, CA. April 29-30, 2003.

International Program of Chemical Safety (IPCS). 1994. Brominated Diphenyl Ethers. Environmental Health Criteria 162. World Health Organization, Geneva.

Norris, J.M.; Kociba, R.J.; Scwetz, B.A.; Rose, J.Q.; Humiston, C.G.; Jewett, G.L.; Gehring, P.J.; Mailhes, J.B. 1975. Toxicology of octabromobiphenyl and decabromodipheny oxide. Environmental Health Perspectives. 11:153-161.

National Toxicology Program (NTP). 1986. Toxicology and carcinogenesis studies of decabbromodipheny oxide (CAS No 1163-19-5) in R344/N rats and B6C3F1 mice (feed studies). NTP technical report series no 309. Research Triangle Park, NC.

Herrick, T. As Flame Retardant Builds Up In Humans, Debate Over a Ban. The Wall Street Journal, October 8, 2003, Vol. CCXLII NO. 70.