Highs, mid-levels and lows of infant exposures to certain toxins seem to correlate closely with highs, mid-levels and lows of autism or ASD traits
Since what follows may seem to many readers to be improbable, or possibly merely random associations, the plausibility of a causal relationship between these toxins and ASD should first be briefly touched on: Experts in the field of developmental toxicology pointed out in 2004 that various chemicals that have become greatly increased in modern environments "have caused contamination of human milk only during the last half century, and long-term health impacts are now being discovered."F Some of those chemicals, according to the EPA and other leading authorities, are neuro-developmental toxins and become concentrated in breast milk in concentrations far exceeding established safe levels.F1
a) First-born children, compared with later-born, have the highest rate of autism,1 and they also have the highest exposure to breastfeeding, in rates,2a in duration,2b and in concentrations of developmental toxins contained in the milk.2c
b) In one U.K. study,9 one Canadian study9a and two U.S. studies,10, 12 breastfeeding rates were found to have been unusually high among children later diagnosed with autism. One of those was a study of data from all 50 U.S. states and 51 U.S. counties, and another studied a population of 127,000; more in item 3.a below. The associations were higher with greater durations of breastfeeding.
c) 4-year-old children with higher levels of PBDEs were found to have over 2½ times the risk of poor social competence (a basic autism-related trait), compared with less-exposed children;5 this should be seen in combination with comparative exposure data such as the nearly 3-to-1 difference in levels of PBDEs in breastfed as compared with formula-fed children at age 4, as reported in what is apparently the only study that has made such a comparison.6
d) The following should be seen together with awareness that hyperactivity and attention deficits have significant overlap with traits of ASD.6b In a study of 3½-year-olds, history of breastfeeding was related to less-sustained attention; that study also found more signs of hyperactive behavior associated with higher postnatal levels of PCBs, which in turn were mainly predicted by breastfeeding duration. 6a In a study of 4-year-olds, higher risk of attention deficits was associated with current body burden of PBDEs;5 remember from above the far higher levels of PBDEs in breastfed than in formula-fed 4-year-olds.
e) Many studies have found high mercury levels in those diagnosed with autism.3 (The studies that have failed to find this association have (a) focused on thimerosal, which contains only ethylmercury, one of many species of that chemical, (b) measured mercury levels in children far past the highly vulnerable early-postnatal period, or (c) assessed effects at too young an age to properly judge the long-term results.) High mercury levels in those with autism should be seen together with the findings in two studies of doubling or tripling of infant mercury levels resulting from breastfeeding, compared with levels in non-breastfed children; compatible findings were reported in other studies.4, Such increases of mercury in breastfed children take place during the infants’ periods of rapid brain growth and development.(see chart) (Seeing the postnatal increases in cells shown in this chart, note that studies “have clearly demonstrated that when proliferation is actively occurring in a given region of the brain, it is vulnerable” to toxins.4a)
f) ASD apparently increased in the U.S. during recent decades while the children being diagnosed had been breastfed at increasing rates;7 concentrations of PBDEs (a strongly-suspected neurodevelopmental toxin) in the breast milk also greatly increased during that period.8
b) No neurological harm to children from maternal methylmercury was found in a country (Seychelles) with exceptionally low exclusive breastfeeding; this is noteworthy in that maternal methylmercury has been uniformly, authoritatively found in studies in other countries to harm neurological development of the children. (The explanation required on this point is lengthy and therefore is placed at 2.b cont., to allow promptly going on to the other main points of this article.)
c) ASD prevalence among 8-year-olds was found to be stable in the U.K. during the most recently-assessed period (2004-2010),10a which followed approximately eight years after a time of stable breastfeeding rates there.11 So, during the general period of the infancies of the U.K. children whose autism rates were not increasing, breastfeeding rates were also basically level. This stable level of autism prevailed in the U.K. while autism rates were reported to have increased in the U.S. along with increases in breastfeeding rates.11b The difference between countries in autism trends was sufficiently noteworthy to be the central finding of a study in the journal, BMJ Open; and it was apparently also considered by the organization, Autism Speaks, to be newsworthy, as opposed to being seen as a merely random fluctuation.11a
3. Highs through to lows, including mid-levels, with intermediate data filling out the middle areas of correlations as found in large-scale studies:
a) Autism risk declines progressively from first-born to second-born, to third-born children, and continues downward to fourth-born children;1 and breastfeeding rates, duration and concentrations of toxins contained in breast milk decline from first to later children.2a, 2b, 2c
(Toxin levels are reduced as a result of excretion to earlier-born infants during previous nursing.)
At a quick first glance, the chart below could be a graphical representation of autism rates according to birth order.
Neurological toxins typically ingested in infancy decline with birth order, as shown above. The close resemblance of this decline to the decline in autism by birth order might not be coincidental.
In addition to the declines in concentrations of PCBs and DDT with
birth order as shown above, concentrations of dioxins in breast milk
have also been found to decline with subsequent births, and in percentages
similar to those shown in the chart above, as found in a German study described
in a 2001 American review article.2d (Note that, according
to a study by an EPA senior scientist, breastfed infants are typically exposed
to dioxins, a known neurodevelopmental toxin, in doses scores to hundreds of
times higher than established safe levels.36)
b) Autism prevalence was found in a study by a highly-published scientist (R.J. Shamberger) to correlate with breastfeeding rates and duration, on the basis of data for all 50 U.S. states and 51 U.S. counties. This included findings that "exclusive breast-feeding shows a direct epidemiological relationship to autism" and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism."12
c) Another U.S. study found that 37% of children with autism had been breastfed for at least 6 months, as compared with 13% in the comparison group.10
d) A U.K. study of 1189 children with ASD found an unusually high percentage of ASD cases had been exclusively breastfed for more than four weeks: 65%, in a low-breastfeeding country in which about 28% would have been normal for that duration of breastfeeding.9
e) A 2010 Canadian study, drawing data from a population-based “clinically-rich perinatal database,” investigated a very large cohort of nearly 130,000 births. In that respect, it was second only to the Shamberger study, in studies on this topic. Data from almost 127,000 of those children (those without identified genetic risk of autism) went into the study’s finding that there was a 25% increased risk of autism among children who were breastfed at discharge from the hospital, compared with those who were not.9a
Note in c, d, and e above what appear to be effects’ varying in relation to duration of exposure: When the dividing line for comparison purposes was at discharge from the hospital, the increase in autism for breastfed infants was 25%. When the cutoff was at four weeks, the increase in autism was 132% (65% divided by 28%). When the cutoff was at six months, the increase was 185% (37% divided by 13%). Remember also from b) above the finding, in a study covering an extremely large, diverse geographic area, that autism prevalence correlates with duration of breastfeeding.
4. Strong associations between higher/lower autism prevalence and higher or lower exposures to toxins that probably become concentrated in mothers’ milk: More specifically, various studies have found associations between autism prevalence and higher or lower exposures to atmospheric pollutants, especially diesel and vehicular emissions, approximately at time of birth;13 those toxins probably become concentrated in human milk, as implied by the following: diesel emissions contain the neurodevelopmental toxins, dioxins, PCBs, and PBDEs,14 which become concentrated in human milk to levels over 30 times higher than in infant formula.15
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.”17n In relation to that, according to the ATSDR, “the predominant neuropathological feature (of effects of methylmercury exposure) is degenerative changes in the cerebellum.”17a As mentioned earlier, many studies have found high mercury levels in those diagnosed with autism.3 Bearing the above in mind, note what is said in the next paragraph about the means by which infants are exposed to high levels of mercury.
