A recent study apparently in conflict with the general view about mercury hazard to infants:  Should child-bearing women be cautious about seafood consumption, or does this study show that to be unnecessary?


According to a publication of the National Scientific Council on the Developing Child, on a Harvard University website, At levels frequently measured in our environment, heavy metals (which include mercury) interfere with the construction of the basic framework of the maturing brain as well as with its function. These toxic effects include disruption of neural cell migration from one part of the brain to another, as well as the formation of synapses….”1  Lead is one of the heavy metals that is well known for its neurodevelopmental toxicity, but mercury is another one whose toxic properties are also well established.  One especially toxic form of mercury, methylmercury, is present in significant concentrations in the typical human body, mainly as a result of consumption of fish and seafood that contain it.2  Long-term, low-dose exposure to methylmercury stemming from maternal consumption of fish and seafood is recognized as neurodevelopmentally toxic to the fetus/infant.3  Strong basis for that belief is reflected in a 2010 systematic review of 48 articles about studies conducted in the U.S. and four other countries,4 and in other studies as well.5  Developmental neurotoxicity of organic mercury (which includes methylmercury) “has been observed at very low exposure levels,” according to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR).6   At least five published studies have found high levels of mercury in those with ASD.7  For additional specific evidence about harmful effects of methylmercury, go to Appendix B.


Additional evidence that everyday exposures of infants to mercury are at hazardous levels:  The maximum mercury concentration allowed in bottled water, according to U.S. Federal Regulations, is 2 ppb (parts per billion).8  In contrast with that, the U.S.  ATSDR, based on the available information from various countries of the world, estimated that the mean concentration of mercury in breast milk of non-exposed women is 8 ppb.9  Notice that this figure applied to women without unusual exposure to mercury; it is important to bear in mind that large numbers of people in the general population are in the more-exposed category, including those who eat larger amounts of fish and seafood (especially of certain species), many people working with art materials, some who work in dental offices, recycling facilities or laboratories, those with large numbers of dental amalgam fillings, those who live or work in buildings painted on the inside with mercury-containing latex paints or who use certain cosmetics, and many who live or work near or downwind from coal-burning power plants, municipal or medical incinerators, or waste disposal sites; mercury is also present in vehicle emissions, especially in diesel emissions,10 which is very significant in that a major 2013 study found that autism prevalence correlates closely with geographic locations where diesel emissions are known to be high.11, and two California studies have found autism to be increased near freeways.


Considering all of the above, it has been with good reason that child-bearing women have been cautioned by public health authorities to minimize ingestion of mercury by avoiding excessive consumption of fish and seafood, especially certain species, since that is known to be the main avenue of human ingestion of methylmercury.  Given that, it may have been puzzling to read about the findings of major studies carried out in the Republic of Seychelles, where fish consumption is high, which detected no association between high mercury levels in mothers at or near the time of birth and later neurological problems in their children.12


The designated committee of the U.S. National Research Council, in its National Academies publication in the year 2000, considered the high quality and size of a 1990’s study, also carried out in the Seychelles, that did not find toxic effects of maternal mercury.  They compared that with the even more substantial evidence to the contrary from other human (and animal) studies; they were trying to determine a safe level of exposure to this chemical, and they stated that the “conflicting results (the Seychelles study conflicting with studies conducted elsewhere) present a vexing choice.”13  The National Research Council decided not to use the Seychelles study in determining risk of methylmercury exposure simply because its findings were in apparent conflict with the weight of evidence provided by the other high-quality studies.(p. 299 of reference 14)  The expert on neurodevelopmental toxicology, D.C. Rice, called the Seychelles study “anomalous” in comparison with the findings of eight other studies.15  A similar apparent conflict arose again in 2013 when another highly-authoritative study, also carried out in the Seychelles, again arrived at a conclusion that seemed to disagree with the established body of knowledge about toxicity of maternal methylmercury.16 


But there is no need to be vexed by what seems to be repeated disagreement between the Seychelles studies and all the rest of the studies on effects of maternal methylmercury.  There wasn’t really disagreement; one only needs to be aware that (a) there was extremely little lactational exposure of infants to methylmercury in the Seychelles (details below), and (b) lactational exposure is likely to be the major source of harm.  To read about the authoritatively recognized vulnerability of an infant’s neurological development to postnatal toxic exposures, as well as evidence that lactation is effective at transferring most of a grown person’s accumulations of developmental toxins to a developing infant, as part of a postnatal surge, see “Postnatal vulnerability to toxins” below.  Add to that the evidence that transfers of mercury by lactation are in doses normally exceeding established safe levels by hundreds of per cent.(see paragraph 2 above and reference 17)  


