To gain an understanding of the toxicity of mercury we must first separate the different types of mercury and their effects on the human body. All forms of mercury are toxic but each have slightly different effects and thresholds.
The EPA defines inorganic mercury as;
“Mercury in elemental form is a silver-coloured metal that exists as a thick liquid at room temperature, familiar to most people as the silver liquid inside mercury thermometers.”
Another name for inorganic mercury is elemental mercury, either term may be used for referencing the same substance in this article. Though it must be noted that there are non-elemental forms of inorganic mercury which are explained in the EPA document linked above.
With the exception of dental amalgams, environmental exposure to inorganic mercury is not high for most people.
Dental amalgams have been shown to release mercury vapour when in a moist environment by chemist Dr. Boyd Haley. Dr. Haley’s lectures have been uploaded on this topic and are available on youtube.
Mercury burden of human fetal and infant tissues. Eur J Pediatr 153:607-610 (1994)
Multiple studies have shown that inorganic mercury can and does, cross the placenta.
Safe exposure levels are listed by the EPA as 0.0003 mg/kg for chronic oral exposure.
Minimal risk level for inhalation is listed as 0.007 mg/kg.
Half life in the human brain is seen to be years to decades.
The retention time of inorganic mercury in the brain — A systematic review of the evidence doi:10.1016/j.taap.2013.12.011 PMID: 24368178
“Reports from human case studies indicate a half-life for inorganic mercury in the brain in the order of years—contradicting older radioisotope studies that estimated half-lives in the order of weeks to months in duration. This study systematically reviews available evidence on the retention time of inorganic mercury in humans and primates to better understand this conflicting evidence. A broad search strategy was used to capture 16,539 abstracts on the Pubmed database. Abstracts were screened to include only study types containing relevant information. 131 studies of interest were identified. Only 1 primate study made a numeric estimate for the half-life of inorganic mercury (227–540 days). Eighteen human mercury poisoning cases were followed up long term including autopsy. Brain inorganic mercury concentrations at death were consistent with a half-life of several years or longer. 5 radionucleotide studies were found, one of which estimated head half-life (21 days). This estimate has sometimes been misinterpreted to be equivalent to brain half-life—which ignores several confounding factors including limited radioactive half-life and radioactive decay from surrounding tissues including circulating blood. No autopsy cohort study estimated a half-life for inorganic mercury, although some noted bioaccumulation of brain mercury with age. Modelling studies provided some extreme estimates (69 days vs 22 years). Estimates from modelling studies appear sensitive to model assumptions, however predictions based on a long half-life (27.4 years) are consistent with autopsy findings. In summary, shorter estimates of half-life are not supported by evidence from animal studies, human case studies, or modelling studies based on appropriate assumptions. Evidence from such studies point to a half-life of inorganic mercury in human brains of several years to several decades. This finding carries important implications for pharmcokinetic modelling of mercury and potentially for the regulatory toxicology of mercury.”
Mercury, Cadmium, and Lead Levels in Human Placenta: A Systematic Review Environ Health Perspect; DOI:10.1289/ehp.1204952
Background: Placental tissue may furnish information on the exposure of both mother and fetus. Mercury (Hg), cadmium (Cd), and lead (Pb) are toxicants of interest in pregnancy because they are associated with alterations in child development.
Objectives: The aim of this study was to summarize the available information regarding total Hg, Cd, and Pb levels in human placenta and possible related factors.
Methods: We performed a systematic search of PubMed/MEDLINE, EMBASE, Lilacs, OSH, and Web of Science for original papers on total Hg, Cd, or Pb levels in human placenta that were published in English or Spanish (1976–2011). Data on study design, population characteristics, collection and analysis of placenta specimens, and main results were extracted using a standardized form.
Results: We found a total of 79 papers (73 different studies). Hg, Cd, and Pb levels were reported in 24, 46, and 46 studies, respectively. Most studies included small convenience samples of healthy pregnant women. Studies were heterogeneous regarding populations selected, processing of specimens, and presentation of results. Hg concentrations > 50 ng/g were found in China (Shanghai), Japan, and the Faroe Islands. Cd levels ranged from 1.2 ng/g to 53 ng/g and were highest in the United States, Japan, and Eastern Europe. Pb showed the greatest variability, with levels ranging from 1.18 ng/g in China (Shanghai) to 500 ng/g in a polluted area of Poland.