Typical mercury in breast milk is eight times the WHO relatively-safe guideline value for drinking water;15b there is also considerable other evidence of high levels of mercury in breast milk.4, 17 What becomes of those developmental toxins in women’s bodies and in their milk (when and how heavily infants could be affected by the toxins) 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;15d
-- 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.17
-- a 2007 study of 82 mother-infant pairs found that mercury levels in mothers’ hair decreased 57% during six months of lactation;15e
-- 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 present in circulating blood (5 L]0.3 lg/L) would be transferred to the milk every day.” 15f
-- different studies have estimated that concentrations of dioxins in breast milk decline in the range of 48% to 70% during 6 months of breastfeeding.15c
Given this evidence of rapid postnatal transfer of most of a grown person’s accumulations of developmental toxins such as mercury to a breastfeeding infant, it is especially relevant to carefully consider the following statement by the highly-published expert, P. Grandjean, in an article in the American Journal of Epidemiology: “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.”15g Statements by WHO, the U.S. ATSDR, the U.S. EPA, and the U.S. National Research Council all say essentially the same thing about postnatal vulnerability of infants to developmental toxins. (see section 5.a below)
Many studies have found harmful effects of (presumably) “prenatal” exposures judging by measurements of toxins in umbilical cord blood. But there is no reason to think that those cord levels aren’t also indicators of exposure of the infant to toxins via breastfeeding, since most infants have been breastfed in recent decades. In some cases, the supposedly “prenatal” exposures are determined only by measuring contents of breast milk; and there is no acknowledgement that exposure via breast milk (instead of prenatal exposure) could account for the health associations that were found. Note that exposures to toxins via breastfeeding (a) come at a specific time when the brain’s development is authoritatively known to be “particularly vulnerable” to their effects, and (b) are far higher than prenatal exposures. (10 to 20 times -- see expert statement early in next section.)
The probable inaccuracy in judging the timing of the genuinely harmful mercury transfers is in line with likely similar confusion regarding transfers of other toxins as well. But not all studies have fallen into the usual pattern of measuring maternal levels of toxins at time of birth and assuming that those are merely indications of prenatal exposures of the developing brain; at least 30 published studies have carefully distinguished between prenatal and postnatal exposures, and have found associations of postnatal exposures to various environmental toxins with harmful neurological effects while finding either less or no harmful effects associated with prenatal exposures to those same substances.30a That includes two studies that found evidence of toxicity of postnatal exposure to mercury while finding no evidence of toxicity of prenatal exposure to that toxin.26
5. Abruptly high ingestion of toxins via human milk (at initiation of breastfeeding), then two or more months pass, then eye contact “derails” in children who will later have ASD. (Suddenly high exposure + latent period => suddenly high effect)
In a 2013 study (Jones et al.), decline of eye contact, beginning two months after birth, was found in infants who were later diagnosed with ASD. This was not merely failure to develop, it was considered to be a derailment of initially satisfactory development.14a The study’s authors saw this to be especially significant since “deficits in eye contact have been a hallmark of autism since the condition’s initial description.” There is good reason to look into environmental toxins that could be causes of these downturns: A 2014 review found that 92% of the studies of the relationship between exposure to environmental toxins and ASD reported a significant association between the two, and 14 studies found a dose-effect relationship.14b Note that initiation of breastfeeding brings a sudden, major increase in toxins ingested, compatible with abrupt later appearance of negative effects, as indicated by the following: according to leading experts in the field, 10 to 20 times as much of a mother's body burden of developmental toxins such as dioxins and PBDEs is transferred to the infant via the milk as by the transplacental route;16 the surge in mercury exposure at initiation of nursing has already been mentioned, with references (section 1.e above).
There is a common pattern of a child’s development apparently going well initially, even for years, followed by emergence of ASD traits; the Jones study found (by means of advanced equipment) emergence of ASD traits at the early end of the time range in which problems are first detected. Methylmercury fits well in this picture, since its effects are well known to emerge after latencies ranging from months to years. (more on this in item “g)” below)
To understand how this sudden high exposure can explain the subsequent sudden decline, one should be aware of the following:
a) The early-postnatal period is widely, authoritatively recognized to be a period of special vulnerability to toxins such as are present in breast milk:
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.”17c1 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.”17c5 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).17c1 An expert statement (by P. Grandjean) in the American Journal of Epidemiology refers to particular vulnerability to neurodevelopmental toxins during the early postnatal period.15g A commission of the U.S. National Research Council (of the National Academies) refers to “specific periods in development when toxicity can permanently alter the function of a system;” such periods of special vulnerability apply to development of the brain, which the commission says “may demonstrate particular sensitivity during the postnatal period.”17c6
b) Methylmercury, concentrated in breast milk, is known to have effects similar to many traits of ASD, including eye-control problems:
Continuing from the above-quoted ATSDR document, “the major effects (of methylmercury) that are seen across the studies include motor disturbances, such as ataxia and tremors, as well as signs of sensory dysfunction, such as impaired vision.” 17a Visual dysfunction is an important part of the first specific effect of mercury that is stated by the ATSDR -- ataxia; according to an authoritative definition, “Ataxia is a lack of muscle coordination which may affect speech, eye movements,.. and other voluntary movements.”17a1 It is not hard to see a possible relationship between visual dysfunction/ impaired eye control and the loss of eye contact that has been found to begin months after birth among those who will later be diagnosed with ASD. Many other effects of mercury that closely resemble traits of ASD are indicated below, in paragraph e.
c) Toxins including mercury are present in human milk in concentrations that greatly exceed established safety guidelines:
As mentioned earlier, typical human milk has mercury concentrations that are eight times WHO’s guideline for drinking water safety; 15b levels are often substantially higher among women with special dietary, occupational, or regional exposures. (Concentrations of mercury in human milk are also apparently over a hundred times higher than levels in infant formula.17k) Typical human milk in the U.S., at initiation of breastfeeding, also has levels of the known neurodevelopmental toxin, dioxin, that are hundreds of times higher than the EPA’s RfD (estimated relatively safe dose).17i
d) At least six published studies have found high levels of mercury in those with ASD, including correlations between degrees of autism severity and increasing hair levels of mercury.17p
e) Other known neurological effects of methylmercury exposure are also similar to traits of ASD:
In addition to the above-mentioned impairments in speech and eye-movement control associated with exposure to mercury, with similarities to traits of ASD, also note the following:
Impaired social interaction is “the hallmark feature of ASD,” according to the NIH’s Autism Fact Sheet.17b3 A scientist and MD (D.T. Wigle) writing in a publication of the Oxford University Press, points out that relatively low developmental exposures to mercury cause “abnormal social behavior….”17b4
Clumsiness: According to the U.N. Environmental Programme (UNEP), other symptoms of methylmercury poisoning include cerebellar ataxia (lack of muscular coordination) and gait disturbance,17q Those effects of mercury are quite compatible with the deficits in gross and fine motor skills and the unusual gait typically observable in those with ASD.17r
Hyperkinesia (pathologically increased muscular movement) is a normal characteristic of mercury poisoning,17s and people who have had much contact with those with ASD will be familiar with that problem.
Deficits in language, attention, and memory were associated with higher mercury exposure among children in the Faroes Islands, where mercury ingestion is elevated due to a diet including considerable seafood.17w It should not be hard to see that these effects of mercury are compatible with traits of many of those with ASD.
Other observed effects of methylmercury toxicity, which will sound familiar to people who have lived or worked with people with autism, include the following: “talked little…moved slowly,… often did the same thing repeatedly…. placed vases in a straight line… often impolite, too friendly to others,… restless, sensitive, easily became angry… attention was distracted…. startled easily to stimuli such as sound.”17x It may need to be repeated that the above characteristics were observed effects of methylmercury toxicity, not traits of ASD, since the effects reported above could easily be confused with descriptions of many or most people with ASD. Note also that these are not general traits, but instead are mostly distinctive and fairly specific to autism.
Other sensory problems:
According to the U.N. Environmental Programme (UNEP), other symptoms of methylmercury poisoning include visual-field constriction and hearing impairment.17q In a Vanderbilt University study, 41% of those with ASD in a hearing test “responded in such a way as to indicate that they did not hear normally for at least one test stimulus…”17b5 Also, it is common for those with ASD not to respond when their names are called.
Paresthesia (feeling of burning, prickling, skin crawling, itching or numbness17v) is another common effect of mercury exposure; very likely connected with that, a problem that has been reported to affect about 30% of children with ASD at some point is self-injurious behavior such as hand-biting and head banging;17z such behavior could reasonably be seen as a manifestation of a kind of sensory impairment, a sensorily-impaired person’s equivalent of vigorously scratching an itchy insect bite -- rough activity in response to an irritation. Actions that would be painful to others may be felt as an improvement by somebody with impaired tactile perception who is trying to deal with a feeling of irritation or pain.
