[1] Ropeik (2004) European Molecular Biology Organization Reports, vol. 5 (special issue), S56-S60.

[2] Ropeik (2004) continues that “As argued for by Matthew Adler and others (2003), the effects of fear are harmful to health, no less than the physical harm from some toxic agent or pollutant, and these can and should be measured and economically quantified to help identify the most efficient approaches to improving public health.”

[3] Kraepiel, A. M., Keller, K.., chin, H.B., Malcolm, E.G., & Morel, F.M. (2003). Sources and variations of mercury in tuna. Environmental Science & Technology, 37, 5551-5558. Miller,, et al, (1972). Mercury concentrations in museum specimens of tuna and swordfish, Science, 175, 1121-1122.

[4] Ibid.

[5] Tsubaki, T., & Irukayama, K. editors (1977). Minamata Disease: Methylmercury poisoning in Minamata and Niigata, Japan. Elsevier Publishing Company: New York.

[6] Ibid.

[7] Developmental Disabilities Following Prenatal Exposure to Methyl Mercury from Maternal Fish Consumption: A Review of the Evidence, Meyers, et al. (2006), University of Rochester Medical Center, correspondence.

[8] In clinical studies, laboratory rats exposed to PCBs (but not MeHg) showed adverse neurological effects, while rats exposed to MeHg (but not PCBs) showed no effects. Rats exposed to both PCBs and MeHg (as in the Faroe study and the U.S. Great Lakes) showed greater adverse effects than those rats exposed to PCBs only. (J. Bemis and R. Seegal, 1999, “Polychlorinated Biphenyls and Methylmercury Act Synergistically to Reduce Rat Brain Dopamine content in Vitro,” Environmental Health Perspectives, vol. 107: 879–885.)

In a letter to EPA, Dr. Kenneth Poirier and Dr. Michael Dourson, former EPA RfD/Reference Concentration Work Group co-chairs, provided these scientific findings to the Technical Information Staff at EPA.

[9] Meyers, et al., op. cit.

[10] Minamata disease, sometimes referred to as Chisso-Minamata disease, is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision and damage to hearing and speech. In extreme cases, insanity, paralysis, coma and death follow within weeks of the onset of symptoms.

[11] Ibid.

[12] Tsubaki, op. cit..

[13] Saito,H. (2004a). Congenital Minamata disease: a description of two cases in Niigata. Seychelles Medical Dental J.7(1), 134-137.

[14] Watanabe, C. & Satoh, H. (1996). Evolution of our understanding of methylmercury as a human threat. Environmental Health Perspectives, 104 Supplement 2, 367-379.

[15] Moriyama, H. Takizawa, Y. (2001). Assessing low-dose effects on children exposed in utero to methylmercury – protocol for on-the-spot re-inspection for Minamata and Niigata data at early stage. In Methylmercury poisoning in Minamata and Niigata, Japan. Edited by Takizawa, Y. and Osame, M. Tokyo: Japan Health Association, 54-60.

[16] Saito, et al., (2004b). Prenatal and postnatal methylmercury exposure in Niigata, Japan: adult outcomes. Seychelles Medical Dental J, 7(1), 138-145.

[17] Saito, H. (2004a), op. cit.

[18] Sakamoto et al. (2006) Environmental Research, in press (available online May 2, 2006).

[19] As determined by MeHg contents in their birth cord tissues. It should be noted that mercury content in both cord blood and cord tissue are in general some tens to hundred times lower than that measured in hair. The Sakamoto et al. (2006) data are able to confirm that the mean total mercury content in hair samples of the 115 Japanese women is about 1.62 ppm, with the 25th-75th percentiles ranging from 1.18 to 2.20 ppm, which in turn is significantly higher than the overly restrictive EPA RfD of about 1 ppm for hair mercury content.

[20] Coincident to the peak period of acetaldehyde production in Minamata before the installation of waste water management systems.

[21] Akagi et al. (1998) Environmental Research, vol. 77, 98-103.