Conclusion: The use of the placenta as a biomarker to assess heavy metals exposure is not properly developed because of heterogeneity among the studies. International standardized protocols are needed to enhance comparability and increase the usefulness of this promising tissue in biomonitoring studies.
Placental DNA Methylation Related to Both Infant Toenail Mercury and Adverse Neurobehavioral Outcomes Environ Health Perspect; DOI:10.1289/ehp.1408561
Background: Prenatal mercury (Hg) exposure is associated with adverse child neurobehavioral outcomes. As Hg can interfere with placental functioning, and cross the placenta to target fetal brain, prenatal Hg exposure can negatively impact fetal growth and development directly and indirectly.
Objectives: To examine potential associations between prenatal Hg exposure assessed through infant toenail Hg, placental DNA methylation changes, and newborn neurobehavioral outcomes.
Methods: The methylation status of >485,000 CpG loci was interrogated in 192 placental samples using Illumina’s Infinium HumanMethylation450 BeadArray. Hg concentrations were analyzed in toenail clippings from a subset of 41 infants; neurobehavior was assessed using the NICU Network Neurobehavioral Scales (NNNS) in an independent subset of 151 infants.
Results: 339 loci were identified with an average methylation difference >0.125 between any two toenail Hg tertiles. Variation amongst these loci was subsequently found to be associated with a high-risk neurodevelopmental profile (omnibus p-value=0.007) characterized by the NNNS. Ten loci had p<0.01 for the association between methylation and the high-risk NNNS profile. Six of ten loci reside in the EMID2 gene and were hypomethylated in the 16 high-risk profile infants’ placentas. Methylation at these loci was moderately correlated (correlation coefficients range -0.33 to -0.45) with EMID2 expression.
Conclusions: EMID2 hypomethylation may represent a novel mechanism linking in utero Hg exposure and adverse infant neurobehavioral outcomes.
Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury Neuroreport. 2001 Mar 26;12(4):733-7 PMID: 11277574
Inhalation of mercury vapor (Hg0) inhibits binding of GTP to rat brain tubulin, thereby inhibiting tubulin polymerization into microtubules. A similar molecular lesion has also been observed in 80% of brains from patients with Alzheimer disease (AD) compared to age-matched controls. However the precise site and mode of action of Hg ions remain illusive. Therefore, the present study examined whether Hg ions could affect membrane dynamics of neurite growth cone morphology and behavior. Since tubulin is a highly conserved cytoskeletal protein in both vertebrates and invertebrates, we hypothesized that growth cones from animal species could be highly susceptible to Hg ions. To test this possibility, the identi®ed, large Pedal A (PeA) neurons from the central ring ganglia of the snail Lymnaea stagnalis were cultured for 48 h in 2 ml brain conditioned medium (CM). Following neurite outgrowth, metal chloride solution (2 ìl) of Hg, Al, Pb, Cd, or Mn (10ÿ7 M) was pressure applied directly onto individual growth cones. Time lapse images with inverted microscopy were acquired prior to, during, and after the metal ion exposure. We demonstrate that Hg ions markedly disrupted membrane structure and linear growth rates of imaged neurites in 77% of all nerve growth cones. When growth cones were stained with antibodies speci®c for both tubulin and actin, it was the tubulin/ microtubule structure that disintegrated following Hg exposure. Moreover, some denuded neurites were also observed to form neurobrillary aggregates. In contrast, growth cone exposure to other metal ions did not effect growth cone morphology, nor was their motility rate compromised. To determine the growth suppressive effects of Hg ions on neuronal sprouting, cells were cultured either in the presence or absence of Hg ions. We found that in the presence of Hg ions, neuronal somata failed to sprout, whereas other metallic ions did not effect growth patterns of cultured PeA cells. We conclude that this visual evidence and previous biochemical data strongly implicate Hg as a potential etiological factor in neurodegeneration.
Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000 Jan;74(1):231-6 PMID: 10617124
Concentrations of heavy metals, including mercury, have been shown to be altered in the brain and body fluids of Alzheimer's disease (AD) patients. To explore potential pathophysiological mechanisms we used an in vitro model system (SHSY5Y neuroblastoma cells) and investigated the effects of inorganic mercury (HgCl2) on oxidative stress, cell cytotoxicity, beta-amyloid production, and tau phosphorylation. We demonstrated that exposure of cells to 50 microg/L (180 nM) HgCl2 for 30 min induces a 30% reduction in cellular glutathione (GSH) levels (n = 13, p<0.001). Preincubation of cells for 30 min with 1 microM melatonin or premixing melatonin and HgCl2 appeared to protect cells from the mercury-induced GSH loss. Similarly, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cytotoxicity assays revealed that 50 microg/L HgCl2 for 24 h produced a 50% inhibition of MTT reduction (n = 9, p<0.001). Again, melatonin preincubation protected cells from the deleterious effects of mercury, resulting in MTT reduction equaling control levels. The release of beta-amyloid peptide (Abeta) 1-40 and 1-42 into cell culture supernatants after exposure to HgCl2 was shown to be different: Abeta 1-40 showed maximal (15.3 ng/ml) release after 4 h, whereas Abeta 1-42 showed maximal (9.3 ng/ml) release after 6 h of exposure to mercury compared with untreated controls (n = 9, p<0.001). Preincubation of cells with melatonin resulted in an attenuation of Abeta 1-40 and Abeta 1-42 release. Tau phosphorylation was significantly increased in the presence of mercury (n = 9, p<0.001), whereas melatonin preincubation reduced the phosphorylation to control values. These results indicate that mercury may play a role in pathophysiological mechanisms of AD.
Methylmercury - elemental mercury that has oxidized and then had a methyl group added.
Frequent exposure through food, predominantly fish. Up to 95% absorption rate when ingested.
Biological half life in the blood is 50 days, only 1 - 10% goes into the blood, prefers fatty tissues with up to 50% of dose found in the brain. Slowly demethylated to become inorganic mercury in the body, methylmercury takes about 70-80 days to be eliminated from the body with the inorganic remaining in the fatty tissues.
Safe levels for chronic oral exposure are considered to be 0.1 mg/kg, no data available for other routes of exposure. The EPA did an IRIS write up that you can view here and another on the health effects of methylmercury can be seen here: http://www.epa.gov/hg/effects.htm.
Ethylmercury - Most frequent exposure source is biological pharmaceutical products and dry fungicides. A much longer list can be found here.
In Dr. Magos paper, Answers to Questions on the Toxicity of Ethylmercury he explains that ethylmercury degrades into inorganic mercury at a significantly faster rate than methylmercury. We also learn that studies comparing methyl and ethyl mercury exposure have found that ethylmercury exposed rats have much higher levels of inorganic mercury in their brains compared to the rats exposed to methylmercury.
Safe exposure levels have not been established. Ethylmercury has a biological half life of 30 - 50 days. Inorganic mercury resulting from the breakdown of ethylmercury will remain in the fatty tissues.
A systematic study of the disposition and metabolism of mercury species in mice after exposure to low levels of thimerosal (ethylmercury). doi:10.1016/j.envres.2014.07.009 PMID: 25173055
“Thimerosal (TM) is an ethylmercury (etHg)-containing preservative used in some vaccines despite very limited knowledge on the kinetics and direct interaction/effects in mammals׳ tissues after exposure. Thus, this study aimed to evaluate the kinetics of Hg species in mice in a time course analysis after intramuscular injection of TM, by estimating Hg half-lives in blood and tissues. Mice were exposed to one single intramuscular dose of 20 µg of Hg as TM. Blood, brain, heart, kidney and liver were collected at 0.5 hour (h), 1 h, 8 h, 16 h, 144 h, 720 h and 1980 h after TM exposure (n=4). Hg species in animal tissues were identified and quantified by speciation analysis via liquid chromatography hyphenated with inductively coupled mass spectrometry (LC–ICP-MS). It was found that the transport of etHg from muscle to tissues and its conversion to inorganic Hg (inoHg) occur rapidly. Moreover, the conversion extent is modulated in part by the partitioning between EtHg in plasma and in whole blood, since etHg is rapidly converted in red cells but not in a plasma compartment. Furthermore, the dealkylation mechanism in red cells appears to be mediated by the Fenton reaction (hydroxyl radical formation). Interestingly, after 0.5 h of TM exposure, the highest levels of both etHg and inoHg were found in kidneys (accounting for more than 70% of the total Hg in the animal body), whereas the brain contributed least to the Hg body burden (accounts for <1.0% of total body Hg). Thirty days after TM exposure, most Hg had been excreted while the liver presented the majority of the remaining Hg. Estimated half-lives (in days) were 8.8 for blood, 10.7 for brain, 7.8 for heart, 7.7 for liver and 45.2 for kidney. Taken together, our findings demonstrated that TM (etHg) kinetics more closely approximates Hg2+ than methylmercury (meHg) while the kidney must be considered a potential target for etHg toxicity.”