Note also that, in addition to many studies that have found evidence of neurodevelopmental toxicity of low-dose postnatal exposure to mercury, there have been at least two that found evidence of toxicity of postnatal exposure to mercury while specifically finding no evidence of toxicity of prenatal exposure to mercury.18  


After knowing the significance of lactational exposure to mercury, completing the picture started above only requires awareness that exclusive breastfeeding is extraordinarily low in the Seychelles.  Exclusive breastfeeding at 6 months in the Seychelles in 2008 was one-eighth as high as in the U.S.;19 and the U.S. in turn was fifth from the bottom of an authoritative 2003 chart of initial breastfeeding rates in 86 countries of the world.20  The major studies from which the National Research Council drew its principal evidence of harmful developmental effects of mercury were carried out in the Faroes Islands and New Zealand; both of those countries have high breastfeeding rates.21, 22


The above is worth focusing on for a moment:  The Seychelles had a breastfeeding rate one-eighth as high as the equivalent rate in one of the world’s lowest-breastfeeding countries.  If breastfeeding is an important means of transferring serious doses of mercury to infants, during a period when neurological development is vulnerable to mercury (see Postnatal vulnerability to toxins” below), consider the significance of that extremely low rate of breastfeeding in Seychelles.  Should it be a surprise that harm resulting from developmental mercury exposure is hard to find there?


So the authoritative Seychelles studies, in apparent conflict with studies conducted elsewhere, aren’t really in conflict with the other studies after all; they merely help clarify the exact stage at which the most harmful transfers of mercury are probably taking place.


To re-state the basic point explained above:  No harmful effects of high maternal levels of a well-recognized neurodevelopmental toxin (methylmercury) were found in children in a country with exceptionally low breastfeeding.  The authorities who were trying to determine which exposures are unsafe didn’t really need to be vexed by the seemingly conflicting studies, they merely needed to abandon their assumption that the potentially harmful exposures are prenatal, and then look into comparative breastfeeding rates. There was no lack of effect of mercury in the case of the Seychelles, instead there was lack of transfer of mercury to the infant during the especially vulnerable time.


Postnatal vulnerability to toxins:

The highly-published expert, P. Grandjean, in an article in the American Journal of Epidemiology states:  “The nervous system is particularly vulnerable to effects from neurotoxicants such as methylmercury during the last two trimesters of pregnancy and during early postnatal life.”23  Statements by WHO, the U.S. ATSDR, and the U.S. EPA all say essentially the same thing about postnatal vulnerability of infants to mercury. (See Appendix A)


As mentioned earlier, typical breast milk has mercury concentrations four times the level that is permitted by law in U.S. bottled water, and many women have higher concentrations.  What becomes of the mercury in women’s bodies (how heavily infants could be affected by it) is worth thinking about: 

-- a 1998 German study found that concentrations of mercury in breast milk of 85 lactating women at two months after birth had declined by an average of over 70% from their levels at time of birth;24


-- According to researchers contracted by the EPA, "a wealth of information" indicates that lactational transfer of maternal mercury during the first 15 days of lactation is equal to about a third of the total transfer of mercury that takes place during gestation.25


-- a 2007 study of 82 mother-infant pairs found that mercury levels in mothers’ hair decreased 57% during six months of lactation;26


-- According to a 1999 Swedish study, “there was a marked decrease in I-Hg (inorganic mercury) in (the mothers’) blood and urine during lactation, most likely related to the excretion of I-Hg in milk…. About 10% of the Hg (mercury) present in circulating blood (5 L]0.3 lg/L) would be transferred to the milk every day.”27   (Obviously, the mother also keeps taking in mercury.)


-- Evidence from the Iraqi poisoning incident showed that lactation decreased blood mercury clearance half-times in women by 44%.(27a)


-- In addition to infants’ high ingestion of mercury via breastfeeding, absorption of mercury also appears to be high while the infant is on a milk-based diet, as indicated in an experiment with monkeys.(27b)


 -- In a study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.(27c) 


--  Another study found over-200% increases in infant mercury levels due to 6 months of breastfeeding.(27d)


 Based on considerable earlier research, a 2013 study in the National Library of Medicine generalized, “the cerebellum has emerged as a region of interest in autism studies because of converging findings from human postmortem research, human neuroimaging studies, and animal models…. Evidence appears to support cerebellar dysfunction…as a contributor to the autism phenotype.”28   In relation to that, according to the ATSDR, “the predominant neuropathological feature (of effects of methylmercury exposure) is degenerative changes in the cerebellum.29  As mentioned earlier, many studies have found high mercury levels in those diagnosed with autism. 