[22] Meyers, et al., op. cit.

[23] Meyers, et al., op. cit..

[24] Meyers, et al., 2006, “Development Disabilities…”, International Review of Research in Mental Retardation, Vol. 30.

[25] Dourson, et al., Toxicology Excellence for Risk Assessment, ALEC, December 3, 2000.

[26] See “Making Sense of State Fish Advisories” (http://ff.org/centers/csspp/pdf/20050228_hgfishadvisories.pdf)

[27] Dourson et al. (2001) Neurotoxicology, vol. 22, 677-689 and see additional discussions from CSPP's publications at http://www.scienceandpolicy.org/.

[28] The Danish Ministry of Environment's National Environmental Research Institute's Technical Report (2004) No. 525, "Screening of 'new' contaminants in the marine environment of Greenland and The Faroe Islands". CSPP thanks Professor Gary Myers of the University of Rochester for this communication.

[29] One might ask about Weihe’s cited connection between the Faroes study and Harvard. It is only that Phillippe Grandjean of Denmark, who led the Faroes Study, then moved to Boston for an adjunct position at Harvard Med School. Harvard had nothing to do with neither the original study nor the follow up analyses.

[30] Comments of the Utility Regulatory Group to EPA (69 Fed. Reg. 12398 [March 16, 2004]), Docket ID No. OAR-2002-0056.

[31] The State of California vs. Tri-Union Sea Foods. April 17, 2006

[32] Ibid. p 40. “Effects of PCB Exposure on Neuropsychological Function in Children”

[33] Ibid. p. 40, 41

[34] Grandjean et al. (2001) Neurotoxicology & Teratology, vol. 23, 305-317

[35] 1997, Neurotoxicology and Teratology, vol. 19, 417-428

[36] J. Bemis and R. Seegal, 1999, “Polychlorinated Biphenyls and Methylmercury Act Synergistically to Reduce Rat Brain opamine content in Vitro,” Environmental Health Perspectives, vol. 107: 879–885.

[37] Meyers, et al., “Developmental Disabilities Following Prenatal Exposure to Methyl Mercury from Maternal Fish Consumption: A Review of the Evidence” International Review of Research in Mental Retardation, 2006.

[38] Methylmercury (MeHg). EPA's Integrated Risk Information System available at http://www.epa.gov/iris/subst/0073.htm.

[39] Clarkson TW, Cox C, Davidson PW, Myers GJ. “Mercury in Fish.” Letter to the editor Science. 279:459-460. 1998

[40] 2001, Neurotoxicology, vol. 22, 677-689

[41] p. 1692 of Myers et al. (2003) The Lancet, vol. 361, 1686-1692.

[43] Meyers et al., op cit

[44] Kjellstrom et al. (1986, 1989)

[45] Meyers, op cit

[46] Dourson et al. 2001, Neurotoxicology, vol. 22, 677-689.

[47] Crump et al., 1995, Risk Analysis, vol. 15, 523-532.

[48] Crump et al., 2000, Environmental Health Perspectives, vol. 108, 257-263.

[49] Weis (2004) Environmental Research, vol. 95, 341-350.

[50] http://www.marchofdimes.com/prematurity/5413_11560.asp

[51] Ibid.

[52] Ibid.

[53] Olsen and Secher (2002) British Medical Journal, vol. 324, 447-450.

[54] Smuts et al., 2004, Obstetrics and Gynecology, vol. 101, 469-479.

[55] Olsen and Secher (2002) British Medical Journal, vol. 324, 447-450.

[56] July 24, 2002 FDA food advisory committee on methylmercury, transcript available at http://www.fda.gov/OHRMS/DOCKETS/ac/02/transcripts/3872t2.htm

[57] Hibbelin (2002) Journal of Affective Disorders, vol. 69, 15-29.

[58] Daniels et al. (2004) Epidemiology, vol. 15, 395-402.

[59] Richardson and Montgomery (2005) Pediatrics, vol. 115, 1360-1366.

