The Comparable Dangers of Ethylmercury and Methylmercury

Government health agencies, such as the CDC, maintain that ethylmercury is less toxic than methylmercury because it is broken down and excreted more quickly. Accordingly, as the CDC states on its website, ethylmercury is much less likely to “accumulate in the body and cause harm.” 334 The World Health Organization states that the half-life of ethylmercury—that is, the length of time half of a given dose remains in the body—is “short (less than one week) compared to methyl mercury (1.5 months), making exposure to ethylmercury in blood comparatively brief.” 335

The scientific literature, however, does not unanimously support these statements. Research on human beings that might firmly answer questions about methylmercury and ethylmercury toxicity is not ethical, of course. Many of the best insights that are available, however, into the toxicology of both ethylmercury and methylmercury in humans come from poisoning events several decades ago.

In addition to the well known Minamata and Iraq methylmercury-poisoning, many other large-scale food poisonings have occurred involving ethylmercury fungicides in Iraq in 1956 and 1960, in Pakistan in 1961, and in Russia in the 1960s as well. 390 391 392 393 These episodes resulted in maladies ranging from basic tissue injury to heart and brain injury and even death. 394 395 396 397 398 399

Derban reported in 1974 on 144 cases of mercury poisoning from the use of ethylmercury fungicide on a southern Ghana state farm. 400 Multiple other studies based on these poisoning events showed, as stated in a 1977 study by David Fagan, that the long-term neurological consequences produced by the “ingestion of either methyl or ethyl mercury-based fungicides are indistinguishable.”401 402 403

Ethylmercury compounds easily cross the placental barrier into human fetuses and into breastfeeding children for three to four years after maternal exposure, according to a 1968 study.404 In 1977, Mukhtarova examined Russian adults who ate meat and dairy over a course of two to three months that had been exposed to ethylmercury-contaminated grain, containing mercury in micrograms or tenths of a microgram per kilogram. Many of the Russian patients still had clinical evidence of neurological injury, including vertigo, decreased vision and hearing, decreased memory, and pain and numbness in hands and feet, at least three years after exposure.405

A 1979 case report concerned a fifteen-year-old boy who had eaten the meat of a pig that had fed on ethylmercury fungicide−treated seed. Documented effects on the boy included debilitating brain damage and loss of coordination, with high toxicity for the brain as well as the spinal motor neurons, peripheral nerves, skeletal muscles, and heart muscle. The boy died about one month after becoming ill.406

Ethylmercury’s use as pesticide was eventually banned in many countries, including the United States and those in the European Union, and for good reason: A 1977 study gauged ethylmercury chloride’s relative toxicity as a pesticide as the fifth most toxic of thirty substances tested, with a score of 12.7. That grade score almost matched that of DDT, at 14.2, an infamous pesticide banned in 1972.407 408 409

The US EPA Guidelines for exposure to Methyl Mercury

In 1995, based on research from outbreaks of poisonings and other research from the Faroe Island and New Zealand, the EPA established a safe “reference dose” for methyl mercury (RfD). An RfD is defined as “an estimate of a daily exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of adverse effects when experienced during a lifetime,” according to the EPA.341

The EPA adopted for methylmercury an RfD of 0.1 microgram of mercury per kilogram of the individual’s body weight per day.342 343  Other health agencies set their own recommended limits for methylmercury exposure, such as the FDA in 1979, the World Health Organization in 1989 and the US Agency for Toxic Substances and Disease Registry (ATSDR) in 1999. The highest of these limits was the WHO’s, at 0.47 microgram per kilogram of body weight per day.344 345

In 1999 the US Congress directed the EPA to contract with the nonprofit, independent National Research Council (NRC) to prepare recommendations on an updated and appropriate RfD. The EPA commissioned the National Academy of Sciences (NAS) and the NRC to carry out a study on toxicological effects of methylmercury compounds. The goal was to review the process used by the EPA to establish national safety standards. The committee evaluated the literature, which demonstrated methylmercury compounds’ high toxicity to brain tissue, even at minute levels. The NAS ultimately agreed with the EPA’s originally conceived RfD, which remains in place today.346

An RfD has never been established for ethylmercury, presumably because there is not a common environmental exposure or route of ingestion as with the methylmercury in seafood. Ethylmercury, however, unlike methylmercury, is injected into the human body as part of Thimerosal.

