Doing Harm –The Mercury Scare 

A critical, Science‐based Analysis of the Chicago Tribune 

“Mercury Menace” Series (December 11-13th, 2005)

www.scienceandpublicpolicy.org 

[202] 288‐5699 

 

Robert Ferguson  

July 2007 

By 

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Table of Contents

Foreword 6 General Overview and Summary Conclusions 8 Introduction and Background 10 Why this response? Contextual background on mercury toxicity and epidemiology: Japan and Iraq Japanese fetal exposures Iraq exposures Exposure history What constitutes real “development disability? Section 1: The Phantom Menace 15 EPA’s Mercury Reference Dose Definition and description The Problematic Faroe Islands Study Inappropriateness Boston naming test problems Summary of Faroe Islands study problems Superior Seychelles Islands Studies An appropriate study Highlights of Seychelles children studies The New Zealand Study Iraqi Poisoned Grain-based RfD Miscellaneous Fish and Human Health The heartbreak of pre-term delivery Postpartum depression and low seafood consumption Improved fetal and child development Breast cancer Kidney disorders Stroke in men and women Adult type 2 diabetes Alzheimer Disease (AD) and adult cognitive abilities Prostate cancer Summary of health findings Dietary benefits Conclusion Section 2: An Extraordinary Popular Delusion: Myth of the Mercurial Hundred Thousands 33 Statistical Manipulations Revisit the RfD Additional Considerations

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No Bright Line of Harm General Summary of mercury RfD talking points Conclusion Section 3: Misrepresenting the FDA 40 Conclusion Section 4: How Safe is “Safe”? 44 Freshwater Sport Fish Conclusion Section 5: Mercury, Mercury Everywhere…Forever 49 Burying the lead Mercury Deposition in Illinois Accounting for Natural Sources From Hg to MeHg Section 6: Poisoning Sophie 55 The Sophie Chabon Case Poisoned tuna? The Waldman confessional Conclusion Section 7: The NRC and the Mercury RFD 59 Unscientific Policy Proposal The NRC Panel Conclusion Section 8: Cardiac Arrest 62 Study Problem Cardioprotective Benefits Conclusion Section 9: Understanding the Hightower Paper 68 Personal Opinions are not Science “Treating” Sophie Contradictions Reinterpreting the RfD Conclusion Section 10: Through the Looking Glass 72 Political Wonderland Bad Science Section 11: The Selenium (Se) Factor 76 Swordfish Guidelines vs. Confiscation The Canadian Approach The Selenium Factor

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Conclusion Section 12: Fish Boom? 83 An Absence of Concern Section 13: Attacking the FDA 85 More Confusion A Letter from the Senate Section 14: False Limits 88 More RfD Confusion Eat More Fish! Amazonia Conclusion Section 15: Sources of Ocean Fish Mercury 92 Canned Tuna The Real Issue – Natural Sources of Mercury Conclusion Section 16: Meaningless Tests 96 Just the Facts Meaningless Tests Section 17: More Congressional Confusion 99 Section 18: Man-made vs. Natural Sources of Mercury 101 Section 19: The NESCAUM Report 103 Section 20: Where are all the Victims? 106 Where are the victims of fish poisoning? Exhibits that argue for lack of victims FDA Tuna Monitoring Section 21: Hypothesis Rejected 111 Garbage in, Garbage out A Vital Need for Essential Answers Illinois Hot Spot? Swamped in Florida Conclusion End Notes 118

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“We cannot give up science. It is in the breath of our nostrils. Even if Joshua were to appear and forbid it we would not obey him. For we have a warranty which outweighs them all, that is to say Maimonides, who recommended it and impressed it upon us. We are ready to set our goods, our children and our lives at stake for it.” - Rabbi “Penini” (Jedaiah ben Abraham Bedersi 1270 – 1340)

“Nonscientists generally do not want to bother with understanding the science. Claims of consensus relieve policy types, environmental advocates and politicians of any need to do so. Such claims also serve to intimidate the public and even scientists...there is a clear attempt to establish truth not by scientific methods but by perpetual repetition.” - Dr. Richard Lindzen, MIT, (6-26-06)

 Note:  This paper was written by the author while he served as Executive Director for the Center for 

Science and Public Policy (CSPP), before founding the Science and Public Policy Institute (SPPI) in 

March of 2007. Questions regarding its content can be directed to SPPI. 

   

 

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Foreword

enerally, the level and quality of information on mercury and health appearing in most public literature and media reports is based on misunderstanding and misleading interpretations of the science.

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As one example, in the context of mercury-related sciences, the Chicago Tribune (CT) series “The Mercury Menace” from late 2005 was based on questionable or mistaken presumptions. That is to say, it is so permeated with stunning inaccuracies and important omissions that it should not be relied on in any policymaking arena. The entire series and follow-up articles seem largely drawn from previously published materials in the non-science literature, largely without attribution. For example, the story concerning the reputed “poisoning” of little Sophie Chabon and her “treatment” by Dr. Jane Hightower earlier appeared in the San Francisco Chronicle. Critical comments about the FDA appear drawn from various “mercury-activist” web sites. Tragically, regarding public health, the Tribune series itself and the information upon which it is based may do more harm than good. The series could cause people to avoid fish consumption altogether, thereby missing out on the significant nutritional benefits fish consumption provides – especially for women and their babies. In this regard, we direct attention to a paper by Sandy Szwarc, When Mercury Fears Harm, found at (http://ff.org/centers/csspp/pdf/szwarc_072006.pdf). It examines the risks of mercury alarmism: “Fears about mercury are directed at our most vulnerable — pregnant women, babies and young children — but the evidence indicates they are most harmed by fears, endangering the neurological development of babies and young children and increasing risks for pregnancy complications and preterm deliveries.” By this, she means that discouragement of fish consumption also “eliminates the health benefits from eating fish, which help reduce those very same fear-induced health concerns among adults and growing children.” More broadly, even a cursory examination of the evolving peer-reviewed literature reveals a plethora of significant health benefits that could result from intake of omega-3 polyunsaturated fatty acids, vitamin E, selenium, protein, iron, zinc, calcium and other essential nutrients available in a fish-rich diet. Each reader of the Tribune series is getting older every day. Many encounter the difficult impacts of old age, either in themselves or in friends and family members. Emerging literature indicates that increased fish consumption is associated with more positive outcomes for a variety of diseases often associated with old age, including cardiovascular disease, type II diabetes, and even Alzheimer’s – to name only a few (see Sec. 1).

Scares ultimately divert our attention from real opportunities to enhance life and longevity. What an incredible waste of time, resources, and human potential.

Overall, the Tribune series doesn’t report the critical and balanced information required for either public or personal informed decision-making.

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This paper not only represents a quest for the truth and a defense of science, but seeks to improve the basis for public policy decision-making and the improved health and well-being of all people, especially women and all our children. We agree with the observation of former Surgeon General C. Everett Koop: “Scares ultimately divert our attention from real opportunities to enhance life and longevity. What an incredible waste of time, resources, and human potential.” In the face of an expansive and robust body of scientific literature and the growing potential for misinformation doing great harm to public health, the continued purveyance of unwarranted mercury alarmism is highly troubling. Willful ignorance is no longer an excuse.

Robert Ferguson

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GENERAL OVERVIEW AND SUMMARY CONCLUSIONS

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. -- Ropeik et al., 2004

n its apparent haste to dispraise the FDA, the tuna industry and the power generation industry, the Chicago Tribune’s "Mercury Menace" series – and the activist claims upon which it heavily relies – achieves little except frightening some people away

from eating highly nutritious fish meals. I

If the naturally-occurring micro-traces of mercury in fish sold in the restaurants and supermarkets of Chicago were as harmful as reported, then there would exist an epedimic of fish-mercury poisoning in the Chicago area. Not a single case has reported. Average Americans consume between 2 to 10 times below the daily intake of essential omega-3 fatty fish oils, compared to consumers in Japan, Singapore, Scandinavia and Spain. Americans need more, not less fish consumption; the overwhelming health benefits clearly outweigh recently conjured, exaggerated risks unsupported by science. Misinformation in the CT series is troublesome: 1) According to a breadth of studies, the claimed evidence of

"learning disabilities in children and neurological problems in adults" from eating fish simply does not exist.

Americans need more, not less fish consumption.

2) Fear and alarmism appear substituted for critical analysis and responsible

interpretation of available research data on nutrition and health. 3) The FDA has executed its fish advisory role based on a balancing of the risks and

benefits of fish consumption. This has resulted in a well-executed strategy that protects all Americans, including the sensitive sub-populations of women and young children.

4) Claims that fish mercury exposure counteracts the well-known cardio-protective

properties of fish oils are not well-supported. 5) Activist literature consistently ignores the complex and nonlinear chain of mercury

processes within the ecosystem food web. These processes make it difficult to claim that an active capture of the majority of elemental and ionic mercury emitted from coal-fired power plants -- however “cheap”, urgent or feasible -- will lead to beneficial lowering of the concentration of MeHg in fish.

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6) The CT has conducted a rather unremarkable analysis of mercury content in fish sold

in Chicago. Consumers should also consider the rich variety of important, essential nutrients (especially the disproportionately higher selenium content) and vitamins from fish intake.

7) The EPA’s current “safe” mercury exposure standard is based on highly conservative

assumptions and is therefore overly restrictive. 8) The CT focuses on whether some yellowfin tuna is canned as light tune. There is no

demonstrated harm resulting from consuming yellowfin tuna either as canned or fresh/frozen steaks. Seafood mercury content varies depending on many factors beyond human management or control. In fact, yellowfin tuna and other ocean fish mercury levels are likely naturally derived, and not from emissions of mercury from coal-fired power plants or other anthropogenic sources.

9) CT has wrongly accused EPA of (1) downplaying the benefits of reduced mercury

pollution and (2) suggesting that the Harvard Center for Risk Analysis report was submitted too late for drafting the power plant mercury rule.

10) The Illinois governor’s proposal for a 90% mercury reduction at state coal-fired

power plants should be critically examined regarding health benefits and the real costs of increased electric rates.

11) The much ballyhooed “independent” fish mercury measurements are not

unprecedented, having been done previously in a 2003 San Francisco Chronicle series. Results are not outside the bound of data already published by FDA, EPA and the fish industry.

Finally, in evaluating the health consequences of exaggerated fears, the director for risk communication at the Harvard Center for Risk (Ropeik, 2004)1 reported:

“[T]he cumulative load of modern threats may be creating an even greater risk that is largely overlooked: the risk that arises from misperceiving risks as higher as or lower than they actually are. As a result of some of the decisions we make when we are fearful, some of the choices we make when we are not fearful enough and because of the ways our bodies react to chronically elevated levels of stress, the hazards of risk misperception may be more significant than any of the individual risks about which we fret.”2

It is the underlying finding of this review that the Chicago Tribune, in league with mercury “activists”, appears engaged in an unscientific fear campaign about mercury in fish; and by doing so, is itself doing terrible harm.

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Doing Harm –The Mercury Scare 

A critical, Science-based Analysis of the Chicago Tribune “Mercury Menace” Series (December 11-13th, 2005)

Introduction and Background

Why this response?

he “Mercury Menace” is a series of 3 articles published in Chicago Tribune (hereafter as CT) by investigative reporters Sam Roe and Michael Hawthorne, including:

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Toxic risk on your plate (December 11, 2005) U.S. safety net in tatters (December 12, 2005) How safe is tuna? (December 13, 2005)

The CT articles were broadly reprinted in various media outlets across the country and have since triggered a plethora of in-house editorials and articles in the Chicago Tribune itself:

Kirk urges FDA to boost effort (December 13, 2005) Citizen readers and policy makers relying on the CT series for choices will be disappointed and likely harmed.

Something fishy in the tuna aisle (December 15, 2005) States fight emission rule (December 20, 2005) FDA to check tuna (December 31, 2005) Governor seeks 90% mercury reduction (January 5, 2006)

Despite serious factual errors, misinformation, and missing contexts throughout, the Chicago Tribune printed only 3 rebuttal letters to the editor (from fish-related industry representatives) while printing 8 supportive letters mostly adding to the misinformation and confusion. Tragically, misinformed consumers restricting regular seafood nutrition out of “poisoning” fears may be needlessly endangering both their health and lives. Most at risk are fetuses of pregnant women, children and the elderly. Policy makers rushing to “do something” in reaction to the alarmism saturating the CT series, will likely only waste energy and resources better allocated to more real and immediate public needs.

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Following is a critical examination of the more key statements and claims made in the CT series. We have attempted to synthesize the most current science findings across a spectrum of issues and disciplines converging on the factual understanding of mercury’s environmental cycle. For easier reference, the “responses” are organized into numbered sections. In each section, the claim or statement by CT is presented, follow by a response. It is suggested that interested persons read the original Tribune series and then read and re-read the entire paper and endnotes in order to synthesis the issues toward a broader understanding. Some repetition of facts between sections has been necessary for providing immediate context. Unfortunately, the Chicago Tribune’s Mercury Menace series appears largely agenda driven. Regardless of motive, the only actual “menace” is the almost certain broad harm being inflicted by injecting fear and disinformation into the public square. Contextual Background on Mercury Toxicity and Epidemiology: Japan and Iraq The chemical element mercury (Hg) is abundant and naturally occurring in the earth’s crust, air and water systems. It commonly occurs in two inorganic forms, elemental mercury (a silvery liquid metal at room temperature) and divalent mercury (much more easily combined into chemical compounds). In aquatic systems various microorganisms such as bacteria methylate a tiny fraction of existing divalent Hg into methyl mercury (MeHg). Once present in these bacteria, MeHg can then be taken up by larger organisms to bioaccumulate and bioconcentrate up the aquatic food chain. Consequently, all aquatic organisms including fresh and saltwater fish contain and always have contained some level of MeHg, and the billions of peoples past and present who have consumed fish or other seafood are all exposed. Specific levels of micro-traces of background MeHg, which depend on fish age and size, appear to have been present since fish evolved and appear not to have changed despite increasing modern industrialization (see Sec. 15).3

A molecule of mercury is not an Ebola virus.

A molecule of mercury is not an Ebola virus. Proximity does not assure exposure, and exposure does not assure harm. [See Sec. 1 for discussion of EPA’s mercury reference dose (RfD)]. Among exposures to the different forms of mercury, the organic form MeHg is of particular concern because it results in measurable toxic effects at sufficiently high dose rates (amount and time rate of intake of MeHg). Japanese fetal exposures As for infant or fetus exposures, it should be understood at the outset that fewer than 100 instances of prenatal MeHg poisoning have been documented in the world literature.

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Only a few of these included reliable exposure data.4 All cases resulted from direct poisoning events either as treated seed grain or seafood directly contaminated with industrial waste containing a mixture of MeHg hundreds of times higher than background levels and other known toxic chemicals, such as occurred in Minamata, Japan (MeHg at 47 parts per million [ppm] in fish tissue5) and Niigata, Japan. The actual factory waste dumped near shore was known to contain large amounts of silicon, iron, aluminum, calcium, magnesium, potassium, sodium, ammonia, copper, arsenic, manganese, chlorine, phosphorus, sulfur, and lead.6 With the attribution of Minamata disease symptoms to MeHg exposure only, the contribution of the concomitant toxic exposures was never determined. Iraq exposures Then in the early 1970s in Iraq there was an outbreak of general MeHg poisoning from the ingestion of MeHg-fungicide-treated wheat grains. The isolation of rural populations meant that actual exposure levels were never measured concurrently with exposure incidents, but rather reconstructed later from subject hair mercury levels. Subsequent research led to the hypothesis that lower levels (as low as 10 ppm) of prenatal MeHg exposure from fish might present a subtle risk to the developing brain.7 The interpretation of these various studies with conflicting results continues to be controversial. Keep in mind that the Iraq exposure was not from fish consumption, and therefore provided none of the protective benefits of selenium found abundantly in fish, and believed to protect against MeHg toxicity (see Sec. 11).

There has never been a documented and verified case of MeHg poisoning from fish consumption in the United States.

Exposure history Again, it is factually certain that there has never been a verified report of frank MeHg intoxication from fish consumption outside of the Japanese industrial waste discharge events. Also, there has never been a poisoning from Japan absent the confounding effects8 of those high levels of multiple toxic chemicals discharged into near-shore waters.9 Thus, there has never been a documented and verified case of MeHg “poisoning” from fish consumption in the United States (see Sec. 6). Of the 22 Minamata, Japan reported cases of fetal Minamata disease10, all the affected children reportedly had severe neurological deficits including microcephaly, intellectual disability, cerebral palsy and seizures. There were no children with just mild or moderate disability, let alone any “subtle” deficits as reported in the Faroe Islands study relied on by EPA for deriving its highly conservative mercury exposure reference dose of 5.8 ppb in cord blood and about 1.0 ppm in hair. (see Sec. 1, 2, and 7). And the Minamata children’s prenatal exposure levels to either MeHg or other chemicals were not determined.11 However, mercury levels in the ill children’s (all over one year of age) hair ranged from 5 to 100 ppm, and the mothers’ from 1 to 191 ppm. Inexplicably, the hair mercury content

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of healthy – absent symptoms – infants (all under one year of age) at the same time ranged from 0 to 158 ppm!12 Following a similar industrial chemical pollution near Niigata, Japan only one infant was formally diagnosed with congenital MeHg poisoning. Her total hair mercury level (THg), measured shortly following birth, was an astounding 77 ppm. (Remember, EPA’s hair RfD – “safe” level – is only about 1.0 ppm.) Her mother’s THg measured 293 ppm, although she reported no ill health affects!13 Other toxic chemical levels were not determined. Health authorities offered abortions to 12 other women who recorded hair Hg levels between 51 and 115 ppm.14 All 12 women chose to deliver their infants. All of those infants and mothers appeared healthy at birth. At five years of age all 12 children were examined and reported normal.15 Adult follow up of these same children reported no sign of Minamata disease. Three had completed middle school, six completed high school, and one each completed nursing school, business school an

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isease (“mercury poisoning”).

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evidence for MeHg poisoning of babies simply because their mothers eat lot of fish.

u Japan remains today – as it has been for centuries -- a high fish consuming culture, with 87% of its population exceeding EPA’s mercury RfD. The last case reported ofsy ood was a child born in Japan in 1965.17 In terms of potentially dangerofetal exposure to MeHg from maternal fish consumption, currfindings by Japanese scientists (including those from the JapaneNational Institute for MinamaDisease) confirm the generaimprobability of fetuses in contemporary fish-eating populationbeing exposed to MeHg levelsor exceeding those estimated necessary for inducing Minamatad Following a survey of 115 healthy Japanese pregnant women and their child births in 1996, Sakamoto and colleagues18 confirmed (see Fig. 1) that current baby MeHg exposure19 is about 20 tibelow that associated with the 1950-1965 births20 of the 24 children diagnosed with congenital or infantile Minamata disease.21 This important result, together with the that the past and current Japanese population ranks among the world’s highest fish consumers, should place a useful upper limit on fetal MeHg exposure risk for other fish eating populations, especially U.S. consumers. Also, the new findings may help explain why there is no

Contemporary babies for the high‐fish‐eating Japanese population are exposed to MeHg 20 times below those diagnosed with congenital or infantile Minamata Disease.

1.63 ppm

0.083 ppm

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1950‐1965 births: 24 children with Minamata Disease (Akagi et al. 1998)

1996 births: 115 babies from healthy Japanese pregnant women (Sakamoto et al. 2006)

a

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If serious and frightening accusations that consumption of market-available fish with natural levels of MeHg is poisoning people today are true, then where are the world-wide legions of victims? If the alarmism by the Chicago Tribune were remotely scientifically credible, MeHg would account for a substantial portion of all children and adults with developmental disabilities in Chicago and elsewhere. Where are they? (see Sec. 20) What constitutes real “developmental disability”? And finally, the CT and its sources make the extraordinary leap of equating exceeding the EPA mercury RfD as placing the child at “developmental risk.” But what constitutes a “developmental disability?” Writes Dr. Gary Myers, professor of Pediatric Neurology at the University of Rochester, and co-author of the Seychelles Child Development Study:

The term “development disability” is a political one. The definition presented by the Center for Communicable Diseases of the U.S. Department of Health and Human Services is “Developmental disabilities are a diverse group of severe chronic conditions that are due to mental and /or physical impairments. People with development disabilities have problems with major life activities such as language, mobility, learning, self-help, and independent living. Development disabilities begin anytime during development up to 22 years of age and usually last throughout a person’s lifetime.”22

The reputed “subtle” difference in cognitive performance in the Faroe Islands’ Boston Naming test, partly relied on by the EPA and NRC for development of a mercury RfD and resulting emissions regulations – even if valid (see Sec. 1) -- could not be considered a development disability or any other clinical health problem.23 Dr. Myers, concludes,

“There is no evidence that exceeding the [EPA] RfD (about 1.0 ppm in hair), even on a regular basis, would place the child at risk of having a developmental disability. Nor do we believe that current evidence supports the presence of [even] subtle adverse effects on child development from the consumption of ocean fish at prenatal exposures below 10 ppm measured in maternal hair.”

This, and what follows, constitutes critical health information that CT fails offering expectant mothers.

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THE MERCURY MENACE – A RESPONSE

SECTION 1: THE PHANTOM MENACE

“These data [from the Seychelles children studies] do not support the hypothesis that there is a neurodevelopment risk from prenatal MeHg [methylmercury] exposure resulting solely from ocean fish consumption.”

- Professor Gary Myers, University of Rochester Medical Center

“We question the wisdom and the validity of the scientific basis of these advisories. Highly restrictive generic fish consumption advisories such as the ones issued by the EPA and the FDA, can cause harm by unnecessarily warning people not to consume fish. Alaska’s public health response to EPA/FDA advisories has been to recommend unrestricted consumption of fish caught in Alaska waters.”

- Arnold et al. (2005)

Chicago Tribune: Supermarkets throughout the Chicago area are routinely selling seafood highly contaminated with mercury, a toxic metal that can cause learning disabilities in children and neurological problems in adults, a Tribune investigation has found. (December 11, 2005) Response:

his is a scientifically incomplete and inaccurate statement, invoking needless alarm leading to potentially health threatening nutritional decisions.

Like almost any substance, including drinking water, mercury's potential for toxicity depends on dose -- how much one takes, over a time interval.

T Apart from the few well-reported acute direct mercury poisoning cases in the past – such as occurred in Minamata, Japan – there has been no convincing finding that regular consumption of fish with historically natural levels of mercury has caused "learning disabilities" in children. The best “evidence” presented for this claim is derived from a challenged study in the Faroe Islands, commonly used to suggest that prenatal exposure to micro-trace mercury might cause subtle deficits in neuropsychological performance.

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EPA’s Mercury Reference Dose (RfD)

Definition and description The U.S. Environmental Protection Agency's (EPA) dose level of concern is called a mercury reference dose (RfD). Understanding it is essential to sorting out the entire mercury debate and discussion which follows below. An RfD is an estimated (“with uncertainty spanning perhaps an order of magnitude”) amount of methylmercury one can consume every day, over a life time of 70 years without appreciable risk of deleterious effects. It is based on a worse case scenario of chronic, low level exposure that leads to a blood concentration of 58 parts per billion (ppb), and then divided by an extremely conservative factor of 10 as an "uncertainty" or safety cushion.

EPA's current mercury RfD seems arbitrarily the most restrictive in the world.

For context, EPA determined that its mercury reference dose should be set at 0.1 µg/kg/day. The FDA dose was established at 0.4, the Agency for Toxic Substances and Disease Registry (ATSDR) at 0.3, and the newly revised FAO/WHO level at 0.21.24 Viewed alternatively, EPA's mercury RfD “safe” dose is intake of 0.1 (µg/kg-day), reflected as 5.8 ppb (parts per billion) when measured in human blood, and about 1.0 ppm (parts per million) when measured in human hair. The estimation of a “safe” dose involves several judgments such as (a) the choice of the most appropriate No Observed Adverse Effect Level (NOAEL) or Benchmark Dose (BMD) of the critical effect, and (b) the choice of the appropriate uncertainty factors based on a review of the entire database.25 EPA’s rather extreme uncertainty factor of 10 exceeds those of other medical bodies and institutions.

EPA’s “safe” level of MeHg consumption is set at 0.1 μg/k/day(this includes a safety factor of 10 – the original level was 0.45 to 1.9)

This translates into once a week consumption of a fish meal (4 ounces) with MeHg level of 0.2 to 0.3 ppm (tuna) by an adult woman (60 kg)

EPA’s “safe” MeHg consumption level is 3 to 5 times more conservative than WHO, ATSDR and FDA’s recommendations.EPA’s recommendation “may do more harm than good” to public health because of the potential lack of consideration from multiple benefits of fish consumption from effects of selenium, vitamin E as anti‐oxidants and omeg‐3 polyunsaturaed fatty acids (recommended by the American Heart Association, Kris‐Etherton et al.., Circulation, 2002)

What EPA’s “safe” level of MeHg exposure means

EPA's current mercury RfD seems arbitrarily the most restrictive in the world. (See also, Section 2) That is to say, EPA appears to have set the stage for alarm by (a) setting “low” estimates of safe levels, making things look worse than reality, and (b) setting “high” estimates of exposure, making things look worse than reality. The combination of the two can be

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highly deceptive. The alarm is compounded when concerned State officials, agitated by activists, decide to set even lower fish tissue concentration standards for triggering fish advisories.26 Perhaps, more appropriate would be establishing a realistic “safe” range instead of a single number beset with confusion and wide latitude for statistical mischief.

The Problematic Faroe Islands Study

Inappropriateness EPA’s mercury RfD is further problematic because it is based on inappropriate studies of people inhabiting the Faroese Islands who consume both fish (found to be generally low in mercury) and pilot whale meat and blubber (a unique practice no one in the US pursues) containing multiple, confounding chemicals (PCBs, cadmium, pesticides, persistent organic pollutants, DDT, etc.) of which mercury is only one. 27 (And even here, the subtle effects ascribed to low MeHg doses do not constitute developmental disabilities as described by Dr. Myers above.) Adding to this chemical cocktail, a report recently released by the Danish government also found significantly high levels of perfluorooctane sulfonate (PFOS), perfluorooctane sulfonamide (PFOSA), polychlorinated naphthalenes (PCNs), and polybrominated diphenyl ethers (PBDEs) in pilot whales from the Faroe Islands.28 Regardless of the scientific debate (examined below) about whether the interpretation of the Faroese data constitutes sound or reliable evidence, it is clear that the study is simply inappropriate for EPA use in determining safe fish mercury exposure to Faroese children, let alone U.S. children. Dr. Pal Weihe, co-researcher of the Faroe study and Chief Physician of the department of occupational and public health for the Faroese hospital system implicitly agreed with this assessment in a letter to the Boston Herald dated February 9, 2004:

In the Boston Herald, Friday, February 6, 2004, p. 20 the following was stated about a mercury study in the Faroe Islands conducted in cooperation with the Harvard University29: “A fish industry spokesman said that the Harvard study was flawed because Faroe Islands women typically eat far more mercury-tainted fish than do Americans” As the researcher in charge of the mercury studies on children in the Faroe Islands since 1985 I want to correct this statement. The Faroese children are not exposed to methylmercury by eating fish. They are exposed to mercury by the traditional consumption of pilot whale meat. Fish normally consumed in the Faroes, e.g. Cod and haddock, are low in mercury and do not, to my opinion constitute any threat to the

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health of the Faroese children. In the contrary the fish consumption most likely is beneficial to their health. (Emphasis added)

This poses the question, how can EPA or the National Research Council (NRC) (see Sec. 7) seriously cling to the Faroe study as a basis for their RfD formulation when the lead author of the study states that it has nothing to do with MeHg in fish, but only in whale meat and blubber; and that both were highly contaminated with a mixture of known neurotoxins?