[60] Gago-dominguez et al., 2003, British Journal of Cancer, vol. 89, 1686-1692.

[61] Terry et al., 2003, American Journal of Clinical Nutrition, vol. 77, 532-543.

[62] Donadio and Grande, 2002, New England Journal of Medicine, vol. 347, 738-748.

[63] He et al., 2002, JAMA, vol. 288, 3130-3136.

[64] Iso et al., 2001 JAMA, vol. 285, 304-312.

[65] Quillin, How to Reverse Diabetes, 2005, p. 7.

[66] U.S. Department of Health and Human Services, Food and Drug Administration, Center for Food Safety and Nutrition, Food Advisory Committee. Methylmercury Meetings, July 23-24, 2002.

[67] Salmeron et al., 2001, American Journal of Clinical Nutrition, vol. 73, 1019-1026.

[68] Circulation, Mar 2003; 10000062. American Heart Association: http://www.americanheart.org/

[69] Morris et al., 2003, Arch. Neurol.., vol. 60, 940-946.

[70] Friedland et al., 2003, Arch. Neurol., vol. 60, 923-924.

[71] Kalmijin et al., 2004, Neurol., vol. 275-280.

[72] Morris et al. (2005) Archives of Neurology, vol. 62, 1849-1853.

[73] Weil et al. (2005) Journal of the American Medical Association, vol. 293, 1875-1882.

[74] Sappy C et al. (1994), Journal of Aids Research and Human Retrovirology 10, 1451-1461.

[75] Margaret P. Rayman, The argument for increasing selenium intake, Proceedings of the Nutrition Society (2002), vol 202-215.

[76] Terry et al., The Lancet, vol. 357, 1764-1766.

[78] USDA and HHS recommended an approximate total of 8 ounces per week

[80] "Blood Mercury Levels in Young Children and Childbearing-Aged Women ---United States, 1999--2002" report available at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5343a5.htm.

[81] In reality, even this single woman may not exceed the RfD because it is unlikely her long-term mean average is as high as 7.7 ppb. If so, she would have to be extraordinary for Americans by eating regular fish meals. Or she could easily have consumed a high-end mercury fish like shark for swordfish shortly before the blood test, which would have given her a short term “mercury spike.” Mercury clears the human body in about 60 days on average.

[82] Yasutake et al. (2004) Journal of Health Science, vol. 50 (2), 120-125.

[83] Yasutake et al. (2003) Tohoku Journal of Experimental Medicine, vol. 199, 161-169.

[84] From the December 21, 2005's China Post article "People in Taiwan free from mercury poisoning, EPA says" (available at http://www.chinapost.com.tw/i_latestdetail.asp?id=33723) .

[85] McDowell et al. (2004) Environmental Health Perspectives, vol. 112, 1165-1171.

[86] p. 2 of Taipei Times on August 30, 2005 “Taipei residents’ mercury content is too high, tests say” (available at http://www.taipeitimes.com/News/taiwan/archives/2005/08/30/2003269687) quoting mainly Hsu Ming-Lun, director of the Taipei City Health Bureau’s laboratory.

[87] Walker et al. (2006) Environmental Research, in press (available online August 3, 2005).

[88] pp. 47-48 of "Methodology used to generate deposition, fish tissue methylmercury concentrations, and exposure for determining effectiveness of utility emission controls" available at http://www.epa.gov/ttn/ecas/regdata/Benefits/Final_Effectiveness.pdf.

[89] What the Agency apparently means is a sort of one-sided bright line: below the RfD there is no risk; above it there may be some risk, magnitude undetermined, but increasing in some unknown manner as the distance above the RfD increases.

[90] The FDA's mean mercury level for orange roughy is similar to CT's 18-sample mean but the FDA mean level of 0.55 ppm for grouper is significantly higher than CT's 0.26 ppm.