The evidence base showing the toxicity of mercury is large, however some have tried to dismiss any ideas that say there is a risk with Thimerosal. Given the evidence that shows the breakdown of ethylmercury into inorganic mercury we are left with the personal burden of verifying or dismissing the risks for ourselves. Let us start looking at some studies comparing exposures.
Identification and distribution of mercury species in rat tissues following administration of thimerosal or methylmercury. 2010 Nov;84(11):891-6. doi: 10.1007/s00204-010-0538-4. PMID: 20386881
Methylmercury (Met-Hg) is one the most toxic forms of Hg, with a considerable range of harmful effects on humans. Sodium ethyl mercury thiosalicylate, thimerosal (TM) is an ethylmercury (Et-Hg)-containing preservative that has been used in manufacturing vaccines in many countries. Whereas the behavior of Met-Hg in humans is relatively well known, that of ethylmercury (Et-Hg) is poorly understood. The present study describes the distribution of mercury as (-methyl, -ethyl and inorganic mercury) in rat tissues (brain, heart, kidney and liver) and blood following administration of TM or Met-Hg. Animals received one dose/day of Met-Hg or TM by gavage (0.5 mg Hg/kg). Blood samples were collected after 6, 12, 24, 48, 96 and 120 h of exposure. After 5 days, the animals were killed, and their tissues were collected. Total blood mercury (THg) levels were determined by ICP-MS, and methylmercury (Met-Hg), ethylmercury (Et-Hg) and inorganic mercury (Ino-Hg) levels were determined by speciation analysis with LC-ICP-MS. Mercury remains longer in the blood of rats treated with Met-Hg compared to that of TM-exposed rats. Moreover, after 48 h of the TM treatment, most of the Hg found in blood was inorganic. Of the total mercury found in the brain after TM exposure, 63% was in the form of Ino-Hg, with 13.5% as Et-Hg and 23.7% as Met-Hg. In general, mercury in tissues and blood following TM treatment was predominantly found as Ino-Hg, but a considerable amount of Et-Hg was also found in the liver and brain. Taken together, our data demonstrated that the toxicokinetics of TM is completely different from that of Met-Hg. Thus, Met-Hg is not an appropriate reference for assessing the risk from exposure to TM-derived Hg. It also adds new data for further studies in the evaluation of TM toxicity.
Comparison of organic and inorganic mercury distribution in suckling rat. J Appl Toxicol. 2006 Nov-Dec;26(6):536-9 PMID: 17080402
Thimerosal is used as a preservative in vaccines given to small children. The metabolic product of thiomersal is ethylmercury and its distribution and kinetics are still not known, especially at this early age. The purpose of this study was to compare the body distribution of two forms of mercury: organic (thimerosal) and inorganic (mercury(2+) chloride) in very young, suckling rats. Mercury was applied subcutaneously three times during the suckling period on days 7, 9 and 11 of pups age, imitating the vaccination of infants. A single dose of mercury was equimolar in both exposed groups, i.e. 0.81 µmol Hg kg−1. At 14 days of age the animals were killed and the total mercury analysed in blood and organs (kidney, liver and brain). The analytical method applied was total decomposition, amalgamation, atomic absorption spectrometry. The results showed that the level of mercury was higher in the liver and kidney of the inorganic mercury group than in the thimerosal exposed group. However, the brain and blood concentrations of mercury were higher in the thimerosal exposed group. These results need to be clarified by additional data on the kinetic pathways of ethylmercury compared with inorganic mercury.