There are additional serious issues of inappropriateness for the underlying epidemiological data from the Faroe Island children studies; not the least of which is the refusal of the Faroe Islands researchers and the Danish government to release their raw data for independent statistical analyses and verification. By continuing to rely on this black-boxed data, both EPA and the NRC violate EPA’s own data quality guidelines.30 The Boston Naming Test problems Nevertheless, CT and activists continue to rely heavily on the 2000 NRC Report, which concludes that the Boston Naming Test results of the Faroe Islands study are an appropriate basis for EPA’s mercury RfD. However, following a lengthy trial, a San Francisco Superior Court found in May 2006 that:

“[T]he NRC failed to cite a critical paper in which the Faroe Islands authors state that a new cohort was being formed in the Faroe Islands to study the role of PCBs. Following the publication of the NRC report, four papers have been published discussing the high levels of PCBs in the Faroe Islands. When investigators controlled for concurrent PCB exposure, there was no statistically significant correlation between methylmercury exposure and performance deficits on the Boston Naming Test. The authors of the Faroe Islands study recognized the impact of PCBs rather than methylmercury on the results of the Boston Naming Test, noting that ‘especially for the Boston Naming Test, the PCB concentration appeared to be an important predictor’ of the children’s performance.31 (Emphasis added)

Former EPA official and co-author of the mercury RfD, Dr. Deborah Rice, published a paper in 2003 in which she herself concluded that PCBs caused the reported performance deficiencies measured by the Boston Naming Test.32 However, according to the Judge’s findings, during the San Francisco trial, Rice inexplicably denied ever writing the paper. When shown the article in court, Dr. Rice then “admitted to reviewing and approving it, and that the article was published under her name.”33 Finally, the authors of the Faroe study themselves admitted to PCB confounding:

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Prenatal exposure to PCBs was examined by analysis of cord tissue from 435 children from a Faroese birth cohort... The association between cord PCB and cord-blood mercury (r=0.42) suggested possible confounding. While no PCB effects were apparent in children with low mercury exposure, PCB-associated deficits within the highest tertile of mercury exposure indicated a possible interaction between the two neurotoxicants. The limited PCB-related neurotoxicity in this cohort appears to be affected by concomitant methylmercury exposure.34

Considering the actual data itself, Fig. 1-A shows the rarely presented “smoking gun” evidence adopted by EPA and the NRC 2000 review to support claims of negative neuro-developmental impacts from prenatal exposure through marine consumption. The result was drawn from the Faroe Islands children study originally published by Grandjean et al.35 and the particular endpoint test is the so-called cued Boston Naming Test (not to be equated with IQ; an IQ test was never administered to the Faroe cohort).

Fig. 1-A clearly suggests a significant scatter in the test scores as the MeHg exposure level changes. In this curve fitting, there appears no strongly discernable trend even around 100 ppb, let alone at 5.8 ppb. In other words, EPA’s adopted MeHg RfD of 5.8 ppb shows a clear disconnect to the underlying data. Again, these data led Judge Robert Dondero to conclude after expert testimony that “The Boston Naming Test has no statistically significant relationship to methylmercury exposure.” It would be interesting to see a similar quantification of response functions to PCB exposure. It is worth repeating that this particular endpoint is among the best evidence relied upon by EPA and the NRC to suggest negative impacts with increasing MeHg exposure. (For more on the BNT, see Sec. 7) Figure 1-A contributes to the distinction between actual “potential levels of harm” or concern for MeHg in prenatal exposure and the hypothetical, ultra-precautionary level of safety set by EPA’s RfD. No equivalent epidemiological data has been produced demonstrating serious health concerns in adults

Evidence for neuropsychological problems inthe Faroe islands children study is not strong

Budtz‐Jorgensen et al. (2003) Environmetrics, vol. 14, 105‐120

Cued Boston Naming Test

These tendencies for curving downward are what were referred to as “adverse neuro‐developementalproblems.” It appears more an exercise in visual curve‐fitting, especially at levels below 100 ppb.  The raw data have not been released for verification.

better test scores

worsening test scores

Increasing levels of exposure to meHgthrough mother

5.8 ppb: this is EPA’s ultra-conservative RfD level!

Figure 1‐A

20

from chronic exposure to methylmercury through dietary fish consumption. In fact, growing evidence exists for just the opposite (See Fish and Human Health below). Summary of Faroe Islands study problems

Unique dietary habits of consuming pilot whale meat and blubber, making the Faroese an inappropriate subject group for an American RfD.

Pilot whale contamination with multiple chemicals, some known neuro-toxins. Claimed “subtle deficits” weak and not fitting CDC definition of “developmental

disabilities.” Mercury concentrations in samples of pilot whale livers have been 5,000 times

greater than the Japanese government's limit for mercury contamination of 0.4 ppm.

Reports that concomitant exposure to MeHg and PCBs has synergistic toxicity.36 PCB exposures of pregnant women among the highest ever measured in humans. PCBs are an important confounder that can lead to a false and misleading

correlation between MeHg and childhood development. Pilot whales are lower in mercury-sequestering selenium that is abundant in ocean

fish. (see Sec. 11) Faroe researcher stated “children are not exposed to dangerous levels of MeHg by

eating fish.” EPA and NRC ignored confounding chemical contamination in pilot whales, and

rejected the Seychelles study which found no adverse effects from pre-natal exposure resulting from heavy maternal fish consumption.

Faroese researchers and the Danish government refuse to release study’s raw data for independent analysis and scrutiny.

The BNT end-point test relied on by EPA and the NRC for setting an RfD is so weak and unconvincing that after hearing testimony a California Court judge found it non-credible.

Potential post-natal contamination by children eating whale products up until age 7, when tests were administered.

Some mothers of test subjects smoked and/or consumed alcohol during pregnancy.

Evaluations of children after 7 years of age no longer double-blind. Results contradicted by better studies. Faroes fish relatively low in MeHg. Cord blood used only detects levels of MeHg in last few weeks of pregnancy.

Recent whale intake could spike and skew test results. An association of cord blood Hg and brain mercury levels have not been reported.

Some of the tests, such as finger tapping during a 15-second interval, have no clinical relevance for an individual.

One of the reputedly strongest pieces of evidence for a detectable MeHg exposure is the BAERS (brainstem auditory evoked responses) test at 14-years of age. But there are “no data to suggest that a change of 1/100,000th of a second would

21

constitute a significant impairment in auditory processing and it would certainly not constitute a development disability.” 37

Diets and source of exposure differ from Seychelles studies. Seychelles diet of fish, fruit and vegetables. Faroe diet included fish, whale meat and fat.

Problematic study design. Additional deficiency findings of San Francisco Superior Court Judge in

California vs. Tri-Union Seafoods: * The Faroe Islands Study has no exposed or reference groups * Lacks a reliable ascertainment of exposure * Suffers from incomplete follow-up * Does not adequately identify or quantify biases and confounding factors * Does not adequately separate prenatal from postnatal effects * The NRC report, which endorsed reliance on the Faroe Islands Study, was published in 2000, before a series of articles focused on PCBs in the Faroes

Again, it is critical to repeat that EPA defines its RfD for methylmercury as "an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime."38 Further, EPA didn’t account for the research showing fish are rich in selenium, which likely counteracts MeHg in fish. Pilot whales, on the other hand, are selenium deficient (see Sec. 11). Further clarification of EPA's RfD is discussed in Sec. 2 and 7.

The Superior Seychelles Mercury Studies An appropriate study In sharp contrast to the Faroe Island study, the Seychelles Child Development Study (SCDS) “was specifically designed to test the validity of [the] hypothesis [of adverse neurodevelopment effects] in a well-nourished population exposed to MeHg only from high consumption of unpolluted [other chemicals] ocean fish.” The Seychelles Island results are clearly superior for deriving RfD exposure to methylmercury for the U.S. population. This is so simply because that study is without toxic confounders and the Seychelles Island mothers consumed about 10 times the amount of fish as U.S. mothers39 - ocean fish containing MeHg concentrations comparable to those consumed by the general U.S. population, including Chicago area residents. This evaluation was confirmed in a post NRC (2000) analysis. Dourson et al.40 restated that “The Faroe Islands data are from exposures to a mixture of chemicals. The Seychelles Island data are from exposures to primarily one chemical, methyl Hg...We would...encourage EPA to use the Seychelles Island data as the basis of its methyl Hg RfD.” Dr. Dourson is the former EPA RfD/Reference Concentration Work Group co-chair.

“For now, there is no reason for pregnant women to reduce fish consumption below current levels, which are probably safe.”

22

The SCDS authors from the University of Rochester recently concluded that:41

“[SCDS] longitudinal assessment at 9 years of age indicates no detectable adverse effects in a population consuming large quantities of a wide variety of ocean fish. These results are consistent with our earlier findings in the same children examined at 6, 19, 29 and 66 months of age. In Seychelles, fetal exposure was continuous through frequent consumption of ocean fish containing concentrations of MeHg comparable to those consumed by the general population in the USA. We recorded effects from covariates known to affect child development, but did not find an association with prenatal mercury.” (Emphasis added)

Constantine Lyketsos of the John Hopkins Hospital offered a professional overview on the implications of the Seychelles study, concluding that:

“On balance, the existing evidence suggests that methyl mercury exposure from fish consumption during pregnancy, of the level seen in most parts of the world, does not have measurable cognitive or behavioural effects in later childhood....If there is subtle association that could only have been detected in a much larger sample or through the use of more sensitive tests, it can reasonably be argued that the effect would be small enough to be essentially meaningless from the practical point of view. For now, there is no reason for pregnant women to reduce fish consumption below current levels, which are probably safe.” 42 (Emphasis added)

Highlights of Seychelles children study

Uncontaminated (by non-mercury compounds) ocean fish are sole source of exposure – no sea mammals in diet or fresh water fish in diets.

Measured levels of PCBs were undetectable in the Seychelles. The ocean fish consumed have mercury levels similar to commercial fish sold in

the U.S. The cohort had extensive evaluations at 6, 19, 29, 66, and 107 months of age. There have no consistent adverse associations with mercury exposure present. Mothers in the study consumed fish 12 times per week. Prenatal exposure averaged 6.9 ppm (1-27 ppm) in hair mercury or about 40 ppb

in blood mercury. (EPA’s RfD is 5.8 ppb) EPA needs to reconsider and reset upwards its mercury RfD.

The study has been conducted double blind for nearly 20 years with no clinical investigators or anyone in the Seychelles knowing the mercury exposures.

Study provided no support for an adverse association between child neurodevelopment and prenatal exposure to MeHg from maternal consumption of ocean fish at the levels being studied (5.8 – 156 ppb).43

Thus, at best, the Faroe Islands studies are useful for understanding a mixed chemical exposure, especially for PCB. The Seychelles Islands studies are very good at understanding exposures to primarily methyl mercury.

23

In the interest of public health and wellbeing, EPA needs to reconsider - based on more recent science - and reset upwards its mercury RfD.

The New Zealand Study

The first studies of prenatal low-level MeHg exposure were reported from New Zealand.44 There were two technical reports and one peer reviewed journal paper. The studies were discounted by most investigators, including EPA, until 1998 when the data were reanalyzed by Crump and published in a peer reviewed journal. The studies reported decreased performance on scholastic and psychological tests associated with high prenatal MeHg exposure. Results were included in a 2000 review conducted by the National Research Council (NRC) at the request of the EPA. Some researchers are cautious about relying on the NZ findings due to shortcomings:

Primary exposure through shark meat, some with up to 4 ppm of Hg. Original study not peer-reviewed. Second paper reviewed but had complications with design. Small sample size of only 74 (age 4 years) mother/child pairs. Introduced a variety of confounders by including three different ethnic groups,

each with a distinct and different culture (European, Maori and other Pacific Islanders).45

Testing of controls and subjects who were at different ages. Adverse association present only when one child with very high level of exposure

but no adverse effect (whose mother’s hair mercury was 89 ppm) was excluded. NRC rejected the study for an RfD, but used it to say that more studies than just

the Faroes had found adverse effects.

Iraqi Poisoned Grain-based RfD

In 1995, EPA established a consumption RfD based on an episodic MeHg exposure from the Iraqi seed grain poisoning incident in which people ate grain treated with a preservative of MeHg instead of planting it for crops. Later, realizing a lack of relevance of the Iraqi incident for mercury in fish, EPA shifted the basis of its RfD to the Faroe Islands study in 2001, urged on by the 2000 NRC report. Despite the drastic switch in the basis for the RfD derivation and with different rationale for the “less-than-default” uncertainty factor of 10, the new value of the RfD (5.8 ppb) suspiciously remained the same.46 In 2000, Crump noted that EPA’s early derivation of RfD from the Iraqi study was based on a Benchmark Dose Lower Limit (BMDL) value of 11 ppm in maternal hair. But a full assessment of the child data on age first walked, talked, and a neurological test by Crump et al. (1995)47 yielded BMDL values of 54 to 152 ppm, which is consistent with “other analysis of the Iraqi data that there was no

There was no conclusive evidence of a mercury effect below a maternal hair level of 80 ppm.

24

conclusive evidence of a mercury effect below a maternal hair level of 80 ppm”48 (EPA’s current RfD is only about 1.0 ppm for hair). Miscellaneous Closer to home for the Chicago Tribune, a new study seeking to confirm potential health problems in children from consuming fish from the Canadian Great Lakes was simply "unsuccessful".49

Fish and Human Health

In sharp contrast to the Chicago Tribune’s lack of scientific evidence of harm from eating fish, beneficial effects of fish and fish oil consumption are well documented. Such health information is critical for making informed dietary decisions. Perhaps no one group is more at risk from

mercury/fish alarmism than mothers. The heartbreak of pre-term delivery Perhaps no one group is more at risk from mercury/fish alarmism than mothers. [for a more detailed discussion, see When Mercury Fears Harm at: http://ff.org/centers/csspp/pdf/szwarc_072006.pdf]. Claims of concern for fetal and child health by EPA, the CT and mercury activists largely fail to properly balance concerns and adequately inform women of the extraordinary benefits of fish nutrition during and after pregnancy.

Continued trends for preterm and low birthweightstatistics in the U.S. from the latest CDC’s National Vital Statistic Reports (vol. 53, no. 9, November 23, 2004)

Figure 1‐B

Premature birth is so serious an outcome for women that the March of Dimes organization has adopted it as a primary cause.50 More than 500,000 babies are born prematurely every year in the U.S. The infants aren’t just small; they’re developmentally “unfinished.”51 The March of Dimes

25

provides these facts on prematurely born babies:

Pre-mature births have increased by 29 percent since 1981 (Fig. 1-B) Accounts for 12 percent of all live births Can happen to any pregnant woman Is the leading killer of babies in their first month of life Is a major cause of long-term health problems, including cerebral palsy, mental

retardation, blindness, chronic lung problems, respiratory distress syndrome and bleeding in the brain

Is the number one obstetrical problem in the country Robs families of the full potential of their children, society of their future leaders

and our nation of strong and healthy citizens Places tremendous financial burdens on everyone. Hospital charges for infants

with a principle diagnosis of prematurity average $75,000, and add up to billions of dollars each year.52

Recognizing the critical role fish nutrition plays in helping prevent the tragedy of pre-term delivery, the March of Dimes is funding research. The research team of Olsen and Secher (2002) found that:

“Low consumption of fish was a strong risk factor for preterm delivery and low birth weight. In women with zero or low intake of fish, small amounts of n-3 fatty acidsprovided as fish or fish oilmay confer protection against preterm delivery and low birth weight.” 53 [Emphasis added]

Olsen et al. suggested that higher fish intake by Faroe Island women compared with Danes was the reason for longer gestation in Faroese pregnancies. The researchers demonstrated that fish intake of 2.7g per day provided increases in gestation of 4 days for healthy women and 8.5 days for healthy women with a previous pre-term delivery.54

Fish intake during pregnancy Has the potential to improve fetal development.

Further, Olsen and Secher found that women who consumed fish or seafood at least once a week during the first 16 weeks of pregnancy have one-third the normal risk of low-birth weight or premature births.55 Dr. Charles Lockwood, chairman of Obstetrics and Gynecology at the Yale School of Medicine observed:

[T]here are lots of health benefits of eating fish and it is a relatively cheap source of protein. There may be additional benefits of reducing oxidative stresses that might induce pre-eclamsia or pre-term delivery; may affect fetal growth restriction by impairing placentation. So, there are lots of reasons to think that fish might be useful for pregnant women to take in…56

26

Postpartum depression and low seafood consumption Research by Dr. Joseph Hibbelin of the National institutes of Health calls attention to another serious risk for mothers associated with low intake of fish nutrition – postpartum depression. Available cross-national statistics strongly suggest a greater risk of postpartum depression with both low seafood consumption and low DHA content in the nursing mother’s milk (Fig. 1-C) Dr. Hibbelin reported that the “data suggest that the nearly 50-fold difference in prevalence rates of major postpartum depressive symptoms across countries is substantially associated with omega-3 fatty acid nutritional status.”57

Higher Prevalence Rates of Postpartum Depression With Low Seafood Consumption and DHA Content in Mother’s Milk

Hibbeln (2002) Journal of Affective Disorders, vol. 69, 16-29

“Both lower DHA content in mother’s milk and lower seafood consumption were associated with higherrates of postpartum depression. Interventional studies are needed to determine if omega-3 fatty acids can reduce major postpartum depressive symptoms.”

Figure 1‐C

USA

USA

A further concern for postpartum depression is its sometime association with suicidal ideation. Improved fetal and child development A group of scientists from the National Institute of Environmental Health Sciences and the Institute of Child Health at the University of Bristol, UK reported important conclusions about the beneficial effects of marine fatty acids on the well being of young children:

27

“Fish intake by the mother during pregnancy and by the infant postnatally, was associated with higher mean [child] development scores [in a cohort of 7421 British children]. For example, the adjusted mean MacArthur [vocabulary] comprehension score for children [15 months old] whose mothers consumed fish four or more times per week was 72 ... compared with [a score of] 68 among those whose mothers did not consume fish. ... Although the total cord mercury levels increased with maternal fish intake, our data did not suggest adverse developmental effects associated with mercury. In a small study of subjects in [this] ALSPAC [Avon Longitudinal Study of Parents and Children] study, maternal DHA levels were associated with improved visual stereoacuity among offspring at 3.5 years of age. ... Fish intake during pregnancy has the potential to improve fetal development because it is a good source of iron and long chain omega fatty acids, which are necessary for proper development and function of the nervous system.” 58 [Emphasis added]

The Tribune series also clearly missed the positive news for children with developmental coordination disorder (DCD) as reported in the May 2005 of the professional journal Pediatrics. Researchers found that:

Mounting evidence suggests that a relative lack of certain polyunsaturated fatty acids may contribute to related neurodevelopmental and psychiatric disorders such as dyslexia and attention-deficit/hyperactivity disorder...Fatty acid supplementation may offer a safe efficacious treatment option for educational and behavioral problems among children with DCD. 59

Breast Cancer Recent research suggests that high fish consumption is associated with low incidence of breast cancer. Coastal and rural-dwelling Japanese and Eskimos, who traditionally consume large quantities of fish, have low breast cancer rates. A study of Singapore Chinese women aged 45-74 suggested that an intake of approximately 40g of fish/shellfish per day can reduce breast cancer risk by 25%.60 Another study in Japan found that women who consumed about 5 servings of fish per week had a 10-20% lower risk than women consuming only 1 serving per week. A Norwegian study reported that women who consumed 5 servings of poached fish per month exhibited a 30% lower risk than did those who ate poached fish about 2 times per month.61

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Kidney disorders A large, randomized and placebo-controlled trial reported that treatment for two years with a daily dose of EPA and DHA lowered the risk of death or end-stage renal disease by 67%. These benefits persisted after 6.4 years of follow-up.62 Stroke in men and women A large prospective study among 43,671 male health care professionals (aged 40-75 years) observed a 40% lower risk of ischemic stroke in those who consumed fish once per month or more compared to those who ate less often.63 Another prospective cohort study of 79,839 women aged 34-59 indicated that higher fish consumption is associated with a 48% reduced risk for thrombotic infarction among women who ate fish 2 to 4 times per week.64 Adult, type 2 diabetes Many observers see a modern epidemic of adult diabetes - diet and life-style induced. Diabetes affects an estimated 18,200,000 people and there are another 15,000,000 not yet diagnosed, just in the United States alone. Currently diabetes is the third leading cause of death in the United States. Common complications include eye damage and blindness; kidney failure; nerve damage to bladder, intestines, sexual organs, hands and feet; and heart problems. About 80% of type II diabetics die from heart disease. According to one report, the Pima Indians of the Southwestern United States had one case of diabetes in 1908. Today, 60% of all Pima adults suffer from type 2 diabetes.65 Dr. John Middaugh, State Epidemiologist of Alaska, reported to the FDA that many native Alaskan communities abandoned traditional fish diets since the FDA’s 2001 mercury advisory, with a subsequent increase in diabetes, heart disease and vitamin A and D deficiencies.66 A study by Salmeron et al. (2001)67 estimated that incidence of type 2 diabetes in women could be reduced about 40% by increased intake of omega-3 fatty acids (DHA + EPA) available in fish. And another study found that regular fish consumption led to a 64% reduction in the risk of heart disease in women with type 2 diabetes.68 Alzheimer Disease (AD) and adult cognitive abilities A large prospective study in a biracial Chicago community of 815 participants aged 65 to 94 years found that fish intake was associated with reduced risk of incident AD. Persons who consumed at least 1 fish meal per week had 60% less risk than persons who rarely ate fish. This study supports the protective associations found in two previous studies.69

29

Friedland et al. (2003) reports that Hendrie et al. found a low risk of AD from fish intake by Cree Indians in NE Canada. At the same time, Friedland and colleagues found a high prevalence of AD in the Arab population in Israel with a low rate of fish consumption.70 Kalmijn et al. reports that “the notion that dietary factors influence cognitive functions and subsequently the risk of dementia is growing.” Various studies have shown that even mild cognitive impairment progresses to dementia or AD at a rate of 10-15% per year.71 A study of 1613 men and women aged 45-70 years found fish consumption associated with better overall cognitive function and speed.

For most people, the risk from mercury by eating fish and shellfish is not a health concern.

Positive results were also recently reported from the Chicago Health and Aging Project at the Rush University Medical Center. In the December 2005 issue of the Archives of Neurology, Martha Morris and colleagues found that:

Dietary intake of fish was inversely associated with cognitive decline over 6 years in this older, biracial community study [of 3718 adults 65 years and older at Chicago]. The rate of decline was reduced by 10% to 13% per year among persons who consumed 1 or more fish meals per week compared with those with less than weekly consumption. The rate of reduction is the equivalent of being 3 to 4 years younger in age. 72

Other new results were reported by Weil et al. (2005)73 in the Journal of the American Medical Association. It was the first study attempting to assess the potential association of mercury exposure with adverse neurobehavioral outcomes for older adults in the general U.S. population. In this study, 474 participants were randomly selected from the larger pool of 1140 residents aged 50 to 70 years of the Baltimore Memory Study in order to confirm any potential associations of adverse neurobehavorial performance as functions of mercury levels measured in their blood. Weil et al. (2005) concluded that:

“Overall, the data do not provide strong evidence that blood mercury levels are associated with worse neurobehavorial performance in [the] population of older urban adults [from their Baltimore Memory Study].”

Finally, the abundance of Selenium (Se) found in fish seems to be a crucial nutrient for HIV-infected subjects. It is a potent inhibitor of HIV replication in vitro.74 Rayman reports that Se is a strong predictor of the outcome of HIV infection; that Se-deficient patients are 19.9 times more likely to die from HIV-related causes that those with adequate Se levels.75

The message from current research seems pole star clear that older Americans should eat lots of fish and not be dissuaded by mercury alarmists.

30

Prostate cancer A recent study found that moderate or high fish intake could be associated with decreased risk of prostate cancer. The study examined a cohort of 6,272 Swedish men.76 These findings should be of particular concern to African-American males, who suffer a disproportional higher incidence of prostate cancer. Summary of health findings Clearly, the medical and nutritional literature on dietary fish consumption is rich with potential mitigations for a host of serious health concerns, especially those related to child birth and physiological and mental development of infants and young children. These include:

Pre-term delivery and low birth weights, and physiological and mental development of infants and young children

Cardiovascular disease (CVD) Coronary heart disease (CHD) and sudden death Breast Cancer Post partum depression, major depression, bipolar disorders, schizophrenia and

suicidal ideation Prostate cancer

Autistic Children Are Deficient in Essential Fatty Acids (EFAs): The Case of Scottish Children

(Bell et al., 2004, Prostaglandins, Leukotrienes & Essential Fatty Acids, vol. 71, 201‐204)

Numbers of autistic children are increasing in Scotland

Figure 1‐D Endometrial (inner lining of the uterus) cancer

Kidney disorders Rheumatoid arthritis Type 2 diabetes in

women and CHD in type 2 diabetic women

May lessen effects of dyslexia, hyperactivity and attention deficit disorder

Stroke Auto-immune

conditions Autism (Fig. 1-D) Allergies Migraines Skin conditions Crohn’s disease

31

Sleep disorders Aggressive behavior in young adults Enhanced protection from viral infections Reproductive health Mood disorders Thyroid function Bipolar disorders

Dietary benefits These scientific health findings -- ignored by CT -- support the general conclusion of the 2005 Dietary Guideline for Americans:

For most people, the risk from mercury by eating fish and shellfish is not a health concern.77

The scientific results also clearly support the latest recommendation on fish consumption by National Oceanic and Atmospheric Administration Fisheries group (emphasis added): “Backed by compelling science that links seafood consumption to reduced risk of disease, the U.S. government this week is recommending that all Americans - especially pregnant & nursing women and children - eat two seafood meals per week78 that are rich in omega-3 fatty acids. This recommendation is included in USDA's 2005 dietary guidelines and is being reiterated by the National Oceanic and Atmospheric Administration. ... By eating the right kinds of seafood, pregnant and nursing women pass to their baby important nutrients that aid in brain development and may lessen the effects of dyslexia, autism, hyperactivity and attention deficit disorder, according to scientists presenting at the conference. [Note this international conference

was sponsored by the governments of the United States, Canada, Iceland and Norway with technical assistance from the Food and Agriculture Organization of the United Nations.]

Average American needs more fish oils (DHA+EPA omega-3 fatty acids)

0.1 to 0.2

0.650.8

1.21.0

3.0

0

0.5

1

1.5

2

2.5

3

Daily DHA+EPA fatty acids (g/d)

US current intake

NIH 1999 workshop

NATO workshop

British Nutrition Foundation

AHA for patients with CHD

AHA for patients needing triglyceride lowering

Figure 1-E

Recommended intake of fatty acids

Sources: Kris-Etherton et al. (2000, Am. J . Clin. Nutr., vol. 71, 179-188); Kris-Etherton et al. (2003, Arterioscler. Thromb. and Vasc. Biol., vol. 23, e20-e30); Din et al. (2004, Brit. Med. J ., vol. 328, 30-35)

Salmon appears to be the king of fish, especially for pregnant and nursing women.