[91] Burger and Gochfeld (2004) Environmental Research, vol. 96, 239-249. CSPP further notes from the manuscript submission, acceptance and appearance dates (November 2004) that there is clearly no acceptable excuse for the Rutgers researchers to simply ignore the well-publicized results from the FDA's 2002/2003 mercury measurements for 2 canned tuna products (albacore and " light") and 12 different species of fish.

[92] From the September 19, 2005 presentation by Donald Kraemer, the acting director of FDA's Office of Seafood at the EPA's 2005 Fish Forum available at http://epa.gov/waterscience/fish/forum/2005/.

[93] See for example the June 2001 EPA fish advisory fact sheet (EPA-823-F01-011) available from the EPA's Office of Water web: http://epa.gov/ost/fishadvice/mercupd.pdf.

[95] Carrington et al. (2004) Regulatory Toxicology and Pharmacology, vol. 40, 272-280.

[96] See "Making sense of state fish advisories" report by CSPP available at http://www.scienceandpolicy.org.

[97] From the fact sheet of Canadian Food Inspection Agency dated May 2002 at http://inspection.gc.ca/english/corpaffr/foodfacts/mercurye.shtml/.

[97] The 38 eastern U.S. states are AL, AR, CT, DC, DE, FL, FA, IA, IL, IN, KS, KY, LA, MA, MD, ME, MI, MN, MO, MS, NC, ND, NE, NH. NJ. NY, OH, OK, PA, RI, SC, SD, TN, TX, VA, VT, WI, and WV.

[99] Knobeloch et al. (2005) Environmental Research, vol. 97, 220-227.

[100] Cole et al. (2004) Environmental Research, vol. 95, 305-314.

[101] Morrissette et al. (2004) Environmental Research, vol. 95, 363-374.

[102] It is rather remarkable to find the "regulatory affair manager" of Springfield, Illinois's City Water, Light and Power (CWLP), Bill Murray, appearing in public suggesting that their "Dallman generators were able to remove about 90 percent of the mercury contained in coal, while a third extracted about 82 percent." In case you may be confused on what sort of control technology the mercury extraction may constitute, consider this next quote. "CWLP's Dallman units were tested last summer in preparation for new federal regulations scheduled to go into effect in 2010, Murray said. ... But Murray emphasized that the test was conducted using complex mathematical calculations and does not guarantee each unit's performance on a continual basis. Measuring devices that gauge mercury constantly are not on the market, he said." Somewhat later further confusing statements: "Still, Murray said he's not convinced that the difference between the Blagojevivh proposal at 90 percent and federal regulation at 79 percent is ultimately going to mean much to the environment. "The quantity of mercury we're talking about is very minute, he said. "Trying to remove mercury from a stack or a combustion process from coal is like if you filled the Astrodome with ping-pong balls and you painted one of them silver. What you are trying to do is find that silver ball in all those balls in the Houston Astrodome. The technology to do that is tough." " (Read this January 6, 2006 news article at http://www.sj-r.com/sections/news/stories/75499.asp by reporter Chris Wetterich and with contribution by the Associated Press.)

[103] It is instructive that Roe and Hawthorne, like other activists insist on labeling Hg entering the system as a “pollutant” only in reference to anthropogenic sources. Are the vastly larger natural sources also pollutants”? What does one then do about Yellowstone National Park which has for centuries likely emitted more Hg into the air than all Wyoming’s coal-fired plants combined?

[104] Krug and Winstanley (2004) Hydrology & Earth System Sciences, vol. 8, 98-102.

[105] Pat E. Rasmussen, Environ. Sci. Technol., Vol. 28, No. 13, 1994

[106] A.S.Astakhov, G.I.Koruykin, M.V.Ivanov, Pacific Oceanological Institute, Vladivostok, Russia, PANGEA Inc., Moscow, Russia

[107] Pat E. Rasmussen, Environ. Sci. Technol., Vol. 28, No. 13, 1994

[108] Pacyna et al. 2003, Freidli et al. 2003

[109] The 58,000 tons of natural mercury emission annually with better accounting for major geological sources from previous study is from the 2001 report "Critical Review on Natural Global and Regional Emissions of Six Trace Metals to the Atmosphere" by Richardson et al. as a technical report prepared for the International Lead Zinc Research Organization, International Copper Association, and the Nickel Producers Environmental Research Association.