Ethyl Mercury Exposure Levels Based on Methyl Mercury Guidelines  

A single Thimerosal-preserved flu vaccine contains 25 micrograms of ethylmercury. If the EPA RfD for ingested methylmercury is applied to this injected ethylmercury figure, an individual would have to weigh more than 250 kilograms (551 pounds) for the 25 microgram exposure to be considered safe. Young children are commonly given half-doses of Thimerosal-preserved flu shots nowadays, working out to approximately fourteen times a safe daily exposure for a 20-pound (9-kilogram) individual. Back in the 1990s, a two-month-old child could have received 62.5 micrograms from three vaccines in a single doctor’s visit. Assuming the child weighed about 5 kilograms (11 pounds), he or she would have received 125 times the EPA RfD for methylmercury.

At least one study has suggested that the methylmercury RfD should be set lower for infants and also for fetuses. In 1995, Steven Gilbert and Kimberly Grant-Webster wrote: Available information on the developmental neurotoxic effects of MeHg [methylmercury], particularly the neurobehavioral effects, indicates that the fetus and infant are more sensitive to adverse effects of MeHg. It is therefore recommended that pregnant women and women of childbearing age be strongly advised to limit their exposure to potential sources of MeHg. Based on results from human and animal studies on the developmental neurotoxic effects of methylmercury, the accepted reference dose should be lowered to 0.025 to 0.06 MeHg [microgram]/kg/day.347

What might this mean for a fetus today? We’ll take the low end of that estimate and apply it to an average 1.15-kilogram (2.54-pound) fetus at the start of the third trimester.348 A fetus exposed to 25 micrograms of mercury via a Thimerosal-preserved flu shot administered to its pregnant mother would be subject to 870 times the proposed lower reference dose.

Newer research supports older data that “safe” levels of ethylmercury exposure might indeed be lower than the EPA’s RfD. A 2012 Italian study, for instance, showed that ethylmercury-containing Thimerosal diminished the viability of human cells in the lab at a concentration one-fiftieth that of methylmercury. 351

Japanese research on rats in 1968 showed that ethylmercury compounds, such as ethylmercuric chloride from which Thimerosal is made, clear the body more slowly than the mercury compounds mercuric chloride and phenylmercuric chloride. 352

A book chapter in 1972 by Staffan Skerfving, an emeritus professor at Lund University in Sweden, reviewed literature on methylmercury versus ethylmercury, noting several instances where compounds of the latter appeared more toxic than the former in animal studies. 353

For example, ethylmercury chloride killed off half of a test population of mice—a classic “LD50” (lethal dose) study—within a week at a concentration of 12 milligrams of mercury per kilogram of body weight; methylmercury chloride’s LD50, meanwhile, lethal to half the mice was 14 milligrams.354 355

Further examples abound. Pig studies by Tryphonas and Nielsen in 1973 showed that ethylmercury “proved much more toxic” than methylmercury.356 Meanwhile, another 1973 study that emerged from a 1971 international conference found the toxicity of ethylmercury compounds comparable to or even greater than that of methylmercury, as well as more persistent in the brain.

An advisory committee at the conference reported that the International Committee on Maximum Allowable Concentration for Mercury and Its Compounds grouped ethylmercury with methylmercury, and observed that accounts of human intoxication with ethylmercury have usually described neurological and other symptoms similar to those of methylmercury. The report noted that in studies of patients transfused with a commercial product of human plasma containing 0.01 percent Thimerosal, as well as in studies of mice injected with an ethylmercury solution, the increased level of inorganic mercury added to the mercury already existing in the body resulted in a “longer biological half-life of total mercury than that reported for methylmercury injection.”357

Why do the CDC and WHO Report that Ethyl Mercury Exposure is Safe?