To sum up the above: Methylmercury exposure, such as is known to often be well above established safe levels in human milk, has been found to cause many symptoms that closely resemble traits of ASD.
g) The latency range for effects of methylmercury following exposure is very compatible with the time range for emergence of symptoms of ASD after birth:
According to the ATSDR, there is “a slow but inevitable trapping of mercuric ions” in the brain, which “may lead to the mercury-induced delayed central nervous system toxicity observed months to years after exposure ceases.”17c2 The latent periods known to follow mercury exposure are quite compatible with the typical time range of appearance of ASD symptoms following birth. The two-month postnatal periods that preceded the first of the above-mentioned eye-contact “derailments” were near the early end of the range of latencies of methylmercury. Later appearances of ASD symptoms, which are also well within the range of latencies of mercury effects, are often referred to as “regression” (following earlier progress) or “late emergence.”17b
The ATSDR also says there is good evidence that methylmercury has “delayed neurotoxicity observable many years after cessation of exposure.”17c4 A study of data concerning 2568 children with ASD in the CDC’s 2002 ADDM network found that 27% of the cases had not been identified through age 8.17c Considering how far into their school years so many children (who would later be diagnosed with ASD) had progressed without being identified as having ASD, it would be surprising if late emergence of symptoms would not have been a valid description of what took place in many or most of those cases. Bear in mind the above authoritatively-reported evidence of “many years” of latency after methyl-mercury exposure, and remember that most infants are known to be exposed to methylmercury in doses recognized to be far above recognized safe levels. (see section 4(b) above)
To sum up some of the above: Mercury, including in relatively low doses, has harmful effects that are very similar to characteristics of ASD. That chemical very often begins to be ingested by newborns in doses far exceeding established safe levels at a time when the infant brain’s development is going through a period that is authoritatively recognized to be “particularly sensitive” to effects of mercury; and that exposure is taking place during the months preceding the first signs of ASD. The range of ages at which ASD symptoms emerge is very compatible with the known range of latency of methylmercury, assuming the first weeks after birth as the beginning of exposure. The findings in several studies that most of a grown woman’s accumulations of developmentally-toxic mercury are rapidly excreted to her developing infant in breast milk (section 4, item c above, also 4, 17) should be of concern.
Remember that, according to EPA researchers, studies “have clearly demonstrated that when proliferation (cell division) is actively occurring in a given region of the brain, it is vulnerable” to toxins.4a Then note in this chart that the cerebellum, which coordinates muscle (and eye) movement, is growing especially rapidly in the year after birth and is therefore quite vulnerable to toxins in this period.
Note the following about the brain’s still greater vulnerability to some specific toxins during that same period of rapid growth:
a) an EPA-contracted research group has stated that the brain is especially vulnerable to metals during the brain growth spurt;17g
b) 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 (Sect. 9.3.2 in ref.17b6); “abnormal neuronal migration” and actual destruction of neurons are other likely effects that those same experts attribute to methylmercury. (About half of mercury in breast milk is methylmercury.17d) Those authors’ principal concern was with effects of mercury exposures at levels that are frequently present in the environment.
Abnormal neuronal migration (as an effect of methylmercury exposure) is especially significant to discussion of origins of autism, since disorganization of brain cells, which could result from defective migration, was found in a 2014 study to be normally present in brains of children with ASD. Disorganized patches of cells were found specifically in two brain regions in which considerable development is known to take place postnatally.17e1 An EPA report to Congress stated that “neuronal migration, a process specifically affected by methylmercury…continues until five months after birth.”17e
Given the above, regular initiation of breastfeeding months before beginnings of derailments of eye contact could well be more than mere coincidence. And it could be of great significance to origins of autism.
No harmful effects from maternal mercury in children in a country with exceptionally low breastfeeding:
Long-term, low-dose exposure to methylmercury stemming from maternal consumption of fish and seafood is recognized as neurodevelopmentally toxic to the fetus/infant.18 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,19 and in other studies as well.20 Providing additional confirmation from animal studies, developmental neurotoxicity of organic mercury (which includes methylmercury) “has been observed at very low exposure levels,” according to the U.S. ATSDR.20a
But one country stands out in which major studies have found that high maternal mercury levels from seafood consumption did not lead to neurological problems in the children -- the Republic of Seychelles. 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 in the Seychelles that did not find toxic effects of maternal mercury, and 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 (Seychelles study conflicting with studies conducted elsewhere) present a vexing choice.”21 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 21b) The expert on neurodevelopmental toxicology, D.C. Rice, called the Seychelles study “anomalous,” in comparison with the findings of eight other studies carried out in other countries.21c 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.22
But there is no need to be surprised 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 may well be the major source of harm. Remember from section 4 above the recognized vulnerability of an infant’s neurological development to postnatal toxic exposures, as well as evidence that lactation is effective at rapidly transferring most of a grown person’s accumulations of developmental toxins to a small, developing infant. Add to that the evidence that transfers of three of those toxins (including mercury) by lactation are in doses normally exceeding established safe levels by hundreds of per cent.F1, 4 , 15b
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 while specifically finding no evidence of toxicity of prenatal exposure to mercury.26
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.;29 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.30 There is additional evidence of a long-term, cultural bias against breastfeeding in this African region.30c The major studies from which the National Research Council drew its strongest 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.29a, 29b
It therefore appears that there has been unusually little transfer of toxins to the developing brain taking place in the Seychelles during the important postnatal phases of the brain’s development; and the postnatal period may well be the more vulnerable time for certain toxins, for reasons explained above.
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 likely to be 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. This caused vexation among authorities who were trying to determine which exposures are unsafe for developing brains, since those people were assuming that the potentially harmful exposures are prenatal, to which all developing brains would be exposed. This limited focus blinded them to the major differences that exist between the Seychelles and other countries in prevalence of lactational transfers from mother to infant. The effects of presumably “prenatal” exposures to methylmercury that were found in other countries, as estimated on the basis of time-of-birth measurements, were probably actually results of the far greater early-postnatal transfers to infants of those same maternal toxin concentrations. (see section 4) There was no lack of effect of mercury in the case of the Seychelles, instead there was lack of transfer to the infant at what is probably the most vulnerable time, and especially lack of transfer at the stage when the transfers are by far the greatest.
Other recognized environmental toxins that are also linked with neurodevelopmental harm
The above emphasis on mercury should not detract from the importance of other toxins to which infants are also exposed in doses far exceeding recognized safe levels. The following is a very brief introduction to other relevant toxins:
-- dioxins, in human milk in concentrations exceeding the EPA’s Reference Dose (estimated reasonably safe dose, or RfD) by scores to hundreds of times;36
-- PBDEs, in breast milk in concentrations normally well above and sometimes up to 40 times the EPA’s RfD;37 and
-- PCBs, in human milk in concentrations about 20 times the maximum allowed by law in U.S. public water supplies.38
All three of the above developmental toxins are present in infant formula in average concentrations no more than 4% as high, and usually less than 1% as high, as their concentrations in human milk.39
Notice on the right the difference (shown in the gray area) between the PCB exposure of a breastfed child and that of a cow’s-milk-formula-fed child. (This chart is from a 2011 study, Quinn et al.,40 by a Canadian-Swedish-Norwegian team of scientists; very similar data is provided in a 2015 study.40a) Seeing the peak at 6 months, corresponding with the 6-month duration of breastfeeding assumed for this chart, consider how much higher the PCB exposure would be if the infant were to be breastfed for (the often-recommended) 12 months or longer. Also bear in mind that PCBs are only one of four developmental toxins to which breastfed infants are exposed in doses far exceeding established safe levels, and at far higher levels than formula-fed infants. (see above, including mercury earlier)
Effects of the above toxins:
PCBs: A large team of German scientists and doctors, studying 171 healthy mother-infant pairs, found "negative associations between (human) milk PCB and mental/motor development ... at all ages, becoming significant from 30 months onwards." Also, "negative associations with PCB increased with age." They found no significant association of the children’s neurological development with PCB levels in umbilical cord blood, whereas they did find association with breast milk PCB concentrations and duration.41 For results of many other studies showing associations of postnatal PCB exposure with adverse neurological effects, including three other studies that at the same time found no effects of prenatal exposures to PCBs, see “PCBs” in Appendix A of www.breastfeeding-research.info/postnatal-effects.htm.
Dioxins: A study by an international research team found that learning disability and attention deficit disorder (which overlap with ASD) were 133% and 202% higher among children with higher levels of dioxins -- that is, over two and three times the risk compared with children with lower exposures.42 The elevated levels of dioxins associated with such dramatic increase in risk of neurological disorders were quite common -- found in 27% to 31% of children -- by no means exceptional exposures. The children tested were 12 to 15 years old; that relatively advanced age means that their adverse outcomes were unusually indicative of long-term effects, compared with almost all other studies of effects of developmental toxins. Breastfeeding exposure to dioxin is quite relevant to this age group, given the authoritative determination that accumulated exposure to dioxins would still be twice as high among ten-year-old children breastfed for six or more months compared with non-breastfed ten-year-olds.43 It is reasonable to consider the main determinant of the increased levels of dioxins in the 12-to-15-year-olds (and therefore the place of origin of the toxins’ apparent harmful effects during development) to have been breastfeeding.