[110] Richardson et al. (2003) Environmental Reviews, vol. 11, 17-36.

[111] http://teacher.scholastic.com/researchtools/articlearchives/volcanoes

[112] http://newsdesk.inel.gov/press_releases/2003/10-21mercury_testing.htm

[113] Shannon and Voldner (1995) Atmospheric Environment, vol. 29, 1649-1661.

[114] Article dated November 23, 2003 by Jane Kay entitled "Toxic Fish Alert-Survey finds mercury in 4 species at markets in Bay Area" available at http://www.sfgate.com/cgi-bin/article.cgi?file=/c/a/2003/11/23/MNGIO394FI1.DTL.

[115] Hightower and Moore (2003) Environmental Health Perspectives, vol. 111, 604-608.

[116] Dorea et al., 2003, Environmental Research.

[117] “Over the past few months I have found myself enjoying more and more the process of blogging. I'd written personal essays before, but never on this scale -- never so often and with such, er, honesty. (If by honesty I mean slashing my wrists and hemorrhaging all over the computer screen). By far the best part has been meeting people in the comments section and through emails.”

[118] http://bad-mother.blogspot.com/

[119] Tang, S., et al., Mercury speciation and emissions from coal combustion in Guiyang, southwest China, Environm. Res. (2007), doi:10.1016/jenvres.2007.03.008

[120] Walker, et al., 2005, “Maternal and umbilical cord blood levels of mercury, lead, cadmium, and essential trace elements in Arctic Canada”, Environmental research.

[121] “EPA MACT Rulemaking Not Justified by Science’, Center For Science and Public Policy (http://ff.org/centers/csspp/pdf/mercurywhitepaper.pdf)

[122] Meyers, et al., 2006, “Development Disabilities…”, International Review of Research in Mental Retardation, Vol. 30.

[123] EPRI Comments on EPA Proposed Emission Standards, Docket ID No. OAR-2002-0056, June 16, 2004.

[124] Ibid.

[125] US EPA, Comments of the Utility Air Regulatory Group, Docket ID No. OAR-2002-0056, June 29, 2004. See also: http://ff.org/centers/csspp/pdf/mercurywhitepaper.pdf

[126] http://ff.org/centers/csspp/pdf/20050119HGHeart.pdf

[127] We have recently granted the request of a major university to achieve this paper and make it permanently available to students, faculty and researchers.

[128] Salonen et al (1995) Circulation, vol. 91, 645-655 and Salonen et al. (2000) Atherosclerosis, vol. 148, 265-273.

[129]Virtanen et al. (2002) poster presentation entitled "Hair content of mercury and risk of cardiovascular and coronary heart disease mortality: The Kupio Ischaemic Heart Disease Risk Factor (KIHD) Study" in the April 23-26, 2002 American Heart Association, Asia Pacific Scientific Forum at Honolulu, Hawaii.

[130] Virtanen et al. (2005) Arteriosclerosis, Thrombosis, and Vascular Biology, January, doi: 10.1161/01.ATV.0000150040.20950.61.

[131] Guallar et al. (2002) New England Journal of Medicine, vol. 347, 1747-1754.

[132] Stern (2005) Environmental Research, vol. 98, 133-142.

[133] Clarkson (2002) Environmental Health Perspectives, vol. 110 (supplement 1), 11-23.

[134] See When Fears Harm, by Sandy Szwarc, at www.scienceandpolicy.org

[135] Agren et al. (1988) Lipids, vol. 23 (No.10), 924-929.