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Studies also have presented a link between these nutrients and increased intelligence in infants and young children. Species that are rich in these nutrients - omega-3 fatty acids, iodine, iron and choline - include wild and farmed salmon, cod, shrimp and canned light tuna. Salmon appears to be the king of fish, especially for pregnant and nursing women; it is exceptionally low in mercury and exceptionally high in omega-3 and selenium (see Sec. 11). Women will not put their babies at risk – even under EPA’s extreme RfD – if they avoid eating shark, swordfish, tilefish, king mackerel, tuna steaks and whale meat until after they have delivered and stopped breast feeding, scientists said. Exposure to mercury found in those species during the sensitive stages of fetal brain development may cause neurological damage. As an extra precaution, women who plan to become pregnant should avoid those species for six months before conception. These are conservative guidelines, considering the 10-fold safety margin built in for precaution, and the fact that mercury is eliminated from the body in about 60 days. Scientists reiterated that there is no evidence of health risk to the rest of the population, including children and the elderly, from eating seafood. To the contrary, studies have shown seafood consumption to help people live longer, healthier lives. Seafood cuts the risk for heart disease, cancer, Alzheimer's, stroke, diabetes, and inflammatory diseases such as rheumatoid arthritis. Further, studies show that nutrients found in whole fish and shellfish – not fish oil supplements – help the body heal after cancer treatments, and ward off auto-immune conditions, allergies, asthma, migraines, skin conditions, and Crohn's disease. Studies have found that people with omega-3 fatty acid deficiencies are also at greater risk for sleep problems, depression, stress, schizophrenia and aggressive behavior. 79

Conclusion

Any calls for reductions in fish consumption, inherent in ill-informed fish advisories or unbalanced alarmist claims by activists and the press, must take extreme precaution against promoting widespread public health threats. The most fundamental principle must be to do no harm in the first place.

The most fundamental principle must be to do no harm in the first place.

The CT series does not measure up. It has clearly failed to report from a vast, current literature that there are far greater, real risks from restricting or avoiding fish, and that the supposed evidence for "learning disabilities in children and neurological problems in adults" from eating fish is weak or simply does not exist. By this, CT is doing great harm.

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SECTION 2: AN EXTRAORDINARY POPULAR DELUSION - MYTH OF THE MECURIAL HUNDRED THOUSANDS

“There is no opinion, however absurd, which men will not readily embrace as soon as they can be brought to the conviction that it is generally adopted.” - Schopenhauer The number [of children born each year to mothers exceeding EPA’s blood mercury RfD] should not be interpreted as an estimate of the annual number of cases of adverse neuro-developmental effects. The Committee (NRC, 2000) does not believe it is possible to estimate a meaningful number of children that might be affected within the “at risk” population. - Robert Goyer, Chair of NRC Committee on Toxicological Effects of Mercury

Chicago Tribune: No one knows how many people in the U.S. have been harmed by mercury in fish. But a recent government study estimated 410,000 babies are born each year at risk for mercury poisoning because of high levels in their mothers' bodies. (December 11, 2005) Response:

Statistical Manipulations

he first sentence is true, and the “no one” includes Roe and Hawthorne. They did not produce a single, clinically verified case of harm. If anything approaching their claims were sound, they could have found an epidemic just in

the Chicago area. T

The second sentence is a variation on the most emotive refrain driving the mercury alarmism campaign. It initially exclaimed that "630,000 American babies are born each year" with elevated concentrations of mercury in their blood, with the potential for "permanent brain damage and learning disabilities." CT has now reduced that number to 410,000 without any explanation as to why. Perpetual repetition of various perturbations of this baseless claim does not establish truth. It does, however, fuel the politically clamorous fires of maternal fear about fish consumption. Infants are said to be "poisoned" at birth because their mothers consumed fish containing micro traces of mercury. The statistic represents hypothetical pregnancies unjustifiably derived by mutating EPA’s RfD “safety threshold” into an actual risk calculation. Such a precise number derived

34

from a sea of uncertainty and contrary data should have been the first clue that statistical mischief was afoot. The genesis of the calculation was the 2003 Centers for Disease Control release of its results from the 1999-2000 nutrition and health survey. It was reported that 8% of women of childbearing age (16-49 years old) had blood mercury concentrations above EPA’s RfD. Since there are over four million births in the U.S. annually, mercury opponents and several government scientists unofficially extrapolated that at least 320,000 babies born

are "at risk" in the U.S. each year due to "unsafe" mercury levels in their mother's blood. There is no official “government study” making this claim anywhere, as far as we know.

There is no official “government study” making this claim anywhere, as far as we know.

Then, in January 2004, an EPA employee revised the number of babies born at risk upward to 630,000, based on "new information” that mercury in maternal cord blood (shared with the fetus) is more concentrated (by about a factor of 1.7 to 2.0) than in body blood. But the information was not "new," it was a double-counting, since EPA earlier accounted for the blood-concentration difference in 2001, helping justify its "safe" mercury dose (a factor of 10) as the most stringent in the world.

Dramatic drop in percentage of U.S. women with blood mercury levels above EPA’s RfD for MeHg

7.8% (of 1709 women)

3.9% (of 1928 women)

1.8% (of 1824 women)

0

2

4

6

8

10

12

14

1999-2000 Survey 2001-2002 Survey 2003-2004 Survey

% of women of childbearing age with blood mercury above EPA’s RfD for “safe” MeHg consumption

From the important CDC’s update on November 5, 2004 at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5343a5.htm + J uly 2006 updates

± 4%

± 2%

Figure 2-A

Next, CDC released its 2001-2002 health survey results.80 The results should have suggested caution to the truly thoughtful.

Instead of finding 8% of 1,709 women as surveyed in 1999-2000 above EPA’s “safe” mercury level, the CDC reported only about 5% of the 1,928 women surveyed

in 2001-2002 exceeding EPA’s RfD. Extrapolating an average of 6% for the full 4 years of survey data yields an estimate of “410,000” (i.e., 0.06 times 1.7 times 4 millions).

The clearest fact is that, all things considered, there is not a single woman or child at actual risk in these data.

And now, the CDC has released its most recent blood mercury survey results. No more than 2% of the 1,824 women (16-49 year-olds) surveyed have MeHg levels exceeding EPA’s RfD. So the fraction above the RfD continues dropping dramatically - from

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around 8% for the first two years of data to about 5% in the next two and to about 2% currently. Thus, as world-wide, man-made Hg emissions rise (principally from China, India and South Africa), the reputed numbers of babies “born at risk” for mercury “poisoning” continues its dramatically precipitous decline. What is a possible explanation for this seeming inverse relationship for increased power plant emissions and declining human exposure levels? Isolating the response data for actual pregnant women seems to indicate they are indeed being frightened away from fish meals. The change in survey data-sets from 1990-2000 to 2001-2002 reflected a sharp drop in pregnant women above EPA’s mercury RfD. The most recent 2003-2004 survey data show a continuing decline such that only a single pregnant woman of the 255 in the survey exceeded the RfD. Her level was measured at about 7.7 ppb. 81 If only pregnant women (the focus of concern) are considered, then the number of babies claimed to be “born at risk” drops to statistical insignificance – 1/1824. Further, given that the EPA RfD of 5.8 ppb has an excessive safety factor of 10-fold, even she has an enormous safety cushion for actual risk.

No woman (aged 16‐49) in the CDC’s NHANES blood mercury survey (1999‐2002) has blood mercury above NRC/EPA’s own chosen statistical benchmarks: BMD or BMDL

Adapted from EPA’s Technical Supporting Document: Methodology Used to Generate Deposition, Fish Tissue Methylmercury Concentrations, and Exposure for Determining Effectiveness of Utility Emission Controls (March 18, 2005)

Even more significantly, the latest CDC data show that only one out of 911 children (ages 1 to 5 years) surveyed has a blood mercury concentration above EPA’s excessively stringent limit. This compares to only 11 of the 1,577 children previously surveyed in 1999-2002. The clearest fact is that, all things considered, there is not a single woman or child at actual risk in these data, let alone 410,000.

Data outlier?(with no fish consumption reported)

blood Hg for 3637 U.S. women of childbearing age: mean = 0.92 ppb 212 ppb: level for mothers of

children with Minamata Disease

Figure 2-B

levels of health concern?

safety factor of 10 applied to get EPA’s conservative RfD at 5.8 ppb

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This misleading statistical exercise perpetuated by the Tribune – and the alarming claims bred from it – first originated with the 2000 NRC Committee on the toxicological Effects of Methylmercury. On page 327 of their report they stated, “The committee estimates that over 60,000 children are born each year at risk for adverse neurodevelopmental effects due to in utero exposure to MeHg.” After the report was published, Dr. Robert Goyer, Chair of the committee, wrote that the number representing offspring of mothers considered “at risk” should “not be interpreted as an estimate of the annual number of cases of adverse neurodevelopmental effects. The committee does not believe it is possible to estimate a meaningful number of children that might be affected within the ‘at risk’ population.” But by then the damage was done. The “410,000” claim suffers from a number of additional, major problems.

Revisit the RfD

Additional considerations As already pointed out in Sec. 1, a number of issues suggest EPA’s underlying RfD is almost certainly too conservative, inappropriately derived, non-transparent and should be revised upward. There has been a persistent pattern of suspicious behavior noted for many years. In a 1994 National Academy of Science report, the panel found, “In the absence of convincing scientific knowledge or data, EPA relies on assumptions [default options], often conservative in nature, about such questions as how exposure to low doses of a contaminant affects human health.” A 2006 Govt. Accounting Office investigation reported that “EPA should more transparently communicate which default assumptions were used in risk assessments, why the defaults were chosen, and what judgments EPA was making when it employed certain methods.” In this context of suspicion, first consider that a recent peer-reviewed survey reported that over 5,900 Japanese, 87% of the sample, including 74% of child-bearing aged women, had mercury concentrations above EPA’s “safe” level.82 Yasutake et al. (2003) cautioned that these levels do not present a hazard to the fetus:

“The present hair mercury data would reflect a portion of the food habits of the current Japanese population. Although it was suggested that a large proportion of the Japanese population is exposed to [MeHg] at doses over the EPA/NRC [U.S. National Research Council] recommended level through the daily intake of fish/shellfish, this does not necessarily imply that they are exposed to doses with a substantial hazard to a fetus. However, a very little portion (0.4%) of females at reproductive ages, that show hair mercury levels above 10 [ppm or ten times above the EPA's RfD], may have to change the amount or species of fish consumed in their daily life concerning pregnancy to avoid possible adverse effects on a developing fetus. The results of the present study should be helpful to establish a healthy diet with an appropriate consumption of fish and

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shellfish, which are nutritionally outstanding foods containing valuable nutrients such as n-3 polyunsaturated fatty acids.” 83

Similarly, a recent hair-mercury survey of 1,066 Taiwanese in 23 counties and cities84 yielded a mean hair mercury level of about 2.4 ppm. These results are similar to the Japanese ones, but significantly higher compared to the average level of 0.2 ppm for U.S. women of childbearing age.85 These results confirmed that 80% of Taipei residents86 surveyed had hair mercury levels exceeding the U.S. EPA's RfD, without reports of derived health complaints. Still, another recent survey by the Faroes investigators found 56% of Inuit cord blood samples87 exceeded the EPA’s RfD, without reported harm. Logically, one must either conclude generations of Japanese, Taiwanese and the Canadian Intuits are “brain-damaged,” suffering “severe and permanent” learning deficits, or that EPA’s “safe” mercury dose is too stringent, extreme and untrustworthy for safe and effective policy outcomes. In other words, CT needs to account for the absence of generational epidemics that would have long characterized these societies if its series of reports were remotely scientifically evident. (see Sec. 20) Secondly, the “safe” level of mercury exposure established by EPA is widely recognized as the most stringent in the world by at least 10 times any actual levels of concern or harm established elsewhere. To repeat, by a reasonable safety margin, no women in the CDC 1999-2002 survey (the blue data curve in Fig 2-B) had blood mercury above levels of actual harm or concern (vertical purple lines). The mean level was 0.92 ppb, with a data outlier (red circle) around 40.0 ppb reporting no fish consumption at all. By comparison, no cases of Minamata disease were recorded for any child whose mother had mercury levels below 212 ppb (upper blue arrow). Third, the CDC’s own ethical guide lines do not require notifying survey participants of potential harm until a blood concentration of 200 ppb is exceeded. What does the CDC know that EPA apparently doesn’t? Fourth -- and almost never reported -- the CDC also surveyed actual blood mercury levels for children ages 1-5 years. The 1999-2000 survey documented only 7 out of 705 (or 1%) above the EPA’s RfD, while the 2001-2002 survey found only 4 out of 872 (or 0.5%) exceeding it. As noted above, the latest 2003-2004 survey by CDC reported only one out of 911 (0.1%) children aged 1-5 has blood mercury above EPA’s limit. Even the highest measurement for the entire 6-year survey still enjoyed a safety cushion of more than 500%. None of the representative U.S. children were exposed to mercury levels even approaching the threat of mental retardation, even within the limits of EPA’s RfD.

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No Bright Line of Harm In other words, EPA’s mercury safety factor is unjustifiably stringent, and carries no credible justification for morphing it into a bright line of harm. This was confirmed in EPA's own technical document, "Methodology used to generate deposition, fish tissue methylmercury concentrations, and exposure for determining effectiveness of utility emission controls" dated March 18, 2005:88

“The RfD does not represent a "bright line" above which individuals are at risk of significant adverse effects. Rather, it reflects a level where EPA can state with reasonable certainty that risks are not appreciable. The Agency further notes that a number of other national and international scientific bodies have assessed the health effects of methylmercury and have adopted other health-based benchmarks greater than EPA's RfD. Health Canada established its Tolerable Daily Intake (TDI) level at twice the EPA's RfD. Their benchmark is 0.2 micro-g/kg bw/day. The agency for Toxic Substances and Disease Registry (ATSDR) has set a Minimal Risk Level (MRI) of 0.3 micro-g/kg bw/day – three times EPA's RfD level. The World Health Organization's (WHO) benchmark is set at 0.23 micro-g/kg bw/day. Of these major agencies, EPA's RfD has established the lowest risk benchmark to define levels of exposure that are without appreciable risks. As exposure levels increase beyond RfD, the possibility of deleterious effects increases, but the point at which they become "unacceptable" must be determined on a case-by-case basis. In making this determination, the Agency considers a number of factors including: Confidence in the risk estimate: How certain is the scientific

information supporting the link between possible health effects and exposures?

The effects of concern: How serious are the health effects? The size of population at risk, as well as distribution of risk within the

population. The Agency has considered these factors in the case of mercury and has concluded that the exposures above the IDI [Index of Daily Intake] described elsewhere in this chapter do not constitute an unacceptable risk.”89 [Emphasis added]

A general summary of mercury RfD talking points:

It is inappropriate to speak of a linear relationship between MeHg and IQ (or other neurological effects).

Exposures in U.S. do not even approach the NOEL (Non-Observed Effect Level) in Faroes.

MeHg RfD is based on limited, non-transparent and inconsistent data from a study of people who are exposed from consuming pilot whales.

Whales contain PCBs and other pollutants in addition to Hg.

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Whales are not consumed in the U.S. The RfD is based on the Boston Naming Test and there is no evidence it indicates

neurological damage or even is associated with success in life. It is a test originally designed to evaluate traumatic brain injuries in war veterans and not children.

The EPA has not seen or evaluated the data from the Faroes study. Consequently, they cannot know the accuracy or reliability of the data upon which their RfD is based.

Epidemiological studies are difficult to conduct and interpret. When evaluating psychological endpoints this is especially true since so many social, family and other factors can influence them.

Health benefits of lower-level reduction cannot be measured/demonstrated. Mechanism for IQ/behavior effect from low-level Hg is unknown. Weakness of data behind MeHg RfD suggests extreme caution against drastic or

costly interventions.

Conclusion In sum, the Chicago Tribune’s reporting apparently fails at any depth of critical analysis. Tragically, the Mercury Menace series itself may represent the real menace to public health. Its wide, continuing distribution will misinform and frighten off a population already remarkably deficient in fish nutrition – especially pregnant women and a vulnerable, aging population.

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SECTION 3: MISREPRESENTING THE FDA

Consistent with its mission and practice, FDA has studied carefully the issue of methylmercury in fish for more than twenty-five years and has developed substantial expertise in analyzing both the scientific and consumer education aspects of the issue. Accordingly, FDA is uniquely qualified to determine how to advise consumers on the issue of methylmercury in fish. - Hon. Robert L. Dondero, San Francisco Superior Court Judge

Chicago Tribune: The newspaper randomly selected supermarket chain stores and fish markets in the Chicago area and bought 18 samples each of eight kinds of fish, including two types of canned tuna. The samples were sent for analysis to a laboratory at Rutgers University, which has performed some of the nation's only studies of mercury in store-bought seafood. ... The FDA has issued warnings for canned albacore tuna, which has averaged 0.35 parts per million in the agency's testing. Yet the agency has not issued warnings for orange roughy, which averaged 0.57 parts per million in the Tribune testing, or walleye, which was at 0.51. (December 11, 2005) Response:

he facts suggest that CT has clearly misrepresented the efforts by the FDA and confused the information listed on the FDA fish mercury website.

Ignored was the available FDA mercury data for orange roughy and grouper (with mean levels of 0.54 and 0.55 ppm respectively, measured mainly in the 2002/2003 period.90 CT seems compelled to deprecate the FDA's monitoring and measurement efforts on mercury for fresh and canned tuna (see Sec. 20), following the lead of Rutgers University researchers.91 Burger and Gochfeld (2004) had also chosen to highlight only dated FDA tuna measurements from the 1991 era while ignoring 2003 data and other complimentary tuna-mercury monitoring programs under FDA jurisdiction.

T

The manuscript submission, acceptance and appearance dates (November 2004), of Burger and Gochfeld (2004) suggests no acceptable excuse for Rutgers researchers or CT reporters ignoring the well-publicized results from the FDA's 2003 mercury measurements for 2 canned tuna (albacore and " light") or 12 different species of fish, including orange roughy and grouper. CT should explain why, as late as December 2005, Roe and Hawthorne base their criticisms of the FDA's mercury measurement and monitoring efforts on older data from a 1991 survey, while apparently ignoring the updated 2002/2003 data. A discussion of FDA's tuna mercury data is given in Sec. 20. However, it is noted that mercury levels in albacore and yellow-fin steaks as compared to the skipjack tuna species

41

was well accounted for in the FDA/EPA well-publicized fish consumption advisory issued of March 2004. The summary of tuna data in Fig. 20-C and Fig. 20-D below clearly demonstrate that CT's own tuna data is unremarkable and falls within the range of FDA numbers. The CT also failed to properly inform its readers that FDA's seafood safety program has the following mercury measurement and monitoring activities in place:92

The Total Diet Study properly focuses on average, rather than extreme, dietary intake of mercury from fish/seafood, including canned tuna.

The FY05 Toxic Elements Program to monitor mercury, lead, cadmium and arsenic in a 160 imported samples of striped bass, salmon, flounder, herring, sardine, cod, bluefish, halibut, Alaska pollack, crab, oyster, squid, scallop and lobster.

FY05 Mercury Assignments to measure total mercury levels in 29 species of fish, 100 fresh/frozen tuna and 50 samples of canned tuna.

CT correctly reported FDA’s 4 mercury measurements of walleye, as listed in its public database entitled "Mercury in Fish: FDA Monitoring Program (1990-2003)" (http://www.cfsan.fda.gov/~frf/seamehg2.html). This reporting evidences CT reporters must have been fully aware of the FDA data from 2002/2003 measurements. However, they did not make sufficiently clear to their readers that freshwater fish advisories fall under EPA jurisdiction, or that EPA mercury data for walleye is extensive. EPA measured levels for walleye93 range widely, depending on size and location, from 0.005 to 16 ppm -- with a mean of about 0.43 ppm. These data again evidence that CT's 18-sample mean of 0.51 ppm (ranging from 0.11 to 1.74 ppm) is neither unusual nor alarming. It is further puzzling that CT faults only FDA for a joint EPA-FDA fish advisory. More to the point, the Tribune’s accusations of neglect toward sensitive subgroups in the March 2004 advisory are unconvincing. The advisory actually stated:94

“By following these 3 recommendations for selecting and eating fish or shellfish, women and young children will receive the benefits of eating fish and shellfish and be confident that they have reduced their exposure to the harmful effects of mercury. (1) Do not eat Shark, Swordfish, King Mackerel, or Tilefish because they contain high levels of mercury (2) Eat up to 12 ounces (2 average meals) a week of a variety of fish and shellfish that are lower in mercury: Five of the most commonly eaten fish that are low in mercury are shrimp, canned light tuna, salmon, pollock, and catfish. Another commonly eaten fish, albacore ("white") tuna has more mercury than canned light tuna. So, when choosing your two meals

42

of fish and shellfish, you may eat up to 6 ounces (one average meal) of albacore tuna per week. (3) Check local advisories about the safety of fish caught by family and friends in your local lakes, rivers, and coastal areas. If no advice is available, eat up to 6 ounces (one average meal) per week of fish you catch from local waters, but don't consume any other fish during that week.”

Again, there is failed recognition that EPA and FDA are advising a complete avoidance of high-mercury species while encouraging healthy consumption of low-mercury fish and seafood. The advisory also specifically points out the difference between albacore and light canned tuna.

Top-26 Seafood Consumed in the U.S. Accounts for over 93% of the Commercial Market

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Figure 3-A

CT statements that the FDA/EPA advisory did not specifically target orange roughy, grouper and walleye species, is addressed in Sec. 4 below. The short answer is that average Americans are not consuming much of these fish, and certainly not enough to

43

meet EPA’s RfD criteria of every day consumption for a lifetime before raising concern – not danger, but concern. In other words, no advisory is directed at these fish species for the same logical reason one is not directed at pilot whales, even though they contain very high levels of potentially toxic substances, including methylmercury - nearly no Americans eat them. Fig. 3-A verifies that orange roughy, grouper and walleye are not even among the top 26 seafood types consumed in the U.S. which account for over 93% of market share. Orange roughy and grouper combined account for no more than 0.5%, according to the 2001 National Marine Fisheries Service landings data summarized in Carrington et al. (2004). Even under an adjusted ranking utilizing mean mercury exposure from commercial market share in the U.S. (i.e., multiplying the mean mercury content in each fish species by percent market share consumed by Americans), neither orange roughy nor grouper make the top-15 species list, and are ranked lower than mercury exposure from shark intake.

Conclusion In conclusion, it appears CT has misrepresented FDA’s reasonably well-executed advisory role in maintaining a balance between assuring public nutritional health from fish consumption and mercury warnings for the most-sensitive sub-populations of women and young children.

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SECTION 4: HOW SAFE IS “SAFE”?

“The global cycling of mercury, along with the processes of biomethylation and bioaccumulation, implies that humans must have consumed methylmercury in fish dating back to times before Homo sapiens evolved. It could be argued that environmental levels of mercury vapor were much higher in an earlier period of earth’s history when oxygen had not yet appeared in the atmosphere [i.e., the appearance an oxygen atmosphere was timed roughly to 2.45 to 2.22 billion years ago]. As levels of oxygen began to rise, increasing amounts of the vapor would be converted to the ionic form. Life forms at those Archean times [roughly 3.8 to 2.5 billion years ago] had to protect themselves not only from this new toxic gas, oxygen [i.e., because of its reactivity], but also from ionic mercury [i.e., Hg2+] pouring down in rainwater. Perhaps it is no coincidence that those proteins and antioxidant molecules present in today’s cellular machinery to protect against oxygen also are our main line of defense against mercury. - Tom Clarkson, University of Rochester Medical Center

Chicago Tribune: The simple question "Is fish safe to eat?" depends on many factors. What kinds of fish do you eat? How much do you eat? How often do you eat it? How much do you weigh? ... Shoppers have no way of knowing, for instance, if one piece of orange roughy in a supermarket display case has a widely different amount of mercury than the orange roughy fillet next to it. The same is true for canned tuna and many other kinds of fish. ... For example, 15 of the orange roughy samples the Tribune bought had high levels. The testing also indicates mercury levels can vary widely even within a given species. A sample of orange roughy from Dominick's in suburban Crestwood had seven times more mercury than a piece from Jewel on North Elston Avenue in Chicago. ... FDA officials said it is impractical to test individual swordfish to weed out those that are heavily contaminated. Issuing warnings is a better way to protect at-risk groups, such as young children and pregnant women, the officials said. "Rather than saying, `You can eat swordfish as long as it has been tested,' we're saying, `Don't eat those fish,'" Acheson said. Though it is unclear whether a single high-mercury meal could harm a fetus, experts say the developing nervous system is so sensitive to toxic substances that caution should prevail. "You only get one chance to develop a brain," Hightower said. (December 11, 2005) Response:

ere, CT advances the somewhat sophistical notion that without implementation of impractical testing and labeling of every individual piece of fish sold in US markets or restaurants, any fetus may miss its “one chance to develop a brain.”

Equally questionable is the “expert” claim of non-clarity regarding “whether a single high-mercury meal could harm a fetus.” It is highly doubtful that Dr. Jane Hightower –

H

45

neither a toxicologist nor epidemiologist – would make such an extraordinary leap against the huge body of literature to the contrary (see Sec. 9). Such CT claims, here and throughout the series, compels the question as to how is it possible that thousands of generations of humans the world over have consumed large

quantities of a variety of sea foods and still managed to escape a pandemic of brain damage? Ultra-trace levels of mercury have likely been present in fish and fish-eaters around persistent and current levels since either evolved.

Ultra-trace levels of mercury have likely been present in fish and fish-eaters around current levels since either evolved.

The data briefly presented in Sec. 1 and Sec. 8 clearly support the findings that fish and fish oil consumption is highly beneficial and that average Americans are far below optimal levels (1) consumed in other countries or (2) recommended by medical and nutrition professionals. The real benefits of fish consumption clearly far outweigh hyperbolic risk claims. Any such risk concerns need to be rationally evaluated on a case-by-case basis for extreme situations or consumption patterns. For example, a recent analysis by Carrington et al. (2004)95 suggests the optimal strategy for reducing MeHg exposure is to restrict fish consumption to no more than 12 ounces a week while avoiding the high-mercury species as recommended in the joint EPA/FDA fish advisories. Their analysis indicated that if the U.S. population took the further precautionary step of eating only the low-mercury species like shrimp, canned light tuna, salmon, pollock and catfish, even individuals with unusually high blood mercury could achieve reductions below a wide range of proposed safety standards, including the most stringent by EPA (see Figure 5 in Carrington et al. 2004). Pseudoscience calls for almost-zero risk tolerance in fish consumption is untenable and ignores the optimal approach taken by FDA in minimizing risk. In the above quote, the CT appears to blink at the principle of averages, failing to allow for the fact that occasionally crossing EPA’s stringent methylmercury threshold does not even faintly constitute a known health threat. According to EPA's own RfD definition, fish consumers would have to persistently beat incredible odds for randomly selecting only high-mercury content fish, day after day, for a lifetime to risk being “poisoned.” Practically, total public avoidance for occasionally eating a “high” mercury meal is unlikely, regardless of resources expended. Again, CT impugns the FDA as having purposely neglected its public health responsibilities, this time by comparing Canadian policy. CT appears to lament that the Canadian mercury actionable level (0.5 ppm) for prohibiting sale of commercial fish is twice as stringent as FDA (1 ppm). [As an aside, it should be noted that EPA's threshold advisory for freshwater fish is 0.3 ppm (see CSPP’s Making Sense of State Fish Advisories96).