The WHO’s conclusion that ethylmercury is safer because of its “short” half-life may be based on observations that ethylmercury disappears from blood samples quicker than methylmercury. This tendency may be evidence not of ethylmercury’s comparative safety, but of its greater danger if, as science has suggested, ethylmercury is not leaving the body but simply migrating more rapidly to the organs, including the brain. Indeed, studies have shown that an ethylmercury compound’s short residence in the blood stems from its ability to more easily pass into the organs, where it can remain for long periods and possibly cause injury.

For example, A. M. J. N. Blair in 1975 dosed squirrel monkeys intranasally with saline or Thimerosal daily for six months, finding that, compared to the saline group, mercury concentrations in the Thimerosal group were significantly raised in the brain, liver, muscle, and kidney, though not in the blood. Although there were no signs of toxicity in the animals, Blair concluded that the “accumulation of mercury from chronic use of thiomersal-preserved medicines is viewed as a potential health hazard for man.”358

In 1985, Laszlo Magos showed that the neurotoxicity of both mercury types was broadly comparable. Higher levels of inorganic mercury were found in the kidneys and brains of rats that were fed ethylmercury, though more brain damage was seen in the methylmercury-fed rats.

Lower concentrations occurred in those same organs of organic and total mercury in the ethylmercury-treated rats.359

Beyond a possibly greater capacity to have inorganic mercury accumulate in organs, Thimerosal also passes more easily from a mother’s bloodstream through the placenta into a developing baby than does methylmercury. That was the evaluation made in a 1983 review study by A. Leonard.361 In addition, a 1995 study demonstrated that both ethylmercury and methylmercury cause mutagenic changes at similar concentrations in bacterial cells.362

With these and other studies as background, an important study in humans took place in the early 2000s. The study, by Michael Pichichero of the University of Rochester Medical Center and published in The Lancet in 2002, lent some apparent scientific credence to the idea that ethylmercury is safer than methylmercury.363 364. The study assessed mercury levels in the blood, urine, and feces of forty infants ages six months or younger three to twenty-eight days after they had received Thimerosal-preserved vaccines (DTaP, HepB, and in some cases Hib). For comparison, twenty-one similar infants who received Thimerosal-free vaccines were also evaluated. Although infants who received Thimerosal-preserved vaccines had higher levels of mercury in their blood, urine, and feces than did the infants who received Thimerosal-free vaccines, the authors concluded that the levels of mercury detected were not greater than what is considered safe. Most of the mercury from the injected Thimerosal seemed to have left the children’s bloodstreams more rapidly than methylmercury found in the blood of those eating fish in previous studies; the researchers estimated a half-life of seven days for ethylmercury in the blood. Pichichero concluded that ethylmercury, therefore, did not remain in children’s bodies long enough to possibly cause damage.

In a number of respects, though, this well-known study that is often cited as evidence of the safety of thimerosal, was seriously flawed. For example, every child in the study was tested only once. The infants were not followed for any length of time, so there was no possibility of seeing a change in the children’s mercury levels, or whether any mercury poisoning effects occurred in later years.365 The study also did not indicate whether any of the children had low levels of the antioxidant glutathione, a substance that helps clear mercury from the body. Glutathione deficiency has been associated with sensitivity to Thimerosal, according to studies by Gotz Westphal, and a 2007 study by Geier and Geier found deficiencies in glutathione pathways in a small group of children with autism who had received Thimerosal-preserved vaccines.366 367 368 369  The Pichichero study’s cohort size of just sixty-one infants was too small to likely include individuals with an autism spectrum disorder (based on an estimated prevalence in the early 2000s of 1 in 166), who again as studies have suggested are poor excreters of mercury.