The EPA-contracted research group referred to earlier provides good reason to be especially concerned about postnatal infant ingestion of mercury, which is that "the brain is especially vulnerable (to metals) during the brain growth spurt."(30)  Notice in this chart that most of the brain growth spurt, especially in the cerebellum, takes place in the year after birth.  And note that this period of maximum vulnerability to metals occurs at the same time as a breastfed infant is ingesting a surge of mercury that will transfer to the infant much or most of a grown person’s accumulation of that toxin. (see the indented section above)  And remember from the previous paragraph the close connection between cerebellar dysfunction and autism, as well as the harmful effect of methylmercury on the cerebellum.


While noting in this chart the major amount of growth of the brain taking place postnatally, note that tissues undergoing growth (to which cell division is important) are especially vulnerable to methylmercury, since “methylmercury is known to inhibit cell division by causing metaphase arrest,” according to a WHO publication (31)



There are many close similarities between known effects of mercury and traits of ASD.  Those include (a) mercury’s known latency (of months to years) after exposure before effects become apparent, which is relevant to autism’s pattern of late emergence and/or regression, (b) abnormal social behavior, and (c) many others, which can be read about in section 5.b of


Timing of the brain’s maximum vulnerability to toxins in general:   According to EPA researchers, an organ is generally at its greatest vulnerability to environmental toxicants if exposure to the toxins occurs during development of that organ.32  Note in the above chart the similarity between the period of breastfeeding (with its transmission of high levels of other toxins as well as mercury -- see below) and the period of the greatest amount of growth of the brain.


Laboratory experiments with animals are widely conducted to find effects of various potential toxins on the brain, under carefully-controlled conditions.  An experiment with prairie voles (which have similarities to humans in social interaction) found that chronic ingestion of mercury in environmentally-relevant doses substantially reduced social contact by male voles when they were given a choice between isolation or contact with an unfamiliar same-sex mole. The effects of metals ingestion were specific to males: no effects of metals exposure were seen in females.  The authors concluded, “thus, an ecologically relevant stimulus (mercury ingestion) produced two of the hallmark characteristics of autism – social avoidance and a male-oriented bias…..”32a


Although most of this article deals with mercury and its effects, it should also be pointed out that there are other important toxins that could also be contributing to problems in neurological development of infants.  Some that stand out are dioxins (including their chemical relatives, PCBs) and PBDEs; those appear to be the only other developmental toxins (besides mercury) that are known to be ingested in concentrations that (like mercury) are known to greatly exceed established safe levels in typical human milk. (See  As indicated at that website, with authoritative sources, most of those toxins (including mercury) are present in infant formula in concentrations less than 2% as high, and usually less than 1% as high, as in human milk.


Some may wonder why human milk should be so much higher in mercury than cows’ milk or infant formula.  Aside from fish and other seafood, the principal source of mercury in typical human bodies is absorption of matter originating from dental amalgam, which is about 50% mercury.  See the second paragraph at the top of this article about other sources that especially affect many mothers, including residence near municipal or hospital waste incinerators, being near diesel emissions or high vehicle traffic, working with certain art materials or in dental offices or some laboratories, use of certain cosmetics, being inside buildings with certain kinds of paint, etc.  It should therefore not be surprising that products of cows and soybean fields do not have the mercury concentrations that are found in human milk. The only readily-found survey of mercury in infant formula products (in Canada, 2003) found the average mercury level in milk-based, ready-to-use formula to be 0.028 ng/g (=.028 billionths of a gram per gram, or 0.028 ppb).33  This is well below one percent of the mercury concentration in average breast milk, going by the best available data as quoted above.  In addition:  A study (Hapke, 1991) found that “cattle are able to demethylate mercury in the rumen and thus absorb less mercury.”


The question is also likely to come up as to why serious effects of postnatal exposure to mercury should be found, considering the widespread impression that neurodevelopmental harm resulting from toxins is likely to occur from prenatal exposures.  The answer to that question is somewhat lengthy, including the recognition by many experts and health-related government agencies of harmful effects of postnatal exposures to toxins, the tremendous increases in exposures to toxins postnatally compared with prenatal exposures, the large number of published studies that have found neuro-developmental harm to result from specifically postnatal exposures, and explanation of how incorrect impressions grow. For a complete statement on the above subject, go to


Another logical question is, why should levels of mercury and other toxins in breast milk be a source of developmental harm these days when they weren’t in earlier times?  Aside from exposures to mercury via dental amalgam, by far the largest proportions of human exposures to these toxins in the environment originate as products of modern combustion (of fossil fuels) and industrial processes.  Mercury is naturally present in the environment, but humans receive little exposure to it except from sources that originate from modern human activity.  Mercury emitted by coal-fired power plants drifts for thousands of miles and settles into bodies of water, where it builds up in the tissues of fish and seafood, reaching much higher levels in larger fish that are higher up in the aquatic food chain, thereby becoming the other major source of mercury in humans.  Despite efforts by the EPA, mercury in the environment has only been increasing at a less rapid pace than otherwise.  According to a document on mercury of the U.S. Agency for Toxic Substances and Disease Registry on their website in December of 2014, “environmental levels of mercury are continuing to rise.”(33a)