For several other studies indicating associations of postnatal dioxin exposure with adverse effects, including two studies that found no effects of prenatal exposures to the same toxins, see the “Dioxins” section of Appendix A at www.breastfeeding-research.info/postnatal-effects.htm.
PBDEs: A Spanish study assessed PBDE levels in mothers and found that gestational exposure had no significant adverse effect on 4-year-olds, but exposure to those same mothers' PBDE levels via breastfeeding did have substantial effects, including an 80% increase in relative risk of attention-deficit problems and a 160% increased relative risk of poor social competence.44 (“Poor social competence” is a way of describing a basic characteristic of people with autism spectrum disorders, or ASD.) Note that this study was carried out in Europe, where PBDE levels have been found to be only one-tenth (or less) as high as in the United States.45 For additional studies finding associations between postnatal PBDE exposure and adverse neurological effects, see the “PBDEs” section of Appendix A at www.breastfeeding-research.info/postnatal-effects.htm.
Correlation between hazardous exposures of infants to developmental toxins and the toxins’ presence in human milk:
The three toxins dealt with in the previous section, combined with mercury as discussed earlier, make a total of four toxins to which infants are exposed in concentrations far exceeding established safe levels. Infants are apparently exposed to all four of those developmental toxins in such high concentrations only via breast milk. Nobody seems to be aware of any other widespread exposures at such hazardous levels by any means other than in breast milk.(see below).
The author of this article has asked Alycia Halladay (Autism Speaks senior director of environmental and clinical sciences) and seven other scientists at that organization if they were aware of any other toxins (besides the above-mentioned four) to which developing brains are widely exposed in concentrations that greatly exceed established safe guidelines; three replies have been received as of several months later, and none have included mention of any other toxins to which developing brains are widely exposed at levels known to exceed established safe guidelines.
So there appears to be an extremely high correlation between hazardous infant exposures to toxins and the lactation process, which mobilizes toxins that have been stored in a mother’s body fat and excretes them to the infant in highly-concentrated form. People who should be knowledgeable about such matters seem to know about no such high exposures except for those that take place via breastfeeding.
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 early-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 toxins30b could be avoided by parents’ reverting to bottle feeding of infants, which was the predominant feeding type in the mid-20th century,31 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.32
-- 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,33 and causes of those epidemics and increases have not been determined.
-- 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, 34 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;35 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.
Comments or questions are invited. At the next link are comments and questions from readers, including a number of doctors. Some of the doctors have been critical but at least four have been in agreement with us, including two with children of their own with health problems and one who says she has delivered thousands of babies; they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications. Also, we have responded to many readers’ questions and comments, including about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option. To read the above, with a link for sending your own comments or questions, go to www.pollutionaction.org/comments.htm If you have criticisms, please be specific about any apparent inaccuracies, rather than merely saying you don’t like what is said here. Note that we don’t feel obligated to present the favorable side of the breastfeeding debate, since that is already very amply (and one-sidedly) presented in many other, widely-distributed publications as well as in person by numerous enthusiastic promoters.
Since many negative considerations about breastfeeding are being pointed out here, we should provide at least the following concerning the major alternative to breast milk: a link to guidance in choosing which infant formula to feed an infant. There is a good section on that in the website of Healthy Child Healthy World, at http://healthychild.org/easy-steps/find-safer-baby-formula. (That organization, in line with widespread opinion, encourages breastfeeding as the preferred feeding method.)
* For information about Pollution Action and the author of this article, please go to www.pollutionaction.org
F) Grandjean and Jensen, Breastfeeding and the Weanling’s Dilemma Am J Public Health. 2004 July; 94(7): 1075. PMCID: PMC1448391 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448391
F1) Regarding dioxins: At www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day." (that is, O.7 pg of TEQ/kg-d) In the EPA’s “Glossary of Health Effects”, RfD is defined: “RfD (oral reference dose): An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure of a chemical to the human population (including sensitive subpopulations) that is likely to be without risk of deleterious noncancer effects during a lifetime.”
The RfD (from above) should be seen in relation to levels of dioxins found in typical human milk (including 242 pg of TEQ/kg-d at initiation of breastfeeding) as stated in: Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber (Senior Scientist at EPA) and Phillips Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH) at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
Considerably more information about high concentrations of environmental toxins in human milk, citing authoritative sources, can be found at www.breastfeeding-toxins.info. Also presented there is information about the far higher exposures to toxins received via breastfeeding as compared with formula feeding.
1) Durkin et al., Advanced Parental Age and the Risk of Autism Spectrum Disorder, Am J Epidemiol. 2008 December 1; 168(11) Table 3’s “Birth order” section, at www.ncbi.nlm.nih.gov/pmc/articles/PMC2638544; this study was referred to in 2009 as the largest of its kind (in “US researchers find link between age, birth order and autism,” theguardian.com, 7 January 2009); it studied a birth cohort of over 250,000. Durkin et al. also referred to two other studies that supported the correlation of increased autism with earlier birth order:
-- Glasson et al. Perinatal factors and the development of autism. Arch Gen Psychiatry. 2004;61(6):618–627.) and
-- Croen et al., Maternal and paternal age and risk of autism spectrum disorder. Arch Pediatr Adolesc Med. 2007;161(4):334–340.
-- A later meta-analysis (Gardener et al., 2011 at http://pediatrics.aappublications.org/content/early/2011/07/06/peds.2010-1036) found similar results but with the decline in autism risk starting after the second child.
-- Another later study, based on data from a very large population (5750 with ASD or intellectual disability out of 398,000 children in Western Australia) also found that “the odds for ASD with and without ID were reduced for those second or later born.” Of particular interest, the study also found that, in contrast with the ASD correlation, “the odds for children with mild-moderate and severe ID (intellectual disability) were increased for later born children.” (Leonard et al., Autism and Intellectual Disability Are Differentially Related to Sociodemographic Background at Birth, PLoS One. 2011; 6(3): e17875. Published online Mar 30, 2011 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068153) Along similar lines, an early Dutch study (taking data from periods before ASD became significant), based on records of 200,000 children, found that risk of low-level school failure became greater with later birth order. (Belmont et al., Birth order, family size and school failure, Dev Med Child Neurol. 1976 Aug;18(4):421-30. at at http://www.ncbi.nlm.nih.gov/pubmed/955306) The latter two findings, both based on studies of large populations, contradict the idea that the lower rate of ASD among later-born children might merely be a normal tendency, resulting from something such as parents’ curtailing subsequent births after a child turned out to be impaired. There is a well-established greater risk for neurological impairment with older parental age, and that effect prevails in the case of general intellectual disability. The greater risk with greater parental age is also found in the case of ASD, but an inverse relationship between later birth order and impairment risk stands out only in the case of ASD; the latter could be logically explained on the basis of ASD being caused by environmental toxins, exposures to which are reduced for later-born children. The fact that non-ASD intellectual disability is greater with later birth order may reflect the greater likelihood of birth complications after multiple births as well as the greater risk with older parental age; but non-ASD intellectual disability apparently is affected little if any by the declining levels of developmental toxins with later birth order. By contrast, however, there is good reason to see that ASD apparently is affected by postnatal exposures to toxins (which decline with later birth order 2a, 2b, 2c).
A very small (39 cases), earlier study (Piven et al., 1993) found that fourth-born children had equal risk with first-borns (after decline in risk for second and third children); aside from the large chance of this being merely random occurrence in such a small study, it could also reflect greater risk of birth complications with later births, as well as the known increase in ASD and intellectual disability with increasing parental age.
Note that what is discussed here is risk related to birth order in general, not birth order in “multiplex” families (families with multiple children with ASD).
2a) (Likelihood of being breastfed, by birth order): Ryan et al., Program for Women, Infants, and Children Participants, 1978 -2003: Lower Breastfeeding Rates Persist … in journal Pediatrics, at http://pediatrics.aappublications.org/content/117/4/1136.full.pdf+html , Table 2, “Parity” section.