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Also, see Sec. 17 highlighting the confusion in Representative Mark Kirk's "dear Colleague” letter suggesting that Canada banned the sales of walleyes above 0.5 ppm level while FDA has ignored the situation.] This is an odd claim considering the FDA (and EPA) advocates the far more restrictive advisory of no consumption for the high-mercury fish species like swordfish, shark and fresh and frozen tuna steaks. Health Canada’s guidelines for high-mercury fish species state: 97

“Certain fish species sold in Canada, namely, shark, swordfish, and fresh and frozen tuna, contain mercury at levels that are known to exceed the 0.5 ppm guideline. Mercury levels for these species generally remain between 0.5 and 1.5 ppm, allowing for occasional consumption. Therefore, these species (Note: not canned tuna) are exempted from the 0.5 ppm guideline and, in their case, another risk management strategy is followed, namely, issuance of advisories recommending appropriate restrictions on (amounts and frequencies of) consumption. In this way, these species can continue to be enjoyed by consumers as part of an occasional diet. Consumption of shark, swordfish and fresh and frozen tuna should be restricted to one meal per week. For young children, pregnant women, and women of child-bearing age, consumption should be limited to one meal per month. Because of the nutritional value of fish, these species continue to be available to Canadian consumers, with advice to limit consumption to avoid exposure to hazardous levels of mercury.” (Emphasis added)

Again, by advising total avoidance of high-mercury fish for pregnant women, FDA is more conservative, even though Health Canada’s legal limit for banning commercial fish is 2 times higher that the guideline set by the Canadian Food Inspection Agency.

Freshwater Sport Fish How safe is freshwater sport fish consumption? First, an Electric Power Research Institute report of May 2003 assumed a large upper bound of 10% of all fish consumed in the U.S. being from “wild, freshwater fish.” However, utilizing statistics from the U.N. Food and Agriculture Organization, our macroeconomic estimate indicates that only about 0.5% of all fish consumed in the U.S. is from freshwater catch. For those concerned about mercury exposure consumption levels for freshwater fish, Fig. 4-A displays recent EPA exposure estimates from researchers at RTI International. The results clearly show that mean daily intake of MeHg from local freshwaters for the 38 eastern U.S. states98 - including Illinois - fall safely below EPA's recommended ingestion

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rate. These empirical findings confirm that alarmism over “toxic exposure” to MeHg from consumption of freshwater fish caught in U.S. lakes and rivers is largely unwarranted.

Also, a collaborative project between the Wisconsin Department of Public Health and Maine’s Bureau of Health99, assessing mercury awareness in 12 States, found that only 29% of the 3,015 women of childbearing age surveyed had eaten any sport-fish. Hair mercury levels [measured for 414 women in the sample] ranged from 0.005 to 4.62 ppm and were positively correlated to fish consumption rates (P<0.0001). Women who ate sport-caught fish did not have significantly higher hair mercury levels than others (mean 0.51 vs. 0.48 ppm). Among women who ate sport fish, advisory awareness had no effect on their mercury exposure. “Demographic indicators associated with higher hair mercury levels included residence in northeastern USA, marital status of married, college education, annual household income greater than $75,000, and Asian race.” These researchers also documented that 50 women (12% of the 414 women sampled) had a hair mercury level greater than the 1 ppm safety guideline established by EPA’s MeHg RfD, and that most of these women did not consume sport-caught fish; their exposures are largely explained by consumption of commercially sold fish, including frequent meals of canned tuna. Additional research results were recently reported from Canada. Cole et al. (2004) reported relevant findings for anglers and sport-fish eaters from Ontario, Canada.100 Surveys among 176 anglers

consuming their catch had a mean blood total mercury level of 2.8 ppb – well below EPA’s RfD of 5.8 ppb. These findings are also consistent with the estimates

shown in Fig. 4-A, indicating that mercury exposure through the consumption of locally-caught freshwater fish is not a predominant route, when compared to commercial seafood. The authors concluded, “Given the nutritional and social benefits of fish consumption, prudent species and location choices should continue.”

New Estimates of Mercury Exposure for Women of Childbearing Age From Consumption of Noncommercial Freshwater Fish in the U.S. Suggests Low Intake Levels

1.81

2.92

6

0

1

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6

Mean Mercury Ingestion Rate (g/day)

Mean of Women from Illinois

EPA’s MeHg RfD Safe Level for 60 kg (~130 lbs) Women

Data Source: “Assessment of Mercury Exposures to Women of Childbearing Age From Consumption of Noncommercial Freshwater Fish in the U.S.” Report (Draft Dated November 2004) prepared by RTI International for EPA under contract number 68-D-00-265

Mean of Women from 38 Eastern U.S. States

Figure 4-A

Be smarter about advisories and stop scaring sport fish consumers.

Similar results were reported by Morrissette et al. (2004) after monitoring actual blood and hair mercury exposures in pregnant women living in the region of the St. Lawrence

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lakes, St. Francois and St. Louis.101 Their analyses showed that “during pregnancy market fish (fresh, canned, and frozen) were more important sources of Hg exposure than were fish from the St. Lawrence River.” They concluded, “These results should be taken into account for future advisories and intervention strategies, which should consider Hg levels in different species from all sources in order to maximize the nutritional input from fish and minimize the toxic risk (emphasis added).” In other words, be smarter about advisories and stop scaring sport fish consumers. Also, these findings by Morrissette and colleagues are encouraging because they show that the primary mercury exposure path for these Canadian pregnant women was not from locally-caught fish. It is further encouraging to find that none of these pregnant Canadian women are significantly at risk from exposure to total, organic and inorganic mercury since all measured concentrations, including those notably more concentrated levels in cord blood, ranged from non-detectable to no more than 1.6 ppb, and total maternal hair mercury level below 0.3 ppm.

Conclusion All the above findings point to a relatively less important exposure risk through sport fish than the CT series suggests. This should have direct implications for active proposals by Illinois, Connecticut, Massachusetts, Minnesota, New Hampshire, New Jersey, North Carolina and Wisconsin calling for stringent cuts up to 90%102 on mercury emissions from local power plants. There is almost zero chance, even were 100% emission cuts achieved, that these states will be able to lower the methylmercury content in any of the popular fish consumed. This is more specifically examined under Sec. 5, 10, and 21.

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SECTION 5: MERCURY, MERCURY EVERYWHERE...FOREVER

[T]he hypothesis that most Hg in Illinois and the USA soils is of anthropogenic origin is rejected. - Krug and Winstanley The relative contribution made by natural sources, versus those of anthropogenic origin, is typically ignored in environmental regulation…some data indicate that planned reductions in Hg industrial emissions, without consideration for natural sources, will result in no significant decline in levels of biotic contamination. - Richardson et al. (2003)

Chicago Tribune: Almost all the mercury that people are exposed to comes from eating fish. And almost all fish contain some amounts of the metal, much of which falls into oceans, lakes and streams from air pollution. Some of that pollution can travel around the world before falling to the ground. So emissions from a factory in China can pollute a lake in America and vice versa. Mercury also occurs naturally in rock and soil and is continually being released into the oceans through erosion and underwater volcanoes. In water, bacteria chemically alter mercury, creating a highly toxic form called methylmercury, which the tiniest fish eat or absorb. As bigger fish eat smaller fish, mercury accumulates up the food chain, with the largest predators, such as shark and swordfish, generally containing the most. (December 11, 2005) Response:

Burying the Lead

nce CT finally came to bat discussing sources of mercury cycling through the environment, they fouled out to left field.

Mixing metaphors, the weights of several scientific facts crumble the footings underlying their entire construction of industrial loading of MeHg to fish tissue. The principal fact is that annual total mercury entering the bio-sphere from natural sources dwarfs anthropogenic sources into near insignificance. Natural sources are not only immense and overwhelming, but are persistent over geological time. This stubborn fact has been resolute in the literature for decades, and doggedly ignored by mercury activists. Thus, readers are being misled about some of the most crucial science allowing for a rational policy approach to the issues.103

O

Mercury Deposition in Illinois

To verify this, CT would have had to look no further than to experts within their own state.

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Critical findings by Edward Krug and Derek Winstanley of the Illinois State Water Survey clearly show that man-made mercury from atmospheric deposition is a very small contributor to the huge amount of natural mercury already contained in the soils of Illinois specifically and the nation generally.104 After measuring mercury soil content, they estimated that it would take 9,000 years at current atmospheric deposition rates alone to account for all the mercury present in just the top 380-cm of Illinois soils. Similar analysis for a composite of U.S. soils yielded an estimate of 14,000 years of present atmospheric deposition required to attribute U.S. soil mercury content to man-made "air pollution." Krug and Winstanley made their point polar-star clear:

“When widespread Hg pollution first became a popular concern, global anthropogenic Hg was compared to global soil Hg as part of a larger literature that criticized the common presumption that the principle source of Hg in the environment is anthropogenic. Regarding world soil Hg content, these early analyses reported that anthropogenic activities could have increased world soil Hg content by 0.02 percent. Despite this early seminal literature and a persistent stream of publications in following decades, the presumption that anthropogenic Hg is the principle source of Hg in the soils that mantle landscapes is still common and exerts a powerful effect on scientific and public perception of the role of anthropogenic atmospheric Hg deposition on the environment of Illinois and the USA. [In this work,] the hypothesis that most Hg in Illinois and the USA soils is of anthropogenic origin is rejected.” [Emphasis added]

It would take 9,000 years at current atmospheric deposition rates alone to account for all the mercury present in just the top 380-cm of Illinois soils.

Accounting for Natural Sources

Part of the earlier literature to which Krug and Winstanley alluded pointed out the critical importance of getting the natural/anthropogenic equation right. In a 1994 review paper105, the researcher stated:

“The most valuable information for assessing the impact of anthropogenic [mercury] activity is an understanding of natural processes.” “All [current] global estimates ...refer to atmospheric emissions only. Geological processes supplying Hg to soil, oceans, and inland water bodies also need to be quantified to complete the global natural cycle.”

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Added Russian researchers:

“The natural mercury emission from Earth’s Crust is an important factor controlling mercury distribution in marine water and atmosphere along with anthropogenic pollution. Main sources of mercury to seas are submarine volcanoes, mud volcanoes and cold gas vents.”106

Some literature reviews estimate all-source natural contributions of mercury to the global environment in a range of 38,000 – 211,600 tons per year.107 This compares to estimated annual anthropogenic atmospheric contributions of around 2,700 tons.108 Likely the most reliable current estimates of natural mercury emissions (58,000 tons/yr) were recently reported by Mark Richardson of the Risklogic Scientific Service. 109 Mercury sources included direct emissions from volcanoes, soil evasions, soil particles, plants, marine evasion, fire freshwater evasion, meteoritic dust and sea salt to the air -- all substantially underestimated by previous “best-estimates” utilized by EPA.

Natural Hg emissions have been underestimated

58,000 tons/yr

2500 tons/yr

0

10000

20000

30000

40000

50000

60000

Richardson et al. (2001, 2003) Nriagu (1989)

Hg emissions from natural sources (tons/year)

Outdated estimate

Sources: Richardson et al. (2003) Environmental Reviews, vol. 11, 17-36; Richardson et al. (2001), “Critical Review on Natural Global and Regional Emissions of Six Trace Metals to the Atmosphere”, Risklogic Scientific Services, Inc. Report (for International Lead Zinc Research Organization et al.)

“The most reliable estimate of natural source emissions to date”

Figure 5‐A

These important results (shown in Fig. 5-A), if proven correct, have serious implications for the efficacy of legislative and regulatory proposals aimed at removing mercury from the environment through mandatory reductions in emissions from coal-fired power-plants. (See discussion in Sec. 21) The above findings taken together with similar estimates by Richardson et al. (2003)110 for natural mercury emissions just in Canada and the US (shown in Fig. 5-B), pose reasonable questions concerning control of mercury in

Natural Hg emission sources from U.S. and Canada dominate the smallerman-made sources from the U.S.

4500 tons/yr

1100 tons/yr

107 tons in 2000

0

1000

2000

3000

4000

5000

Sources: Richardson et al. (2003) Environmental Reviews, vol. 11, 17-36; Richardson et al. (2001), “Critical Review on Natural Global and Regional Emissions of Six Trace Metals to the Atmosphere”, Risklogic Scientific Services, Inc. Report (for International Lead Zinc Research Organization et al.)

Natural Hg emissions in US and Canada versus man-made source in US (tons/year)

U.S. total man‐made Hg emissions appear insignificant (0.02%) compared to total natural emissions from North America

Figure 5-B

Natural U.S.emissions

Natural Canadianemissions

U.S. man‐madeemissions

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the environment. Momentarily setting aside issues of toxicology and epidemiology, even if 100% capture of man-made Hg emissions were technologically and economically feasible, would it make any difference in the persistent, historical levels of micro-trace MeHg present in fish? (See Fig. 5-A) Richardson addresses this question:

“There is an on-going regulatory concern for metals [including Hg] in the environment, and numerous regulations have been implemented globally, or are being developed, to control or curtail industrial metal emissions. However, the relative contribution made by natural sources, versus those of anthropogenic origin, is typically ignored in environmental regulation, or dated publications are cited as evidence that natural sources are relatively insignificant. ... The primary citation concerning the contribution made by natural sources to environmental metal contamination remains Nriagu (1989).

Nriagu presented an analysis of available data suggesting that natural contributions of metals and metalloids made up generally less than 50% of

the total emissions to the atmosphere. ... Regulatory agencies are now preparing to introduce or enact legislative initiatives to reduce industrial metal emissions, with no clear understanding of the relative contributions of anthropogenic and natural sources, and the uncertainties therein. Such legislation has been conceived on the basis of these earlier uncertain estimates of natural source contributions. For example, Canada is developing pollution abatement initiatives for Hg (soil, air and water quality guidelines, phase-out of products containing Hg, emissions reduction targets, etc.) on the assumption that natural and anthropogenic sources contribute approximately equally (50:50) to the environmental Hg problem. Some data indicate that planned reductions in Hg industrial emissions, without consideration for natural sources, will result in

no significant decline in levels of biotic contamination. It is apparent, therefore, that a need exists to update the estimate of natural source contributions with the spate of recent research on the emission of elemental Hg from surface waters, soils, faults and geologic deposits.” [Emp

The relative contribution made by natural sources, versus those of anthropogenic origin, is typically ignored in environmental regulation.

Some data indicate that planned reductions in Hg industrial emissions, without consideration for natural sources, will result in no significant decline in levels of biotic contamination.

hasis added]

ver

CT’s passive acknowledgment of mercury emissions from natural sources such as "underwater volcanoes," failed to follow Richardson’s strong counsel to consider the size and scope of dominant, natural sources. Volcanic degassing may serve as a significant source of ocean and

atmospheric mercury. According to the Smithsonian Institution,111 there are well o

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5,000 surface and submarine volcanoes in the world, with about 50 to 60 eruptions eachmonth. Perhaps more important is the constant, non-event venting of mercury-ladenheated water at seafloor vents, such as the black smokers in the Easte

r Pacific Rise.

Park

ing’s ed power plants combined.

At Roaming Mountain, Wyoming, researchers measured mercury emanating from the clay hillside at up to 2,400 nanograms per square meter per hour. By comparison, background levels away from geothermal areas range from zero to 10! So, Hg emissions from active geothermal areas could range from tens to hundreds times more than from other background areas. At Yellowstone Lake, researchers have discovered submerged faults, explosion craters, domal features, hydrothermal vents, lava flows extending far out into the lake and much more. Therefore, it is hardly surprising that a report issued by the Idaho National Engineering and Environmental

Lab112 showed that several places in Yellowstoneemit higher levels of airborne mercury than power plants. Researchers estimated that Yellowstone could equal or exceed mercury emissions from Wyomeight coal-fir

Mercury from black smokers

An ocean floor hydrothermal vent -'Black Smoker'

Perhaps the most dramatic examples of natural metal transport and deposition are the hot metal‐rich aqueous solutions erupting at mid‐oceanic ridge environments to form ʹblack smokersʹ, characterized by the exhaling plumes of crystalline metal sulphide particles.

Figure 5-C

Researchers estimated that Yellowstone could equal or exceed mercury emissions from Wyoming’s eight coal-fired power plants combined.

Instead of reporting these findings, CT artfully wrote that “much” of the mercury that people become exposed to through fish ingestion comes from anthropogenic “air pollution.” The insinuated, false paradigm seems clear: natural sources of mercury are unimportant; remove the Hg from human activities, and one sufficiently removes MeHg from fish to make them “safe” again.

From Hg to MeHg Finally, CT touches on the bio-transformation of raw (Hg) mercury into methylmercury (MeHg). Again, the substance and relevance of the science is ignored. A fuller discussion of these issues follows in Sec. 21. Suffice it here to observe that it is a highly complex process; that the biochemical transformation of Hg into MeHg, and its ultimate bioaccumulation up the food chain, is not easily predictable. Neither is the process simply dependent on manipulation of raw Hg inputs, regardless of source or magnitude. To demonstrate this complexity and the uncertainty it introduces, following is a partial listing from the literature of variable and interactive conversion and transformation factors:

(1) levels of MeHg are independent of raw Hg levels (Marvin-DiPasquale et al. 2003; Paller et al. 2004; Bonzongo & Lyons 2004) (2) pH and sulfate (Bonzongo & Lyons 2004)

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(3) leaf litter inputs and microbial growth (Balogh et al. 2003) (4) roles of visible light (Seller et al. 1996), UVA (Lalonde et al. 2004), diurnal MeHg and solar radiation (Siciliano et al. 2005) (5) experimental treatments with sulfate (Harmon et al. 2004) (6) sulfate, organic matter, and bacterial activity (Mason et al. 2005) (7) water temperature and fish body weight (Trudel and Rasmussen 1997) (8) algal bloom-induced biodilution of MeHg in zooplankton Daphnia (Pickhardt et al. 2002) (9) dependence of MeHg on species of zooplankton (Masson & Tremblay 2003) (10) “MeHg accumulation paradox” (Schaefer et al. 2004) (11) seasonal cycle of MeHg before and after control flooding (St. Louis et al. 2004) (12) 48 environmental variables including land use, various catchment areas and lake characteristics, lake water chemistry and fish stocks (Soneston 2003)

As a more local illustration of mercury cycling complexity facing would-be regulators, consider that quantitative estimates of elemental mercury revolatilization in the Great Lakes of about 2.3 to 13.7 tons per year. Estimated direct deposition of all species of mercury from the atmosphere is estimated at only 4.7 tons per year.113 This suggests the perplexing management accounting in which natural revolatilization output exceeds total input.

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SECTION 6: “POISONING” SOPHIE

“When I went to my shrink for the first time I told him that...I was worried about my daughter, and about how mean I was to her. For some reason, all my craziness channeled itself in her direction.” - Ayelet Waldman, Sophie’s mother

Chicago Tribune: “The fact that we poisoned our air and our oceans to such an extent that we can't eat a damn tuna sandwich is just diabolical," said Ayelet Waldman, a noted mystery author whose daughter was diagnosed with mercury poisoning at age 5 after frequently eating tuna. Waldman, of Berkeley, Calif., said that when her daughter, Sophie, was 5, she seemed to stop learning. She had trouble sounding out words she had already learned. She forgot how to tie her shoes. During a heavy metals screening in 2000, Sophie showed high mercury levels, her mother said. After Sophie's mother consulted with a San Francisco internist, Dr. Jane Hightower, one of Sophie's favorite meals was identified as the culprit: She was eating a tuna sandwich a week made with canned albacore. Further tests by Hightower confirmed high mercury levels in Sophie, the doctor said. When Sophie quit eating tuna, she started learning again, her mother said. "She seemed to us like she was a different kid." Waldman, Sophie's mother, said that if there had been proper warnings years ago, she never would have fed so much canned tuna to her daughter, now 11. Today, Waldman said, she keeps track of how much fish her daughter eats and consults an environmental group's Web site to find mercury levels in various fish. (CT - December 11, 2005) Response:

t is highly disturbing that CT would worry mothers and seek to influence public policy by uncritically recycling the anecdotal "poisoning" of Sophie Chabon, daughter of novelists Michael Chabon and Ayelet Waldman. The story originally

appeared several years earlier in the San Francisco Chronicle, and has since become a staple for mercury-alarm journalism.114

I

The Sophie Chabon Case Poisoned tuna? A more serious examination of the Sophie Chabon case poses the question whether she could have actually suffered -- and quickly recovered -- from acute MeHg poisoning after ingesting small amounts of tuna over a short span. Scientifically, nothing about the case makes any sense.

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The San Francisco Chronicle earlier reported Sophie’s miraculous recovery, as recounted by Waldman:

[Five-year old Sophie’s’] lively progress in reading and other accomplishments dipped. "She was happily tying her own shoes, and suddenly she just lost that skill. She seemed like she was beginning to read. Then she plateaued. She never progressed for a year,'' Waldman recalled. Sophie's hair was odd. "It was brittle, and wouldn't grow beyond a certain length,'' Waldman said Waldman conducted her own research. She found Hightower, who took Sophie off fish. "Sophie's mercury level dropped to normal levels in two months. She could tie her shoes again and was suddenly able to read. It might have been a coincidence, but it didn't seem it at the time. She had plateaued academically, and then she sort of spurted ahead. It was remarkable to see,'' Waldman said.” [Emphasis added]

First, according to Professor Tom Clarkson, the nation’s foremost expert on health impacts of mercury toxicity, Sophie’s reputed symptoms and reversal are not characteristic of any known kind of MeHg poisoning. Clinically diagnosed effects of developmental brain damage due to mercury poisoning are permanent. Also, even though Hightower and Sophie’s parents say that changes in hair clued them to mercury, in actual incidents of Hg poisoning changes in hair (brittleness, falling out) have never been reported as symptomatic. Secondly, CT left unreported and unexamined the measured mercury levels for the other Chabon children and Ayelet Waldman herself.

Reviewing the paper by Hightower and Moore (2003)115 (discussed in Sec. 9), one can easily identify blood mercury levels recorded for Sophie Chabon (13 ppb), her younger brother Zeke Chabon (less than 5 ppb) and Ayelet Waldman (7.4 ppb). Also, Hightower listed Sophie as having consumed about eight 6-oz. servings of canned tuna per month, or about two cans of tuna per week for one year duration -- not the single albacore tuna sandwich a week reported by CT .

Zeke, 3 years old at that time, had not consumed any fish meals, yet his mercury level was recorded at <5 ppb. This level is significantly higher than the mean (0.3 ppb) for children aged 1-5 surveyed by the CDC.

Levels for both Sophie and Ayelet Waldman exceeded EPA's conservative RfD (5.8 ppb in blood, or 1.0 ppm in hair), but were no where near lowest levels (216 ppb) recorded for Minamata-like symptoms. Also remember, EPA’s RfD is based on 70 years of daily consumption. Sophie was only five years old, so there was no increased or decreased risk.

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The essential and paramount point is, nothing in the vast mercury literature reports clinical manifestations for mercury poisoning at levels recorded for Sophie, after any duration of consumption.

Even Amazon rainforest natives with hair levels at mean average of 21 ppm, and as high as 302 ppm, showed no signs of toxicity.116 Surveys report that 87% of Japanese exceed EPA’s RfD; so merely exceeding this level does not mean MeHg poisoning. Also, compare Sophie’s tuna consumption rate of 8 servings per month with the 12-14 fish meals per week in the Seychelles Islands. Then factor that Hong Kong Chinese children have one of the highest seafood consumption rates in the world, with no reported harm. If the case of Sophie Chabon is an actual one, where is the epidemic of developmental disabilities that should be present in persistent fish consuming societies like Japan, Seychelles, Hong Kong, Amazonia or even the Faroes? Answer: nowhere, at no time. (see Sec. 20) Directly put, the Sophie case seems little more than a single anecdotal report from a couple of parents about one child – so what?

The Waldman confessional

However, perhaps the more serious omission by CT – particularly for mothers and pregnant women – is Waldman’s openly self-reported tragic relationship with Sophie. Ayelet Waldman’s volitional public117 introspections recorded on her internet blog,118 Salon.com and elsewhere may reveal that little Sophie’s perceived arrested development at age five could reasonably be attributed to something other than tuna sandwiches. A few excerpts suffice [some emphasis added]:

So when Sophie was still painstakingly sounding out words at age 7, I ended up calling my mother, completely distraught. "She's only reading at a first-grade level!" I wailed. There was silence on the other end of the line for a few moments. Finally my mother said, "Honey, she's in first grade." When our children fail to meet our unrealistically high expectations -- when they behave, instead, like normal, average kids -- we feel disappointed.” (October 2003 issue of Child Magazine) I'm afraid that all my unmedicated years taking out my bipolar disorder on Sophie will cause her to write me off and make disparaging comments about me on her blog. (January 24, 2005) When I went to my shrink for the first time I told him that...I was worried about my daughter, and about how mean I was to her. For some reason, all my craziness channeled itself in her direction. I couldn't bear the idea that I would damage her. I have a little marker that tells me when my meds aren't working. When I lose it with Sophie, when I scream at her, when I grab her and drag her up the stairs, when I toss her into her room, when I slam her door, I know that things are bad and I need to get...into the

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doctor's office for an adjustment. I always tell her that it's not her fault, that it's mommy's fault. That I'm sick, that my pills are screwing up, but how often does she have to deal with this crap? Those shoulders are awfully skinny for such a heavy burden. (January 26, 2005)

Waldman herself implies that one could not be faulted for wondering if any child could function normally in the difficult social setting and interactions described, let alone excel or meet high parental expectations – tuna sandwiches or not.

Conclusion The Tribune series represents what the late Julian Simon called ‘false bad news.” Its price in economic loss, loss of public confidence, misguided policies and damage to public health – particularly of women and their children – has yet to be fully calculated. But those costs are potentially fearfully high, and growing. By not exploring and reporting the context and veracity of Ayelet Waldman’s anecdotal “evidence” for her daughter’s reputed “poisoning” by tuna ingestion, the Chicago Tribune's readers and public officials have been seriously mislead by the celebrated, unlikely mercury "poisoning" of Sophie Chabon.

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SECTION 7: THE NRC AND THE MERCURY RFD

Selecting an appropriate outcome to focus upon presents a substantial challenge to investigators and those interpreting their studies to use in making public policy. - Dr. Gary Meyers, Seychelles Children Study investigator The role of science, from Galileo to Newton and through the centuries, has been to debunk the consensus and move us forward. But now science has been stripped of its basis in experiment, knowledge, reason and the scientific method and made subject to the consensus created by politics and bureaucrats. - Terence Corcoran

Chicago Tribune: Solving the mercury problem ultimately will require reducing levels of the pollutant in the environment, according to the National Academy of Sciences, the nation's leading scientific advisory body. For now, though, the academy says consumers can best protect themselves by eating low-mercury fish. (CT - December 11, 2005) Response:

Unscientific policy proposals

ssertions of a linear improvement in public health from reductions in anthropogenic mercury sources is not supported by the science. Various species of mercury are continually being exchanged and re-transformed among sources

from, and within the reservoirs of air, water, soil and terrestrial vegetation without any direct connection to the "pollutant in the environment," by which is meant coal-fired power plant emissions (see Sec. 5 and 21).