One implication of the above is that, if we want to avoid transferring the most harmful doses of toxins to infants, we should seek to minimize the postnatal transfers. The most effective way to do that would be to depart from the breastfeeding recommendations that have been increasingly followed in recent decades.  But those policies have considerable support in the population and among doctors. However, there are additional good reasons for reconsidering those recommendations:


-- High infant exposures to serious developmental toxins could be avoided by means of parents’ reverting to bottle feeding of infants, which was the predominant feeding type in the mid-20th century,35 without negative health effects being apparent as of a half-century later. (See below for comparisons with later periods.)


 -- Four decades of historical child health data (mainly from the CDC) have shown that the major increases in breastfeeding rates since 1971 have been followed by substantial increases in all but one of the disorders that are alleged by the U.S. Surgeon General to be reduced by breastfeeding.36


-- Epidemics and increases of other childhood disorders (diabetes, asthma, allergies, obesity, ADHD and apparently mental retardation and autism) came about following the transition from low to high breastfeeding rates.37


-- Good reason to see a reversion to mainly bottle-feeding as a reasonable alternative, compared with the type of infant feeding that is high in known neuro-developmental toxins, can be found in

-- the historical record (see above),

-- the 50+ studies that have found adverse effects of breastfeeding,38 and

-- the increasingly wide acceptance of the “hygiene hypothesis” as an explanation for the increases in immunity-related diseases (including asthma, allergies and type 1 diabetes) among children;39 according to this hypothesis, microbial exposure in contemporary developed countries is already too low to provide the needed stimulus for proper development of children’s immune systems, due to increases in hygiene in recent times; the additional shielding of infants from microbes as provided by the immune cells in breast milk should be seen in that light.



In closing, it is interesting to note the results of another study of effects of mercury that was carried out in the Seychelles (Davidson et al., 201039a), as follows: Fig. 3

Investigating children exposed to mercury by way of high seafood consumption, it was found that prenatal exposures had no significant effects, but postnatal exposures did appear to have substantial adverse effects on male children when tested at ages 9 and 17. (See charts.)



On the left are large sections of Figures 1 and 2 from the above-mentioned study, consolidated here.  Results are shown for a number of different scholastic achievement tests administered to children who had varying levels of mercury; for six of those tests, results were indicated by gender (as seen in these charts).  The tests that were not broken down by gender showed no consistent associations of mercury with achievement, in contrast with the results that were shown separately for males and females, in these charts.  The authors acknowledged what is undeniable in these charts by saying, “we did find significant adverse associations between recent postnatal MeHg (methyl mercury) hair level and outcomes” in boys only, which they said was compatible with a report of “some adverse effects” of postnatal MeHg exposure.  But beyond that they said little more than that the gender effects were “intriguing,” that their “findings are sporadic and not consistent,”(!) and that “this outcome does not constitute evidence of any pattern of associations between MeHg and achievement.”  While reading those surprising words about “sporadic and not consistent” findings and about lack of any pattern, note that these charts are the only reports in this study that provided results for males and females separately.


The above would seem to be a good illustration of researchers’ only seeing or reporting things that fit their preconceived ideas.  It is apparent that there is a widespread, firmly-held but unjustifiable notion among many scientists that only prenatal, rather than postnatal, toxic exposures contribute significantly to adverse neurological effects in children.  When other scientists or medical professionals read only the abstracts or news reports about studies such as this, the preconceived notions are inappropriately reinforced. 


 At a time when diagnoses of both autism and ADHD have been increasing rapidly, with both affecting males overwhelmingly, it would seem that results such as those in all of these charts should not be merely dismissed as “sporadic,” and (by implication) not significant.  But it appears that many scientists (and peer reviewers) will not be able to see the obvious until progress is made in overcoming the groupthink belief that only prenatal exposures have serious developmental effects.



Appendix A:  More on postnatal vulnerability to toxins:

The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) refers to the “particularly sensitive” periods of children’s neurological development to effects of mercury, which include “the early months after birth.”40  The EPA’s Science Advisory Board advised the Agency, regarding developmental effects of mercury, that ““there is sufficient data to conclude that the developing organism is vulnerable during the entire period of development and that in utero as well as early postnatal exposure to methylmercury is of concern.”41  WHO recognizes the special neurodevelopmental vulnerability to mercury of newborns and young children; WHO’s concerns in this matter include vulnerability to atmospheric pollutants and to frequently-occurring dietary exposure (especially to fish and seafood).40 