Furthermore, Pichichero, who helped develop the HiB vaccine and previously received grants and honoraria as a consultant for Eli Lilly and other vaccine makers, did not declare these potential conflicts of interest in a statement in his paper, as would seem to be required by The Lancet’s peer review rules.370 371 372 373 374

Notable concerns about the study were voiced in a 2003 letter to The Lancet by Neal Halsey, of the Institute for Vaccine Safety at Johns Hopkins Bloomberg School of Public Health, and Lynn Goldman, also of the Bloomberg School of Public Health. Halsey and Goldman pointed out that Pichichero and colleagues “did not measure the peak blood concentrations that occurred within hours after the injections.” The concentration listed for one child in the study of 20.55 nanomoles per liter was obtained five days post-vaccination. Assuming Pichichero’s own estimate of an ethylmercury half-life in the blood of seven days, the peak blood concentration for this child was 29.4 nanomoles per liter—exceeding the conventional safety threshold of 29.0 nanomoles per liter, and casting doubt on the study’s claim that “no children had a concentration of blood mercury exceeding 29 nmol/L.” The child in question had received 37.5 micrograms of ethylmercury rather than the possible maximum exposure of 62.5 micrograms. In the latter scenario, the child’s peak blood mercury concentration would have hit 48.3 nanomoles per liter.

Another child in the study registered a 7 nanomole per liter blood concentration 21 days post-vaccination; extrapolating backwards, this child’s peak mercury level might have reached 42 nanomoles per liter. Halsey and Goldman’s letter further pointed out that the children in the study—some already with no margin of safety for further mercury exposure—seemed to have come from a population with low background environmental and maternal exposure to methylmercury.375

Soon after Pichichero’s study came out, new evidence emerged that ethylmercury lingers in the body. Boyd Haley, then-chairman of the chemistry department at the University of Kentucky and Mark Blaxill reviewed Pichichero’s data, and in an unpublished letter submitted to Pediatrics came to a very different conclusion. Pichichero and colleagues had measured the excretion levels of mercury in the stools of 22 healthy infants exposed to Thimerosal-containing vaccines. A range was found for the infants aged two and six months of 23 to 141 nanograms per gram of stool (dry weight). Blaxill and Haley wrote: “The authors interpreted these levels, mere parts per billion, as positive evidence of mercury elimination.” When considering the amount of mercury the children might have been exposed to, though, and the expected volume of their stool, this rate of mercury elimination from the body would seem far too low to support a claim of “rapid excretion.” Blaxill and Haley considered the 187.5 micrograms of ethylmercury a child could have received by six months of age during the 1990s, and infant stool volumes ranging from 6 to 18 grams (dry weight) per day covering the newborn to six-month age period. Assuming the excretion rate reported by Pichichero, Blaxill and Haley demonstrated that it could take children with low excretion rates of mercury in their stool almost four years to eliminate a 187.5 microgram mercury burden from their bodies.376

In 2006, Luis Maya and Flora Luna expanded the critique of Pichichero’s study. The authors pointed out that while Pichichero’s team had found ethylmercury to be excreted in appreciable quantities in the feces, the researchers did not study other body parts beyond the blood, such as the central nervous system. In agreement with Halsey and Goldman, Maya and Luna criticized Pichichero for neglecting to measure the peak serum levels of ethylmercury after the first hours of inoculation, though other investigations had documented substantially elevated blood concentrations in the first forty-eight to seventy-two hours after administration in pediatric vaccines. Maya and Luna also pointed out that the study was small and measured variables of pharmacokinetics (the actions of a drug within the body over time), so it was not designed to measure the biological effect of Thimerosal as a preservative.381

After such attacks on their methodology and conclusions, Pichichero and his colleagues conducted a similar analysis on a larger group of infants at two and six months as well as newborns. This second paper in 2008 concluded that the half-life of ethylmercury in the blood was about four days. Pichichero and his colleagues wrote that “our measurements are unable to determine the fate of the mercury after it leaves the blood”; they also pointed out that “exposure guidelines based on oral methylmercury in adults may not be accurate for risk assessments in children who receive thimerosal-containing vaccines [because] of the differing pharmacokinetics of ethyl and methylmercury.”382