Mercury deposition in suckling rats: comparative assessment following parenteral exposure to thimerosal and mercuric chloride. J Biomed Biotechnol. 2012;2012:256965. doi: 10.1155/2012/256965 PMID: 22899883
Due to the facts that thimerosal-containing vaccine is still in use in many developing countries, and all forms of mercury have recognised neurotoxic, nephrotoxic, and other toxic effects, studies on disposition of ethylmercury and other mercury forms are still justified, especially at young age. Our investigation aimed at comparing mercury distribution and rate of excretion in the early period of life following exposure to either thiomersal (TM) or mercuric chloride (HgCl2) in suckling rats. Three experimental groups were studied: control, TM, and HgCl2, with 12 to 18 pups in each. Both forms of mercury were administered subcutaneously in equimolar quantities (0.81 μmol/kg b.w.) three times during the suckling period (on the days of birth 7, 9, and 11) to mimic the vaccination regimen in infants. After the last administration of TM or HgCl2, total mercury retention and excretion was assessed during following six days. In TM-exposed group mercury retention was higher in the brain, enteral excretion was similar, and urinary excretion was much lower compared to HgCl2-exposed sucklings. More research is still needed to elucidate all aspects of toxicokinetics and most harmful neurotoxic potential of various forms of mercury, especially in the earliest period of life.
Thimerosal-containing hepatitis B vaccination and the risk for diagnosed specific delays in development in the United States: a case-control study in the vaccine safety datalink. N Am J Med Sci. 2014 Oct;6(10):519-31. doi: 10.4103/1947-2714.143284 PMID: 25489565
Background: Within the first 3 years of life, the brain develops rapidly. Its development is characterized by critical developmental periods for speech, vision, hearing, language, balance, etc.; and alteration in any of the processes occurring in those critical periods can lead to specific delays in development.
Aims: The present study evaluated the potential toxic effects of organic-mercury exposure from Thimerosal (49.55% mercury by weight) in childhood vaccines and its hypothesized possible relationship with specific delays in development.
Materials and Methods: A hypothesis testing case-control study was undertaken to evaluate the relationship between exposure to Thimerosal-containing hepatitis B vaccines administered at specific intervals in the first 6 months among cases diagnosed with specific delays in development and controls born between 1991-2000, utilizing data in the Vaccine Safety Datalink database.
Results: Cases were significantly more likely than controls to have received increased organic-mercury from Thimerosal-containing hepatitis B vaccine administered in the first, second, and sixth month of life.
Conclusion: Though routine childhood vaccination may be an important public health tool to reduce the morbidity and mortality associated with infectious diseases, the present study supports an association between increasing organic-mercury exposure from Thimerosal-containing childhood vaccines and the subsequent risk of specific delays in development among males and females.
A Case-Control Study Evaluating the Relationship Between Thimerosal-Containing Haemophilus influenzae Type b Vaccine Administration and the Risk for a Pervasive Developmental Disorder Diagnosis in the United States. Biol Trace Elem Res. 2015 Feb;163(1-2):28-38. doi: 10.1007/s12011-014-0169-3 PMID: 25382662
Thimerosal is an organic mercury (Hg)-containing compound (49.55 % Hg by weight) historically added to many multi-dose vials of vaccine as a preservative. A hypothesis testing case-control study evaluated automated medical records in the Vaccine Safety Datalink (VSD) for organic Hg exposure from Thimerosal in Haemophilus influenzae type b (Hib)-containing vaccines administered at specific times within the first 15 months of life among subjects diagnosed with pervasive developmental disorder (PDD) (n = 534) in comparison to controls. The generally accepted biologically non-plausible linkage between Thimerosal exposure and subsequent diagnosis of febrile seizure (n = 5886) was examined as a control outcome. Cases diagnosed with PDD received significantly more organic Hg within the first 6 months of life (odds ratio (OR) = 1.97, p < 0.001) and first 15 months of life (OR = 3.94, p < 0.0001) than controls, whereas cases diagnosed with febrile seizure were no more likely than controls to have received increased organic Hg. On a per microgram of organic Hg basis, cases diagnosed with a PDD in comparison to controls were at significantly greater odds (OR = 1.0197, p < 0.0001) of receiving increasing organic Hg exposure within the first 15 months of life, whereas cases diagnosed febrile seizure were no more likely than controls (OR = 0.999, p > 0.20) to have received increasing organic Hg exposure within the first 15 months of life. Routine childhood vaccination is an important public health tool to reduce the morbidity and mortality associated with infectious diseases, but the present study provides new epidemiological evidence of a significant relationship between increasing organic Hg exposure from Thimerosal-containing vaccines and the subsequent risk of PDD diagnosis in males and females.
Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats. Behav Brain Res. 2011 Sep 30;223(1):107-18. doi: 10.1016/j.bbr.2011.04.026 PMID: 21549155
The neurotoxic organomercurial thimerosal (THIM), used for decades as vaccine preservative, is a suspected factor in the pathogenesis of some neurodevelopmental disorders. Previously we showed that neonatal administration of THIM at doses equivalent to those used in infant vaccines or higher, causes lasting alterations in the brain opioid system in rats. Here we investigated neonatal treatment with THIM (at doses 12, 240, 1440 and 3000 μg Hg/kg) on behaviors, which are characteristically altered in autism, such as locomotor activity, anxiety, social interactions, spatial learning, and on the brain dopaminergic system in Wistar rats of both sexes. Adult male and female rats, which were exposed to the entire range of THIM doses during the early postnatal life, manifested impairments of locomotor activity and increased anxiety/neophobia in the open field test. In animals of both sexes treated with the highest THIM dose, the frequency of prosocial interactions was reduced, while the frequency of asocial/antisocial interactions was increased in males, but decreased in females. Neonatal THIM treatment did not significantly affect spatial learning and memory. THIM-exposed rats also manifested reduced haloperidol-induced catalepsy, accompanied by a marked decline in the density of striatal D2 receptors, measured by immunohistochemical staining, suggesting alterations to the brain dopaminergic system. Males were more sensitive than females to some neurodisruptive/neurotoxic actions of THIM. These data document that early postnatal THIM administration causes lasting neurobehavioral impairments and neurochemical alterations in the brain, dependent on dose and sex. If similar changes occur in THIM/mercurial-exposed children, they could contribute to neurodevelopmental disorders.
Maternal thimerosal exposure results in aberrant cerebellar oxidative stress, thyroid hormone metabolism, and motor behavior in rat pups; sex- and strain-dependent effects. Cerebellum. 2012 Jun;11(2):575-86. doi: 10.1007/s12311-011-0319-5 PMID: 22015705
Methylmercury (Met-Hg) and ethylmercury (Et-Hg) are powerful toxicants with a range of harmful neurological effects in humans and animals. While Met-Hg is a recognized trigger of oxidative stress and an endocrine disruptor impacting neurodevelopment, the developmental neurotoxicity of Et-Hg, a metabolite of thimerosal (TM), has not been explored. We hypothesized that TM exposure during the perinatal period impairs central nervous system development, and specifically the cerebellum, by the mechanism involving oxidative stress. To test this, spontaneously hypertensive rats (SHR) or Sprague–Dawley (SD) rat dams were exposed to TM (200 μg/kg body weight) during pregnancy (G10–G15) and lactation (P5–P10). Male and female neonates were evaluated for auditory and motor function; cerebella were analyzed for oxidative stress and thyroid metabolism. TM exposure resulted in a delayed startle response in SD neonates and decreased motor learning in SHR male (22.6%), in SD male (29.8%), and in SD female (55.0%) neonates. TM exposure also resulted in a significant increase in cerebellar levels of the oxidative stress marker 3-nitrotyrosine in SHR female (35.1%) and SD male (14.0%) neonates. The activity of cerebellar type 2 deiodinase, responsible for local intra-brain conversion of thyroxine to the active hormone, 3′,3,5-triiodothyronine (T3), was significantly decreased in TM-exposed SHR male (60.9%) pups. This coincided with an increased (47.0%) expression of a gene negatively regulated by T3, Odf4 suggesting local intracerebellar T3 deficiency. Our data thus demonstrate a negative neurodevelopmental impact of perinatal TM exposure which appears to be both strain- and sex-dependent.