[136] The summary provided by the commercial fish oil website at http://www.oilofpisces.com/hearthealth.html (reaccessed January 11, 2006) further explained that: “A 15-week experiment involving 62 students was carried out to determine if a regular diet of freshwater fish affects coronary heart disease risk factors. The students were divided into three groups: a fish eating group who made no other changes to their diet, a fish eating group who also decreased their overall fat intake and a control group (19 students) who ate a typical western diet. The special diet consisted of one fish meal a day (in addition to the regular diet) and provided about 0.25 g/day of eicosapentaenoic acid [EPA fatty acids] and 0.55 g/day of docosahexaenoic acid [DHA fatty acids]. Serum cholesterol was found to decrease in fish eaters who also decreased their lipid intake but not in the other groups. Blood triglyceride levels decreased significantly in the fish eating groups, but not in the control group. Levels of apolipoproteins A1 and B were lowered in both fish eating groups as was the formation of thromboxane B2 during incubation of whole blood. In the fish eating groups, the proportion of omega-3 fatty acids increased significantly in erythrocyte ghosts and platelets at the expense of omega-6 fatty acids. The results of the study support the contention that moderate fish consumption has a protective effect against coronary heart disease.”

[137] Plante and Babo (2003) New England Journal of Medicine, vol. 348, 2151-2152.

[138] Albert et al. (2002) New England Journal of Medicine, vol. 346, 1113-1118.

[139] Leaf et al. (2003) Circulation, vol. 107, 2646-2652.

[140] Siscovick et al. (2003) Circulation, vol. 107, 2632-2634.

[141] From the August 26, 1998 news article "COMMERCIAL FISH: EAT UP, DESPITE LOW LEVELS OF MERCURY" from the University of Rochester available at http://www.rochester.edu/pr/releases/med/mercury.htm.

[142] April 10, 2004, NY Times article by Jennifer Lee

[143] Mozaffarian et al. (2004) Circulation, vol. 110, 368-373.

[144] In an earlier publication (Mozaffarian et al., 2003, Circulation, vol. 107, 1372-1377), Mozaffarian and colleagues pointed to the importance of types of fish meal consumed, finding that fried fish or fish sandwiches may not offer the same level of protection for the heart as broiled or baked fish.

[145] Calo et al. (2005) Journal of the American College of Cardiology, vol. 45, 1723-1728.

[146] Hightower is a San Francisco doctor who's apparently become a magnet for people who feel vaguely bad, but who want a more fashionable diagnosis than chronic fatigue syndrome. There are a slew of articles on her in the SF Chronicle, most written by the environmental writer, not the medical or science writer who might have known the distinction between a clinical physician and an epidemiologist. Most would agree she is simply not qualified to be drawing any conclusions about mercury. Sorting out the causes of subjective and subtle symptoms is not something a lone physician can do. There would need to be a very carefully controlled double-blind protocol where independent investigators took a random representative sample of people and classified them by symptoms without knowing their mercury status, and then matched them with their tested mercury levels. People who were aware of mercury and the supposed symptoms it causes would need to be disqualified from the study.

[147] Hightower and Moore (2003) Environmental Health Perspectives, vol. 111, 604-608.

[148] Schoen (2004) Environmental Health Perspectives, vol. 112, p. A337; and Hightower's further commentary on p. A337-A338.

[150] Hightower and Moore (2003) Environmental Health Perspectives, vol. 111, 604-608.

[151] State of Alaska Epidemiology bulletin No. 11 (December 2, 2004). Anyone seriously interested in the risk perspectives of fish in a healthy diet should read this bulletin found at: http://www.epi.hss.state.ak.us/bulletins/docs/rr2004_11.pdf

[152]The exposure in Faroes was to pilot whale meat and blubber that also contains PCBs (one of the highest exposures known), pesticides and other persistent organic pollutants. The Seychelles exposure was from fish consumption with PCBs below detectable levels. (See Section 1)

[153] Further, there were no control subjects in the Faroes study - that is no unexposed children. The subjects were divided into quintiles of mercury hair levels in mothers at birth. The quintile boundaries were selected to include roughly the same number of subjects in each quintile. The difference in median response time on a computer image recognition test between highest and lowest quintile exposures was a mere “72 milliseconds”. On such are regulatory empires built.

