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Response to Comment on “Global Assessment of Polybrominated Diphenyl Ethers in Farmed and Wild Salmon” We thank Hardy for her interest in our paper about polybrominated diphenyl ethers in farmed and wild salmon (1). We appreciate her comments, which articulate clearly the views of one of the major U.S. manufacturers of brominated flame retardants. Hardy’s criticism is that we did not distinguish sufficiently between the less-brominated diphenyl ethers (such as BDE-47) and the fully brominated congener (BDE-209 or DecaBDE). We agree that this distinction is important given that the flame retardant industry is stopping production of the former but continuing production of the latter, but we are not sure how we could have been more clear. The Experimental Section of our paper listed the congeners we measured; we even added post-release text to indicate that DecaBDE was not present above our limit of detection in the farmed or wild salmon samples (although it was sometimes present in significant amounts in the feed samples). We (and many others) are gratified that the brominated flame retardant industry has stopped production of the lessbrominated diphenyl ether products in the United States. However, it is clear that these compounds will be contaminating people and the environment for years to come. Two examples illustrate this point: First, the production of polychlorinated biphenyls (PCBs) stopped in the United States in 1976, but PCBs are still present in the environment, and their concentrations are only slowly decreasing (halflives of 5-10 yr) (2). Second, the production of polybrominated biphenyls (PBBs), a flame retardant that is structurally analogous to PBDEs, stopped in 1977, but PBBs are still present in fishes from the Great Lakes, and their concentrations are only slowly decreasing (half-lives of >19 yr) (3). From these and many other examples, it is apparent that the environment will remain contaminated with these persistent organic pollutants for many years; the elimination of the source of contamination is only the first step in solving these problems. Although it was not the focus of our paper, Hardy argues for the continued production of DecaBDE. The arguments she makes to support this proposition seem to rest on three claims: (i) Hardy points out that DecaBDE saves lives by acting as a flame retardant. We agree, but we note that there are alternate products that would have the same beneficial social effects without contaminating the environment. Phosphatebased flame retardants, for example, are less environmentally persistent. (ii) Hardy claims that DecaBDE is not available biologically and does not accumulate in the environment. This is not true. DecaBDE is present in the particle phase of the atmosphere (4); in sediment from the United States and Canadian Great Lakes, and from European estuaries (5); and in the tissues of occupationally exposed people (6, 7). These results indicate that DecaBDE can accumulate in the ambient environment and in people and that DecaBDE is, in fact, available biologically. Incidentally, we suspect that the presence of DecaBDE in the environment and in people is under-reported because this compound has been rarely measured in these samples; thus, good data are not yet available to assess either DecaBDE’s concentrations in the 10.1021/es0484045 CCC: $30.25 Published on Web 12/03/2004
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environment and in people nor to track concentration changes over time. (iii) Hardy says that DecaBDE is not toxic and poses no risk. To support this argument, Hardy suggests that the toxicological database on PBDEs is extensive. It is not. The National Academy of Sciences (8) compilation, to which Hardy refers, cites the paucity of human epidemiological data on all PBDE congeners, including DecaBDE. The few studies on critical reproductive and developmental effects cited by the NAS are nearly 30 years old. More recently, a variety of PBDE congeners, including DecaBDE, have been evaluated for their developmental neurotoxicity (9). While there are questions regarding the statistical analysis used in some of these studies, the results suggest that there is a critical “window of sensitivity” for PBDE exposure that coincides with the period of rapid brain growth. Hardy emphasizes the NAS (8) conclusion that no further studies are needed to assess consumer health risks. She fails to state, however, that the NAS risk characterization was for direct human exposure to DecaBDE from its use in furniture. The NAS did not assess risks associated with ambient environmental exposures to PBDEs, including DecaBDE, nor did they consider the mounting evidence of increasing PBDE levels in the human tissues associated with environmental exposure. This is particularly important because there is evidence that DecaBDE degrades to less-brominated congeners (discussed fully in ref 9). For example, there is increasing evidence that some animals, including