Letters to the editor: Risks and Benefits of Seafood Consumption

interest, and impugns the credibility and objectivity of these studies. Note: We acknowledge funding support for portions of our work on farmed and wild salmon from the Pew Charitable Trusts, Philadelphia PA. Jeffery A. Foran, PhD David O. Carpenter, MD David H. Good, PhD M. Coreen Hamilton, PhD Ronald A. Hites, PhD Barbara A. Knuth, PhD Steven J. Schwager, PhD Midwest Center for Environmental Science and Public Policy, and School of Public Health, University of IllinoisChicago (Foran), Milwaukee, Wisconsin; Institute for Health and the Environment, University at Albany (Carpenter), Rensselaer, New York; School of Public and Environmental Affairs, Indiana University (Good, Hites), Bloomington, Indiana; AXYS Analytical Services Ltd. (Hamilton), Sidney, British Columbia, Canada; Department of Natural Resources, Cornell University (Knuth), Ithaca, New York; and Department of Biological Statistics and Computational Biology, Cornell University (Schwager), Ithaca, New York

References 1. Willett WC. Fish: balancing health risks and benefits. Am J Prev Med 2005;29:320 –1 (editorial). 2. Hites R, Foran JA, Carpenter D, Hamilton MC, Knuth BA, Schwager SJ. Global assessment of organic contaminants in farmed salmon. Science 2004;303:226 –9. 3. Bell JG, Henderson RJ, Tocher DR, Sargent JR. Replacement of dietary fish oil with increasing levels of linseed oil: modification of flesh fatty acid composition in Atlantic salmon using a fish oil finishing diet. Lipids 2004;39:1–10. 4. Bell JG, McGhee F, Dick JR, Tocher DR. Dioxin and dioxin-like PCBs in Scottish farmed salmon: effects of replacement of dietary marine fish oil with vegetable oils. Aquaculture 2005;243:305–14. 5. Foran JA, Good D, Carpenter D, Knuth BA, Hamilton MC, Schwager SJ. Quantitative analysis of the benefits and risks of consuming farmed and wild salmon. J Nutr 2005;135:2639 – 43. 6. Cohen JT, Bellinger DC, Connor WE, Shaywitz BA. A quantitative riskbenefit analysis of changes in population fish consumption. Am J Prev Med 2005;29:325–34. 7. Foran JA, Hites R, Carpenter D, Hamilton MC, Mathews-Amos A, Schwager SJ. A survey of metals in farmed and wild salmon. Environ Toxicol Chem 2004;23:2108 –10. 8. Huang X, Hites RA, Foran JA, et al. Consumption advisories for salmon based on cumulative risk of cancer and non-cancer health effects. Environ Res 2006. In press. 9. Foran JA, Carpenter D, Hamilton MC, Knuth BA, Schwager SJ. Risk-based consumption advice for farmed Atlantic and wild Pacific salmon contaminated with dioxins and dioxin-like compounds. Environ Health Perspect 2005;113:552– 6. 10. Cohen JT, Bellinger DC, Shaywitz BA. A quantitative analysis of prenatal methyl mercury exposure and cognitive development. Am J Prev Med 2005;29:353– 65. 11. Rice DC. The US EPA reference dose for methyl mercury: sources of uncertainty. Environ Res 2004;95:406 –13. 12. Konig A, Bouzan C, Cohen JT, et al. A quantitative analysis of fish consumption and coronary heart disease mortality. Am J Prev Med 2005;29:335– 46. 13. Albert CM, Hennekens CH, O’Donnell CJ, et al. Fish consumption and risk of sudden cardiac death. JAMA 1998;279:23– 8. 14. Asherio A, Rimm EB, Stamphfer MJ, Giovanucci EL, Willett C. Dietary intake of marine n-3 fatty acids, fish intake, and the risk of coronary heart disease among men. N Engl J Med 1995;332:977– 82.

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15. Hu FB, Bronner L, Willett WC, et al. Fish and omega–3 fatty acid intake and risk of coronary heart disease in women. JAMA 2002;287:1815–21. 16. DiPietro B. Did NFI and Tuna Foundation money influence Harvard seafood mercury study? October 21, 2005. Available at: www.intrafish.com. Accessed January 31, 2005. 17. U.S. Tuna Foundation. Harvard study finds life years gained by eating more fish. October 19, 2005 press release. Available at: www.tunafacts.com/ press/2005/oct19.cfm. Accessed January 31, 2005.