2b) (Duration of breastfeeding, by birth order): CDC chart at www.cdc.gov/breastfeeding/data/NIS_data/2006/socio-demographic.htm
2c) (Concentrations of toxins in breast milk, by birth order): Jiyeon Yang et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants, Chemosphere 46 (2002) 419–428); also Judy S. LaKind, et al., Infant Exposure to Chemicals in Breast Milk in the United States: Children's Health Review Environmental Health Perspectives • Volume 109 | Number 1 | January 2001, p. 81, referring to an average 20-30% decline in dioxins from first to second child, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1242055/pdf/ehp0109-000075.pdf Also Thompson et al., Multiple environmental chemical exposures to lead, mercury and polychlorinated biphenyls among childbearing-aged women (NHANES 1999–2004): Body burden and risk factors, Environ Res. Author manuscript; available in PMC Feb 21, 2013. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578119/
2d) LaKind, et al., Infant Exposure to Chemicals in Breast Milk in the United States: Children's Health Review Environmental Health Perspectives • Volume 109 | Number 1 | January 2001, p. 81, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1242055/pdf/ehp0109-000075.pdf
3) 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 http://researchbank.swinburne.edu.au/vital/access/manager/Repository/swin:9302 Also see reference 13 below. Also see 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, www.ncbi.nlm.nih.gov/pubmed/20628441.
-- Also 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 www.ncbi.nlm.nih.gov/pubmed/17237965
--- See also reference 17 below.
4a) Rice and Barrone, Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models, EPA National Center for Environmental Assessment, 2000,at www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807
5) Gascon M et al., Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of age. Environ Int. 2011 Apr;37(3):605-11. doi: 10.1016/j.envint.2010.12.005. Epub 2011 Jan 14 found at www.ncbi.nlm.nih.gov/pubmed/21237513)
6) Re: PBDE levels in breastfed vs formula-fed children: Near end of Section 5.6.2 ("Impacts to Infants from Consumption of Breast Milk"), p. 5-79, of An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R-08/086F. online at http://www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
Re PBDEs in breast milk, 1,056 pg/g wet weight: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520, 4th paragraph from end, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425 and
PBDEs in infant formula, 32 and 25 pg/g wwt: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment; EPA/600/R-08/086F. online at www.epa.gov/ncea or directly at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
6a) S Patandin et al., Effects Of Environmental Exposure To Polychlorinated Biphenyls And Dioxins On Growth And Development In Young Children: A Prospective Follow-Up Study Of Breast-Fed And Formula-Fed Infants From Birth Until 42 Months of Age Section 7.5 at http://www.sciencedirect.com/science/article/pii/S0022347699703690 or (free, as of 4/14) at repub.eur.nl/pub/19721/990106_PATANDIN,%20Svati.pdf
6b) Banaschewski et al., Autism and ADHD across the life span. Differential diagnoses or comorbidity? Nervenarzt. 2011 May;82(5):573-80. doi: 10.1007/s00115-010-3239-6. [Article in German] at www.ncbi.nlm.nih.gov/pubmed/21484168
7) Surgeon General's Call to Action to Support Breastfeeding, 2011," at www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf
8) Sec. II.B of Brominated Flame Retardants, Third annual report to the Maine Legislature, 2007, D Rice et al. www.maine.gov/dep/waste/publications/legislativereports/documents/finalrptjan07.pdf, citing Li et al., 2005a
-- Table 3 of Developmental Neurotoxicity of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Costa et al., Neurotoxicology. 2007 November; 28(6): NIHMS34875 at www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052
-- Schecter A et al., Polybrominated diphenyl ethers (PBDEs) in U.S. mothers' milk. Environ Health Perspect. 2003 Nov;111(14):1723-9 www.ncbi.nlm.nih.gov/pubmed/14594622
9) Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14 Paul Whiteley (Faculty of Applied Sciences, University of Sunderland, UK), et al. Autism Insights 2009:1 3-17 at http://www.la-press.com/redirect_file.php?fileId=2425&filename=1725-AUI-Trends-in-Developmental,-Behavioral-and-Somatic-Factors-by-Diagnostic-.pdf&fileType=pdf Whitely et al. looked at a comparison figure of 54%, but that figure was unrealistically high, since it came from a study (Pontin et al.) of breastfeeding by mothers largely from “more affluent families”, who breastfeed at unusually high rates in the U.K. For breastfeeding prevalence data that would apply to the general U.K. population, the authors of the Pontin study referred the reader to Infant Feeding 1995 (Foster et al.); examination of the data in that book reveals that a figure in the upper 20’s of percents would apply at just after four weeks, compared with 65% of children with ASD who had been exclusively breastfed for that length of time, as found in the Whitely study.
9a) Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (2011) 41:891–902 DOI 10.1007/s10803-010-1114-8, Table 6, at http://autism.medicine.dal.ca/research/documents/2011DoddsetalJAutDevDisord.pdf
10) Breastfeeding and Autism P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot, found at https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html) This study found that 37% of children with autism had been breastfed for at least 6 months, as compared with 13% in the comparison group.
10a) Taylor et al., Prevalence and incidence rates of autism in the UK: time trend from 2004–2010 in children aged 8 years, BMJ Open. 2013; 3(10): e003219. Published online 2013 October 3. doi: 10.1136/bmjopen-2013-003219 PMCID: PMC3808754 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3808754
11) Infant Feeding Survey 2010: Summary, IFF Research, Univ. of Dundee, on behalf of Health and Social Care Information Centre. found at catalogue.ic.nhs.uk/publications/public-health/surveys/infant-feed-surv-2010/ifs-uk-2010-sum.pdf , Ch. 2, p.13. Stable autism prevalence was recorded for U.K. 8-year-olds for the years 2004-2010; breastfeeding data that would apply to the years of the infancies of those 8-year-olds should ideally cover the years 1996 to 2002. The closest years for which that data is available for the U.K. are 1995 to 2000. According to the UK's National Health Service (see footnote just above), breastfeeding prevalence past initial breastfeeding in the hospital did not increase between 1995 and 2000. After those years of stable breastfeeding, the first data point at which an increase is shown is 2005.
11a) Oct. 16, 2013 report of Autism Speaks,at http://www.autismspeaks.org/science/science-news/study-finds-autism-prevalence-has-leveled-united-kingdom
11b) U.S. CDC: Breastfeeding Among U.S. Children Born 2000–2010,CDC National Immunization Survey
at http://www.cdc.gov/breastfeeding/data/nis_data/index.htm That page shows a 72% increase in breastfeeding at 12 months between 2000 and 2010.
12) Autism rates associated with nutrition and the WIC program. Shamberger R.J., Phd, FACN, King James Medical Laboratory, Cleveland, OH J Am Coll Nutr. 2011 Oct;30(5):348-53. Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621
13) Roberts et al., "Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants," (Environ Health Perspect; DOI:10.1289/ehp.1206187 online at http://ehp.niehs.nih.gov/1206187)
14) Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 11: 709–715, 2011 ISSN: 1680-8584 print / 2071-1409 online doi: 10.4209/aaqr.2011.05.0058 at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf
14a) Jones et al., Attention to eyes is present but in decline in 2-6-month-old infants later diagnosed with autism : Nature:(2013) DOI:doi:10.1038/nature12715 at http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12715.html
14b) Rossignol et al., Environmental toxicants and autism spectrum disorders: a systematic review, Transl Psychiatry. Feb 2014; 4(2): e360. Published online Feb 11, 2014. PMCID: PMC3944636 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3944636
15) Infant Exposure to Dioxin-like Compounds in Breast Milk, Lorber (Senior Scientist at EPA) et al., Vol. 110 No. 6 June 2002, Environmental Health Perspectives at www.ncbi.nlm.nih.gov/pmc/articles/PMC1240886
Re: PBDEs ingested by breastfed infants: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425
Re: dioxins in formula less than 1% of dioxins in breast milk:
- U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
- Compatible figures were found in Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants. Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
Re: PBDEs in formula less than 3% of concentration in breast milk:
-Section 4.7 , 2nd paragraph (citing Schechter et al.) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
For much more information on the subject of early-postnatal vulnerability to developmental toxins, see www.autism-research.net/postnatal-effects.htm .