In addition to being four times the legal limit that applies to bottled water, typical mercury in breast milk is eight times the WHO relatively-safe guideline value for drinking water. 17 


A 2006 study determined that, of the three sources of infant mercury exposure, ingestion (breast milk), inhalation, and dermal exposure, the largest contribution was from breast milk, providing 96 to 99.6% of the total exposure.43 



Appendix B:  More evidence about effects of Methylmercury:

Methylmercury is one of the “environmental agents with the property of killing neurons as they are born,” according to a study referred to by the NIH.44   Rats exposed to methylmercury on postnatal day 7 were found to have brain cell death induced by one exposure to methylmercury at a level “that begins to approximate human exposure;” and this dose was “equivalent to a single daily exposure” at a level that is estimated to be chronic for many humans.45    Methylmercury accumulates in the brain, and has been found to reach levels over seven times the levels in the blood.46, 47   The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) refers to “deranged neuronal cell migration” that may result from the developing nervous system’s exposure to methylmercury, during particularly sensitive periods of children’s neurological development occurring in the early months after birth as well as prenatally.48   An EPA report to Congress concurs with that description.49






       *For  information about Pollution Action, and to see a listing of our many free online publications, go to  




     1) National Scientific Council on the Developing Child, Early Exposure to Toxic Substances Damages Brain Architecture, 2006, p. 3, at


2) EPA web page at concerning exposure source;  Agency for Toxic Substances and Disease Registry web page at


3) Grandjean et al., Methylmercury and brain development:  imprecision and underestimation of developmental neurotoxicity in humans.  Mt Sinai J Med. 2011 Jan-Feb;78(1):107-18. doi: 10.1002/msj.20228.  at  Also, The National Academies Press,  Toxicological Effects of Methylmercury (2000) at   Discussing the effects of “chronic, low-dose prenatal MeHg exposure from maternal consumption of fish”  (p.4),..  “there is a large body of scientific evidence showing adverse neurodevelopmental effects, including well-designed epidemiological studies.” (p. 6)


4) Koren et al., Fish consumption in pregnancy and fetal risks of methylmercury toxicity, Can Fam Physician. Oct 2010; 56(10): 1001–1002.  PMCID: PMC2954077 at


5) Studies with similar findings from other countries can be found by doing a search with the phrase “maternal methylmercury effects on children,” at


6) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury,  at, Section, p. 146


7)  Geier DA et al., Blood mercury levels in autism spectrum disorder: Is there a threshold level?  Acta Neurobiol Exp (Wars). 2010;70(2):177-86,    Also see footnotes 6, 15, 16, and 29  in D. Austin, An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis’, International Journal of Risk and Safety in Medicine, 20 (2008) 135-142  at

8) Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at

9). U.S. ATSDR document on mercury at, p. 443

10)  2004 International Emissions Inventory Conference, Air Toxics Session, Clearwater, Florida, Mercury Emissions from Motor Vehicles, at

        Also,  Hoyer et al., Mercury Emissions from Motor Vehicles (EPA publication), esp. p 4, at


      11) Roberts et al., Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, published June, 2013 in Environmental Health Perspectives, at


12) Wijngaarden et al., Prenatal methyl mercury exposure in relation to neurodevelopment and behavior at 19 years of age in the Seychelles Child Development Study, Neurotoxicol Teratol. 2013 Sep-Oct;39:19-25. doi: 10.1016/ Epub 2013 Jun 14, at


13) p. 313 of The National Academies Press,  Toxicological Effects of Methylmercury (2000) at   All studies that were considered had been conducted in countries where exposures were “within the range of the general U.S. population exposures.” (p. 5)


14) p. 299 of The National Academies Press,  Toxicological Effects of Methylmercury (2000) at of The National Academies Press,  Toxicological Effects of Methylmercury (2000) at


15) Statement by Dr. D.C. Rice before U.S. Senate Committee on Environment & Public Works, 07/29/2003 at


16) Myers et al., Effects of prenatal methylmercury exposure from a high fish diet on developmental milestones in the Seychelles Child Development Study, Neurotoxicology. 1997;18(3):819-29.  at;

    van Wijngaarden et al., Prenatal methyl mercury exposure in relation to neurodevelopment and behavior at 19 years of age in the Seychelles Child Development Study,  Neurotoxicol Teratol. 2013 Sep-Oct;39:19-25. doi: 10.1016/ Epub 2013 Jun 14. at


17)  Mercury is typically present at 8 parts per billion in breast milk, according to U.S. ATSDR document on mercury at, p. 443,  which compares with1 microgram per liter (1 microgram per billion micrograms), or 1 part per billion, the WHO guideline value for drinking water:  (WHO, Mercury in Drinking-water Background document for development of WHO Guidelines for Drinking-water Quality  WHO/SDE/WSH/03.04/10  at  p. 8   Accessed 4/8/2014)