[154] Morel et al. (1998) Annual Review of Ecology and Systematics, vol. 29, 543-566.

[155] Can mercury from a thermometer pollute a lake? http://www.junkscience.com/feb01/wallacemercury.htm

[156] The FDA's fish mercury directory is accessible here: http://vm.cfsan.fda.gov/~frf/sea-mehg2.html.

[157] See Table 2 of Mahaffey (2004) Environmental Research, vol. 95, 414-428.

[158] Mendez et al. (2001) Journal of Food Composition and Analysis, vol. 14, 453-460.

[159] There is another reasonable RfD value available alternative to the most restrictive one by EPA. A panel of risk assessment experts – convened in January and February of 1998 – derived a set of “site-specific” MeHg RfDs ranging from 0.3 to 1.0 mg/kg (b.w.)/day, with the median value of 0.54 mg/kg (b.w.)/day. This range of values is believed more appropriate for fish-eating populations, like those in Lacava Bay, Texas. Accordingly, if this expert-derived RfD mean value of 0.54 mg/kg (b.w.)/day were adopted, then a threshold value of fish tissue MeHg as high as 2 ppm would be tolerable before triggering a fish advisory or any confiscation of seafood. (The panel was convened under the leadership of Michael Dourson of the non-profit organization, Toxicology Excellence for Risk Assessment (TERA). Two reports generated for the derivation of this site-specific RfD are available at http://www.tera.org/peer/MeetingReports.html —look under Methylmercury RfD).

[162] Mahaffey (2004) Environmental Research, vol. 95, 414-428.

[163] Raymond and Ralston (2004) Seychelles Medical and Dental Journal, Special Issue, vol. 7, 72-77.

[164] Burger and Gochfeld (2005) Environmental Research, vol. 99, 403-412.

[165] Plessi et al. (2001) Journal of Food Composition and Analysis, vol. 14, 461-467.

[166] Meyers, et al. (2006), Developmental Disabilities Following Prenatal Exposure to Methyl Mercury from Maternal Fish Consumption: A Review of the Evidence, International Review of Research in Mental Retardation, Vol. 30, 141-169.

[167] Jan Robinson, MSc; Jude Shroff, BSc, Observations on the levels of total mercury (Hg) and selenium (Se) in species common to the artisanal fisheries of Seychelles,SMDJ Seychelles Medical and Dental Journal, Special Issue, Vol 7, No 1, November 2004, p.56-57.

[168] Dorea (2003) Environmental Research, vol. 92, 232-244.

[1]69 Lima et al. (2005) Environmental Research, vol. 97, 236-244.

[170] Rayman (2000) The Lancet, vol. 356, 233-241.

[171] Margaret P. Rayman, The argument for increasing selenium intake, Proceedings of the Nutrition Society (2002), vol 202-215.

[172] p. 72 and 75 of Raymond and Ralston (2004) Seychelles Medical and Dental Journal, Special Issue, vol. 7, 72-77.

[173] Ralston. Physiological and Environmental Importance of Mercury-Selenium Interactions. Energy & Environmental Research Center Fish Forum 2005, September 19, 2005 (http://www.epa.gov/ostwater/fish/forum/2005/presentations/Monday%20Slides%200919/afternoon/Ralston%20Presentation.ppt)

[174] Ganther et al. (1972) Science, vol. 175, 1122-1124.

[176] http://ff.org/centers/csspp/pdf/20050228_hgfishadvisories.pdf

[177] p. 682 of Dourson et al. (2001) Neurotoxicology, vol. 22, 677-689.

[178] McDowell et al. (2004) Environmental Health Perspectives, vol. 112, 1165-1171.

[179] Mahaffey 2004

[180] Dorea et al., 2004, “Hair mercury (signature of fish consumption) and cardiovascular risk in Munduruku and Kayabi Indians of Amazonia”, Environmental Research, p. 8.