A Proposals mandating costly 90% mercury emission reductions from coal-fired power plants need to scientifically demonstrate that such actions will yield any measurable improvements to public health (see Sec. 21). This is particularly required in light of new research coming out of China. China has long been regarded as one of the largest man-made mercury emission sources (from coal combustion in particular). Pacyna and Pacyna (2002) estimated that China’s emissions from coal combustion contributed more than 25% to the total global man-made mercury emissions in 2002. Tang, S., et al. (2007) report that just in Guiyang province in southwest China the annual mercury emissions from coal consumption in power plants will increase to “about 32 tons in 2015, which is comparable to the [current] annual coal combustion mercury emissions in the whole USA.”119

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The NRC panel Three pre-natal exposure studies (Faroe Islands, New Zealand and Seychelles Islands) were included in a review conducted by a U.S. National Research Council panel at the request of EPA (see Sec. 2). The panel’s task was to investigate the toxicological effects of MeHg in relation to the review of MeHg exposure reference dose recommendations.120 The panel rejected the NZ endpoints and the Connors Continuous Performance Test before settling on the Boston Naming Test. Deeming the Boston Naming Test as sufficiently reliable, the panel preferred an estimated benchmark dose lower limit (BMDL) of 58 ppb. The panel also recommended an uncertainty factor of no less than 10. The EPA incorporated these recommendations in its MeHg oral reference dose assessment (U.S. EPA, 2001) against the strong objections of others, including members of the U.S. Senate, other relevant agencies and Dr. Michael Dourson and Dr. Kenneth Poirier, former co-chairs of EPA’s own RfD/Reference Concentration Work Group.121 "Solving the mercury problem" is a policy judgment and was certainly not the charge of the NRC committee panel on the Toxicological Effects of Methylmercury. In fact, "the panel was not [even] charged to calculate an RfD for MeHg." One of the reasons that the Boston Naming Test from the highly confounded and non-transparent Faroe Islands study [focused on pilot whale consumption] was selected as a basis for a mercury RfD was because it claimed “subtle” negative findings. The NRC’s reliance on the Boston Naming Test (BNT) seems little justified122:

The BNT was developed to detect aphasis and brain damage in adults and is not a standard part of child neuropayschological testing.

No biological reason has been proposed as to why the BNT should be particularly sensitive to prenatal MeHg exposure.

Halperin et al. (1989) had concluded that, in children, the BNT score relates more to acquired word knowledge than to word retrieval or fluency, and that verbal memory appears to be independent of these linguistic functions.

In terms of educational findings, the BNT appears to be significantly related to reading comprehension rather than verbal memory or word retrieval.

Three different seemingly correct interpretations by professional psychologists of the scoring methods publish by Kaplan et al. (1983) for the BNT resulted in large, clinically significant differences in the total score (Lopez et al., 2003).123

Assuming the BNT mean score for U.S. 7-year olds is 38.83 (Halperin et al., 1989), the expected mean score for the approximately 300,000 children exposed per year at the RfD is 38.73 – a decrement of 0.1 point that is clearly not detectable, and not meaningful given the standard deviation of 4 to 6 on BNT scores.124

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Added to all this, the Faroe investigators themselves acknowledged concerns that PCB concentrations appeared an important predictor for the BNT results; cord PCB concentration was associated with deficits on the BNT. Even so, the NRC discounted PCB confounding by relying on a statistical analysis performed by the Faroe researchers. Yet, the NRC panel failed to address the most obvious question as to why the Faroe study reportedly observed no significant effects from PCB contamination when PCB exposures were at levels twice as high as the lowest observed effect level for those compounds. Thus the NRC and EPA avoided having to demonstrate some identifiable health risk to some segment of the population at some defined level of predicted exposure – the precise legislated requirement for regulatory consideration. 125 This plowed a wide field for the future unjustifiable alarmism and exaggerated claims.

Conclusion If the NRC and EPA had properly included and weighted the Seychelles research findings, a higher RfD would likely have been derived, resulting in no pretext for regulatory action. By discounting the more appropriate Seychelles findings while resorting to the troubled Faroe paper, the NRC panel seems to have fabricated for EPA a unique sieve that retained dross findings of the Faroe study and allowed the gold of the Seychelles results to slip free. (see discussion in Sec. 1) The consequences are that women and their babies are the poorer for it.

The NRC panel seems to have fabricated a unique sieve that retained the dross and allowed the gold to slip free.

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SECTION 8: CARDIAC ARREST

If, as Guallar et al. suggest, mercury increases the risk of myocardial infarction by more than 100 percent when the hair mercury level reaches 2 ppm, how can one explain the absence of effects at doses greater than 100 ppm? - Plante and Babo (2003) Eating lots of ocean fish isn’t much of a hazard compared to missing out on the benefits from not eating fish. A slew of scientific reports have shown that eating fish helps protect against cardiovascular disease and enhances brain development before and after birth. Overstating the almost negligible risk of mercury could adversely affect millions of people who face the risk of heart disease. -Dr. Tom Clarkson, University of Rochester Seychelles researcher

Chicago Tribune: Other studies suggest the heart benefits of eating fish might be offset by mercury. Though the American Heart Association recommends eating fish twice a week to "benefit heart health," two major European studies found that mercury exposure can increase the risk of fatal heart attacks in men. (CT - December 11, 2005) Response:

Study Problems

he results of the European studies referred to have been found, upon subsequent review, to be weak and to perhaps have not accounted sufficiently for cross-cultural differences and other confounders. An easily accessible reference is

CSPP’s paper, “Fish, Mercury and Cardiac Health”126, in which specifically examined is the question, “Does the trace amount of mercury in fish overwhelm the nutritional benefits for heart health?”127 A brief summary follows.

T First, a description of the two European studies claiming negative cardiac health associated with fish consumption. (1) The Finnish Study published in Salonen et al. (1995, 2000)128 + update in Virtanen et al. (2002)129 + latest update in Virtanen et al. (2005)130. This study of 2005 men from Kuopio, eastern Finland found that men in the highest quarter (> 2.5 ppm) of Hg exposure had a 1.6-fold risk of CVD death and 1.7-fold risk of CHD death when compared to men in the lowest three quarters after adjusting for numerous risk factors including age, LDL (bad) cholesterol + triglyceride, intake of saturated animal fatty acids, etc. (2) The European/Israeli Study by Guallar et al. (2002)131.

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This is a case-control study of 684 men with 724 controls that reported increasing toe nail mercury levels from 0.11 to 0.66 ppm (about 0.34 to 2 ppm in equivalent hair mercury levels) is associated with a doubling of the risk of myocardial infarction after adjusting for numerous risk factors like age, family history of heart attack, smoking status, alcohol intake, diabetes, history of hypertension, selenium intake and etc. Numerous risk factors other than MeHg in fish more likely explain most of the findings in both Salonen et al. (1995, 2000) and Guallar et al. (2002). Specific criticisms on Salonen et al. (1995, 2000) include the following:

(1) Salonen et al. (1995)’s own admission: “Theoretically, our findings could be specific only for men in Eastern Finland, who traditionally have a high intake of meat, fish, and saturated animal fat and a low intake of selenium and vitamin C and, most likely, other vegetable-derived antioxidants.”

(2) The Kuopio population has one of the highest recorded rates of CHD and high consumption of animal fat with high measured levels of LDL (bad) cholesterol. (See Fig. 8-A)

Statistics of mortality from Coronary Heart Disease: Men of Eastern Finland are especially vulnerable

Menotti et al., 1999, European J ournal of Epidemiology, vol. 15, 507-515

Table 1: Age-standardized 25-year death rates per 1000 from CHD in 16 cohorts of the Seven Countries Study. Standard error of rate in parenthesis.

Cohorts N CHD (death rates/1000)

US Railroad, USA 2571 160 (7)

(3) Stern (2005)132 pointed out that even in the first report of Kuopio study by Salonen et al. (1995) as long as 9 years already elapsed between the collection of hair + urine samples and the recording of a CVD + CHD + death event. An updated report of KIHD Hg-related results in Virtanen et al. (2002) extends the elapse time to as long as 16 years and hence

East Finland, Finland 817 268 (15)

West Finland, Finland 860 180 (13)

Zutphen, The Netherlands 878 169 (13)

Crevalcore, Italy 993 93 (9)

Montegiorgio, Italy 719 60 (9)

Rome Railroad, Italy 768 87 (10)

Dalmatia, Croatia 671 54 (9)

Cohorts N CHD (death rates/1000)

Crete, Greece 686 25 (6)

Corfu, Greece 529 48 (9)

Tanushimaru, Japan 508 30 (8)

Ushibuka, Japan 502 36 (8)

Velika Krsna, Serbia 511 43 (9)

Zrenjanin, Serbia 516 116 (14)

Belgrade, Serbia 536 106 (13)

Slavonia, Croatia 696 89 (10)

“[T]he intake of diary products, potatoes, butter, and sugar products was very high in . A similar but lower intake pattern was observed in The Netherlands. Fruit, meat and pastry consumption was high in the USA. Cereals and wine consumption was high in Italy, while bread consumption was high in Yugoslavia with the exception of the Belgrade cohort. In Greece, the intake of olive oil and fruit was very high, while the J apanese cohorts were characterized by a high consumption of fish, rice, and soy products.”

Figure 8-A

Finland

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contributes to a serious potential misclassification of causes and effects. The latest updates in Virtanen et al. (2005) covered deaths through 2002 and thus extends the elapse time another 2 years. (4) Clarkson (2002)133 noted that highest recorded hair level is 15.7 ppm, more than 6 standard deviations from the mean and only a small % of the population has high hair Hg. Yet high-value points may play a major role in this type of study, “it would have been of interest to see if these correlations persisted when the very high mercury levels were excluded.” (5) No clear accounting for stress—which is believed to be a major risk factor.134

It is relevant that in an earlier experimental study of 62 healthy students from the same region (Kuopio, Finland), Agren et al. (1988) 135 had instead found:

“A moderate intake of fish-containing meals has some beneficial effects on plasma lipid and prostanoid metabolism, when coronary heart disease risk factors are considered.”

Also relevant, the selected Kuopio students ate fish an average of 3.7 times per week, for 15 weeks. These meals consisted of 87% locally caught freshwater fish (vendace, pike, perch and rainbow trout) and 13% Baltic herring from brackish water. The largest decrease in CHD risk was found for those 21 students which consumed freshwater fish and restricted their lipid intake, compared to two other groups.136 In other words, health benefits were reported for the University of Kuopio students who both restricted intake of saturated fatty acids, and consumed freshwater fish. Criticisms of Guallar et al. (2002) include the following:

(1) It is contradicted by results from Yoshizawa et al. (2002), a 5-year follow-up study of 33,737 U.S. male health professionals. The Yoshizawa study examines a wider range of toenail mercury levels, from 0 to 14.6 ppm (or about 45 ppm in equivalent hair), and that these levels were not significantly associated with risk for CHD. (2) Why is LDL cholesterol not measured and identified as a risk factor (while HDL and total cholesterol were measured)? (3) Guallar has been seriously challenged by Plante and Babo (2003)137: “Patients with Minamata disease and hair mercury levels above 100 ppm did not have a higher rate of death from heart disease than controls, nor did they have a higher degree of arteriosclerosis. In the Minamata region of Japan, a population of approximately 50,000 with an average hair mercury level of 50 ppm did not have a higher rate of death from heart disease than a reference population of 800,000 with an average level of 9

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ppm. ... Cree Indians with an average hair mercury concentration of 10 ppm have a lower risk of death from circulatory disease than the rest of the population in Quebec, in which the average hair mercury level is 0.5 ppm. If, as Guallar et al. suggest, mercury increases the risk of myocardial infarction by more than 100 percent when the hair mercury level reaches 2 ppm, how can one explain the absence of effects at doses greater than 100 ppm?” [Emphasis added]

Cardioprotective benefits In sharp contrast to the suspect European studies relied upon by CT, there exists indubitable evidence that consumption of fish and omega-3 fatty acids provides numerous cardioprotective benefits. Notably, clinical evidence demonstrates that fish consumption lowers risk for “sudden death”:

“The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease. As compared with men with levels of long-chain n-3 fatty acids in the lowest quartile, those with levels in the highest quartile had an 81 percent lower risk of sudden death.” (Albert et al., 2002)138 “[W]e have summarized the growing clinical evidence that these n-3 fatty acids are antiarrhythmic and can prevent sudden cardiac death in humans. These n-3 fatty acids have been part of the human diet for some 2 to 4 million years ... They are safe and have been listed on the GRAS (‘generally regarded as safe”) list according to the Food and Drug Administration in amounts up to 3.5 g of fish oil per day.” (Leaf et al. 2003)139 “Alexander Leaf and colleagues ... suggest a hypothesized cellular mechanism through which n-3 polyunsaturated fatty acid (PUFAs) affection channels to reduce the risk of arrhythmia. The messages ... are clear. For clinicians, it is time to implement the current American Heart Association dietary guidelines that recommend the dietary intake of 1 to 2 fish meals, particularly fatty fish, each week. For policymakers, there is a need to consider new indication for treatment with low-dose n-3 PUFAs supplements ...” (Siscovick et al., 2003)140 [Emphasis added]

Eating lots of ocean fish isn’t much of a hazard compared to missing out on the benefits from not eating fish.

Speaking on cardiac risk concerns, Professor Tom Clarkson, Distinguished Professor of Environmental Medicine at the University of Rochester commented:141

“Eating lots of ocean fish isn’t much of a hazard compared to missing out on the benefits from not eating fish. A slew of scientific reports have

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shown that eating fish helps protect against cardiovascular disease and enhances brain development before and after birth. Fish is a rich source of low-fat protein and is full of fatty acids known to lower cholesterol. Overstating the almost negligible risk of mercury could adversely affect millions of people who face the risk of heart disease.”

Dr. Eric Rimm, Professor of Epidemiology and Nutrition at Harvard School of Public Health agreed:

“The message of fish being good has been lost and people are learning more about the hypothetical scare of a contaminant than they are of the well-documented benefits of coronary disease reduction. The danger of the tuna fish is not well documented compared to the potential dangers for a 50-year-old male or female who are at a much higher risk of coronary health.”142

Also, there are the findings in “Fish Intake and Risk of Incident Atrial Fibrillation,” published in the American Heart Association’s journal, Circulation. In a 12-year follow-up for a cohort of 4,815 men and women over age 65 (in 4 U.S. communities), Mozaffarian et al. (2004)143 reported that adults consuming tuna or other broiled or baked fish144 1 to 4 times per week had 28% lower risk of developing atrial fibrillation when compared to those who ate fish less than once per month. Those eating fish five times or more per week showed a 31% lower risk. Mozaffarian et al. (2004) concluded that “fish intake may influence risk of this common cardiac arrthymia” that affects more than 2 million individuals in the United States.

The use of omega‐3 fatty acids significantly reduced the incidence of postoperative occurrence of atrial

fibrillation (AF) and was associated with a shorter hospital stay after coronary artery bypass graft surgery

Calo et al. (2005) Journal of the American College of Cardiology, vol. 45, 1723‐1728

Less AF in fish‐oil‐treated group

Figure 8-B

Finally, in a recent study by Calo et al. (2005)145, researchers report that the use of the omega-3 PUFAs was significant for reducing the incidence of postoperative atrial fibrillation (AF) in patients undergoing coronary artery bypass graft surgery. Risk reductions were 18% absolute and about 54% relative (See Fig. 8-B). The use of omega-3 fatty acids was also associated with a shorter hospital stay. Calo et al. (2005) explained:

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“The main hypothesis of our study was that antiarrhythimic properties of PUFAs could also extend to the atrial myocardium, thereby protecting against the occurrence of AF. [O]ur findings represent the first direct evidence that PUFA supplementation may, indeed, be effective in preventing AF. Furthermore, our findings are in keeping with a recent study in which the consumption of tuna, and other broiled or baked fish, was associated with a 30% lower incidence of AF in a 12-year follow-up [i.e., the study of Mozaffarian et al. (2004) discussed above].”

Conclusion

Uncritical repetition of worrisome claims, such as examined above, exposes a demographically aging, at-risk society to unnecessary harm, and maybe preventable “sudden death.”

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SECTION 9: UNDERSTANDING THE HIGHTOWER PAPER

Hightower and Moore investigated the relationship between methyl mercury exposure, fish consumption, and the U.S. EPA's RfD -- not the relationship between methyl mercury and health effects. - Schoen (2004)

Chicago Tribune: Hightower is one of the few American physicians who have diagnosed and treated people with elevated mercury levels. After discovering that some of her patients had complaints suggesting mercury poisoning, such as headaches, fatigue and loss of concentration, she tested 123 children and adults who had symptoms or who reported eating fish. In a peer-reviewed study published in 2003, Hightower reported that 89 percent of the patients showed high mercury levels in their blood. (CT - December 11, 2005) Response:

Personal opinions are not science

T implies that Dr. Jane Hightower146 is successfully fighting an epidemic of fish mercury poisoning in the higher than average fish-consuming population of San Francisco; that nearly nine of every ten patients suffer some level of poisoning;

that the successful treatment consists simply of reducing or removing fish from their diets. CT further attempts to add scientific authority to the Hightower paper with the qualifier “peer reviewed.” Fact-checking again exposes these claims as problematic.

C First, it is highly doubtful that Dr. Jane Hightower has ever actually seen anyone with true mercury poisoning. She has apparently been treating a laboratory value and assuming it is mercury poisoning. Her comment (2003) that hair loss first alerted her to heavy metal toxicity is revealing; it is not a symptom that has been reported in mercury poisoning according to expert knowledge. Secondly, San Franciscans eat seafood. Not finding ultra-trace mercury in their bodies would be surprising. Nearly everyone consulting a physician presents complaints, many of them variations on the symptoms listed by Hightower and reported by CT. The key issue is not a correlation between mercury presence and complaints. After all, flu outbreaks and winter holiday seasons are highly correlated, but one cannot militate against the flu by banning celebration of Thanksgiving, Christmas, Hanukkah and lunar calendar’s New Year. The real question is whether Hightower demonstrated that mercury has caused poisoning episodes, as CT clearly implies. The answer is no because Hightower never even investigated this relationship!

It is highly doubtful that Dr. Jane Hightower has ever actually seen anyone with true mercury poisoning.

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Dr. Hightower did not try to establish causality. Experts point out that she merely developed a hypothesis based on a study of her patients (high-end fish consumers) and expressed her personal opinion about causality. An actual study of causality would have required a longitudinal scientific investigation with blinding to exposure. For example, in a post-publication commentary on Hightower and Moore (2003) 147, Schoen (2004)148 states:

“Hightower and Moore investigated the relationship between methyl mercury exposure, fish consumption, and the U.S. EPA's RfD -- not the relationship between methyl mercury and health effects. Not all readers of EHP [Environmental Health Perspectives, the journal that printed Hightower and Moore, 2003] will appreciate the difference between documenting exposure levels and providing evidence for health effects, and not every reader will have followed the ongoing international controversy over the health effects of methyl mercury for fish consumers.” [Emphasis added]

Another way of stating Schoen is that Hightower performed a descriptive (cross sectional) study of fish consumption and blood mercury levels, which, by definition, cannot be used to infer causality.149 Even so, people do it all the time; it just isn’t good science. Cross sectional studies can be used to develop a hypothesis, but then a proper study is required to prove it. Schoen’s elucidation is actually verified by Hightower herself:

“Cause and effect regarding symptoms was not fully addressed in this study for the following reasons. A chart of symptomatology on all patients presenting to the office in the 1-year period of the study was not done. Therefore, a comparative analysis for the purpose of control is not available. Many patients who present to their doctor have symptoms that may be caused by other conditions. It is difficult to determine whether mercury is causing or exacerbating these symptoms, especially in the case of autoimmune phenomena, chronic fatigue syndrome, fibromyalagia, depression, sinusitis, coronary artery disease, and menopause, to name but a few [to say nothing of controlling for diet or health-damaging behaviors such as smoking or drug and alcohol abuse] where there is either a possible link to or an overlap of symptoms with mercury exposure. Second, the subjective nature of symptoms makes standardization difficult. Last, because only mercury was tested in these individuals, other contaminants [or non-contaminants such as diabetes, depression, thyroid malfunction, etc.] responsible for symptoms cannot be ruled out. Often the clinician recommends elimination of diets [or more likely, further tests] to establish whether the patient is affected by an exposure. It is important to demonstrate the normalization of blood mercury levels for clinicians who

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may want to try this as a diagnostic approach for certain individuals.” [Emphasis and comments added]

The critical point is that Hg may have no relationship to Hightower’s findings whether there is or is not an association. Hightower is saying – albeit in a somewhat obfuscatory way – that she did not study cause and effect. That is, she cannot be sure the relationship between mercury and the symptoms is real. In addition, she doesn't know if mercury even contributes to the symptoms. She then goes on to imply that trying an elimination diet will help the physician sort out the issue. In sum, she is simply presenting her opinion with no evidence to back up a causal relationship.

Hightower is saying – albeit in a somewhat obfuscatory way – that she did not study cause and effect. That is, she cannot be sure the relationship between mercury and the symptoms is real.

An elimination diet is not proof. To repeat, proving a relationship would be quite complicated and require blinding of exposure and the return of symptoms when exposed again. Additionally, by leaving out “a chart of symptomatology on all patients” Hightower and Moore were able to claim improvement with treatment without the burden of showing what was actually improved. Dropping someone’s blood mercury level – or any other measurable parameter – is not a cure; it is simply changing a measurement result. Dr. Hightower also fails to mention that average exposures in other countries (Japanese at 2 ppm, Faroese at 4 ppm, Seychellois at 6 ppm) occur without the reported symptoms seen in her patients (see Sec.6).

“Treating” Sophie Remember, Hightower was Sophie Chabon’s treating physician. There is no scientific validity for persisting in the popular claim that Sophie was “poisoned” by eating tuna. Not even Hightower herself makes such claims.

Contradictions It is also highly relevant that Hightower and Moore (2003)150 revealed some contradictory findings. They reported a reasonable scenario correlating higher consumption of swordfish with elevated blood mercury levels. There is nothing astonishing or alarming about this – not even for 550-year old mummified remains of native, marine-eating Alaskans with mercury levels twice those of living Alaskans.151 However, they also reported the puzzling and highly inconsistent scenario that the more red snapper and sole their patients ate, the lower their blood mercury levels! In the face of such contradiction, Hightower and Moore (2003) loosely offered their caution that "cause and effect regarding symptoms is not addressed in this article."

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Also, CT’s noting that 89 percent of Hightower’s patients recorded “high” mercury levels is, by implication, another unfortunate misuse of EPA’s RfD for methylmercury. An RfD is defined as a “safe” dose to consume daily over a lifetime . ( see Sec. 1)

Reinterpreting the RfD Of serious concern is reinterpreting the meaning of the RfD; to emotively insinuate that anything above the RfD presents risk of “permanent brain damage” in fetuses or young children. Rarely clarified is that EPA built in a safety factor of 10 (1/10 of what EPA considered risky – 58 ppb in blood, a number itself open to question). It is misleading to assert that anything exceeding the RfD is risky. Even the Faroes152 studies from which the RfD is derived don’t say the children examined had a disability [the finger tapping difference between controls and exposure was one finger tap153]. Further, results from the extensive Seychelles studies have consistently found no adverse effects from prenatal exposure to MeHg in fish among a population consuming on average about 10 times the daily intake of Americans. Another unreported numerical confusion in Hightower and Moore (2003) is the apparent unjustified lowering by them of EPA's RfD equivalent for mercury in hair to 5.0 ppb from 5.8 ppb. This problem extended to the next one: while the abstract of the Hightower and Moore (2003) paper claimed that 89% of their 89-subject sample exceeded the RfD, the discussion on the subsequent page suggests that 82 subjects and hence 82/89 = 92% of their sample had blood mercury above 5 ppb. The often quoted value of 89% apparently was derived from a larger sample of 103 patients with levels above 5.0 ppb, itself from an initial sample of 116 patients. One can understand how this confusion spilled over to a congressional "Dear Colleague" letter by Representative Mark Kirk of Illinois (see Sec. 17).

Conclusion The terminal problem with the Hightower report is that there is nothing to link exposure with symptoms. She did a cross sectional descriptive study that is useful for developing

hypotheses. However, such studies tell us nothing about causation. If she believes there is a causal relation she should find and report it.

In sum, misrepresentations of the work of Jane Hightower provide confusion, not scientific insight regarding the potential toxicity or epidemiology of mercury. The enthusiastic miscasting of her work often introduces confusion and lack of clarity. This is hardly a sound or confident basis for urging public policy responses.

The fatal problem with the Hightower report is that there is nothing to link exposure with symptoms.

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SECTION 10: THROUGH THE LOOKING GLASS

Alice was startled to see the Cheshire Cat sitting in a tree just ahead of her. The Cat grinned when it saw Alice, but did nothing more. “Cheshire Cat,” Alice began timidly, “would you tell me, please, which way I ought to go from here?” “That depends a good deal on where you want to go,” the Cat replied. “I don’t much care where...” began Alice. “Then it doesn’t matter which way you go,” said the Cat. - Louis Carroll

Chicago Tribune: That may sound like a tiny amount, but mercury is so toxic that, by one estimate, a teaspoon of the metal is enough to contaminate a small lake. (CT - December 11, 2005) Response:

Political Wonderland

n Political Wonderland perhaps this claim has substance, but not within the realm of physical science. Mercury is not an Ebola virus.

The statement is a variation on a theme pervasive in mercury news articles, activists’ literature and websites.

I The extraordinary claim is most often composed as, “The mercury in one thermometer – about a gram – is enough to pollute [contaminate] [poison] an entire 20-acre [averaged sized] [small] lake for a year and render all the fish inedible, according to the U.S. Environmental protection agency.” This menacing statement invokes exactness (one gram, 20-acre lake, all fish, and one year) and the authority of the EPA and state government agencies (it still shows up repeatedly in official documents of EPA and state agencies). Major policy decisions are based on its truthfulness. Surely, it must derive from extensive, peer-reviewed studies? No. There has never been any study making these claims. Hundreds of documents show everybody quoting each other, and no one citing an original source.

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Bad science It is bad science. Contamination is a function of volume, not surface area. The surface area of a 20-acre lake is 871,600 square feet. At an average depth of 30 feet, the lake volume is 26,148,000 cubic feet, or about 200 million gallons of water. Can half a gram of elemental mercury “poison” 200 million gallons of water? (see Fig. 10-A) Such a claim misrepresents the toxicity of mercury by simplifying the complex processes of bio-conversion and bioavailability in aquatic systems and bio-accumulation in fish (Sec. 21). As pointed out in Sec. 5, these processes are highly complex, not fully understood and not easily predictable. Neither process is so simply dependent on or responsive to manipulation of raw Hg inputs, regardless of quantity or source. Again, more precisely, given the full complexity of diverse ecosystems, their multiple and overwhelming sources of natural mercury and the variables controlling the biomethylation and bioaccumulation of methylmercury, how likely can a gram or teaspoonful of metal mercury (Hg) from a thermometer impact ["contaminate"] the content of methylmercury (MeHg) in the water, sediment, organic matter, various species and sizes of zooplankton and fish in a entire lake?

Source: Swain et al. (1992) Science, vol. 257, 784-787 (plus a public corrective clarification issued on October 2002 available from edward.swain@pca.state.mn.us) + UGSG Factsheet 216-95 by Krabbenhoft & Rickert (1995) + Robert Rio (2003) New England’s Environment Magazine, vol. 9, issue 4, July/August issue

This droplet of mercury (Hg) spread over one year can not “contaminate” about 200 million gallons of water in a 20‐acre lake with depth of about 30 feet.