18) A study in Taiwan (H.C. His et al.) examined effects of exposure of 3-year-olds to mercury linked with fish consumption, distinguishing between prenatal and postnatal exposures; the authors found that prenatal exposure was not associated with neurological harm, whereas postnatal exposure was found to be associated with low scores in expressive language; note that language impairment is one of the principal characteristics of autism. (His et al., The neurological effects of prenatal and postnatal mercury/methylmercury exposure on three-year-old children in Taiwan, Chemosphere. 2014 Apr;100:71-6. doi: 10.1016/j.chemosphere.2013.12.068. Epub 2014 Jan 23  at


-- In tests of neuromotor functions, current mercury levels, but not pre-natal, were associated with increased action tremor amplitude in preschool children (Despres et al.,  Neuromotor functions in Inuit preschool children exposed to Pb, PCBs, and Hg, Neurotoxicol Teratol. 2005 Mar-Apr; 27(2):245-57 at


-- The following study of Chinese children with elevated mercury levels due to fish consumption found that the children with mercury concentrations above a certain level (one-sixth of the level considered to be poisoning) had a 9.7 times higher risk of having ADHD, after adjustment for confounding variables. (Cheuk et al., Attention-Deficit Hyperactivity Disorder and Blood Mercury Level:  a Case-Control Study in Chinese Children  Neuropediatrics 2006; 37: 234–240  at


-- A study with mice provided additional support for seeing the toxic effects of methylmercury exposure to be greater in the later period of brain development than in the earlier period (specifically in the cerebellum, and early-postnatally in human-equivalent time, although later in the nursing period for mice).   (Stringari et al., Postnatal Methylmercury Exposure Induces Hyperlocomotor Activity and Cerebellar Oxidative Stress in Mice: Dependence on the Neurodevelopmental Period, Neurochemical Research  April 2006, Volume 31, Issue 4, pp 563-569 at


--  A study in Spain found substantial adverse cognitive effects of postnatal exposure to mercury linked with fish consumption as late as age 4, even past the early-postnatal period of greatest vulnerability. (Freire et al., Hair mercury levels, fish consumption, and cognitive development in preschool children from Granada, Spain,  Environ Res. 2010 Jan;110(1):96-104. doi: 10.1016/j.envres.2009.10.005   at


-- A 2003 study found reduction of growth in infants in a dose-response relationship with duration of breastfeeding (with methylmercury from seafood consumption being considered to be the causal agent); that is only a very small step away from seeing neurological harm to result from postnatal exposure to mercury, since (a) mercury is recognized to be neurodevelopmentally toxic and (b) there is very considerable brain growth taking place that is subject to attenuation during the early-postnatal period.  (P. Grandjean et al., Attenuated growth of breast-fed children exposed to increased concentrations of methylmercury and polychlorinated biphenyls,  FASEB J. (February 5, 2003) 10.1096/fj.02– 0661fje  at


-- A Brazilian-U.S. research team generalized about postnatal mercury exposure on the basis of examination of other studies, “MeHg exposure is associated with a wide range of central nervous system dysfunctions in both children and adults,” and also referred to “increased susceptibility of the developing nervous system to low level exposures; judging by their own research, “The magnitude of the effects increased with hair mercury concentrations, consistent with a dose-dependent effect.”  Yokoo et al., Low level methylmercury exposure affects neuropsychological function in adults,  Environ Health. 2003; 2: 8. Published online Jun 4, 2003. doi:  PMCID: PMC165591at



Other studies have found associations of methylmercury exposure from fish consumption with adverse neurological effects specifically in adults:

-- Carta et al., Sub-clinical neurobehavioral abnormalities associated with low level of mercury exposure through fish consumption, Neurotoxicology. 2003 Aug;24(4-5):617-23, at


and in a dose-effect relationship:

-- Carta et al., Neuroendocrine and neurobehavioral effects associated with exposure to low doses of mercury from habitual consumption of marine fish, Med Lav. 2002 May-Jun;93(3):215-24. at


19) Report on the Situation of Infant and Young Child Feeding in Seychelles, August 2011, IBFAN, The Committee on the Rights of the Child  The data from the Seychelles (1.5% exclusive breastfeeding at 6 months in 2008) should be compared with the11.9% exclusive breastfeeding at 6 months in U.S. in 2008, according to CDC data at, top of 2nd page.  This is from what is unfortunately the only readily-available data source regarding breastfeeding rates in Seychelles.  If anybody knows of any other data source on this topic, please notify


20) See the “World” breastfeeding rates chart, taken in 2012 from the website of LaLeche League International, now shown at (the LLLI does not show such a chart currently).  This is compatible with Chart CO1.5.A:  Proportion of children who were “ever breastfed”, around 2005, from the OECD Family Database at 


21) Jensen et al., Effects of breast feeding on neuropsychological development in a community with methylmercury exposure from seafood,  Journal of Exposure Analysis and Environmental Epidemiology (2005) 15, 423–430  at, showing a 92% breastfeeding rate for the Faroes.

