106
Another study entitled “Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA” explains how ethylmercury damages mitochondria:
We find that ethylmercury not only inhibits mitochondrial respiration leading to a drop in the steady state membrane potential, but also concurrent with these phenomena increases the formation of superoxide, hydrogen peroxide, and Fenton/Haber-Weiss generated hydroxyl radical. These oxidants increase the levels of cellular aldehyde/ketones. Additionally, we find a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks.107
Because the oceans are polluted with it, methylmercury is typically found in fish and shellfish. The larger the fish and the longer the lifespan, the more mercury is accumulated; the most contaminated include tuna, swordfish, king mackerel, and shark. The EPA warns that nearly all fish are tainted with at least trace amounts of mercury. Some of the more health-conscious grocery stores even include warnings on store shelves about methylmercury in tuna, and many recommendations caution people from eating tuna more than once a week (pregnant women are cautioned to eat it sparingly, if at all).
MINAMATA DISEASE: MERCURY POISONING VIA INDUSTRIAL POLLUTION IN JAPAN
The most significant mass acute mercury poisoning in recent history was seen in cases of Minamata disease in Japan, officially attributed to industrial contamination. Wastewater dumped into Minamata Bay containing high levels of inorganic mercury was converted to methylmercury through biological processes, bioaccumulated up the food chain, and ingested in large quantities by local residents.
In the short term, about one hundred people were killed by intense industrial-based mercury poisoning. Decades later, thousands of people from the region had been officially diagnosed with Minamata disease, while over one thousand of those diagnosed have died from the effects of mercury poisoning since the 1950s.1
Mercury’s debilitating effects include sensory damage, muscle weakness, paralysis, coma, and possible death. The Chisso Corporation, responsible for the pollution, has paid out more than $80 million in damages to tens of thousands of affected people and has been ordered to clean up the sources of waste.2
Meanwhile, numerous other sources of toxic mercury pollution remain barely noticed and under-regulated.
Thimerosal in vaccines
The ethylmercury preservative thimerosal is found in personal care products like lotions, cosmetics, and contact lens solution; over-the-counter medications including some nasal and throat sprays; and in some vaccines including many widely available flu shots officially recommended to pregnant women. Because a vaccination is injected directly into the bloodstream, all of the ingredients are allowed to bypass the digestive tract where many of the body’s natural defenses are located.
According to the state of Wisconsin’s Department of Natural Resources, “Vaccines with 1:10,000 or 0.01 percent thimerosal have about 50 mg/L mercury, which exceeds the 0.2 mg/L hazardous waste toxicity characteristic regulatory level for mercury.” This means that discarded vaccines containing the preservative may need to be officially handled as a hazardous waste per state and federal standards.108 The Environmental Working Group (EWG) has listed thimerosal as a 10, or high hazard, on the organization’s health hazard scale—the highest ranking an ingredient can receive.109 The CDC continues to assert that thimerosal in vaccines is safe and denies links to adverse health effects including autism on the insistence that ethylmercury is much less dangerous than methylmercury.
Shorter half-life for ethylmercury
Part of this argument rests on the observation that ethylmercury has a shorter half-life in the blood, but some researchers have advised caution in making ethylmercury safety determinations based on this criterion. A comparative ethyl- to methylmercury toxicology study found little difference between the neurotoxicities of either compound, and detected concentrations of inorganic mercury in treated rats was higher after an ethylmercury dose.110 Further research corroborated these findings.
A 2005 study assessing human ethylmercury risk noted that much higher levels of inorganic mercury were found in the brain than with methylmercury, where it remains much longer than organic mercury at a half-life of more than a year. The author cautioned that neurotoxic potential in developing brains exposed to inorganic mercury “are unknown” and that thimerosal risk assessments based on blood mercury measurements alone may be invalid and require further research.111 Researchers reviewing medical literature in combination with U.S. government data have concluded that thimerosal induces autism and related its symptoms in some children who suffer the effects of mercury poisoning due to the preservative.112
Mercury in high-fructose corn syrup (HFCS)
High-fructose corn syrup (HFCS) is a highly processed sweetener made primarily from corn and found in a plethora of food and beverages on grocery store shelves. The U.S. Department of Agriculture’s Economic Research Service estimated in 2011 that the average consumer per capita consumes nearly 42 pounds of high-fructose corn syrup per year.113 Not one, but two studies in 2009 found that HFCS commercially produced in America and American-bought HFCS products were tainted with mercury.
The first study published in the peer-reviewed journal Environmental Health found that, of twenty samples collected and analyzed from three different manufacturers, nine, or 45 percent, came back tainted with mercury.114 The second study by watchdog group Institute for Agriculture and Trade Policy (IATP) purchased fifty-five food items from popular brands off grocery store shelves in the fall of 2008—items in which HFCS was the first or second principal ingredient—and detected mercury in nearly a third of them.115 The contamination may have been due to the fact that mercury cells are still used in the production of caustic soda, an ingredient used to make HFCS.
The HFCS-mercury plot thickens, however. Online news outlet Grist reported that the lead researcher in the Environmental Health study, Renee Dufault, previously worked as an FDA researcher. Dufault had apparently turned over the information contained in her HFCS-mercury study to the agency back in 2005, but the FDA reportedly sat on it and did nothing, so Dufault went public with it after she retired in 2008.116
A breakthrough in converting dextrose to fructose with the use of a microbial enzyme in 1957 set the stage for a commercially viable process to produce what became known as high-fructose corn syrup. The development was pursued by the Clinton Corn Processing Company, which was later acquired by Archer Daniels Midland in 1982.
The Clinton Corn Processing Company’s work in the mid-1960s with the Japanese Agency of Industrial Science and Technology led to the discovery of HFCS in 1966 by Dr. Yoshiyuki Takasaki, who was granted a patent on the substance in 1971 alongside development of the sugar substitute’s commercialization.117,118
HFCS is created through a complex process in which cornstarch undergoes acid hydrolysis and becomes dextrose,119 the glucose sugar produced from corn. A secondary process uses the enzyme glucose isomerase to convert glucose into fructose.
Clinton Corn created different formulas of HFCS, including a 42 percent fructose concoction that contains 58 percent glucose, which is frequently used to sweeten solid foods, as well as a purified 90 percent fructose formula (with only 10 percent glucose) that is rarely used directly. Instead, the 42 percent and 90 percent fructose formulas are blended to create a high-fructose corn syrup that is 55 percent fructose and 42 percent glucose (or alternately 45 percent glucose and 52 percent fructose).120 This liquid corn-derived 55 percent fructose variety is the most widely
