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Doing Harm –The Mercury ScareA critical, Science-based Analysis of the Chicago Tribune“Mercury Menace” Series (December 11-13th, 2005) Introduction and Background Why this response? The “Mercury Menace” is a series of 3 articles published in Chicago Tribune (hereafter as CT) by investigative reporters Sam Roe and Michael Hawthorne, including: • Toxic risk on your plate (December 11, 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) 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. 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). 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. Only a few of these included reliable exposure data. 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 tissue ) 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. 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. 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). 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 effects of those high levels of multiple toxic chemicals discharged into near-shore waters. 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 disease , 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. 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 of healthy – absent symptoms – infants (all under one year of age) at the same time ranged from 0 to 158 ppm! 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! 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. 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. 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 and university. 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 of clinical symptoms from consumption of sea food was a child born in Japan in 1965.  In terms of potentially dangerous fetal exposure to MeHg from maternal fish consumption, current findings by Japanese scientists (including those from the Japanese National Institute for Minamata Disease) confirm the general improbability of fetuses in contemporary fish-eating populations being exposed to MeHg levels near or exceeding those estimated necessary for inducing Minamata disease (“mercury poisoning”). Following a survey of 115 healthy Japanese pregnant women and their child births in 1996, Sakamoto and colleagues confirmed (see Fig. 1) that current baby MeHg exposure is about 20 times below that associated with the 1950-1965 births of the 24 children diagnosed with congenital or infantile Minamata disease. This important result, together with the fact 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 evidence for MeHg poisoning of babies simply because their mothers eat a lot of fish. 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.” 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. 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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