22) Essex et al., Breastfeeding rates in New Zealand in the first 6 months and the reasons for stopping. N Z Med J. 1995 Sep 8;108(1007):355-7.  at, showing a 94% exclusive breastfeeding rate at birth in a study published in 1995. Breastfeeding rates as of 2012 were higher than in 1995.  (  Also National Breastfeeding Advisory Committee of New Zealand’s advice to the Director-General of Health, National Strategic Plan of Action for Breastfeeding 2008–2012,  at

23) P. Grandjean,  Methylmercury Exposure Biomarkers as Indicators of Neurotoxicity in Children Aged 7 Years,  American Journal of Epidemiology 1999,  The Johns Hopkins University School of Hygiene and Public Health  at


24) Drexler et al., The mercury concentration in breast milk resulting from amalgam fillings and dietary habits,  Environ Res. 1998 May;77(2):124-9. at  The concentrations were also positively associated with fish consumption, which implies that a high percentage of the mercury in the breast milk was in the form of methylmercury, which is the most toxic form and the form chiefly present in fish;   another study found various forms of mercury in mothers’ blood and urine declined during lactation, and said that was probably attributable to excretion during breastfeeding. (Vahter, Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Volume 84, Issue 2, October 2000, Pages 186–194


25) Exploration of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section,  at  

The highly effective transfer of mercury from mother to infant via breastfeeding is also compatible with the finding that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, due to excretion in breast milk. (Wigle, D.T., MD, PhD, MPH:  Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 106, typically available through Ebsco Host at local libraries)


26) Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines.Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  at  


27) Vahter et al., Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Section A 84, 186}194 (2000) at


27a)  According to the U.S. Hazardous Substances Data Bank of the National Library of Medicine's TOXNET system, at


27b) Lok, E. 1983. The effect of weaning on blood, hair, fecal and urinary mercury after chronic ingestion of methylmercuric chloride by infant monkeys. Toxicology Letters, Volume 15, Issues 2–3, February 1983, Pages 147–152, abstract at


27c)  P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993

27d)  Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured  in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months.  Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding,(43) the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.

28) Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors,  Autism Res Treat. 2013; 2013: 731935 PMCID: PMC3787615   at


29) Section of U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at  

See also Section of International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990) at

For ataxia-producing effect of methylmercury, see also p. 6-21 of U.S. EPA, Mercury Report to Congress, Vol. VII, Dec. 1997, EPA-452/R-97-009  at


30) Exploration of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section,  at   See reference 17d below about mercury exposure in humans being mainly methylmercury.

The highly effective transfer of mercury from mother to infant via breastfeeding is also compatible with the finding that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, due to excretion in breast milk. (Wigle, D.T., MD, PhD, MPH:  Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 106, typically available through Ebsco Host at local libraries)


31) International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990)  at  Sections 9.1 and 9.42


32) Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at


32a) Curtis et al., Chronic Metals Ingestion By Prairie Voles Produces Sex-Specific Deficits In Social Behavior: An Animal Model Of Autism, Behav Brain Res. 2010 Nov 12; 213(1): 42–49.  Published online 2010 Apr 28. doi:  10.1016/j.bbr.2010.04.028  PMCID: PMC2880538 at


33).  Food Additives & Contaminants: Part B: Surveillance  Volume 5, Issue 1, 2012  Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada  DOI: 10.1080/19393210.2012.658087  at


33a) U.S. ATSDR, “Mercury”, p. 355, at


34) See for a more complete statement about those toxins


35) International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990)  at  Section 9.3.2


35)  American Academy of Family Physicians website at

36)  See, where numerous peer-reviewed studies are cited in support of this statement.


37) CDC’s MMWR National Surveillance for  Asthma -- United States, 1980-2004, Table 29, at

Re allergies: CDC’s Health United States 2011, Table 46, p. 3, at  

Type 2 Diabetes in Children and Young Adults:  A “New Epidemic”  Francine Ratner Kaufman, MD  CLINICAL DIABETES • Volume 20, Number 4, 2002  at 

Re ADHD:  see for substantial evidence about the time trend of ADHD in the U.S.

Re mental retardation trend: National Center for Health Statistics, Healthy People 2000 Review, 1997.  Public Health Service. Lib. of Congress Cat. No. 76-641496, Figure R, found at

Also see, where numerous peer-reviewed studies are cited in support of this statement .


38)  See, where over 50 peer-reviewed studies are cited in support of this statement.