[181] Ibid.

[182] Storelli et al. (2002) Food Additives and Contaminants, vol. 19, 715-720; and Storelli and Marcotrigiano (2004) Food Additives and Contaminants, vol. 21, 1051-1056.

[183] Kraepiel et al. (2003) Environmental Science & Technology, vol. 37, 5551-5558.

[184] Zhang et al. (2002) Ambio, vol. 31, 482-484.

[185] p. 5551 Kraepiel et al. (2003) Environmental Science & Technology, vol. 37, 5551-5558.

[186] Environmental Science and Technology, 2004, 38, 4048

[187] Barber et al. (1984) Environmental Science & Technology, vol. 18 (no. 7), 552-555.

[188] p. 1122 of Miller et al. (1972) Science, vol. 175, 1121-1122. There is a puzzling attempt in a recent report (Code RL32420 entitled Mercury in the Environment: Sources and Health Risks) by Linda-Jo Schierow of the Congressional Research Service (CRS) to discredit this important pioneering paper by Miller et al. (1972). The June 3, 2004 CRS report claimed in its footnote 48 that Miller et al. (1972) “reported the study in a letter to the editor of Science, it was not peer-reviewed, and is [thus] an insufficient basis for drawing any conclusions.” This is clearly mistaken. The March 10, 1972 Miller et al.’s contribution is a peer-reviewed REPORT rather than a LETTER TO EDITOR for Science magazine. One of the members of this 1972 Miller et al. team is F.S. Rowland, the co-recipient of the 1995 Nobel Prize for Chemistry.

[189] For a more in-depth examination of EPA’s CAMR, see CSPP’s “EPA NODA Comments” at

[190] California vs. Tri-union Seafoods, Superior Court of California, San Francisco, April 17, 2006.

[191] Hightower and Moore (2003) Environmental Health Perspectives, vol. 111, 604-608. Another paper in press for the journal Environmental Health Perspectives by Dr. Hightower and colleagues is entitled "Blood mercury reporting in NHANES: Identifying Asian, Pacific Islander, Native American, and multiracial groups" (available online September 21, 2005). Although this paper is not a topic of discussion for this claim, CSPP notes that Hightower now identifies the EPA's RfD blood mercury threshold to be 5.8 ppb, rather than 5.0 ppb previously used in Hightower and Moore (2003) discussed in reply # 9 in the main text.

[192] Mason et al. (2005) Environmental Science and Technology, vol. 39, A14-A22.

[193] NESCAUM claims peer review, but it was only an internal review by a few selected EPA staff.

[195] Actually listed in the EPA (1997) report as 0.206 ppm but rounded off to 0.21 ppm in Mahaffey (2004).

[196] All 8 volumes of reports are available here http://www.epa.gov/mercury/report.htm.

[197] Yess (1993) Journal of AOAC International, vol. 76, 36-38.

[198] see the presentations "Mercury levels in Fish-Recent FDA data" by David Acheson (January 26, 2004) and "National Mercury Advisory: Description of Existing Advisory & August 2003 FDA FAC Recommendations" by David Acheson and Denise Keehner (January 26, 2004) available at http://epa.gov/waterscience/fish/forum/2004/.

[199] From the September 19, 2005 presentation by Donald Kraemer, the acting director of FDA's Office of Seafood at the EPA 2005 Fish Forum available at http://epa.gov/waterscience/fish/forum/2005/.

[200] Burger and Gochfeld (2004) Environmental Research, vol. 96, 239-249.

[202] with a formal publication as Cohen et al. (2004) Environmental Research, vol. 95, 247-265.

[203] Dr. Cohen is also noted to have briefed Rep. Mark Kirk (R-Il) on "Atmospheric Mercury and the Great Lakes" on June 29, 2005.

[204] Dr. Mason is currently at the University of Connecticut.

[205] Mason et al. (2005) Environmental Science & Technology, vol. 39, A14-A22.