To the editors: The analysis by Cohen et al.1 of possible public health impacts of warnings about mercury and other contaminants in seafood, and the accompanying papers analyzing benefits and risks of seafood consumption, address an important and timely question with innovative analytical methods. The Harvard research team deserves credit for tackling this issue and for correctly stressing the need for balanced and accurate risk communication, a goal all stakeholders with an interest in mercury issues should support. However, the analysis has some significant methodologic shortcomings. The projected health risks and benefits of changes in seafood consumption patterns are derived from a series of hypothetical scenarios. Such scenarios are only as good as the assumptions on which they rest. The pivotal assumptions made by Cohen et al.,1 and the central basis for their conclusions that the negative health impacts of mercury warnings might outweigh the benefits, were, first, that all pregnant women (in their Scenario 2), and, second, that the entire U.S. adult population (in Scenario 3), would reduce their fish consumption by 17%, because of misunderstandings about mercury advisories. Cohen et al.1 based these assumptions a single study by Oken et al.2 But the latter study offers tenuous support at best for such severe, worst-case assumptions. Oken et al.2 studied the fish consumption of women in a large Boston obstetricsgynecology practice before and after the first Food and Drug Administration (FDA) advisory on mercury in fish was issued in March 2001.3 Women surveyed reduced their total fish intake from 7.7 to 6.4 meals per month in the 11 months after the advisory. Most of their total reduction (0.8 meals per month) came from eating less canned tuna, their most heavily consumed fish product, and one that contains moderate mercury levels. The women also ate 0.2 fewer meals per month of “dark meat fish,” a group including swordfish, a high-mercury species. Consumption of “white meat fish,” which generally are relatively lower in mercury, also dropped by 0.2 meals per month, and intake of shellfish, generally even lower in mercury, did not change. In short, the women studied by Oken et al.2 substantially decreased their intake of types of fish known to be significant sources of mercury exposure; they also, to a smaller extent, reduced their consumption of some varieties not generally associated with mercury risk. Although these changes in eating patterns did not perfectly match current FDA advice, they showed a reasonable trend in that direction. Cohen et al.1 might arguably have used the data collected by Oken et al.2 to support their Scenario 1—in which women accurately followed the current advisory and selectively eliminated high-mercury fish from their diets. But Cohen et al.2 ignored the finding by Oken et al.2 that women differentiated among the types of fish they ate less of, and instead used the study to support their assumption, in Sce-

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nario 2, that women would reduce their consumption of all types of fish by 17%. That assumption is also questionable for other reasons. The women Oken et al.2 studied were presumably influenced by the 2001 FDA advisory, a straightforward warning to avoid four specific high-mercury fish varieties. In 2004, the FDA and the U.S. Environmental Protection Agency (EPA) issued a new joint advisory, which conveyed much more balanced and nuanced information.4 The current advice stresses the benefits of eating fish and lists low-mercury fish to choose, as well as high-mercury fish to avoid. FDA and EPA were aware of the study by Oken et al.2 and explicitly aimed to avoid unintended consequences of their advice when developing the new advisory.5 The assumption by Cohen et al.1 that all U.S. women will react to current FDA/EPA advice the same way that a group of women in Boston did to a simpler, scarier warning 4 years ago seems quite far-fetched. Even less tenable is the assumption by Cohen et al.1 that all adults, including the elderly men who would lose the most in terms of cardiovascular health benefits, would decrease fish consumption by 17%, their basis for Scenario 3, which projects the most profound negative health impacts. Oken et al.’s2 study looked only at women of childbearing age; it provides no evidence to support this assumption. In fact, while Cohen et al.1 acknowledged this limitation in their published paper, Harvard’s press release about the study specifically ignores this critical caveat, claiming that “it is not difficult to imagine that other adults, not targeted by the advisory, cut back on fish based on misperceptions about the risks.” The key (and apt) word there is “imagine.” The 17% decrease in fish consumption that leads to the net negative public health impact in the scenarios by Cohen et al.1 is an imaginary risk. Unfortunately, the authors, Harvard’s press office, and media stories have treated it as if it were real. While the projected negative cardiovascular health impacts based on an imagined worst-case scenario have drawn the most public attention, another conclusion in the study by Cohen et al.1—and one with a more substantial basis in scientific evidence— has gone virtually without public comment. In their campaign to neutralize the impact of mercury warnings, fishing interests have stressed that the omega–3 fatty acids in fish are beneficial for neurologic development. (Cohen is also quoted on this specific point in Harvard’s press release.) The tuna industry, in particular, has repeatedly claimed that the benefits of fish consumption, including benefits to the developing fetal brain, vastly outweigh any risks associated with “trace” amounts of mercury in fish.6 The analysis by Cohen et al.1 specifically examined this risk–risk trade-off.7 Hazards of mercury exposure and benefits of omega–3 intake with respect to brain development were two of the four health outcomes projected in their scenarios.1 The results show that the mercury effects on the fetal brain (IQ points gained from reduced methyl mercury exposure, or IQ points lost due to increased mercury exposure following increased fish consumption) are much greater than omega–3 effects (IQ points gained from fish consumption, IQ points lost due to decreased fish intake). In Scenario 1, the mercury IQ effect is almost ten times greater than the omega–3 IQ effect; in the other scenarios, it is three times as great.8 In short, the Cohen et al.1 analysis suggests rather forcefully that, in this particular risk–risk trade-off, the harm done to