15a) Surgeon General's Call to Action to Support Breastfeeding, 2011, Figure 1, at http://www.surgeongeneral.gov/library/calls/breastfeeding/calltoactiontosupportbreastfeeding.pdf
15b) typical 8 parts per billion in breast milk, according to U.S. ATSDR document on mercury at http://www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, 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 http://www.who.int/water_sanitation_health/dwq/chemicals/en/mercury.pdf p. 8 Accessed 4/8/2014)
15c) Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber (Senior Scientist at EPA) and Phillips VOLUME 110 | NUMBER 6 | June 2002 • Environmental Health Perspectives (a peer-reviewed journal published by the National Institute of Environmental Health Sciences of NIH) http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
15d) 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 http://www.ncbi.nlm.nih.gov/pubmed/9600805. 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
15e) Marques 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 http://www.ncbi.nlm.nih.gov/pubmed/17237965
15f) 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 http://www.detoxmetals.com/content/FISH/FISH/Hg%20in%20pregnant%20urine%20and%20cord.pdf
15g) 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 http://aje.oxfordjournals.org/content/150/3/301.full.pdf
16) Jensen, A.A. et al, Chemical Contaminants in Human Milk, CRC Press, Inc., Boca Raton, Ann Arbor, Boston, 1991, p 15. This is fully compatible with the statement by two other experts, as follows: “Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs, accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.” (Grandjean P, Landrigan PJ., Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at
For more on toxins in human milk, including comparisons with levels of toxins in infant formula, see www.breastfeeding-toxins.info.
16a) Weiss et al., Silent Latency Periods in Methylmercury Poisoning and in Neurodegenerative Disease, Environmental Health Perspectives • Volume 110 | Supplement 5 | October 2002 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241259/pdf/ehp110s-000851.pdf
17) 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 126.96.36.199, at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF 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)
See also Section 188.8.131.52 of International Programme On Chemical Safety, Environmental Health Criteria 101: Methylmercury (a publication of WHO, Geneva, 1990) at http://www.inchem.org/documents/ehc/ehc/ehc101.htm#subsectionnumber:9.1.2
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 http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf
17a1) (From a web page of Medical News Today, at http://www.medicalnewstoday.com/articles/162368.php)
17b) Ozonoff et al., The Onset of Autism: Patterns of Symptom Emergence in the First Years of Life, Published in final edited form as: Autism Res. Dec 2008; 1(6): 320–328. Author manuscript at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857525
17b2) CDC Biomonitoring Summary for Mercury at http://www.cdc.gov/biomonitoring/Mercury_BiomonitoringSummary.html
17b3) (NIH Autism Fact Sheet , at http://www.ninds.nih.gov/disorders/autism/detail_autism.htm#243523082
17b4) (D.T. Wigle, MD, PhD, MPH: Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 103,106, typically available through Ebsco Host at local libraries) Note that the studies referred to by the author normally based their observations of effects of “prenatal” exposures on umbilical cord blood levels of mercury, or both cord blood and maternal hair mercury levels, all of which would be good indicators of levels in breast milk.
17b5) A.M. Tharpe, Auditory Characteristics of Children with Autism, Lippincott Williams and Wilkins, 2006, at http://www.mc.vanderbilt.edu/root/pdfs/pedauditory/auditory_characteristics_autism.pdf
17b6) International Programme On Chemical Safety, Environmental Health Criteria 101: Methylmercury (a publication of WHO, Geneva, 1990) at http://www.inchem.org/documents/ehc/ehc/ehc101.htm Sections 9.1 and 9.42.
17c) Shattuck et al., The Timing of Identification among Children with an Autism Spectrum Disorder: Findings from a Population-Based Surveillance Study, J Am Acad Child Adolesc Psychiatry. Author manuscript at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188985
Also World Health Organization (WHO), U.N. Environment Programme, "Guidance for Identifying Populations at Risk form Mercury Exposure" August 2008 at http://www.who.int/foodsafety/publications/chem/mercuryexposure.pdf?ua=1, 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.
17c5) p. 5-18 in Mercury Study Report to Congress, Vol. VII, EPA-452/R-97-009
December 1997, at http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf
17c6) Pesticides in the Diets of Infants and Children, Commission on Life Sciences, National Research Council, National Academy Press, Washington, D.C. 1993, p. 25 at http://www.nap.edu/openbook.php?record_id=2126&page=43
17d) Mercury levels in studies of humans are normally not speciated, but they are mainly methylmercury, an organic form; among U.S. women with mercury concentrations in the highest 10% of those tested in the 1999-2000 NHANES survey, 92% of the mercury in their blood was methylmercury. (Mahaffey et al., Blood Organic Mercury and Dietary Mercury Intake: National Health and Nutrition Examination Survey, 1999 and 2000, top lines ofTables 2 and 4, at www.ncbi.nlm.nih.gov/pmc/articles/PMC1241922/pdf/ehp0112-000562.pdf)
17f) Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors, Autism Res Treat. 2013; 2013: 731935 PMCID: PMC3787615 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3787615
17g) 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 184.108.40.206, at www.epa.gov/raf/publications/pdfs/PPKFINAL.PDF
17h) Re: Mercury levels in breast milk:
- U.S. Agency for Toxic Substances and Disease Registry (ATSDR) document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443
- Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?fr=165.110
Concerning dioxin levels in human milk in the U.S. at initiation: Lorber (Senior Scientist at EPA) and Phillips, Infant Exposure to Dioxin-like Compounds in Breast Milk, Volume 110 | Number 6 | June 2002 • Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download
For more information about toxins in human milk, including comparisons with levels in infant formula or cows’ milk, see www.breastfeeding-toxins.info.
17k) The U.S. ATSDR, based on information from various countries of the world, estimated that the mean concentration of mercury in breast milk of non-exposed women is 8 ppb (parts per billion) .(U.S. ATSDR document on mercury at http://www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443) Notice that the above figure applied to people 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 many people working with art supplies, some who work in dental offices, recycling facilities or laboratories, 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. (See Appendix of www.breastfeeding-toxins.info))
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).(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 http://www.tandfonline.com/doi/full/10.1080/19393210.2012.658087#tabModule)
17m) The University of Chicago Hospitals web page for Ataxia at http://www.uchospitals.edu/online-library/content=P08765
17n) Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors, Autism Res Treat. 2013; 2013: 731935 PMCID: PMC3787615 at www.ncbi.nlm.nih.gov/pmc/articles/PMC3787615
17p) 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 http://researchbank.swinburne.edu.au/vital/access/manager/Repository/swin:9302
Also Adams JB et al., Biol Trace Elem Res. 2013 Feb;151(2):171-80. doi: 10.1007/s12011-012-9551-1. Epub 2012 Nov 29.Toxicological status of children with autism vs. neurotypical children and the association with autism severity. at http://www.ncbi.nlm.nih.gov/pubmed/23192845
Also 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, http://www.ncbi.nlm.nih.gov/pubmed/20628441
17q) UN Environmental Programme: Chemicals: Mercury Programme, Global Mercury Assessment, Chapter 3 Toxicology at http://www.chem.unep.ch/mercury/Report/Chapter3.htm
17s) M. Harada, Minamata Disease: Methylmercury Poisoning in Japan Caused by Environmental Pollution, CRC Press, 1995, Sec. V.A. http://meghanbabin.com/school/Reading/Sept%2027%20week%203/Minamata%20Disease_Japan_Environment_Pollution.pdf
17u) Damstra, Environmental Chemicals and Nervous System Dysfunction, The Yale Journal of Biology and Medicine 51 (1978), 457-468 at www.ncbi.nlm.nih.gov/pmc/articles/PMC2595611/pdf/yjbm00133-0026.pdf
17u1) Statement by Dr. Margaret Souders as reported in an Autism Speaks blog, “Sleep, Glorious Sleep (or lack thereof!)” Posted: 03 Jun 2014 08:26 AM PDT; also see Autism Speaks blog at http://feeds.feedburner.com/AutismSpeaksBlog and Katz et al., Solving Sleep Problems in Children with Autism Spectrum Disorders
17v) NIH web page at http://www.ninds.nih.gov/disorders/paresthesia/paresthesia.htm
17w) D.T. Wigle, MD, PhD, MPH: Child Health and the Environment, Oxford University Press, 2003, Ch. 5.
