Environ. Sci. Technol. 2005, 39, 2415-2416
Response to Comments on “Polybrominated Diphenyl Ethers Contamination of United States Food” We are responding to the comments from Hardy (1) of the Albemarle Corporation, a manufacturer of brominated flame retardants. In her letter, she comments on our recently published article on levels of PBDE brominated flame retardants in a market basket survey of U.S. food (2). We are surprised by her critical comments because all information in the article and draft versions of the article were shared with senior representatives of Albemarle prior to submission, and their comments were solicited by us. There was no response from Albemarle suggesting any problems with our data or our conclusions at that time. We shared our information and drafts months before publication with our colleagues in industry because we value their opinions. We are also puzzled by Hardy’s contention that no further study of levels of PBDEs in US food is indicated. There is clearly a legitimate public health concern about the potential health damage that could occur from these toxic and persistent organic compounds, the concentrations of which are rapidly increasing in the environment (3-10). These compounds toxicologically and structurally resemble PCBs, which are known to be toxic to humans and other vertebrates in a number of ways. PCBs and other persistent organic pollutants have been implicated in cancer, endocrine disruption, reproductive and developmental disorders, immune deficiency, central and peripheral nervous system pathology, liver damage, skin disorders, and elevation of cholesterol and triglycerides in blood (11, 12). In addition, toxicology studies in animals with PBDEs show nervous system damage, reproductive and developmental damage, and endocrine disruption and cancer following high doses of Deca-BDE in feed (13-22). Contamination of the U. S. food with toxic and persistent chemicals is certainly a matter of considerable public health importance. There are a number of chemicals including PBDEs, PCBs, dioxins, and others which are found at greater or lesser levels in U. S. food, especially food of animal origin (23-26). These chemicals individually or in combination can contribute to adverse health consequences in humans. Because of the potential for health effects, not wanting to know the levels of contamination of toxicants in food is difficult to understand. Knowing where contamination exists, of which compounds and at what levels, is critical public health information. EPA has been able to reduce the amounts of dioxins, PCBs, and lead in humans by determining past levels, determining their sources and routes of contamination and by acting to decrease these levels. By doing so, levels of dioxins, PCBs and lead in humans in the U. S. have dropped considerably in the past decades contributing to improved public health (27-31). Food PBDE levels contribute to the finding that PBDE levels in nursing mothers’ milk in the U. S., including BDE 209 found in three recent studies (31-33), are the highest in the world today, 10-100 times higher than European levels. In fact, the margin of exposure for several adverse health effects (e.g., developmental neurotoxicity in mice and rats, developmental reproductive effect in rats; 34, 35) is low for women whose breast milk concentrations are at the high end of the general population (36). Although the production of the commercial Penta and Octa PBDE products was phased out in the United States by 10.1021/es058001k CCC: $30.25 Published on Web 02/12/2005
2005 American Chemical Society
the end of 2004, these mixtures and their environmental and biological breakdown products will persist in the environment for a long period of time, leading to exposure of humans and wildlife for many future decades. The commercial Deca PBDE product, which is largely BDE 209, continues to be produced and used worldwide. BDE 209 has been reported by many laboratories to be present in biological materials, including invertebrates, fish, birds, and mammalian wildlife. There is growing evidence of its breakdown to lower brominated compounds: photolytically (37), microbially (38), and metabolically (39, 40). Industry, government, academia, and the public all have a common need to learn as much as possible about health aspects of the PBDEs. We are all exposed to these compounds at rapidly increasing levels (3-9). The appropriate response to the growing body of information demonstrating the environmental occurrence, exposure to wildlife and humans, and potential for effects is for all of the stakeholders to work together to address this issue. This letter does not reflect U. S. Environmental Protection Agency policy.
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(31) Schecter, A.; Pavuk, M.; Pa¨pke, O.; Ryan, J.; Birnbaum, L.; Rosen, R. Polybrominated diphenyl ethers in U.S. mothers’ milk. Environ. Health Perspect. 2003, 111, 1723-1729. (32) Northwest Environment Watch. http://www.northwestwatch.org/toxics/PBDEs_in_NW.pdf; (accessed December 23, 2004). (33) Environmental Working Group. http://www.ewg.org/reports/ mothersmilk/ (accessed December 23, 2004). (34) Viberg, H.; Fredriksson, A.; Eriksson, P. Investigations of strain and/or gender differences in developmental neurotoxic effects of polybrominated diphenyl ethers in mice. Toxicol. Sci. 2004, 81, 344-353. (35) Kuriyama, S.; Talsness, C.; Grote, K.; Chahoud, I. Developmental exposure to low dose PBDE 99: Effects on male fertility and neurobehavior in rat offspring. Environ. Health Perspect. (in press); available at http://ehp.niehs.nih.gov/members/2004/ 7421/7421.pdf (accessed December 23, 2004). (36) McDonald, T. Distribution of PBDE levels among U.S. women: Estimates of daily intake and risk of developmental effects. Third International Workshop on Brominated Flame Retardants, June 6-9, 2004, Toronto, Canada; pp 433-446. (37) Soderstrom, G.; Sellstrom, U.; de Wit, C.; Tysklind, M. Photolytic debromination of decabromodiphenyl ether (BDE 209). Environ. Sci. Technol. 2004, 38, 127-132. (38) Parsons, J.; Zegers, B.; Skoczynska, E.; de Voogt, P. Reductive debromination of decabromodiphenyl ether (BDE 209) by anaerobic sediment microorganisms. Organohalogen Compd. 2004, 66, 2272-2274. (39) Mo¨rck, A.; Hakk, H.; O ¨ rn, U.; Klasson-Wehler, E. Decabromodiphenyl ether in the rat: Absorption, distribution, metabolism, and excretion. Drug Metab. Dispos. 2004, 31, 900907. (40) Stapleton, H. M.; Alaee, M.; Letcher, R. J.; Baker, J. E. Debromination of decabromodiphenyl ether by juvenile carp. Organohalogen Compd. 2003, 61, 21-24.
Arnold Schecter* and Kuang-Chi Tung University of Texas Health Science Center School of Public Health Dallas Regional Campus Dallas, Texas 75390
Olaf Pa1 pke ERGO Research Hamburg, 22305 Germany
Daniele Staskal University of North Carolina Curriculum in Toxicology Chapel Hill, North Carolina 27599
Linda Birnbaum U.S. Environmental Protection Agency National Health and Environmental Effects Research Laboratory Research Triangle Park, North Carolina 27709 ES058001K