By then, other research had clarified that while ethylmercury disperses quickly from the bloodstream, this is not evidence of safety. For example, a 2004 study by G. Jean Harry of the National Institute of Environmental Health Sciences noted that mice injected with Thimerosal accumulated mercury in both the brain and kidneys.383 “By seven days” post-treatment, the study authors wrote, “mercury levels decreased in the blood but were unchanged in the brain” compared to levels measured just twenty-four hours after treatment, indicating slow clearance.384

A particularly significant study in this regard was conducted by the University of Washington’s Thomas Burbacher and was published in 2005.385 The researchers compared mercury levels in the blood and brains of infant macaques injected with Thimerosal-containing vaccines with monkeys who ingested equal amounts of methylmercury hydroxide via a feeding tube. The former group of primates were exposed to 20 micrograms of ethylmercury per kilogram of body weight on the day they were born and when they were seven, fourteen, and twenty-one days old, which was estimated to be within the range of doses that children at different developmental stages were receiving in the United States. The dosing methods were selected to mimic the routes of exposure in humans who eat mercury-containing foods and receive mercury-containing vaccines.

Subsequent tests showed a faster disappearance of mercury from the bloodstream of Thimerosal-injected monkeys than from the methylmercury group. Total mercury amounts in the brain were also threefold less for the Thimerosal-treated monkeys. However, the Thimerosal-injected monkeys had a higher ratio of brain-to-blood levels of mercury than the methylmercury group. In general, the primates injected with Thimerosal in the Burbacher study retained twice the level of inorganic mercury—a breakdown product of Thimerosal that has been suggested to be responsible for the brain damage associated with methylmercury—in their brains as the methylmercury-exposed primates. While all seventeen monkeys given Thimerosal had “readily” detectable levels of inorganic mercury in their brains, only nine of the seventeen exposed to methylmercury had detectable levels. Burbacher cited previous research ranging the half-life of inorganic mercury in various brain regions of primates from 227 to 540 days. In either case, that is a long time period for the toxic element to remain, especially if at higher levels from ethylmercury deposition versus methylmercury.

Burbacher and his colleagues wrote in summary that “[methylmercury] is not a suitable reference for risk assessment from exposure to thimerosal-derived [mercury]” and that: Data from the present study support the prediction that, although little accumulation of [mercury] in the blood occurs over time with repeated vaccinations, accumulation of [mercury] in the brain of infants will occur. Thus, conclusion [sic] regarding the safety of thimerosal drawn from blood [mercury] clearance data in human infants receiving vaccines may not be valid, given the significantly slower half-life of [mercury] in the brain as observed in the infant macaques.386

A more recent 2012 study by Croatian researchers took a similar approach as Burbacher’s study, but in suckling rats, and further evidences that the claims of ethylmercury’s comparative safety to other forms of mercury is unwarranted. Maja Blanusa and colleagues gave rat pups either Thimerosal or inorganic mercury three times in their first 11 days of life, mimicking human infant vaccination schedules. The scientists then assessed the total retention of mercury and excretion over six days. The Thimerosal-exposed rats showed higher mercury retention rates in their brains, in line with some other results described in this chapter. Furthermore, these Thimerosal-exposed rats exhibited similar fecal excretion and much lower urinary excretion compared to the inorganic mercury-exposed rats. That second group also demonstrated higher retention rates of mercury in organs other than the brain.387

Two additional studies in the last few years by researchers in Brazil and Germany show, again, that methylmercury in particular should not be considered summarily more dangerous than ethylmercury. The studies found that cells similarly take up both forms of mercury. The former, by Luciana Zimmermann and colleagues, showed in 2013 that the methyl- and ethylmercury entered cultured rat cells in roughly equal measure and display similar toxicities.388 The 2014 German study led by Christoph Wehe used novel laboratory techniques in concluding that methylmercury and ethylmercury in the form of Thimerosal accumulated in equal measure in a type of cultured human neural cell.389

Many studies, as we have seen, present substantial evidence that ethylmercury could well be more invasive, more persistent in the brain, and ultimately more toxic than methylmercury, in direct contrast with the CDC’s position. It only seems logical that our U.S. Federal agencies and the WHO should follow the precautionary principle and move forward with phasing out the use of thimerosal in all medical products, including vaccines.

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