17x) Ekino et al., Minamata disease revisited: An update on the acute and chronic manifestations of methyl mercury poisoning, Journal of the Neurological Sciences 262 (2007) 131–144at http://www.institute-of-mental-health.jp/thesis/pdf/thesis-02/thesis-02-18.pdf WebMD lists “jumpiness or easily startled” as symptomatic of both ASD and autism, at http://symptomchecker.webmd.com/multiple-symptoms?symptoms=jumpiness-or-easily-startled|loss-of-coordination&symptomids=441|278&locations=66|66
18) 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 http://www.ncbi.nlm.nih.gov/pubmed/21259267 Also, The National Academies Press, Toxicological Effects of Methylmercury (2000) at www.nap.edu/openbook.php?record_id=9899&page=4 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)
19) 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 www.ncbi.nlm.nih.gov/pmc/articles/PMC2954077
20) Studies with similar findings from other countries can be found by doing a search with the phrase “maternal methylmercury effects on children,” at www.pubmed.gov.
21) p. 313 of The National Academies Press, Toxicological Effects of Methylmercury (2000) at www.nap.edu/openbook.php?record_id=9899&page=4 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)
21b) p. 299 of The National Academies Press, Toxicological Effects of Methylmercury (2000) at of The National Academies Press, Toxicological Effects of Methylmercury (2000) at http://www.nap.edu/openbook.php?record_id=9899&page=299
21c) Statement by Dr. D.C. Rice before U.S. Senate Committee on Environment & Public Works, 07/29/2003 at http://www.epw.senate.gov/hearing_statements.cfm?id=212850
22) The following is only the latest of at least two major studies based on this island population that have failed to find adverse neurological effects of relatively high levels of maternal mercury from seafood consumption: 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/j.ntt.2013.06.003. Epub 2013 Jun 14. at http://www.ncbi.nlm.nih.gov/pubmed/23770126
24) 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 http://www.epa.gov/ttn/oarpg/t3/reports/volume7.pdf
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 www.ncbi.nlm.nih.gov/pubmed/12216063 or full text at http://www.nchh.org/Portals/0/Contents/Article0201.pdf
25) 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 www.ncbi.nlm.nih.gov/pmc/articles/PMC1637807 “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.”
Hygiene and Public Health at http://aje.oxfordjournals.org/content/150/3/301.full.pdf : “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 http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf, Section 1.6
26) 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 http://www.ncbi.nlm.nih.gov/pubmed/24461425)
-- 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 http://www.ncbi.nlm.nih.gov/pubmed/15734276/)
-- 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 http://www.uni-kiel.de/medinfo/material/seminar_ws0809/Artikel%20Statistische%20Modelle%20WS%202008_09.pdf)
-- 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 http://link.springer.com/article/10.1007/s11064-006-9051-9)
-- 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 http://www.ncbi.nlm.nih.gov/pubmed/19909946)
-- 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 www.fasebj.org/content/17/6/699.full.pdf)
-- 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 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC165591
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 http://www.ncbi.nlm.nih.gov/pubmed/12900074
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 http://www.ncbi.nlm.nih.gov/pubmed/12197271
27) It should be apparent from this 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 http://data.euro.who.int/hfadb)
28) 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 www.ncbi.nlm.nih.gov/pmc/articles/PMC1637830/pdf/envhper00312-0050.pdf
28a) The WHO authors provide a major discussion on a topic that they say is about effects on “developing tissues” (that is their only category other than effects on adult tissues), but their heading for that section is “Prenatal Exposure.” (International Programme On Chemical Safety, Environmental Health Criteria 101: Methylmercury (a publication of WHO, Geneva, 1990) at http://www.inchem.org/documents/ehc/ehc/ehc101.htm#subsectionnumber:9.1.2 Sections 9.1 and 9.42.)
29) Report on the Situation of Infant and Young Child Feeding in Seychelles, August 2011, IBFAN, The Committee on the Rights of the Child www.ibfan.org/art/IBFAN_CRC58%20-2011_Seychelles.pdf 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 www.cdc.gov/breastfeeding/pdf/2008BreastfeedingReportCard.pdf, 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 mailto:firstname.lastname@example.org. See also footnote 30c, below.
29a) 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 http://www.nature.com/jes/journal/v15/n5/full/7500420a.html, showing a 92% breastfeeding rate for the Faroes.
29b) 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 http://www.ncbi.nlm.nih.gov/pubmed/7566772, showing a 94% exclusive breastfeeding rate at birth in a study published in 1995. Breastfeeding rates as of 2012 were higher than in 1995. (http://www.stuff.co.nz/life-style/life/7377846/More-Kiwi-mothers-breastfeeding). 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 http://www.health.govt.nz/system/files/documents/publications/breastfeeding-action-plan.pdf
30) See the “World” breastfeeding rates chart, taken in 2012 from the website of LaLeche League International, now shown at www.breastfeeding-rates.info (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 www.oecd.org/els/social/family/database)
30a) See Section 3.cont. of www.breastfeeding-research.info/postnatal-effects.htm.
30c) The Republic of Seychelles, an island nation off the coast of Kenya, has a population mainly of African origin. (Bovet et al., [Health situation and issues in the Seychelles in 2012]. Med Sante Trop. 2013 Jul-Sep;23(3):256-66. doi: 10.1684/mst.2013.0222, at http://www.ncbi.nlm.nih.gov/pubmed/24103919). There is a relevant quote from “The Breastfeeding Answer Book,” p. 543, referred to by the La Leche League: “Despite the near universality of breastfeeding in Africa, the rate of exclusive breastfeeding is estimated to be 0 to 17 percent.” (at http://www.llli.org/docs/543.pdf) Also relevant is a quote from the web page of a La Leche League Leader in Gabon (Donna M. Nance, in LEAVEN, Vol. 37 No. 1, February-March 2001, p. 19-20 found at http://www.llli.org/llleaderweb/lv/lvfebmar01p19.html), reporting on “the perception (in Gabon and other developing countries) that artificial milks are superior and embraced by the economically advantaged. While mothers who have no economic choice do breastfeed their babies for at least a short while, others who are more economically privileged often do not breastfeed. Or, if they do, the duration of breastfeeding is likely to be very, very short - perhaps only one week or less.” (italics added) Relevant to economic advantage, it is noteworthy that, aside from a few oil-rich countries, Seychelles has the highest per capita income of the entire Africa and Middle East regions (owing to its status as a tourist destination). (U.S. CIA’s World Factbook accessed October, 2014, at https://www.cia.gov/library/publications/the-world-factbook/rankorder/2004rank.html) Also, until recent years, “fostering” of children was reported to be common in Seychelles, in which a woman would give away her first child to the grandmother or an aunt; “this fostering occurred in all classes.” (Countries and Their Cultures: Seychelles, at www.everyculture.com/Sa-Th/Seychelles.html) This practice would probably cause exclusive breastfeeding rates to be even lower than the low level that would be normal for a high-income African country.
31) American Academy of Family Physicians website at www.aafp.org/about/policies/all/breastfeeding-support.html
32) See www.breastfeedingprosandcons.info, where numerous peer-reviewed studies are cited in support of this statement.
33) CDC’s MMWR National Surveillance for Asthma -- United States, 1980-2004, Table 29, at www.cdc.gov/mmwr/preview/mmwrhtml/ss5608a1.htm
Re allergies: CDC’s Health United States 2011, Table 46, p. 3, at www.cdc.gov/nchs/data/hus/hus11.pdf
Type 2 Diabetes in Children and Young Adults: A “New Epidemic” Francine Ratner Kaufman, MD CLINICAL DIABETES • Volume 20, Number 4, 2002 at http://clinical.diabetesjournals.org/content/20/4/217.full.pdf+html
Re ADHD: see www.breastfeeding-and-ADHD.info 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 www.cdc.gov/nchs/data/hp2000/2k97.pdf
Also see www.breastfeeding-health-effects.info, where numerous peer-reviewed studies are cited in support of this statement .
34) See www.breastfeeding-studies.info, where over 50 peer-reviewed studies are cited in support of this statement.
35) http://www.fda.gov/biologicsbloodvaccines/resourcesforyou/consumers/ucm167471.htm 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. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448690/ 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 http://www.nature.com/cr/journal/vaop/ncurrent/full/cr201265a.html
Also, "About Allergies/ Why Are Allergies Increasing?" at http://fooddrugallergy.ucla.edu/body.cfm?id=40
36) Re: EPA’s RfD for dioxin: At www.epa.gov/iris/supdocs/dioxinv1sup.pdf in section 4.3.5, at end of that section, "...the resulting RfD in standard units is 7 × 10−10 mg/kg-day." (that is, 0.7 pg of TEQ/kg-d)
Re: breastfed infants’ exposures to dioxins, in U.S. and internationally:
- Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber (Senior Scientist at EPA) et al., VOL. 110 No. 6 June 2002, Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download, showing typical 242 pg of TEQ/kg-d at initiation of breastfeeding, but declining over months of breastfeeding.