Figure 10-A

First, the claim is rooted in an original, unrelated estimate done by Dr. Edward Swain of the Minnesota Pollution Control Agency in 1992. Dr. Swain issued the following corrective clarifications in October 2002 on why thermometer mercury would not be able to "poison" any lake:

“The atmosphere brings about one gram of mercury each year to a 20 acre lake, EQUIVALENT to one fever thermometer per year. But throwing a broken thermometer into a lake wouldn't have the same effect because: 1) fish contamination is the result of many years of mercury pollution [that is to say, Hg deposition from air and land, predominately of natural origin], not just one year, and 2) liquid mercury wouldn't disperse in the environment the same way as mercury in rain (liquid mercury isn't water soluble, but mercury washed out by rain is water soluble - mercury in the air is slowly converted to Hg (II), a water soluble-form).” (Comment added)

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Secondly, Dr. Morel of Princeton University has addressed this issue of the complex roles and transformation paths for various mercury chemical species in the full ecosystem and food web:154

“[T]he average proportion of MeHg [methylmercury] over total Hg increases from about 10% in water column to 15% in phytoplankton, 30% in zooplankton, and 95% in fish. The accumulation of MeHg in higher organisms results mainly from the ingestion of MeHg-containing food rather than direct uptake of MeHg from the water. The structure of the food web determines the efficiency of transfer from algae to top predators. To yield high concentration in fish, mercury must not only be taken up efficiently by the microorganisms that are at the bottom of the food chain, it must also be retained by these organisms and passed on to their predators. Many trace metals are efficiently accumulated in planktonic bacteria and microalgae, but most are not biomagnified: Their concentrations in the biomass do not increase (they often decrease) at high levels in the food chain. A key to understanding mercury bioaccumulation is provided by the contrast between Hg0 [elemental mercury], Hg (II) [ionic mercury], and Me2Hg [di-methylmercury], which are not bioaccumulated, and MeHg [methylmercury], which is. Hg0 and Me2Hg are not bioaccumulated, simply because they are not reactive and thus are not retained in phyto- or bacterio-pico-plankton: They diffuse out as readily as they diffuse in [cell membranes].”

In a letter to the editor of the Portland Press Herald155, Dr. Kevin Wallace cast his own aspersions on the claim. Wallace, a medical toxicologist, is director of the Occupational & Environmental Toxicology Clinic at Good Samaritan Regional Medical Center in Phoenix, Arizona. Dr. Wallace wrote:

Not entirely satisfied...I pursued a further description of the pollution risk assessment methods used to characterize the environmental/biologic impact of mercury pollution. I obtained a copy of a recently published document, "MPCA Mercury Policy" (Proposed October 12, 2000), through the agency's website (www.pca.state.mn.us). In "Appendix D" of that document, the authors address the lack of confidence scientists have - and perhaps the rest of us should have - in the "use of models to predict the local contamination of surface waters": “If the model goes on to calculate the risk to humans or wildlife of the mercury emissions, it makes assumptions about the size and species of fish eaten, the number of fish meals per unit time, the body weight of the consumer, and the sensitivity of the consumer to methylmercury. This information is often unobtainable, although the processes undoubtedly occur. In the absence of information, models use reasonable assumptions

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that often yield reasonable but unverifiable predictions. As with all models, the conclusions are generally as uncertain as the assumptions.” [Emphasis added]

Dr. Wallace concluded:

[I]t appears that the EPA, in this instance, has cast a "tattered net" with regard to the environmental impact of mercury thermometers. Contrary to what is implied by the EPA's "twisted" assertion, the mercury contained in a single fever thermometer would not be expected to have significant impact on the content of methylmercury in fish in a 20 acre lake...While I will be one of the first to admit that mercury thermometers are something we can do without, I am bothered by an authoritative governmental agency's failure, in this case, to accurately and reasonably represent what is known AND NOT KNOWN about this issue. And, I cannot help but wonder where, and at what cost, such distortions of truth have taken us in the past and will take us in the future. [Emphasis in original]

We agree.

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SECTION 11: THE SELENIUM (Se) FACTOR

Measuring the amount of mercury present in the environment or food sources may provide an inadequate reflection of the potential for health risks if the protective effects of selenium are not also considered. - Raymond and Ralston (2004) Perhaps it is no coincidence that those proteins and antioxidant molecules present in today’s cellular machinery…are our main line of defense against mercury [toxicity]. - Dr. Tom Clarkson (2002)

Chicago Tribune: Swordfish showed the highest mercury levels in the Tribune tests, averaging 1.41 parts per million, well above the 1.0 limit at which regulators can confiscate fish. In FDA testing, swordfish has averaged 0.97 parts per million. (December 11, 2005) Response:

Swordfish Guidelines vs. Confiscation

he Tribune here states the common as though rare, and the well-known as though concealed.

That it to say, reporting that high-end predators such as swordfish carry higher levels of MeHg in tissue and internal organs is well-known, especially since the FDA, EPA, and other federal and state agencies have advisories for these fish.

T CT reported mercury levels from a small sample of 18 Chicago area swordfish, ranging from 0.47 ppm to 3.07 ppm, with an average of 1.41 ppm. These levels are neither unusual nor remarkable when compared to the 605 swordfish samples taken by FDA over the 1990-2002 periods. 156 This larger sampling showed a range from 0.1 ppm to 3.22 ppm, with a mean average of 0.97 ppm. FDA's mean mercury concentration for swordfish agrees well with the mean of 0.95 ppm reported by the EPA.157 From the literature, Mendez et al. (2001) recently analyzed 192 specimens of Southwest Atlantic swordfish ranging from 10 to 412 kg by weight.158 They found total mercury values of between 0.04 and 2.21 ppm with a mean of 0.62 ± 0.35 ppm. They also reported levels for two groupings by fish body weight. Those weighing less than 100 kg had a mean of 0.53 ppm ± 0.02 ppm; those weighing more than 100kg had a mean of

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0.94 ± 0.06 ppm. These findings emphasize the importance of size and weight for determining likely mercury tissue levels. CT’s sampling and analysis is highly inferior to that of the FDA (18 samples versus 605) or Mendez et al., promotes a statistically biased mean of 1.41 ppm and calls for confiscation of the swordfish. Once again, EPA’s RfD definition (daily consumption over a 70 years period before discernible concern) is missing, providing no context for evaluating the meaning of CT’s data; which practical meaning is that Chicago consumers would have to daily -- for a lifetime running – select and eat only swordfish above the mean before exceeding EPA’s RfD. The odds of this happening are likely near zero. On top of this, EPA’s ultra-conservative RfD provides a safety cushion of 10 fold and does not consider the anti-oxidant role of selenium (discussed below).

The Canadian approach From a public health perspective, a zero-mercury/zero-risk regime encouraging widespread banning of all fish with mercury content above the numerical threshold of 1.0 ppm159 would be counter-productive, even harmful. Instead, the Canadian approach seems more sensible:

Health Canada has established a guideline level of 0.5 parts per million (ppm) for mercury in most commercial fish. This guideline is enforced by the Canadian Food Inspection Agency (CFIA). It was first set in the 1970's and, based on a recent re-evaluation, is still considered appropriate to ensure that the health of Canadians is protected from the toxic effects of methyl mercury. Certain fish species sold in Canada, namely, shark, swordfish, and fresh and frozen tuna, contain mercury at levels which are known to exceed the 0.5 ppm guideline. Based on current data available, average mercury levels in these species are at or near 1.0 ppm [the current guideline for methyl mercury in the United States] with a typical range of 0.5 - 1.5 ppm. Application of the 0.5 ppm mercury guideline to these species would virtually eliminate these types of fish from the Canadian diet. 160

Health Canada continues with highly conservative guidelines:

Therefore, these species [Note: not canned tuna] are exempted from the 0.5 ppm guideline and, in their case, another risk management strategy is followed, namely, issuance of advisories recommending appropriate restrictions on (amounts and frequency of) consumption. In this way, these species can continue to be enjoyed by consumers as part of an occasional meal. Fish are an excellent source of high-quality protein, and are low in saturated fat, which makes them a healthy food choice. Because of

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nutritional value, fish continue to be available to Canadian consumers, with advice to limit consumption to avoid exposure to hazardous levels of mercury. Specifically, pregnant women, women of child-bearing age and young children are advised to limit their consumption of shark, swordfish and fresh and frozen tuna to no more than one meal per month. For others in the population, a consumption level of no more than one meal per week is recommended for these species. 161

As noted in Sec. 3, the FDA/EPA joint fish advisory urged even more strict precaution for pregnant women, women of childbearing age and young infants and children to avoid fish species with high mercury contents, listing particularly swordfish, shark, king mackerel and tilefish (also called golden bass or golden snapper). Another key consideration is that in the marine consumption guidelines by Arctic rim nations and the State of Alaska, there is the persistent, fundamental concern that an unbalanced focus on mercury content risks an unhealthy disregard for benefits of essential daily nutrients and vitamins. These include high-quality protein, lysine, iodine, sulfur-containing amino acids, copper, calcium, zinc, iron, manganese, selenium, omega-3 polyunsaturated fatty acids, vitamin E (anti-oxidants) and more.

The Selenium (Se) Factor Some studies (Raymond and Ralston - 2004) have suggested that proportionally higher selenium levels in consumed ocean fish may counteract the toxicity of fish tissue MeHg. Swordfish for example, while higher in MeHg, is a superior source for omega-3162 fatty acids and selenium.163 A recent survey of 11 commercial sea foods in New Jersey confirmed that selenium concentrations exceeded those of mercury; for some species the selenium to mercury ratio was as high as 23.164 An analysis of 39 types of commonly consumed fish and shellfish in Modena, Italy by Plessi et al. (2001) also confirmed "a large excess of selenium in relation to mercury".165

Both fish selenium and amino acids are well-documented for helping reduce toxicity by inhibiting entry/transport of MeHg into brain cells.

Both fish selenium and amino acids are well-documented for helping reduce toxicity by inhibiting entry/transport of MeHg into brain cells. This critical finding may suggest why Minamata-like poisonings have not been diagnosed from chronic MeHg-exposures through large daily intake of fish not directly contaminated with multiple chemicals.166 For example, Robinson et al. write:

Per capita fish consumption in Seychelles is known to be high by world standards, and it is understood that Hg exposure results primarily from high rates of fish consumption. The ongoing Seychelles Child Development Study (SCDS) has initiated a nutritional study (Seychelles Child Development Nutrition Study) that focuses on mothers during

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pregnancy and offspring in early childhood…Results from the SCDS have shown that, despite considerable and continuous prenatal exposure to methyl mercury (MeHg) through the regular consumption of fish, there is no evidence suggesting that child development in the main cohort (tested at 6, 19, 29, 66 and 107 months) has been adversely affected. These consistent findings suggest that other constituents of the Seychellois diet might protect against the toxic effects of Hg. Experiments have shown that Se can reduce the neurological toxic response resulting from exposure to Hg.167

Also, among the Amazonian population of Rio Tapajós’s gold-mining region no typical symptoms of Minamata disease were detected at mean MeHg hair levels of 13.8 ppm or 21 ppm. Even an individual with the extreme exposure value of 303 ppm presented with no symptoms of Minamata-like illnesses.168 The scientific hypothesis that selenium plays a key role for naturally limiting the toxicity of methylmercury for these Amazonian fish eaters was recently clarified by Lima et al. (2005):

Mercury is a major public health concern because of its widespread occurrence in the environment and its toxic effects on humans, mainly through fish ingestion. On the other hand, selenium is known by its antioxidant effect....Our study demonstrated that the presence of Hg in fish is positively correlated to the concentrations of Se [see Fig. 11-A]. As previously mentioned, the correlation between these metals was also reported in riverside communities, hair samples from the Amazon, which confirms the exposure via consumption of fish to be a significant source of human exposures. Thus, the high contents of Hg found in this work and the absence of official reports on mercury poisoning in the inhabitants of Amazon region suggest that Se can be acting as a detoxification agent. 169 [Emphasis added]

Fig. 11-A illustrates that as mercury content increases with weight for two freshwater species taken from rivers and artificial lakes in the Cachoeira do Piria Municipality of ParaState, the selenium content increases disproportionately more. The measurements by Lima et al. (2005) confirm that the selenium-to-mercury ratios are generally greater than one and range from 1.28 to 17 for a wide variety of carnivorous, omnivorous and herbivorous fish species. So, what are the key biochemical roles played by selenium and related selenium-based proteins and enzymes, and how does selenium interact with mercury for reducing toxic outcomes? First, selenium, as selenoprotein/seleno enzymes (including 2 of the 22 primary amino acids), is known as an important determinant for maintenance of human health regarding (a) immune function, (b) protection from viral infection, (c) reproduction, (d) mood, (e)

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thyroid function, (f) cardiovascular health, (g) oxidative-stress or inflammatory conditions, and (h) cancer prevention (Rayman 2000).170 About 35 Se-containing proteins are present in the cells of the human body. While there are other enzymes that assist the seleno-enzymes in detoxifying the free radicals, they are less active in brain tissues. Selno-enzymes are thus known to perform vital functions in brain tissues (Ralston 2003). The role of Se is further underlined by the fact that it is the only trace element to be specified in the genetic code – selenocysteine, now recognized as the 21st amino acid.171

Mercury and selenium concentrations are related in river and lake fish samples from Para State Brazil: A potential resolution for the puzzle of no Minamata symptoms in high-fish

consumption cultures?

Lima et al. (2005) Environmental Research, vol. 97, 236-244

As mercury level increases with fish size the selenium level increases disproportionately more

Figure 11-A

Secondly, regarding selenium’s interaction with MeHg, Raymond and Ralston (2004) offer the following observations:

Measuring the amount of mercury present in the environment or food sources may provide an inadequate reflection of the potential for health risks if the protective effects of selenium are not also considered. Selenium's involvement is apparent throughout the mercury cycle,

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influencing its transport, biogeochexposure, bioavailability, toxicological consequences, and remediation. Likewisnumerous studies indicate that seleniumpresent in many foods (including fish)

protects against mercury exposure. Studies have also shown mercury exposure reduces the activity of selenium dependent enzymes. Whileseemingly distinct, these concepts may actually be complementary perspectives of the mercury-selenium binding interaction. Owing to thextremely high affinity between mercury and selenium, selenium sequesters mercury and reduces its biological availability. It is obviothat the converse is also true; as a result of the high affinity complexformed, mercury sequesters selenium. This is important because seleniuis required for normal activity of numerous selenium dependent enzymThrough diversion of selenium into formation of insoluble mercury-selenides, mercury may inhibit the formation of selenium dependent enzymes while supplemental selenium supports their continued synthesi... In summary, studying the pathology of mercury toxicity may require amore insightful question than simply, 'How much mercury is consumThe more appropriate question may be, 'Is a sufficient amount of freselenium available in the cell to create the necessary selenoenzymes or it too much se 172

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ed?' e

is lenium lost by binding to mercury?

Ralston also reports that moderate additions of Se to lakes in Sweden reduced Hg-concentrations in fish by 75%!173

In earlier research Ganther et al. reported:

The implications of this study are that the danger for man of Hg in tuna may be somewhat less than anticipated, and that total Hg contents in the diet or even in the blood may not be valid criteria [for deciding toxicity]….It thus appears that Hg and Se tend to be accumulated together in tuna. Selenium in tuna, far from being a hazard in itself, may lessen the danger to man of mercury in tuna.174

This critical science (missing from the CT series and the activist literature) may, in part or whole, point to an evolution of bio-adaptability for persistent, natural exposure to mercury – environmental mercury present since the earth formed 4.5 billions years ago. Reporting on interactions between selenium and mercury, Raymond and Ralston (2004) speculated upon a novel explanation that may contribute insight as to why the Faroe Children Study (discussed in Sec. 1) reported detecting "adverse neuropsychological" problems in association with prenatal exposure to methylmercury, but the better-designed study conducted in the Seychelles Islands did not yield any consistent effects, despite years of careful research testing. Raymond and Ralston (2004) observe:

Numerous studies indicate that selenium, present in many foods (including fish), protects against mercury exposure.

Studying the pathology of mercury toxicity may require a more insightful question than simply, 'How much mercury is consumed?'

Mercury concentrations in samples of pilot whale have been 5,000 times greater than the Japanese government's limit for mercury contamination of 0.4 ppm.

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“The diet consumed by the Faroe Islanders includes [Pilot] whale where the Seychelles Islanders' diet does not. Whale is known to contain PCBs as well as possibly other toxins not typically found in fish. [See the list of chemicals in Sec. 1] Additionally, the amount of MeHg in some types of whale meat analyzed has been reported to be exceedingly high. The concentration of mercury present in whale rises continually with and can exceed the selenium content. This is seen in high-end predator whales such as pilot whales rather than filter feeders such as bowhead whales. (see Fig. 11-B)175 Mercury concentrations in samples of pilot whale have been 5,000 times greater than the Japanese government's limit for mercury contamination of 0.4 ppm. In contrast to whales, methylmercury concentrations in fish rise with age, but as their mercury contents increase, so do their selenium concentrations. To our knowledge, there are no reports of mercury exceeding selenium concentrations in any ocean fish.”

0

5

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ole

Flo

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r

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mon

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lock

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ibut

Cod

Snap

per

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uper

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ordf

ish

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aver

age

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t Wha

le

Mercury

Selenium

Molar concentrations of mercury and selenium in SeafoodAside from pilot whale (Aside from pilot whale (JulshamnJulshamn et al. 1987) and swordfish (Friedman et al. 1978), data depicteet al. 1987) and swordfish (Friedman et al. 1978), data depicted d originate from Hall et al. (1978). originate from Hall et al. (1978). 

Ralston. Physiological and Environmental  Importance of Mercury‐Selenium Interactions. Energy & Environmental Research Center Fish Forum 2005, September 19, 2005 

Figure 11-B

nmol/g

Conclusion Through out, CT has failed to contextually inform readers of the rich variety of essential nutrients and vitamins contained in swordfish and other popular seafood species, including the important protective role played by selenium. The mercury-attenuating effect of selenium needs particular consideration.

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SECTION 12: FISH BOOM

"Dose makes the poison."

- Paracelsus

Chicago Tribune: Announcing the change in the Federal Register in 1979, the FDA said new data showed that consumers were not exposing themselves to as much mercury as officials had estimated when they set the more stringent 0.5 guideline a decade earlier. The FDA said the new data came from a report by the National Marine Fisheries Service, an arm of the Commerce Department. ... The report proved to be prophetic. With the relaxed rules in place, the seafood industry boomed. After decades of stagnant growth, fish consumption grew 20 percent from 1980 to 1990. (December 12, 2005) Response:

An absence of concern

he fact that fish consumption has “boomed” may well be explained by the boom in research revealing just how vital fish nutrition is for total physical and mental

wellness (see Sec. 1). The advent and dissemination of this knowledge, not any FDA actions, is more likely responsible for a rational increase in fish consumption rates by Americans -- although still far below world standards for recommend nutritional needs.

T

In "Making Sense of State Fish Advisories"176 we thoroughly discuss FDA and EPA fish mercury guidelines. FDA legal guidelines, that commercial fish mercury content is not to exceed 1 ppm, is not a bright line for safety. The FDA, joining with EPA, issued a cautious fish consumption advisory (March 2004) calling for optimal consumption of low-mercury fish of about 12 oz. per week. Such advisory seems sensible in light of the analysis in Carrington et al. (2004), cited in Sec. 4. Fig. 12-A shows the available U.S. fish consumption data from 1980, updated through 2004. It posses the question as to why CT specifically ignored data from 1991 through 2004 when flagging a 20% growth in fish consumption from 1980 to 1990. While total per capita consumption of commercial fish and shellfish in the U.S. shows an even higher value by 2004, Americans still fall far short of recommended intake of omega-3 fatty acids (see Sec. 14).

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12.4

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1982

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US Annual per capita consumption   

(pounds)

Data Source: National Marine Fisheries Service’s “Fisheries of the United States 2004” report (November 2005)

high point in 2004

Figure 12-A

The Chicago Tribune selected two annual points (1980 and 1990) to flag a 20% growth in seafood consumption

In short, it remains rather troubling that CT seems intent on discounting the good faith of both the FDA and seafood industry while intimating a lack of concern about the need for increased fish consumption levels in Americans.

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SECTION 13: ATTACKING THE FDA

It has come to our attention that both the Food and Drug Administration (FDA) and the National Marine Fisheries Service (NMFS) have submitted comments to the EPA critical of the scientific methodology in the EPA’s [draft] report. The FDA, which has federal statutory authority to ensure seafood safety, stated in a letter to the EPA dated February 16th that “the serious public misunderstanding about the safety of seafood which could result from the issuance of this report in its current form would be a disservice to the public and could lead to a further loss of confidence in government. - U.S. Senate letter to EPA, March 14, 1996

Chicago Tribune: During these years, the FDA did virtually nothing to warn people of the mercury threat. Nor did the agency test any fish for mercury throughout the 1980s, according to FDA data. The agency also conducted little basic research, such as studies to determine which fish have the most mercury or whether there were high-mercury "hot spots" in the oceans that fishing boats should avoid. It took a sharply critical 1991 report from the National Academy of Sciences, the nation's leading scientific advisory body, to coax the FDA to resume significant testing of fish for mercury. The agency promised several times during the 1990s to re-evaluate its mercury limit in fish. But the FDA never changed it, even though other government scientists were concluding the metal was far more harmful than previously thought. Once again, an important calculation--this one aimed at determining how much mercury can be safely consumed--was at the center of a debate. In 1997 the EPA, the agency responsible for monitoring recreationally caught fish, recommended a mercury-exposure limit in people based on the most recent scientific studies about the health risks. The EPA took a far stricter approach than the FDA did in setting its safety standard for mercury, concluding that a person could safely ingest only 0.1 grams of mercury per kilogram of body weight each day. The FDA's equivalent was 0.4. (December 12, 2005) Response:

More Confusion

gain, CT appears confused. T

than CT rephe level should be 0.1 micro-grams, an amount one million times smaller orted. Such a numerical error is equivalent to suggesting that a woman of

childbearing age with an average body weight of 161 lbs could “safely” consume up to 375,000 lbs of canned albacore tuna (mean mercury level of 0.3 ppm) per week. The

A

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numerically correct consumption rate would be no more than 6 oz. for an exposure level below EPA’s highly restrictive guidelines. More seriously, CT fails to emphasize that EPA’s “safety” standard is drawn from a Faroe Islands study concerned with consumption of whale meat and fat, not fish (see Sec. 1 and 7). Pilot whale meat in the Faroes catches has highly elevated concentrations of MeHg. Pilot whale fat, or blubber, also consumed by Faroese mothers, contains a mixture of toxic chemicals including PCBs and DDT. It has been estimated that Faroese infants may have been exposed to PCB levels exceeding EPA standard by 600 times.177 This is why, contrary to popular belief, the basis for EPA's mercury standard is viewed as highly flawed and certainly neither directly applicable nor appropriate for fish-consumption standards in Chicago or anywhere else in the U.S. From the beginning, it has not been universally accepted that EPA used the “best” or most recent science in forging its “safety” standard (see Sec. 1, 2 and 7).

A letter from the Senate As another example, in the year prior to issuing the recommendations referred to by CT, EPA received a stern letter from the U.S. Senate expressing not only concerns over EPA’s “scientific methodology,” but also its by-passing normal procedures for guarding against “crucial errors.” The letter intimates deep concerns among other federal agencies that the Browner/Clinton EPA might itself be posing a public health risk; concerns which have proved prophetic. Here are excerpts from the March 14, 1996 Senate letter:

It has come to our attention that both the Food and Drug Administration (FDA) and the National Marine Fisheries Service (NMFS) have submitted comments to the EPA critical of the scientific methodology in the EPA’s [draft] report. The FDA, which has federal statutory authority to ensure seafood safety, stated in a letter to the EPA dated February 16th that “the serious public misunderstanding about the safety of seafood which could result from the issuance of this report in its current form would be a disservice to the public and could lead to a further loss of confidence in government.” [Specifically, EPA] Similarly, NMFS also wrote to the OMB in a letter dated November 28, 1995, that “the public may become unduly alarmed and perceive the report as recommending against the consumption of fish.” We believe it is inappropriate to issue a report which could do great harm to the domestic seafood industry without resolving the concerns of these agencies and incorporating the Seychelles and Faroe Islands studies.

We share a final concern that the agency has not submitted this congressionally mandated report to its Scientific Advisory Board (SAB)

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for review prior to release. In the past, the SAB has been crucial identifying errors before publication. We believe it is critical that the mercury study be fully reviewed by the SAB, from a scientific standpoint, and to ensure that the report is based on the best available peer-reviewed science.

We urge you to delay sections of this report which address seafood safety until the report incorporates the Seychelles and Faroe Island studies, fully addresses the concerns of other agencies, and is reviewed by the SAB. The accuracy and careful analysis of this scientific information greatly outweighs a premature release of these sections of the report. [Emphasis added] Sincerely, [Signed] Murkowski (R-AK), Stevens (R-AK), Hollings (D-SC), Kerry (D-MA), Breaux (D-LA), Inouye (D-HI), Snowe (R-ME), Cohen (D-ME), Johnston (D-LA), McConnell (R-KY), Lott (R-MS), Mack (R-FL)

To our knowledge, EPA never did submit its draft to the SAB for review. Its “incorporation” of the far more appropriate Seychelles findings, contradictive of the Faroe data, consisted solely in discounting them.

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SECTION 14: FALSE LIMITS

It doesn’t tell us there’s a hazard [if one has mercury levels above EPA’s RfD]. - Tom Sinks, CDC Epidemiologist The whole idea of a safety factor is to protect people. You can’t turn it around to use as an indication of who’s at risk. If you are just above it, you aren’t necessarily in trouble. - Dr. Tom Clarkson, University of Rochester

Chicago Tribune: But the FDA warning did not reflect the EPA's science on what constitutes acceptable exposure to mercury. Based on the FDA's own testing, many consumers following the agency's advisory still could absorb too much of the toxic metal. For example, if a 161-pound woman--the average weight of U.S. females of childbearing age--ate 12 ounces of lobster in a week, she would expose herself, on average, to twice as much mercury as what the EPA considered acceptable. If she ate 12 ounces of orange roughy, or about two meals, she would be three times over the limit. (December 12, 2005) Response:

More RfD confusion

he Tribune monotonously repeats confused claims of being “over EPA’s limit,” suggesting a lack of understanding of EPA’s own definition of an RfD.

Further assessing EPA’s RfD as overly restrictive (see Sec. 2), we offer additional considerations.

T Another sign of extremity in EPA’s MeHg RfD?

Senn, Lincoln & Spengler  (2005) SEJ Mercury Biomarker Study Report [available at http://www.hsph.harvard.edu/water/SEJHgStudy.pdf] (a project funded by the Heinz Endowment)

EPA hair MeHg RfD=1 ppm

27% of SEJ members above EPA’s RfD of 1 ppm

3.4 ppm = John Spengler’s hair mercury level

Figure 14-A

First, it is clear from the ethical guidelines established by the Institutional Review Board of the National Center for Health Statistics of the CDC (the governing body which approved the recent National Health and Nutrition Examination Survey –NHANES -- mercury survey for U.S. women and children) that caution notices must be issued to NHANES participants only if their total hair mercury levels exceed 15 ppm or total blood

89

mercury exceeds 200 ppb (see McDowell et al., 2004).178 By contrast, EPA considers hair levels “safe” only below 1 ppm, and blood levels “safe” only below 5.8 ppb.

Secondly, consider informal survey results (funded by the Heinz Endowment) of hair mercury levels for 260 members of the Society of Environmental Journalist (SEJ) attending a December 2004 meeting in Pittsburgh (Fig. 14-A). Up to 27% (n = 70) of attendees tested hair mercury levels above what is considered “safe” by EPA. Applying these levels to CT’s standard for harm, is one then justified in assuming a large portion of environmental journalists may be neurologically impaired, or is EPA’s MeHg RfD simply overly conservative and misapplied by alarmists?