fish, can metabolize DecaBDE to less-brominated congeners (10). Hardy’s most troubling statements are associated with her interpretation of the NAS (8) assessment of the toxicology of DecaBDE. Hardy fails to report that the NAS concluded that DecaBDE induced thyroid hyperplasia in male rats, thyroid follicular cell hyperplasia in male mice (which was induced at the lowest concentration tested), liver changes in male rats and mice (some of which, again, occurred at the lowest concentrations tested), and most importantly, cancer in rats and mice. More than one type of cancer, hepatocellular adenomas and carcinomas and thyroid gland follicular cell adenomas and carcinomas, occurred in laboratory carcinogenicity studies of DecaBDE. Hardy also fails to acknowledge the U.S. EPA’s weight-of-evidence cancer classification of DecaBDE as “possible human carcinogen” (based on the EPA’s 1986 guidelines) and “suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential” based on the EPA’s 1996 draft guidelines. The NAS (8) stated that they could not conclude that DecaBDE is a carcinogen in humans but that a conservative approach is justified to be protective of human health. The NAS even went so far as to develop a cancer potency factor for DecaBDE. Incidentally, Hardy suggests incorrectly that we misstated European actions to regulate PBDEs. In paragraph 6 of our Results and Discussion section (1), we state clearly that, while DecaBDE and other BDEs were considered for regulatory action, Europe banned only the Penta- and OctaBDE products. In summary, we agree that studies of PBDEs should report congener-specific information, as we did in our evaluation of PBDEs in farmed and wild salmon. We also agree that the toxicological evidence should be assessed for specific congeners; however, it is important to note that humans or the environment are not exposed to a single congener. Therefore, ambient monitoring and toxicological evaluation should include all PBDE congeners, including DecaBDE. The absence of a particular congener, such as DecaBDE, in environmental media does not support the safety of that congener, VOL. 39, NO. 1, 2005 / ENVIRONMENTAL SCIENCE & TECHNOLOGY
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particularly where monitoring data for that congener are lacking or where that congener may degrade to lower homologues, which may be more toxic.
Literature Cited (1) Hites, R. A.; Foran, J. A.; Schwager, S. J.; Knuth, B. A.; Hamilton, M. C.; Carpenter, D. O. Global assessment of polybrominated diphenyl ethers in farmed and wild salmon. Environ. Sci. Technol. 2004, 38, 4945-4949. (2) Buehler, S. S.; Basu, I.; Hites, R. A. Gas-phase polychlorinated biphenyl and hexachlorocyclohexane concentrations near the Great Lakes: An historical perspective. Environ. Sci. Technol. 2002, 36, 5051-5056. (3) Zhu, L. Y.; Hites, R. A. Temporal trends and spatial distributions of brominated flame retardants in archived fishes from the great lakes. Environ. Sci. Technol. 2004, 38, 2779-2784. (4) Strandberg, B.; Dodder, N. G.; Basu, I.; Hites, R. A. Concentrations and spatial variations of polybrominated diphenyl ethers and other organohalogen compounds in Great Lakes air. Environ. Sci. Technol. 2001, 35, 1078-1083. (5) Hites, R. A. Polybrominated diphenyl ethers in the environment and in people: A meta-analysis of concentrations. Environ. Sci. Technol. 2004, 38, 945-956. (6) Stanley, J. S.; Cramer, P. H.; Thornburg, K, R,; Remmers, J. C.; Breen, J. J.; Schwemberger, J. Mass spectral confirmation of chlorinated and brominated diphenylethers in human adipose tissues. Chemosphere 1991, 23, 1185-1195. (7) Sjo¨din, A.; Hagmar, L.; Klasson-Wehler, E.; Kronholm-Diab, K.; Jakobsson, E.; Bergman, A. Flame retardant exposure: Polybrominated diphenyl ethers in blood from Swedish workers. Environ. Health. Perspect. 1999, 107, 643-648. (8) National Academy of Sciences. Toxicological Risks of Selected Flame Retardant Chemicals; National Academy Press: Washington, DC, 2000. (9) Birnbaum, L. S.; Staskal, D. F. Brominated flame retardants: Cause for concern? Environ. Health. Perspect. 2004, 112, 9-17. (10) Kierkegaard, A.; Balk, L.; Tja¨rnlund, U.; deWit, C.; Jansson, B. Dietary uptake and biological effects of decabromodiphenyl ether in rainbow trout. Environ. Sci. Technol. 1999, 33, 16121617.
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Ronald A. Hites* School of Public and Environmental Affairs Indiana University Bloomington, Indiana 47405
Jeffery A. Foran Midwest Center for Environmental Science and Public Policy Milwaukee, Wisconsin 53202
Steven J. Schwager Department of Biological Statistics and Computational Biology Cornell University Ithaca, New York 14853
Barbara A. Knuth Department of Natural Resources Cornell University Ithaca, New York 14853
M. Coreen Hamilton AXYS Analytical Services Ltd. P.O. Box 2219 2045 Mills Road Sidney, British Columbia, Canada V8L 3S8
David O. Carpenter Institute for Health and the Environment University at Albany Rensselaer, New York 12144 ES0484045