39)  Also Clin Exp Allergy. 2006 April; 36(4): 402–425.  Blackwell Publishing Ltd  "Too clean, or not too clean: the Hygiene Hypothesis and home hygiene,"  SF Bloomfield et al.   Also Cell Research advance online publication 24 April 2012; doi: 10.1038/cr.2012.65  "Early exposure to germs and the Hygiene Hypothesis"  Dale T Umetsu  Division of Immunology, Karp Laboratories, Children's Hospital Boston, Harvard Medical School, Boston,MA

Also, "About Allergies/ Why Are Allergies Increasing?" at


39a) Davidson et al., Fish Consumption, Mercury Exposure, and Their Associations with Scholastic Achievement in the Seychelles Child Development Study, Neurotoxicology. Author manuscript; available in PMC Sep 1, 2011, Published in final edited form as:Neurotoxicology. Sep 2010; 31(5): 439–447. Published online May 31, 2010. doi:  10.1016/j.neuro.2010.05.010, PMCID: PMC2934742  at


40)  U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at, Section 1.6  

Also World Health Organization (WHO), U.N. Environment Programme, "Guidance for Identifying Populations at Risk form Mercury Exposure" August 2008 at,  Section 2.7 and Executive Synopsis item 17.  In this document (item 166), WHO says that “the fetus, the newborn and young children are especially susceptible to mercury exposure because of the sensitivity of the developing nervous system.”  See item 127 about inhalation exposure.


41) p. 5-18 in Mercury Study Report to Congress, Vol. VII, EPA-452/R-97-009 December 1997, at


43) Chien LC, et al., Analysis of the health risk of exposure to breast milk mercury in infants in Taiwan. Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at 

44) Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at

45) Sokolowski et al., Methylmercury (MeHg) elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures, Neurotoxicology  2011  at 

46)  U.S. Agency for Toxic Substances and Disease Registry web page at, saying "Methyl mercury is the most toxicological form of the element and, by its accumulation in the central nervous system (CNS), may result in neurotoxic effects…."

 Also Berlin M. 1979. Mercury. Handbook on the Toxicology of Metals. Amsterdam: Elsevier.


      47) Burbacher et al., Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal,  (Oral Mg Kinetics section)  Environ Health Perspect. 2005 August; 113(8): 1015–1021, PMCID: PMC1280342  at


48) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at,  p. 214 re “deranged” neuronal migration.  Also Section 1.6 re particularly sensitive periods of neurological development.


49)  EPA-452/R-97-009 December 1997  p. 5-29 (Section 5.6.1) at




See also: 


Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environ. Health Perspectives, accepted Oct. 1993  




Weiss et al., Silent Latency Periods in Methylmercury Poisoning and in Neurodegenerative Disease, Environmental Health Perspectives • Volume 110 | Supplement 5 | October 2002 at


Section 2.6 of U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury, p. 302  at,


It should be apparent from the above WHO chart that most infants in recent decades have been breastfed, especially considering that the percentage breastfed for 3 months (shown here) is always far lower than the percentage breastfed for several weeks.  It should also be apparent that most countries’ breastfeeding rates have been rising in recent decades, especially among those that were not already high.

(Chart generated at WHO’s European Health for All Database, March 25, 2014,rat


 G.J. Myers and P.W. Davidson, Does Methylmercury Have a Role in Causing Developmental Disabilities in Children?  Environmental Health Perspectives   Vol 108, Supplement 3  June 2000   at


Section 6.4.2 of Mercury Study Report to Congress c7o032-1-1,  Office of Air Quality Planning & Standards and Office of Research and Development  Volume VII  at

    also  Mendola  P et al, Environmental factors associated with a spectrum of neurodevelopmental deficits, Ment Retard Dev Disabil Res Rev. 2002;8(3):188-97  abstract at or full text  at


Rice and Barone, Critical Periods of Vulnerability for the Developing Nervous System:  Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, 2000, at, p. 515. Quoting from p. 518, “It is apparent from the summary of these specific developmental processes that ontogeny (origin and development) of different parts of the brain occurs at different times during the prenatal and postnatal period, thus broadening the temporal window of vulnerability and the number of developmental processes that may be affected by exposure to xenobiotics.”

   Also, P. Grandjean,  Methylmercury Exposure Biomarkers as Indicators of Neurotoxicity in Children Aged 7 Years,  American Journal of Epidemiology 1999,  The Johns Hopkins University School of

Hygiene and Public Health  at :  “The nervous system is particularly vulnerable to effects from neurotoxicants such as methylmercury during the last two trimesters of pregnancy and during early postnatal life.”

   Also, The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) refers to “particularly sensitive” periods of children’s neurological development to effects of developmental toxins, which include “the early months after birth.” (U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at, Section 1.6


U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at  p. 417





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