- Wittsiepe J, PCDD/F and dioxin-like PCB in human blood and milk from German mothers. Chemosphere. 2007 Apr;67(9):S286-94. Epub 2007 Jan 10. www.ncbi.nlm.nih.gov/pubmed/17217986
- Focant et al., Levels of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in human milk from different regions of France, Science of The Total Environment, Volumes 452–453, 1 May 2013, Pages 155–162 abstract at http://www.sciencedirect.com/science/article/pii/S0048969713002404
- Yang J, et al., PCDDs, PCDFs, and PCBs concentrations in breast milk from two areas in Korea: body burden of mothers and implications for feeding infants. Chemosphere. 2002 Jan;46(3):419-28. At www.ncbi.nlm.nih.gov/pubmed/11829398
- Bencko V et al., Exposure of breast-fed children in the Czech Republic to PCDDs, PCDFs, and dioxin-like PCBs. Environ Toxicol Pharmacol. 2004 Nov;18(2):83-90. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/21782737/
- Nakatani T, et al., Polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and coplanar polychlorinated biphenyls in human milk in Osaka City, Japan Arch Environ Contam Toxicol. 2005 Jul;49(1):131-40. Epub 2005 Jun 22. Found at http://www.ncbi.nlm.nih.gov/pubmed/15983863
- Deng B, et al., Levels and profiles of PCDD/Fs, PCBs in mothers' milk in Shenzhen of China: estimation of breast-fed infants' intakes.Environ Int. 2012 Jul;42:47-52.. At www.ncbi.nlm.nih.gov/pubmed/21531025
- Chovancová J, et al., PCDD, PCDF, PCB and PBDE concentrations in breast milk of mothers residing in selected areas of Slovakia Chemosphere. 2011 May;83(10):1383-90. doi: 10.1016/j. At www.ncbi.nlm.nih.gov/pubmed/21474162
- J Grigg, Environmental toxins; their impact on children’s health, Arch Dis Child 2004;89:244-250 doi:10.1136/adc.2002.022202 at http://adc.bmj.com/content/89/3/244.full
37) Re: PBDEs ingested by breastfed infants:
-Table 5-4 of EPA (2010) An exposure assessment of polybrominated diphenyl ethers. National Center for Environmental Assessment, Washington, DC; EPA/600/R 08/086F. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404, Schechter study in first page of table, showing 306 ng/kg-d as exposure for breastfed infants.
- Costa et al.,Developmental Neurotoxicity Of Polybrominated Diphenyl Ether (PBDE) Flame Retardants, Neurotoxicology. 2007 November; 28(6): 1047–1067. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118052 Last paragraph of “Relevance to Humans” section, re up to 4.1 micrograms (4100 ng)/kg-day exposure of infants
Regarding prevalence of tetraBDEs, see Costa LG, et al., Polybrominated diphenyl ether (PBDE) flame retardants: environmental contamination, human body burden and potential adverse health effects. Acta Biomed. 2008 Dec;79(3):172-83 at www.ncbi.nlm.nih.gov/pubmed/19260376.
-- RFD for PBDEs: EPA Technical Fact Sheet on Polybrominitated Diphenyl Eithers (PBDEs) and PBBs, p. 4 re RfD of 1 x 10-4 mg/kg/day (100 ng/kg-d) for BDE-47 and BDE 99 at www2.epa.gov/sites/production/files/2014-03/documents/ffrrofactsheet_contaminant_perchlorate_january2014_final_0.pdf
38) U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf This ATSDR report quotes a range of concentrations of PCBs in human milk as from 238 to 271 ng/g lipid weight. 1 g lipid weight = about 25g whole weight (assuming 4% fat in human milk). So the concentrations found in the studies were about 250 ng/25g whole weight, which = 10ng/g whole weight. 1 g (gram) = 1 ml of water., so the 10 ng/g whole weight is the same as 10ng/ml. That is the same as 10,000 ng per liter, which is the same as .01 mg/liter. So the levels of PCBs in human milk seem to be about .01 mg/liter, compared with .0005 mg/liter, the maximum allowed by law in U.S. public water systems. (U.S.EPA, Drinking Water Contaminants, National Primary Drinking Water Regulations, at http://water.epa.gov/drink/contaminants/index.cfm#Organic) That is, about 20 times the concentration that would be allowed in public water systems.
39) Re: dioxins in formula less than 1% of dioxins in breast milk:
- Re dioxins in breast milk, Infant Exposure to Dioxin-like Compounds in Breast Milk Lorber (Senior Scientist at EPA) and Phillips Vol. 110., No. 6 June 2002 • Environmental Health Perspectives at http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download 242 pg at initiation; this should be compared with data from following: U.K. Food Standards Agency Food Survey Information Sheet 49/04 Mar. 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
Compatible figures were found in Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants, Chemosphere 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
- Re dioxins in formula: U.K. Food Standards Agency Food Survey Information Sheet 49/04 MARCH 2004, Dioxins and Dioxin-Like PCBs in Infant Formulae, found at http://www.food.gov.uk/multimedia/pdfs/fsis4904dioxinsinfantformula.pdf
- Compatible figures were found in Weijs PJ, et al., Dioxin and dioxin-like PCB exposure of non-breastfed Dutch infants. Chemosphere. 2006 Aug;64(9):1521-5. Epub 2006 Jan 25 at www.ncbi.nlm.nih.gov/pubmed/16442144
Re: PBDEs in formula about 3% of concentration in breast milk:
- Re PBDEs in breast milk, 1,056 pg/g wet weight: Schecter et al., Polybrominated Diphenyl Ether (PBDE) Levels in an Expanded Market Basket Survey of U.S. Food and Estimated PBDE Dietary Intake by Age and Sex, Environ Health Perspect. Oct 2006; 114(10): 1515–1520, 4th paragraph from end, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1626425 This study was cited in the EPA document below, Section 5.6.2, 2nd paragraph.
- In formula: Section 4.7 , p. 4-77, 2nd paragraph (citing Schechter et al., finding of 25 and 32 pg/g wwt, ) of U.S. EPA (2010) An exposure assessment of polybrominated diphenyl ethers. http:/cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404
Re: Mercury in formula less than 1% as high as in human milk:
Mercury levels in breast milk:
- U.S. ATSDR document on mercury at www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443
Mercury in infant formula:
- 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
Re: PCBs in infant formula typically less than 1% but up to about 4% as high as in human milk:
- In breast milk: About 250 ng/g lipid weight. In soy-based formula: about 10 ng/g lipid weight. U.S. Agency for Toxic Substances and Disease Registry, Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000, pp. 560, 573, at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf Data does not appear to be available for PCBs in cow’s-milk-based infant formula, but data for whole milk could give an approximation, as follows: adding together the figures for the two kinds of PCBs in this study provides a range of 52 to 2455 ng/kg fat, which equals .05 to 2.45 ng/g fat (lipid) (Krokos et al., Levels of selected ortho and non-ortho polychlorinated biphenyls in UK retail milk, Chemosphere. 1996 Feb;32(4):667-73. at www.ncbi.nlm.nih.gov/pubmed/8867147)
40) Quinn et al.,Investigating Intergenerational Differences in Human PCB Exposure due to Variable Emissions and Reproductive Behaviors, Environ Health Perspect. May 2011; 119(5): 641–646. at www.ncbi.nlm.nih.gov/pmc/articles/PMC3094414
40a) Measured Prenatal and Estimated Postnatal Levels of Polychlorinated Biphenyls (PCBs) and ADHD-Related Behaviors in 8-Year-Old Children, Environ Health Perspect; DOI:10.1289/ehp.1408084 , Vol. 123, Issue 9, Sept. 2015, at http://ehp.niehs.nih.gov/1408084
41) Jens Walkowiak et al., Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood. Lancet 2001: 358: 1602-07 Abstract at www.thelancet.com/journals/lancet/article/PIIS0140-6736(01)06654-5/abstract
42) Lee et al., Association of serum concentrations of persistent organic pollutants with the prevalence of learning disability and attention deficit disorder, J Epidemiol Community Health 2007;61:591–596. doi: 10.1136/jech.2006.054700 at http://jech.bmj.com/content/61/7/591.full.pdf+html.
* For information about Pollution Action and the author of this article, please go to www.pollutionaction.org