Neonatal administration of thimerosal causes persistent changes in mu opioid receptors in the rat brain. Neurochem Res. 2010 Nov;35(11):1840-7. doi: 10.1007/s11064-010-0250-z PMID: 20803069
Thimerosal added to some pediatric vaccines is suspected in pathogenesis of several neurodevelopmental disorders. Our previous study showed that thimerosal administered to suckling rats causes persistent, endogenous opioid-mediated hypoalgesia. Here we examined, using immunohistochemical staining technique, the density of μ-opioid receptors (MORs) in the brains of rats, which in the second postnatal week received four i.m. injections of thimerosal at doses 12, 240, 1,440 or 3,000 μg Hg/kg. The periaqueductal gray, caudate putamen and hippocampus were examined. Thimerosal administration caused dose-dependent statistically significant increase in MOR densities in the periaqueductal gray and caudate putamen, but decrease in the dentate gyrus, where it was accompanied by the presence of degenerating neurons and loss of synaptic vesicle marker (synaptophysin). These data document that exposure to thimerosal during early postnatal life produces lasting alterations in the densities of brain opioid receptors along with other neuropathological changes, which may disturb brain development.
Integrating experimental (in vitro and in vivo) neurotoxicity studies of low-dose thimerosal relevant to vaccines. Neurochem Res. 2011 Jun;36(6):927-38. doi: 10.1007/s11064-011-0427-0 PMID: 21350943
Neurotoxic effects of thimerosal at vaccines doses on the encephalon and development in 7 day-old hamsters. An. Fac. med. [online]. 2007, vol.68, n.3, pp. 222-237. ISSN 1025-5583.
An assessment of the impact of thimerosal on childhood neurodevelopmental disorders. Pediatric Rehabil 6: 97-102, 2003. PMID: 14534046
Full copy here:
A meta-analysis epidemiological assessment of neurodevelopmental disorders following vaccines administered from 1994 through 2000 in the United States. Neuro Endocrinol Lett. 2006 Aug;27(4):401-13 PMID: 16807526
Full copy here:
An Evaluation of the Effects of Thimerosal on Neurodevelopmental Disorders Reported Following DTP and Hib Vaccines in Comparison to DTPH Vaccine in the United States DOI:10.1080/15287390500364556
Effect of thimerosal, a preservative in vaccines, on intracellular Ca+2 concentration of ra cerebellar neurons. Toxicology 195: 77-84, 2004. PMID: 14698570
Thimerosal and Animal Brains: New Data for Assessing Human Ethylmercury Risk Environ Health Perspect. 2005 Aug; 113(8): A543–A544 PMCID: PMC1280369
BIOMEDICAL ASPECTS OF EXPOSURE TO MERCURY AND ORGANIC MERCURY COMPOUNDS Dr. Boyd Haley
The comparative toxicology of ethyl- and methylmercury. Arch Toxicol. 1985 Sep;57(4):260-7 PMID: 4091651
This was the shortest I could make the list of studies, with the clearest studies out of the ones I found. If you made it through even a fraction of these studies then you know from the research that Ethylmercury prior to breakdown is more toxic to the kidneys, and Methylmercury prior to breakdown is more toxic to the brain. After breakdown into inorganic mercury both are toxic to the brain (and other organs). Ethylmercury breaks down into inorganic mercury much faster than methylmercury, resulting in more inorganic mercury being caught in the fatty tissues and faster clearance from the blood.
The EPA declares in their handout on organic mercury that there is “no data” on the toxicity of thimerosal. If this was true that would mean that it was used in vaccines and other products without any safety studies being done. That alone is a significant problem. At this point most vaccines do not contain thimerosal after the manufacturer's voluntarily removed it for PR reasons. However we know that inorganic mercury can persist in the fatty tissues for decades and that it crosses the placenta. We also know that using methylmercury is inappropriate for measuring the risks of ethylmercury in thimerosal. This poses serious questions about past vaccines having adverse consequences for babies being born now and their heavy metal burdens at birth.
Additionally, despite claims saying that thimerosal is safe we can see that injuries from thimerosal occur and are compensated.
The Federal Claims Court has in their summary for the year 10/01/2013 - 09/30/2014 many cases pertaining to thimerosal specific injuries.
In closing, I feel the need to ask why these studies and many others are being ignored by governing bodies on the health policies around the world… What is to be gained by a chronically ill population? And why are the very one’s entrusted with our health, doctors, remaining ignorant of even a fraction of this information?