Average American needs more fish oils (DHA+EPA omega-3 fatty acids)

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NIH 1999 workshop

NATO workshop

British Nutrition Foundation

AHA for patients with CHD

AHA for patients needing triglyceride lowering

Figure 14-B

Recommended intake of fatty acids

Sources: Kris-Etherton et al. (2000, Am. J . Clin. Nutr., vol. 71, 179-188); Kris-Etherton et al. (2003, Arterioscler. Thromb. and Vasc. Biol., vol. 23, e20-e30); Din et al. (2004, Brit. Med. J ., vol. 328, 30-35)

Average American needs more fish oils (DHA+EPA

omega-3 fatty acids)

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Sources: Kris-Etherton et al. (2000, Am. J . Clin. Nutr., vol. 71, 179-188); Iso et al. (2001, J AMA, vol. 285, 304-312); Terry et al. (2003, Am. J . Clin. Nutr., vol. 77, 532-543); Gago-Dominguez et al. (2003, Brit. J . Cancer, vol. 89, 1686-1692)

Daily DHA+EPA     fatty acids (g/d)

US current intake (and UK+Italy)

Canada, New Zealand

Spain, Norway, Finland, Sweden

Singapore Denmark J apan Greenland (Eskimos)

10.5 g/d (!)

Figure 14-C

In response to the findings, the coordinator for the SEJ survey, Professor John Spengler of the Harvard School of Public Health, appeared to answer the question. Upon discovering his hair mercury level to be 3.4 ppm -- more than 3 times the EPA limit! Spengler appropriately reasoned:

“But I’m not going [to be] apoplectic about it because I know if I just watch my consumption, I can moderate that over time...and there’s that safety margin [i.e., a

90

factor of 10]...that I suspect I’d have to be much higher for much longer to really have symptoms” [i.e., at least 58 ppb daily, for a lifetime]. [Emphasis and comments added]

In other words, Spengler does not strictly interpret EPA’s RfD as a bright line above which is unsafe.

Eat more fish! A third consideration relates to real concerns for potential public harm flowing from a cresting tide of alarmism and misinformation. The average American needs more, not less, fish nutrition -- despite an encouraging trend of recently increased per capita fish consumption in the U.S (Fig. 12-A). Fig. 14-B and Fig. 14-C suggest elevated U.S. susceptibility to potentially life-threatening diseases due to current dietary deficiencies for EPA+DHA omega-3 polyunsaturated fatty acids. U.S. consumption is already 3 to 6 times lower than recommendations by the National Institutes of Health (NIH) and the American Heart Association (AHA). American children and adults are likely void of the health benefits proffered by omega-3 fatty acids, compared to people from the high fish-consumption nations like Japan, Singapore, Hong Kong and Scandinavia. This is why fear-based restriction or avoidance of fish intake will likely spawn increasing, negative public health consequences (See Sec. 1). Even the recent trend for shrimp overtaking canned tuna as the top seafood consumed per capita in the U.S. may not be an entirely positive outcome (Fig. 14-D). Shrimp has, on average, a lower content of total omega-3 DHA + EPA fatty acids than does canned tuna species (0.33 to 0.44 grams per 100 grams consumed versus 1.48 to 1.6 grams, respectively179).

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2000

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US Annual per capita consumption  of tuna and 

shrimp (pounds)

Data Source: National Marine Fisheries Service’s “Fisheries of the United States 2004” report (November 2005)

Figure 14-D U.S. Tuna consumption in decline.Shrimp consumption up in last 5 years.Means less intake of omega‐3 fatty acids.

tuna consumption

shrimp

91

Amazonia

Lastly, Dorea et al. (2004) report that:

There is evidence of fishing villages in the Amazon dating back eight millennia. In Brazilian times, there are no cases of required medical attention due to [mercury] health problems cause by fish consumption. Regarding neurobehavioral changes, the special fishing skills of some Amazonian native people do not suggest the existence of a compromising problem. Some Amazonian tribes fish with bow and arrow in turbid waters where they have to remain still for hours, apparently demonstrating good peripheral vision and outstanding motor coordination.180 [Emphasis added]

Dorea further reports that these Amazonian populations experience chronic MeHg exposures, through large daily intake of fish, far exceeding any level likely ever experienced by Chicago residents or other Americans. For example, in the Rio Tapajos gold-mining region, researchers detected hair levels reached 13.8 ppm and 21 ppm, with one value reaching 303 ppm! Riparian populations of the Rio Maderia region showed a prevalence of 3% with hair Hg above 50 ppm. And there has never been reported poisonings or Minamata-like illness among these peoples. By comparison, EPA’s RfD is only about 1.0 ppm.

Conclusion “The health implications of any diet are determined by the balance between essential nutrients and toxic substances that are naturally present in the food consumed.”181 Misunderstanding and misapplication of EPA’s restrictive and controversial mercury RfD for fish consumption leads to diminished public health. Failure to properly discern risks may prove fatal.

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SECTION 15: SOURCES OF OCEAN FISH MERCURY

The data for both tuna and swordfish lend support to the contention that the mercury levels now being found in wide-ranging ocean fish are not primarily the consequence of man-made pollution but are of natural origin.” - Miller et al., 1972 The relatively high concentrations of mercury found in marine fish that inhabit the surface and deep waters of the open ocean result from natural processes, not 20th century industrial pollution. - Barber et al., 1984 Our findings that the concentration of mercury in tuna…has not changed over a period of time during which anthropogenic mercury inputs…have increased supports the idea that the source of methylmercury in tuna is not in surface waters. [This] provides prima facie evidence that this concentration is not responding to anthropogenic emissions irrespective of the mechanisms by which mercury is methylated in the oceans and accumulated in tuna. - Kraepiel, et al., 2004

Chicago Tribune: Albacore tuna is a big fish and therefore tends to have higher mercury levels. The government has warned young children and pregnant women to limit how much albacore they eat. There are no warnings for light tuna, because most of it is made with skipjack, a relatively small species with lower levels of mercury. But some canned light tuna comes from another species: yellowfin. While the mercury content of yellowfin varies, industry testing found the average to be equal to that of albacore. (December 13, 2005) Response:

Canned tuna

o anyone even slightly familiar with the issue, it is well known that larger, longer lived species of tuna have relatively higher levels of natural residual mercury. Warm-blooded albacore, yellowfin or even bluefin tuna of matured size, weight

and age from certain ocean basins - the Mediterranean for example182 - have relatively higher mercury levels. (The issues of mercury in canned tuna are further discussed in Sections 16 and 20.)

T

The Real Issue: Natural Sources of Mercury However, all of this seems a diversion from the real issue: a missing context of mercury source and bioaccumulation in any species of ocean tuna ultimately found in canned tuna

93

products. In other words, how did the mercury in tuna get there in the first place, and can human intervention remove it? (The other key contextual issue of whether present levels are toxic is discussed repeatedly in this review paper.) The general impression with which CT leaves readers is that present mercury levels in tuna are a recent “menace,” with attribution to human activities. However, available fish mercury data challenge the premise that anthropogenic industrial Hg emissions deposited to air and water has led to heightened levels of MeHg in ocean fish over time. In rejecting the hypothesis, evidence strongly suggests that (1) MeHg has always been present in fish, (2) MeHg levels in fish vary naturally over time, and (3) the natural production (and destruction) of MeHg is not limited by the amount of Hg available in aquatic systems, regardless of sources. Hence, theoretical modeling claims of a linear connection between ocean fish MeHg levels and minor (compared to natural emissions, Sec. 5) power plant Hg emissions confirm a serious misunderstanding of or disregard for the emerging science derived from real-world observations.

No increase in mercury levels for Yellowfin tuna caught in 1998 relative to a similar sample caught in 1971

1971 Yellowfin Tuna with mean Hg = 0.218 ppm (n=71)

1998 Yellowfin Tuna with mean Hg = 0.206 ppm (n=66)

Expected increase of 9 to 26% in mercury levels between 1971 and 1998 was not observed

Kraepiel et al., 2003, Environmental Science & Technology, vol. 37, 5551-5558

Figure 15-A

Pacific Yellowfin tuna data provide but one example. Fig. 15-A shows recent results by Kraepiel et al. (2003) 183

finding no increase

in MeHg levels for Yellowfin tuna caught in 1998 relative to a similar cohort caught in 1971. The theoretical expectation (similar to EPA’s) was that methylmercury concentrations “should have increased by 9 to 26%” over the interval “if methylation occurred in the mixed layer or in the thermocline [of the Pacific Ocean].” The theory was not proven. Integral to the Kraepiel findings, Zhang et al. (2002)184

has estimated that China’s

mercury emissions alone from coal combustion are increasing at the rate of 5% per year (from available data from 1978 through 1995), which is consistent with the theoretical expectation of increased amounts of methylmercury in the waters of the Pacific Ocean if the Hg-to-MeHg conversion process in the oceans is sensitive to industrial emissions loading. To the contrary, Kraepiel et al. (2003) clearly concluded that “[s]uch an increase is statistically inconsistent with the constant mercury concentrations measured in tuna.” 185 [Emphasis added] The following year (2004), the authors strongly reconfirmed:

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Our findings that the concentration of mercury in tuna...has not changed over a period of time during which anthropogenic mercury inputs...have increased supports the idea that the source of methylmercury in tuna is not in surface waters. This provides prima facie evidence that this concentration is not responding to anthropogenic emissions irrespective of the mechanisms by which mercury is methylated in the oceans and accumulated in tuna.186 (Signed) Francois Morel, Princeton University; Klaus Keller, Penn. State University; Elizabeth Malcolm and Henry Chin, NFPA; Anne Kraepiel, Princeton University.

The Kraepiel findings are supported by similar research. A study by Barber et al.187 confirmed that although one can find clear increases of MeHg concentration in western Atlantic blue hake as fish length increases, one can not find significant changes in the fish mercury-size relation between fish samples caught in 1880s and samples caught in the 1970s. The authors concluded:

“This result supports the idea that the relatively high concentrations of mercury found in marine fish that inhabit the surface and deep waters of the open ocean result from natural processes, not 20th century industrial pollution.”

[Emphasis

added]

A third study188 compared mercury levels in various samples of tuna, including data from canned tuna more recently compiled by FDA and EPA. Dated fish samples (fig. 15-B) from the Smithsonian museum (1878-1909) indicate a relatively elevated mercury level associated with past sources and exposure unrelated to modern power plant mercury emissions. These old samples contain a mean level of about 0.38 ppm, significantly exceeding the mean levels of 0.29 ppm and 0.15 ppm for the 1971-1972 samples and the large FDA (1993) 220-canned tuna samples, respectively. The authors of this important research concluded:

0

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Old 'Modern' NMFS FDA

maximum

meanminimum

Mercury concentration (ppm)

(1878-1909) 7 samples

(1971-72) 5 samples

(1978) 250 samples

(1993) 220 canned samples

Data Sources: Miller et al. (1972), Science, vol. 175, 1121-1122; Carrington et al. (1997), Water, Air and Soil Pollution, vol. 97, 273-283

Hg levels in tuna (marine fish) had been naturally higher in the past!

0.21 ppm EPA (1997) mean level today

0.38 ppm mean level of Smithsonian Museum 1878‐1909 samples

Figure 15-B Mercury levels in tuna:  Old (museum) versus new specimens

95

“The data for both tuna and swordfish lend support to the contention that the mercury levels now being found in wide-ranging ocean fish are not primarily the consequence of man-made pollution but are of natural origin.” [Emphasis added]

Finally, using human-remains mercury levels as proxy for past available fish levels definitively confirm persistent mercury presence in marine life as long ago as the fifth century A.D. (Fig. 15-C). This is not surprising since Hg and MeHg have been present in the marine environment since before fish evolved.

Conclusion Thus, it seems reasonable to conclude that an appropriate science-based response to the Tribune’s mercury testing and reporting for small samplings of local fish is, “So what?” The above research findings clearly suggest that MeHg concentrations in ocean fish are not likely derived from human activities nor are they likely to be modified by small alterations from inorganic Hg sources (either anthropogenic or natural). This is why claims that EPA’s proposed Clean Air Mercury Rule (CAMR) – or even the stronger regulations being pressed by some states – will lead to a measurable reduction in MeHg accumulated in fish are factually misleading.189

Mercury in Humans‐Historical EvidenceArcheological data of ancient human hair demonstrate past exposure 

Barrow, Alaska:  total mercury 4.8 ppm in a 25 year‐old and 1.2 ppm in a 50‐year‐old mummy dating back to 1460 A.D

5th and 12th century

 15th century

 1170 A.D. to 1660 A.D.

 1450 A.D

. (Toribara et al. 1984). 

In Canada:   methylmercury levels ranged from 0.8 ppm to 3.7 ppm with a mean level of 1.7 ppm among eight individuals (Wheatley et al. 1988). 

In Greenland: the mean total hair mercury level ofmummies was 3.1 ppm among six adults and 10.0 ppm among 2 children (Hansen et al. 1989). 

Kodiak, Alaska: mean total mercury concentration in sixteen human hair samples dated in was 1.33 ppm (Egeland et al. 1999). 

Alaska’s Aleutian Islands:  dating to about . , average level of methylmercury in 4 adults was 1.2 ppm and in 4 infants 1.4 ppm.

State of Alaska Epidemiology Bulletin No. 11 (December 2, 2004)

Figure 15-C

Thus, it seems reasonable to conclude that an appropriate science-based response to all the CT hand waving accompanying its mercury testing and reporting for small samplings of local fish is, “So what?”

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SECTION 16: MEANINGLESS TESTS

This court is persuaded on balance that virtually all of the methylmercury in tuna originates from natural sources, while a small amount may be attributable to human activity. - Findings of Fact, San Francisco Superior Courts, California vs. Tri-Union Seafoods, 2006.

Chicago Tribune: The Tribune tested 18 cans of albacore and 18 cans of light tuna for mercury. After learning that yellowfin is often used in canned light, the newspaper analyzed 18 cans of gourmet tuna in a second round of testing. The gourmet cans showed low levels of mercury: 0.06 parts per million--even lower than regular canned light and far lower than the average reported by the tuna industry. Stiker said he was surprised by the findings. He speculated that Chicago had received shipments of gourmet cans made with small, juvenile yellowfin that would be low in mercury. Yellowfin range from 10 to 200 pounds, he said, "so you can certainly get some yellowfin that are low in mercury." When the newspaper tested tuna steak made with yellowfin, it averaged 0.35. Canned light tuna averaged 0.11 parts per million and albacore 0.30. Mercury content varied widely within most species tested. One can of light tuna had 0.31 parts per million of the toxic metal--in the range of albacore and other high-mercury fish. One can of StarKist had 10 times more mercury than another can of exactly the same kind of tuna. (December 13, 2005) Response:

Just the Facts

gain, consider even a few contextual facts reported in a wide body of scientific literature which appears studiously ignored by CT:

A

The monotonous listing of local test results is meaningless…none of the fish mercury levels reported by the Chicago Tribune are unusual, unnatural, extreme or dangerous to public health.

A minimum of a 10-fold safety level in EPA’s RfD(and likely larger).

Whole cultures eat 12-14 fish meals per week with higher levels than here listed, with only health benefits reported.

Extremely small sample sizes used by CT. CT samples employ no sampling controls for age and weight of fish. MeHg levels in same-cohort samples do not increase over centuries. Mercury is most likely methylated in the deep ocean – there is no evidence that

methylation occurs in the mixed layer or thermocline. There is more than enough MeHg generated in deep ocean vents to account for

MeHg levels in ocean fish without anthropogenic attribution. Thus, current mercury levels in fish have probably existed since prehistoric times.

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Even at exaggerated EPA RfD levels, one would have to always and only eat highest mercury level fish daily for a lifetime of 70 years before encountering potential concern.

CT lacks accounting for the higher anti-toxicity effects of selenium, vitamin E and omega-3 polyunsaturated fatty acids in larger and older fish.

That there is not now, nor ever been reported a world-wide mercury pandemic. Meaningless Tests

Chicago Tribune articles containing the words

"mercury" and "tuna"

(the data for 2006 is through June 26th)

0

5

10

15

20

25

1985

1986

1987

1988

1989

1990

1991

1992

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1994

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2001

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Year

An

nu

al N

um

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of

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icle

s

Source:  Chicago Tribune archives

Figure 16‐A

Thus, the monotonous listing of local test results is meaningless, unless one is uninformed or credulous enough to be persuaded that one molecule of MeHg is like an Ebola virus. The stubborn fact remains that none of the fish mercury levels reported by the Chicago Tribune are unusual, unnatural, extreme or dangerous to public health, as Sec. 20 further elucidates. Nonetheless, CT reporting seems increasingly focused on creating alarm concerning the trace levels of mercury in tuna. (see Fig. 16-A). We have already considered implications for findings of unchanging mercury levels in a variety of ocean fish (see Sec. 5, 15 and 20). Again, why did these mercury levels remain so consistent over time, during decades of enhanced industrial emissions, particularly from India and China? We repeat, the most plausible scientific hypothesis is that the methyl mercury bioaccumulated in these fish are not of anthropogenic origin, but are instead necessarily attributed to geological sources such as deep-ocean floor sediments surrounding hydrothermal vents. That is to say, “the best scientific evidence supports the conclusion that virtually all of the MeHg in tuna [and other commercially sold ocean fish] originates from deep ocean sources. This conclusion is based on (1) published data that shows an increase of monomethylmercury and dimethylmercury at depth; (2) samples of seawater from deep sea vents collected and analyzed…showing an amount of MeHg sufficient to account for all MeHg in tuna; and (3) evidence that a chemical process can create MeHg in hydrothermic vents.”190

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So, reporting naturally present micro-traces of mercury in fish, and comparing types of fish at such levels, only alarms without informing.

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SECTION 17: CONGRESSIONAL CONFUSION

Not all readers of EHP [Environmental Health Perspectives, the journal that printed Hightower and Moore, 2003] will appreciate the difference between documenting exposure levels and providing evidence for health effects, and not every reader will have followed the ongoing international controversy over the health effects of methyl mercury for fish consumers. - Schoen et al., 2004

Chicago Tribune "Kirk urges FDA to boost efforts" (Article, December 13, 2005). Response:

his article apparently reports on a December 12, 2005 congressional “Dear Colleague" letter from Representative Mark Kirk of Illinois. It states that Dr. Jane Hightower tested "129 children" for mercury and found that “89 percent had

elevated levels of mercury in their blood." The purpose of the in-house missive is to persuade Members of Congress that a serious health hazard exists; but how accurate are the claims?

T The statement reflects common confusion about, and misrepresentation of Hightower’s findings (see Sec. 9). Epidemiologists found the single paper by Hightower and Moore191 proved nearly irrelevant for health effects of dietary methylmercury exposure. The two reported having tested 123 patients of which only 7 were children, not 129. Of the 7 children listed in Table 2 of Hightower and Moore (2003), 4 had blood mercury above 5.0 ppb – a sample irrelevantly small. What’s more, Hightower herself clearly stated that these children were "not used for statistical analysis." Hightower and Moore (2003) did conclude that "89%" of 123 patients had blood mercury levels exceeding their own arbitrarily chosen 5.0 ppb RfD (instead of the actual 5.8 ppb established by EPA). There is nothing extraordinary about these levels. The "Dear Colleague" letter from Rep. Kirk contained two additional claims: "The U.S. government recently estimated that about 410,000 American babies were

born last year with a high risk of mercury poisoning." "The Tribune has found very high levels of mercury in walleye on sale in stores (with

no FDA warnings), while Canada already banned the sale of this fish due to mercury contamination."

The first relies on the CT claim (December 11th) that "a recent government study estimated 410,000 babies are born each year at risk for mercury poisoning.” Neither the

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CDC, EPA nor any government entity has ever issued such an official estimate. This is thoroughly examined in Sec. 2. As for the second claim, it is shown above (Sec. 4 and 11) that the Canadians have not banned any sale of walleye recently; but this is a minor point. Whatever the source of the confusion, those receiving the letter were misinformed.

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SECTION 18: MAN-MADE VS. NATURAL SOURCES OF MERCURY

[D]ecision makers need more than mercury concentrations to be able to ensure defensible interpretation of the indicators, such as MeHg in fish. - Mason, et al., 2005

Chicago Tribune: It doesn't matter who catches or sells the fish. The mercury is everywhere - oceans, rivers and lakes - thanks mainly to man-made pollution. (December 15, 2005) Response:

he Kafkaesque attribution to “man-made pollution” in this statement is scientifically indefensible, and is addressed throughout this critique (see Sec. 5). We repeat,

“The weights of several scientific facts crumble the footings underlying their entire construction: one such fact is that annual total mercury entering the bio-sphere from natural sources dwarfs anthropogenic sources into near insignificance. These sources are not only immense and overwhelming, but are persistent over geological time. This stubborn fact has been resolute in the literature for decades, and doggedly ignored by mercury activists.”

T

Further, it is well recognized that the processes of bio-conversion from Hg to MeHg is reversible, depending on multiple factors, including levels of sulfate, organic matter and even selenium levels in a particular ecosystem. According to Mason et al. (2005),192 the correlated factors of sulfate-organic-matter and bacterial activity alone could “possibly cause an increase in fish mercury concentration even as atmospheric deposition decreases”. [Emphasis added]

There are already extant millions of tons of naturally occurring Hg in Earth’s waters, crust, soils and sediments ever available for conversion into MeHg.

The decisive point is that science-based observations reveal that both the production and destruction processes of MeHg ending up in fish are not exclusively dependent on the amount of Hg available in a water system. Hence, key biological, geological and chemical processes driving Hg environmental abundance, methylation/demethylation and the ultimate bioaccumulation of MeHg in fish tissue overwhelm the relatively insignificant contributions of elemental, ionic and particulate Hg from U.S. power plant emissions. This is because there are already extant millions of tons of naturally occurring Hg in Earth’s waters, crust, soils and sediments ever available for conversion into MeHg. This explains why it is neither difficult nor surprising to find high, even extremely high, levels

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of MeHg in both fish and humans in the past several centuries, at times lacking mercury emissions from power plants or other industrial activities. For example, a comparison of MeHg levels in ancient and modern Alaskans found a higher mean level in 550-year old mummies.

Figure 18-A

Number of  samples

Total mercury (ppm)

World Health OrganizationNo Observed Effect level = 14 ppm

Exposure to MeHg in Alaska today vs. 550 years ago: Today’s distribution of pregnant women (n=177) in Alaska with a mean of 0.7 ppm (or median value of 0.47 ppm)

Compare this 0.7 ppm to the mean level of MeHg in 550‐year old Aleutian mummies:

1.2 ppm (mean of 4 adults)

1.44 ppm (mean of 4 infants)

One mummy with MeHg as high as 4.6 ppm!

State of Alaska Epidemiology Bulletin No. 11 (December 2, 2004)

Figure 18-A shows pregnant Alaskan women today with mean hair levels of 0.7 ppm, compared to 550-year old mummified adults with a mean of 1.2 ppm and one as high as 4.6 ppm. While this sample number is small, it demonstrates the point and is supported by other Arctic Circle remains dating some as long ago as the fifth century A.D. (see Sec. 15). So, while CT is correct about mercury being naturally ubiquitous, it is clearly incorrect to categorically state that anthropogenic sources of mercury are predominant.

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SECTION 19: THE NESCAUM REPORT

The NESCAUM report attempted to quantify the marine exposure pathway but used assumptions that are not supported by the literature on marine fate and transport of Hg, likely resulting in an overestimate by an unknown amount. - EPA, Evaluation of NESCAUM Report, 2005

Chicago Tribune: Illinois and 14 other states are challenging the Bush administration's proposal for regulating mercury emissions from power plants, arguing the rule fails to adequately protect Americans from exposure to the toxic metal. Citing a recent Tribune series on mercury in fish, the states filed comments Monday taking issue with the U.S. Environmental Protection Agency's conclusion that pollution from coal-fired power plants has little effect on seafood. The states also pointed to a Harvard University study commissioned by the EPA that found the health benefits from reducing mercury emissions would be 100 times greater than the agency projected when it issued the rule earlier this year. By underestimating the benefits of reduced mercury pollution, the states said, the EPA gave utilities a break. If the rule takes effect, many power plant owners likely won't need to install new equipment to curb mercury emissions. ... They also cited a study by the Harvard Center for Risk Analysis, paid for by the EPA and co-written by an agency scientist, that concluded the health benefits from reducing mercury emissions would be far greater than the agency's estimates--$5 billion a year rather than $50 million. Consumer advocates and environmental groups have criticized the Harvard center as being "pro-industry," and the Bush administration has frequently cited its work on other regulatory matters. But the EPA said the mercury study was submitted too late to be considered in drafting the power plant rule. (December 20, 2005) Response:

T here implies that (1) the report produced by the Harvard Center for Risk Analysis (which was submitted to EPA by NESCAUM) was submitted too late to be

considered in drafting the power plant rule and (2) EPA downplayed the benefits of reduced mercury emissions.

C First, the so-identified study is actually a non-peer-reviewed193, yet-unpublished report signed by Glenn Rice, an EPA employee. Rice performed the analysis as part of his doctoral thesis, along with Dr. James Hammitt, Director of the Harvard Center for Risk Analysis. The report, Economic Valuation of Human Health Benefits of Controlling Mercury Emissions from U.S. Coal-Fired Power Plants" is dated February 2005, and was submitted to EPA's rulemaking docket (as item OAR-2002-0056-5749) by the Northeast States for Coordinated Air Use Management (NESCAUM) by February 22, 2005. Second, it is true that this study was funded by EPA through contract to NESCAUM.

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Third, it is an unsubstantiated view that EPA had not considered the study or been thoroughly informed about the NESCAUM report in time for its rule making decision published March 29, 2005:

Rice and Hammitt, presented to EPA officials a 41-pp. power point presentation entitled "Assessing Power Plant Mercury Control Issues" on August 19, 2004.

In docket OAR-2002-0056 dated January 3, 2005, NESCAUM submitted to EPA the conclusions of the report, issued February, 2005.

From the timing, it appears obvious the actual NESCAUM report was submitted on time to the EPA docket for the consideration by EPA.

Finally, section 9 entitled "Evaluation of NESCAUM Report" of EPA's Technical Support Document Revision of December 2000 Regulatory Finding on the Emissions of Hazardous Air Pollutants From Electric Utility Steam Generating Units; Standards of Performance; Proposed Rules194 dated October 21, 2005 clearly shows that EPA had considered and evaluated NESCAUM's health benefit analysis. Some of EPA's key criticisms of the NESCAUM report included:

For example, the NESCAUM report attempted to quantify the marine exposure pathway but used assumptions that are not supported by the literature on marine fate and transport of Hg, likely resulting in an overestimate by an unknown amount. [I]t does not appear that the NESCAUM report took into account the timeframe for reduced exposure to MeHg. This omission alone leads to the benefits in the NESCAUM Report being overstated by at least a factor or two.

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SECTION 20: WHERE ARE ALL THE VICTIMS?

“[Their] findings should have been reported as good news for consumers because the mercury levels are very low and fall within the limits set by FDA. -- David Burney, US Tuna Foundation

Chicago Tribune: The Food and Drug Administration will investigate whether tens of millions of cans of tuna sold each year contain potentially hazardous levels of mercury. Responding to a Tribune series this month on mercury in fish, the FDA said it will review the possibility that there are elevated mercury levels in some cans of "light tuna," one of America's best-selling seafoods and a product the agency has recommended repeatedly as a low-mercury choice. (December 31, 2005) Response:

s previously noted, the menacing phrases, “potentially hazardous levels of mercury” and “elevated levels of mercury” are meaningless without context.

Elevated co A

mpared to what? Third International Mathematics and Science Study (TIMSS) Results (41 nations)

Grade 4 Grade 8 Grade 12 *

1. Singapore Singapore Netherlands2. Korea Korea Sweden3. Japan Japan Denmark4. Hong Kong Hong Kong Switzerland5. Netherlands Belgium Iceland12

Where are the Victims of

Fish Poisoning?