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the developing brain by mercury in fish greatly outweighs the benefits to the brain from the associated omega–3 intake. This is exactly the opposite of a prominent claim stressed in current industry public relations efforts. Neither the authors of the study nor the fishing industry interests that paid Harvard to do the analysis have focused public attention on this central result, which clearly supports the need for and the appropriateness of the health advisories that prompted their study in the first place. Edward Groth, III, PhD Groth Consulting Services, Pelham, New York 1. Cohen JT, Bellinger DC, Connor WE, Shaywitz BA. A quantitative riskbenefit analysis of changes in population fish consumption. Am J Prev Med 2005;29:325–34. 2. Oken E, Kleinman KP, Berland WE, Simon SR, Rich-Edwards JW, Gillman MW. Decline in fish consumption among pregnant women after a national mercury advisory. Obstet Gynecol 2003;102:346 –51. 3. U.S. Food and Drug Administration. An important message for pregnant women and women of childbearing age who may become pregnant about the risks of mercury in fish. Washington DC: U.S. Food and Drug Administration, March 2001. 4. U.S. Environmental Protection Agency. What you need to know about mercury in fish and shellfish. March 2005. Available at www.epa.gov/ waterscience/fishadvice/advice.html. Accessed November 21, 2005. 5. U.S. Food and Drug Administration and U.S. Environmental Protection Agency. What you need to know about mercury in fish and shellfish. Available at: www.epa.gov/waterscience/fishadvice/advice.html. Accessed November 21, 2005. 6. U.S. Tuna Foundation. Harvard study finds life years gained by eating more fish. Press release, October 19, 2005. Available at: www.tunafacts.com/press/ 2005/oct19.cfm. Accessed November 21, 2005. 7. Cohen JT, Bellinger DC, Shaywitz BA. A quantitative analysis of prenatal methyl mercury exposure and cognitive development. Am J Prev Med 2005;29:353– 65. 8. Cohen JT, Bellinger DC, Connor WE, Shaywitz BA. A quantitative analysis of prenatal intake of n–3 polyunsaturated fatty acids and cognitive development. Am J Prev Med 2005;29:366 –74.

To the editors: Konig et al.1 performed a meta-analysis of fish consumption and coronary heart disease (CHD) mortality, and in doing so referred to our recent meta-analysis publication on the same topic.2 We would like to offer a few corrections regarding references made to our previous work. In their discussion, they stated that two studies (Osler et al.3 and Yuan et al.4) included in our previous analyses should not have been included in a meta-analysis because Osler et al.3 did not use the lowest intake group as reference and Yuan et al.4 did not report the combined relative risk for all CHD mortality. They apparently did not recognize that we requested the original data from the relevant studies and had obtained de novo results from Osler et al.3 As for Yuan et al.,4 we pooled the relative risks of CHD death by weighting the inverse of variances derived from Yuan et al.,4 and used the pooled relative risks in the overall quantitative analyses. These facts were noted in our methods and acknowledgments.2 We believe that Konig et al.1 might have lost important information by excluding these two large cohort studies that we were able to include. We also note that Konig et al.1 assigned a serving size (100 g/day) to all included studies, even though some studies reported portion size, used absolute amount of fish consumption, or the portion size could be derived from the published information. We believe that this approach may cause misclassification bias in fish consumption. Contrary to what the

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