. USA  USA  USA

 USA

 USA  USA

Math

Science

A relevant question is: if “tens of millions of cans” of tuna sold in the U.S. are truly hazardous, then likely so are all cans of tuna currently or ever in the past consumed world-wide because MeHg levels in fish have been consistent for centuries (see Sec. 15); and there should have long ago presented a dramatically evident mercury poisoning pandemic. In fact, indigenous populations would long ago have abandoned eating fish.

28. 19.

Grade 4 Grade 8 Grade 12 *

1. Korea Singapore Sweden2. Japan Czech Republic Netherlands3. Japan Iceland4. Austria Korea Norway5. Australia Bulgaria Canada

17. 16.

* Inexplicably, Some of the superior countries in grade 8 (especially the Asians) 

were not included in published 12th grade results. Source: http://4brevard.com/choice/international‐test‐scores.htm (excerpted from a speech  by Pascal D. Forgione, Jr., Ph.D. U.S. Commissioner of Education Statistics.

International standardized tests in math and science (4th through 12th grades) score high fish consuming cultures at the top.

Figure 20‐A

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Exhibits That Argue for Lack of Victims Exhibit A - We witness children from the highest fish-consuming cultures dramatically – some might say appallingly -- eclipsing U.S. children in international standardized tests for math and science (Fig 20-A.). These statistics have little to do with different curriculum approaches: if a child is “permanently brain damaged” as alarmists claim, no amount of time in a classroom will compensate for a toxicity-induced “disability.” One simply can not have it both ways. Exhibit B – Seychelles Island study.

About twice the MeHg exposure levels of Faroe Islands mothers 12-14 fish meals per week – U.S. consumers average one or less per week No harm found to children, only benefits: better eyesight; less hyperactivity;

better brain function; better heart function Dr. Clarkson: “In our results…to date we have not found adverse effects from

prenatal exposure to MeHg in fish in a population consuming on average about 10 times the daily intake of the USA.”

Exhibit C – Bristol, England study found no harm, but instead benefits of prenatal fish consumption:

Higher child mental development scores Better eyesight “Our data did not suggest adverse developmental affects associated with

mercury.” Exhibit D – Norwegian study (Helland and colleagues) found that the nutrients in fish oil ingested during pregnancy and lactation “improves the intelligence of children at 4 years of age.” Exhibit E – Amazon rainforest native study (Dorea, et al.) reported that although natives eat lots of fish from Hg-rich areas, there is “no evidence that shows that freshwater…fish cause neuropathies (brain problems).” Hair levels at mean average of 21 ppm, and as high as 303 ppm (EPA RfD = 1.0 – 1.2 ppm) present no sign of toxicity effects. Exhibit F – 87% of Japanese are above EPA “safe” level of exposure, with no cases of poisoning reported since the cessation of large industrial chemicals discharges into surrounding waters. Exhibit G – Hong Kong children have one of the highest levels of seafood consumption in the world. They have a mean mercury hair level of 2.2 ppm, but seriously outperform U.S. children (mean hair level of 0.12 ppm) on international standardized tests for math and science (see Fig. 20-B). Exhibit H – The search by the Faroe researchers for “subtle neurobehavioral deficits” in children from prenatal exposure to MeHg failed detection in Inuit children from Greenland. The average mercury concentration in children’s’ hair was 5 ppm (0.6 – 1.0

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ppm in Faroese children at age 7 to 14 years, for comparison) and 15.5 ppm in Inuit mothers (4.2 ppm in Faroese mothers, for comparison). Recent measurements revealed that Hong Kong children 

(4 to 11 years) have relatively high mercury levels in their blood and hair. Yet, they outperformed U.S. children in math & science test scores.

Ip et al. (2004) Pediatric International, vol. 46, 715-721; McDowell et al. (2004) Environmental Health Perspectives, vol. 112, 1165-1171

The 1999‐2000 NHANES survey reported that mean hair mercury level for young (1 to 5 years old) U.S. children is only 0.12 ppm, compared to 2.2ppm for Hong Kong children.

Figure 20‐B

Exhibit I – Officials from the international Arctic Monitoring and Assessment Program have pointed out their mistrust of the U.S. EPA’s RfD because it only considers the hypothetical potential risks and does not take into account the well-known actual benefits of fish consumption. For example native women of Nunavik have average blood levels of 16.6 ppb (2 ppb-112 ppb) and suggest no restrictions at all because they know that a seafood diet is rich in selenium and vitamin E, which strong antioxidants are known to protect against mercury toxicity. Exhibit J – Alaska uses exposure guidelines from Health Canada and WHO, and will not issue any fish advisories for restricted consumption of fish from its waters. It encourages pregnant women to eat all the seafood they can from Alaskan waters because of multiple health benefits to the woman and her fetus, including enhanced brain development and cognitive abilities.

FDA Tuna Monitoring As explained above (see Sec. 3), the persistence in falsely painting the FDA (and the fisheries industry, including the tuna canners) as irresponsible toward public health is unjustified and misleading. In the case of tuna products (from fresh/frozen steaks to canned varieties), EPA reports a composite of "tuna" to have a mean of 0.21 ppm, published as late as in Mahaffey (2004)

195. The source of this information can be traced to pp. 3-24 to 3-25 of EPA's Mercury Study Report to the Congress (1997, volume III),196 listing the composite number as the average of 3 types of tuna: albacore tuna (0.264 ppm), skipjack tuna (0.136 ppm), and yellowfin tuna (0.218 ppm). FDA merely took a similar approach regarding "tuna." It was absolutely clear about the distinction between albacore, skipjack and yellowfin as sources for canned tuna in its 1991 large, survey of mercury content in canned tuna products, which ultimately was published in Yess197. Yess reported in detail that:

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"A total of 220 samples of canned tuna were collected and examined for methyl mercury. Of those, 50 test samples contained <0.10 ppm methyl mercury (expressed as Hg). Statistical values of methyl mercury (expressed as Hg) found in the 220 samples were as follows: average, 0.17 ppm; median, 0.14 ppm; range <0.10 -0.75ppm; and 90th percentile value, 0.42 ppm. ... In the FDA survey, levels of methyl mercury in solid white and chunk white tuna were significantly higher (analysis of variance) than in those products categorized as chunk light or chunk (0.26 and 0.31 ppm vs. 0.01 and 0.10 ppm, respectively). The influence of oil or water on these methyl mercury levels cannot be assessed, because there was relatively few oil packed products (5 solid white, 5 chunk, and no chunk white). There were 26 oil-packed chunk light tuna samples, with an average methyl mercury level of 0.06 ppm, compared with 0.11 ppm for 80 samples of water-packed tuna. There was no significant difference in methyl mercury levels for the different size cans in which the tuna was packed. ... Between 1978 and 1990, FDA determined methyl mercury in a total of 42 samples of canned tuna. The findings ranged from <0.10 to 0.67 ppm methyl mercury expressed as Hg with an average of 0.14 ppm; these results are similar to those of the 1991 survey. In 1973, FDA conducted a survey of canned tuna for total mercury. The average level of total mercury was 0.24 ppm for 253 samples. The ratio of total mercury to methyl mercury may vary among species. Hall (1974) found that 89% (range, 64-119%) of the mercury in canned tuna was methyl mercury. If that relationship is assumed, then the average value for the 1973 survey analyses would be 0.21 ppm methyl mercury, somewhat higher than the results from the 1991 FDA survey."

The alarming phrases, “potentially hazardous levels of mercury” and “elevated levels of mercury” are meaningless without context.

Once again, the facts sharply contradict CT’s attack on the FDA. FDA has expertly and carefully measured and monitored canned tuna for quite some time now. By the time of FDA's 2002/2003 mercury in tuna assignment reported in the January 2004's EPA Fish Forum,198 FDA had distinctly reported mercury contents from the wide variety of canned and fresh/frozen tuna tests on its webpage. CT further failed to properly inform its readers that FDA's seafood safety program has the following mercury measurement and monitoring programs in place:199

The ongoing Total Diet Study to focus on average, rather than extreme, dietary intake of mercury from fish/seafood, including canned tuna. (This study yields averaged mercury values of 0.163 ppm and 0.130 ppm for canned tuna in oil and in water [drained], respectively, as well as detection of very low mercury levels in homemade tuna casserole and 277 other popular foods consumed in the U.S. market baskets.)

The FY05 Toxic Elements Program to monitor mercury, lead, cadmium and arsenic in the 10 domestic, 160 import samples of fresh

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or frozen striped bass, salmon, flounder, herring, sardine, cod, bluefish, halibut, Alaska pollack, crab, oyster, squid, scallop and American lobster.

The FY05 Mercury Assignments to measure total mercury levels in 29 species of fresh/frozen of domestic and import fish and 100 fresh/frozen tuna and 50 samples of canned tuna.

As pointed out in Sec. 3, CT may be misinformed due to reliance on the research paper by their Rutgers University's source/contact of Burger and Gochfeld (2004). That paper200 oddly focused only oFDA's canned tuna measurements from the 1survey as published in Yess (referred to above) whilignoring subsequent FDA monitoring of mercury incanned tuna, especially the well-publicized new data from the

n

991

e

2002-2003.

Mercury levels in canned “light” tuna: 

Chicago Tribune results compared

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

ChicagoTribune

Burger &Gochfeld

FDA FDA

maximummean

minimum

Mercury concentration (ppm)

(2005)               18 samples

(1998‐03) 45 samples

(2003) 119 samples

(1993)                   220 “composite”canned samples

Data Sources: Chicago Tribune (2005) Mercury Menace Series 12/11/05-12/13/05;Burger and Gochfeld (2004), Environmental Research, vol. 96, 239-249; Acheson (2004) EPA Fish Forum January 26, 2004; Yess (1993) Journal of AOAC International, vol. 76, 36-38

0.21 ppm  EPA (1997) mean level for “composite”canned tuna

Figure 20-C

It is clear that mercury concentrations in all commercial seafood varies with size, weight, age and area fished. Fig. 20-C confirms that the average mercury concentration in "light" canned tuna remains low regardless of the information source, including CT’s tiny, 18-sample results.

Mercury levels in canned albacore/white tuna: 

Chicago Tribune results compared

0

0.2

0.4

0.6

0.8

1

1.2

ChicagoTribune

Burger &Gochfeld

FDA FDA

maximummean

minimum

Mercury concentration (ppm)

(2005)               18 samples

(1998‐03)      123 samples

(2003) 70 samples

(1993) 220 “composite”canned samples

Data Sources: Chicago Tribune (2005) Mercury Menace Series 12/11/05-12/13/05;Burger and Gochfeld (2004), Environmental Research, vol. 96, 239-249; Acheson (2004) EPA Fish Forum January 26, 2004; Yess (1993) Journal of AOAC International, vol. 76, 36-38

0.21 ppm  EPA (1997) mean level for “composite”canned tuna

Figure 20-D Likewise, Fig. 20-D presents a summary of available measurements for canned albacore tuna. Occasional monitoring of the mercury levels in canned tuna will likely still be performed; however, level comparisons shown in Figures 20-C and 20-D suggest that available resources might be better spent elsewhere, such as better, fact-based public health education.

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In this regard, evaluation of the CT series by David Burney, executive director of the U.S. Tuna Foundation, appears reasonable:

“[Their] findings should have been reported as good news for consumers because the mercury levels are very low and fall within the limits set by FDA. But unfortunately, the findings were used to raise concerns about eating tuna when the real risk to the public is not getting enough canned tuna and other fish in the American diet.”

Burney’s last point is fully consistent with the scientific analyses highlighted in Secs. 1, 8 and 14. Fish remains the primary protein source for much of the world’s peoples, and offers a nutritious wonder-food for all Americans.

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SECTION 21: HYPOTHESIS REJECTED

It is not clear whether changes in mercury input will result in a linear change in mercury methylation [i.e., creating MeHg]. Computer models, such as one developed for the Florida Everglades, tend to predict a linear response, but there are little data to support the predictions… - Mason, et al., 2005 The hypothesis that most Hg in Illinois and USA soils is of anthropogenic origin is rejected. - Krug and Winstanley, 2004

Chicago Tribune:

Some recent research suggests that mercury levels in fish can drop significantly once emissions from nearby sources of the metal are reduced. For instance, after Florida imposed tough regulations on waste incinerators, the top source of mercury in that state, levels of the metal in largemouth bass and wading birds in the Everglades dropped more than 60 percent. The Blagojevich administration thinks the same thing could happen in Illinois, since about two-thirds of the mercury that falls in the state is estimated to come from coal plants and other sources within state borders. (January 5, 2006)

Garbage in, Garbage out

Response:

uch unfounded claims are based almost exclusively on speculative computer

modeling, not empirical findings. Secs. 5, 15 and 16 present the case that cutting all man-made sources of Hg emissions within Illinois would not change MeHg levels in albacore, yellowfin, skipjack tuna, sword fish, orange roughy, grouper, walleye or salmon consumed in Chicago. We refer again to the scientifically defensible work of the Illinois State Water Survey office which found that, “The hypothesis that most Hg in Illinois and the USA soils is of anthropogenic origin is rejected."

Data used by EPA to support recent Clean Air Mercury Rule

Illustration courtesy of Mark Cohen, NOAA (based on his ppt talk April 21, 2005)

Figure 21-A

S

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To add context for Illinois deposition rates, total mercury deposition in the U.S. from emissions originating from U.S. utility generators has been estimated at 13.5 tons in 2001 (Fig. 21-A). This amount pales compared to the estimated deposition of 327 tons originating outside the U.S. and the naturally occurring amounts in situ available from aquatic and geological reservoirs. As is the case in Illinois, neither total mercury deposition nor total system burden is measured across the U.S.

A Vital Need for Essential Answers Before issuing costly state targeted mandates of 80 to 90% Hg reductions, it seems responsible for Illinois regulatory authorities to answer some fundamental questions regarding perceived objectives and methodology for targeted outcomes; similar questions should be required collectively or individually from Connecticut, Massachusetts, Minnesota, New Hampshire, New Jersey, North Carolina and Wisconsin, so say nothing of EPA itself. Put simply, what gain for all the pain? How much total mercury is deposited and in situ within Illinois? How much mercury in rivers and streams comes from natural sources in watersheds? How will drastic state actions exceeding EPA’s Clean Air Rule change the deposition

rates for Illinois’ own 23 coal-fired power plants? How will such action change methylmercury levels in local fish or in the top-25 sea

foods consumed? What are the designated indicators that costly proposed actions will enhance the lives

and health of women, infants, young children or the elderly? What system of monitoring and measuring will verify results? How long before results should be evident? If prescribed end-results stemming from reductions never materialize, then what? Let’s examine in more detail the reliability of the rather affirmative premises for State action as reported by the CT (January 5, 2006). The two major premises are:

(1) "About two-thirds of the mercury that falls in the state is estimated to come from coal plants and other sources within state borders,” and (2)"after Florida imposed tough regulations on waste incinerators, the top source of mercury in that state, levels of the metal in largemouth bass and wading birds in the Everglades dropped more than 60 percent."

Illinois Hot Spots?

It appears the CT source material for these premises is the December 2003 Environmental Defense (ED) publication, "Out of Control and Close to Home."201 It states:

"Local emissions of mercury are largely responsible for mercury deposition hot spots (locations where mercury deposition is high), providing an excellent opportunity for effective reductions. [A claim

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contradicted by results in Fig. 21-A] Recent modeling [by EPA's Dwight Atkinson whose results are shown and clarified in Fig. 21-B] suggests that at mercury hot spots pollution sources within the state can account for large portions of the deposition (Figure B). [Note: Figure B of the ED report shows the "top 8 worst hot spot states" in the order of MI, MD, FL, IL, SC, NC, PA and TX.] At hot spots across the United States, local sources often account for 50% to 80% of the mercury deposition. As shown in Figure B, for example, local pollution sources account for over 60% of the deposition in hot spots in Michigan, Maryland, Florida, and Illinois. [Confirmed to be 63% in the single (!) hot spot centered on the Chicago area clarified in Fig. 21-B] In another recent analysis in south Florida, dramatic reductions in mercury pollution from local incinerators were accompanied by a lowering of mercury concentrations in large mouth bass by 60-75%, indicating the importance of controlling local sources to reduce local contamination." (Emphases and [comments] added)

ED has relied on the modeling efforts distributed by EPA’s Dwight Atkinson. Another computer modeling analysis202 was carried out by Dr. Mark Cohen203 of the NOAA Air Resources Laboratory at Silver Spring, MD. However, to date, no credible simulations are suggesting that two-thirds of Illinois mercury deposition originates from in-state emissions sources.

Contributions to Hg at site of maximum IL Hg deposition

IL63%

Boundary26%

IN9%

WI1%

MI<1%

MO<1%

Canada<1%

Other states1%

Fate of IL Hg emissions deposited in domain

IL41%

IN13%

MN1%

MI6%

OH2%

WI4%

Region 79%

Region 46%

Region 32%

Other states3%

Coastal waters*

2%

Great Lakes5%

Other domain6%

Modeling Domain

IllinoisTotal annual Hg deposition:– at site of max. state dep. 70 g/km2

– at site of max. total dep. 70 g/km2

Total annual Hg from state:– deposited in domain 1,253 kg– advected out of domain 5,318 kg– airborne at end of year 26 kg

__________Total annual emissions: 6,597 kg

REMSAD Mercury Deposition - 1998

* Waters within 200 mi of US coastline

( on map)

Adopted from the presentation by Dr. Dwight Atkinson of the EPA’s Office of Water (communicated December 22, 2003)

Figure 21‐B

Note: only a single “hot spot” in Illinois

We say “no credible” quantification because Dr. Cohen's model assumed only man-made sources of mercury from U.S. and Canada is emitted into the modeled atmosphere. This is of course dubious because such a first-step assumption inexplicably and unjustifiably ignores enormous sources of atmospheric mercury from (1) other anthropogenic emissions, principally Asian (2) re-emissions from natural sources within

It seems highly problematic to assert that any mercury emission cuts by the state of Illinois will lead to significant reductions in the deposition of mercury to Illinois soil and waters.

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the U.S. and Canada (see Fig. 5-B) and (3) other world-wide natural emissions from volcanoes and geological and oceanic reservoirs (see Fig. 5-A). Thus, it seems highly problematic to assert that any mercury emission cuts by the state of Illinois will lead to significant reductions in the deposition of mercury to Illinois soil and waters, the Great Lakes area or even regions further away. Fig. 21-B clarifies the misleading claim that two-thirds of Illinois deposition originates from in-state anthropogenic emissions. As shown in Atkinson’s re-scaled model, there is essentially only a single “hot spot” in Illinois, around Chicago (top left). Even this result may simply be an artifact of EPA’s model assumptions which may over-prescribe the role of dry atmospheric deposition relative to wet deposition. Other parts of the state are less impacted because about 81% of Illinois emissions are transported out of the modeling domain. Even according to Atkinson’s results, only a tiny amount (i.e., 63 kg or no more than 0.1%) of Illinois' annual Hg emissions fall back to the Great Lakes. Also consider that only a fraction of that amount may be transformed into MeHg. This all raises serious doubts about claims for MeHg reductions in Great Lakes fish, even if Illinois emitted zero mercury from its coal-fired power generation plants.

Patterns in industrial Hg emission sources in South Florida

From p. 76 of Florida EPA’s November 2003 report on Hg Cycling in Everglades http://www.floridadep.org/labs/mercury/index.htm

If local emissions directly affected local deposition and substantial changes in mercury content in largemouth bass, then would a sudden rise in atmospheric deposition imply rebounding emissions?

Sharp rise and drop in local emissions that need not correspond directly to increase or decrease of the deposition of mercury in local areas

Figure 21‐C

Swamped in Florida

What about the seemingly encouraging news for Illinois from the Florida Everglades study (i.e., the expectation that lowering mercury emissions from Illinois power plants can lead to a substantial reduction of MeHg in locally caught fish)? On p.12 of "Out of Control and Close to Home," ED states:

"An ambitious analysis of mercury pollution, deposition and fish contamination in Florida provide on-the-ground evidence that corroborates the importance of local sources. Because of tighter standards on medical and municipal waste incinerators that took effect in mid-1992, South

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Florida's total estimated local emissions of mercury declined by about 93% between 1991 and 2000. During this same period, mercury deposited via rain and other precipitation declined in South Florida by about 25%. Concentrations of mercury in largemouth bass have also decreased significantly, 60-75% since the early 1990s. The data strongly suggest that reducing local mercury pollution will lower concentrations in local water bodies, and in turn reduce contamination in fish and the risk of human exposure."

The “strong suggestion” is in serious doubt. A distinguished team of researchers led by the University of Maryland’s R. Mason204 recently issued a warning to decision makers’ about reliance upon unproven modeling efforts, such as in the Florida Everglades:

“It is not clear whether changes in mercury input will result in a linear change in mercury methylation [i.e., creating MeHg]. Computer models, such as one developed for the Florida Everglades, tend to predict a linear response, but there are little data to support the predictions…. [D]ecision makers need more than mercury concentrations to be able to ensure defensible interpretation of the indicators, such as MeHg in fish. Other necessary information includes land use; food-web structure; the introduction of exotic species; point-source discharges; changes in climate, atmospheric chemistry, and acidic deposition; and hydrological regimes (e.g., retention time and water level fluctuation). ... Other factors, such as sulfate and organic matter that impact bacterial activity, could also possibly cause an increase in fish mercury concentration even as atmospheric deposition decreases.” 205 [Emphasis added]

Annual-mean mercury wet deposition for South Florida

5

10

15

20

25

30

1996 1998 2000 2002 2004 2006

EvergladesNat. Park

Andytown

EvergladesNutrientRemov.Proj.

Data Source: National Atmospheric Deposition/Mercury Deposition Network http://nadp.sws.uiuc.edu/mdn/maps/

Hg Deposition (g/m2)

Year

Neither the decrease nor the increase in Hg deposition at these sites is consistent with the trend of industrial Hg emission in south Florida

A “surprising” return to high Hg deposition in 2003!

Figure 21-D

(first update for 2003 in 2004, second update for 2004 in Oct. 31, 2005)

Mason’s warning seems to have proven out for Florida, raising serious questions about ED’s interpretations of the data. Has local deposition actually diminished in response to local emissions reductions? The answer is no.

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First, there was a sharp drop (Fig. 21-C) in mercury emissions from medical waste facilities from 1991 to about 1997. But a key question is, if the MeHg content in largemouth bass from the Everglades really decreased as an instantaneous consequence of the decline in south Florida medical waste emissions as described by ED, then prior to that time (between 1980 and 1991) when emissions were dramatically increasing did anyone report correlated large increases in MeHg levels for largemouth bass, or any area predator fish species? Secondly, recent wet deposition data from three Florida monitoring sites including the Florida Everglades (Fig. 21-D) strongly suggest that the sharp fluctuations over time are not consistent with or correlated to trends for industrial Hg emissions in South Florida. Note that deposition rates returned to sharply higher levels in 2003. Thus, the “hot spot” remediation hypothesis for South Florida as claimed by ED is neither convincing nor proven. This poses several questions for policy makers. First, if, as claimed, MeHg levels in largemouth bass declined in response to a mandated reduction of industrial emissions (Fig. 21-C), have mercury levels now sharply increased in any predatory fish in concert with the dramatic rebound in deposition rates (Fig. 21-D)? Secondly, if local emissions and deposition rates actually are tightly correlated, does the 2003 rebound in deposition (Fig. 21-D) point to a return of higher local man-made emissions? In other words, what’s again firing up the “hot spot” in the absence of those sharply curtailed incinerator emissions (Fig. 21-C)? Another puzzle is worth considering. Florida is ranked only 18th nationally in Hg emissions (about 1 ton) from coal-fired power plants, yet the levels of Hg wet deposited at several locations in Florida are among the highest in the U.S. By comparison, Texas ranks first nationally (5 tons), yet its Hg wet deposition rates are neither high nor especially alarming (Fig. 21-E). Also, the biggest signal in these data is a sharp decline in Hg wet deposition from the Gulf Coast to the Canadian border. The highest values are along the Gulf Coast, not in the Ohio Valley where coal-fired power plants are abundant. This further undermines ED’s “strong suggestion” that local emissions reductions guarantee consistent local deposition control. Contrary to ED’s assertions, when chemical, meteorological and climatic processes are accounted for, evidence is stronger that significant Everglades’s deposition sources are foreign, out of state and/or natural within the state. Another ED misstep is discounting the complexity of the cycling process for various species of mercury, especially methyl mercury. (See Sec. 5) It is well known that municipal and waste incinerators release mostly the oxidized or ionic form of mercury, which is water-soluble and easily rain-washed out into local rivers and lakes.

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Total mercury wet deposition, 2001-2004Figure 21‐E

By contrast, elemental mercury emitted from coal-fired plants is not readily water-soluble. Also, power plant chimneys are typically higher than incinerator chimneys, generally aiding in wider dispersal away from a local point of origin.

Conclusion In conclusion, the proposed policy action by Illinois appears hasty, unscientific and ill-advised, apparently fueled by confusion and misinformation. There appears no convincing evidence for sketching a scenario whereby a mandated lowering of Illinois industrial Hg emissions would ultimately improve human health through a concomitant lowering of MeHg in local fish, let alone imported sea foods. Sadly, the most likely result will be a spectrum of unintended negative consequences, resulting in severely diminished public health and wellbeing.206

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END NOTES

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

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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. 42 Lyketsos (2003), The Lancet, vol. 361, p. 1668. 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.

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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. 77 p. 31 of Dietary Guideline for Americans 2005 available at http://www.health.gov/dietaryguidelines/dga2005/document/. 78 USDA and HHS recommended an approximate total of 8 ounces per week 79 See http://www.nmfs.noaa.gov/docs/Conference%20final.pdf (December 8, 2005 press release). 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.

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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. 94 http://www.cfsan.fda.gov/~dms/admehg3.html. 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/. 98 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

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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 http://www.billingsgazette.com/index.php?display=rednews/2003/10/22/build/wyoming/25-mercury.inc 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. 129Virtanen 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

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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. 149 Lancet 2002: 359: 145-9 150 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 152The 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.

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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 g/kg (b.w.)/day, with the median value of 0.54 g/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 g/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). 160 http://www.hc-sc.gc.ca/ahc-asc/media/advisories-avis/2001/2001_60_e.html. 161 http://www.hc-sc.gc.ca/ahc-asc/media/advisories-avis/2002/2002_41_e.html. 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. 169 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. 175 Ralston, Fish Forum, op cit. 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

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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 http://ff.org/centers/csspp/pdf/EPANODAComments-121804.pdf 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. 194 Available from http://www.epa.gov/ttn/atw/utility/TSD-112-final.pdf. 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. 201 Available from http://www.environmentaldefense.org/pdf.cfm?ContentID=3370&FileName=MercuryPowerPlants.pdf. 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. 206 See When Fears Harm, by Sandy Szwarc, at www.scienceandpolicy.org

Robert Ferguson has 26 years of Capitol Hill experience, having worked in both the House 

and Senate.  He served in the House Republican Study Committee, the Senate Republican 

Policy Committee; as Chief of Staff to Congressman Jack Fields (R‐TX) from 1981‐1997, Chief 

of Staff to Congressman John E. Peterson (R‐PA) from 1997‐2002 and Chief of Staff to 

Congressman Rick Renzi (R‐AZ) in 2002.  He also served as the Executive Director of the 

Center for Science and Public Policy.  He has considerable policy experience in climate change 

science, mercury science, energy and mining, forests and resources, clean air and the 

environment.  His undergraduate and advanced degrees were taken at Brigham Young 

University and George Washington University, respectively.